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Step 1: General Principles

The Step 2 exam will ask to either identify the rhythm or choose Normal Sinus
an intervention. In order to identify the rhythm, follow these S. Tach
simple principles. 1) Determine the rate: tachycardia is > 100,
bradycardia < 60. 2) Determine the QRS complex: wide is > IVF

.12msec and means its a ventricular rhythm while narrow is < Sxs O2
.12msec and means its an atrial rhythm. These two things will Monitor
give you 80% of the answers on the test. The third and final
decision is if the rhythm is regular or irregular. Of course, to
determine any of this an ECG, preferably a 12-lead, is needed. Stable
Any other SYS BP < 90
With the ECG ask if theres an arrhythmia or not. Note that there symptoms CP, SOB
are two, maybe three, rhythms that arent arrhythmias. Normal
Sinus Rhythm is what everyone should be in. Sinus tachycardia Stable Unstable
is typically a normal, physiologic response to an underlying
stressor. Sinus bradycardia may be a normal rhythm in a DRUGS ELECTRICITY
competitive athlete, though they usually do not appear in a Fast + Narrow Adenosine Fast Shock
vignette or in the hospital as an arrhythmia. Fast + Wide Amiodarone Slow - Pace
Slow Atropine
Step 2: Symptoms or No Symptoms
Ask, are there symptoms? An arrhythmia without any
symptoms does not warrant attention. Simply: if there are no RATE CONTROL
symptoms then do nothing. Nothing means routine care: IV, B, CCB
O2, and Monitor. Likely, this will be a question about rhythm
Tachy Rhythms
Step 3: Stable vs Unstable - Sinus Tachycardia
If the patient has symptoms decide whether theres time to stay - Supraventricular Tachycardia
and play or if definitive therapy is needed right now. Stability is Atrial
- Multifocal Atrial Tachycardia
a product of your own comfort. But for a test, if theres chest - Afib Narrow
pain, shortness of breath, altered mental status, or a systolic - Aflutter
BP < 90, then the patient is considered unstable. If theyre - Vtach
unstable use electricity. - Vfib
- Torsades Wide

If instead the patient has symptoms, but not any one of those listed Brady Rhythms
- Sinus Bradycardia
above, the patient is stable. A patient who is stable has time to fix Varying degree
- 1o Block
the rhythm. Theyre not going to die at this moment; - 2o Block of PR intervals
pharmacotherapy can be used. - 3o Block
- Junctional
Step 4: Choose an intervention - Idioventricular
If youve chosen unstable/electricity only one question needs to
be asked - fast of slow. If the rhythm is fast + unstable then
shock. If the rhythm is slow + unstable then pace.

If youve chosen stable/electricity its a slightly more difficult Intervention Heart Rate QRS Complex Stability
task. For stable rhythms, there are three, maybe four, options. 1 - Pacer Brady Any Unstable
If the rhythm is fast + narrow + stable use adenosine. 2 - If the Cardioversion Tachy Any Unstable
rhythms fast + wide + stable use amiodarone. 3 - If the
Atropine Brady Any Stable
rhythms slow + stable use atropine (epi drips can also be used
Adenosine Tachy Narrow Stable
in the new ACLS roll out). 4 - If the rhythms Afib/Aflutter (note
this is the only rhythm that actually had to be identified to do the Amiodarone Tachy Wide Stable
right intervention), rate control is preferred. If they were Rate Control Tachy Afib/Flutter Stable
unstable shock them since afib usually presents as a tachycardia.
By rate control we mean Beta Blockers or Calcium Channel Rate Control = Verapamil / Diltiazem, Metoprolol

Cardiology [MORE ON RHYTHMS]

Supraventricular tachycardia is an aberrant reentry that

bypasses the SA node. Its narrow (atrial), fast (tachycardia), and Fast Heart Rate
will be distinguished from a sinus tachycardia by a resting heart
rate > 150 + the loss of p-waves (can you tell p-waves from t- EKG
waves?). It responds to adenosine. Narrow QRS Wide QRS

SVT AFib Torsades Vtach

Ventricular Tachycardia is a wide complex and regular Adenosine x3 Rate Control Magnesium Amio
Rate Control (CCB, B) (Amio) (Lido)
tachycardia. Look for the tombstones. Since its ventricular
there are no paves at all - just the QRS complexes. It responds to
amiodarone (newer/better) or lidocaine (older/cheaper)

New or SHOCK
Recent Afib
Atrial Fibrillation can be identified by a narrow complex
tachycardia with a chaotic background, absent p-waves, and an Stable
irregularly irregular R-R interval. It has a special treatment
algorithm. In the acute setting (ACLS in a nutshell) simply decide Rate Consider
Control Cardioversion
between shock and rate control. Rate control is just as good as
rhythm control (cardioversion). But, you have to weigh risks and CCB
benefits in each patient. If the goal is rhythm control Timing
(cardioversion) its necessary to determine how long the Afibs <48 hrs >48 hrs
been present. Simply cardioverting an Afib thats lasted > 48 hrs
runs the risk of throwing an embolism (and a stroke). If < 48hours Cardiovert TTE TEE
cardioversion is ok. But if its been present > 48 hours the patient
needs to go on warfarin for four weeks. At the end of four weeks,
the TEE is done. If no clot is found, cardioversion is done and the . Cardiovert Warfarin
patient remains on warfarin for another 4 weeks. If you decide to Amio or Shock x 3 weeks
do rate control (beta blockers and calcium channel blockers)
anticoagulation may still be needed. Decide this using the
CHADS2 score. The higher the score the higher the risk of
embolism and the more likely the patient is to benefit from
warfarin (2+ CHADS2). Now, the Xa- or Thrombin-inhibitors
can be used instead (1+ CHADS2). Examples include apixiban
or dabigatran.
Slow Heart Rate


Sinus bradycardia is simply a slow normal sinus rhythm. The

blocks are a worsening of that normal bradycardia. Almost
everything responds to Atropine until it gets really bad - then
only pacing will do.
Sinus 1o Block 2o Block 2o Block 3o Block Idio-
Brady Type I Type II ventricular
Atropine Atropine Atropine Pace
o Pace Pace Pace Pace Pace Pace
1 AV Block is characterized by a regularly prolonged PR
Nothing Nothing Nothing Pace Pace Nothing
interval. Theres no change in the interval between beats, but
each is prolonged. There are no dropped beats.

Cardiology [MORE ON RHYTHMS]

2o AV Block Type I is a normal rhythm with a constantly

prolonging PR interval with each beat, until a QRS complex is
finally dropped. The signal comes from the atria so there is a
narrow QRS complex.

2o AV Block Type II has a normal PR interval but simply drops

QRSs randomly. The signal comes from the atria so the QRS
complexes are narrow. This is the most severe a rhythm can be
before atropine no longer works.

30 AV Block. Theres total AV node dissociation. The Ps march

out (regular interval between P waves) and the QRSs march out
(regular interval between QRS complexes). At times, the P waves
may seem lost or dropped; the QRS complex occurs at the same
time and obscures the p wave. Because the impulse comes from
the ventricles its a wide QRS complex. In general, avoid
atropine (just pace). This is controversial.

Idioventricular Rhythm is a rhythm without atrial activity. Only

the ventricles are contracting, only the ventricles have electrical
activity. It looks like a 3o block, but without p waves. Avoid
atropine (it wont work), as there is no atrial conduction at all, so
just pace.

This is not every rhythm you could see, but its way more than
you need to be prepared for the USMLE. Youll see a rhythm,
MAYBE two on the test. MAYBE.


When dead, remember 1 thing: compressions. Everything is based 2 minutes of CPR 2 minutes of CPR
around 2 minutes of CPR. 2 minutes of CPR, check a pulse, check
a rhythm, shock if indicated. Shock is indicated only in VT/VF Epinephrine Amiodarone Epinephrine Amiodarone
Vtach/Vifb arrest. Always start with Epi. Only in VT/VF can you
shock, and so too only in VT/VF can antiarrhythmics be used.
Thats it. This is almost never tested on Step 2 but is here for PEA/
Epinephrine Atropine Epinephrine Atropine
completeness. Asystole


There are three very distinct mechanical diseases of the heart.
Anything that causes the heart to not work right (cardio = heart,
myo = muscle, pathy = bad or broken) is a cardiomyopathy.
Whether its Afib, MI, infection, toxins, autoimmune disease -
it doesnt matter. Its the hearts response to these stressors that
defines the cardiomyopathy. Thats our discussion.

1) Dilated Cardiomyopathy
The heart works by overlying actin and myosin filaments. If they
start too close together theres nowhere for them to contract.
Conversely, if they start too far apart theres no overlap to
generate contraction. When the heart dilates the wall gets
stretched out (so its thin) and has a decreased contractility
(producing a systolic heart failure). The heart becomes a bag of
blood rather than a pump. The etiologies are vast: ischemia, valve
disease, idiopathic, infectious, metabolic, alcoholic,
autoimmune, etc. The point is that diagnosis and management
Thin walls, weak contraction
are the same, regardless of the etiologies. A Chest X-ray will
show an enlarged heart, while Echo will show the dilated
ventricle. The patient will present with heart failure symptoms
and gets heart failure treatment. Getting the underlying etiology
is an academic exercise and beyond the scope of this course.

2) Hypertrophic Cardiomyopathy (HCM)

An autosomal dominant mutation of myocyte sarcomeres, this
causes an asymmetric hypertrophy of the septal wall. Since it
occludes the aortic outlet it presents just like an aortic stenosis
except that its heard at the apex and improves with increased
preload. Why? Because increased preload causes the ventricular
chamber to fill, pushing the septum away from aortic outlet and
letting blood flow. This is the opposite of aortic stenosis. Also, The hypertrophied septum, By increasing preload the
HCM is found in young people while AS is found in the elderly. growing from the normal chamber fills, pushing the
Symptoms may be SOB (most common), angina, or what people septum overrides the aortic septum away from the aortic
know it for: sudden death in athletes. Treat this by avoiding opening opening
dehydration and with -Blockers to allow an increase in
ventricular filling.

3) Restrictive Cardiomyopathy
Heart muscle should be able to contract and relax. Dilated
cardiomyopathy has trouble with contractility - getting the blood
OUT (systolic failure). Restrictive cardiomyopathy has trouble
relaxing - getting blood in (diastolic failure). It cant relax to
accept blood because theres junk in the way. Its caused by
Sarcoid, amyloid, hemochromatosis, cancer, and fibrosis as
well as other causes that are really rare. Treatment is tricky its
necessary to maintain an adequate preload while not overloading All the junk in the myocardium
the pulmonary vasculature. Gentle diuresis and heart rate wont let the heart relax / fill
control are essential. Transplant in refractory cases.


Cholesterol is needed for cells to exist. The problem is that too
much cholesterol leads to the development of plaques, the things
that cause atherosclerosis. There is bad cholesterol (LDL) that is
responsible for bringing the cholesterol to the periphery. Too
much of it makes plaques form. The good cholesterol (HDL)
clears those plaques and brings the cholesterol back to the liver
for processing. It makes sense that wed want to decrease the LDL
and increase the HDL. Turns out thats not true. The goal is to get
people on a statin.

Why Statins
Although controversial, the most recent lipid guidelines have said
that targeting a specific number did not improve outcomes. What
improved outcomes (stroke, heart attack, and death) was to be on
a high-intensity statin. Its empiric.

Who Gets a Statin When it is an option, the right answer is always:

There are four groups of people who should be on a high- 1. Lifestyle = Diet / Exercise
intensity statin (atorvastatin or rosuvastatin). 1 Anyone with any 2. Adherence = Medication and Lifestyle
vascular disease (stroke, coronary artery disease, peripheral
vascular disease, or carotid stenosis) or 2 LDL > 190. If a patient Who Needs a Statin?
has vascular disease or an LDL > 190, regardless of anything else, 1. Vascular Disease = MI, CVA, PVD, CS
theyre on a statin. It gets a bit trickier when one of these two 2. LDL > 190
criteria isnt present. 3. LDL 70-189
+ Age
If the patient has an LDL < 70 they do NOT need a statin. + Diabetes
Vascular disease and LDL > 190 trump this statement, though the 4. LDL 70-189
intensity will likely be decreased. + Age
+ Calculated Risk = Risk Factors
So groups 3 Diabetes and 4Calculated risk go something like this.
If the patient has an LDL 70-189 AND are Age 40-75 AND are Risk Factors for Coronary Artery Disease
either a diabetic or have a 10-year calculated risk, they get a statin. 1. Diabetes
That 10-year calculated risk thing just means do you have 2 or 2. Smoking
more vascular risk factors but in a more convoluted way you 3. Hypertension
shouldnt memorize. 4. Dyslipidemia
5. Age > 55 for women, > 45 for men
What Statin Should You Give?
The goal is to be on high-intensity statin. Start a moderate-
intensity and increase the dose to high-intensity.

If theres liver disease or renal disease, start at and stay on a High-Intensity Moderate-Intensity Low-Intensity
moderate-intensity statin. Atorva 40, 80 Atorva 10, 20 ---------------
Rosuva 20, 40 Rosuva 5, 10 ---------------
If there are signs of statin-toxicity during treatment, stop the --------------- Simvastatin 20,40 Simvastatin 5, 10
statin until the signs go away. Then restart the statin at a lower --------------- Pravastatin 40, 80 Pravastatin 10,20
dose. Anaphylaxis would be an exception, though the incidence --------------- Lovastatin 40 Lova 20
is so low it essentially doesnt count.

Evaluation of Statins What and When Monitoring Statin Therapy

Baseline values of Lipids, A1c, CK, and LFTs are required before Baseline Routine Symptoms
starting a statin. You want to know what their baselines are to Lipids q1y --------------
allow comparison if something happens. A1c DM = q3mo --------------
CK -------------- Muscle Sxs
Lipids are assessed annually (NOT q3months). LFTs -------------- Hepatitis
CK and LFTs are NOT checked routinely. Assess them only Statin-Myositis Stop Statin Start a lower dose
when theres evidence of disease. Myositis presents with Statin-Hepatitis Stop Statin Restart at a lower dose
soreness, weakness, or muscle pain. Hepatitis presents with right
upper quadrant abdominal pain or jaundice.


So You Cant Use A Statin
The way the test will go after your knowledge of other lipid
medications (which is still viable test fodder) is by giving a
patient who, for whatever reason, CANT take a statin. Then the
door opens to follow the previous lipid guidelines of reducing the
LDL to < 100 with medications. Of course, lifestyle modifications Drug Effect Mechanism Side Effect
and adherence become paramount, but the test is going to get you Statins LDL TG HMG-CoA Myositis
to answer questions about medications. reductase LFT
Fibrates TC HDL Lipoprotein Myositis
Some highlights: Lipase LFT
Ezetimibe LDL Cholesterol Diarrhea
Fibrates are the second line to statins. They have the same side Absorption
effect profile but are also really good at getting the LDL down Niacin HDL LDL Fatty Acid Release Flushing (treat
and the HDL up. They make sense. LDL Synthesis with ASA)
Bile Acid LDL Bile Acid Diarrhea
Niacin is a board favorite because it causes flushing. While Resins Reabsorption
Niacin has not been shown to have mortality benefit, it makes for
a great test question. Treat the flushing with Aspirin prophylaxis.

Bile Acid resins and Ezetimibe block absorption of fatty-related

stuff. That leads to a fatty stool. Fatty stool causes osmotic


Coronary artery disease is blockage in the heart arteries. Its
caused by chronically progressive atherosclerosis (the plaque)
that obstructs the lumen, decreasing the ability of the arteries to
perfuse the myocardium. This produces ischemia when cardiac Stable Unstable NSTEMI STEMI
demand increases; theres an imbalance in the demand to supply Angina Angina
ratio. For these conditions, both reperfusion (getting rid of the Pain Exercise @ rest @ rest @ rest
plaque) and reducing the workload of the heart will improve Relief Rest +
symptoms. When an acute thrombus forms from endothelial Nitrates
injury the lumen can quickly become occluded, resulting in a
ST s
supply ischemia; no amount of demand reduction will save this Pathology 70% 90% 90% 100%
tissue. Reperfusion is required to prevent myocardial death.
Sxs Assoc Sxs Risk Factors
The spectrum of coronary artery disease begins with stable 1. Substernal Dyspnea Diabetes
angina where the coronary artery disease is known and the patient 2. Exertional N/V Smoking
knows how far they can go before symptoms start. Unstable 3. Relieved with Presyncope HTN
angina is worsening of symptoms with less work, more pain with NTG
the same work, or pain refractory to nitroglycerin. NSTEMI is HLD
still demand ischemia, but theres elevation of the troponins. 3/3 = Typical Family Hx
2/3 = Atypical Age > 45 M
STEMI implies acute thrombosis and transmural infarct.
> 55 F
0-1 =
Risk Factors Nonanginal
CAD is just vascular disease in the heart arteries; the risk factors
are the same for all vascular disease. Diabetes, Smoking,
Hypertension, Dyslipidemia, and Obesity are modifiable risk
factors. Age (M > 45, F > 55) and family history of early Chest Pain
vascular disease are non-modifiable risk factors.
ST Emergently
Patient Presentation
The Diamond classification identifies patients risk of coronary STs
artery disease based on the symptoms. There are three
Biomarkers NSTEMI CATH
components. 1Substernal chest pain, 2 Worse with Exertion, and Troponin
Better with Nitroglycerin. 3/3 is called typical, 2/3 is called
atypical, and 0-1 is called non-anginal. The more positives, the
higher the likelihood that this chest pain is anginal. The classic Cardiac CP?
description is a crushing, retrosternal chest pain that will
radiate down the arm and up the jaw.
Stress Test
Associated symptoms are also useful. The presence of dyspnea, Treat with
nausea/vomiting, or diaphoresis with the onset of the chest pain medications
Stress Tests then
increases the suspicion of myocardial ischemia.
Treadmill ECG
Consequences of the infarct may also be identified. Congestive Pharm Echo Medically
heart failure (pulmonary edema, JVD, poor distal perfusion) and Nuclear
arrhythmia (especially heart blocks and ventricular tachycardia)
can be seen, but are often absent. If the person cant walk for any reason, use pharmacologic
stress (either dobutamine or adenosine)
Rule out the most severe disease (STEMI) first with a 12-Lead If the person has a normal ECG, use ECG
ECG looking for ST-segment elevations or a new LBBB. If the person has an abnormal ECG, use Echo
STEMI goes to emergent cath. If negative rule out NSTEMI with If the person has an abnormal Echo or CABG, use Nuclear
biomarkers (Troponin-I). NSTEMI goes to urgent cath. If both
the troponins and the ECG are negative, youre left considering if
this pain is coronary in nature at all. This can be determined using
the stress test. If the stress test is positive, go to elective cath.


Diagnostic Modalities
1. The stress test Cant Exercise: Peripheral Vascular Disease, Claudication,
Regardless of the mechanism used, its looking for the same vasculitis, diabetic ulcers, SOB at rest, etc.
thing: evidence of ischemia under stress. The goal is to get the
patient to target heart rate (85% of their maximum) and have them Cant Read ECG: Any BBB or old infarct
sustain it. The test is positive if theres chest pain during stress or
the imaging modality is positive. For ECG test, look for ST Dead Things Dont Move
segment changes (T wave inversion or ST segment elevations).
For the Echo, look for dyskinesia (also called akinesis) thats Stress
present on stress but absent at rest (this is at-risk but not dead
tissue). Nuclear stress tests demonstrate perfusion with Thallium.
The reversibility (normal perfusion at rest, compromised with Normal
stress) identifies salvageable tissue. Whenever the stress test is Wall Akinesis Akinesis
positive, the next step is catheterization. Motion

2. Catheterization No Dz Ischemia Infarct

This is the best test for the diagnosis of coronary artery disease.
It assesses the severity of stenosis AND helps rule out
Prinzmetals angina (clean coronary arteries producing Normal Normal
ischemia as a product of vasospasm - treat with CCB). Wall Wall Akinesis
Motion Motion
Acute Treatment
Patients presenting with angina need Aspirin, first and foremost.
Nitrates can be given to alleviate pain, but must be avoided in
At Rest
right-sided infarcts (II, III, AvF). Beta-blockers reduce
myocardial work and prevent ventricular arrhythmias (the thing
that kills patients in the first 24 hours). ACE-inhibitors have long Acute Presentation: MONA-BASH
Morphine Beta-Blocker
term benefits. Statins are the mainstay of therapy for cholesterol.
Oxygen ACE-inhibitor
If its certain this is Acute Coronary Syndrome, therapeutic Nitrates Statin
heparin and clopidogrel load should be used as well. Oxygen Aspirin Heparin
and morphine are used prn.
Treatment When to use it Goals
Chronic Therapy Statins Any ACS LDL < 70 HDL > 40
1. Adjust risk factors -Blockers Any ACS SBP < 140 DBP < 90
a. HDL High potency statin. Old LDL goal < 100. Now, start ACE-i Any ACS SBP < 140 DBP < 90
statin. ASA Any ACS No goal
Clopidogrel ASA allergy or No goal
b. DM tight glucose control to near normal values (80-120 or
HgbA1C < 7%) with oral medications or insulin. stents
c. HTN regular control of blood pressure to <140 / <90 with Angioplasty ST or + Stress; 1 or 2 vessel disease
Beta-Blockers (reduce arrhythmias) and ACE-inhibitors. CABG ST or + Stress; Left-Mainstem or 3 vessel disease
Titrate heart rate to between 50-65 bpm and 75% of the heart tPA ST or + Stress; no PCI available, no transport
rate that produced symptoms on stress test. Heparin ST or + Stress; contraindication to tPA
2. Reduce Risk of Thrombosis
Aspirin (Cox-Inhibitor) is the standard therapy. Clopidogrel Indication Duration
(ADP-inhibitor) can be used, but is indicated for stents only. Drug Eluding Stent Clopidogrel x 12 months
3. Surgical Management Bare Metal Stent Clopidogrel x 1 month
Angioplasty Alone No Clopidogrel
Surgical management choices are Stent or CABG. The decision
is made based on the severity of occlusive disease. If its really
bad (i.e. requires multiple stents) do a CABG. If the
atherosclerosis is global, distal, or microvascular then medical
1,2 Vessel Left Mainstem
management only may suffice. Angioplasty CABG
4. Thrombolytics (PCI) 3 Vessel Disease
Either the administration of tPA (within 12 hours of onset) or
heparin is done only when catheterization is not available AND
Surgery = Left Mainstem OR 3-vessel disease; surgery = CABG
theyre in an acute disease (NSTEMI or STEMI).
Angioplasty = 1,2 Vessel Disease

Cardiology [HEART FAILURE]

Heart failure is enormously complex. There are multiple types,
manifestations, causes, and treatments. You need to consider the
chronic management of a regular heart failure then decide what
to do with an acute exacerbation.

Types of Failure
The first consideration to understand is systolic vs diastolic.
Systolic failure arises when the heart cant push blood forward. It
can go backwards (a leaky heart), be floppy (dilated
cardiomyopathy), or be dead (secondary to myocardial
ischemia). Plain and simple - systolic failure is a broken pump.
The heart fills in diastole, hence, diastolic failure is when the
heart cant fill. If something prevents the heart from relaxing and
accepting blood it produces a diastolic failure. This might be from
hypertrophy or infiltration.

The second consideration is left versus right failure. Left Right failure = backup in Left failure = backup in
Ventricular Failure is a failure to pump blood into the periphery; the veins of the periphery the veins of the lungs
theres a backup of blood into the lungs. Right Ventricular
Failure causes a backup of blood into the venous circulation.
Most of the time its a combination of both.

Pathogenesis and Etiology

The typical chronic failure that occurs insidiously is by far the
most common. Its caused by hypertension. High blood pressure Failure Path Etiology EF
causes an increase in systemic vascular resistance; the heart has Systolic Forward Leaky valves = any regurgitation
to pump harder and harder to push the blood. It gets bigger and Failure failure Dead Heart = Ischemia / infarction
beefier to compensate. But just like any muscle, it putters out and Floppy muscles = EtOH, HTN, Drug
eventually fails. The heart gets bigger, rounder, and eventually Diastolic Filling Pericardium = Pericardial Tamponade
goes floppy. Pathologically, constant overstimulation by Failure failure Constrictive Pericarditis
catecholamines first helps the heart overcome the hypertension. Cardiomyopathy = Restrictive
It eventually leads to neural hormonal remodeling, cardiac Hypertrophic
toxicity, and then fibrosis. Other etiologies are simply a matter
of memorization.
Diastolic CHF (CHF with preserved ejection fraction) is caused Left Ventricular Failure Right Ventricular Failure
by the things that prevent relaxation. Generally, its a Orthopnea, Crackles, Rales Hepatosplenomegaly, JVD
hypertrophic or restrictive cardiomyopathy. Pericardial disease Dyspnea on Exertion, S3, Peripheral Edema,
and deposition disease can do it too. Paroxysmal Nocturnal Dyspnea Dyspnea on Exertion, JVP

S3 and JVD poor prognostic sign in acute exacerbation

Symptoms arise from where the fluid backs up. The classic
patient is the triad of Exertional Dyspnea, Orthopnea, and
Paroxysmal Nocturnal Dyspnea. Exertional dyspnea is
Chronic NYHA Class
shortness of breath limiting walking. Orthopnea is shortness of
I Limited Symptoms
breath thats worse when lying flat. Paroxysmal Nocturnal
II Slight Limitations Comfortable at rest and walking
Dyspnea is when the patient wakes up in the middle of the night III Moderate Limitations Comfortable at rest only
gasping for breath. Because most patients have left and right IV Totally Limited Bed bound, sxs @ rest
failure together, rales (fluid on the lungs) may get mixed with
peripheral edema and hepatomegaly. Symptoms like an S3 The ACC/AHA has a class A-D, based on the presence of
heart sound and Jugular Venous Distension are signs of acute structural heart disease. Dont use the A-D model, use I-IV
exacerbation. In the chronic setting, its critical to determine what
class they are. Here, we use NYHA, as it directs treatment.

Cardiology [HEART FAILURE]

CHF sxs
When first attempting to diagnose CHF there are two tests that of any kind
should be used. The BNP is useful to say, volume overload or
not. Its a blood test and requires no advanced training to
interpret. The standard test is the 2D echocardiogram, which can Dia dysfxn ECHO
distinguish between systolic failure (ejection fraction <55%) and EF
diastolic failure (preserved ejection fraction). There are more
definitive tests available. A nuclear study calculates the exact Diastolic Systolic
ejection fraction and identifies areas of ischemia (its a stress Dysfunction No heart Dysfunction
test). Left Heart Catheterization (even more definitive of EF failure
and coronary artery disease) can be performed with a right heart
cath to demonstrate elevated pulmonary artery pressures. ECG
(demonstrates old ischemia / arrhythmia), CXR (demonstrates
cardiomegaly or pulmonary edema), and troponins (acute
ischemia) arent inappropriate, but theyre also not necessary.

Treatment with Reasoning

There are two goals: reduce fluid (preload) and reduce afterload.
To reduce fluid, its important to restrict salt intake (< 2g/day of
NaCl) and reduce fluid intake (< 2L H20/day). Everybody gets
this. Once the patient reaches class II, keep the fluid off by using
diuretics like furosemide. At class III, Isosorbide Dinitrate is
Patient Treatment
Afterload reduction is achieved with ACE-inhibitors (also Everybody Salt <2g per day
Angiotensin Receptor Blockers). When CHF gets really bad H2O < 2L per day
ACE-i or ARB (best mortality benefit)
(Class III and greater), add Spironolactone or Hydralazine.
Isosorbide Dinitrate (preload) and Hydralazine (afterload) are Preload Diuretics such as Furosemide
given as a combination medication BiDil. Reduction Nitrates such as Isosorbide Dinitrate
Dietary Modifications (NaCl, H2O)
When the situation is dire (class IV) its time to add inotropes Afterload ACE-i or ARB
like Dobutamine (which is a continuous infusion) while Reduction Hydralazine
preparing for a transplant or ventricular assist device bridging Spironolactone
them to transplant. Ambulatory infusion devices are available.
Special Treatment
EF < 35% AICD (must be Class I-III)
To reduce the risk of sudden cardiac death, Beta-blockers are
Ischemic ASA and Statin
used to reduce arrhythmia and neuro-hormonal remodeling. Other Class IV Inotropes like Dobutamine (ICU)
considerations are the placement of an AICD if the EF < 35% VAD bridge to transplant
and theyre NOT class IV. Digoxin can be used if theres need of Transplant
symptom relief (knowing it wont change mortality).

Acute Exacerbation CHF sxs

The precipitant of a CHF exacerbation (which usually means of any kind
volume overload) can be a product of dietary noncompliance,
medication noncompliance, blood pressure control, ischemia or
arrhythmia. The goal is the same as for chronic management: r/o Acute Ischemia
afterload reduction (aka blood pressure control) and preload
Consider CXR ABG MI
reduction (diuresis and nitrates). Ruling out acute ischemia Another Echo BNP
(which should be treated as an MI) and other causes of dyspnea Troponins CATH
is important. But the person who is overtly overloaded (JVD, Morphine Beta-Block

crackles, peripheral edema) with an elevated BNP needs Oxygen ACE-i
aggressive diuresis with IV Furosemide and blood pressure Nitrates Statin
CHF Aspirin Heparin
control. Never start or increase a Beta-Blocker during an
Lasix (furosemide)


Hypertension, low blood pressure, is defined by a systolic blood
pressure >140 or diastolic blood pressure > 90 mmHg.
Hypertension itself is a silent disease; the patient doesnt feel it.
But its a risk factor for atherosclerotic diseases: peripheral
vascular disease, stroke, heart attack. The goal is to modify this
risk factor, to gain control of the disease, and to prevent
development of heart disease.

Diagnosis Stage SYS DIA Initial Tx

Hypertension is diagnosed with two separate blood pressures Normal 120 80 Lifestyle and Diet
taken at two separate office visits with the systolic or diastolic Pre-HTN Lifestyle and Diet
blood pressure being elevated. The best form of diagnosis is Stage I 140 90 Thiazide > ACE > CCB
ambulatory blood pressure monitoring, though since the vitals are Stage II 160 100 Comorbid Specific
taken at each office visit, its often diagnosed in clinic. According Urgency 180 110 PO Meds (Hydralazine)
to JNC-8, there is no more staging of hypertension, though that Emergency Alarm Sxs IV Meds (Labetalol)
discussion is still included at the end of this topic with an
explanation for why it is useful. Start with Normal. Add 20 to systolic, 10 to diastolic to reach
the minimum BP required for the next stage. It is an OR
Hypertensive urgency is any blood pressure >180 systolic or statement if either the SYS or DIA is in a stage, you call it
>110 diastolic without evidence of end organ damage. This is the highest qualified stage.
seen in the clinic, urgent care, or ED. Its managed with oral
Dz Medications
Hypertensive emergency is any blood pressure >180 systolic or CAD BB + Ace ISMN, CCB
>110 diastolic with evidence of end organ damage. Its treated CHF BB + Ace ISDN + Hydralazine, Spironolactone
with intravenous infusions to control MAP. The goal is to use CVA Ace-i
intravenous nitrates or calcium channel blockers to get the MAP DM Ace-i
25% in the first 2-6 hours, then to normal ranges with oral CKD Ace-i Thiazides dont work after Cr > 1.5
medications in 24 hours.
Comorbid conditions often dictate the medications chosen,
I still teach the 20, 10 symptom rule, Stage I, Stage II, urgency, and may be directly opposing JNC-8 recommendations
and Emergency because it suggests how many medications youll (CAD and CHF in particular)
need to gain control + JNC-7 focused on comorbid conditions.
This is included to the right.

JNC-8 Management JNC-8 Recommendations in a Nutshell

JNC-8 has made the management of hypertension quite simple. 1. >60 + No Dz = 150 / 90
While hypertension often exists with comorbid conditions that 2. Everyone else = 140 / 90
require stricter blood pressure goals, JNC-8 has clarified the 3. CCB, Thiazide, Ace/Arb
management of hypertension. 4. Old (>75) or AA = No Ace-i
5. CKD Ace/Arb (overrides #4)
The goal for Age > 50 is 150/90, and for everyone else 140/90. 6. Dont use Beta-Blockers for Hypertension

To treat, use your choice of CCB (Amlodipine), Thiazide

(HCTZ) or Ace-i. If they cant tolerate an Ace, an ARB can also
be used. It doesnt matter which is chosen or in which order.

Except: old people (>75) and African Americans dont get an

Ace-I / Arb to start.

Except: CKD (even if you are old or AA) patients get an Ace-I /
Arb as the first medication.


Medications Class Side effect Indication
You should learn the indications, contraindications, and side CCB Peripheral JNC-8, Angina
effects of each of the medications. This information is included to Edema
the right. ACE K, Cough, JNC 8 AA X
Angioedema Old X
Major highlights that are worth remembering: CKD Y
Ace-I induce angioedema. If they do, the person must never again Ace-intolerance
be on an ACE. ARB is ok. Thiazide K JNC-8
Stop if GFR
Ace-I induce a chronic dry cough. Switch to an ARB if this Loop K Renal Failure
happens. Both ACE and ARBs cause hyperkalemia. CHF II-IV
Beta Blocker HR CAD, CHF
Beta-blockers reduce the heart rate. While its considered a side Art Dilators Reflex Tachy CHF
effect, its often intended (as in CHF and CAD) to reduce the Venodilator Sildenafil unsafe CHF
workload of the heart. drop in BP
Aldo K, CHF
Spironolactone causes gynecomastia and hyperkalemia. If the Antagonists Gynecomastia
gynecomastia becomes a problem, switch to eplerenone. Clonidine Rebound HTN NEVER USE

Secondary Hypertension Class Examples

Rather than attempt to impart all the nuances of the differential CCB Amlodipine, Felodipine
for secondary hypertension here, which would certainly be ACE Lisinopril, Quinapril, Benazepril
overwhelming, we introduce the topic and expect you to be able ARB Losartan, Valsartan
to identify someone who may have secondary hypertension. Thiazide HCTZ, Chlorthalidone
Loop Furosemide
Hypertension before the age of 35 (though this has been Beta Blocker Metoprolol, Carvedilol, Nebivolol
challenged by the rise of childhood and early adult obesity) or any Art Dilators Hydralazine
hypertension thats refractory to 3 medications where one is a Venodilator Isosorbide Dinitrate, Mononitrate
diuretic should be considered for secondary causes. As the fourth Aldo Spironolactone (gynecomastia)
medication is reached, alternative causes should be considered. Antagonists Eplerenone (no gynecomastia)

The most common secondary cause is CKD / ESRD. If the Type History Workup
patient has this condition no workup need be done. Hyperaldo Refractory HTN or Aldo:Renin > 20
(1o Aldo) HTN and HypoK CT Pelvis
If they dont, then the tests to do and the order to do them in is Hyperthyroid Weight Loss, Sweating, TSH, Free T4
dependent on the clinic picture. Assessing for clues in the history, Heat intolerance,
physical, and typical labs guide where to start. The chart is Palpitation,
included to the right for reference. Hypercalcemia Polyuria, AMS, Free Ca
moans, groans, bones,
Conns (Primary Hyperaldosteronism), Pheochromocytoma, kidney stones
and Cushings are discussed in endocrine adrenals lecture and Aortic Children = warm arms, X-ray of Chest
are reviewed in surgical hypertension in the Surgery: Specialty Coarctation cold legs, claudication Angiogram, CT
series. Adults = Rib notching, angio
BP differential in legs
Renovascular Hypertension and Aortic Coarctation are also and arms
discussed in surgical hypertension in the Surgery: Specialty Renovascular DM or CrCl
series. glomerulonephritis BMP
Young woman = FMD Aldo:Renin < 10
Old guy = RAS U/S Renal
Renal Bruit, Hypo K Artery
Pheochrom- Pallor, Palpitations, 24-Hr Urinary
ocytoma Pain, Perspiration, metanephrines,
Pressure CT
Cushings Diabetes, HTN, Central Low-dose Dexa
obesity, Moon Facies ACTH Level
High-dose Dexa
OSA Obesity, daytime Sleep Study
somnolence, improved
with CPAP


The etiologies of all pericardial diseases are the same. We could Etiology Categories
memorize 50+ causes of pericardial disease, but its better to Infections Viral (coxsackie)
simply learn categories and keep a reference nearby to obtain the Bacterial (Strep/Staph)
specifics. Infections, autoimmune diseases, trauma, and TB
proximate cancers (lung, breast, esophagus, and mediastinum) Fungus
cause pericardial disease. If acute, they cause an inflammatory Autoimmune Lupus, Rheumatoid, Scleroderma
condition (pericarditis). If they happen to make fluid they cause Procainamide, Hydralazine, Uremia
an effusion, or in its worst form, tamponade. If chronic, the Trauma Blunt, Penetrating
inflammatory condition can be around long enough to cause Cancers Lung, Breast, Esophagus, Lymphoma
fibrosis, which leads to constrictive pericarditis. Focus on Others Many
identification and treatment rather than etiology.
Disease Treatment
1) Pericarditis Pericarditis NSAIDs + Colchicine
Pericarditis is an inflammatory disease with an inflammatory Pericardial effusion Pericarditis
treatment. It presents as pleuritic and positional (better when Recurrent Effusion Pericardial Window
leaning forward) chest pain that will have a multiphasic friction Tamponade Pericardiocentesis
rub. Caused by an inflammation of the sac around the heart, every Constrictive Pericarditis Pericardiectomy
heart beat causes irritation, producing constant pain. An ECG
will show diffuse ST segment elevation (caution MI), but what
is pathognomonic is PR segment Depression. An Echo will show
ST elevation
an effusion but not the inflammation. Echo is the wrong
answer. Theoretically, MRI is the best radiographic test, but is
often not needed. The treatment is NSAIDs + Colchicine. There
may be times where either NSAIDs or Colchicine cant be used;
in that case monotherapy is used. Steroids are used in refractory PR depression
cases, but associated with recurrence; theyre usually the wrong

2) Pericardial Effusion / Tamponade Heart Pericardial

When fluid accumulates in the pericardial space theres Space Pericarditis
pericardial effusion. If that effusion is slowly developing or
small in size, it may just be an incidental finding on echo. If it
progresses quickly or gets large, there may be symptoms. These
symptoms will be those of CHF: dyspnea on exertion, orthopnea,
and PND. Diagnose the effusion with an echocardiogram. Effusion Tamponade
Pericardial effusions are secondary to an underlying cause. Treat
the effusion by treating the cause. Most often an effusion
develops in the setting of pericarditis; treating the pericarditis
treats it. But if the effusion is large, refractory, or recurrent a
pericardial window (literally a hole in the pericardium) can be
Loose fluid produces Tight fluid crushes
made so that the fluid drains into the chest rather than into the
rub, compromise ventricle, compromise
pericardial space.

If the effusion is rapid (or theres ventricular hemorrhage) the

pericardium fills without time to compensate. This produces
tamponade. Becks triad (JVD, Hypotension, Distant Heart Pericardial window
Sounds), clear lungs, and pulsus paradoxus >10mmHg make allows fluid to drain
the clinical diagnosis. Do EMERGENT pericardiocentesis. An
echo facilitates the diagnosis but is neither necessary nor
3) Constrictive Pericarditis
If an inflammatory process is left untreated long enough, fibrosis
will set in. The loose membrane of the pericardium becomes fixed Normal
and rigid. It causes no trouble with contractility, but the heart
relaxes into a rigid box, limiting filling. As the heart expands into
too-small-a-space, it strikes the walls of the box and causes a
pericardial knock. Diagnosis is made with an echocardiogram.
Treat by removing the rigid pericardium with a pericardiectomy. Constrictive

Cardiology [SYNCOPE]

Syncopes a symptom defined as a transient loss of
consciousness due to global cerebral hypo perfusion. The heart is
a pump; it pushes blood into the vasculature, the tank. The brain
is at the top of the tank. Gravity works against the heart by pulling
the blood towards the ground. Thus, its necessary to have a
strong pump, a normal sized tank, and enough blood to fill the
tank to get the blood to the brain. If blood cant get up to the brain,
we pass out, i.e. syncope. It all comes down to blood pressure -
a product of multiple factors (equation to right). The etiologies of
syncope are vast; each affects one of these elements directly. But
they all can be narrowed down to: a broken pump, too big a tank,
and not enough fluid. Its important to realize how the history and Hemorrhage Vasodilation Broken Pump
physical relates to the potential etiology and the tests that need to (Volume Down) (ANS) (Heart Failure)
be done to confirm suspicions.
Neurocardiogenic (Vasovagal) HR x SV
The vagus nerve goes everywhere: visceral organs, blood vessels,
and the brain. Its both afferent and efferent. Its signal to the blood
vessels causes them to dilate, reducing systemic vascular
resistance. The signal given to the heart is bradycardia. If the
Vagus nerve activates more than it should (for whatever reason),
it can cause bradycardia (cardio-inhibitory) or hypotension
(vasodepressor). In both cases blood pressure falls, blood to the
brain falls, and the person passes out. Lots of things can cause the
Vagus to fire: visceral stimulation, such as cough / defecation /
micturition, an overactive carotid sinus as in turning the head
or shaving, and, because the vagus nerve comes from the brain,
- Overactive Vagus HoTN, Bradycardia
psychotropic causes such as the sight of blood. Vasovagal is both
- Situational Syncope
situational and reproducible. Do a tilt-table test to confirm o Visceral Cough, Defecation, Micturition
suspicions. o Turning Head/ Shaving
o Site of blood Psychogenic
Orthostatic Hypotension - Tilt Table
Normally, when going from sitting to standing the blood follows
gravity and pools in the legs. The person does not feel it but
theres a drop in blood pressure. Its sensed by the same
baroreceptors that could go overactive in vasovagal. These
carotids send a signal that causes an almost immediate
compensatory vasoconstriction and increased heart rate (which is
why we dont pass out every time we stand). But this reflex can - Failure of Reflex Sympathetics
fail if theres insufficient sympathetic tone or volume. If the o Elderly/DM Broken ANS
autonomic nervous system is broken (as in the elderly or a o Sepsis Inflammatory Cytokines
diabetic) or theres something fighting against the sympathetic o Anaphylaxis Same as sepsis
tone (such as sepsis) there can be no reflex sympathetics to o Addisons Disease
compensate, causing a person to pass out. In other words - SVR - Hypovolemia
is insufficient. However, if theres insufficient preload to begin o Hemorrhage
with, standing up exacerbates the condition; CO is insufficient. A o Dehydration
decreased preload is seen in people with hypovolemia (diuretics, o Diuretics
diarrhea, dehydration and hemorrhage). In both cases vital signs - Postural Hypotension
are highly suggestive of the disease. A decreased systolic BP of o Laying Standing
20, a decrease diastolic BP of 10, an increase in HR of 10, or o SysBP 20, DiaBP 10, HR 10
symptoms when moving from a laying position to a standing one
o Rehydrate or Add Constrictors
give away the diagnosis. This person is said to be orthostatic.
Give back the volume with IVF if volumes down, or give

Cardiology [SYNCOPE]

Mechanical Cardiac Disease

This is a rare cause of syncope. If theres a giant obstruction to
outflow from the heart (saddle embolus, aortic stenosis, HOCM,
LA Myxoma) the cardiac output suffers. Because the patient is
- Structural Lesion
living, syncope occurs with an increase in cardiac demand, i.e.
o PE, AS, HOCM, LA Myxoma
sudden onset with exertion. There might be an audible murmur, - Post Exertional Syncope
but these diseases are structural so get an Echo. Cardiac output - ECHO
suffers because theres an obstruction to outflow. For a more - Treatment Etiology dependent
thorough discussion of this phenomena please see hypertrophic
cardiomyopathy in the cardiomyopathy section.

Arrhythmias are typically a disorder of automaticity. If the heart - Sudden onset syncope, without prodrome
goes too fast, theres not enough time to fill ( preload). If the - Rapid change in CO
heart goes too slow, heart rate suffers + with it BP. Syncope will o Too fast = Preload
o Too slow = HR
occur suddenly, without warning. An ECG will show the
arrhythmia IF symptoms are occurring at the time of ECG, but it
- Antiarrhythmics or Defibrillator
usually requires a 24-hr Halter monitor to catch symptoms
occurring with the arrhythmia. This will require antiarrhythmics
or an AICD to flip them into a normal rhythm.

Some things LOOK like a syncopal episode but actually arent. If
you see someone pass out, consider these diseases. This section
is even more brief than usual; only one neuro cause is actually
syncope. Decreased blood flow to the posterior circulation -
vertebrobasilar insufficiency may result in the patient passing
out. Diagnose it with a CT Angiogram by looking at the
vertebrobasilar arteries.

If the patient is post-ictal after passing out they may have had
a seizure. Diagnose with an EEG. If the patient has a focal
neurologic deficit they may have had a stroke. Diagnose with a
CT or an MRI. If the patient simply falls asleep and wakes
refreshed consider narcolepsy; treat with amphetamines and
regularly scheduled naps.

Put it in practice - handling syncope: Woman 3-2-1 PE

History Physical Diagnosis

VV (Vaso Vagal) Situational, often Vagal stimulation Tilt Table
- Visceral Organs (micturition, defecation, cough) Reproducible, with produces asystole
- Carotid Stimulation (turning head, shaving) a positive prodrome or a SYS BP of
- Psychogenic (site of blood) 50 mmHg
Orthostatics Orthostatic Defined as Volume and Reassess, chase
- Volume Down hypotension SYSBP by 20 causes of hypotension if
- Autonomic Nervous Dysfunction DIA BP by 10 refractory to fluid
HR by 20
Sxs of orthostasis
Mechanical Cardiac Exertional syncope Murmur Echo
Arrhythmia Sudden Onset, None 24-hour Holter
Neuro (vertebrobasilar insufficiency) Sudden Onset, Focal Neurologic CTA
unprovoked, very Deficit
Pulmonary Embolism PE PE Wells Criteria, CT scan
Electrolytes (bG, Tsh) None None BMO


Cardiac murmurs occur as a result from increased turbulence.
Theyre caused by increased flow across a narrowed lumen -
either from a stenotic valve or a regurgitant one. The location
and timing within the cardiac cycle are useful for identification
of the murmur before imaging. Confirmatory diagnosis is always
with echocardiogram. The good news is not all murmurs are
pathologic. If the murmur is < grade 3 (out of 6), systolic, and
asymptomatic it needs no investigation. Any diastolic,
symptomatic, or > grade 3 requires a workup. The goal should
be to identify on auscultation, understand treatment and
maneuvers (which mirror one another), and then learn the nuances
found on history or physical.

Mitral Stenosis
Mitral stenosis represents an obstruction to flow across the
mitral valve during diastole. Atrial pressures are near to 0, with Blood backs up in
blood normally just falling into the ventricle. Now forward flow the lungs +
is impeded - blood backs up in the lungs and you get CHF / SOB atria dilates
symptoms. Because theres also an atrial stretch, a resultant

Afib is possible. Caused almost exclusively by rheumatic fever,
its imperative that strep throat be treated appropriately. The
auscultation will reveal an opening snap followed by a
decrescendo murmur in diastole - the worse the stenosis the
earlier the snap. Treatment is initiated when symptoms begin. Afib
Pulmonary from stretch
Do not wait for congestive heart failure to set in! Because more Edema
flow = more murmur, treat this with preload reduction. For
severe disease balloon valvotomy or valve replacement is
required. If there is resultant afib, anticoagulate and cardiovert
after the lesion is identified. Commissurotomies arent performed

Aortic Stenosis
Aortic stenosis is an obstruction in getting blood out of the
ventricle during systole. Because the most common cause is
calcification (even in the case of congenital bicuspid valves,
where calcification is just accelerated), and calcification takes
decades to set in, this disease occurs in elderly men. The most
common presentation is angina, especially on exertion (old men
have coronary artery disease AND now they have calcification
Huge afterload from stenotic valve
too). Syncope is classic, especially as cardiac demand increases
(as in with exertion). The worst symptom is active CHF, implying
Makes for a big beefy heart that eventually fails leaving the
the worst prognosis - a 1-3 year survival from diagnosis. Heard
heart full of blood
best at the aortic region, its a crescendo-decrescendo murmur.
Because it will cause hypertrophy and eventual failure (as the left
ventricle pushes against an enlarged afterload), treatment is a
must. Start with preload reduction so theres less to push. A
valve replacement is required sooner rather than later. In this
case, a commissurotomy or valvotomy is not possible, because
the calcifications are too thick. A valve replacement will result in
the ostea being lost; it prompts a CABG regardless of CAD


Mitral Regurgitation
Blood should exit the left ventricle though the aortic valve. The
mitral valve prevents it from going back into the atria. When the
mitral valve fails, blood shoots from the high pressure left
ventricle to the low pressure left atrium. This causes atrial
stretch (potential Afib), pulmonary congestion (full blown
pulmonary edema to CHF), and a decreased forward flow Blood shoots back into the atria
(cardiogenic shock). The process may be acute (rapid, sudden,
devastating) and is a result of valve destruction. Causes include
ruptured papillary muscle or Chordae Tendinae (via Pulmonary Atrial
myocardial ischemia), infective endocarditis, or direct trauma. Congestion Dilation
Onset will be sudden and the symptoms fulminant.
Rapid identification and surgery is required. In the chronic
(slowly developing - time for compensation) condition, usually
secondary to ischemia or mitral valve prolapse, the onset is
gradual and the symptoms are simply exertional dyspnea or
fatigue. Heart failure may be controlled with normal medications,
but replace before CHF / Afib / Dilation occur. Treat it when
its found. This is the classic holosystolic murmur radiating to
axilla heard best at the cardiac apex.

Aortic Insufficiency
Blood should not fall back into the left ventricle during diastole.
In fact, aortic contraction maintains diastolic blood pressures. If
the aortic valve is floppy (ischemia or infection) as the aortas
contractility squeezes blood, it will squeeze it back into the
ventricle rather than forward into the periphery. This presents
with dilated heart failure if chronic or cardiogenic shock if
acute. Some end-stage findings have been characterized and Blood pours back into the Cardiac Dilation
left ventricle + Systolic Dysfxn
named. Impress the attending with their knowledge but the valve
should be replaced before that happens. This is a decrescendo
murmur heard best at the aortic valve.

Mitral Valve Prolapse

Generally, mitral valve prolapse is a congenital defect of the
valve leaflets. They are too big for the annulus; they pooch into
the atria. The murmur sounds like mitral regurgitation but the
pathogenesis and treatment is far different. Expanding
intravascular volume and allowing the heart to fill will stretch the
annulus and make the leaflets fit better. Look for the pregnant
woman (whose decreased venous return exacerbates this Blood pooches into atria, Expanding the ventricle
murmur). rather than lock, allowing pulls the valve together
back flow
Murmur Location Leg Raise Valsalva Tx Path Presentation Def Tx
Mitral Apex Worsens Improves Preload Rheumatic Fever Afib, CHF Replace
Stenosis Reduction SOB
Aortic Aortic to Worsens Improves Preload Calcification Angina, CHF Replace
Stenosis Carotids Reduction Bicuspid Syncope
Mitral Apex to Worsens Improves Preload Infxn CHF Replace
Regurg Axilla Reduction Infarction
Aortic Aortic Worsens Improves Preload Infxn CHF Replace
Regurg Reduction Infarction
HCOM Apex Improves Worsens Increase Congenital SOB, Sudden Replace
Preload Death
Mitral Apex Improves Worsens Increase Congenital CHF Replace
Valve Preload

Pulmonology [COPD]

COPD is a combination of emphysema and bronchitis that produces Shortness of Breath and Wheezing by Age
airway inflammation and irreversible bronchoconstriction. The
primary cause of COPD is cigarette smoking. Because only 20%
of smokers get COPD but 90% of COPDers were smokers, there Allergic Nonallergic COPD
must be other contributing factors: genetic (as in 1-AntiTrypsin Asthma 18 Asthma 65
deficiency) and/or environmental factors influence the final
disease. Emphysema is the destruction of alveolar walls at the
terminal bronchiole (i.e. in the small airways) with fibrosis. Loss of
elasticity causes air trapping - allowing air in on inhalation while
preventing air out on exhalation. Bronchitis is defined as a
productive cough for more than 3 months in 2 consecutive years.
Its characterized by mucous production that obstructs the large

Together, therell be ciliary loss, goblet cells, mucous

production, increased smooth muscle hypertrophy (narrowing the Bronchitis Emphysema Normal
airways and resistance to flow), accumulation of interstitial
inflammatory infiltrates (causing gas exchange as a result of Hypoxia (blue, cyanosis) Air Trapping
decreased diffusional area), and a loss of elasticity leading to airway RV Strain CO2 Retention
collapse during expiration. The chronic hypoxia in alveoli leads to RVF (edema) Barrel Chest
an pulmonary vascular resistance and subsequent pulmonary Hyperresonant
Pursed Lips

Pathology to Presentation
A patient presenting with COPD will present with wheezing and
dyspnea. Risk factors for COPD (as opposed to asthma) are
smoking ~40 pack-year history, age > 45, and the physical signs of Finding to Pathology
symptoms of COPD not present in Asthma. With bronchitis the so- Finding Pathology
called blue bloaters, the chronic cough combined with the Barrel-Chest AP Diameter, Accessory muscle hypertrophy
cyanosis and edema predominate. Bronchitis produces hypoxia and Hyperresonant Air-Trapping
the subsequent increase in pulmonary vascular resistance. Signs of Flattened Air-Trapping
clubbing and edema of the digits indicates chronic hypoxia. The Diaphragm
Hyperlucency Air-Trapping
result is right heart failure that manifests with JVD, edema, and
on CXR
hepatosplenomegaly. Emphysematics suffer from air trapping, Weight Loss Accessory Muscle hypertrophy, work of
which causes the barrel-chest of an increased AP diameter and breathing
hyperresonance on percussion. Theyll breathe through pursed Prolonged Overcoming Airway Resistance
lips to prolong expiration and reduce the resistance of airflow out Expiration
of their lungs. Because its a struggle to get air out of the lungs the Pursed Lips Overcoming Airway Resistance
hard work of breathing causes weight loss and accessory muscle Hypoxia Interstitial Inflammation, Bronchiolar Mucous
Edema Hypoxia Pulmonary HTN R heart failure
hypertrophy. The trapped air reduces expulsion of carbon dioxide.
RVH Hypoxia Pulmonary HTN R heart failure
RAD R Heart Failure OR Rotated Silhouette
Diagnosis Cyanosis and Hypoxia
The only diagnostic modalities that can diagnose COPD are the Clubbing
pulmonary function tests. Other tests will be performed as a result Erythrocytosis Hypoxia
of the chief complaint and can be suggestive of the underlying Hypercapnia Chronic CO2 retention
Pulmonary Irreversible Bronchoconstriction and
disease. They can also be used to indicate severity of an acute flare.
Function Tests inflammation separates wheezing of COPD from
The CXR will show flattened diaphragms, translucent lung wheezing of Asthma. Asthma can be reversed
fields (both from increased air in the lungs), and a rotated heart with bronchodilators. Not COPD
silhouette. The EKG might show RVH (from cor pulmonale) or a
Right Axis Deviation (from RVH or rotation from

Pulmonology [COPD]

er-inflation). An ABG will show a hypoxic hypercapnic Exacerbation

respiratory acidosis and is useful to direct treatment (see later). When a patient has a drop in SpO2 or in productive cough the
Finally, PFTs will show an irreversible obstructive airway patient may be presenting with acute exacerbation. The goal is
disease: FEV1 FEV1/FVC, RV, TLC, and a DLCO. first to help them breathe, cover a potential infection, then figure
Finally, even if there are no outwards signs, a CBC may show an out what caused the exacerbation. The first line therapy is, of
erythrocytosis in response to the hypoxia. course, Oxygen while a diagnosis is made. In a patient with acute
dyspnea the worry of decreasing hypoxic drive is far
Treatment overshadowed by the patients need for oxygen. Then, nebulized
Treatment of stable, chronic COPD is based on an escalation of therapy is crucial. Ipratropium > Albuterol (for the test), but
severity. Many medications can be swapped for each other and this the two are usually given together in practice. IV Steroids
process is much more convoluted (aka personalized) on a patient by (methylprednisolone 125mg)) or PO Steroids can follow if theres
patient basis. You should learn the mnemonic COPDER and no improvement with the nebulizers. No taper is required for
memorize the escalation of therapy we suggest here (knowing that COPD. Antibiotics are indicated if theres purulent sputum or
its more complicated than this). sputum production is increased. Use anything that will cover for
the typical bugs (amoxicillin, trimethoprim-sulfa,
Short Acting Bronchodilators (ipratropium, albuterol) are used for azithromycin, doxycycline, on a rotating schedule). If theres
acute symptoms relief. Long acting muscarinic antagonists no improvement admission to the ICU with mechanical
(tiotropium) is added for initial maintenance therapy. Long acting ventilation may be required.
beta agonists (formoterol, salmeterol) are added for further
maintenance. Inhaled Corticoteroids (budesonide, another one)
are added to reduce readmissions. Newer medications such as the
PDEV-inhibitors (roflumilast) are a last ditch effort to avoid oral
steroids. Oral steroids are used in refractory disease. Notice that in
Asthma ICS are added before LABA, but in COPD LABA is before
ICS. Leukotriene antagonists are used in Asthma, but not in COPD.

Corticosteroids are given in the form of inhaled corticosteroids and

oral steroids. Oral steroids are often reserved for acute
exacerbations of COPD and should be avoided in chronic Treatment Goals and Methods
management given the risk of hyperglycemia, hypertension, and C Corticosteroids Inhaled maintenance, IV exacerbation,
osteopenia. change in mortality unless infection
O Oxygen When PaO2 <55 or SpO2 <88% titrating to
PaO2 55-60 SpO2 >90%
Oxygen: To give or not to give - that is the question. Due to the risk
P Prevention Vaccines: Pneumovax (q5y) and Flu (q1y)
of eliminating hypoxic drive (chronic hypercapnia results in Smoking cessation
respiratory drive driven solely by low levels O2 rather than high Mortality
levels of CO2) there are strict criteria for starting home oxygen. If D Dilators Anticholinergics > Beta-Agonists
the pO2 < 55 on ABG or SpO2 < 88% on a pulse Ox at rest, activity, Rescues Nebs Continuous (Inpt only)
or exercise, then chronic home O2 is indicated with a goal of E Experimental Out of our scope
R Rehabilitation Exercise tolerance,
titrating SpO2 > 88-92%.
Dyspnea and fatigue
Change in Mortality
Prevention comes down to smoking cessation and vaccinations.
Patients required the annual flu vaccine and the pneumococcal
vaccine, once before 65 and once after 65. Smoking cessation, in
addition to home O2, is the only intervention that will prolong life.
However, because theres a lag time between smoking cessation Interventions in COPD
and inflammation the patient may initially get worse. Agent Dose Comments
Ipratropium 0.5mg NEB q4 First Line
Dilators include any of those listed above: LAMA, LABA, SABA. Albuterol 2.5mg NEB q4 First Line
Corticosteroids Methylprednisone 125mg IV Exacerbation
Prednisone 40mg PO
Experimental therapy is beyond the level of this course.
Oxygen Titrate to SpO2 88-92% or Home and In
PaO2 55-60 patient
Rehab consists of improving exertional capacity but does not Intubation and Last Resort
improve mortality. Ventilation


Pulmonary embolism should be considered one continuous disease
with a deep venous thrombosis. The etiology of DVT / PE is Stuck!
Virchows Triad: 1) Venous Stasis, 2) Hypercoagulable State, 3)
Endothelial Damage. Risk goes up with the classic risk factors (bed
rest and surgery), hypercoagulable disorders (cancer, OCPs, and Embolus
genetics), and HTN/Dissection/IV sites. The thrombus forms in the Traveling
deep veins; its typically in the popliteal or femoral veins. Since >2 cm difference in
theres valves in the deep veins, should a piece of a clot should calf circumference
break free (the embolus) it can travel up the IVC and into the lungs.
It gets stuck in a small vessel of the lung. This has two
consequences. 1) Because good blood is unable to get to the alveoli,
theres a limitation of gas exchange. 2) Because theres less piping
to pump blood through theres an increase in pulmonary vascular
resistance, creating a right heart strain.

Yet even the smallest embolus can cause profound dyspnea. A small
clot doesnt cause heart strain or significantly impact gas exchange
(relative to the size of the lung). How these small emboli cause such Wells Criteria Building the Wells Score
profound dyspnea is through platelet-derived mediators leading to PE most likely diagnosis, s/s DVT 3 each
lung-wide inflammation. This allows fluid to leak out around the HR > 100 1.5
alveoli. The fluid is a barrier to the diffusion of oxygen but NOT Immobilization 1.5
Surgery w/i 4 weeks 1.5
carbon dioxide. Thus, as the respiratory rate increases CO2 is blown
Hemoptysis 1
off while Oxygen cant get in. Malignancy 1
h/o DVT or PE 1.5
Presentation Wells Score for V/Q Scan Interpretation
The classic patient will present with a shortness of breath, Score <2 Score 2-6 Score > 6
tachypnea, tachycardia, a pleuritic chest pain, and a Clear Chest Small Probability Moderate Probability High Probability
X-ray. The difficulty with PE is that theres no clinical finding that
Modified Wells do I do a CT Scan?
screams PE Here, so the goal is to identify risk factors and rule
Score < 4 Score > 4
out other diseases. The presence of a Homans Sign (pain on passive Dont Do It Do It
flexion of the foot) is highly suggestive for DVT but its absence
means nothing. As such, always at least consider PE when a patient
complains of shortness of breath. All thats left is to use the Wells Shortness of Breath +
Tachycardia + Clear CXR
Criteria to decide what type of test to do and how to treat it.

Diagnosis Unlikely Wells Criteria Likely

During the workup of SOB the typical tests of CXR, EKG, and
ABG may show soft signs of PE. The CXR is normal - the EKGS
show S1Q3T3 indicative of Right Heart strain - and the ABG may Unlikely Likely
show a hypoxemic respiratory alkalosis (the increased respiratory
rate because of hypoxia drives venting of CO2). The absence of these D-Dimer Can they
mean nothing, however. A D-Dimer is usually 1st, but is only useful Yep
get a CT?
if normal (rules out PE though does not rule in anything and can be
falsely elevated). A lower extremity ultrasound is great if positive
(rules in but not out, as the clot may have already embolized). The Med Prob
two tests that can absolutely diagnose a PE are Spiral CT and PE CT Scan V/Q Scan
Angiogram. The spiral CT is the modality of choice because its Stop
non-invasive. The Angiogram is invasive and isnt superior to the High Prob
Spiral CT. However, if the patient cant have IV Contrast a CT scan
is really useless. Instead, do a V/Q Scan to stratify risk into high,
medium, and low.
Low Prob


Treatment is really based on the severity of the disease.

If theres a massive embolism that has compromised cardiac Pulmonary Embolism

function (hypotension) its imperative to jump right to emergent Path: Virchows Triad
intra-arterial tPA or thrombectomy. Pt: Shortness of Breath, Tachycardia, Clear CXR
Dx: D-Dimer, CT Scan, V/Q Scan
In most cases there are two treatment goals. One is to shut off those Tx: Heparin to Coumadin
platelet mediators using heparin. Heparin is the mainstay of
therapy; even if a PE is suspected start it. The second goal is to
prevent recurrence with an anti-coagulator like warfarin. To put
a patient on heparin they need a heparin to warfarin bridge. The
target INR is 2-3; give heparin to help the patient right now and to
prevent the procoaguable effects of early warfarin.

Those patients who cant tolerate warfarin or who have DVT/PE

while therapeutic require the placement of a Greenfield filter in
the IVC.

Obviously, the first step in treatment will be to give a dyspneic

patient oxygen.

Warfarin can cause hypercoagulability and thus requires a heparin
bridge in the first few days. Likewise, INR must be maintained
between 2-3 to avoid bleeding (if it gets too high) and clotting (if it
gets too low). While in the hospital, heparin can induce a heparin-
induced thrombocytopenia (HIT). This usually occurs within 7
days on first exposure and 3 days on repeat. Draw a HIT panel, stop
the Heparin, and give Argatroban.

Pulmonology [LUNG CANCER]

Lung cancer is a common malignancy and a common cancer killer.
Its very tightly linked to smoking. While exposure to radiation,
heavy metals, and some other environmental exposures (like
Asbestosis) do contribute to lung cancer, you should align
Smoking and Lung Cancer as essentially synonymous
(especially in regards to the test).

Screening and Prevention

Primary prevention is about not smoking. Those who dont smoke
shouldnt start, while those who do should quit today. Even those
who dont smoke should avoid other people who do (second hand
smoke) as all smoking exposure increases the risk of lung cancer.

Screening is with an annual Low Dose CT scan of the chest. The

people who get screened are those who have a 30 pack year history,
quit less than 15 years ago, and are between 55-80 years old.

Pulmonary Nodule
Regardless of whether a pulmonary nodule was found because of a
screening CT scan or from imaging of the chest for some other
reason, the investigation process is the same.

Step one is to compare old films. If theres been no change in 2

years, the nodule is said to be stable; no further investigation or
follow-up is required.

If the nodule has changed, its said to be unstable and you have to
decide if this can be followed with serial CT scans (for two years
until it becomes stable) or needs to be biopsied right now. The
things that make the risk increase or decrease are listed below.
Weve come up with the Ss as a means of helping you remember
which cancers are caused by smoking and to remind you that the
analysis of a nodule is made using Size, Surface features, Smoking
history, and the patients Age (Self).

Making a Diagnosis of Lung Cancer

Lung cancer can occur in different places in the lung and often
spreads through lymph nodes prior to metastasizing. The major rule
of lung cancer is to avoid poking the lung if possible; make the
diagnosis some other way. Ideally, that means stage the cancer and
make the diagnosis by choosing a site that is extra-pulmonary.

But for intrapulmonary lesions without evidence of spread, there are

still a number of ways to get a piece of tissue. The Bronchoscopy
(now upgraded to include an ultrasound probe called EBUS) is used
to biopsy proximal lesions. Rigid bronchoscopy alone allows us to
sample lesions that are intraluminal in large airways, while EBUS
allows for more accurate sampling of the lymph nodes or masses on
the outside of the lumen (in the chest / lung). Percutaneous CT
guided biopsy is chosen when the lesion is peripheral. Video
Assisted Thoracoscopic Surgery (the laparoscopy of the chest) can
be used to sample lesions not assessable by EBUS or Percutaneous

Still other methods exist. Thoracentesis revealing malignant cells

is Stage IV, metastatic disease. And lesions that are very clearly
malignant can be diagnosed with resection.
Pulmonology [LUNG CANCER]

Lung Cancer Presentation

The classic symptoms of an advanced lung cancer include fever,
hemoptysis, and weight loss. These are constitutional symptoms
seen in Lymphoma and in TB. But if the person is old and has a
personal history of smoking, youre being guided towards Lung
Cancer. Often the workup begins with a Chest X-ray, done not
because its lung cancer (Chest X-ray is poorly sensitive for Lung
Cancer), but as an inexpensive and accessible means of looking at
the chest. If lung cancer is suspected, go straight to CT scan.

If that chest x-ray is unrevealing, but there are paraneoplastic

syndromes get a CT. If the X-ray reveals an effusion, perform
thoracentesis. If the CT scan shows a malignancy, refer to the
diagnostic approaches listed above. Surgery Alone Surgery and Adjuvant Chemo Radiation
Chemo WITHOUT surgery
Staging is done with PET-CT. before a treatment plan is made, Ia Ib > 4cm Mass IV (N2, N3 nodes)
pulmonary function tests are required to assess if the patient can Ib, <4cm mass II (N0 or N1 nodes) IV (Mets)
tolerate surgery. Then, ultimately chemo, radiation, and surgery are III (N0 or N1 nodes) IV (Pleural effusion)
chosen based on the stage.
Squamous Cell Carcinoma
Caused by smoking, the lesion is typically central. Classic warning
signs (hemoptysis and weight loss without fever) are the tipoff. A
CXR may show a large lesion or repeated PNA (caused by
obstructing lesion). EBUS with Biopsy gets the diagnosis. The
cancer may produce PTH-rp (parathyroid-like hormone) causing a
hypercalcemia. Squamous cell carcinoma can also cause an Eaton-
Lambert paraneoplastic syndrome see Neuro, Weakness.

Small Cell Carcinoma

Also caused by smoking, its a central lesion thats typically
metastasized at the time of diagnosis. Its too small to be seen on
X-ray so it requires a CT scan to make the diagnosis. EBUS with
Biopsy confirms the diagnosis. The tumor should NOT be resected;
its exquisitely sensitive to chemo. Because its a neuroendocrine
tumor it can produce ADH (SIADH) or ACTH (Cushings). It does
not get large enough to cause obstructive pneumonias or

This is the lung cancer that people get when they dont smoke. It
typically occurs in the periphery of the lung and is stuck to the
pleura causing it to pucker. Its either spontaneous or secondary to
a remote asbestos exposure or other non-cigarette exposure.
Smoking makes it more likely, and worse, but is not necessary.

Carcinoid is a rare neuroendocrine tumor that may occur in the small
intestine or the lung. It produces serotonin, which degrades to 5-
HIAA and gets secreted into the urine (how its diagnosed). Because
the serotonin originates in the lung it will cause a left-sided valve
fibrosis along with the flushing, wheezing, and diarrhea typical of
the intestinal carcinoid. Since the serotonin is degraded by the liver,
the right side of the heart is spared.
Cancer Path Location Histology Paraneoplastic Dx Tx
Small Cell Smoking Sentral Neuroendocrine granules ADH - SIADH Bronch, EBUS Chemo + Rad
on EM ACTH Cushings (no matter the stage)
Squamous Cell Smoking Sentral Intracellular Bridges, PTH-rp Bronch, EBUS Surgery
Keratin Pearls
Adenocarcinoma Asbestos Peripheral Mucin Glands - Perc CT Surgery
Carcinoid Smoking Anywhere Salt and Pepper Serotonin Syndrome U 5-HIAA Surgery

Pulmonology [ASTHMA]

Introduction and Pathology
Asthma is a reactive obstructive airway disease caused by an Risk Factors
inflammation and bronchoconstriction that results in increased - h/o Allergic Rhinitis, Nasal Polyps, Eczema
resistance to airflow. Its an allergic disease (Asthma, Allergy, Atopy) - Exposure to known precipitants
and is likewise IgE / Mast cell mediated. - Nocturnal Wheezing / Cough (Caution for GERD)
- #of ED Visits, Hospitalizations, and Intubations
Patients will complain of cough, wheezing, and dyspnea; they may
also claim chest tightness during an acute attack. The constricted
airways produce air trapping; air can get in on inhalation, but cant get
out on exhalation. Physical exam reveals wheezing and a prolonged
expiratory phase with a potentially hyperinflated or hyperresonant
chest (an ominous sign). Signs of severe dyspnea (accessory muscle Wheezing, Cough, Dyspnea
use or the absence of lung sounds) signal the presence of status
asthmaticus - a medical emergency. Obtaining a history and physical
as well as risk factors is crucial for the decision making that follows.
FEV1/FVC Pulmonary Function Tests FEV1/FVC
Between attacks, the lungs usually sound normal.

If someone comes in with an acute onset of wheezing and dyspnea Active Dz Active Dz
SKIP the diagnosis and move directly to treatment. In the outpatient
setting there are a number of diagnostic modalities, of which
Pulmonary Function Testing is by far the best. If the patient has Methacholine Bronchodilator
active airway disease at the time of the test the FEV1/FVC will be Challenge PFT
decreased. They can be reversed with bronchodilators to
definitively diagnose asthma. A normal patient does not rule out
asthma. A patient suspected of having asthma but a normal FEV1/FVC Non-
Inducible Inducible Irreversible Reversible
can be given the methacholine challenge test to provoke
bronchoconstriction. There are other ancillary tests that come up from
time to time that may be suggestive of asthma. Eosinophilia on a CBC Asthma Dz Something Asthma
or Sputum sample, Charcot-Leyden Crystals or Curschmanns Else
Spirals on sputum, and Allergen Skin Testing are useful, but you (COPD)
should rely on the PFTs for diagnosis. Use Allergen Skin Testing when
severe, refractory, or to assess which exposures trigger the disease.
These tests should not be routinely performed.

Besides diagnosis, severity of disease is a critical element to evaluate

as itll drive patient management. Its determined by frequency of
daytime symptoms, nocturnal symptoms, and severity of the PFTs.
They are broken down into steps, or grades, indicating which
- Bronchoconstriction Theophylline, SABA/LABA, Leukotrienes
medications need to be added. - Inflammation Inhaled / PO Corticosteroids
- Stabilizing Cromolyn / Nedocromil
Treatment targets the two elements of asthma: decreasing
inflammation and reversing bronchoconstriction. Inflammation is
conquered by steroids, bronchoconstriction by beta agonists. Then,
Step Daytime Nocturnal PFTs Treatment
there are a few drugs that have been added to the mix. Symptoms Symptoms (FEV1)
Intermittent < 2 /wk <2/month >80% Rescue Inhaler
Patients who have symptoms infrequently can use a rescue inhaler Mild < 1 /day >2/month >80% Low Dose ICS
(short acting -Agonists or even Anticholinergics) as needed. As the Persistent
severity of disease increases medications are added. Daily Inhaled Moderate > 1/day >1/week 60-80% Low Dose ICS
Corticosteroids will decrease the inflammation while rescue inhalers Persistent and LABA
can control the bronchoconstriction. For frequent symptoms Long Severe > 1/day frequent < 60% High Dose ICS
Acting Beta-Agonists (LABA) are added to Inhaled Corticosteroids Persistent and LABA
(and must NEVER be used on their own). From this point, the dosage Refractory Refractory Severe Persistent PO Steroids
of steroid increases from low-dose steroids to high-dose steroids, and
then to PO steroids.

Pulmonology [ASTHMA]

Be aware of other drugs that can be used in place of or in addition to Treatment Progression
the LABAs. The new guys to the market are the Leukotriene 1. SABA
Antagonists. For all intents and purposes, a Leukotriene Antagonist is 2. SABA + ICS
an Inhaled Corticosteroid and can be used interchangeably. They 3. SABA + ICS + LABA
should not be used together. 4. SABA + ICS + LABA
5. SABA + ICS + LABA + Oral Steroids
Theophylline is a po Adenosine Antagonist. Its pretty old but is still
in use. This is never the right answer on the test. It may still be used in ICS = LTA
patients because of the cost of inhalers, but this is ALWAYS WRONG Before adding an inhaler, asses to make sure the patient
Knows how to use and is using the inhalers correctly.
for your exams.

For exercised induced asthma with known triggers the IgE/Histamine

Stabilizers (Nedocromil or Cromolyn Sulfate) can be used
immediately before known exposure but with limited use.

Spend a lot of time on the treatment progression listed to the right, then
just know other treatment options exist.

Acute Exacerbation
When someone presents to the ED with acute or refractory symptoms
they need to be treated and stratified. Evaluation involves Peak Wheezing, Cough, Dyspnea
Expiratory Flow Rates (PEFR), the Physical Exam, and an ABG. A
Chest X-ray isnt useful but often done to rule out other causes of
O2 target SpO2 >90%
Albuterol/Ipratropium q20 x3
Treatment begins immediately with O2, Albuterol/Ipratropium
Steroids IV or PO
Nebulizers (to reverse bronchoconstriction) and corticosteroids (to
For 3 Hours
reverse the inflammation). Peak flow, CO2 retention, oxygen
saturations, and lung assessment should be repeated after the initial
intervention. PEFR > 70% PEFR > 50-70 PEFR<50%
Symptoms Mild to Mod Sxs Wheezing
Rescue therapy for refractory disease involves Racemic Epinephrine
Dyspnea Dyspnea
PaCO2 > 42
Nebulizers, Subcutaneous Epinephrine, and Intravenous
Magnesium. These are added in an attempt to avoid intubation.
Ultimately, if there are signs of rising CO2, decreasing pH, or the
absence of lung sounds, intubation is required.
Reversal Incomplete Severe
When they first arrive in the ED a Peak Flow should be performed. If Go Home
theres no improvement after 3 hours of continuous nebulizer
treatment they go to the ICU; if better (100% improvement and
Floor / Obs ICU
symptom free) they go home. Anywhere in between gets admitted to
the hospital for further management. Further management really Check q8H Intubation
means Albuterol + Ipratropium every four hours with ongoing oral or NEBS q4H IV Steroids
IV steroids. d/c in AM (High Dose)

Pulmonology [ARDS]

Pathogenesis and Introduction

ARDS is a noncardiogenic pulmonary edema that results from
Normal gas exchange
increased permeability of capillaries permitting the
and no leaky
transudation of fluid from capillaries into the interstitium. This capillaries in the
causes a barrier to diffusion preventing gas exchange resulting in normal state
a hypoxemia. It looks and feels like CHF but the cardiovascular
function is intact, hydrostatic pressures are normal (meaning that
the capillary wedge pressure is normal), and its the capillary
permeability that drives disease. Too many leaky capillaries then Impaired oxygenation
leads to pulmonary edema and alveolar derecruitment. as a product of
increased diffusion
Presentation barrier from leaky
This is a patient with pulmonary edema (SOB, cough, crackles) capillaries in ARDS
and a nasty looking CXR (bilateral white out). The patient is
also one without a reason for CHF (MI, HTN, Arrhythmia, Fluid)
and has instead a really sick presentation (as in the ICU). To
PEEP provides
cause capillary permeability to increase so significantly requires alveolar recruitment
GNR septicemia, burns, TRALI, or drowning. These patients and improves
usually present to the hospital then crash in the ICU, rather than a diffusion of oxygen by
person presenting in florid pulmonary edema. reducing diffusion
A patient with a systemic disease and pulmonary edema
(especially someone volume down or hypotensive) is likely
enough for the diagnosis. A CXR will show white out bilaterally. Alveolus
However, to definitively diagnose ARDS vs CHF a measurement
of capillary-wedge pressures via a Swan-Ganz cath is required. Blood
This will show a decreased or normal wedge (no backup of
fluid) and an increased or Normal LV function (not heart Blood
failure). Both findings are in direct contradiction to CHF.
Generally, its not done for CHF (patients arent sick enough to Gas Exchange Impaired Edema impairs Gas Exchange
get a Swan-Ganz), though there are certainly HF patients sick
enough to make it to the ICU. A patient with ARDS will be
intubated, full of lines, and ripe to do the assessment on. A PaO2
to FiO2 ration will be < 200.
J = K [Pcap Pint ) (cap int)]
Fluid movement across a capillary
Intubation and Oxygenation are crucial as first line therapy.
ARDS causes in K, fluid leaks out
With intubation, application of PEEP increases the interstitial
PEEP causes in Pint, pushes fluid back in
pressures, forcing the fluid back into the capillaries. The vessels
remain leaky and only close once the underlying disease is
Exacerbating HTN, MI Sepsis, Burns,
Monitoring/Complications Factors Fluid Overload Drowning, TRALI
When someones put on PEEP its possible to induce Chest X-Ray Bi Pleural Effusions Total White Out
barotrauma or induce pneumothorax. If the patient suddenly Bi Hazy Infiltrates Severe Bi Infiltrates
presents with worsening SOB after PEEP, suspect barotrauma. Capillary Wedge (25) Normal (10)
However, if a patient becomes hypotensive and has a LV Function Normal
mediastinal shift (tracheal deviation) a tension pneumo should Treatment Diuresis, PEEP
Control of HTN, Intubation
be suspected. Confirm the diagnosis with a CXR and treat with
PEEP if severe Tx Underlying Dz
needle decompression and chest tube.


There are two types of effusions: transudates and exudates. A
Intravascular Pleural Effusion Extravascular
transudate is a lot of fluid and not much else. Its caused by
Hydrostatic Oncotic Pressure
intravascular pathology; either an Hydrostatic Pressure (CHF) Oncotic
or Oncotic Pressure (Nephrotic syndrome or cirrhosis) from
within the blood vessels. These are usually distributed evenly across
the lungs and are thus bilateral. An exudate is a lot of stuff in the
parenchyma drawing the fluid out. Its caused by extravascular Transudate Exudate
pathology - generally an Oncotic Pressure of the interstitium
outside the blood vessels (infection, malignancy, PE, TB, CHF, Nephrosis, Infxn, Malignancy, PE, TB,
Cirrhosis Hemothorax, Chylothorax
Hemothorax, Chylothorax, or some Zebras). Since this doesnt
necessarily distribute evenly it may be unilateral.
Upright Chest X-ray
Diagnosis < 250cc Not visible
Pleural effusion is on the differential for shortness of breath or 250cc Blunting of the costovertebral angle
pleuritic chest pain. However, the diagnosis does not become >250cc Meniscus line rises, air-fluid level
apparent until the Chest X-ray. Once blunting of the
Recumbent Chest X-ray
costovertebral angles (which requires at least 250cc) is seen the
Free fluid vs loculated (Layers out or doesnt)
diagnosis is made. If more than that is present the air-fluid level (the Volume required for thoracentesis (>1 cm)
meniscus) rises. After the chest X-ray perform a recumbent X-ray
to assess if the fluid is free moving (not loculated) and in sufficient Thoracentesis Findings
quantity (>1cm from chest wall to fluid level) to do a thoracentesis. Transudate LDH < 2/3 Upper Limit of Normal (~200) and
A loculated effusion can;t be safely tapped and needs surgical Total Proteineffusion / Total Proteinserum<0.5
intervention. With thoracentesis the Lights Criteria (comparing Total Proteineffusion / Total Proteinserum<0.5
the Serum Protein and Serum LDH to the Pleural protein and the Exudate LDH > 2/3 Upper Limit Normal (~200) or
LDHeffusion / LDHserum > 0.6 or
Pleural LDH) can be performed. It shows the exudates vs
Total Proteineffusion / Total Proteinserum>0.5
transudates (see the table to the right). The next need is to get a
complete characteristic of the pleural fluid for definitive diagnosis CT Scan
(WBC, RBC, pH, and Glucose). If underlying conditions require for evaluation or diagnosis

CT scan or bedside ultrasound can also assess for loculation. The
CT may also give insight into the cause of the effusion. However, Effusion Ultrasound is taking
if the patient has CHF and the diagnosis is leaning that way theres the place of this test
no need to any workup. Simply diurese and monitor.
Upright and
Treatment Decubitus
If theres a loculated effusion a thoracostomy (chest tube) is XRay
required. Parapneumonic effusions that are loculated may form a Loculated < 1cc
rind, called empyema. This requires thoracotomy (surgery) with
decordication. Repeat effusions may be treated with pleurodesis - a
chemical or surgical elimination of the pleural space. If a pathology Thoracotomy Tappable Observe
is identified on the thoracentesis, treat the underlying condition. If
the condition is already known, no tap need be done (for example, Chest Tube Observe Only
CHF getting diuresis only).
No CHF? Yes
1) Find an effusion on CXR Determine Tappability Thoracentesis CHF
2) a. If loculated, thoracotomy failure thoracotomy
Diuresis and
b. If not loculated >1cc Tap, if <1cc Observe
Lights Observe
3) If they have CHF diurese and monitor - do NOT tap
4) Light Criteria for Transudate vs Exudate Criteria
5) If transudate treat the underlying disease
Transudate Exudate Full Workup
6) If exudates get complete workup, tx as diagnosed
7) If all else fails consider Pulmonary Embolism
Treat the Work it up Glucose, Amylase, Cytology,
cause Cell count, culture, Gram
stain, AFB, TB antigen;
Gastroenterology [ACUTE DIARRHEA]

Introduction and Definitions Bloody Diarrhea Common Acute Diarrhea
Diarrhea itself is defined by > 200g stool / day. Unfortunately, no M edical Disease Medical Disease
E. coli (EHEC) E. coli (ETEC)
one is going to measure their stool every day in a bucket at dry
S higella Bacillus cereus toxin
weight. Clinically, its defined as frequency or consistency S almonella Viruses (Adeno, Roto)
of stools. Acute diarrhea is any diarrhea with a duration < 2 Y ersinia histolytica Giardia
weeks. Chronic diarrhea is a duration > 4 weeks. Subacute is Staph aureus toxin
in between. When talking about an acute diarrhea it really C. difficile
means infectious diarrhea. Most causes of diarrhea are A moeba histolytica
C ampylobacter C. difficile = Hospital Acquired
infectious and self-limiting. Its your job to know when to do Vibrio cholera = Rice-Water Stools
A eromonas
additional tests and when to give antibiotics. In real life, thats ETEC = Travelers Diarrhea
rarely ever. Enterotoxic Staph aureus = Proteinaceous Foods
Bacillus cereus = Reheated Rice, Buffets
Leukocytosis Giardia = Hiker Drinking Fresh Water
Invasive bacteria get into the mucosa which causes fever + Fever
leukocytosis. They destroy the endothelium and produce a Infectious Bloody Stool
bloody diarrhea with WBC in stool. This is easy to spot but may Diarrhea Watery Stool
be confused for one of the chronic diarrheas, as they can cause an Shigella = Hemolytic Uremic Syndrome
Salmonella = Raw Chicken/Eggs
inflammation as well. Lactoferrin is the most sensitive test. Invasive Amoeba histolytica = HIV/AIDS
Campylobacter = MC Bloody Diarrhea
Leukocytosis EHEC (0157:H7) = Uncooked Meat
Enterotoxic bacteria produce a compound that turns the
absorptive gut to a secretory gut. This may be in the form of an Bloody Stool
active toxin (vibrio) or a preformed toxin (staph). In any case, Abd Pain
theres no fever, leukocytosis, or blood but there is watery stool.
The history can alert and point to a specific agent; corresponding Diarrhea
antigens should be investigated (reheated rice, protein dip,
shellfish). However, because this person is pooping a lot right
now, theres little ability to trace their last 72 hrs of eating, Viral Yes No Investigation
presuming there was a preformed toxin somewhere in their Gastroenteritis?
history (its likely they will have risk factors for several Rehydrate
- Fever > 104o - Duration >3days (PO > IV)
organisms in any given 72 hr period). Since these are usually self-
- Severe Dehydration - Abd Pain Loperamide
limiting, treatment centers around hydration and loperamide. Be
- Blood, Pus - Antibiotics
cautious - do NOT give loperamide to diarrhea resulting from an
- Recent Travel - Hospitalization
invasive organism as it will make it worse!
C. difficile
C. diff is part of the normal gut flora. When exposed to
C. Diff NAAT
antibiotics, C diff wins and causes diarrhea. Its diagnosed with C. diff? C. diff
a C. diff NAAT (not toxin, not colonoscopy). There are two
presentations. The first is a watery diarrhea with a tell-tale C. diff MTZ or PO Vanc
smell. This is treated with oral medications. Oral metronidazole
is essentially equivocal to oral vancomycin, but metronidazole is Fecal Leukocytes
cheaper. For repeated recurrences use fidaxomicin. For Fecal Occult Blood
refractory cases a fecal transplant can be performed. The second
presentation is severe C. diff, presenting with toxic megacolon,
renal failure, and overt sepsis / shock. This person requires IV WBC Blood
metronidazole AND oral vancomycin. Non-Invasive Invasive

Hemolytic Uremic Syndrome

In the presence of anemia + worsening Cr + Bloody Diarrhea Ova + Parasites Stool Cx, Bx
dont assume the Cr is rising from dehydration. Suspicion of
Bx Bx
Shigella and the Shiga toxin must be high. If suspected, get a
O+P Cx Cx
serum shiga toxin assay and E.coli O157:H7 culture. Treatment
is with supportive care, dialysis, and plasma exchange.
Medications or Parasites Invasive Inflammatory
Enterotoxic Bacteria Bacteria Bowel
O+P Speciate Speciate 5-ASA compounds
and and and
Treat Treat Steroids

Gastroenterology [CHRONIC DIARRHEA]

Secretory vs Osmotic vs Inflammatory
Chronic diarrhea is persistent or recurrent symptoms for > 4 Secretory Osmotic Inflammatory
weeks; its usually the result of a chronic underlying condition. It Secretagogues: VIP, Absorption = Fat,
becomes initially important to differentiate pathologically and Gastrin, Toxins Protein, Osmolar Load,
Nrml Osmotic Gap Osmotic Gap Blood
clinically. The Osmotic Gap, Blood/Mucous, and Pattern of
Blood Mucous Blood Mucous Mucous
Bowel Habits provide clues to clinically separate the different
Nocturnal Sxs Nocturnal Sxs
types. Change with NPO Change with NPO
Normal Fecal Fat Fecal Fat
The Secretory type of diarrhea is caused by molecules that
transform the normal absorptive gut to a secretory one. This may
Measure Stool Osmoles Calculated Stool Osmoles = Osmotic Gap
be via hormones (VIPoma, Gastrinoma) or a persistent infection
(reported value) (Stool Na + Stool K) *2
(enterotoxins). It produces an enterotoxigenic picture: Normal
280 110 = 170, Osmotic
Osmotic Gap (not osmotic), no blood or mucous (not
280 278 = 2, Secretory
inflammatory), and because the toxin is already there, no changes
in BM after NPO.

The Osmotic diarrhea is caused by something being in the lumen Chronic Diarrhea Medications
that draws water out of the body and into the lumen. This is
usually a product of malabsorption (lactose, gluten, fat, protein).
There wont be an inflammatory picture (no blood or mucous), Laxatives Laxatives
Is it a classic cause
but something other than Na + K will make up the osmolarity of of chronic diarrhea?
stool, thus there will be an Osmotic Gap. Furthermore, tests Lactose Test Lactose Def.
will likely find Fecal Fat (a byproduct of malabsorption). If the
osmotic load is taken away (that is, go NPO), this diarrhea gets a
lot better. Infection
Stool Culture
Really Need W/U
The Inflammatory diarrhea looks like acute inflammatory
diarrhea: Blood and Mucous. But because it recurs, or has
been chronic, its likely due to a medical disease (like IBD). Stool Osmolar Gap
Fecal Fat
Specific Diseases within Chronic Diarrhea Fecal WBC
Osmotic diarrheas have been discussed in the malabsorption Fecal FOBT
syndromes lecture. Inflammatory diarrhea is discussed in the NPO
acute diarrhea (Bloody Diarrhea) and in the Inflammatory Bowel
Disease content (Crohns and UC). Lets cover some secretory
Normal Gap Gap Blood
diseases here.
Fat Fat WBC
Blood WBC w/ NPO
i. Gastrinoma Mucous
Change NPO
Persistent ulcers despite treatment with diarrhea raise suspicion
for Zollinger-Ellison syndrome and the presence of a gastrin-
producing tumor. First, measure a serum gastrin then allow for Secretory Osmotic Inflammatory
an increased gastrin on secretin stimulation. Do a CT scan or a
Hormone Levels EGD w/ Bx Colonoscopy
SRS (Somatostatin Receptor Scintillography) to find the tumor,
Colonoscopy Secretin Test
then resect (see GI Gastric Disorders).
Toxins Specific Tests
ii. VIPoma
Chronic diarrhea without a real presentation to go along with it.
High Serum VIP is sufficient for diagnosis. Resect it. VIPoma Celiac, Whipples, Crohns
Gastrinoma Tropical Sprue, Ulcerative Colitis
iii. Carcinoid Carcinoid Lactose Deficiency, Radiation Colitis
A tumor usually found in the small intestine that has no C. difficile Biliary /Pancreatic Diverticulitis
symptoms until it metastasizes to the liver. There, serotonin Insufficiency Invasive Infxn
enters the blood stream causing right heart failure, flushing, and (See Malabsorption) Ischemic Colitis
Diarrhea. Get a Urinary 5-HIAA to confirm the diagnosis and
resect (see GI Cancers).


Definition and Introduction Cirrhosis Etiologies = VW HAPPENS
A cirrhotic liver is one thats been annihilated, replaced by Viral Hep B/C
extensive fibrosis, and now has minimal regenerating nodules. Wilsons Eyes, Liver, Basal Ganglia (Cu)
Its the end-stage of liver disease - regardless of the etiology. It Hemochromatosis Bronze Diabetes (Fe)
Alpha-1 Anti-trypsin Emphysema and Cirrhosis
produces a number of complications that become targets of
therapy. Once cirrhotic, the only option is transplant. Knowing Primary Sclerosing Men with Crohns
etiology, presentation, and the unique considerations is key to Cholangitis
mastering cirrhosis. Primary Biliary Women, Autoimmune, AMA,
Cirrhosis Biliary Cirrhosis is for Bitches
Presentations and Labs Ethanol Drinkers
NASH/NAFLD Fat people
The liver does a lot of things. It clears bilirubin - failure causes
Something Rare
jaundice and sclera icterus. It produces bile - accumulation of
bile causes pruritus. It also produces coagulation factors - a Function Effect of Cirrhosis
deficiency produces bleeding. Because all blood flow from the Bilirubin Jaundice, Scleral Icterus, Dark Urine
visceral organs flows through the liver, a cirrhotic liver, like a Bile Pruritus
plug, resistance, which causes portal hypertension. This HTN Coagulation Bleeding = PT, PTT, INR (coags)
causes porto-caval shunting (hemorrhoids, caput medusa, Protein Hypoalbuminemia Ascites, Edema
esophageal varices) and transudation of fluid (ankle edema and Blood Flow Porto-caval shunt, Ascites
(Portal HTN) (hemorrhoids, caput, esophageal varices)
ascites). Ascites is exacerbated by a protein production
Estrogen Gynecomastia, Palmar Erythema
(hypoalbuminemia, Total protein ). Estrogen is degraded and Nitrogen Asterixis and AMS/Coma
converted to testosterone while estrogen excess produces
gynecomastia, palmar erythema, and spider angioma. Finally, **Also: Parotid Enlargement, Dupuytrens Contracture,
the liver controls ammonium metabolism. Excess ammonium clubbing, axillary hair loss**
can cause asterixis (flapping tremor) and encephalopathy. Get
an Ultrasound (1st, to identify cirrhosis), a CT /MRI to evaluate J = K (Part Pint) + (int art)
nodules or masses, and finally a biopsy (best) to confirm the
diagnosis and etiology. Acute hepatitis causes an elevation of
liver enzymes. A cirrhotic liver is burned out; the AST/ALT will
be low or smoldering just above elevated. The MELD score
(calculated using the bilirubin, INR, and creatinine) show how
sick a liver is. 1 is normal, 40 is death. Transplant workup starts Pint art int
at 15. Part

The full workup of a liver involves the LFTs (AST, ALT, Alk
Phos, Bili, TP, Albumin), Coagulation Factors, Ultrasound, CT Parterial int or K
scan, and Transjugular Biopsy. Portal HTN Related Non-Portal HTN Related
SAAG > 1.1 SAAG < 1.1
Ascites and SAAG Cirrhosis Cancer
Fluid in the abdomen (ascites) has multiple etiologies - one of R-sided CHF Peritoneal TB
Budd-Chiari Nephrotic Syndrome
which is cirrhosis. The patient will have flank dullness, a fluid
Portal/Splenic Thrombosis Protein-Losing Enteropathy
wave, and shifting dullness on physical exam. To detect fluid an Schistosomiasis Post-Op Lymphatic Leak
Ultrasound may be performed. Fluid may also be detected via Bowel Obstruction
CT/MRI (which helps with differentiation). What we worry
about is a 1st time presentation (etiology unknown) or a return Cirrhosis Na < 2g/day
customer with a fever or abdominal pain. For both cases do Ascites H2O < 2L/day
paracentesis first to get a SAAG score (Serum Albumin Therapy Diuresis with spironolactone 100, Lasix 40
Ascites Albumin) and an AFTP (cirrhosis vs cardiac ascites). If a Tap 4-6L off requires Albumin infusion
TIPS blood flow, NH4, Asterixis, AMS
SAAG is > 1.1 its from portal HTN (cirrhosis, R Heart Failure,
(should not be used for ascites)
Budd-Chiari). If a SAAG is < 1.1 its non-portal HTN related,
with risk of TB and malignancy. The result will direct the
workup. The goal is to treat the underlying causes. If secondary
to cirrhosis, treat is by restricting fluid + salt and supplementing
with diuretics. Everyone with ascites gets Na Intake (2g
max/day), limiting H2O (2L /day). Some people get


diuretics (high dose spironolactone and furosemide). To treat the
symptoms of distention, repeated therapeutic paracentesis can 1st Presentation OR Fever
be performed. A TIPS procedure can relieve ascites, but because ? Every Hospitalized Pt with Ascites
of the risk of hepatic encephalopathy its often avoided except in
treatment of refractory varices. Treatment or vaccination against Cx Polymicrobial
SBP TAP Secondary SBP
any Hepatitis virus is critical. The patient must stop drinking >250 PMNs >250 PMNs
alcohol. Finally, avoid NSAIDs, as they may GFR and Ceftriaxone Ceftriaxone
Diuresis. (FQ) Cx <250 PMNs +
Spontaneous Bacterial Peritonitis (SBP)
A whole bunch of fluid sitting in the abdomen is a nidus for PPX with FQ or Sterile
infection. So the first step is rule out infection - especially in a Bactrim DS
Treat Ascites Imaging + Ex-Lap
first time case or a return with fever. Do a paracentesis and get a
Laboratory Findings
cell count and Gram Stain / Culture / Sensitivity. The cutoff is AST/ALT Moderately Elevated in smoldering
250 cells; 250 neutrophils to diagnose SBP. No introduction site dz
may be present (why its called spontaneous) and its usually Normal or Low in cirrhosis
70% GNR (E. coli, Klebsiella), sometimes 30% GPC (Strep Alk Phos Moderately Elevated in smoldering
pneumo). Treat with ceftriaxone for double coverage dz
(fluoroquinolone ok if pen allergy) and prophylax with Normal or Low in cirrhosis
Coags INR deficiency of 2,7,9,10
fluoroquinolone. Since this disease can go from asymptomatic to
Platelets Thrombocytopenia most sensitive
fatal rather quickly, tap all hospitalized patients with ascites. The (CBC) test
MELD goes up, tap. The patient has a fever, tap. The patient has Total Protein Low Total Protein synthesis failure
pain, tap. Albumin Low Albumin synthesis failure
U/S Nodules, Vein Patency, Fatty Liver
If the tap is done and finds 250 polys, make the diagnosis of SBP. strongly indicative of cirrhosis or not
BUT, if the tap then comes back polymicrobial, it means the CT Scan Nodules, Masses, and Ascites, even
low amount undetected by U/S or
diagnosis is actually a secondary bacterial peritonitis (NOT
spontaneous) with inoculation from visceral organs. In this case Biopsy Definitive Diagnosis by histologic
its necessary to add metronidazole to ceftriaxone to cover confirmation, evidence of underlying
anaerobes. Go find the perforation with an Ex-Lap. The risk of etiology, specimen for analysis
SBP increases with a Total Protein < 1.0 in fluid, so put these
patients on prophylaxis. Varices HCC
Path: Portal-Caval Path: Cirrhosis
If they've had SBP they get fluoroquinolone prophylaxis. If they Esophagus Hep B
Pt Asx Screen Pt: ASx screen
havent had SBP, but total protein is <1.0, they get
Vigorous Bleed
fluoroquinolone prophylaxis. Dx: EGD Dx: U/S + AFP q6mo
Triple Phase CT
Other complications of Cirrhosis Tx: Banding (acute) Tx: Resection
Varices can bleed. Screen for them with an EGD. Use nadolol or Nadolol (chronic) Transplant
propranolol as an outpatient. If they bleed, they must be banded RFA, TACE
to stop the bleeding. Also give ceftriaxone and octreotide.

Hepatocellular Carcinoma is screened q6month. Obtaining a Hepatic Encephalopathy SBP

RUQ Ultrasound and AFP will likely alert/flag the potential Path: Ammonium Path: Strep
diagnosis. A triple phase CT scan is sufficient to diagnose HCC Gram Neg Rods
- no biopsy is needed. Pt: AMS Pt: Asx
Asterixis Fever, Abdo Pain
Hepatic Encephalopathy is treated with lactulose. A patient Dx: Clinical Dx: Paracentesis
> 250 Polys
with hepatic encephalopathy has altered mental status, asterixis,
Tx: Lactulose Tx: Ceftriaxone
and cirrhosis. Backup medications are rifaximin and zinc. Rifaximin
Hepatorenal syndrome is fatal. Treat a patient with renal failure PPx: FQ or TMP-SMX if
and cirrhosis by holding the diuretics, giving albumin and then SBP or TP < 1.0


Wilsons Disease (Cu) Cirrhosis Etiologies AST/ALT in the 1000s:
Wilsons is a genetic disease of copper excretion resulting from Viral Autoimmune Hepatitis
a defective transport in the biliary system. It prevents extrusion Wilsons Acetaminophen Toxicity
of copper, which results in copper retention. Copper gets Hemochromatosis Aflatoxin (rare)
Alpha-1 Anti trypsin Acute Viral Hepatitis (A, B)
deposited in the liver (cirrhosis), basal ganglia (chorea) and
Deficiency Shock Liver (hypotension)
eyes (the Kayser-Fleischer Rings). Copper studies will show a Primary Sclerosing Budd-Chiari
Serum Ceruloplasmin (its all bound up trying to decrease Cholangitis
the serum copper) and an Urine Copper. Serum copper is Primary Biliary
useless. Performing a slit-lamp exam on the eyes will show the Cirrhosis
rings and is diagnostic. Confirmation requires a Liver biopsy Ethanol
showing > 250ugCu/g Liver Dry Weight. The goal is to get the
Something Rare
copper out so use penicillamine to chelate Cu and excrete it in
the urine. Transplant is curative of cirrhosis and Wilson's.

Hemochromatosis (Fe) Patient has... Key Facts and Diagnosis

A disease of Iron Absorption. Theres no off signal and the Cirrhosis and A1-AT deficiency
gut absorbs all iron. The classic triad is Bronze Diabetes: COPD Get a biopsy = PAS + Macrophages
Cirrhosis, Diabetes, and Hyperpigmentation. While a Cirrhosis, Hemochromatosis
transferrin (>60% men, >50% women) is most sensitive, its Diabetes, Get a ferritin (very high) or transferrin
common to start the diagnosis with Ferritin (very elevated) and Tan Skin then get a biopsy
Transplant cures the cirrhosis, not the
confirm it with a liver biopsy. The goal is to eliminate iron so
chelate it with deferoxamine or serial phlebotomy titrating to Cirrhosis, Wilson's Disease
an Fe sat <30 or ferritin < 50. Transplant cures the cirrhosis but Chorea, and Start with a slit lamp (Kayser-Fleischer)
not the Hemochromatosis. "Black Liver on MRI." the "eye" Do NOT get Serum Copper - this is wrong
Either ceruloplasmin or urine copper
1-Antitrypsin Deficiency Transplant cures cirrhosis and disease
These patients have a mutation in a protease inhibitor that Cirrhosis and Primary Sclerosing Cholangitis
Inflammatory Start with an MRCP
prevents release of 1-AT from the liver. It results in junk
Bower Biopsy / ERCP is NOT needed
accumulating in the liver (cirrhosis) and overactive elastase in Disease Do NOT STENT - ursodeoxycholic acid
the lungs (emphysema). To confirm, take a biopsy and see the Can recur in transplant
PAS Hepatocytes or do PCR + phenotyping. PiZZ is the Cirrhosis and Alcoholic cirrhosis
worst phenotype, while PiMM is normal. Since the problem is alcohol Stop drinking alcohol
with the liver a transplant is curative. 1-AT replacements consumption Transplant curative
will help the emphysema but not with the cirrhosis. Cirrhosis and Viral hepatitis
positive Treat Hep B, Treat Hep C
serology Vaccinate against A and B
Primary Sclerosing Cholangitis Cirrhosis and NASH
An autoimmune disease that affects males and causes fibrosis a long list Diagnosis of exclusion
of extrahepatic ducts (macroductal disease). Theres a high ensuring Treat symptoms and transplant
association with Ulcerative Colitis. It presents with an everything is
obstructive picture of the biliary system that may involve the negative
pancreas. Screen suspected patients with an ANCA. The MRCP
is essentially diagnostic, showing a beads on a string pattern.
Serology Diagnosis on the TEST
ERCP and biopsy is NOT required, but will show onion-skin
fibrosis if performed. Do NOT place a stent to alleviate
obstruction (it just makes transplant harder) though symptoms ANA Nothing... Dont be fooled
should be treated with cholestyramine or ursodeoxycholic acid. Ceruloplasmin Decreased in Wilson's Disease
Ferritin Elevated in Hemochromatosis
Primary Biliary Cirrhosis Hep B, Hep C Viral Hepatitis
An autoimmune disease that affects females and causes Smooth Autoimmune Hepatitis
fibrosis of intrahepatic ducts (microductal disease). Since these
Anti-LKM Autoimmune Hepatitis
are small structures MRCP will look normal. Patients are
otherwise asymptomatic young women with cirrhosis. Screen EtoH cirrhosis and NASH are essentially diagnoses of
with an AMA, confirm with a biopsy. Immunosuppression to exclusion. Viral hepatitis has a positive serology.
start, then transplant - though it may recur even after transplant.

Gastroenterology [COLON CANCER]

Pathogenesis Disease Presentation Pathology Treatment
Colon cancer is typically a disease of > 50 yr olds thats a Familial 1000 polyps by 18, APC gene PPX
progression of either genetic errors (see the chart to the right) or Adenomatous Cancer by 40, Mutation Colectomy
long term inflammation (Crohns, UC) into cancerous growth. Polyposis Death by 50
The mechanism is important, but theres loss of the APC, ATM,
Hereditary 3 family members DNA Screening
and p53 genes - in that order - that eventually turns a Nonpolyposis 2 generations Mismatch Start at 20.
premalignant polyp into an invasive carcinoma. The process Colorectal 1 under 50 Repair Or 10 years
(polyp Cancer) occurs over 3-7 yrs. Cancer Colon Cancer AND prior to
(HNCC) reproductive organs first CRC.
Patient Turcot GI tumors and Brain Tumors Turcot, Turban (head)
Gardner GI Tumors + Jaw Tumors
The initial presentation can be highly variable. The best way to
Peutz-Jeghers Nonmalignant polyps and hyperpigmented buccal
discover colon cancer is with appropriate screening (see next mucosa + small intestine tumors (hamartomas)
section). Think colon cancer if you see any of these three
presentations. 1 A post-menopausal female or any male with Iron
Deficiency Anemia, 2 alternating bowel habits (diarrhea and Asx Screen
constipation) with change in the caliber of their stool (generally
to "pencil thin"), or finally, there may be nothing to tip you off -
Colonoscopy Low Risk
the initial presentation is 3 a metastasis to the liver or lung.
Colonoscopy q10y
Polyps + FOBT q1y
Colonoscopy is the golden standard done q10y unless Precancer
abnormalities are found, at which the frequency is increased. This
will identify adenomatous polyps which will be removed and Ca Noninvasive
analyzed. Sessile, Villous polyps have an increased risk of Curative Biopsy Curative
malignant transformation, while pedunculated, tubular polyps Colonoscopy q5y + Colonoscopy q5y +
have a lower risk. Colonoscopy is required in order to visualize FOBT q1y FOBT q1y
the entire colon because only 50% of polyps are Left sided Cancer
(opposed to rigid sigmoidoscopy). In communities where
colonoscopy isnt available screening with FOBTx3 annually or Mets Mets
FOBT q3 yrs with Flex Sig q5yrs is also appropriate. Barium Stage I / II Stage > Stage III
Nodes Nodes
Enema is NOW NEVER the right answer as it only detects colon Resection FOLFOX
cancer at > Stage III disease (incurable with resection). If either (Chemo)
the barium enema or the flex sig are positive a colonoscopy must
be done anyways to get a biopsy.
In someone with severe disease all thats necessary is a barium
enema to reveal the apple core lesion (dont do it, but still a test
question because of the radiograph). The best test is colonoscopy. Mega Mega Mega Mega
If theres invasive disease a metastatic workup (CT
q10y q5-10y q1-3y Q2-6
chest/abdomen/pelvis) is required for staging. Intraoperative
1-2 polyps > 3 polyps month
staging can be performed. Disease regression or relapse is > 1cm
< 1cm
followed by the CEA levels its never diagnostic. Tubular Villous
Low-Grade High-Grade
This is dependent on staging. If theres extracolonic
involvement (Lymph Nodes or Mets) the treatment is FOLFOX
(5-Fu + Leucovorin + Oxaliplatin) or FOLFIRI. Recently added
to improve remission is Bevacizumab, a VEGF Inhibitor. If
theres no extracolonic involvement a simple resection is Small (<2cm)
Pedunculated Large (>2cm),
Tubular Sessile,

Low Risk Polyp High Risk Polyp


Diverticulosis is the actual pocket - the physical outpouching of
the colon caused by luminal pressure inside it. Its typically
the result of a diet rich in red meat and deficient in fiber.
Repeated constipation causes the colon to contract against hard
stool, resulting in pressures and eventually outpocketing of the
colonic mucosa. Its a very common condition in the United
States thats asymptomatic and often an incidental finding on
routine screen. By eating a higher fiber diet and reducing red meat Diverticuli. The normal colon (left) generates intraluminal
the disease and its complications (conditions listed below) can
pressures (the arrows) as a result of low fiber and chronic
be prevented. Diverticuli are typically a disease of the elderly (> constipation. At select locations, the wall of the colon
50 yo). They occur more often on the left than the right because
protrudes, stretching the mucosa (right)
stool is harder on the left. They can be an incidental finding on
CT scan, but are definitely diagnosed by colonoscopy. Spasm:
Px: Diverticulosis + Continued Poor Diet
Diverticular Spasm = Symptomatic uncomplicated Diverticulosis Pt: Elderly pt + LLQ post prandial pain
This is caused by a spasm of the diverticulum - especially when relieve with BM
diet hasnt been changed. It will present as an LLQ post- Dx: Clinical, Severe disease r/o
prandial pain thats relieved by a bowel movement. The Tx: High Fiber Diet
question stem will read like IBS but in an elderly patient. Its
treated with a high fiber diet to prevent future spasms.
Diverticular Hemorrhage Px: Arteriole at the dome of diverticuli tears
An arteriole in the dome of the diverticulum gets stretched, tears, Pt: Elderly bright red bleed from rectum
and bleeds. This presents as a brisk, painless bleeding per Dx: (1) r/o UGIB w/ NGT + EGD
rectum. It isnt the FOBT of Iron Deficiency Anemia slow bleed (2) Colonoscopy ( Bleeding)
its a severe GI bleed with rapid blood loss. Itll be diagnosed Arteriogram (Brisk Bleeding)
by first ruling out an upper GI Bleed (NG Tube / EGD) and found Tagged RBC (Slow Bleeding)
either on colonoscopy, tagged RBC scan, or Angiogram (see GI Tx: Embolization, Cautery, Resection
Bleeding for details). Diverticuli bleed from the right colon more
often than the left (but diverticula occur on the left more than on
the right). Fecalith, obstruction,
Px: Diverticulitis + Fecalith + Perforation
infxn, inflammation
Pt: LLQ Pain in an elderly pt w/ acute onset
and mild to severe fever + leukocytosis
Diverticulitis has a similar pathogenesis and presentation as a
Dx: (1) r/o Perforation/Ileus with KUB
Left Sided Appendicitis of the elderly. A fecalith forms across
(2) CT Scan for severity
a diverticulum causing obstruction, inflammation, and the
(3) Avoid Colonoscopy
compromise of the blood supply to the diverticulum. This results
Tx: Mild = PO FQ + MTZ + Liquid Diet
in infection, inflammation, and perforation. The presentation is
Severe = NPO, IVF, IV Abx
highly variable - from a mild inflammation (low fever, mild
Abscess = Drainage
leukocytosis, and abdominal tenderness) to florid peritonitis or Perforation, Refractory = Colectomy
perforation (high fever, massive leukocytosis, rebound,
guarding). Diagnosis is made by first ruling out a surgical
emergency with a KUB to ensure no free air or ileus, then via a LLQ Abd Pain
CT scan to identify the extent of the disease. Avoid Colonoscopy
until 2-6 wks after acute disease has resolved (to minimize the Free Air Air-Fluid Levels
risk of perforation). Treatment is dependent on the severity. Mild Perforation KUB Obstruction
Dz is treated with oral antibiotics and adequate bowel rest (liquid Surgery Surgery
diet only). In more severe disease use NPO, IVF, and IV
Antibiotics. Multiple combinations are acceptable as long as they
get gram negatives and anaerobes (Ampicillin-Gentamicin and
Mild CT Scan Abscess
Metronidazole, Ciprofloxacin and metronidazole, OR
Mild Dz Severe Abscess
pip/tazo). If theres an abscess on the CT it needs to be drained.
Finally, colectomy is indicated in severe or refractory disease. Liquid Diet Severe Dz NPO, IV
Amp-Gen + MTZ
Cipro + MTZ

Gastroenterology [ESOPHAGITIS]

If a patient presents with Odynophagia, dysphagia, or chest Causes of Esophagitis = Piece of the Esophagus
pain, one consideration should be an inflammation of the Pill Induced NSAIDs, Abx, NRT
esophagus. Infectious HIV, CMV, Herpes, Candida
Eosinophilic Asthma, Eczema, Food Allergy
Pill-Induced Esophagitis Caustic Alkali (Drain Cleaner), Acid
Prolonged direct exposure of the esophagus mucosa cause erosive Everything else GERD, Rare causes
esophageal ulcerations. Some drugs are notorious: NSAIDs,
Anti-retrovirals, and Antibiotics (Doxycycline, Clindamycin,
Sulfamethoxazole/Trimethoprim aka Bactrim) - especially the
cheaper, non-enteric coated pills. Because its a direct result of
constant exposure, patients should take pills with 4oz H2O and
while erect and upright. After exposure occurs endoscopy can
reveal and allow removal of the tablet or pill, but it takes time to
heal after pill removal.

Infectious Esophagitis Bug Finding Treatment

Infections of the esophagus arent common. The patient must Candida Thrush Nystatin and Fluconazole
have a risk factor that makes them immuno-suppressed such as: Herpes Oral Ulcers (Val)Acyclovir or Foscarnet
organ transplant, leukemia or lymphoma, steroids, or HIV/AIDS. CMV - (Val)Ganciclovir or Foscarnet
Concurrently, theyll get opportunistic infections like candida,
HSV, and CMV. While an Endoscopy with Biopsy is needed to
get a definitive diagnosis, certain physical findings can enhance
the chances of pre-procedural diagnosis. Oral ulcers (herpes
labialis) are linked to Herpes while thrush is associated with
Candida. Treatment for the infections is dependent on the
infectious agent (see the chart to the right).

Eosinophilic Esophagitis
This is an allergic reaction in the esophagus. Look for the history
of Asthma, Atopy, and Allergies with Esophagitis. Get an
endoscopy with biopsy showing eosinophilia (>15/hpf). Even if
you see the eosinophils, treat it like GERD with PPI. If PPI fails,
then use swallowed aerosolized steroids.

Caustic Esophagitis
Diagnosis Review
Caustic Esophagitis is covered in detail in the toxic exposure Pill Induced Pt: NSAIDs, NRTs, Abx (clinda, doxy, Bactrim)
lecture (in surgery trauma), so the review will be brief here. Either Dx: Endoscopy
accidently (children) or purposefully (adult suicide) drinking Tx: Pill removal, time, PPIs for comfort
caustic substances (i.e. alkali-like lye, drain cleaner, or any acid) PPx: Enteric Coating, Erect Ingestion, 4oz H20
ruins the esophagus. The burning of the esophagus produces chest Infectious Pt: Immunocompromised, Thrush, Ulcers
pain + odynophagia, leading to the avoidance of swallowing, Dx: Endoscopy with Biopsy
Tx: Cause dependent, Antifungal, Antiviral
resulting in drooling. Burning of the larynx causes stridor or
Eosinophilic Pt: Child with Asthma, Eczema, Odynophagia
wheezing. The first thing to remember is that one should NEVER Dx: Endoscopy with Bx shows Eosinophilia
induce vomiting to expel a caustic ingestion. An endoscopy is Tx: Remove foods then reintroduce, PPIs
done within 24 hrs to evaluate the severity. Low Severity (edema, Caustic Pt: Children (accident) Adult (suicide)
erythema, shallow ulcers) can be moved from liquid to solid diet ingestion of caustic alkali or acid,
in the first 24-48 hrs. High severity (deep ulcers, circumferential presenting with drooling, odynophagia
Dx: endoscopy within 24 hrs
burns, black necrosis) has a high incidence of perforation,
Tx: High Severity: NPO x 72 hrs (risk perf)
bleeding, strictures, and fistulas so must remain NPO for 72 hrs, Low Severity: Liquid Solid w/i 48 hrs
with constant monitoring for the development of complications. Everything Consider GERD, cancer, other
70% develop strictures while 2-3% develop cancer (surveillance Else mechanical/motility disorders
required 15-20 years later).

Gastroenterology [ESOPHAGUS]
Solid then Liquid Solid and Liquid
Introduction Progressive Progressive
The purpose of the esophagus is to carry food from the mouth to the
stomach - AKA swallowing. So its no surprise that disorders of the Mechanical Motility
esophagus present as dysphagia (difficulty swallowing) or (Obstructive) (Functional)
odynophagia (pain on swallowing). An important initial step is to
separate the motility/functional dysphagia from the
mechanical/obstructive dysphagia. The former is dysphagia to
everything at once, while the latter is dysphagia progressive from Rings Stricture Cancer Achalasia Scleroderma Spasm
foods to liquids.
1st: Barium Swallow 1st: Barium Swallow
MOTILITY Best: EGD w/ Bx Then: Manometry
Achalasia Best: EGD w/ Bx
This is a failure of the LES to relax and presents as dysphagia to
solids and liquids. Food enters the esophagus, moves just fine to the Dilated
stomach, but cant fit through a tightened LES. Patients describe a Esophagus
knot or ball of food behind their sternum along with dysphagia. A Esophageal
Tightened Activity
diagnosis can be made on barium swallow, demonstrating a birds
beak. Its confirmed with a manometry that shows hyperactive
contraction and inactivity of the rest of the esophagus. An EGD Sustained LES
must be done to rule out cancer (pseudoachalasia) and to reveal the Contraction
absent myenteric plexus. For treatment, the LES has to be opened. Achalasia depiction and manometry studies. LES contracts
Botulinum must be repeated and is used for poor surgical as normal but cannot relax, producing sustained
candidates. Dilation carries perforation risk. The preferred contraction.
treatment is myotomy.

Scleroderma is an autoimmune disorder of collagen deposition.
Whether CREST or Systemic Sclerosis, collagen in the esophagus
means the LES cannot contract. The patient will present with
relentless GERD. A definitive diagnosis is made with manometry
showing a relaxed esophagus ( tone) and pressure in the LES.
Treat symptomatically with PPIs.
Scleroderma depiction and manometry studies. LES is
persistently relaxed permitting regurgitation of acid
Esophageal Spasm
contents. LES has no activity at all.
This looks like an MI at first glance. It presents with a crushing,
retrosternal chest pain thats relieved with nitrates but isnt an MI.
On first presentation, rule out MI with ECG and troponins.
Thereafter, esophageal spasm is diagnosed by manometry showing
erratic, diffuse spasm unrelated to eating, drinking, or position. A
barium swallow done at the time of pain may show multiple
regions of spasm, the corkscrew esophagus (though it will be
normal if not experiencing pain). Treat this with Calcium Channel
Blockers or Nitroglycerin as needed.
Esophageal Spasm depiction and manometry. Diffuse,
MECHANICAL uncoordinated, painful contractions of the esophagus.
Schatzki Ring
A fibrous ring located at the LES causes only large diameter Ring occludes lumen
foods to get stuck. This will be a very episodic (months in between) New Lumen is smaller
dysphagia with odynophagia. Since most food is cut or chewed
well theyll get by the ring. Only once every so often does the food Steakhouse Dysphagia
get stuck - hence episodic. A barium swallow will show a
narrowed lumen and an EGD will yield definitive diagnosis with
visualization and biopsy. Breaking the ring will alleviate symptoms.
Pl Schatzki Ring depiction. Only once in a while does large
caliber food get stuck. Thus, it is the critical diameter food
that makes this disease

Gastroenterology [ESOPHAGUS]

Plummer-Vinson Syndrome New Lumen
Esophageal Rings + Esophageal Webs + Iron Deficiency
Anemia, typically in a woman, is Plummer-Vinson. Note that these
patients have a special type of ring located in the upper esophagus.
They also have an risk of squamous cell carcinoma of the
esophagus. Theres no treatment but the patient needs screening
EGDs to screen for cancer. Prophylactic esophagectomy is NOT Esophageal Webs side view and cross-section. Webs can
indicated. occur anywhere in the esophagus. They stay within the
lumen, and can be of any size
Stricture New Lumen
Potential consequences of long-standing GERD is Barretts and Circumferential Scar
Cancer. Another, considered grade 4 GERD, is a stricture. So
much inflammation over such a long period causes scarring.
Another cause of stricture is caustic ingestion (harsh acid or base). GERD
The scarring enters the lumen. This is a progressive history of
GERD or remote history of ingestion followed by motility
dysphagia. There may be weight loss (b/c they cant eat as much,
distracting you towards cancer). Diagnosis is initially made with a
barium swallow then confirmed by EGD with Biopsy for
definitive diagnosis. Treatment is the aggressive management of Stricture side view and cross-section. GERD causes
GERD (high dose PPI) and resection of the stricture. stricture at lower esophagus, ingestion can be anywhere,
usually at entrance. Scar is circumferential with a new,
Cancer smaller lumen in the center
Cancer presents as progressive weight loss and progressive
Fungating Mass
dysphagia in an older person with GERD (adenocarcinoma) or in
New Lumen
a smoker/EtOH (squamous cell). Theres often an associated
weight loss. Progressive = obstructive, weight loss = cancer, risk
factors = which cancer. A barium swallow is done first to identify
the area of the lesion and to rule out cancer high in the esophagus
(which might perforate if an EGD is done first). Follow up the
swallow with an EGD and Bx. If positive, stage with a (PET)CT.
Resection and chemo is the treatment as most of the cancers are Cancer side view and cross-section. GERD causes
invasive at the time of diagnosis. Because acid refluxed from the adenocarcinoma in the distal esophagus. Toxic exposure
stomach into the bottom of the stomach, adenocarcinoma is at the causes sqaumous cell in the proximal esophagus. Fungating
1/3 of the esophagus. Because smoke and hot drinks enter at the mass eats into the lumen from a single focus, new lumen is
top of the esophagus, squamous cell is at the 1/3. oddly shaped. This tumor is depicted as having invaded the
wall of the esophagus.
In a really old guy with bad breath who has trouble eating Zenkers. False lumen with an
(coughing + gurgling at the start of eating) suspect a Zenkers undigested stick figure in it. This
diverticulum. The diagnosis is sealed if the patient regurgitates figure will leap out at night onto the
undigested food days after eating it. The diverticulum is a false pillow. It will first make this old mans
diverticulum caused by decades of pressure. Do a barium breath smell terrible and itll be hard
swallow to identify and an EGD if need be. Treat with resection. for him to eat.

Disease Presentation Classic Sxs 1st Test Best Test Treatment

Achalasia Motility Knot or Ball of Food at esophagus Manometry Dilation, Botox, Myotomy
Scleroderma Motility CREST, Female GERD tx, cure
Esophageal Spasm Motility CP better with Nitro, CCB NTG, CCB prn
Schatzki Ring Mechanical Episodic to Large caliber foods Resection
Plummer Vinson Mechanical Iron Def Anemia, Webs, Female , Monitor for Cancer
Stricture Mechanical GERD with Weight Loss or Resection
h/o Caustic Ingestion EGD Bx
Zenkers Mechanical Old Man, Halitosis, regurgitation Resection
Cancer Mechanical GERD Weight Loss Resection
Or + Chemo
Smoking + EtOH

Gastroenterology [GALLBLADDER DISEASE]

Gall Stones
There are two major types of stones. Cholesterol Stones are
caused by cholesterol and appear green. The person who is at risk
for these types of stones are the 5 Fs: Fat, Female, Forty, Fertile,
and Native American (ok, so that last one wasnt an F). The other
stone is Pigment Stones caused by hemolytic disease. Theyre
black in color and coincidentally occur in African Americans
more often. In reality, most people have a combination, called
mixed stones.

When the gallbladder contracts against these stones, it hurts.
Cholelithiasis is simply the presence of stones in the gallbladder.
Theres no obstruction, inflammation, or risk of death just pain.
Gallstones will present with a Colicky RUQ Pain that radiates
to the shoulder made worse by fatty foods. Eating, and fatty
foods in particular, cause the gallbladder to contract. Most people
who have gallstones are asymptomatic and dont require
prophylactic cholecystectomy. Better diet, exercise, and
cholesterol can prevent the stones from becoming symptomatic.
Symptoms arise at a rate of about 30% every 2 years. Diagnosis Normal Anatomy of the Asx Gallstones present,
is made with the RUQ U/S showing stones in the gallbladder. Hepatobiliary system without obstruction
Treat with cholecystectomy (surgery) or ursodeoxycholic acid
for non-surgical candidates.

When a gallstone gets stuck in the cystic duct an inflammatory
process develops in the gallbladder. This shifts from the colicky
abdominal pain to a constant RUQ pain. As the name implies, -
itis means inflammation, and so the pain is often accompanied
by a mild fever and mild leukocytosis. Murphys Sign is positive
(this test is better when performed with an ultrasound probe over
Neg Dz Pos Dz
the gallbladder). Diagnose with an ultrasound (pericholecystic
fluid, gallstones, and gallbladder thickening). If the U/S is

equivocal, use a HIDA scan. Upon diagnosis NPO, Intravenous
Fluids, and IV antibiotics are started. The goal is urgent Acute Cholecystitis. Gallstone HIDA scan. Normal on left has
cholecystectomy (within 72 hours). Waiting only worsens lodges in Cystic Duct, inducing tracer throughout biliary system.
outcomes. Cholecystostomy (a tube) is possible for poor surgical Inflammation of the Gallbladder. Obstruction on right prevents filling
candidates, but its rarely the answer on the test. No hepatic/pancreatic of the gallbladder. Positive study.
involvement There is involvement

Dz Path Pt Dx Tx
Stones Cholesterol = the Fs ASX U/S, Diagnosis not required None
(Lithiasis) Pigmented = Hemolysis
Cholecystitis Cystic Duct Obstruction RUQ Pain, Murphys Sign U/S HIDA Urgent
mild fever , mild leukocytosis Cholecystectomy
Choledocholithiasis Common Bile Duct Obstruction RUQ Pain, Murphys Sign + U/S HIDA ERCP,
(koh-lee-doh-koh) = Hepatitis and/or Pancreatitis AST/ALT, Lipase/Amylase mild fever, mild leukocytosis Cholecystectomy
Ascending All of the above PLUS RUQ Pain, Murphys Sign + U/S HIDA ERCP Emergent,
Cholangitis Infection behind the stone Labs, T >104, Leukocytosis severe fever and leukocytosis Cholecystectomy


Gastroenterology [GALLBLADDER DISEASE]

A stone in the common bile duct has a number of potential
consequences. The first, painful jaundice is classic for gallstone
obstruction of the biliary tree. Depending on the severity and
location of the stone, stones in the biliary tree can lead to hepatitis
or pancreatitis. Gallstone pancreatitis is the second most common
cause of pancreatitis in the US. Theres often (but need not be)
mild inflammation, presenting with low-grade fevers and mild
leukocytosis in addition to the symptoms of the associated organs

- Hepatic obstruction = pruritus, jaundice, and LFTs.

Choledocholithiasis. Obstruction of Choledocholethiasis. Obstruction
- Pancreatic obstruction = Pain, N/V, Amylase, Lipase
common duct proximal to pancreas. of common duct distal to pancreas.
Pancreas not involved, liver is. Both involved. AST/ALT, Cong
Diagnosis begins with RUQ U/S which should show dilated
AST/ALT, Cong Bili Bili, Amylase, Lipase
ducts. If the ducts arent dilated, but Choledocholithiasis is
suspected, do an MRCP.

Treatment is with ERCP and stone retrieval. Prophylactic

antibiotics awaiting the procedure are generally recommended,
sticking with the NPO, IVF, IV abx theme for acute disease.
Eventually a cholecystectomy should be performed, but this can
be done in the urgent to elective period if an ERCP is done.

Ascending Cholangitis
Ascending Cholangitis
Bile stasis is a nidus for infection. Most infections of the biliary
Choledocholithiasis + Infxn Proximal to
tree (except when surgical intervention has been performed) will
obstruction. Chills, High Fever, Severe
be isolated to gut flora: E. coli, Klebsiella, or Enterobacter.
These are gram negative organisms and can present with quite a
sick patient. The combination of Painful Jaundice + High Fever >
Charcots Triad (Cholangitis):
104 F is Charcots Triad (RUQ pain, Jaundice, Fever). If the
1) RUQ Pain
patient has also hypotension and altered mental status, then
2) Fever
they have Reynolds Pentad. Immediate resuscitation with IV
3) Jaundice
Abx + IVF + NPO should be performed. Diagnosis can be
facilitated by Ultrasound showing dilated ducts. The patient
Reynolds Pentad (Cholangitis):
must receive emergency ERCP to remove the stone and allow
1-3) Charcots Triad
biliary flow. Cholecystectomy can be performed once the patient
4) Hypotension
recovers from their severe illness.
5) AMS

Antibiotic Choice
The organisms of the biliary tree are the organisms of the GI tract
- primarily Gram Negative Rods and Anaerobes. Multiple
regimens exist. Ciprofloxacin + Metronidazole, Ampicillin-
Gentamycin + Metronidazole, and Pip/Tazo are appropriate.
Particularly, Pip/Tazo is correct if skin flora must be considered;
its wrong if considering only GI bugs.


Gastroenterology [GERD]

Gastroesophageal Reflux Disease
GERD is a common disorder of the esophagus that results in
esophagitis. A weakened Lower esophageal sphincter (LES)
allows gastric acid to regurgitate and burn the distal esophagus.

There are two types of symptoms. 1) Typical (Intestinal)

symptoms are a product of acid regurgitation in the esophagus. It
predominates with a retrosternal burning chest pain thats worse
with spicy foods and recumbency, better with sitting up,
antacids, and cold water. 2) Atypical (extra-intestinal)
symptoms are a product of acidic damage to the proximal
esophagus and airways. In this variant hoarseness, cough, and
nocturnal asthma predominate in symptoms.

The first diagnostic step depends on symptoms. If there are no

alarm symptoms then the first test is treat with a PPI and
lifestyle x 6 weeks. Lifestyle modifications are variable and have
mixed benefit; initial therapy must include a PPI. Lifestyle
modifications include 1) avoiding food hours before recumbency,
2) small meals, 3) elevating the head of the bed, 4) avoidance of
LES dilators: alcohol, smoking, peppermint, and chocolate. If
there are any alarm symptoms on presentation OR PPIs fail to
resolve the disease, the next necessary step is endoscopy with
biopsy. Endoscopy allows assessment of severity of the
esophagitis (Grade 1 4), evaluation for ulceration, and enables GERD PPI
us to rule out Barretts and Cancer. The best test is 24-hour pH Barretts High Dose PPI
monitoring, though it is rarely performed. If surgical intervention Dysplasia Ablation
is required for GERD, this test (as well as manometry) should be Adenocarcinoma Resection

The treatment of the disorder is based on the endoscopic findings.

GERD is treated with the lowest dose of PPI possible and Metaplasia Dysplasia
patients may come off the PPI. (Esophagus Duodenum) (Metaplasia Cancer)

GERD Barretts Adenocarcinoma

Metaplasia (Barretts) esophagus is identified on endoscopy as
salmon-colored mucosa and confirmed on biopsy as intestinal Lifestyle + High Dose PPI Resection +
metaplasia (the esophagus changes to the duodenum). This is PPI Chemo
treated with high-dose PPIs. Annual EGD surveillance is
required given the increased risk of adenocarcinoma in Barretts
Esophagus. It can then be spaced out to q3yrs if stable.

Dysplasia is nearing malignancy and treated with local ablative

therapies. The method is up to the provider: cryoablation, laser
ablation, or radiofrequency ablation. This requires more frequent
EGD surveillance than Metaplasia. The severity of the dysplasia
determines the surveillance rate.

Adenocarcinoma is treated with staging and resection vs chemo

and radiation.

If a patient cant tolerate PPIs or doesnt wish to take medications

for life, the Nissen Fundoplication can be performed. Be
cautious as this may result in Achalasia if the wrap is made too

Gastroenterology [GI BLEED]

Upper vs Lower Etiologies and Characteristic Findings
GI bleeding has a wide variety of differential diagnoses and
potential workups. One of the fundamental determinations is UPPER GI BLEED LOWER GI BLEED
Upper (proximal to the ligament of Treitz) versus Lower (distal Ligament of Treitz Ligament of Treitz
Hematemesis and Melena Hematochezia and
to the Ligament of Treitz) Bleed. While no single finding on
N/V Diarrhea
history or physical definitively determines the location, there are 66% of all GI Bleeding FOBT
findings that are more suggestive of one versus the other. 33% of all GI Bleeding
Hematemesis is vomiting blood. The blood must be near the in CAUSES UGIB CAUSES LGIB
hole for it to come back out. Melena is dark tarry stools Oropharyngeal Bleed Diverticular Hemorrhage
indicative of long-standing blood in the GI tract. Nausea, Epistaxis Angiodysplasia
Vomiting, Hematemesis, and Melena are all indicative of an Erosive Esophagitis Colitis
Gastritis or Ulcer Anorectal / Hemorrhoids
Upper GI bleed. Meanwhile, diarrhea, FOBT , and
Varices Polyps
Hematochezia (bright red blood per rectum) are indicative of a Mallory-Weiss / Neoplasm
lower GI bleed. Boerhaave
Dieulafoys Lesion
Initial Management Neoplasm
Determining stability is the 1st order of business; make the things
that will keep the patient alive the priority. Obtaining 2 large bore GI BLEED
IVs, Type + Cross, and CBC are essential. Transfusions may be
required for absolute anemia (Hgb < 7) or symptomatic anemia at 1) Stabilize the
any Hgb. PT/PTT determines if theres a clotting/bleeding Patient
problem or if FFP is required. Finally, EKGs will rule out risk
for mesenteric ischemia. 2 Large Bore IVs
IVF, Type and Cross,
Work-Up = Find the Bleed Blood Prn, Coags/FFP
The simplest test one can do is to place an NG Tube. If the fluid
is green the samples been taken from the stomach and the
duodenum and has effectively ruled out Upper GI bleed. 2) Determine if the
Alternatively, if frank blood or coffee grounds were found its bleeding is UGIB or not
highly suspicious for UGIB. Since blood tends to flow
downstream an Endoscopy is the best test for UGIB. Itll help
identify lesions that are currently bleeding (+ propose a therapy).
for Blood for Blood
If the NG is negative do an EGD in almost all cases. The next LGIB UGIB
step is to move to the colon. Here, the decisions based on if Varices
theres a lot of bleeding (Brisk Bleeding is >2cc/hr or 1Unit AVM
pRBC q4H), slow bleeding (<0.5cc/hr or 1Unit pRBC q1day), Boerhaave
CBC + Endoscopy Gastritis
or no bleeding (none). The idea is since blood is moving
Transfusion Rate Mallory Weiss
downstream, attempting a colonoscopy with brisk bleeding will Aortoenteric Fistula
just visualize a river of blood coming at you (not very useful), Neoplasm
while trying to find the source of a very slow bleed with an <0.5cc/min Dieulafoys
angiogram might not show anything. A tagged RBC study can > q1d 1UpRBC >2cc/min
find the source of the bleed - especially in locations where the Slow H/H > q4H 1UpRBC
colonoscopy cant reach - but is unable to offer any intervention. Rapid H/H
A pill cam is the last resort; its notoriously unsuccessful for Slow Bleed Brisk Bleed
finding a bleed. In general, testing goes like this:
1) Brisk Bleed Angiogram = Possible intervention Colonoscopy Arteriogram
2) Slow Bleed Tagged RBC = Localization only
3) No Bleeding Colonoscopy = Definitive diagnosis
Locate, Diagnose,
Colonic Small Intestine Cauterize/Embolize

Tagged RBC
Colitis Neoplasms
Pill-Cam Endoscopy
Hemorrhoids Diverticular

Gastroenterology [GI BLEED]

Etiologies Management f) Gastritis/Ulcers
NSAIDs (multiple shallow ulcers), Malignant (heaped up
a) Esophageal Varices margins, necrotic core), or Acid-Induced ulcers may erode
Caused by Portal HTN secondary to liver failure, portosystemic into blood vessels or perforate. Diagnose with EGD and treat
shunts form and these veins become engorged. Vomiting or with PPIs or resection. See Gastric Disorders.
retching causes them to bleed, which is NOT self-limiting and
may be fatal. The patient is NG Tube , Hematemesis , and g) Colitis
the EGD shows the definitive diagnosis. In a patient bleeding Ulcerative Colitis, in particular, may present as a bloody
right now with known variceal bleeding, give octreotide. With diarrhea diagnosed by EGD with biopsy. Control the flares
Endoscopy theres the option to do cautery, banding, or a with steroids and control the bleeding. Other forms of colitis,
balloon tamponade. Tamponade is merely a temporary bridge to including bacterial infections, should be excluded with
a TIPS procedure, where the portal pressures are reduced by Stool Culture and treated with antibiotics.
bypassing the cirrhotic liver (which also increases the risk of
asterixis and hyperammonemia). Finally, Propranolol low dose h) Diverticular Hemorrhage
(10mg tiD) may actually shrink varices and decrease the risk of While diverticuli occur more often on the left than the right,
bleeding. hemorrhage occurs on the right more than the left. An
arteriole in the dome of the diverticulum tears, which
b) Mallory-Weiss Tear produces massive LGIB and hematochezia. Resection or
Present in people who go on a drinking binge or are one-time cautery will cure the lesion. See diverticular disease for more
vomiters who produce hematemesis after retching. The details.
bleeding is usually self-limiting; its caused by a tear in the
mucosa only at the GE Junction. Perform an EGD if the patient i) Cancer
presents with active bleeding. Cancer can cause an UGIB if in the stomach or esophagus,
or a LGIB if in the colon. Cancer has its own specific
c) Boerhaave Syndrome screening, diagnosis, and treatment based on which cancer it
Present in Alcoholics or Bulimics who present like a sick is. Regardless, the general principle of a camera (endoscopy
Mallory-Weiss. They have a transmural tear that isnt self- with biopsy or colonoscopy with biopsy) is required for
limiting. Theyll have Hematemesis, Fever, diagnosis. Stage with (PET)CT and treat with resection or
Leukocytosis and Esophageal Crepitus. The Hammans chemo/radiation. See the corresponding sections for
Crunch is a crepitus heard with each heartbeat, indicating theres specifics on each cancer.
air in the mediastinum. These patients require emergent surgical
intervention. Diagnose them with a gastrografin swallow (water j) Mesenteric Ischemia
soluble but less harsh than barium on the mediastinum) and This is the gut's equivalent of a "heart attack." Caused by
follow up with an EGD. See surgery for more details. atherosclerosis or A fib, the mesentery dies. This hurts.
Chronic mesenteric ischemia will present with postprandial
d) Dieulafoys Lesion abdominal pain (intestinal angina) and likely weight loss.
An anatomic variant in the cardia of the stomach, this lesion is Acute mesenteric ischemia presents with pain out of
a superficial artery that becomes easily eroded by gastritis or proportion to the physical exam. An angiogram is
ulcers. It presents as sudden massive UGIB and often requires diagnostic and resection is usually necessary.
subtotal gastrectomies.
k) Ischemic Colitis
e) Esophagitis Ischemic colitis occurs at the watershed areas of the colon
Just a simple inflamed esophagus can bleed - especially as the during periods of hypotension. This is often painful, results
inflammation progresses to cancer. Think of GERD 1st, but also in a self-limiting bleed, and needs a colonoscopy to
consider CMV or Herpes (ganciclovir or foscarnet), Candida definitively diagnose.
(nystatin), and HIV (HAART). Biopsy and culture on EGD yield
diagnosis. See GI - Esophagitis for more details. There are many other causes of GI Bleed. It becomes
paramount to focus on the classic presentations of some of
the more common and identifiable diseases, but most
importantly, on stabilizing the patient before worrying
about which diagnosis it truly is.

Gastroenterology [IBD]

Ulcerative Colitis Crohns Disease
UC is an inflammatory disease is a superficial inflammation Crohns disease is an inflammatory disease of the bowel that
thats limited to the colon. Patients present with bowel urgency, can extend from the mouth to anus and can be discontinuous
frequent bowel movements, and bloody diarrhea. Onset is (skip lesions). Patients present with an insidious onset of
abrupt and patients often remember when the disease first started. symptoms and rarely remember the initiation of the disease. They
Abdominal pain is unusual; it represents a complication. also present with gradually worsening watery diarrhea and
Diagnosis revolves around colonoscopy. UC is a continuous weight loss. Because the inflammation is transmural, its possible
lesion, involving the rectum and then extending variably through to develop fistulas from the bowel to any other organ (entero-
the colon. UC doesnt extend outside the colon. The end of entero, entero-vagina, entero-vesicular) or the skin (entero-
involved tissue is also abrupt. Biopsy of the colon reveals crypt cutaneous). Because the inflammation can occur anywhere,
abscesses and superficial inflammation. symptoms are highly variable, which includes nutritional
deficiencies. Theres a predilection for the terminal ileum
Extraintestinal manifestations include primary sclerosing resulting in B12 deficiency. Diagnosis revolves around
cholangitis (association with p-ANCA), erythema nodosum, and endoscopy and biopsy. Biopsy will reveal transmural
aphthous ulcers. inflammation and noncaseating granulomas.

Unlike with Crohns, surgical removal of UC is curative. Extraintestinal manifestations exist, but arent as specific as in
Because theres a high association with malignant transformation UC. For Step 2, consider Crohns as having, no extraintestinal
of UC, a colonoscopy screening begins at 8 years from disease, though do know that Rheumatologic complaints can
diagnosis and continues annually until resection. exist.

Disease severity dictates medical management. For mild disease, Theres no increased risk of malignancy in Crohns*. Resection
5-ASA compounds are effective in UC (unlike Crohns). For is NOT curative, but can be used on limited stretches of bowel
moderate disease, immune modulators such as Azathioprine and that are refractory or particularly burdensome.
6-mercaptopurine are used; TNF-inhibitors are used should
they fail. Surgery is ultimately curative. 5-ASA compounds are still used in Crohns disease, but theres
increasing evidence that early initiation of disease modifying
agents is superior for the disease course. Azathioprine and 6-
mercaptopurine are used in mild and moderate disease. Anti-TNF
medications are used in severe disease, and, in the absence of
infection, are often successful in healing enterocutaneous fistulas.
Dexa-scans and Calcium repletion are usually needed.

Crohns Flare
UC Flare Flares will present with increased number of bowel movements,
Flares will present with increased number of bowel movements weight loss, and electrolyte abnormalities. For flares, infectious
or worsening blood. For flares, infectious etiologies must be etiologies must be ruled out - specifically C. diff. Flares are
ruled out, specifically C. Diff. Flares are treated with steroids treated with steroids and antibiotics.
and antibiotics.
Perirectal disease, such as perianal abscess, must be drained.

Mild: 5-ASA Compounds designed to prevent Mild: 5-ASA Compounds dont really work for
flare by releasing in the rectum to quiet Crohns disease.
inflammation. These work for UC Sulfasalazine
Mod: Oral steroid taper quells the acute flare Mod: Oral steroid taper quells the acute flare
Then: follow with immune modulators Then: follow with immune modulators
Prednisone Prednisone
Azathioprine / 6-Mercaptopurine Azathioprine / 6-Mercaptopurine
Severe: IV steroids to quell acute flare, then: Severe: IV steroids to quell acute flare, then
For UC Infliximab or Cyclosporine For CD Infliximab
For UC Resection


Fistulas (see surgery topics)
Screening colonoscopy q1y starting at y8.
Antibiotics are good when theres a perirectal
abscess, otherwise no benefit

*severe distal colonic Crohns = Screen like UC

Gastroenterology [JAUNDICE]

Introduction and Differential Prehaptic Hemolysis
Jaundice is a clinical finding where theres yellowing of the Hematoma
sublingual region (1st), the sclera (2nd) and then the skin (3rd). Its Gilberts
a result of elevated bilirubin in the blood. Bilirubin is processed Crigler-Najjar
by the liver and excreted into the small intestine by the biliary IntraHepatic
tree. Defects in any three regions can cause a build up of bilirubin: Rotors
1) PreHepatic, which essentially means hemolysis producing an Cirrhosis
unconjugated bilirubinemia from increased RBC turnover, 2)
Intrahepatic, a defect in anything involving uptake, PostHepatic Gallstones
metabolism, or excretion of bilirubin producing an unconjugated Pancreatic Cancer
bilirubin, and 3) PostHepatic, typically a mechanical PBC
obstruction preventing efflux of conjugated bilirubin. PSC

Conjugated vs Unconjugated
Unconjugated bilirubin comes from broken down red blood cells. UNCONJUGATED CONJUGATED
Glucuronyl Transferase is an enzyme in the liver that conjugates Lipid-Soluble Water-Soluble
the unconjugated bilirubin. Conjugated bilirubin can then be Crosses BBB Cross BBB
excreted in the GI tract. Unconjugated is generally the worse Urinary Excreted Urinary Excretion
type. It cant be renally excreted and can cross the blood brain Kernicterus Kernicterus
barrier because its lipid-soluble. Conjugated on the other hand
is water-soluble and is renally excreted, but cant cross the
blood brain barrier. A conjugated hyperbilirubinemia will
therefore present with dark urine. Congenital or Acquired
(Usually Unconjugated)
1) Hemolysis
See the heme section for all hemolytic anemias. Look for a UDP Glucuronyl
history of transfusions, culpable medications (like Dapsone), or Transferase
African Americans. Since actual hemolytic anemia rarely causes
jaundice, look only for a mild elevation of the bilirubin. A blood RBC Unconjugated Conjugated
smear and Hgb Electrophoresis can distinguish hemolytic Turnover Hemolysis Bilirubin Bilirubin Stool
2) Gilberts and Crigler-Najjar
Disease of uptake of bilirubin. Theyre either fatal early (Crigler-
Najjar) or present as asymptomatic jaundice when the body is Hemolysis or Obstructive Jaundice
stressed (infection, dehydration, etc). Because bilirubin cant Hematoma Reabsorb (mostly conjugated)
enter the liver or get conjugated, theres an unconjugated (mostly unconjugated)
bilirubin. The enzyme deficiencies are for step 1 and arent

3) Dubin-Johnson and Rotor syndrome

Diseases of excretion of already conjugated bilirubin, these cause
an asymptomatic jaundice when the body is stressed just like
Gilberts. However, theres conjugated hyperbilirubinemia so
the urine will be dark and for blood (representing the
bilirubin, not actually hematuria). Being able to separate these
two diseases isnt necessary.

4) Gallstones
Discussed in gallbladder pathology. The patient will present with
a history of colicky RUQ pain and will have either hemolytic
anemia or be fat, fertile, + forty. Diagnosis is made with
ultrasound then treated/confirmed with ERCP to remove stones.
Gallbladder jaundice is painful obstructive jaundice.

Gastroenterology [JAUNDICE]

5) Pancreatic / Biliary Tract Cancer
There will be a painless obstructive jaundice with a conjugated
hyperbilirubinemia. An ultrasound will show a thin-walled,
distended gallbladder. See surgery videos for more information
on obstructive jaundice.

6) Primary Biliary Cirrhosis

PBC is for Bitches, an autoimmune disease affecting females
and intrahepatic ducts. Conjugated bilirubin cant get out,
causing a conjugated hyperbilirubinemia. The only diagnostic
tool is a biopsy and treatment is transplant. See cirrhosis.

7) Primary Sclerosing Cholangitis

An autoimmune disease affecting MALES with an association
with ulcerative colitis (p-ANCA). This affects extrahepatic
ducts, causing a macroscopic pattern of disease. A diagnostic
MRCP can be used to see a beads-on-a-string pattern. Biopsy
(not needed) via ERCP will show onion-skin fibrosis.

8) Stricture
Stricture is the other painless obstructive jaundice. It presents
just like a cancer (insidious, dilated ducts, conjugated
hyperbilirubinemia), but there isnt cancer or PSC. Strictures are
diagnosed with MRCP, confirmed by ERCP and treated with
stenting (do not stent PSC, only stents). To identify a potential
stricture look for iatrogenic causes - especially a history of
manipulation of the biliary tree surgically or with ERCP.

Disease Bilirubin Dysfunction Patient Picture Diagnosis Treatment

Hemolysis or Unconjugated PreHepatic African American, Transfusions, Heme/Onc Lectures
Hematoma Medications
Cirrhosis (any Unconjugated IntraHepatic EtOH, Viral, Wilsons, Hemochromatosis, Diagnose Supportive
acquired form) Acetaminophen toxicity, etc. etic. underlying dz Care
Gilberts Unconjugated IntraHepatic Asx, Unconjugated Hyperbili, Genetics Asx, Tx
Crigler-Najjar Death In Infancy Biopsy
Dubin-Johnson Conjugated IntraHepatic Asx Conjugated Hyperbili MRI, Biopsy Asx, Tx
Gallstones Conjugated PostHepatic h/o colicky pain, RUQ worse with fatty food, U/S RUQ ERCP
Female, Fat, Forty, or Hemolysis ERCP, HIDA
Pancreatic Conjugated PostHepatic Weight Loss and Asx Jaundice U/S RUQ Surgery
Cancer CT Scan
Primary Conjugated PostHepatic MALE with Ulcerative Colitis p-ANCA Transplant
Sclerosing Extrahepatic Dilation MRCP
Cholangitis Biopsy
Primary Biliary Conjugated PostHepatic FEMALE with conjugated hyperbili AMA Transplant
Cirrhosis Biopsy
Cancer Conjugated PostHepatic Weight loss, Painless Jaundice CT scan Resection
EUS biopsy
Stricture Conjugated PostHepatic Previous manipulation of the biliary system, U/S RUQ Stent
painless jaundice MRCP

Gastroenterology [MALABSORPTION]

Introduction Pancreas/Bile Salts
Digestion begins with mastication and amylase in the mouth, Either an obstruction (cystic fibrosis, gallstones) or destruction
continues into the stomach with gastric acid, and completes in the (chronic pancreatitis) causes insufficient digestive enzymes.
duodenum. Absorption then occurs in the lower GI tract south Without them, no digestion or absorption can occur. In an adult it
of the Ligament of Treitz. Fats require bile salts and a terminal causes weight loss, foul diarrhea, and feces that are difficult to
ileum to be absorbed. Fat absorption has to happen for absorption flush (floaters). In a child it causes stunted growth. Giving back
of vitamins ADEK. The proximal bowel is the site of absorption the enzymes the patients lacking will correct the condition.
for the FIC vitamins (Folate, Iron, Calcium). Protein is required
for growth and needs pancreatic enzymes to be digested. Some
general malabsorption syndromes follow.
FATS ADEK and Steatorrhea
Celiac Sprue A = Night Blindness
This is an autoimmune disorder caused by a gluten allergy; the D = Hypo Ca / Osteoporosis
body produces antibodies in reaction to gluten of wheat, rye, and E = Nystagmus
barley. Antibodies cause a destruction of intestinal villi, surface K = Bleeding (2,7,9,10) INR
area and prevent absorption of everything. That yields the classic Protein Weight Loss and Edema
symptoms (chronic diarrhea, weight loss, abdominal distention).
Since the small bowel also absorbs FIC the nonclassic symptoms Proximal FIC vitamins
are anemia ( Folate and Iron) and osteoporosis ( Ca). Diagnosis Bowel Folate = Megaloblastic Anemia
begins with anti-endomysial and anti-transglutaminase Iron = Microcytic Anemia
antibodies (best). Anti-gliadin antibodies arent useful. Calcium = Osteoporosis
Confirmation is made with a biopsy via EGD showing atrophic
villi. Because its an autoimmune disorder, withdrawal of the Malabsorption
offending agent will show improvement - but only after
antibodies diminish (3-4 months). Finally, Dermatitis
Herpetiformis is a cutaneous variant of celiac (all DH have Fecal Fat <14g/24 hrs
celiac, all celiac has DH). Give 100g Fat /day Malabsorption
Take: 72 hrs Stool
Whipple Disease
When malabsorption occurs with systemic symptoms >14g/24 hrs
(malabsorption plus) think Whipple Dz. Theres a
malabsorption with brain, lymph, and joint problems. Caused Malabsorption
by the organism T. whipplei, the bug can either be seen as Pas
Macrophages on EGD Biopsy or via Electron Microscopy.
Additionally, PCR on the Blood/CSF can yield a positive result. D-Xylose
This requires Long-Term Abx to eradicate (pick either Bactrim CT scan
DS or Doxycycline).
Absorbed Absorbed
Tropical Sprue
Intestinal Border Def. Pancreas Deficiency
A distractor for celiac, its also called sprue b/c it causes atrophic
villi on biopsy that occurs in Caribbean farmers. Its likely due to Give Enzymes
an infection and thusly doesnt improve with gluten withdrawal.
However, it does respond to antibiotics. EGD w/ Bx ?
Lactase Deficiency
As the body ages the amount of Lactase decreases. When lactose
(i.e. dairy products) is consumed the sugar is not digested or
absorbed; its passed to the colon. Bacteria in the colon love Sprue
lactase, eat it, and produce lots of gas. Lactose is an osmolar load Enteritis
that draws water into the lumen. This causes foul flatulence, Crohns / UC
diarrhea, and bloating. Immediate improvement can be seen Whipples
by the elimination of dairy or adding lactase. invasive
procedures are required for diagnosis or therapy.
Disease Patient Deficiency Pathology Diagnosis Treatment
Celiac Sprue Adults FIC Autoimmune Antibodies Bx Gluten Free Diet
Tropical Sprue Tropics B12 Infxn Bx Abx + B12
Whipples Dz Tropics CNS, Joints Infxn Bx or PCR Abx (Bactrim)
Lactase Deficiency Asians Dairy Enzyme Relief w/ Tx Lactase or Dairy
Pancreatic Cystic Fibrosis, ADEK Enzymes CT/MRI/Bx Add Enzymes
Insufficiency Gallstones


Gastroparesis (think Gastro-paralysis) is a nerve problem with
the stomach whereby digested food just wont go forward. In
other words, the stomach cant empty. The most common cause
is idiopathic, though it's often associated with autonomic
neuropathy, especially diabetic neuropathy (neuropathy of the
vagus nerve).

Chronic nausea, vomiting, and early satiety is classic for

gastroparesis. Severe abdominal pain isnt typical it. However,
on inpatient medicine rotations youll encounter patients
suffering with intractable pain secondary to their gastroparesis.

The diabetic with gastroparesis must have peripheral neuropathy

in their feet for the diagnosis the longest nerves are affected
first. Often theyll be poorly controlled as well. Control of the
blood sugar is paramount to limit diabetic gastroparesis.

An endoscopy is often performed for these patients because

they present with chronic nausea and vomiting. While this can
rule out other diagnoses (such as malignancy and gastric outlet
obstruction), the EGD is non-diagnostic for gastroparesis. To
diagnose it, a gastric emptying study is performed.

The treatment of gastroparesis uses prokinetic agents as the

cornerstone of therapy. Oral Metoclopramide is best used for
chronic management while intravenous Erythromycin is used
for acute exacerbations. Consuming small meals with little
fiber also helps. Avoid opiates and anticholinergic

Severe, refractory cases may result in the use of gastric

stimulators or tube feeds that bypass the pylorus. In extreme
cases, parenteral nutrition may be required.

The good gastric cancer, this is a Gastric Lymphoma. Its
caused by infection by H. pylori. Its found and diagnosed by
endoscopy with biopsy. Treating the H. pylori treats the cancer.
Use triple therapy (see peptic ulcer disease for more).

Gastric Adenocarcinoma
One of the rarer forms of malignancy in the United States, the
pathogenesis of Gastric Adenocarcinoma is poorly understood.
Japanese diets, particularly those rich in nitrate preservatives
increases the risk. Hence, most new gastric adenocarcinomas are
diagnosed in East Asia, particularly China and Japan. There is
currently no screen for Gastric Cancer. When advanced, the
symptoms will be early satiety, weight loss, and bowel
obstruction. The test of choice is endoscopy to diagnose, then
PET-CT to stage. Most (80-90%) of adenocarcinomas are
metastasized at the time of diagnosis; prognosis is poor.

Gastroenterology [ACUTE PANCREATITIS]

Pancreatitis is caused by autodigestion of the pancreas by
proteolytic digestive enzymes that are released or activated P arathyroid Hormone
prematurely within the pancreatic parenchyma. A lcohol
N eoplasia
Etiologies C alcium
R ocks (Gall Stones)
The most common causes of pancreatitis are gallstones (#1) and
E strogens
EtOH (#2); they account for nearly 80% of all cases. For the A CE-i
wards, also look for iatrogenic / trauma (from ERCP), T triglycerides
medications / toxins (HIV meds), and hypercholesteremia. The I nfarction (Ischemia)
mnemonic Pancreatitis reminds you that there are many other T rauma (ERCP, MVA)
Grey-Turner Sign Flank Ecchymosis
etiologies, but they need not be assessed each time. I nfection (Mumps)
S corpionSign
Stings Umbilical Ecchymosis
Pancreatitis presents as a severe epigastric abdominal pain that
will radiate to the back, with relief by leaning forward (sounds Acute Pancreatitis
a lot like a pericarditis). There are also non-specific signs and Path Autodigestion of the pancreas
symptoms such as N/V/Anorexia. Physical exam findings EtOH (#1)
indicative of intraperitoneal hemorrhage, but associated with Gallstones (#2)
pancreatitis are flank ecchymosis (the Grey-Turner Sign) and
Patient Boring epigastric pain radiating to the
umbilical ecchymosis (Cullens Sign). back, relief with leaning forward.
Dx Lipase > 3x ULN
Diagnosis Amylase > 3x ULN (Lipase better)
This is mainly a clinical diagnosis. However, the best test is an CT scan if unsure or for complications
elevated Lipase > 3x Upper Limit of Normal often seen in U/S if stones suspected ERCP
Tx NPO, IVF, Analgesia
conjunction with an Amylase. While amylase is far less sensitive
Feed when ready
(false positives include vomiting and gallbladder disease), if Antibiotics
either are elevated in the clinical scenario the diagnosis should be Early Refeeding
considered positive. A CT scan was once thought to be harmful, ERCP only if worsening gallstone
but is now known to be safe. A CT scan isnt required for the pancreatitis
diagnosis, but can be used when the clinical picture is incongruent
with the laboratories. Routine CT scans are not indicated.

Other diagnostic steps are used more to identify etiologies.

Ultrasound is done to assess for gallstones. MRCP is used to
evaluate the biliary tree and to start work up for pancreatic cancer.

Initial management is NPO Bowel Rest, IVF, and Analgesia.
NPO prevents pancreatic secretion. 3rd spacing can occur so IVF
keeps them perfused. Analgesia keeps them from anxiety and
unnecessary motion which can exacerbate the pain.

Prophylactic Antibiotics arent required. Gallstone Pancreatitis. The obstructing stone prevents the
digestive enzymes from leaving the pancreas, resulting in
Gallstones are removed with ERCP only in the setting of erroneous activation and destruction of the pancreas.
cholangitis or when there is clinical deterioration.

Gastroenterology [ACUTE PANCREATITIS]

Pancreatitis is a pretty nasty disease. But its the many
complications that cause most of the problems.

The Ranson Criteria and the APACHE II scoring systems exist to

help determine the likely prognosis. The Ranson Criteria is easier
to remember, but must be assessed at day 1 and day 3. The
APACHE II score has more entries and is available at day 1.
Clinical Acumen is as good as the scoring systems. DO NOT
MEMORIZE these scoring systems. If pimped, the BUN has the
greatest prognostic information. Complication Dx Tx
Early ARDS CXR Intubation
CT scan is the preferred method for evaluating the pancreas after HypoCa iCa Ca
pancreatitis to monitor for complications. Routine post-diagnosis Prognosis BUN
CT scans are not indicated. Pleural Effusion CXR Tap / Tube
Ascites U/S Tap / Tube
The most commonly tested complication is pseudocyst. Suspect Mid SIRS Day 7 CT
a pseudocyst if theres early satiety or abdominal fullness 3-7
Infection Bx
weeks after acute pancreatitis. These will spontaneous resolve if
<6cm AND < 6weeks old. If both are not met, then there will Late Abscess CT Drain & Abx
Pseudocyst CT >6 cm or > 6wks
likely be no spontaneous resolution. Surgical drainage is
Drain, Bx
required. Percutaneous, pancreaticogastrostomy, or open
procedures can be used. <6cm and <6 wks
Watch and wait
If an infection is suspected, dont do empiric antibiotics unless
an infection is confirmed with biopsy. When choosing empiric
coverage, elect for meropenem.

If there are pleural effusions or ascites, do NOT try to tap or

drain them. If this fluid is a potential infectious source, then it
should be drained, as should an abscess if one is identified.

Chronic Pancreatitis
A patient thats had acute pancreatitis is at risk for developing
chronic pancreatitis. It presents as chronic pain with occasional
acute flares. The pain is identical to acute pancreatitis. The
Lipase will be smoldering (a burned out pancreas cannot produce
substantial elevations) and a CT scan may show calcifications.
The only treatment is pain control, management of endocrine
dysfunction (diabetes), and replacing pancreatic enzymes if
necessary. Surgical resection is ineffective and should be

Gastroenterology [PEPTIC ULCER DISEASE]

Peptic Ulcer Disease Ulcer Clinical / Endoscopic Findings
An erosion is a break < 5mm. An ulcer is a break > 5mm and H. pylori Single large ulcer,
histologically demonstrates going through the mucosa into the ~100% Duodenal ulcers are H. Pylori
muscularis. Peptic ulcer refers to ulcers that occur in the NSAIDs Multiple Shallow Ulcers
duodenum and stomach. Malignancy Necrotic base, heaped margins
Curlings Burn patients
The etiology of Peptic ulcer disease can often be tracked to the Cushings ICP, Ventilated Patients
appearance of the lesion on endoscopy. H. pylori and NSAIDs Gastrinoma Multiple refractory ulcers with diarrhea
account for the vast majority (90%) of peptic ulcers. Others that
are less common are malignancy and what I call the special Ulcer Treatment Back-Up
circumstances: Curlings (Burns), Cushing (ICP) and H. pylori Triple Therapy Quad Therapy
Gastrinoma (Zollinger-Ellison). Their characteristic patterns are NSAIDs PPI Sucralfate,
listed to the right. (stop NSAIDs) Misoprostol,
H2 Blockers
Alcohol and smoking are NOT independent risk factors, but Cancer Resection
worsen ulcer disease when another etiology is present. Curlings PPI PPI PPx
Cushing PPI PPI PPx
Patients with PUD are asymptomatic in 20% of cases, presenting
only with a complication such as bleeding, perforation, or gastric
outlet obstruction. On the tests, those who are symptomatic will
likely present with a gnawing epigastric pain related to food. Gnawing / Boring
Gastric ulcers are worse with food, while Duodenal ulcers are Epigastric Pain
worse 2-5 hours after food. These associations are unreliable in Urea Breath Test
clinical practice. Serology Multiple
Stool Ag EGD w/ Bx Shallow NSAIDs
Diagnosis is made with Endoscopy and Biopsy, which allows for Burns Ulcers
direct visualization to rule out malignancy and definitively Head Trauma Single Stop NSAIDs
diagnose H. pylori. The diagnostic steps for H. pylori are NSAID use Ulcer or
discussed on the next page. Ulcer Add PPI

Treatment revolves around acid-suppression therapy, where

Proton Pump Inhibitors (PPIs) are superior. Treatment for H.
pylori involves Triple Therapy (discussed below). For NSAID- CLO and
induced ulcers, the NSAIDs should be discontinued at the time Pathology
of diagnosis. If they must be restarted after ulcer healing, use PPI
prophylaxis to prevent recurrence of ulcer. PPIs are superior to Ca Ca
sucralfate, misoprostol, and H2 blockers for NSAID prophylaxis. H. pylori

All ulcers are helped by Smoking Cessation, Alcohol Cessation,

and PPIs. Cancer H. pylori
Resect and Stage Triple or Quadruple
Repeat Endoscopy is NOT needed except when the symptoms
are refractory or when cancer is suspected but not diagnosed.

Gastroenterology [PEPTIC ULCER DISEASE]

H. pylori Test Use
Infection with H. pylori is common (about 50% of the world). But Serology Treat if never treated before
of those infected, only 15% will become symptomatic. It causes Urea Breath Test Confirm Infection
a mild pangastritis in 85% of patients, while 15% develop ulcers. Stool Antigen Confirm Eradication
A small percentage (<1%) will develop MALToma. Thus, H. Endoscopy Urease Test (immediate)
pylori is considered a carcinogen. Endoscopy Histology (superior)

Testing for H. pylori is challenging. PPIs and H2 blockers must

be stopped before doing all testing other than serology.

The test and treat strategy is employed for those who havent been Triple Therapy Quadruple Therapy
Amoxicillin* Metronidazole
treated previously and have evidence of PUD or MALToma. In a
Clarithromycin Tetracycline
case with symptoms and positive serology, the next step is
PPI Bismuth
simply to treat. H2-Blocker
*if Penicillin Allergic, use Metronidazole
Urea breath testing is the best noninvasive test to confirm
diagnosis (which means infection).

Stool antigen testing is the best method to confirm eradication.

Endoscopy with biopsy is the gold standard. Either the rapid

urease test (used in real time in the endoscopy suite) or histology
can be used to confirm the presence of the bug.

Triple therapy consists of clarithromycin, amoxicillin, and a

PPI; its superior to quadruple therapy. Ulcers Resolve

Zollinger-Ellison / Gastrinoma
ZE syndrome
In the presence of virulent or refractory ulcers despite adequate Stage with SRS
therapy, consider ZE. This is especially true when considering Resect
Ulcers and Diarrhea together. Caused by a cancer in the head of <250 >1600
the pancreas, this endocrine tumor erroneously secretes Gastrin r/o Gastrin Level Confirmed
causing production of gastric acid. Acid = Mucosal Barrier
Destruction = Ulcers.

Test for this disease by first getting a serum gastrin level. If the Unconfirmed
levels of gastrin are very elevated (in the 1000s) a Secretin
Stimulation Test isnt required. If the value is < 250, the diagnosis
is excluded. PPIs must be held as they can falsely increase Gastrin Gastrin
Gastrin levels. If equivocal follow with a secretin stimulation Secretin
test which will cause an Gastrin. Stimulation

Once confirmed, localize the tumor with a Somatostatin

Receptor Scintigraphy (SRS) scan. CT scans often arent
sensitive enough. HCl HCl

While the gastrinoma itself is benign, it must be resected to

prevent future ulcers. Additionally, high levels of gastrin can G
transform the normal stomach mucosa into a malignant gastric
G cell Gastrin Ectopic Pancreatic Gastrin

Zollinger-Ellison. The normal condition (left) is a balance

between HCl and Gastrin production, HCl inhibiting the
production of Gastrin. The ZE-condition (right) causes
constant HCl production, depression of the G cells, but
unopposed gastrin stimulation of acid.

Gastroenterology [VIRAL HEPATITIS]

Viral Hepatitis is an umbrella categorization of the different
viruses that can cause an infection of the liver. Some are chronic,
others acute, some can be prevented, others only avoided. Lets
talk about each.

Hepatitis A
This is an Acute form of hepatitis spread by fecal-oral Fecal Oral
contamination. It has a 2-6 week incubation and is carried in RNA
contaminated water, shellfish, and daycares. It produces a Vaccine
nonbloody diarrhea and a modest LFT . Since its self-limiting IgM = Active Infxn
a diagnosis is rarely required. However, serologies will show IgM IgG = Immunity
for active infection while IgG indicates immunity. A vaccine is PPX = IgG w/I 2 weeks of exposure
available and given as a child. Boosters are recommended for
travel to endemic regions >2 wks before the trip. Post Exposure
Prophylaxis with IgG can be started with vaccine within 2 weeks
of exposure.

Hepatitis B
This can be both acute and chronic. The stronger the immune
response the less likely its in the chronic carrier state and more
likely its a devastating hepatitis case. Adults acquire it through IVDA/Sex = Adult = Acute
Sex more than IVDA. Because adults are generally healthy (an Baby = Vertical = Chronic
intact immune system) they suffer jaundice, LFTs in the 1000s, HCC/Cirrhosis if chronic
and only the acute phase without chronic carrier state. Fulminant HBsAg initial infxn
Hepatitis is rare (and nearly fatal). Babies acquire it through the HBeAg infectivity
birth canal (vertical transmission) and will likely have IgM HBxAg window period
symptoms (a poor immune system), but are almost always IgG HbeAb waning infection / infectivity
chronic carriers. Since theres chronic inflammation infection of IgG HBsAb long term immunity
the chronic carrier may result in cirrhosis or hepatocellular Vaccine
carcinoma. Screen for HCC with Alfa-fetoprotein (AFP) and PPx = IgG
Ultrasound. To treat the hepatitis infection give peg IFN--2a DNA Virus
for 48 weeks coupled with antivirals (lamivudine, adefovir, Peg-IF--2a + antivirals = HCC Transformation
telbivudine, entecavir) with the goal of eliminating HBeAg.
Theres a vaccine against Hep B so vaccinations are a must to
prevent chronic illness. If a patient isnt vaccinated and gets stuck,
give them vaccine and ppx IgG. Understanding serology is
critical. IgG indicates either past exposure or immunity. IgM is
only during acute infection. The virus has a surface antigen
(HBsAg), a core antigen (HBcAg), and a protein of infectivity
(HBeAg). IgG HBsAb ONLY is a sign of vaccination. IgG
HBeAb but without the presence of Antigen is a sign of immunity
following exposure. HBsAg (the presence of antigen, not
antibody) occurs early and denotes infection. HBeAg indicates
active infection and infectivity. During the window period
where the Antibodies and Antigens cancel each other out (binding
to each other prevents binding of the test antigen), Anti-HBe is
the only indicator of infection. Incubation is generally 1-6

Gastroenterology [VIRAL HEPATITIS]

Hep C
Hep C is the chronic hepatitis that has no vaccine. Until recently
there was also no treatment. Hepatitis C is on its way to IVDA//Blood Transfusions = Chronic
eradication. Good thing too - chronic hepatitis is chronic HCC/Cirrhosis
inflammation, leading to cirrhosis after 20-30 years. Cirrhosis Antibody and HCV RNA = Early Infection
progresses to hepatocellular carcinoma at a rate of 2-5%. Even Antibody and HCV RNA = Resolution (rare)
in the absence of cirrhosis, chronic Hep C can lead to Antibody and HCV RNA = Chronic
hepatocellular carcinoma. Hep C is transmitted by blood and NO Vaccine
essentially not at all by sex (people who sleep with people who PPx = IgG
do IV drugs tend to also do IV drugs, which is how they get the RNA Virus
virus). Blood transmission means IVDA and Blood Peg-IF--2a + Ribivarin = Remission and HCC
Transfusions. The goal with all Hep C is to prevent further Direct Acting Antivirals = Hep C cure (~12 week regimen)
inflammation by abstaining from alcohol and to screen for HCC
with annual Ultrasound and AFP.

There are two treatments for Hep C. If genotype 1b, we can use
Pegylated Interferon with Ribavirin which causes psychosis,
depression, and flu-like symptoms for a year. If genotype 2 or 3,
we have the new Direct Acting Antivirals which all end in vir.
There are many of them and more are coming (theyre extremely
effective, but also extremely expensive expect to talk about

Viral serology is either acute ( Anti-HCV, HCV RNA),

resolved ( Anti-HCV, HCV RNA), or most commonly,
chronic ( Anti-HCV and HCV RNA).

Hep D
This is essentially mini-B. It requires the presence of Hep B
(reliant on one of Hep Bs proteins) and is transmitted the same Requires coinfection with Hep B
way. It causes a more severe hepatitis and a faster progression makes B worse
to cirrhosis.

Hep E
Pregnant ladies in third world countries contract it through fecal- Pregnant ladies in third world countries
oral route. Think of this as Hep A of women in the 3rd world.

Hepatitis Route Acute Chronic Cancer RNA/DNA Vaccine Serology

Hep A Fecal-Oral Always Never Never RNA >2 weeks before N/A
endemic travel
Hep B IVDA, Sex, Strong Weak HCC, Incomplete All @ risk, See Above
Vertical through Immune = Immune = Only with DNA especially health
birthing Acute Chronic chronic infxn care providers

Hep C IVDA, Never Always HCC RNA None See Above

Horizontal, or
through blood
Hep D IVDA, Sex, Never Always HCC DNA None -
requires Hep B
Hep E Fecal-Oral - - - - -

Nephrology [ACID BASE]

Youll be asked to do two things: interpret a blood gas

(which comes later) and decide what to do next. We first You want to talk to someone
about their acid base status.
handle "what to do next," the potential diagnoses that
might be encountered and how to spot them on a vignette.

< 7.4 > 7.4

The first step is to determine what the primary pH
disturbance is. Its discussed in greater detail in gas
interpretation, but basically <7.4 is acidic while >7.4 is Acidemia Alkalemia
basic. Then use the CO2 (with a cutoff of 40) to separate
into respiratory or metabolic. >40 < 40 < 40 >40

Respiratory Acidosis
This is a product of hypoventilation. The less ventilation Respiratory Metabolic Respiratory Metabolic
Acidosis Acidosis Alkalosis Alkalosis
the more CO2 will accumulate. Whether its a low tidal
volume (COPD) or a low respiratory rate (opiate Hypoventilation Hyperventilation
overdose), if either falls the CO2 rises. Look for things Opiates Pain
COPD Anion Gap Anxiety Urine Cl
like wheezing (Obstructive Lung Disease), obesity
Asthma Hypoxemia
(OSA), cyanosis and pinpoint pupils (opiates), or signs of OSA Na - Cl - Bicarb
muscle weakness (like paralysis from GuillainBarr) Muscle Strength
>12 <12 >10 <10

Respiratory Alkalosis
Anion Gap Non Gap Not Volume Volume
Conversely, respiratory alkalosis is from hyperventilation.
Acidosis Acidosis Responsive Responsive
Very few things will do that as a primary disturbance. Itll
either be pain, anxiety or hypoxemia. Lots of things cause Methanol Diuretics
hypoxemia (pneumonia, PE, ARDS) so the patient can get Uremia Urine Dehydration
DKA Anion Emesis
complex, but in terms of acid-base respiratory alkalosis Propylene Glycol NG Suction
means hyperventilation. Iron and INH
Lactic Acidosis Na + K - Cl
Metabolic Alkalosis Ethylene Glycol -
Salicylates +
The only thing that causes this is a high aldosterone. The
decision is if the person is volume responsive - that is, Renal Diarrhea
will giving him/her volume improve their alkalosis? This Tubular
is done in one of two ways: using the history to say he/she HTN
is volume down and give fluids, then recheck the bicarb
OR by checking the urine chloride. The test loves the
urine chloride. If its low (<10) the patient is salt-
Genetic Diseases Hyp
sensitive, or volume responsive, and giving him/her Bartter Renal Artery Stenosis
volume will improve his/her condition. Look for the use Gitelman Conn's Syndrome
of diuretics, emesis or NG suction, or another reason for
them to be dehydrated (looking for insensible water losses Test When To Use It
like sepsis, fever, tachypnea, or tachycardia). pH Start here
pCO2 After pH to get primary disturbance
Anion Gap Metabolic Acidosis
Urine Anion Gap Non-Gap Acidosis
Urine Chloride Metabolic Alkalosis

Nephrology [ACID BASE]

If the Urine Chloride is high (>10) its a condition that UCl < 10 = Volume Responsive
has nothing to do with volume. Its then time to assess for
the presence of hypertension. UCl > 10 = Not Volume Responsive

UCl > 10 and HTN = Inappropriate Aldosterone

If there is + HTN, consider diseases of too much
aldosterone; inappropriate elevations in aldosterone UCl > 10 and no HTN = genetic diseases
levels. Its most likely to be renal artery stenosis or
Conns syndrome (primary hyperaldosteronism). Keep in
mind that the aldosterone was up in volume depletion to
keep the pressure up. In this case its up inappropriately,
so it causes a rise in blood pressure.

If the patient is - HTN, think of Bartter and Gitelman

syndromes - genetic, always present forms of HCTZ and
Furosemide, respectively.

Metabolic Acidosis
Metabolic Acidosis is the hardest to handle; its the most
complex by far in gas interpretation. But its pretty easy ANION GAP: Na - Cl - Bicarb
to get the answer right when trying to make a diagnosis (NO POTASSIUM)
based on the clinical scenario.
Highlights to MUDPILES Diagnoses
First, calculate the anion gap (Na - Cl - Bicarb). A DKA Diabetic who is acidotic. Look for ketones. Treat
with insulin, fluids, and replete potassium
normal gap is 12, or Albumin x 3. If greater, theres an
Methanol Homemade liquor (moonshine), causes blindness,
anion gap acidosis, which can be reminded by a number no cure
of mnemonics. We've chosen MUDPILES in this section Ethylene Crystals in the urine, urine turns color under
(just don't forget about Toluene). In an anion gap Glycol Wood's Lamp. Give either ethanol or fomepizole
Lactic Either Metformin + Acute Kidney Injury or...
metabolic acidosis the diagnosis is made by the rest of Acidosis Patient in shock (fix the shock)
clinical picture. Highlights of the ones you must know are
to the right.

For non-gap acidosis the next step is the urine anion

gap. The urine anion gap is calculated from similar but
not the same electrolytes as the regular anion gap
(frustrating), so be careful. If positive the answer is renal URINE ANION GAP: Na + K - Cl
tubular acidosis. If negative the answer is diarrhea. (No Bicarb)


Gas interpretation of acid-base disturbances is difficult.
There will be one on your shelf. Youre guaranteed at least You get a question about
one on the Step 2 as well. Unfortunately, being able to acid base disturbance. You
ignore the vignette
appropriately interpret a blood gas doesnt always prove
incredibly useful in actual practice. But being able to
master acid base disturbances can lead to an impressive
< 7.4 > 7.4
evaluation (and can impress all your friends since they pH
won't be able to do it). But in reality, if this stuff just takes
too long and you still don't get it, take the hit on the test and Acidemia Alkalemia
move on. Better to randomly guess and get it wrong than
spend 15 minutes on a question you may not get right >40 < 40 < 40 >40
(thereby wasting precious minutes that could have been
used on other questions). With that in mind, let's get
started. Respiratory Metabolic Respiratory Metabolic
Acidosis Acidosis Alkalosis Alkalosis

Follow the Steps

Determining the Primary Disturbance
Step 1: Acidemia or Alkalemia. Use 7.4
Step 1: Acidemia or Alkalemia
- Is the pH < 7.4 (acidemia)
Step 2: Respiratory or Metabolic
- Is the pH > 7.4 (alkalemia) ....
Step 3: is there something else wrong?
Step 2: Respiratory or Metabolic
See CO2 as respiratory and acid. CO2 is the respiratory
acid. If you get rid of CO2 you get rid of respiratory acid;
this should create an alkalotic environment. If you retain
CO2 you hold onto more respiratory acid; it should create
an acidotic environment.

After deciding if theres an Acidemia or Alkalemia ask,

H+ HCO3- CO2 Bicarb
"What do I expect the CO2 to be - high or low?"
H+ HCO3- CO2 Bicarb

If theres a pH < 7.4, expect the CO2 to be higher than

= CO2
normal - that is >40. If it is, the acidemia is caused by a
respiratory acidosis. If it isnt, the acidemia is caused by a
metabolic acidosis. H+ = "Respiratory Acid" = pCO2
HCO3- = "Metabolic Base" = Bicarb
If theres a pH >7.4, expect the CO2 to be lower than
normal (loss of respiratory acid). If it is, the alkalemia is More H+ = More pCO2 = Low pH
caused by a respiratory alkalosis. If it isnt, the alkalemia Less H+ = Less pCO2 = High pH
is caused by a metabolic alkalosis.
More HCO3- = More Bicarb = High pH
This step is SUPER important because it decides what Step Less HCO2- = Less Bicarb = Low pH
3 is going to be. Once the primary disturbance is
determined you then go through that disturbance start to


Step 3a: Check the anion gap. Anion Gap = Na - Cl - Bicarb
Always check the anion gap. Its normally 12. Its actually
about 3* Albumin, normal albumin being 4, so this may Normal Anion Gap = 12... or Albumin x 3
change in real life. When handling acid-base problems,
If the calculated anion gap (Na-Cl-Bicarb) is greater
view them w/ the assumption of a normal anion gap = 12.
than the normal anion gap there is an anion gap
The reason to always check the anion gap is because if
metabolic acidosis
present (regardless of other findings), there must also be an
anion gap metabolic acidosis. Thats true even if it isnt the REGARDLESS of whatever else is going on
primary disturbance.

Respiratory Acidosis

Step 3b: Acute or Chronic For Every "Dime" Change in CO2

If the respiratory acidosis is acute then for every dime pH Bicarb
change (every 10 points) of CO2 the pH should change by If Acute 0.08 If Acute 1
0.08. If the respiratory acidosis is chronic, then for every If Chronic 0.04 If Chronic 3
dime change of CO2 the pH should change by 0.04. Step
3b is to find out which it is: acute or chronic.

To do that, find out how many dimes from normal the CO2 Formula for memorizers:
is. Multiply that by 0.08 and subtract from the normal pH
7.4 - (Dimes * 0.08) = pH if acute
of 7.4. Do it again multiplying by 0.04 and subtracting that
7.4 - (Dimes * 0.04) = pH if chronic
from the normal pH of 7.4. Compare both scores to
whatever the pH actually is. Whichever is closer Pick the one closest to the actual pH
determines the chronicity.

Step 3c: Is there a Metabolic Derangement Formula for memorizers:

For respiratory acidosis the bicarbonate should change as
well. For every dime change in CO2 the bicarb should 24 + (dimes * 1) = Expected bicarb if acute
change by 1 point if acute or 3 points if chronic. Bicarb 24 + (dimes * 3) = Expected bicarb if chronic
should change to compensate for the CO2; in a respiratory
acidosis the bicarb should go up.
If actual bicarb > expected bicarb: too many bicarbs =
Metabolic Alkalosis
Multiply the number of dime change of CO2 by 1 (if acute)
and by 3 (if chronic). Add that to a normal bicarb of 24. CO2 Bicarb
Compare to the bicarb you have. If there are more bicarbs CO2 Bicarb
CO2 Bicarb
than expected, theres also a metabolic alkalosis. If there
CO2 Bicarb
are too few bicarbs, however, its an additional metabolic Bicarb Bicarb
If actual bicarb < expected bicarb: not enough bicarbs =
Note that in the example the CO2s don't change. When Metabolic Acidosis
exploring Step3c the only care is the bicarb number (too
CO2 Bicarb
few, enough, too many). The CO2 doesn't matter except CO2 Bicarb
to the extent that we use it to determine how much the CO2
bicarb should have changed. CO2


Respiratory Alkalosis
Its literally the same for respiratory acidosis, except that For Every "Dime" Change in CO2
the bicarb changes by 2 (if acute) or 4 (if chronic) for every pH Bicarb
If Acute 0.08 If Acute 2
dime change. Lets spell it out here. If Chronic 0.04 If Chronic 4

Step 3b: Acute or Chronic

If the respiratory alkalosis is acute then for every dime
change (every 10 points) of CO2 the pH should change by
Formula for memorizers:
0.08. If the respiratory acidosis is chronic, then for every
dime change of CO2 the pH should change by 0.04. Step 7.4 + (Dimes * 0.08) = pH if acute
3b is to find out which it is: acute or chronic. 7.4 + (Dimes * 0.04) = pH if chronic

Pick the one closest to the actual pH

To do that, find out how many dimes from normal the CO2
is. Multiply that by 0.08 and subtract from the normal pH
of 7.4. Do it again multiplying by 0.04 and subtracting that
from the normal pH of 7.4. Compare both scores to
whatever the pH actually is. Whichever is closer
Formula for memorizers:
determines the chronicity.
24 - (dimes * 2) = Expected bicarb if acute
Step 3c: Is there a Metabolic Derangement 24 - (dimes * 4) = Expected bicarb if chronic
For respiratory alkalosis the bicarbonate should change as
well. For every dime change in CO2 the bicarb should
change by 2 point if acute or 4 points if chronic. Bicarb If actual bicarb > expected bicarb:
too many bicarbs = Metabolic Alkalosis
should change to compensate for the CO2; in a respiratory
acidosis the bicarb should go up. CO2 Bicarb
CO2 Bicarb
Multiply the number of dime change of CO2 by 2 (if acute) CO2 Bicarb
and by 4 (if chronic). Add that to a normal bicarb of 24. CO2 Bicarb
Bicarb Bicarb
Compare to the bicarb you have. If there are more bicarbs

than expected, theres also a metabolic alkalosis. If there If actual bicarb < expected bicarb:
are too few bicarbs, however, its an additional metabolic not enough bicarbs = Metabolic Acidosis
CO2 Bicarb
Metabolic Alkalosis CO2 Bicarb
The only way this will happen is if the aldosterone is up. CO2
Dont care about the gas interpretation, but instead whether
its "salt sensitive," which always means, "volume
responsive," which also asks, "are they volume deplete?"
To figure that out simply give the patient volume.

The way Metabolic Alkalosis will appear on an acid-base

interpretation question is as a secondary disturbance to a
respiratory problem or on its own. That's it.


Metabolic Acidosis The Expected CO2 for Bicarb is Winter's Formula

Expected CO2 = Winters = (Bicarb*1.5) + 8 + 2

Step 3a: Check the anion gap. See above.
Bicarb you have constant fudge
Step 3b: is the CO2 appropriate for this bicarb?
Assess if the pCO2 on the ABG is appropriate for the If actual CO2 > expected CO2:
bicarbonate. To do this, multiply the bicarb by 1.5 then add too many CO2s = Respiratory Acidosis
eight to that total. There is some fudge factor here. An
acceptable range of pCO2 is that number plus/minus 2. CO2 Bicarb
CO2 CO2 Bicarb
CO2 CO2 Bicarb
If the pCO2 is in that range then theres no respiratory CO2 Bicarb
If actual CO2 < expected CO2:
If the pCO2 is higher than that range, then there are too not enough CO2s = Respiratory Alkalosis
many respiratory acids, which means an additional CO2 Bicarb
respiratory acidosis. CO2 Bicarb
If the pCO2 is lower than that range, there are too few
respiratory acids, which means an additional respiratory
Add Back Method

Step 3c: is there another metabolic derangement? Actual Anion Gap - Normal Anion Gap = Delta
Youll read about the delta-delta. Stop reading about the Given to you 12 (Alb x 3) = Calculated
delta-delta. Its simple to calculate but requires
memorization to interpret. So we use the add-back method Then...
instead. Delta + given bicarb = expected bicarb

A normal anion gap is 12. Take whatever the anion gap is If actual bicarb > expected bicarb:
right now and find out how many extra acids were needed too many bicarbs = Metabolic Alkalosis
to get there. Current Anion Gap - Normal Anion Gap. That
CO2 Bicarb
number is the number of acids added to solution / the CO2 Bicarb
number of bicarbs that came out of solution. To find out CO2 Bicarb
how many bicarbs we started with before the anion gap CO2 bicarb
Bicarb bicarb
business, add that number to the current bicarb.

If actual bicarb < expected bicarb:
That value is how many bicarbs we started off with.
not enough bicarbs = Metabolic Acidosis
Normal is 24.
CO2 Bicarb
If there are too many bicarbs (>24) there are too many CO2 Bicarb
metabolic bases theres an additional metabolic alkalosis. CO2

If there are too few bicarbs (<24) there are too few

metabolic bases theres an additional metabolic acidosis.
Because we started with an anion-gap acidosis, this must
mean we have an additional non-gap metabolic acidosis.


Approach to Renal Failure

Renal failure, or acute kidney injury, often presents with only Pump: CHF, MI
an elevated creatinine or decreased urinary output. Because Fluid: Diarrhea, Dehydration, Diuresis, Bleed
the kidneys are redundant, unless the GFR gets very low the PreRenal Pipes: Nephrotic, Cirrhosis, Gastrosis
kidneys generally maintain near normal function. That is, until Clog: FMD, RAS
electrolytes get out of control the patient will be asymptomatic. Perfusion
Prolonged Ischemia
Its usually on routine labs that its encountered. ATN Toxins (Drugs, Myoglobin, Ig)
Contrast Induced
Its important to differentiate between pre, post, and intra-renal Acute Muddy Casts
Allergic (NSAIDs, Lactams)
failure. The list of potential diagnoses is epic so it becomes Kidney Intrarenal AIN Infxn (Pyelo)
prudent to develop a system. Injury Infiltrative (Sarcoid, Amyloid)
Intrinsic Injury WBC,
to parenchyma WBC Casts
Prerenal is the result of perfusion - whether it be from cardiac
GN Glomerular Diseases
output, 3rd spacing of fluid, or vessel diameter. In this case, the
kidneys think theyre dehydrated and hold onto salt and urine. RBC Casts
Thus, the urinalysis will show a low urine sodium (UNa<10,
FENa<1%) and a BUN/Cr ratio > 20 (use urea instead of Na if Ureter: Stones, Cancer
a patient is on a diuretic). This should also always be the first step Bladder: Stones, Cancer, Neurogenic Bladder
because its very easy to fix (IVF if dry, diuresis if wet). Obstruction to Urethra: Stones, Cancer, BPH, Foley
Prerenal Azotemia (being a little dry) is the most common cause Outflow
of acute kidney injury in the outpatient setting and should correct
quickly with fluid.
Acute Renal Failure
BUN:CR > 20
On the opposite side of the spectrum is postrenal failure from
UNa < 10
obstruction to outflow. Obstruction results in hydroureter or FENa < 1%
R/O PreRenal PreRenal
hydronephrosis and can be visualized by ultrasound. While CT BUN:CR
can be used to diagnose obstruction, ultrasound is the preferred UNa FENa Give IVF or
test. Obstruction can be at any level. Stones and cancer can Diuresis
cause obstruction throughout, but are most often in the ureters. Hydroureter
BPH, Neurogenic bladders, and kinked catheters most often R/O PostRenal PostRenal
sonogram Hydronephrosis
affect the distal GU system. The goal is to alleviate the Stent or
obstruction, which can be done using various methods. Insertion Remove
of a catheter can relieve obstruction of the distal GU. Stenting, for pre and Obstruction
nephrostomy tubes, and rarely open surgery are used for the post renal
proximal GU system. Diagnosis
Intrarenal U/A Variable
Intrarenal disease is the last consideration. It can be quite
difficult to diagnose. Definitive diagnosis can be made with a
biopsy, but biopsy is rarely (if ever) the right answer. Instead, use Bx
of the clinical history and the urinalysis often provide the
diagnosis. Casts are particularly helpful in differentiating
between the three types of intrarenal disease.


Intrarenal Urinalysis Findings

Once honed to Intrarenal, the damage can be thought of in 3 Pre-Renal BUN/CR >2 0, IVF if dry
distinct regions: UNa < 10; FENa < 1% Diuresis if wet
Post-Renal Urinary Retention Alleviate Obstruction:
1) Tubules (Acute Tubular Necrosis) Hydronephrosis /ureter Catheter, Stent, Surgery
Intra-Renal BUN/CR <10,
Acute Tubular Necrosis is caused by either ischemic damage or
UNa > 20; FENa> 1%
toxin exposure. The tubules necrose, die, and slough off. They ATN Muddy Brown Casts Supportive Care
form the shape of the tubules and present as muddy brown casts.
Allergic Eosinophilia Remove Drug
Theyll go through three phases: the prodrome where creatinine Nephritis
rises but urine output remains the same, an oliguric phase where Pyelonephritis WBC Casts Abx
creatinine rises and urine output plummets (caution fluid Myoglobin Blood, RBC NaHCO3, IVF
overload), and a Polyuric phase where the patient pees a lot. Nephritis
Through this time they need supportive care. Glomerulo- RBC Casts Disease Dependent
a. Contrast Induced ATN Gout Uric Acid Crystals Treat the Gout!
If a patient has pre-existing renal damage or is at
increased risk, and they NEED contrast, give vigorous
hydration, prophylactic N-Acetyl-Cysteine, and Stop
ACE/ARBs and Diuretics prior to contrast. Dialysis is
ineffective at preventing contrast induced nephropathy.

2) Interstitium (Acute Interstitial Nephritis)

AIN is essentially an allergic reaction with invasion of white
cells. Drugs, Infections, and Deposition Disease can cause it.
The urine will present with immune cells: white blood cells,
white cell casts (pyelonephritis), or eosinophils. Removal of the
offending agent is crucial. That means either treat the infection
or stop the drug. Steroids are often ineffective.

3) Glomerulus (Glomerulonephritis)
A patient with RBC casts on urinalysis is indicative of Glomerulonephritis History Blood Test
glomerulonephritis. There are a crap-ton of diseases that can IgA Nephropathy Post-Viral
cause it. The way to tell them apart is with a biopsy - something Post-Streptococcal Post Pharyngitis / Impetigo ASO titer
Lupus ANA, dsDNA, Sxs dsDNA
not often done. Learning the typical histories should be enough
(memorize the chart to the right). What becomes important is to Wegeners Sinus, Lung, Kidney ANCA
rule out Nephrotic Syndrome (>3.5g/24hr urine, Edema, and Goodpasture Hemoptysis + Hematuria Anti-GM
Hyperlipidemia) with a U/A Spot Test or 24-hr urine. This isnt Churg-Strauss Asthma + Hematuria
Henoch-Schonlein Post-Viral (IgA) and
step 1 stuff so dont worry about spending time memorizing
systemic vasculitis
biopsies, stains, or complement levels.

Acute Indications for Dialysis Indications for Dialysis:

The decision to dialyze is NOT based on the Creatinine!
Transplant is another definitive option. A Acidosis
E Electrolytes (Na/K)
The decision to dialyze is based on the severity of the condition I Ingestion (Toxins)
and the presence of one of the AEIOU mnemonic. O Overload (CHF, Edema)
U Uremia (Pericarditis)


Introduction and Physiology
Calcium is regulated by Calcitonin (calci-tone-down) and by
parathyroid hormone. The main level of function is at the CaSR
parathyroid gland via PTH. Calciums detected by calcium
sensing receptors on secretory cells of the parathyroid. PTH
Increased Calcium inhibits PTH release. Thus, decreased 99.9% Bound 0.1% Free
levels permit release. PTH has three effects: it 1) activates
osteoclasts to clear bone, Ca and P 2) directly reabsorbs PTH
Ca and excretes P in the kidney, and 3) indirectly absorbs Ca Albumin = Calcium
and P from the gut via Vitamin D. Calcium in the blood travels 1 0.8
mostly as bound calcium (inactive) with a small proportion as
ionized calcium. We measure total calcium routinely so it must
be adjusted for albumin levels and alkalotic states. For every Vit D
one point of albumin below four correct the calcium by 0.8.

For every disease youll use the PTH, Ca, and P levels to Ca Ca Ca
make a diagnosis. P P P
Pt has Ca
1) Hypercalcemia No
A high calcium may be nothing. If increased on ambulatory Bones, Stones Recheck Stop
screening and asymptomatic, redraw it. Further investigations Groans, Moans
required if its still increased on the redraw or there are
symptoms. Symptoms of hypercalcemia are: bones (fracture, Present
osteopenia), stones (calcium Nephrolithiasis), abdominal Diagnose
groans (nausea vomiting, abdominal pain), and psychic moans Treatment PTH
(altered mental, severe hypercalcemia only, Calcium of 13-15). IVF, Calcitonin, P
Diagnosis is less important if there are symptoms, so treat first. Bisphosphonates, Ca
Intravenous Fluid is always the first line therapy. Furosemide Furosemide
is added to increase naturesis and calcium excretion, but only
AFTER volume status is corrected (dehydration from early Treatment Onset Effect
administration of furosemide is actually HARMFUL). If more IVF Rapid Dilutes Calcium, Prerenal Excretion via
aggressive therapy is required (because symptoms are severe), diuresis
start Calcitonin (acts fast, fades fast) and Bisphosphonates Furosamide Rapid Diuresis = Ca excretion. Use only after IVF
(long term therapy). Calcitonin Immediate Effect fades quickly, gets you through a crisis
Bipshos- Chronic Puts the calcium back on bone, risk of jaw
i. 1o Hyperparathyroidism phonates osteonecrosis, good for fractures only
A single autonomous gland secretes PTH without effective
feedback. Calcium is absorbed ( Ca) while Phos is lost (P).
An additional bone finding is found here - fibrosa cystica (aka
brown tumor) - from overstimulated osteoclasts creating

large bone lesions. The treatment is resection. Use a Adenoma with After Resection, Over Time
radionucleotide scan to identify which gland is autonomous / atrophied normal atrophied glands are Recovery
hypertrophied. Monitor for signs of hypocalcemia after surgery glands unable to produce
(hungry bone syndrome). enough PTH

ii. 2o Hyperparathyroid
While were here lets talk about some other PTH diseases. In 1o Hyper PTH 2oHyperPTH 3oHyper PTH
early renal failure Vit D isnt made. This produces a PTH Vit D PTH
hypocalcemia that then causes PTH and parathyroid gland
hypertrophy. PTH increases in order to maintain a normal Ca, P Ca Ca P PTH
iii. 3o Hyperparathyroid PTH Ca, P
If renal failure continues, eventually parathyroid glands
become autonomous - just like in primary hyperparathyroidism.
This is an autonomous gland in the presence of existing renal
disease. Although resection is required, theres no risk of


iv. Familial Hypocalciuric Hypercalcemia

Caused by an abnormal calcium sensing receptor, theres a
new set point. Theres an Ca and PTH, but the body is just
maintaining its normal. Theyre asymptomatic and require no
treatment. Theres caution with stenotic aortic disease as they
age. Bone Ca PTH
Destruction P
v. Malignancy
Cancer can cause hypercalcemia. It can do it in two ways. Either
metastasis goes to the bone and actively destroys it (releasing
Ca and P) or a cancer can produce PTH-rp (parathyroid like
hormone), turning the cancer into a 10 hyperparathyroidism but PTH-rp Osteoclasts Ca PTH
with a low blood PTH (our tests only captures the real PTH; + Kidneys P
special tests are required to measure levels of PTH-rp). Treat the
cancer and the condition goes away.

vi. Immobilization
For some reason (we think its impact stress) patients who are
bed-ridden have an asymptomatic increase in calcium
secondary to bone turn over. Get them out of bed and walking - Perioral Tingling
the condition will improve. Chvostek or Trousseau
vii. Vitamin D excess
Granulomatous disease (Sarcoid, TB) can turn on Vitamin D Asx Check Critical Emergency
independently of kidneys, which increases calcium, turning off Low Ca Calcium
PTH, resulting in P being unable to be renally excreted. Use Normal IV
steroids to treat the underlying disease. Check Calcium
2) Hypocalcemia
Albumin Albumin
Albumin plays a bigger role in Hypocalcemia. Poor nutrition,
Corrects Correct
cirrhosis, or nephrosis will cause a Albumin. Adjustment for Calcium
albumin usually reveals a normal calcium. Potentially, PTH
Monitor Treat Phos Diagnosis
checking for signs and symptoms is important as it could lead
to catching a life-threatening emergency before it gets there. Ca
PO Ca +
Look for perioral tingling (usually comes first) then signs of Vit D
tetany (both Chvosteks and Trousseaus sign). Treatment is to
replace the calcium. Use PO Calcium and Vitamin D for
nonemergent, IV if emergent.

i. Hypoparathyroidism
Typically iatrogenic, either from an oops Thyroidectomy or Ca PTH Disease PO4 Path
from a parathyroidectomy of an adenoma (hungry bone Hyperparathyroidism PTH = Ca
syndrome) secondary to decreased PTH production of atrophied FHH PTH = Ca
glands. Malignancy Mets Ca = PTH
Malignancy PTH-rp Ca = PTH

ii. Vitamin D Deficiency Immobilization Ca = PTH
Whether its from renal failure or sunlight / diet deprivation, Vit D Excess Ca = PTH
having too little Vitamin D leads to secondary Pseudohypoparathyroidism PTH
hyperparathyroidism. Initially, theres decreased calcium. Vit D Deficiency Ca = PTH
Chronic Renal Failure Ca = PTH
iii. Calcium Sequestration Pancreatitis Ca = PTH
An acute condition thats often in the setting of pancreatitis.
Hypoparathyroidism PTH = Ca
iv. Pseudohypoparathyroidism
An awfully named disease that means PTH-end organ
resistance. Theres a high PTH but everything works normally.
Ignore it.


Chronic Kidney Disease (CKD) Stage Description GFR Tx Goals
When the creatinine remains elevated and wont come back I GFR effect >90 Comorbidities
down, its a case of CKD. Its usually >3 months of reduced II Mild 60-89 Comorbidities
GFR (<60mL/hr, or a Creatinine~2). The stage of renal disease is III Moderate 30-59 Comorbidities / Complications
based on the GFR. We use the creatinine as a surrogate for GFR. IV Severe 15-29 Prepare Dialysis / Transplant
There are a number of equations that can be used to estimate the V Kidney Failure <15 Dialysis required for survival
GFR by the creatinine, but to use any of them the creatinine must
be stable. That is, only in chronic kidney disease can you use the
Creatinine to estimate the GFR.

The overall management of chronic kidney disease is to prevent Intervention Goal Progression
progression and manage complications. ACE-inhibitor BP <130 / <80 HTN
Insulin bG 80-110 DM
Prevent progression
Hypertension and Proteinuria are managed with Ace-
inhibitors and Angiotensin Receptor Blockers. Use either an
ACE-I or an ARB dont combine them. The blood pressure goal Complication Goal Example
in CKD remains more aggressive than traditional hypertension Anemia Hgb > 10 EPO, Iron
management; its <130 / <80. Secondary PTH Calcimimetics
Hyperparathyroidism Phos Binders
Diabetes is managed similarly. All diabetics require annual Osteoporosis Dexa > -2.5 Ca, 1,25VitD
urinalysis to assess for microalbuminuria. The A1c goal remains Volume Overload None Loops
< 7.0. Caution must be used in CKD as insulin is renally excreted. Hemodialysis
Metabolic Acidosis Bicarb > 20 NaBicarb
Manage Complications
Anemia results from decreased erythropoietin. The goal
hemoglobin is 11-12. Anemia in CKD is usually normocytic and
seen in late stage disease. Use Erythropoietin and Iron
supplementation to sustain blood counts. Transfusions with
dialysis can also be done.

Secondary hyperparathyroidism is a product of phosphate

retention (elevated phosphorous stimulates PTH) and Vitamin-
D Deficiency that leads to low calcium (low calcium stimulates
PTH). Thus, phosphate binders such as sevelamer and
calcimimetics such as cinacalcet are used to decrease this risk.

Chronic Kidney Disease Mineral Bone Disorders from secondary

hyperparathyroidism can be protected against by giving Calcium
and 1,25-Vitamin D supplementation.

Volume Overload is caused by the loss of urinary output.

Initially, stimulation of the nephron can be sustained using loop
diuretics such as furosemide. Combination therapy with
metolazone and furosemide is a last ditch effort to maintain
adequate urinary output. Ultimately, dialysis manages volume

Acidosis results in a bicarb between 12-20. Bicarbonate

supplementation is used to reverse this.


Polycystic Kidney Disease
A common disease in the population, its responsible for 5-10% Dz Gene Associations
of ESRD (end stage renal disease) and Dialysis. Its an Polycystic ASD SAH, Liver, Pancreas
autosomal dominant genetic disease that insidiously converts Kidney Hematuria, Flank Pain, Infxn, Stones, HTN
the renal parenchyma to cysts. These cysts have no orientation Disease Ultrasound or CT to see cysts
Polycystic ASR Radially aligned cysts at birth
and can be any size. Eventually, functional nephrons are
Kidney Barely compatible with life (peds only)
obliterated and replaced. Along the way the cysts can bleed Disease
(producing pain and hematuria, commonly mistaken for stones), Simple Incidental finding do nothing
get infected (pyelo), or actually form stones. These cysts also Cyst
retain the ability to activate the RAS and can produce malignant Complex Biopsy to rule out malignancy
hypertension. A symptomatic patient can be diagnosed with an Cyst
Renal Smoking, ESRD, VHL
Ultrasound. Theres no treatment, but manage complications
Cell Flank Pain, Flank Mass, Hematuria
then do dialysis / transplant when they finally fail. Whats Carcinoma Ultrasound or CT scan to find it
critical in this disease is to identify the Extrarenal Needle to biopsy it
manifestations. Cysts can form in the liver (cirrhosis), pancreas Excision, Rads / Chemo available
(pancreatitis) and in the cerebral vasculature; they predispose Epo Paraneoplastic Syndrome or Anemia
the patient to subarachnoid hemorrhage.

Simple Cysts
Sometimes an ultrasound or CT will reveal a cyst. If its simple -
no echoes and just one continuous mass (like a smooth balloon)
theres no need to worry about it. If symptoms develop (see
below) biopsy and then excise.
Polycystic Kidney Disease
Complex Cysts
If that ultrasound or CT reveals a large or septated cyst it must
be biopsied to rule out malignancy. Do a needle-guided biopsy
and treat if its a cancer or for symptomatology.

Renal Cell Carcinoma

A Renal Cell Carcinoma can be detected from the ultrasound or
CT, which is why the biopsys done for complex cysts. However,
if the classic triad of flank pain, hematuria, and a flank mass is Simple Cyst
seen its almost guaranteed to be cancer (though it may not always
be present). Patients are at increased risk with smoking, ESRD,
and with Von Hippel-Lindau. If a hematuria comes up on a U/A,
go ahead and get an ultrasound or CT the flank to visualize the
kidneys. Biopsy the lesions and resect. Since the renal cell
carcinoma spreads hematogenously disseminated spread may
have already occurred. Renal vein thrombosis is a real problem
with this cancer. Finally, there can also be either anemia or Septated Complex Cyst
Polycythemia. Either the cancer is stealing the blood (anemia) or
its actually producing an epo paraneoplastic syndrome.

Renal Cell Carcinoma

Nephrology [KIDNEY STONES]

Kidney stones come in a variety of forms. Theyre caused by the Types of Stones Radio- Risk Factors
precipitation of something - either because their quantity is Calcium Oxalate Opaque Ca - Thiazide
large or due to decreased intravascular volume. Each type has Oxalate - Meat in diet
its own risk factor, which is why there needs to be a close analysis Citrate - Fruit in diet
Magnesium Opaque Alkaline Urine secondary to frequent UTIs
of both the stone and the urine after the stone passes.
Ammonium with Urea-Splitting bacteria (Proteus)
The typical patient will present with colicky flank pain that (Struvite) Creates Massively large stones resection
radiates to the groin and with nausea / vomiting. This Uric Acid Lucent Gout - Allopurinol
presentation may mimic pyelonephritis (look for a fever and Tumor Lysis - Rasburicase
white cell casts) and renal cell carcinoma (look for a palpable Cysteine Lucent Rare inherited rental tubular defect
Hematuria, Colicky Flank
Because of the similarities between diseases, start with a Pain Radiating to the
Groin, Nausea / Vomiting
urinalysis. The absence of casts and the presence of blood (even
microscopic hematuria counts) is indicative of the stone. In the
absence of microscopic hematuria, the likelihood of a U/A
Hematuria Hematuria
symptomatic stone is quite low.

The diagnosis is confirmed with a Non-contrasted CT scan - by Stone Consider Something Else
(Highly Sensitive)
far the best test. There will be times where that test is not
available, as in pregnancy. If pregnant, use ultrasound. While NonCon U/S if
ultrasound may not be as sensitive for distal stones or hydroureter CT Pregnant
as CT, it can be done safely without exposing the fetus to
radiation. KUB should NOT be used for diagnosis, but can be Confirmed
used to track disease progression in known stone disease. Pass Stone
Intravenous Pyelogram is no longer used. IVF + Analgesia Analyze Stone NOW
Treat on Size
Management is based on the size of the stone: 24-hr Urine >6 weeks
If <5 mm the stone will pass spontaneously. Hydration and pain
control is all thats needed.

If <7 mm use medical expulsive therapy. This is achieved with

Calcium Channel Blockers (Amlodipine), Alpha-Blockers
(Terazosin) or both. Path: Precipitates form stone in tubules or ureters
Px: Hematuria, Colicky Flank Pain that Radiates to
the Groin, no fever or leukocytosis
If <1.5 cm, the stone is unlikely to pass on its own and needs to Dx: 1st: U/A
be broken down. Both ureteroscopy (for distal stones) and Best: Non-Con Scan
lithotripsy (for proximal stones) are appropriate. Other: U/S if pregnant
KUB if tracking disease
If >1.5 cm, the stone will need to be resected. This is done either IVP never
Tx: <5mm: IVF + Analgesia
with laparoscopic exploration (proximal stones) or with
<7mm: MET (CCB, Alpha Blocker)
percutaneous anterograde nephrolithotomy (distal stones). <1.5cm: Lithotripsy (proximal), ureteroscopy
If emergent, decompression of the GU system is required. As in >1.5cm: Surgery
the case of obstructive sepsis, either a stent (distal disease) or Sepsis: Nephrostomy (proximal), Stent (distal)
nephrostomy (proximal disease) is indicated. F/U: Strain and Analyze Stone
24-hr urine for Ca, PO4, Urate, Oxalate
Regardless of the way the stones taken out, it needs to be
analyzed. See the chart on the top of the page for composition of
different stones. Then, 6 weeks later analyze a 24-hr urine.
Correct the risk factors and bam! good as new.


Hyperkalemia Iatrogenic K-Sparing Diuretics
(over administered) (ACE/ARB, Aldo-i) Ingestion and CKD
Extracellular potassium is tightly regulated. It doesnt take that
much extra potassium in a syringe to kill someone (death

penalty). The range is typically 3.5 5.5 (>4.0 is normal in High Serum
cardiac patients). There are many causes of hyperkalemia - some RTA K
rare, some common. They all lead to the same symptoms: Hypo Artifact /
areflexia, flaccid paralysis, paresthesia (aka decrease motor aldosterone Hemolysis
Areflexia, Spastic Paralysis,
and sensation) and ECG Changes. Whenever theres an
abnormal potassium level, the first thing to do is repeat the lab Paresthesia
ECG Changes
(the sample could be busted or the cells could have hemolysed).
Yet, the crucial evaluation is the ECG 12-Lead. Remember that Check K
Elevated Normal
everything gets bigger as the K goes up the PR prolongs, Levels
the QRS widens, and the T waves peak. There are 3 phases of

treatment. Theyre dependent on severity and ECG changes. Hyperkalemia Something Else
Phase I is to stabilize the myocardium with IV calcium Rec
heck K Unstable
gluconate. Phase II is to decrease serum K by sequestering it -
Elevated s IV Calcium
hiding it - in the cells. Do that with Insulin and glucose (the
insulin shifts the K, the glucose prevents hypoglycemia) or with Hyperkalemia EKG Insulin/Glucose
Bicarbonate. Phase III is to actually decrease total body K with Confirmed
either K-wasting diuretics or more commonly with Kayexalate. Bicarbonate
If in Renal Failure or the K is extreme, use Dialysis. s
Kayexalate Kayexalate
K comes back high Repeat the draw
on a lab draw
K comes back confirmed high Kayexalate,
but the patient is asx, EKG Stop K-Sparing drugs
Everything gets bigger Symptoms or EKG s IV Calcium, Insulin/Glucose,
With or without elevated K Kayexalate, Consider Dialysis
Renal Failure and Dialysis
Sine Wave any of the above

IV Calcium Stabilize Stabilizes Myocardium
Insulin + Glucose Temporize Shifts K into cells
Bicarbonate Temporize Shifts K into cells
Hypokalemia Kayexalate Total K Total Body K
Less exciting than hyperkalemia but just as deadly, a low Dialysis Total K Total Body K
potassium has multiple potential causes. Its usually going to be
through either GI losses (diarrhea, laxatives, vomiting) or Renal

Losses (hyperaldo states, loop diuretics or thiazide diuretics).
Losses Low Serum GI Losses
Hyperaldosterone K Vomiting
While rechecking the K and checking an EKG could be done, = Bartter
Loops Diarrhea
mostly the K is simply repleted. Repletion is performed with oral Thiazide
= Gitelman
or intravenous potassium. Oral replacement is preferred. If IV Areflexia, Spastic Paralysis,
is to be used, the rate must be <10mEq / hr if by peripheral IV

(PIV), or <20mEq/hr if by central line. ECG Changes

Check K
Decreased Levels Normal

Hypokalemia Something Else

Recheck K Normal
Hypokalemia Sxs Replace
Confirmed PO > IV


Introduction Dehydration
Disorders of sodium are really disorders of water balance.
Normally, there are two compartments - the blood and the brain. HyperNa
These compartments are in equilibrium. If theres a disturbance
in how much stuff is in the blood the water will shift. When Blood Brain
theres too much stuff in the blood, water will move out of the [Na]
cells and into the blood to balance it (Hypernatremia), Time
dehydrating the cells. If theres too much water (less stuff) in
the blood (hyponatremia), the water will move out of the blood
and into the cells to balance it, causing them to swell. Either way, HypoNa
thats bad news for the cells. Its the dehydrating and swelling that
leads to symptoms.
To fix Hypernatremia (which is always a deficiency in water)
the task is easy. PO Water is always the best way to replace a
water deficit. However, there may also be the need for Hypotonic
Solutions such as D5W or 1/2NS. Before replacing the free water Onset Symptoms Treatment
deficit, replace volume with Normal Saline. Mild Asymptomatic HypoNa: Dz-Specific
HyperNa: Po Water
To fix Hyponatremia the task is a bit more challenging. If the
patient is in a severe state (regardless of the diagnosis), use Moderate Nausea, Vomiting, Hypo Na: IV NS
Hypertonic Saline (3%). If not severe, then the management is Headache HyperNa: IV NS
based on the underlying diagnosis. For example, SIADH is (all non-specific) NOT Hypertonic
Acute or Severe Coma, Seizures, HypoNa: IV Hypertonic
treated with volume restriction, volume overload with diuresis,
(Na<110, Hours) Death HyperNa: IV D5W
and volume depletion with volume resuscitation. To determine
which course of action to take, further investigation is required.

Sodium correction should occur no faster than 0.25mmol/hr

unless severe. Correction by 4-6 is all that is required to eliminate
symptoms in most cases. If sodium is corrected to quickly, it may
result in osmotic demyelination syndrome (formerly called
central pontine myelinolysis), leaving the patient a spastic
quadriplegic. Thus, a regular assessment of the Na is required.

Isotonic Hyponatremia = Pseudohyponatremia
Pseudohyponatremia is a product of laboratory artifact. The
calculated osmoles will be elevated, but measured will be
normal. This is a result of fats and proteins. Newer labs rarely
encounter this issue.

Hypertonic Hyponatremia
There can be other stuff in the blood that accounts for osmotic
activity other than sodium. While the measured sodium is low,
the measured osmoles are elevated. This is usually a product of
glucose, BUN, or sugar alcohols. For every 100mg/dL of glucose
above 100 adjust for the Na by 1.6. If the corrected sodium is
normal, correct the osmotic compound alone.


Hypotonic Hyponatremia = True Hyponatremia
If the measured osmoles are low, then the original assessment of
the water status was accurate. Now its up to you to determine the
Low Sodium
underlying etiology and correct it to correct the sodium.

Assessment of the Urine Sodium and Urine Osmolality can be

used to separate most causes of hyponatremia. However, the
clinical scenario often gives the answer. This is especially true on Determine Serum
High Osmoles Normal
a vignette, where there cant be a mystery to have a single correct
answer. If a urine sodium is decreased, the kidney is working and
theres poor perfusion to it. If the urine osmoles are concentrated,

Hypertonic Isotonic
ADH is activated. The appropriateness of this is discussed in the = 1.6 Na True HypoNa PseudohypoNa
Posterior Pituitary lecture. (Fats + Proteins)

Hypervolemic Hyponatremia
Dry Mucous Membranes
JVD, Edema, Volume Status Burns, Fever, Tachypnea,
If the patient is wet (i.e. JVD, edema, CHF, Anasarca), theyre Clinical Picture Hypotension, Orthostatics
CHF, Anasarca
overloaded. The fluid is in the third space and needs to be
mobilized. Treat with diuretics.
Hypovolemic Hyponatremia
If the patient is volume down (dry mucous membranes, burns, IVF, see if it
Normal Volume corrects
fevers, tachypnea, hypotension), then all the patient needs is
Volume resuscitation. The sodium should correct with IVF.

Euvolemic Hyponatremia
If the patient is euvolemic, were left with RATS. Rule out each
disease one at a time. Renal Tubular Acidosis is assessed with a
urinalysis, Addisons disease with cortisol, and Thyroid disease IntraRenal ExtraRenal
with a TSH. Diuretics Fluids
SIADH is a diagnosis of exclusion. Its treated with volume

restriction and gentle diuresis. Refractory cases can be treated
with demeclocycline. Check out the endocrine topics for details.
()*+,-. 123
Serum Osmoles = (2#$%) + +
/0 4.0
Vaptans are absolutely contraindicated in hypovolemic
hyponatremia. Theyre never the right answer.

Fluids are discussed in greater detail in the Intern content.
Volume Maintenance Free Water Nutrition
Volume resuscitation is done with Normal Saline or Lactated LR NS D5 D5W PPN
ringers; its provided as a bolus. NS
Free Water is replaced with hypotonic solutions, given either as
PO free water or D5W. NS is a hypotonic solution and can be
used to administer free water, but I want you to learn it as
maintenance fluid.

Maintenance fluid is administered as any combination of NS,

NS, with or without D5.

Nutrition is provided as PPN or TPN. D5 containing solutions do

not count.


All causes of anemia have the same presentation thats based on the severity and etiology. Theres point in Fatigue, Malaise, SOB,
saying over and over again for each disease the symptomatology. Instead, knowing whats unique in the history and Pallor, Pale Conjunctivae,
then the specific best diagnostic test for each one becomes most important. Presyncope, MI, CVA
The symptoms are listed in the chart at the bottom. The symptoms of anemia are vast - everything from a little fatigue, a
acutely, high output cardiac failure chronically, even death as a result of myocardial infarction. While I have
stroke Hgb/Hct Something Else
them in a nice chart, remember that the symptoms are dependent on the severity and the patients tolerance. It all comes Normal
down to the oxygen delivery. Oxygen delivery is based on three things: Hgb, %Saturation, and Cardiac Output. An Hgb/Hct
old man with COPD (%sat), MI and HF (CO), and on a Beta Blocker has a limited supply as is - any drop in the Hgb
significantly compromises him. Even a drop from 10 to 9 can be fatal. On the other hand, the 25 year old athlete can
Hgb that falls from 13 down to 7. Hell experience only a little fatigue and will compensate with tachycardia.

Microcytic Anemia Thalassemia Normocytic Anemia Macrocytic Anemia

Hgb Electrophoresis
Iron Studies Minor: , Reticulocyte Count Acute Blood Smear
Major: Transfuse LDH Bilirubin Loss

Haptoglobin 5+ Lobes
Plug Hole PMNs
Give Blood

Iron Anemia of Sideroblastic Confirmed Hemolysis Paroxysmal Megaloblastic Nonmegaloblastic
Deficiency Chronic Dz Nocturnal
Give Iron Tx the disease Try B6

Sickle Cell Autoimmune G6PD Def Folate
B12 Folate
Smear, Hgb Electrophoresis Coombs Smear Smear
IVF, O2, Analgesia Steroids G-6-PD Level Osmotic Fragility B12 Def. Folate Def.
Exchange Transfusion Avoid Triggers Splenectomy
Hydroxyurea, Vaccines B12 Folate
Hgb Hct Symptoms
>10 >30 Symptoms Equivocal
24-30 Tired, Fatigue, Malaise Hgb X %Sat X CO
6-8 18-23 Dyspnea on Exertion DO2=
4-6 12-17 Lightheaded, Presyncope, Syncope Old Man No Compensation MMA Normal
<4 <12 Chest Pain, Stroke, High Output Failure Athlete Compensates


Understanding bleeding can be complex. You probably
memorized the entire clotting cascade and PT/PTT valves for
every disease for Step 1. Lets go over the essentials of hemostasis (1) (2) (3) (4)
instead of all the complexities. Primary hemostasis begins with endothelial injury,
releasing von Willebrand factor (1), sticking to platelets via
Primary Hemostasis is a function of platelets that starts with Glyc-Ib, adhesion (2). This activates the platelets and allow
for aggregation through fibrinogen and Glyc-IIb/IIIa. The
endothelial injury. From the endothelium, von Willebrand
end result is a fibrinogen mesh plug of platelets, ripe to be
factor (vWF) is released like sticky Velcro tentacles, snatching activated to fibrin in secondary hemostasis (shown below).
onto platelets via Glyc-Ib via a process called adhesion.
Adhesion activates platelets (release of granules and XII VII
rearrangement of protein surface). This allows fibrinogen to link VII
platelets via glycoprotein IIb/IIIa through a process called IX
aggregation. The end product is a platelet plug that stops the X Plasminogen
bleeding initially, with a fibrinogen mesh ready to start the heavy Prothrombin Thrombin tPA
duty clotting. Plasmin
Fibrinogen Fibrin Fibrin Split
Secondary Hemostasis ends with fibrinogen mesh turning into Products
fibrin. Along the way multiple clotting factors need to be
activated. Factor 7 is by its lonesome in the extrinsic pathway Superficial, Mucosal Patient with Bleeding Deep Bleeding
(measured by PT). Factors 8-12 (except 10) are in the intrinsic
Epistaxis Hemarthrosis
pathway (measured by PTT). The two pathways converge with Hematoma
Gingival Bleed
the activation of Factor 10, which together with Factor 5, turns Prolonged Bleeding
prothrombin to thrombin. Thrombin activates the fibrinogen
mesh on those platelets to activate clotting. The whole deal ends 1o Hemostasis 2o Hemostasis
by the activation of tPA, which dissolves the clot into split (Platelets) (Factor)
products. Youll see how easy all the diseases are to understand
if you can just follow the pictures. Platelet Count Factor VII, VIII
Differential Decreased Normal
People like to jump to coagulation studies with bleeding. For the Platelets Platelet Fxn
most part thats ok. Have a bleed? Get a CBC and Coags. But if
interested in determining the best test for the patient in front of Factor Acquired
you, ask if they have platelet bleeding (superficial bleeding Smear Bernard-Soulier Deficiency Disease
secondary to platelet dysfunction) or factor bleeding (deep H+P Uremia
bleeding secondary to hemostasis dysfunction). Then, if its a BM Bx Drugs vWD Vit K Def
problem with platelets use platelet count and platelet function Hemophilia A Liver Dz
(only if count is normal as a count or function) to get near a Sequestration Hemophilia B DIC
diagnosis. If its factor bleeding use PT, PTT, INR, + Factor
Levels to narrow the differential. From there each disease has its Production Destruction
own detail, confirmatory test, and treatment.
Aplastic Anemia ITP, TTP, DIC
Were going to discuss only highlighted diseases in the coming
section - those commonly tested on Step. Check the intern
section for more on bleeding; its separated into an entire lecture Test Measuring What? Diagnosis / Diseases
for platelet bleeding and another dedicated to factor bleeding. PT Intrinsic Pathway Warfarin, Vit K, Factor 7
PTT Extrinsic Pathway Heparin, Lupus Anticoagulant
Bleeding Time Formation of Plug Platelet Disorder
(Platelet Fxn) Thrombocytopenia
Factor Levels Direct Measure Factor Deficiency
Mixing Study Difference Factor Deficiency
Between Inhibitors
vWF Direct Measure vWD
D-Dimer Indirect Measure of DIC
Fibrinogen fibrinolysis
Fibrin Split


Von WillebrandBut What About?
1. Von Willebrand Disease Glanzmanns Deficiency of GlycIIb/IIIa
A person with a platelet type bleeding and a normal platelet Thrombasthenia
count likely has vWD. If theres vWF, platelets cant adhere. Bernard-Soulier Deficiency of Glyc-Ib
Adhesion = Aggregation = Plug. Start by testing for Uremia Seen in Renal Failure
dysfunction of platelets with a bleeding time (archaic) or the Drugs We give patients medications to limit clotting
newer platelet function test then get a vWF assay. Since vWF ASA, Clopidogrel, NSAIDs, Abciximab
stabilizes Factor VIII there might also be factor type bleeding.
Treat with desmopressin to vWF. If severe, give
cryoprecipitate or Factor VII acutely.

2. Thrombocytopenia Thrombocytopenia
This is a topic all on its own. Get the general idea of each potential TTP Platelets + Fever + Plt+ Exchange Never give
cause and learn what to look for. If all cell lines are decreased AMS + RF + MAHA RBC Transfusion platelets
then its an aplastic anemia (a production problem). If the spleen HIT On Heparin 5-7d hx Plt Stop Heparin Tirofiban
is really big its sequestration (a sequestration problem). The 3-4 d with h/o HIT only
other forms of thrombocytopenia all involve destruction of DIC Any systemic or severe dz, Plt Tx Underlying Plts
platelets. Heparin-Induced Thrombocytopenia (HIT) occurs in s/p OB, s/p trauma oozing PT Disease cryo
patients on Heparin (usually on day 5-7 of tx). To alleviate stop from every hole PTT whole blood
the heparin and get HIT-Antibodies. If the patient has the ITP Female with platelets but Plt Plt<20 or bleeding IVIG
classic pentad (platelets, fever, altered mental status, renal nothing else Plt >20 Steroids
failure, Microangiopathic hemolytic anemia) then they have Refractory: Splenectomy
TTP. Do a plasma exchange and absolutely avoid platelet
transfusion. Finally, if she has a thrombocytopenia and all the
others have been ruled out assume she has ITP - an autoimmune
hemolysis of platelets. Fight with IVIg or Rhogam right now,
steroids chronically, and splenectomy if refractory.

3. Hemophilia
An X-linked recessive (boys only) disorder that affects Factor 7
(type A) or Factor 8 (type B). Its a deep factor type bleeding in
children (hemarthrosis is classic). vWD should be ruled out.
Since Factor VIII doesnt last very long transfuse only when the
patients actively bleeding.

4. Liver Disease + Vitamin K Deficiency

The liver needs vitamin K and Vitamin K needs a liver. Either
way, factors 2, 7, 9, and 10 (also protein C+S) are broken,
messing up both the intrinsic and extrinsic pathways and
producing a factor type bleeding. If the patients cirrhotic,
antibiotics killed intestinal K-producing bacteria, or
iatrogenically we blocked the effect with warfarin there could be
a bleed. The move should be to test for factor levels. Ultimately,
however, K will have to be given. If theres no improvement after
K its liver disease. If it improves they were just lacking vitamin

5. Disseminated Intravascular Coagulation (DIC)

Occurs in significant systemic disease (sepsis, shock,
malignancy) where clotting goes crazy; many clots form where
there should be none. This leaves platelets and clotting
factors for where the holes actually are. This person bleeds from
everywhere. There isnt one single test, but together an PT
PTT (factors), Fibrinogen (except in early disease), a D-
Dimer / Fibrin Split Products and the clinical history give a
strong argument. Treat by giving everything back (platelets,
cryoprecipitate, blood) and fix the underlying disease.


Disease Patient PT PTT Bleeding Diagnosis Treatment

vWD Platelet Bleeding Normal Count - - vWF Assay DDAVP
BS Glyc Ib Assay Factor VII
GT Glyc IIb/IIIa
Uremia + Renal Failure CMP / E-Lytes Dialysis
Drugs Clopidogrel, ASA, NSAIDS Med List Stop
Aplastic in all cell lines - - BM Bx Fix Cause Underlying
Platelet Anemia (hypocellular)
Dysfunction Splenic platelet and a big spleen Splenomegaly ?
Sequestration U/S of Spleen
HIT platelets + Heparin (day 5-7) - - HIT-Ab Stop Heparin, start Tirofiban
TTP Fever, RF, plt, MAHA, AMS - - Clinical Plasma Exchange, NEVER plts
HUS Fever, RF, plt, diarrhea - - Clinical Plasma Exchange, NEVER plts
ITP platelets in a female, everything - - Diagnosis of Exclusion IVIG or Rhogam (acute)
else ruled out Steroids (Chronic) Splenectomy (refractory)
Hemophilia Boys with Hemarthrosis - - Factor Levels, Factors only with Bleeding
r/o vWD
Vit K Antibiotics for gut - Vit K levels or just give Vit K Vitamin K
Deficiency or Leafy Greens
Factor Liver Dz Older, EtOH, cirrhosis, Hep B/C - Vit K, if correction, diagnosis is Stop Drinking, Manage chronic disease,
Dysfunction Liver Dz Manage Complications
Warfarin Pt with Afib, DVT, PE or other - Patient Med List, INR Vit K, Blood is Needed
need for anticoagulation
DIC Sepsis, Trauma, Malignancy, - Fibrinogen Fix underlying disease
Bleeding from everywhere D-Dimer Cryo, FFP, Blood


In dealing with Leukemias we must consider whether theyre
acute (undifferentiated, aggressive) or chronic (differentiated,
indolent). The acute leukemia patients are going to be SICK Asx WBC on
routine labs
(fever, night sweats, bleeding, and infection). Its a product of WBC (60-100)
useless, immature cells crowding out effective cell lines, creating
a pancytopenia. Conversely, Chronic leukemia will be
asymptomatic and found on a routine screen for something else Differential
(unless very late stage). Patients present with an enormous Polys Lymphocytes
number of leukocytes. Which line gets elevated is dependent on
the type of cancer. Myelogenous is Neutrophils, while CML CLL
Lymphocytic is Lymphocytes. In all cases the first test will be a
Imatinib or
smear to rule out acute disease (the presence of blasts). Then, a
differential is done to rule out chronic disease. Definitive
diagnosis is made with a bone marrow biopsy.

1. Acute Myelogenous Leukemia

This is a disease of immature (acute) neutrophils (myelogenous) Cytogenetics
cancer in the blood (leukemia). It can arise de novo after
Confirmatory Dx
exposure to radiation, benzene, or chemo, or be a transformation
(so-called blast crisis) from other marrow cancers (CML,
MDS). The symptoms of bleeding, bruising, petechiae, pallor
and fever set in rapidly. CBC is of no use as all values could be
or . What gives the diagnosis away is seeing blasts on a
peripheral smear. To confirm the diagnosis a Bone Marrow Fever, Bone Pain,
Biopsy showing >20%Blasts is required, as well as cytogenetic Infxn, Petechiae,
analysis showing neutrophils (myeloperoxidase). A special form Bleeding, Anemia
of AML, the M3 type (Promyelocytic), is diagnosed by the
presence of Auer Rods. Treatment with chemotherapy
(idarubicin + Ara-C) can push AML into remission. M3 is
treated with Vitamin A, which induces development out of the Polys Lymphocytes
blast phase by all-trans retinoic acid. >20% blasts on peripheral
blood also makes the diagnosis.
2. Acute Lymphoid Leukemia M3: VitA PPx CNS
This is a disease of immature (acute) lymphocytes (lymphoid) BM
cancer in the blood (Leukemia). Its often found in the pediatric
patient who presents with bleeding and bone pain. As in AML,
look at the smear for blasts then get a Bone Marrow Biopsy to Cytogenetics
confirm >20% blasts and cytogenics. Like AML, its treated with Prognosis
Confirmatory Dix
chemo (cyclophosphamide, doxorubicin, vincristine, and
methotrexate) with a fairly decent sustained remission (90%)
and poor cure rate (50%). Consider doing intrathecal ppx
chemo-radiation with Ara-C or Methotrexate, because the
CNS is a sheltered region for ALL to hide while undergoing
therapy for systemic blood and marrow cancer. >20% blasts on
peripheral blood also makes the diagnosis.


3. Chronic Myelogenous Leukemia
This is a disease of matured (chronic) neutrophils
(Myelogenous) cancer in the blood (leukemia). Its associated
with the Philadelphia chromosome a t(9,22) translocation with
overactive activity of a tyrosine kinase BCR-ABL. It presents as
an elevated white count with an abnormal percentage of
neutrophils (>60 WBC, >90% PMNs). Once the diagnosis is
made confirm with a Bone Marrow Biopsy. Revolutionary
therapy with the tyrosine-kinase inhibitor Imatinib has
prolonged survival and delayed the blast crisis. Newer tyrosine-
kinase inhibitors have been used in imatinib-refractory cancers.
However, inevitably this cancer becomes resistant, progresses to
AML, and the patient ultimately succumbs.

4. Chronic Lymphoid Leukemia

This is a disease of mature (chronic) lymphocytes (lymphoid)
cancer in the blood (leukemia). It occurs in old men most
commonly presenting as an asymptomatic in WBC. A diff will
show an absolute lymphocyte count >50. You might see smudge
cells (artificial rupture of fragile cells during smear preparation)
on smear, but its the diff and subsequent bone marrow biopsy
that defines the disease. The average survival is about ten years.
If theyre old do nothing; theyre more likely to die with it than
from it. If they become symptomatic, treat with chemotherapy:
fludarabine or rituximab-based. If the patient is young (<65)
and theres a donor go ahead and perform a stem cell transplant.

Disease Patient Age Cell 1st Test Best Test Treatment Special
Fever, Ara-C
Bleeding, 7 Lymphoid Smear BM Bx MTX CNS PPx
Petechiae, >20% Blasts Cyclophosphamide
Acute Infection, Doxyrubicin
Bruising 67 Myelogenous Smear BM Bx Auer Rods/M3 = Vit Auer Rods
Bone Pain (Neutrophils) >20% Blasts A
Idarubicin + Ara-C

47 Myelogenous Diff Philadelphia Imatinib Blast Crisis
White (Neutrophils) Chromosome
Chronic Count, t(9,22)
Found on BCR-ABL
routine screen If old or Donor =
87 Lymphoid Diff BM Bx If old and symptomatic = Chemo
If young and donor = BM Transplant


Introduction Nontender Lymphadenopathy
Lymphoma is a malignancy of lymphocytes within lymph nodes. (+ B Symptoms)
A lot of this was covered in step I: translocations, cell types,
histologic subtypes, etc. Thats good information to impress the
attending with. Its used for determining severity of disease,
Metastatic Another Excisional Biopsy ? Consider
prognosis, and targeted therapy when typical chemotherapy fails.
Disease Cancer Resection
However, that level of specificity is better left up to the
hematology oncology boards. Lets focus more on the diagnosis Cancer TB, Fungal
and treatment of lymphomas. Screen Reed Reed Gram Stain, Cx
Sternberg Sternberg
Presentation and Diagnosis
Lymphoma presents as nontender lymphadenopathy. The
presence of B symptoms (fever, night sweats, weight loss) is Hodgkins Non-Hodgkins
used only for staging designation. While its true that B symptoms Lymphoma Lymphoma
are more common in Hodgkins than Non-Hodgkins, it can be
present in either disease and shouldnt be used to change the
diagnosis. Other non-specific or uncommon findings are Pel-
Epstein fevers that come and go over weeks or the painful Staging
lymphadenopathy with EtOH and HSM. These can be additive
clues for a Hodgkins lymphoma, but arent required for diagnosis Chemotherapy
or even suspicion of diagnosis. When a painless lymph node is +
encountered, the first step is to get an excisional biopsy (an FNA Radiation
is insufficient and often equivocal). The excisional biopsy is
required to see the lymph node architecture, giving evidence of Stage
the type of lymphoma as well as allowing detection of Reed- I One Group of lymph nodes
Sternberg Cells. The presence of these abnormal B cells defines II > One Group of lymph nodes on same side of diaphragm
Hodgkins lymphoma versus Non-Hodgkins lymphoma. The III > One Group of lymph nodes on opposite side of
excisional biopsy also allows for cytogenetic testing, but thats diaphragm
beyond our scope. If its negative for lymphoma consider mets IV Diffuse Disease in (blood or bone marrow)
and infection. A = No B Symptoms B = Positive B Symptoms

Staging Hodgkins Non Hodgkins
Once the diagnosis of any lymphoma is made the next step is B Sxs more common No B Sxs
to stage the disease. For simplicity, once its reached > Stage IIb, Spreads Anatomically Non-Contiguous Spread
staging can stop. Start with a Chest X-ray then perform either a Usually IIa or better Usually IIb or worse
Pet/Ct or a CT of Chest/Abd/Pelvis. If everything is negative a Pel-Epstein Fevers (rare) Extranodal Disease
Bone Marrow Biopsy must be performed to exclude bone Chemo is Chemo is R-CHOP and CNS
marrow involvement. The push towards all Lymphoma receiving ABVD and BEACOPP prophylaxis with Methotrexate
systemic chemotherapy has challenged the necessity for Bone
Marrow aspiration, though it is still considered standard of care.

Treatment - Cisplatin Ototoxicity

Lymphoma is treated with chemotherapy and radiation -Bleomycin Pulmonary Fibrosis
regardless of the stage. Hodgkins is treated with ABVD in
almost all instances except for extensive, bulky, or a disease -Adriamycin/Doxorubicin Cardiac
presentation with poor prognostic features (you shouldnt learn Toxicity
what those things are for the test), in which case BEACOPP is Peripheral Neuropathy
used. Non-Hodgkins disease is treated with R-CHOP, a
Rituximab-based regimen or with Rituximab alone. Know the

-Cisplatin Nephrotoxicity
side effect profiles of these drugs using Chemo man to the right. -Cyclophosphamide (Cycle )
Hemorrhagic Cystitis


Adriamycin/Doxorubicin Bleomycin Rituximab
Bleomycin Etoposide Cyclophosphamide
Vinblastine Adriamycin/Doxorubicin Hydroxydoxorubicin
Dacarbazine Cyclophosphamide Oncovorin / Vincristine
Oncovorin / Vincristine Prednisone


Macrocytic anemia is a production anemia reticulocytes will be CBC
reduced despite an anemia. When identified, the reflex test is the
blood smear. In the case of impaired DNA synthesis
(megaloblastic anemia) therell be hypersegmented Anemia
neutrophils. If there are none, its said to be non-megaloblastic.
Nonmegaloblastic dz has some risk factors (below). MCV
Megaloblastic dz is either B12 deficiency or folate deficiency.
Folate Deficiency Macrocytosis
Folate comes from leafy greens and has small storage forms (3-
6 weeks) in the body. Thus, it often presents with higher acuity Blood Smear
than B12. Look for people who arent eating real food - the
chronic alcoholic or the elderly woman on a tea and toast diet. 5+ Lobes PMN Hypersegmentation
There arent symptoms other than the anemia itself. A folate level
will diagnose it and folate supplementation is usually sufficient Megaloblastic NonMegaloblastic
for treatment. In equivocal cases where the folic acid levels are
near normal, ancillary testing may be required. Dont remember
the homocysteine levels theyre elevated in both Folate B12 and
deficiency and B12 deficiency. Hence, not useful. The Folate Folate Folate
methylmalonic acid is unchanged in folate deficiency. Replace
with oral supplementation. B12 Deficiency Folate Deficiency
*Folate supplementation is performed in pregnancy to prevent Folate
neural tube defects in the fetus rather than to protect mom from
anemia. Methyl
B12 Deficiency Acid
B12 comes from animal products. It requires both intact
parietal cells and an intact terminal ileum to be absorbed. The MMA Nrml MMA
body has 3-10 years of stores it takes a long time to develop. The
pathology is either decreased intake (strict vegans) or reduced
absorption (as in those pernicious anemia, Crohns disease
involving the terminal ileum, and gastric bypass). It presents first
with a megaloblastic anemia and then, if left untreated, with
subacute combined degeneration of the cord.
Diagnosis is made with a B12 level. If equivocal, an elevated
methyl malonic acid is indicative of B12 deficiency. Dont use
the homocysteine level to diagnose. The only time a Schilling test
is done is when theres uncertainty about the etiology; its rarely Subacute Combined Degeneration of the cord.
used. If the urine is positive for B12, then there is no problem with
Treatment is with B12 supplementation. If theres impaired
absorption the supplementation must be intramuscular, else oral
is sufficient. Be cautious with Folate administration. Throwing a
lot of Folate at a B12 deficiency can overcome the anemia, but it
wont prevent neurologic symptoms.
Nonmegaloblastic Dz
This isnt that interesting; theres just a list of things that cause it.
Its important to first rule out a B12/Folate deficiency then look
for: Liver Disease, EtOH, Medications (AZT, 5-FU, ARA-C)
and metabolic conditions (Lesch-Nyhan, Hereditary Orotic


Brief Introduction
So we know the patient is anemic; we saw the MCV was low. If CBC
they were unstable wed transfuse them. But we ought to get
some labs first because after transfusion the labs will be based on MCV
the transfused blood only. Step one is to get Iron Studies and go
from there.
Iron Deficiency Anemia
Iron Deficiency Anemia
The most common form of microcytic anemia is iron deficiency.
The normal requirement of iron is 1mg/day with a maximum of Fe Studies Anemia of Chronic Disease
3mg/day. If the body starts to lose blood it may begin using iron Thalassemias
(to replace the lost hemoglobin) at a greater rate than it can be
absorbed. But this also means that it must be a chronic source of
Iron Stores Sideroblastic Anemia
blood loss. Potential causes are GI Bleeds (slow, polyps,
hemorrhoids, etc) or Gynecologic losses (menorrhagia, cancer).
(Available Storage)
Alternatively, decreased uptake of iron in a non-bleeding person
(as in a gastrectomy) is possible. In any male or postmenopausal Fe
female with iron deficiency anemia follow up with a colonoscopy (Iron in the Blood)
to rule out cancer. The best test to diagnose iron deficiency
anemia is a Bone Marrow Biopsy. But its rarely done because
(Iron in the Stores)
Iron studies are so good at diagnosing Iron Deficiency Anemia.
The most sensitive part of the Iron studies is a low Ferritin (if Iron Deficiency Anemia. Iron stores are depleted, plenty of
Ferritin is low, its iron deficiency anemia, period). That is, the storage availability. Iron is low. TIBC, Ferritin, Fe.
iron stores are small. Low stores means high capacity to bind, so
therell be an elevated TIBC. The low stores also means low
serum iron. Stop the bleeding then give iron. It takes 6 weeks to
replace the serum iron and 6 months to replace iron stores.

Anemia of Chronic Disease

When theres inflammation the body is trying to prevent
Iron Stores
whatever its fighting from getting the iron it needs. If its only an
acute process, that helps fight infection. A side effect is that it TIBC
makes the iron unavailable even to the host! Great in fighting an (Available Storage)
infection; awful in a chronic disease. Essentially, what happens Fe
is the connection between the Iron stores and the blood is severed. (Iron in the Blood)
The body has a lot of iron stored so a low capacity to bind but
still has a low serum iron. Treating the underlying disease will Ferritin
fix the anemia (the inflammation goes away, the iron stores can (Iron in the Stores)
be reconnected to the blood). Sometimes, thats not possible
(Lupus, Rheumatoid Arthritis) so help the body utilize iron stores Anemia of Chronic Disease. Theres a disconnect between
with EPO. the blood and the iron stores, but iron absorption is intact.
TIBC, Ferritin, Fe
Something different is going on in thalassemia. Its not the iron
stores that are the problem - its the hemoglobin. Theres a
genetic disease (, chromosome 16, frameshift and ,
chromosome 11, deletion) that leads to production of the normal -Thal -Thal
hemoglobin with 2 and 2; HgbA1 22. It doesnt matter which HgbA1 22
Asx N/A 1 Gene Deleted
portion is broken - the patient is going to have anemia with Minor 1 Gene Deleted 2 Gene Deleted HgbA2 22
normal iron studies. The way to definitively diagnose Major 2 Gene Deleted 3 Gene Deleted HgbF 2 2
thalassemia is with a Dead N/A 4 Gene Deleted Barts y4
HgbH 4


Hemoglobin Electrophoresis (-thal is normal). Heres the Iron Stores
TIBC Normal
kicker; because anemia is based on severity, not etiology,
(Available Storage)
definitive diagnosis is not required except for genetic counseling.
Think of ALL thalassemia patients as minor (do nothing) and Fe Normal
major (routine transfusion). The deal with which hemoglobin it (Iron in the Blood)
is, 1, 2, 3, 4 gene deleted is unnecessary and bogus for the clinical
rotations. Recognize the hemoglobins (A1, A2, Fetal, Barts, Ferritin Normal
HbH) but realize its either do nothing (minor) vs transfuse (Iron in the Stores)
(major). Each bag of blood has 350mg Fe - enough supply for one
year. Frequent transfusion leads to iron overload treated with Thalassemia. The iron stories are normal. The more genes
deferoxamine to prevent Hemosiderosis. Deferasirox is an oral deleted, the more severe the disease. Consider
medication that might pop up on a test or on the wards. Thalassemias as either minor or major only.

Sideroblastic Anemia
Nobody likes Sideroblastic anemia because its hard. Really Iron Stores
its because it sounds terrifying and is named from what it looks Normal TIBC
like on Bone Marrow Biopsy. Its the only microcytic anemia (Available Storage)
with elevated iron. Definitively diagnose it with a bone
marrow biopsy, which will show the ringed sideroblasts. It Fe
has a number of causes (Lead, EtOH, Isoniazid, a pyridoxine (Iron in the Blood)
metabolic disease of B6, and Myelodysplasia / AML). Get the
pt away from lead, give them B6, and do a BM Bx for the
cancer (which, coincidentally, you just did for the diagnosis). Normal Ferritin
(Iron in the Stores)
Sideroblastic. Diagnosis of Exclusion confirmed on bone
marrow biopsy. The tipoff is an elevated iron despite an
anemia with small cells

Anemia Pathology Ferritin TIBC Iron Best Test Tx f/u

Iron Deficiency Blood Loss (Chronic) Ferritin TIBC Fe BM Bx Iron Colonoscopy
Anemia of Any chronic Ferritin TIBC Fe BM Bx Treat the Dz (Steroids) -
Chronic inflammatory disease Try Epo
Thalassemia Chr 16, , Frameshift Normal Normal Normal Hgb Minor: Deferoxamine
Chr 11, , Deletion Ferritin TIBC Iron Electrophoresis Major: Transfuse (transfusions)
Sideroblastic Lead, B6, genetic Dz, Normal Normal Fe BM Bx Give B6, Look for -
Myelodysplasia, Ferritin TIBC (Ringed Cancer
EtOH, Copper Sideroblasts)


When it comes to normal sized anemia there are generally two CBC
things to consider: hemorrhage and hemolysis.

Anemia of Acute Blood Loss Anemia

When the blood loss is acute theres an acute drop in H/H. This
generally has an obvious source (trauma, GI, GYN) and isnt the
slow chronic onset iron deficiency stuff. An underlying anemia
can be exposed with dilution, but you cant dilute a normal
persons H/H to anemia. If a Normocytic anemia is revealed, look Normocytic
for the source of the loss. Fix this by plugging the hole and/or
giving blood.
Hemolytic Anemia Acute Blood Bilirubin
Loss LDH
Red blood cells last 120 days. When they die they release iron and
hemoglobin into the blood. Haptoglobin binds up hemoglobin Retic Count
Plug the Hole
for transport to the liver. Because its bound to hemoglobin (used
Give Blood
up) itll be in hemolysis. There will be an overwhelming of the G-6-PD
conjugation system so there will also be an indirect G-6-PD Levels
hyperbilirubinemia causing jaundice, icterus, and pruritus. Avoid Triggers
There can be a lot of talk of intravascular vs extravascular
hemolysis but lets focus on identifying the diagnosis and
management rather than the basic science details.
Flow Cytometry
Sickle Cell Spherocytosis Autoimmune Steroids, Eculizumab
i. Sickle Cell Anemia Hgb Electrophoresis Osmotic Fragility Coombs
This is a long one with plenty of details - all of which are Folate, Fe, Splenectomy Steroids
important. Its caused by an Autosomal Recessive mutation in Hydroxyurea IVIg
the -Globin and commonly seen in African Americans. When IVF, O2, Analgesia Splenectomy
the patient undergoes an oxidant stress (hypoxia, infection, Exchange Transfuse
DKA, or dehydration) the hemoglobin, termed Hemoglobin S,
polymerizes inducing sickling. It creates a non-deforming cell
that gets trapped in capillaries, which causes hemolysis and
microvascular occlusion. It results in many consequences. One Hgb SS Disease
is a chronic anemia, usually with sufficient reticulocytosis. If
the retic is low, consider either an acute aplastic crisis
(parvovirus 19) or a folate deficiency. For this reason HbSS Oxidant Stress
patients should be on daily folate + Fe. Another consequence is
the vasoocclusive crisis. Microvascular occlusion causes
infarction. Infarction hurts. These people will be on chronic pain
management because their joints hurt all the time. Occasionally,
theyll suffer an acute crisis where they need IVF, O2, and
Analgesia to ride out the attack. If the patient develops an acute Hemolysis Splenic Osteomyelitis
chest (ARDS picture) or priapism, they need an exchange Autoinfarcts
transfusion to get over the severe crisis. But infarction costs them
more than that. Splenic Autoinfarction increases risk for Anemia Encapsulated S. Aureus
infection by encapsulated organisms, requiring annual Folate, Fe PPx Abx PCN Salmonella
vaccinations (PCV, Meningococcus, H. Flu, HBV). Aseptic Hydroxyurea Vaccines
Necrosis of the hip/femur requires dexa scan screening. Finally, Vasoocclusive IVF, O2,
these patients are at Risk for salmonella osteomyelitis. Crisis Analgesia
Decrease the amount of bad hemoglobin (HbSS) by giving
Hydroxyurea (induces fetal hemoglobin, which does not sickle).
Prevent sickling by avoiding stressors and staying hydrated.
Control the pain with analgesia chronically and reduce the Priapism Acute Chest Pain Avascular
anemia with Iron and Folate. But how do we know who has sickle Necrosis
cell disease? Seeing sickled cells on a blood smear is sufficient Exchange Transfusions Analgesia DEXA Scans
for the diagnosis. Definitive diagnosis of the disease or of the
carrier state may be confirmed by Hemoglobin Electrophoresis.


Finally, the carrier state almost never sickles unless under
extreme conditions (such as climbing Mount Everest) and in the
renal vein ( risk for renal vein thrombosis).

ii. G6PD Deficiency

An X-linked genetic disorder prevalent in Mediterranean The Greek man eating dapsone for breakfast, primaquine for
ancestry presenting with a hemolytic anemia after exposure to a lunch, fava beans for dinner, and a bucket of sugar for
oxidant stress: drugs (dapsone, primaquine), infection, DKA, or dessert (to go into DKA) might have a G6PD deficiency
foods (fava beans). Diagnose it with a smear showing Heinz
Bodies and Bite Cells. Confirm the diagnosis with a G-6-PD
level but do it weeks after the attack (doing so too soon may be
artificially normal).

iii. Hereditary Spherocytosis

The cytoskeleton of the RBC is missing a piece (usually spectrin
or ankyrin, band 3.1 or pallidin). This presents just like a
hemolytic anemia. The spherocytes can be seen on a smear,
though they arent pathognomonic. Confirm the diagnosis with an
osmotic fragility test. Because the big bad spleen beats up on the
little spherocytes a splenectomy will stop the anemia. However,
the cells will persist as spheres. Splenectomy has its own
problems so stick with Folate supplements unless its really

iv Autoimmune Hemolytic Anemia

As the name implies, its an autoimmune disease that attacks
RBC. There can be cold AIHA caused by Mycoplasma and Smear = Schistocytes, Helmet cells (not pathognomonic)
Mono, which produces IgM against RBC at cold temperatures.
Avoid the cold and its not a problem. Warm AIHA is caused by
autoimmune disease (any Rheum disease), drugs (PCN, Sulfa,
Rifampin), and Cancer, producing IgG against RBC @ warm
temps. Treat this like any autoimmune disease by giving steroids,
IVIg when acute, and splenectomy if refractory. The smear is
non-diagnostic; the Coombs test is diagnostic.

v. Paroxysmal Nocturnal Hematuria

Caused by a mutation in the PIG-A gene the red blood cells have
no GPI-Anchor, so they cant inhibit complement fixation.
Fixation occurs all the time, but is accelerated by hypoxia (when Flow cytometry shows absence of CD55 + CD59
you sleep). So, while these patients sleep complement fixes, cells
lyse, and they wake up with hematuria. They can also get
venous thrombosis in intra-abdominal veins causing abdominal
pain. Confirm the diagnosis with a flow cytometry and treat with
Anti-Ab Drugs (eculizumab).

Disease Patient Path 1st Test Best Test Treatment

G-6-PD Mediterranean man who G6PD Deficiency, cannot Smear G-6-PD Levels Avoid Oxidant Stress
Deficiency eats dapsone, primaquine, tolerate oxidative stress Heinz Bodies weeks after the
fava beans, and goes DKA X-Linked Bite Cells attack
Hereditary Enlarged Spleen Defective RBC structural Smear Osmotic Fragility Splenectomy
Spherocytosis proteins, Splenic Destruction (Spherocytes) (Spherocytes Remain)
Autoimmune IgG: Drugs, Cancer, Rheum Autoimmune Antibodies Smear Coombs Test Steroids, IVIg,
Hemolysis IgM: Mycoplasma, Mono (Spherocytes) Splenectomy
Paroxysmal Irregular bouts of morning PIG-A gene mutation, failure
Nocturnal hematuria and abdominal to inhibit compliment on - Flow Cytometry Steroids, Eculizumab
Hematuria pain RBC
Sickle Cell African American, chronic Hgb S polymerizes in Smear Hgb Electrophoresis IVF, O2, Analgesia,
Disease pain, acute chest, priapism response to stress (Sickles) Exchange Transfusion


Multiple Myeloma
Multiple Myeloma is a dysfunction of plasma cells, which Monoclonal Ig Recurrent Infections
normally secrete Immunoglobulins in response to antigen vs Phantom Ag M-Spike on Spep
presentation. In multiple myeloma the plasma cells secrete one
antibody against some phantom antigen. This dedicates the entire
Bence Jones Proteins Renal Failure
immune system to fighting something that doesnt exist. There
are multiple consequences. The first is the monoclonal antibody incomplete Ig (Kappa) Detected on Upep
produces overwhelming concentration of useless antibody. It can Osteoclast Activating Factor Non-traumatic Fxs
be detected by Hgb Electrophoresis (Spep) as an M spike. The Bone Turnover Hyper Ca
consequence is when real infection comes theres antibodies to
fight infection; these patients develop recurrent infections. Skeletal Surveys
Sometimes complete Ig arent made, but rather only pieces. They Pathologic Fractures
get deposited in the kidneys and can be detected on Urine Renal Failure
Electrophoresis (Upep). The fact that there are these proteins in Recurrent Infections
the blood (both intact Ig + Bence Jones) means there will be an
elevated protein gap. Any time there are antibodies being made
(HIV, Viral, bacterial infection) the protein gap can increase, but Spep, Upep Something Else
a sustained elevation on routine labs may be a tipoff. Plasma cells
also secrete osteoclast activating factor which causes the bone
resorption to go crazy. It results in hypercalcemia and frail bones <10%
= pathologic non-traumatic fractures - especially in the Plasmacytosis
elderly. So patients will be old, with weird fractures, renal
failure, hyper Ca, and an Protein Gap. The first thing to do is >10%
an Spep for the Mspike and a Upep for Bence Jones. A Bone Plasmacytosis
Marrow Biopsy must show a >10% Plasmacytosis. A skeletal
survey is used to assess for lytic lesions (owing to the lytic nature
of this disease, a bone scan, used to assess for boney metastasis Multiple
of other cancers cant be used). Treatment options are dependent Myeloma
on the age; if <70 + Donor do a stem-cell transplant after Skeletal Survey
chemo. For >70 or No Donor do chemo only. SCT + Chemo

Chemotherapy is often with Melphalan + Prednisone and either

Thalidomide or Bortezomib.
Protein Gap
Monoclonal Gammopathy of Uncertain Significance
<3g/dL Observe
MGUS is when theres a Spep but with Bence Jones, Lytic
Lesions, Renal Failure, HyperCa and a plasmacytosis < M prot
Viral Spep + Upep MGUS
10%. Do everything to rule out multiple myeloma, but then just
monitor for conversion to multiple myeloma (~2% / year). This <10%
probably represents an early version of MM, but the patients who BJ or >3g/dL Plasmacytosis
acquire it are often quite old and often do not require any
Waldenstrom BM Bx
Waldenstroms Macroglobulinemia or MM
This is a myeloma-spectrum disorder that presents quite
differently than myeloma. The marrow secretes IgM rather than >10% Lymphocytes
IgG. Thus, it presents with peripheral neuropathy and Plasmacytosis
hyperviscosity syndrome rather than renal failure and bone
fractures. This too will have an elevated M-Spike on Spep, but MM WM
will lack the lytic lesion on skeletal survey. Bone Marrow
Chemo + HSCT Plasmapheresis
Biopsy shows Lymphoplasmacytic Lymphoma in more than
10% of the marrow. This disease is often left alone if
asymptomatic and elderly. Treatment for hyperviscosity
syndrome requires plasmapheresis. This is treated more like a
lymphoma than a plasma cell dyscrasia; the chemotherapeutic
regimen mirrors Non-Hodgkins Lymphoma with the use of
Disease Minor Sxs Major Sxs 1st Best Follow Up Treatment
Multiple Myeloma Hyper Ca Nontraumatic Spep BM Bx <70 + Donor = Chemo + HSCT
Renal Failure Fx in the elderly Upep >10% plasma Skeletal Survey >70 or Donor = Chemo
Anemia Protein Gap
MGUS Spep BM Bx Annual Screen Observe
Upep <10% plasma for MM
Waldenstroms Peripheral Hyperviscosity Spep BM Bx Serum Viscosity Plasmapheresis for Hyperviscosity
Macroglobulinemia Neuropathy Syndrome Upep >10% Nrml = 1.8, Chemotherapy + HSCT
Lymphoma Abnormal >5-6

Disseminated Intravascular Coagulation
At its core, DIC is the function of fibrin clots that consume both
platelets and factors, which causes both a factor and platelet type DIC TTP
bleeding. Blood shearing across those fibrin clots produces Sick already, then bleeds Normal, then FAT RN
microangiopathic hemolytic anemia (MAHA) and Platelet Platelet
Schistocytes on smear. Clots and inflammation in general can Schistocytes Schistocytes
produce a fever. Clots occur everywhere they shouldnt be and PT / PTT Nrml PT/PTT
D-Dimer Nrml D-Dimer
then cant form where they should. Thus, the patient bleeds (not
Fibrinogen Nrml Fibrinogen
where they should be), but also get thrombosis (from where they Reverse underlying Dz Exchange Transfusion
shouldnt bee). The person who gets DIC is going to be sick from Give platelets, blood NEVER give platelets
something else, and then ends up dropping their platelets and
bleeding. Because these are caused by fibrin clots, fibrinogen is
consumed, factors are chewed up, and theres also a rise in the
split products. The DIC panel reveals low fibrinogen, elevated
PT and PTT, and elevated D-Dimer. Its this part of the panel
that separates DIC by labs (the presence of thrombocytopenia and
schistocytes doesnt). The underlying condition must be corrected
to reverse DIC. In the meantime, give the patient whats missing
Blood, platelets, and FFP.

Thrombotic Thrombocytopenic Purpura

TTP is an autoimmune disease where clots form - just like in
DIC. But these clots are hyaline clots that dont consume factors,
fibrinogen, or platelets. Instead, ADAMTS-13 is deficient. It fails
to cleave vWF multimers, which persist and swallow platelets.
The thrombocytopenia has nothing to do with the clots, but with
these large vWF multimers (at least we think). Theres a classic
pentad for TTP, with the mnemonic FAT RN. Theres Fever,
Anemia, Thrombocytopenia, Renal Failure, and Neurologic
symptoms that wax and wane. Diagnosis is based on a normal
DIC panel despite thrombocytopenia and anemia. Schistocytes
may be present. The Laboratory diagnosis separates them. For
TTP, NEVER give platelets (itll worsen the MAHA). Instead,
do a plasma exchange (take out the antibodies and give back
plasma with a lot of ADAMTS-13), or a plasma transfusion
(give ADAMTS-13 only).

Idiopathic Thrombocytopenic Purpura

ITP is an autoimmune disease of an unknown etiology thats a
diagnosis of exclusion. Look at every other cause first, including
bone marrow biopsy. Once exhausted, its the diagnosis. The
treatment is steroids (long term low dose better than short term
high dose as the patient remains sensitive to treatment), though
IVIg can be started acutely to get platelets up faster. If steroids
fail, a splenectomy is definitive. If splenectomy fails or is
contraindicated, the remaining option is Rituximab.

Heparin-Induced Thrombocytopenia
If the patient is on any heparin there may be an autoimmune
destruction of platelets, typically occurring at day 4-10 (earlier
if second exposure). Stop the heparin, start Argatroban, and
then send out the HIT panel. Treatment before diagnosis in this


The (Anti) Clotting Cascade
Dont worry about memorizing the clotting cascade; dont even

memorize this picture. Just recognize that there are forces in
action trying to prevent the formation of a clot. Protein S
activates Protein C. Protein C binds to Factor V to inactivate it,
reducing the production of Thrombin from Prothrombin.
Antithrombin prevents thrombin from turning the fibrinogen
mesh into fibrin. Easy breezy, right?

Is it so hard to imagine if theres a deficiency in Protein C,

Protein S, or Antithrombin that thered be an unusual amount
of clotting? What if factor V just didnt get the Protein C
message? Say there was a mutation of Factor V that made it
resistant to the activity of protein C. Thats Factor V Leiden -
the most common thrombophilia. Dont forget about
Prothrombin 20210A. These are the named thrombophilias that
you should be able to recognize that you should be able to

Theyre all genetic diseases that require genetic testing to

diagnose. They can all be treated with coumadin (Warfarin).
Theyre all related to factor clotting so induce anti-clotting with
coumadin to counteract the anti-clotting-deficient endogenous For the resident, order:
system. Read that again to make sure you got it. But wait! Doesnt - Protein C Levels
Coumadin inhibit the production of clotting factors and proteins - Protein S Levels
from the liver? Coumadin first inhibits protein C and S, actually - Prothrombin levels
INCREASING clotting when its begun. Thats why its - Antithrombin 20210A Mutation
imperative to always start with a Heparin Bridge. Itll prevent - Factor V Leiden Mutation
the whole thing from getting started. Heparin can be removed - Antiphospholipid Assay
once proteins C, S, and all the liver clotting factors are depleted
(with Coumadin being left on).

But whats the right time to go after these tests and to treat with
Warfarin? The answer is never. If the person has two clots, they
get life-long anticoagulation regardless of a genetic defect or
not. You suspect genetic susceptibility when there are multiple
unprovoked DVTs. and you would be anticoagulated for life

If the person wants to STOP anticoagulation, genetic testing

needs to be performed to assess the risk of being off it. Otherwise,
theyre all treated the same way.

Antiphospholipid Antibody Syndrome APLA / APS

This diagnosis warrants special mention. Caused by the lupus
anticoagulant (which is frustrating because its a procoagulant in
vivo), the patient will present with autoimmune disorders and
bleeding. Theyll have both arterial AND venous thrombosis;
it may also present with a history of early miscarriages. The goal
INR is 2-3 for initial therapy. Repeat clot on warfarin indicates a
rise in the goal INR.

Infectious Disease [ANTIBIOTIC LADDER]

Intro Cephalosporins
The bugs that cause disease largely stay the same; the antibiotics The earlier generations of cephalosporins (the 1st Generation)
that treat them dont. Case in point, Staph aureus was the most were designed to cover strep and staph. As you move up the
common cause of osteomyelitis 50 years ago and still is today. generation ladder the amount of gram negative coverage
Abx Resistance means the drugs to treat are constantly evolving. increases, but the staph coverage decreases.

In general, start with penicillin. Its a cidal (kills bacteria) and 1st Generation Cephalosporins are used to cover skin infections
typically successful. such as regular ole cellulitis. Cefazolin.

There are two pathways from there - those that cover staph and 3rd Generation Cephalosporins have sufficient gram negative
those that cover gram negative rods. and positive coverage. They also cross the blood brain barrier.
Theyre chosen first for meningitis and inpatient pneumonia.
Staph Ceftriaxone.
The Methicillins (oxacillin, cloxacillin, dicloxacillin, and
nafcillin) are very good at killing staph. Unfortunately, theyre all 4th Generation Cephalosporins means only Cefepime; it kills
really good at making MRSA. When sensitive to methicillin, any pseudomonas. Like carbapenems, theyre reserved for
of the cillins should be used. In general, this isnt empiric. neutropenic fever or similarly immunosuppressed or severe
Vancomycin is the typical drug used for empiric coverage of
Staph. It covers MRSA. However, just because its a big gun
doesnt imply it has broad coverage its weak against everything

Linezolid is top of the line. Its the last resort for Vancomycin-
resistant Enterococcus (VRE) or Staph (VSA). Use this sparingly
- resistance to this means theres nothing left.

Gram Negatives
To obtain gram negative coverage start with Amoxicillin or
Ampicillin together ( with or without a beta-lactamase
inhibitor). They dont cover pseudomonas.

If pseudomonas coverage is needed, step up to Ticarcillin or

Piperacillin with a Beta-Lactamase Inhibitor. These also cover
gram positives (minus staph) and anaerobes. Use should be
restricted to pseudomonas to prevent resistance.

The Quinolones (Cipro, levo, gatti, and moxifloxacin) are oral

medications that kill a little bit of this and a little bit of that.
Ciprofloxacin covers gram negatives (UTIs) and has the same
bioavailability PO or IV Moxi has the gram negative coverage
but also gets some gram positives (Pneumonia).

The Aminoglycosides (gentamicin, amikacin) are synergistic

with penicillins but almost exclusively gram negative. This is
rarely the first choice for empiric treatment.

Infectious Disease [ANTIBIOTIC LADDER]

Anaerobic coverage comes in many forms. Zosyn (Pip/Tazo) has
coverage, as do the penems. But when the focus is strictly on
anaerobes there are two options: metronidazole (gut and vagina)
and clindamycin (everywhere else).

Understanding Quinolones
The more advanced the generation of quinolone, the more
coverage it obtains. Thats to say, 1st generation ciprofloxacin has
gram negative coverage only; its used to treat associated gram
negative infections. Third generation moxifloxacin has additional
gram positive coverage, but DOESNT LOSE its gram negative
application. This makes moxi a highly attractive medication to
use (single-agent, covers everything) but it also breeds
resistance. Stay away from medications like this because theyre
rarely the right answer. No Quinolone covers Staph or
Pseudomonas, though Cipro can be used in double-coverage of

Pulling the trigger and going broad

In general, the goals to narrow the antibiotics to exactly whats
being treated. For a staph infection, pick Nafcillin. For MRSA,
pick Vanc. For a UTI, pick Ampicillin or Cipro. For
pseudomonas, pick Zosyn.

But there will be a time when a person is just ill. Theyre super
sick and missing the bug could be fatal. When the person is sick
as shit (think septic shock) its ok to just go broad make sure
you get it all. This is why Vanc + Zosyn is so popular in the
hospital. Its also why it will be the wrong answer on the test.
Once cultures and sensitivities come back, its then possible to
narrow the antibiotics. You can also de-escalate, one antibiotic at
a time, and assess the clinical response.
Condition Drugs
Penicillin Rash: Cephalosporins OK
Real Life Antibiotics Allergic Anaphylaxis: Cephalosporins NOT ok
Memorize the prevalence and patterns of infections and your MRSA Vancomycin, Linezolid, Daptomycin
institutions and use the empirically-derived-data for empiric Pseudomonas Pip/Tazo (Zosyn), Carbapenems, Cefepime
coverage. This is the list to the right. Outpatient Doxycycline, Azithromycin, Moxifloxacin
Inpatient 3rd Gen Cephalosporin + Azithromycin (CAP)
Pneumonia Vancomycin + Zosyn (HAP)
Neutropenic 4th Gen Cephalosporin (Cefepime)
Fever Carbapenems
UTI TMP-SMX, Nitrofurantoin
Meningitis Vanc, Ceftriaxone, +/- Steroids, +/- Ampicillin
Cellulitis Cefazolin, Bactrim, Clindamycin
IV Vancomycin

Infectious Disease [BRAIN INFLAMMATION]

Presentation and Differential Bacterial
Any brain inflammation will present with a backbone of fever + Crypto
Meningitis TB
a headache. This is nonspecific for a particular diagnosis, but
antennae should go up for problem in the brain. Other signs and Rocky Mountain
symptoms that help (photophobia, N/V, and seizures) may be + Stiff Neck Syphilis
present but are likewise nonspecific. There are 3 categories of Listeria
disease - each with their own unique findings. 1Meningitis will
Fever + + FND
have a stiff neck (Kernig and Brudzinskis Signs), 2Abscesses Abscess or Cancer
will present with Focal Neurological Deficits, and 3Encephalitis
will present with encephalopathy (aka confusion).
+Confusion Eastern Equine
Western Equine
Encephalitis St Louis
West Nile
(flaccid paralysis)

Encephalitis is the inflammation of the brain parenchyma itself.
It should present with the fever + headache AND confusion.
Altered mental status is part of the FAILS mnemonic, and so a
CT is performed before the LP. The CT should be normal (the
test may say something about temporal lobe or anosmia,
implying that the question is about HSV). The LP should reveal a
bloody tap (while only 30% are bloody, its still a classic
teaching). What separates it from a subarachnoid hemorrhage is
the presence of white cells. Definitive diagnosis is made with
HSV PCR. Treat empirically with Acyclovir while awaiting the
results of the PCR.

The other association to know is that west nile virus presents with
flaccid paralysis.

Abscess vs Cancer (Mass Lesions)

Since mass lesions present as a fever and a headache with Focal
Neurological Deficits, this will also require a CT scan before the
LP - usually with a dose of ceftriaxone. The CT will come back
for a ring enhancing lesion; itll be contraindicating the
lumbar puncture. Instead, additional investigation of the mass
must take place (i.e. a Biopsy). This will tell us if theres an
abscess requiring drainage and investigation of a primary source,
( organisms) or if its a cancer requiring radiation and chemo.
Thats useful since antibiotics wont work for a cancer, nor will
chemo/radiation work for an abscess.

Theres one exception to jumping to a biopsy - an HIV/AIDS

patient. In a patient with a CD4 count < 200 AND a Toxo
Antibody positive at any time in life, the mass is Toxoplasmosis
90% of the time. For this patient treat empirically with
pyrimethamine and sulfadiazine for 6 weeks. If theres
improvement keep it going. If not, go to biopsy. If treat
empirically isnt an option, look for Toxoplasmosis-Ab.

Infectious Disease [BRAIN INFLAMMATION]

Meningitis Lumbar Puncture Findings
Meningitis is inflammation of the meninges caused by any # of Bug Cell Count Glucose Protein WBC Tx
etiologies. The challenge is to identify which organism is most Bacterial PMNs Ceftriaxone
likely, confirm it, then treat it. The definitive test is the Lumbar Viral - Lymph
Fungal Lymph
Puncture. It gives a wealth of information (glucose, protein,
cells) of the CSF as well as a body fluid for Gram Stain and
Culture. But sometimes you cant just jump straight to an LP. A
CT must be done first if they have any of the FAILS mnemonic.
Hence, two treatment pathways:

1. The LP is UNsafe. This treatment plan uses the blood

culture as a chance at getting a diagnosis. Antibiotics are
given prior to the CT scan and the LP. Cultures are sterilized
after 2-4 hours. Then the CT scan is done; if its normal the
LP follows.
2. The LP is Safe. This strategy uses the CSF culture as the
chance to get a diagnosis (aka the next step is LP).
Antibiotics are given immediately after the LP is performed.

The LP gives a wealth of information, but most of it is useless.

The only thing you care about is the number of cells and what
type they are (lymphocytes or neutrophils). Ignore pH / glucose
/ protein for most questions.

If there are mega (100s to thousands) neutrophils you can be

assured that its a bacterial meningitis. Its treatment revolves
around Vancomycin, High-Dose Ceftriaxone, and Steroids. In
the immunocompromised, include ampicillin to cover for listeria.

If the LP comes back no bacterial then we have a dilemma. Its

easy to find what youre looking for when you know what
youre seeking, but hard to find something if you dont know what
it could be. Repeated from the first Page

Cryptococcal meningitis is found in patients with AIDS and a

CD4 count < 200. There may be seizures. Opening pressure is Bug Suspicious Hx Test Tx
often quite elevated and serial taps may be required to keep the RMSF Rash on hands, Spread Proximal Antibody Ceftriaxone
Lyme Targetoid Rash, Hiker, Ticks Antibody Ceftriaxone
pressure down. Diagnose with a cryptococcal antigen (do NOT
Crypto HIV/AIDS Antigen Amphotericin
use India Ink). Treatment is with induction for 2 weeks with IV TB Pulmonary TB AFB RIPE
Liposomal Amphotericin B and IV Flucytosine, followed by Syphilis STD, Palmar Rash, DCMLS RPR Penicillin
consolidation with PO Fluconazole. Listeria Elderly Neonate on Steroids - Ampicillin
Viral Diagnosis of Exclusion - -
Lyme disease can be suspected if theres a targetoid lesion and
travel to endemic areas such as New England. Theres often NO
tick noticed because theyre so small. Use ceftriaxone for Lyme
meningitis (not doxycycline as you do for non-invasive disease).
Borrelia burgdorferi is the bacteria. Ixodes is the Tick.

RMSF is seen in campers who develop a peripheral rash that

moves towards the trunk. Obtain the antibody on the CSF. If
positive, treat it with ceftriaxone.

TB meningitis is simply extrapulmonary TB. Consider this in

someone who has Pulmonary TB risk factors. Treat with RIPE.

Infectious Disease [EARS NOSE THROAT]

Introduction This is a replica of PEDS ENT and included for
A lot of things go on in the head. Children need to be exposed to bugs completeness if only studying ID. Its getting refreshed
to develop an immune system. That means orifices become potential with PEDS, not ID.
sites for problems to develop, which is why this topic is in peds. Each
disease has its own unique presentation so its usually not a differential URI Bugs
- just know what to do. Most Strep Pneumo Amoxicillin
Common H. Influenza + clavulanate
1) Otitis Media Moraxella
Otitis media is an infection of the middle ear caused by the respiratory Catarrhalis
bugs. The child is going to be in pain. Unilateral ear pain in a child, Otitis Pseudomonas Spontaneous Resolution
with or without fever, leukocytosis, etc. is most likely to be otitis. Kids Externa
will pull on their ear (no pain with pinna manipulation) to relieve the
sensation. The diagnosis is confirmed by pneumatic insufflation (a
little puff of air reveals a tense immobile membrane). Things like a
bulging red angry membrane with loss of light reflex are indicative Ear Pain Otitis Media Visual Inspection
of fluid behind the ear but arent pathognomonic. Dont get tests but Otitis Externa Pinna Manipulation
definitely treat with amoxicillin. Failure to treat can cause spread of the Foreign Body Lidocaine / Retrieval
infection to the mastoid, inner ear, and brain. If the infection does not
clear give amoxicillin and clavulanate. If the infections recur do tubes
to equalize pressure and allow drainage - especially if theres residual Rhinorrhea Viral Sinusitis Cough and < 7 days
fluid behind the ear. Bacterial Sinusitis Culture
Foreign Body Inspection
2) Otitis Externa
Otitis Externa presents as unilateral ear pain (like media), but theres
pain on palpation of pinna (unlike media). Caused by frequent contact Sore Bacterial Rapid Strep Culture
with water (swimmers ear), its commonly caused by pseudomonas Throat Viral
(a bug associated with water). It can also be caused by repeated trauma Mono Monospot
or an infection by Staph aureus. On physical exam an angry
erythematous canal can be seen. It usually improves spontaneously. It
becomes important to educate patients not to put anything in their ear Bloody Digital Trauma Cold compress, lean
and to dry ears after swimming and showering. Nose forward, humidified air,
3) Sinusitis
An infection of the nose and sinuses that occurs in both kids and adults.
Purulent bilateral nasal discharge is a giveaway somethings wrong
nearby. Adults and older kids may complain of a congested, stuffed
feeling with sinus tenderness. The facial tap is a sensitive physical
finding (tapping an inflamed sinus hurts). Radiographs are not Is it viral (wait) or is it bacterial (amoxicillin)?
necessary but will show air-fluid levels and opacification (XR + CT).
Theyre expensive and usually reserved for refractory or recurrent Short Duration Longer Duration
sinusitis to make sure theres no congenital defect. But before doing Low-Grade Fever High Fever
anything make sure this isnt just a cold - a regular viral illness. If its Mild Symptoms Worse Sxs
been >7 days or theres also a cough, simply presume bacterial
infection. This is an URI so treat the URI bugs with amoxicillin.
4) Cold Viral Nasal
Typically caused by rhinovirus and transmitted between people by
large droplets. Its also gives boogers, rhinorrhea, congestion, and
low-grade fever so it looks like sinusitis. Nasopharyngeal washes
with culture (to rule out bacterial infection) and Immunofluorescence
(to rule out viral infection) could be gotten but its better to not do
anything because this will just get better on its own. If its <7 days
AND no cough its likely viral and the patients should wait it out.

Infectious Disease [EARS NOSE THROAT]

5) Pharyngitis Calculating the score

Much like sinusitis, viral pathogens are the most common cause +1 Fever
occurring in kids and adults. The primary complaint will be sore throat +1 Exudates
with pain on swallowing. Like otitis, physical exam findings are +1 Adenopathy
nonspecific for viral versus bacterial (erythematous pharynx, swollen +1 ABSENCE of cough
tonsils, purulent exudates). Because a bacterial infection with Group +1 < 15 years old
A Strep can cause rheumatic heart disease and poststreptococcal -1 >44 years old
glomerulonephritis, we must find out if its bacterial or viral. However, Interpreting the Score
those physical findings are not specific. Instead, we use the Centor < 1 No treatment (viral)
Criteria to help direct our decision making, keeping in mind the risk of 2-3 Throat Culture (Rapid Strep acceptable)
mimicry (PSGN and Rheumatic Heart) are higher in kids, so we are > 4 Empiric Treatment, no testing needed
more likely to treat (most doctors dont). The treatment is amoxicillin-
clavulanate if there is strep, but to do nothing if its viral. Using the
Centor Criteria (right) we can make our decision. Doing a Rapid Strep
Test is specific (if start treatment) but not sensitive (if move onto
culture). Cultures take 2-3 days to come back; treatment does not need
to be started until cultures confirm bacterial infection.

6) Foreign Body
Children: Kids like to stick things places. Things can go into the nose
(producing foul-smelling unilateral rhinorrhea), ear (pain), and
sometimes down their throat (aspiration, covered in the pulmonary
videos). Essentially, the object has to be retrieved with a rigid
bronchoscope and the infection treated.

Adults: One particular foreign body are insects; homeless are aware of
this and sometimes sleep with coins in their ears. Bugs present with a
unilateral scratching or buzzing and should be treated with lidocaine
and retrieval, but never light (they just burrow deeper).

7) Epistaxis
Whether out of habit or because the nose itches, epistaxis is most
commonly caused by digital trauma (nose-picking). Normal
nosebleeds are unilateral and last <30 minutes. Applying a cold
compress (vasoconstriction) and leaning forward (backwards is just
drinking the blood causing a cough breaking the clot) can cause an
active bleed to stop. Look inside the nose to make sure there isnt
anything anatomical or foreign inside. Treat recurrent bleeds with
humidified air. Ultimately, ablation is used to prevent bleeding.

Posterior epistaxis may require packing (essentially a tampon inserted

into the posterior of the oropharynx with prophylactic antibiotics to
prevent toxic shock syndrome).

8) Choanal Atresia
Finally, something isolated to pediatrics. This is an atretic or
anatomically stenosed (i.e. really big tonsils) connection between the
nose and mouth. In severe cases the baby will be blue at rest (nasal
breathing is insufficient) and then pink up with crying (as he/she uses
his/her mouth). If its just partially obstructed there might be a
childhood snore; kids shouldnt snore. If theres complete atresia a
catheter will fail to pass. If its incomplete a fiber-optic scope will
identify the lesion. Surgery is required to remove the tonsils or open
the atretic passage.

Infectious Disease [GENITAL ULCERS]

Genital ulcers can be easily separated from one another based on
the number of ulcers, the presence of pain, and the presence of
affected lymph nodes. Getting to the right answer should be easy;
knowing the details of each disease becomes harder (as does
keeping them straight). Give lots of attention to syphilis as the
others are often distractors against it.

1) Syphilis
Primary Syphilis presents as a painless ulcer called a chancre. It
represents the entry point of the Treponema Pallidum organism,
a spirochete. There may be associated painless
lymphadenopathy. Its too early to use serology so we have to
look for the organisms themselves with a Darkfield Microscopy.
At this point IM PenG will be curative. If the patient is penicillin
allergic, doxycycline can be used instead.

Secondary syphilis is a disseminated targetoid or

maculopapular rash that involves the palms and soles. The rash
is infectious. By this time serology is positive. Screen for syphilis
with a non-treponemal test such as RPR (or VDRL) and confirm
with a treponemal test such as FTA-Antibodies. If FTA-Abs ,
treat with IM PenG.

Tertiary syphilis penetrates the CSF. Look for the Argyll-

Robertson pupil, Tabes Dorsalis, and any neuro symptom. Do
serology, only this time the serology should be on the CSF fluid
following a lumbar puncture. In tertiary syphilis the patient Tests for Syphilis
needs IV Penicillin x 7-14 days. If allergic AND pregnant they RPR Good sensitivity requires > 1 month to be positive
have to be desensitized and given the penicillin anyway; doxy is VDRL Decent sensitivity, False with Lupus
contraindicated. FTA-abs Good specificity, confirmatory for RPR
Darkfield Excellent specificity, only means of diagnosis for primary
If the patient has a positive RPR but no symptoms, its said to
Microscopy chancre, can be used on 2o lesions
be latent syphilis. If its within one year of contraction, its early
Treatment for Syphilis
latent syphilis and is treated as secondary. If the time is unknown
Pen G IM Mainstay of therapy, x1 time primary and secondary
or its > 1 year from contraction, its considered late latent
Doxy If Pen Allergic x7 days for primary and secondary
syphilis and is treated with PenG IM qWeek x 3 weeks.
PenV IV Best treatment for 3o disease x 14 days, or for penicillin
allergic pregnant patients (desensitize)
2) Haemophilus ducreyi
Types of Syphilis
You do cry with ducreyi presenting as a syphilitic chancroid
Primary Painless chancre with Inguinal Lymphadenopathy
that hurts. It will have the ulcer, erythematous base, and inguinal
Secondary Maculopapular Rash on hands and soles (infectious)
lymphadenopathy of syphilis, but this will hurt - syphilis doesnt.
Tertiary Any neurologic complaint (Argyll-Robertson Pupil)
Do a simple gram stain and culture, then treat with antibiotics.
Azithromycin or Cipro will do the job. Early Positive RPR and
Latent < 1 year from contraction
3) Herpes Late Latent Asymptomatic Positive RPRP and
Herpes Hurts like ducreyi, but are often multiple roofed > 1 year from contraction, or unknown
vesicles, each on an erythematous base, whose eruption is
preceded by a painful prodrome. If this classic picture is seen
just treat with acyclovir as the diagnosis is clinical. At times, Dz Presentation Test Treatment
however, vesicles can unroof and become confluent. This makes Syphilis Painless but firm 1o=Dark Field PenG IM or Doxy
clinical diagnosis difficult. Diagnose definitively with an HSV ulcer (singular) 2o RPR Abs PenG IM or Doxy
PCR. The Tzanck prep is no longer recommended given the + Lymphadenopathy 3o LP of 2o Pen IV x 14 days
absence of specificity and sensitivity. Ducreyi Painful (singular) Gram Stain + Azithromycin or
+ Lymphadenopathy culture Ciprofloxacin
4) Lymphogranuloma Venereum Herpes Roofed vesicle on HSV PCR Acyclovir
It is caused by C. trachomatis. It presents as a painless singular an erythematous Valacyclovir
ulcer (much like Syphilis), but has painful lymphadenopathy base after a painful
thats often supportive (pus). While a nucleic acid amplification prodrome
assay will confirm the diagnosis, treatment is often supportive or LGV Painless singular needed Doxy
with simple antibiotics such as doxycycline. ulcer, Pussy LN

Infectious Disease [HIV]

Pathology and Diagnosis
HIV is a Retrovirus that enters CD4 cells via gp120 and gp41
(CCR5, CXCR4 chemokine receptor bearing cells). Once
infected, reverse transcriptase turns the RNA virus into host
DNA, hijacking the nucleus to produce HIV RNA. After
replication, new virions are packaged by proteases and are
released into the blood stream by exocytosis. CD8 responses
cause death/loss of CD4 cells resulting in a major decline.
Diagnosis is based on ELISA confirmed with Western Blot or
Viral Load. During the window period (~6 weeks from infection
to antibodies) only viral load can be used to make the diagnosis.
This is useful in acute retroviral syndrome.

Opportunistic Infection Prophylaxis

As the CD4 count falls the patient becomes vulnerable to
opportunistic infections. We look for these opportunistic
CD4 Count and Viral Load
diseases and treat them. However, we can also prophylax against
CD4 Count Whats Right Now = Infection Risk
three diseases: 1PCP pneumonia at a CD4 <200 with TMP-
Viral Load Whats to come = CD4 change
SMX, 2Toxo at a CD4 < 100 with TMP-SMX and 3MAC at a
CD<50 with Azithromycin. If you cant use TMP-SMX, use
Dapsone. If G6PD deficient, use Atovaquone. TMP-SMX =
CD4 Count Vulnerability Prophylaxis
Opportunistic Infections and Therapy >200 Thrush, TB, Leukoplakia
In spite of limited prophylaxis many patients do get infected with <200 PCP Pneumonia 1st Bactrim
2nd Dapsone
opportunistic infections. Knowing what to look for and what to
3rd Atovaquone
treat based on CD4 count is critical. Be aggressive in the
<100 Toxo 1st Bactrim
treatment of opportunistic infections. It comes down to simple
2nd Pyrimethamine
memorization (the chart to the right) and recognition of
symptoms. <50 MAC Azithromycin

Note that AIDS is defined by a CD4<200 OR Opportunistic

Infection. Since it cant currently be cured the patient will always
Count Infection Treatment
have the label - even if the infection clears or CD4 counts rise to
normal levels. >500 Normal person with Normal
normal infections
HIV is a blood borne illness and a sexually transmitted disease. 200-500 Oral Leukoplakia
Be sure to screen for possible coinfections at high risk. Its the Pulmonary TB (>5mm) INH (Latent), R.I.P.E (Active)
infections seen with the same risky behavior (IVDA and sex) such Pneumococcal PNA 3rd Gen Ceph + Macrolide
as cervical cancer, Hep B and Hep C, Syphilis, and Thrush Nystatin S+S
GC/Chlamydia. <200 PCP Pneumonia Bactrim, Dapsone
Crypto Meningitis Amphotericin + Flucytosine
Antiviral Therapy = HAART Esophageal Candidiasis Fluconazole
Start HAART as soon as HIV is diagnosed. Typical therapy <100 HSV/CMV Esophagitis Acyclovir/Ganciclovir
involves the 2+1 approach. That means 2 Nucleoside Reverse Toxoplasmosis Pyrimethamine Sulfadoxine
Transcriptase Inhibitors and 1 Other thing. The other thing <50 Disseminated MAC Clarithromycin + Ethambutol
could be a Protease Inhibitor (boosted with ritonavir), a Non- CMV Retinitis Valaciclovir, Foscarnet
Nucleoside Reverse transcriptase inhibitor, an Integrase
Inhibitor, or Fusion Inhibitor.
You choose which drug to use based on the patients preference
and the genotyping (the closest to a culture we have). If a patient 2 NRT-I + 1 NNRTI
gets on HAART, stays on HAART, and never misses a dose they 1 PI / r
can lead essentially normal lives. 1 Integrase-i
1 Fusion-i
Prophylaxis to HIV Prophylaxis to Exposure
Both Pre-Exposure prophylaxis (PrEP) and Post-Exposure PrEP = Emtricitabine + Tenofovir
Prophylaxis (PEP) are highly effective at reducing HIV PEP = Emtricitabine + Tenofovir +/- Raltegravir
transmission. Tenofovir + Emtricitabine is typically used. Pregnancy = AZT at time of delivery
Vertical transmission can be prevented with AZT when used at
the time of delivery (and also by treating mom during


Infective Endocarditis (IE) is an infection on the heart valves. To
get infected there must be introduction of bacteria into the blood Major Criteria
stream AND a bad valve. Thus, some risk factors are intravenous Sustained Bacteremia by organism known to cause IE
drug use (most common in the US) or a patient with repeated (Strep, Staph, HACEK)
access (like dialysis). Others are valvular damage (rheumatic Endocardial Evidence by Echo
heart worldwide, congenital defects in the US) and a history of New valvular regurgitation
(increase or change of pre-existing not adequate)
endocarditis (100 fold increase in risk). Once the infection sets
Minor Criteria
up shop on the valve, embolic, vascular and rheumatologic
Predisposing Risk Factor (valve disease or IVDA)
manifestations are possible. Fever > 38 C
Vascular Phenomena
Presentation (septic emboli arterial, pulmonary, and Janeway lesions)
The Dukes criteria (presented to the right) is a useful means of Immunologic Phenomena
building a table you can memorize. However, it was created for (glomerulonephritis, Osler nodes, Roth spots, RF)
study inclusion and isnt a diagnostic tool. Instead, note there are
two types of endocarditis: Acute and Subacute. Definite
Two major criteria (Blood Culture and Echo)
Acute Endocarditis is going to be from virulent organisms One major and 3 minor
(Staph, Strep Pneumo) that will infect normal, native valves. 5 minor
These patients will be sick: persistent bacteremia, valve
1 major and 1 minor (almost every bacteremic patient, btw)
destruction, new murmur; we order a bunch of cultures to watch
3 minor
it clear (or not) and start antibiotics right away. Since the Rejected
presentation is obvious it doesnt take long for the patient to seek Firm alternative diagnosis explaining evidence for IE
medical attention. Thus, theres no time for the rheumatologic Resolution of everything in 4 days
manifestations to start. No pathologic evidence (a BIOPSY!?) at surgery or death
Failure to meet criteria as above
Subacute Endocarditis is caused by less virulent organisms (S.
bovis, S. viridans, HACEK) infecting abnormal native valves. Its
the endocarditis people learn about in second year Roth Spots
(eyes), Janeway lesions (painless hands), Splinter
Hemorrhages (nail beds), Osler nodes (painful distal digit pulp)
etc - subtle clues pointing to endocarditis because the patient isnt
sick enough to warrant attention. This one requires multiple
cultures to make a diagnosis; antibiotics shouldnt be started right

The echocardiogram and blood cultures are the cornerstone of
diagnosis. The TTE is often used first (usually to identify a
valvular abnormality rather than a vegetation) followed by a
Transesophageal Echocardiogram to make the final diagnosis
by identifying the vegetation. The TEE is the best test.

Acute endocarditis: hey, the bacteremia wont clear. Keep

getting cultures until they do. OH NOES! A MURMUR!!! Get a

Subacute endocarditis: my my, look at these interesting rashes. Diagnostic Steps

This one is painless on their hands, their nail beds have these Blood cultures x 3, one Subacute Endocarditis
small splinter like splotches, and their RF is up. I wonder if this hour apart, NO abx
is rheumatoid arthritis? Doesnt sound like RA - get a culture Blood cultures x 2 now, Acute Endocarditis
no get THREE cultures and wait. AHA! BACTEREMIA! start empiric abx, follow-
GET A TEE!!!!!! up cultures
Trans Thoracic Echo If you arent sure
Trans Esophageal Echo If you are sure


Treatment Antibiotics
There are two elements to the treatment of Endocarditis: Native Valve
antibiotics and surgery. All Vancomycin Gentamycin
Antibiotics will be required for a minimum of 6 weeks. Which Prosthetic Valve
antibiotic is chosen will be dependent on the culture and <60 Days Vancomycin Gentamycin Cefepime
sensitivity of the organism. But when treatment is begun we must 60-365 Vancomycin Gentamycin
use empiric coverage. That changes not on the endocarditis, but days
on the patient. See to the right. >365 Vancomycin Gentamycin Ceftriaxone
Surgery is designed to prevent CHF and embolization. Acute
endocarditis can cause valvular insufficiency. The worse the SBE Vancomycin Gentamycin Ceftriaxone
valve or the worse the CHF the sooner the surgery (someone in
cardiogenic shock goes right away while someone who is See the vanc+gent backbone. Just remember which ones
compensated but has severe insufficiency can wait a few days). gets Cefepime, Which one gets Ceftriaxone, and then Native
This is a clinical judgment: how sick the patient is. valves need only Vanc

But embolization isnt clinical. There are fairly well described Vancomycin Daptomycin Linezolid
criteria for who goes to surgery for a vegetation that could (not for bacteremia)
embolize. Note that a stroke or MI would be a contraindication to
any surgery EXCEPT for IE, since failing to go to surgery will
result in further embolization. See to the right. Surgery
Go to surgery if
Prophylaxis >15mm even without embolization
Theres a long list of people that need to be prophylaxed against >10 mm + embolization
IE. But if you instead remember, bad valve and mouth and Abscess
throat youll get it right most of the time. Valve destruction or CHF
Bad Valve means they have a congenital heart defect, previous
endocarditis, or a prosthetic valve.

Mouth and throat means theyre having a dental procedure or a

procedure that would involve bronchoscopy and biopsy of the
respiratory flora. Bad Valve Mouth and Throat
Congenital Heart Disease Dental Procedures
If both are seen, give amoxicillin. If they cant tolerate a Prosthetic Valve Biopsy of the Airway
penicillin, use ceftaz. If that doesnt work go to clinda, but you History of Endocarditis
wont be drilling down to this level of detail as a medical student.

Unique Associations for Bonus Points

Strep bovis comes from the colon. If Strep bovi endocarditis, do

colonoscopy for occult cancer.
Staph aureus comes from the skin. IVDA and tricuspid valve Amoxicillin (1st line)
most often. Ceftaz (back up)
Clinda (last line)
Strep Anything Else comes from the mouth. Look for dental

Infectious Disease [PNEUMONIA]

Organisms and Disease Typing
Whenever theres a fever and a cough consider a lung infection.
There are three lung infections: 1) Abscess, 2) Bronchitis, and 3)
Pneumonia. When learning about Typical Pneumonias and
Atypical Pneumonias for Step 1, the symptoms and CXR
findings may be misleading (neither is specific enough), and
Pneumonia is treated on its severity - not by which type it is.
Instead, use: exposure, the history, and risk factors to orient the
treatment goals. That means the Step 1 studying you did (this
organism leads to that presentation) should be ignored. Rather,
the thinking should be along the lines of, given the patients risk-
factors, what bug could this be? If theres no association with
healthcare the community bugs (not virulent or resistant) are CAP Strep pneumo Most Common
more likely (Community Acquired Pneumonia). Within CAP M. catarrhalis
there are bugs more likely to cause disease. Strep pneumo is H. flu COPD / Smoker
Klebsiella and Aspiration
always the most common; the #2 disease is based on risk factors Anaerobes (EtOH, CVA, MS)
(see the table). If the patient has been near healthcare the S. Aureus Post Viral
virulence and resistance increase; the bugs are more hostile. Treat Legionella Immuno
for HCAP (Health Care Associated Pneumonia). To be HAP Pseudomonas
considered HCAP (which also means HAP and VAP), there must MRSA
be exposure to a healthcare facility within 90 days (HCAP), be Immuno TB
admitted and acquire the pneumonia after 48 hours of admission Fungal
(HAP), or be on a ventilator (VAP). While HCAP, HAP, and
VAP are different bureaucratically, they carry the same
microbiologic risk - MRSA and Pseudomonas so theyre treated Fever + Cough.with
the same. If the patient is Immunocompromised the weird bugs Bronchitis Sputum Production, Nrml CXR
can cause infections (TB, Fungus, MAC, and PCP). Finally, if Abscess Foul Breath, Cavitation CXR
theres a risk for aspiration (MS, Stroke, Diabetic, Alcoholic, Pneumonia Sputum production, Consolidation on CXR
Intubated, Seizures), the oral flora /anaerobes are at risk. PCP Immunocompromised, Hypoxemia, elevated LDH
Flu Myalgias, Arthralgias, body aches
Everybody who presents with a fever and a cough will get a
CXR. Theyll also get an SpO2. Even though the best test is a
culture, sometimes in the lung it doesnt work out. So beyond
CXR + SpO2, theres no clear algorithm.

Sputum Gram Stain and Culture rarely has utility unless obtained
by bronchoscopy (contaminated by floral organisms, useful only
when <10 Squamous and >25 Polys /hpf). Blood Cultures rarely
yield anything, and if positive represent septicemia, but should be
obtained on any patient being admitted to the hospital.
Bronchoalveolar lavage is reserved for acutely ill patients or
those who do not improve after 72 hours of empiric therapy.
Serum, urine antigen, or PCR can be used to identify certain
organisms (legionella, strep pneumo), but these advanced tests are
often not needed. Empiric treatment is usually sufficient to
direct us.

Fever, productive cough, and consolidation on chest x-ray is
classic for pneumonia. In this constellation, one must only decide
between HCAP and CAP; use empiric therapy from there. Be able
to differentiate Pneumonia from Abscess and Bronchitis, as well
as HCAP from CAP. See first section.

Infectious Disease [PNEUMONIA]

Bronchitis Other Bugs to consider
Bronchitis presents as a fever and a cough with a Normal CXR. S. pneumoniae Most Common
This presentation might be a viral pneumonia or an Legionella GI + CNS Sxs Urine Ag
extrapulmonary process, but with a sputum production that can Klebsiella EtOH
Chlamydia Placenta/Sheep Serum Ab
be treated as an ambulatory pneumonia. This means outpatient
Haemophilus COPD/Smoker
therapy with a macrolide (Azithromycin), doxycycline, or
moxifloxacin. Chronic Bronchitis is a productive cough for 2-3
months in 2 consecutive years.

Atypical Pneumonia Bottom Line 1st Line Alternate

This isnt a thing in clinical medicine, but it still comes up on Ambulatory Pneumonia Azithromycin Doxycycline
tests. Atypical pneumonia presents as an insidious onset fever (Bronchitis) Moxifloxacin
and cough with bilateral infiltrates on CXR. These patients Inpatient Community Pneumonia Ceftriaxone + Moxifloxacin
(CAP) Azithromycin
typically dont present as acutely ill - the so called walking
Inpatient Health Care Pneumonia Vancomycin Many
pneumonia. Treat this like a bronchitis, but know the association (HCAP) + Pip/Tazo
between Mycoplasma Pneumonia and IgM cold agglutinin PCP Bactrim None
disease. +/- Steroids
Influenza Oseltamivir None
Abscess / Aspiration Pneumonia
An abscess is going to present as a fever and a cough, plus
cavitation and foul breath. Because of cavitation, lung cancer,
TB, and fungus must be considered. Obtain a CT scan to
facilitate. Clindamycin is crucial to the therapy because oral flora
has anaerobes, but often additional therapy is initiated with the
clindamycin as it still represents a pneumonia. Aspiration
causes abscesses. Aspiration risk essentially means patients with
seizure, alcoholics, and MS/CVA patients with dysphagia
(include PEG tube patients in here too).


If the patient has a subacute pneumonia with bilateral fluffy
infiltrates, give consideration to PCP. An elevated LDH is often
associated with PCP. The diagnosis is made with a silver stain on
induced sputum or bronchoalveolar lavage. The treatment is with
IV Bactrim. If the patient is hypoxemic, add steroids.
Who Needs to be admitted? PORT Score / PSI and CURB-65
Confusion of new Onset A 5-point system. The more
You shouldnt memorize the Pneumonia Severity Index (PSI) nor Urea > 7 (BUN > 19) points, the more severe the
the CURB-65, but since pneumonia is so common at least be Respiratory Rate > 30 patients condition + and
aware of what these are and what they mean. The CURB-65 is an Blood pressure < 90 / < 60 the more fatal it is. Used to
ED Triage Tool, whereby the patient likely needs admission if 65 years or older determine if the patient
any one of the CURB-65 are met. The PSI is an Internal needs to be admitted
Medicine Triage Tool thats quite complex it requires an online
calculator to complete. The higher the score, the more likely the
Pneumonia Severity Index
need for ICU. The lower the score the more likely the person can
I Discharge from ED
be discharged. While clinical acumen is equivalent to these II < 70 Floor Admission (probably)
scores, they provide object evidence for documentation and can III 71-90 Floor Admission (Definitely)
be used to gauge clinical reasoning on severity of disease. THIS IV 91-130 ICU Admission (Probably)
IS NOT FOR THE SHELF. V > 130 ICU Admission (Definitely)

Infectious Disease [SEPSIS]

Introduction SIRS Criteria
An infection usually causes a local inflammatory response with Temperature > 38 or < 36
symptoms. Lung infections cause a cough, while UTIs cause Tachycardia > 90
dysuria. But when an infection jumps the shark and goes systemic Respiratory RR > 20 or PCO2 < 32
WBC > 12 or < 4
- effects are felt systemically - start thinking of sepsis. Sepsis
itself doesnt require septicemia (bacteria in the blood) and
therefore may be culture negative, but the systemic effects of SIRS Types
inflammatory mediators can wreak havoc on the body. SIRS 2 or more criteria met, source
Sepsis SIRS source
SIRS Criteria Severe Sepsis Sepsis with low blood pressure or elevated
The Systemic Inflammatory Response Syndrome (SIRS) must lactic that is responsive to fluids
meet 2 of 4 criteria that signal physiologic responses to Septic Shock Sepsis with low blood pressure or elevated
inflammation. Inflammatory mediators will cause CO ( HR) lactate that is non-responsive to fluid.
MODS Multiple Organ Dysfunction Syndrome, the
either directly on the heart or reflexively from vasodilation.
patient is circling the drain with septic
Tachypnea follows. Fever is a product of IL-6 + TNF-. Finally, shock and multiple organs failing
the response to infection is WBC (leukocytosis). But, because
some infections may WBC or a person can have sepsis in the
presence of HIV, both count. Evaluation beyond sepsis involves Organs in Dysfunction
looking for end organ damage: 1) Renal Failure ( Cr and Hypotension
BUN), 2) liver failure with coags and an LFT 3) Blood Vessels
with a blood pressure, 4) Brain with mental status checks, and 5)
Heart with an ECG or Troponins. Still further, one needs to
evaluate for tissue hypoxemia with a lactic acid level. Depending
on the number and severity of organ dysfunction, the patient is
stratified into a sepsis type. (SIRS, Sepsis, Severe Sepsis,
Septic Shock, MODS). Creatinine

Regardless of type, the treatment is the same: Early Goal
Directed Therapy. This takes place in the first six hours of LFTs, Coags
hospitalization (early) and is designed to Tissue Perfusion,
Tissue Hypoxia, and control the source. Controlling the source
begins by eliminating sources of infection (IV sites, Abscess Other Lactate
Drainage, and Wound Debridement) and starting empiric
antibiotics for the suspected agent. Blood Cultures should be
drawn prior to antibiotics, but do NOT delay the treatment with
broad-spectrum antibiotics. In order to meet tissue perfusion
demands certain criteria should be monitored. To maintain Early Goal Directed Therapy
perfusion (MAP > 65, CVP 8-16) a 30cc/kg bolus is the first CVP 10-12mmHg
MAP >65mmHg
step. If responsive, nothing more needs be done. Failure of the
Uoutput >0.5cc/kg/hr
fluid challenge will require the need for pressors. To maintain SvcO2 >70%
oxygenation (oxygen deliver > oxygen consumption, or SvO2 > 1) Give 30cc/kg IV Bolus
70%) both oxygen and blood (if Hgb < 7) should be given. 2) Remove all source of infection
3) O2 as needed
4) Pressors if fluid bolus fails
5) Empiric abx while waiting for cultures

Infectious Disease [SKIN INFECTIONS]

Cellulitis is an infection of the subcutaneous tissue of the skin.
Its most often caused by infection by the skin flora: Group A
Strep and Staph aureus. The presentation of a cellulitis is
usually red, hot, tender skin thats often well-demarcated (ie
you can draw a pen or marker on the edge and watch it grow or
recede). It usually has a portal of entry (like a scratch, scrape, or
puncture wound). The diagnosis is often clinical it rarely
requires culture or biopsy. If theres an abscess (likely to be
Staph) it should be drained; culture the pus. But without purulent
drainage there should be no attempt to culture the cellulitis, as
what youll likely receive is the polymicrobial sample of the skin.

The treatment for cellulitis is affected by one of two scenarios.

When the person isnt toxic and they walk into clinic without
systemic signs of infection, a 1st generation cephalosporin such Scenario Treatment
as cephalexin, or antibiotics thatll cover community acquired Non-Toxic Outpatient 1st Gen Cephalosporin
MRSA such as TMP-SMX (Bactrim) or Clindamycin can be Non-Toxic CA-MRSA TMP-SMX, Clinda
Toxic (inpatient) Vanc, Dapto, Linezolid
If a person is toxic theres sepsis - its time to reach for the
bigger guns such as vancomycin or linezolid. Daptomycin is an

You know youre winning when the ring of cellulitis recedes

towards the portal of entry. A failure to recede may indicate you
have the wrong bug, the wrong drug, or that theres something
under the skin that cant be seen. Routine imaging isnt required
for cellulitis, but can be done when theres a failure to resolve.

Osteomyelitis Osteomyelitis
Osteomyelitis is infection of the bone. This occurs via Risk Factors Bug
hematogenous seeding or by direct inoculation (trauma, Most Common S. aureus
fracture). If you can probe to bone through a wound, its osteo. Penetrating / Sneakers Pseudomonas
The other way to catch osteomyelitis is in a refractory or recurrent Sickle Cell Salmonella
cellulitis. Gardening Sporothrix
DM/PVD Polymicrobial, cover for
Diagnose with X-ray. If theres osteolytic changes, the diagnosis pseudomonas
is made. Its often negative, because it takes two weeks to turn Oysters + Cirrhotic V. vulnificus
positive. If suspicion of osteo is high, but the X-ray is negative,
the best radiographic test is MRI. Two tests that are usually the
wrong thing to do are Bone Scan (useful only when theres no
overlying inflammation) and Tagged WBC scan, which is
always wrong. Once osteo is identified, take a biopsy. Its the best
way to confirm osteo and is necessary to direct antibiotic therapy.

Treatment is 4-6 weeks of antibiotics, which is why the culture

and sensitivity is wanted. Follow with ESR and CRP weekly to
gauge the response to therapy. DO NOT repeat the MRI. DO NOT
repeat the biopsy.

Infectious Disease [SKIN INFECTIONS]

Gas Gangrene
Gas Gangrene is caused by Clostridium perfringens. The patient
will present with some sort of wound, often a penetrating wound
that gets contaminated. Crepitus will be able to be felt. The
diagnosis begins with an X-ray, showing gas in the soft tissue.
The treatment is debridement and PCN + Clindamycin. Gas
gangrene is induced by a toxin, so clindas ability to interrupt
protein synthesis makes it ideal.

Necrotizing Fasciitis
Neck Fack is a life threatening surgical emergency. Its caused
by the same things that cause cellulitis: Strep and Staph. It
presents as a really bad cellulitis. Look for a cellulitis that is:

1) Rapidly progressive with fast spread

2) Crepitus
3) Pain out of proportion with the physical exam
4) Blue-Grey discoloration of the skin

The diagnosis starts with X-ray, which will show gas in the
tissues. We know from Gas Gangrene that well need to get
surgical debridement right away. If on a limb, often we simply
amputate to prevent the spread of infection through fascial planes.
Broad spectrum antibiotics is required. Its fatal if untreated.

If this process is occurring in the groin (male genitalia or female

perineum) its referred to as Fourniers Gangrene.

Red, Hot,
Tender, Skin
The Effective Workup
When cellulitis is seen you want to think a little bit more about it.
Alarm Symptoms?
If theyre non-toxic its easy treat empirically. But there are
some things that should be on the radar, such as: draining tracts
Crepitus Draining Tracts
and palpable bone (osteo) or crepitus and pain out of Pain out of proportion Palpable Bone
proportion (gas gangrene or necrotizing fasciitis). Cellulitis
Gas Gangrene Osteomyelitis
The x-ray can reveal osteolytic changes of osteomyelitis, or the or Nec Fac
gas of the gas gangrene / nec fac. But, if nothings found and
theres still suspicion of Osteo, get an MRI of the bone plus a Gas in the tissue Osteolytic Changes
biopsy if possible. MRI
Gas Gangrene Osteomyelitis
or Nec Fac
Only give antibiotics to osteo after the culture or if the patient is
toxic. Debridement Biopsy Abx, One-Time Cx
Broad-Spectrum Abx MRI qWeek
Hyperbaric O 2 Tx based on Culture CRP/ESR qWeek
Always give antibiotics to Gas Gangrene and Nec Fec. and Sensitivity

Infectious Disease [TUBERCULOSIS]

Microbiology and Epidemiology
TB is an acid-fast bacillus that stains poorly on Gram stain. Its
spread through the aerosolized respiratory droplets and infects Primary Lesions are
the lungs. Primary TB presents like a pneumonia and localizes usually in middle and
in the middle or bottom lobe. Unable to kill the bacteria, the lower lobes
body forms cavitary lesions (aka caseating granulomas) to wall
off bacteria. Reactivation TB occurs in the apices - where
oxygen tension is highest. Cavitation results in lung Reactivation Lesions are in
fragmentation and hemoptysis. Major risk for the spread of TB is the apices
a place where there are too many people in too small a space
(military barracks, prison, and homeless shelters). Being
immunocompromised risk of contracting and reactivating
chronic disease.
Rate of TB in the US
Patient Presentation
There are two types of patients: those who are asymptomatic but
exposed and those with cavitary pneumonia presenting with night
sweats, fever, weight loss, hemoptysis, and cough. These 1930 1950 1990 2010
patients are going to follow a diagnostic algorithm separate from
each other. PPD screen if:
>5mm Immunosuppressed
Diagnosis HIV / AIDS
The asymptomatic screen is performed on people who arent Organ Transplant
symptomatic but require proof of their absence of exposure. The Steroids
Close Contacts of TB
initial test can be done with a PPD or an Interferon-Gamma
>10mm Exposed
Assay. The PPD is placed today and read in 48-72 hours, where Incarcerated, Homeless
the amount of induration (not erythema) is used to determine if Health Care Provider
positive or negative. The Gamma-interferon test is more Travel to Endemic Areas
expensive but tells yes or no. Theres also no need to return for >15mm Shouldnt Be Screened
the assessment. When the patient has had the BCG vaccine you People from Wyoming whos exposure is on
National Geographic
simply ignore that fact when assessing for pulmonary TB. If
forced, choose Interferon-gamma assay over PPD for those with
Asx Screen
BCG vaccine.

If a patient is symptomatic, has a positive PPD, or a positive PPD

Gamma-Interferon Assay, a chest x-ray is required to assess for
active disease. In these patients, the chest x-ray will also serve as
their annual screen (once the PPD is positive, itll always be Exposure No Exposure
If the CXR and theyve never been treated, they require
Isoniazid + B6 x 9 months.

If CXR an active infection must be ruled out with AFB Infected Exposure Only
smears. This is a good time to isolate the individual. If the AFB INH x 9 mos
Smear , theres an active infection; treat with RIPE. If the AFB +B6
Smear , the patient has latent TB; treat with Isoniazid + B6 x CXR
9 months.

For the acutely ill patient theres no need (or time) to wait the Active TB Latent TB
48-72 hrs of the PPD. First do a CXR looking for apical lesions.
R.I.P.E. INH x 9 mos
However, if theres a CXR its insufficient to rule out active +B6
disease; an AFB Smear and Culture must also be done. If the
disease is suspected a positive confirmation is desired.

Infectious Disease [TUBERCULOSIS]

Send out early morning sputum and at least a total of 3 cultures
8 hours apart. Its essential to ensure its negative so also send out
3 early morning sputums 24 hrs apart. For AFB smear culture
(active disease) treat with RIPE. If AFB smear look for
another diagnosis such as malignancy; it isnt TB thats causing
the symptoms.

The culture thats initially negative, but then comes back 6 weeks
later as positive is non-tubercular mycobacterium. Its like MAC
mycobacterium avian complex.

Other Diagnostic Tests

Nucleic Amplification can be used to ensure that the thing you
thought was TB is really not TB. Excellent sensitivity.

Adenosine Deaminase can be used in pleural effusions, and is

better than an AFB smear and culture.

Anyone with a PPD or CXR is going to get at least 9 months
Isoniazid + B6.
RIPE Side Effects
For active disease we get a trial of Rifampin, Isoniazid, Rifampin Red Urine
Pyrazinamide, Ethambutol (RIPE). Its a good idea to know the INH Neuropathy (Give B6 Ppx)
Pyrazinamide Hyperuricemia, Gout
side effects of these drugs. ALL 4 cause hepatotoxicity. Ethambutol Eye Disturbance
(optic neuritis)
To treat non-tubercular mycobacterium (MAC) treat with
Clarithromycin and Ethambutol. Note that hepatotoxicity is a side effect for all


Presentation and Background Disease Symptoms Test Treatment
UTIs are infections involving anything from the kidneys to the Asx Asx screen U/A UCx Pregnant: Amoxicillin
urethra. Its most common in women aged 18-24 because of their Bacteriuria Procedure, Nitrofurantoin
relatively shorter urethra (women) and frequency of sex (age pregnant
group). Sex, OCP, and Anal intercourse all risk of infections. Urethritis Frequency U/A UCx Ceftriaxone 125mg IM
The UTI is most often caused by fecal flora coming into contact Urgency + DNA +
with the urethra. This means E. coli is likely to be the causative Dysuria Doxy 100 x 7 days or
organism. + Discharge Azithro 250 x 1 po
Cystitis Frequency Clinical TMP-SMX or
Urethritis Urgency Nitrofurantoin or
Urethritis is Cystitis + Urethral Discharge - especially in a Dysuria Fosfomycin
sexually active person. We no longer need the swab; simply just Pyelo Frequency U/A IV Cephalosporin (inpt)
obtain urinary Gc/Chla. The urethral discharge is generally Urgency UCx or
more disconcerting to the patient. The cause? Usually STDs. Dysuria BCx PO FQ (outpt)
Treat Gonorrhea with Ceftriaxone 125 IM x1 and treat + Fever
Chlamydia with Doxycycline 100 x 7days or Azithromycin 250 + CVA Tender
x 1. Treat both, even if you only find one.
Abscess Pyelo that does CT or U/S Drainage + Abx
not improve (same as Pyelo)
Asymptomatic Bacteriuria
Bottom line, dont treat asymptomatic bacteriuria, defined as
no symptoms but > 105 colonies. The exception to this are
Pregnant Side Note
pregnant females and anyone with a urologic procedure. If you
Confirmation of eradication is required only in pregnancy. Its justified by
screen AND theres a reason to treat (pregnancy or procedure)
then yes, treat. But all other permutations are NOT treated. On being another screen, > 2 infections means PPx Abx in pregnancies
medicine, dont treat. On OB, do treat. In pregnancy, its treated thereafter.
to prevent progression to pyelo and to clear GBS. Use amoxicillin
as the front line agent and nitrofurantoin if penicillin allergic.

Presenting with frequency / urgency / dysuria, cystitis (bladder
infection) is the most common of the UTIs. Systemic symptoms
like N/V, Fever, and Chills are absent. The diagnosis is clinical.
With a clear diagnosis its fine to just treat. A urinalysis can be
performed to confirm and cultures are almost always
unnecessary. If its an uncomplicated UTI, treat for 3 days. If
its a complicated UTI, treat for 7 days. The antibiotics of choice
are TMP-SMX (Bactrim), Nitrofurantoin, or Fosfomycin.
Ciprofloxacin should NOT be used for cystitis. Complicated
means the presence of any of the Ps listed to the right and

Pyelonephritis should be considered a systemic disease, often
presenting with florid infection. There will be urgency,
frequency, and dysuria PLUS CVA tenderness and a fever.
These patients are often toxic. The U/A will show white blood
cell casts (pathognomonic for Pyelo). The urine culture will
direct ongoing antibiotics. The learning pt is pyelo gets admitted
and receives IV Ceftriaxone or IV Amp + Sulbactam. Bonus - Testing Notes
Theres the condition called ambulatory pyelo where a young U/A Leukocyte Esterase
healthy woman can tolerate po, so she gets PO Cipro. This is the Nitrites
only indication for PO Cipro on the board exams. U Micro + WBC
- Epithelial Cells
Abscess U Culture Pregnant
The person who comes in with pyelonephritis who does not Procedure >105 colonies = Treat
improve probably has an abscess. Either CT scan (preferred test) Pyelo
or an Ultrasound (if pregnant) will reveal it. Drain it and ?? Diagnosis, ?? Organism
continue IV antibiotics. CT scan is best, but avoided in patients CT Screen for Abscess if non-pregnant
with renal failure or pregnancy. In those scenarios an ultrasound U/S Screen for Abscess if non-pregnant
is an acceptable alternative.


Cushings Syndrome Clinical Symptoms of Cushings
A disease of excess cortisol, its caused by one of four conditions:
1) Iatrogenic (most common, taper off to fix), 2) Pituitary tumor 24 Hr Free Urine Cortisol Cushings
(Cushings disease), 3) Adrenal Tumor, or 4) Ectopic ACTH. The and
patient will present with a Cushingoid appearance: central Low Dose Overnight DST
obesity, moon facies, extremity wasting, a buffalo hump, glucose
Cushings Syndrome
intolerance or diabetes, and hypertension. When faced with this
condition, get a 24-hr free cortisol level and confirm with 1mg Adrenal
Low Dose Dexamethasone Suppression test. If cortisol is its ACTH
Cushings. Follow that with an ACTH level to distinguish adrenal High ACTH Low ACTH
( ACTH) from extra-adrenal ( ACTH). If adrenal, spot it with a Adrenal Tumor Adrenal Tumor
CT/MRI of the Adrenals. If extra-adrenal, perform a high dose MRI/CT Abd
dexamethasone suppression test to determine pituitary High Dose DST Resect
(suppresses) vs ectopic ( suppression). Confirm pituitary Suppression Suppression
Cushings with an MRI followed by transsphenoidal resection. If Cortisol Cortisol
Low Then High
ectopic, find it with CT/MRI of 1) Chest (Lung Ca), 2) Abd Ectopic ACTH Cushings Disease
(Pancreatic ca), then 3) Pelvis (adrenals). Remember Low-Dose CT MRI/CT Abd
ACTHen High-Dose. Lung/Abd/Pelvis Resect

Hyperaldosteronism Refractory HTN HTN+Hypokalemia

Aldosterone causes resorption of Na and H2O producing an
Aldo, Renin, Aldo:Renin
expanded vascular volume and hypertension by ENa in the
collecting tubules, trading Na for K. This produces a refractory Aldo Aldo Aldo
Renin Renin Renin
HTN or a Diastolic HTN and Hypokalemia. Differentiate
Aldo:Renin > 20 Aldo:Renin <10
between: primary (a tumor or adenoma called Conns Syndrome)
where aldosterone production is independent of Renin, secondary Mimickers Likely 1o Likely 2o
(renovascular disease, edematous states of CHF, Cirrhosis, Renovascular Dz
CAH Salt Suppression
Nephrotic Syndrome) where the production of aldosterone is Cushings CHF, Cirrhosis,
Test Nephrotic Syndrome
dependent on renin and is an appropriate response to renovascular Licorice
flow, and mimickers (CAG, Licorice, or exogenous mineral Liddles Aldo Garters
corticosteroids). When suspected, perform 8am levels for Iatrogenic Primary Gitelmans
Aldosterone, Renin, and Aldo:Renin Ratio. Ensure any
hypertension medication is discontinued (ACE, CCB, Diuretics CT or MRI
Lesion Lesion
confound the test). If elevated (>20 Aldo and >20 Aldo:Renin), its
likely primary. Confirm with the salt suppression test (where aldo Local Adrenal NonLocal
Cancer Hyperplasia
will not decrease after a 200g Na load). The tumor is found by CT Vein
or MRI. If early AM levels are elevated a different disease is
likely provoking the aldosterone increase.

Pheochromocytoma Palpitations Pressure Pallor Pain Perspiration

An overproduction of catecholamines produces either a sustained
refractory HTN or Paroxysmal Five Ps which are 1) Pressure 24-hr Urinary Metanephrines
(HTN), 2) Pain (Headache or Chest Pain), 3) Pallor or Ruled Out Dz
(vasoconstriction), 4) Palpitations (tachycardia, tremor), and 5) Urinary VMA
Perspiration. This follows the rule of 10 percents (excellent
pimping question, useless for practice). Screen for this disease with Pheochromocytoma
24 hr urinary metanephrines or Urinary VMA (metanephrines
is better, VMA is cheaper). If , do an MRI/CT of the pelvis. They
should be easy to spot. If not, a MIBG Scintigraphy can be done. CT / MRI MIBG
The treatment is resection but with caution; touching one can cause -Blockade Scintography
release of catecholamines. Pretreat first with -blockade to prevent
-Blockade Diagnosis
unopposed -action with -blockade, then -Blockade, then


Adrenal Incidentalomas r/o With
These are asymptomatic adrenal masses found on CT scan for Cushings Dexamethasone Suppression test
something else - an incidental finding. Its important to rule out Pheo 24-Hr Urine
functioning adenomas (pheo, aldo, cortisol, androgen) from Conns Aldo/Renin
nonfunctioning adenomas. All above findings must be done to
rule out Cushings (DST), Pheo (24-hr urine metanephrines) and
Aldo (plasma renin and Aldo). A direct needle biopsy should
NOT be done until pheo is ruled out. Its ok to watch and wait if
<4cm, but intervene with treatment if >4cm or theres an increase
in size over time.

Adrenal Insufficiency Hypotension + Hyperkalemia + N/V

The loss of adrenal function may be from a variety of etiologies,
and may be sudden/acute with multiple presentations. The most
3am Cortisol Ruled Out Dz
common cause in the US is autoimmune adrenalitis; its TB
worldwide. In the setting of sepsis there may be bilateral adrenal <3
destruction from hemorrhage (Waterhouse-Friderichsen). Weird Adrenal Insufficiency
deposition disease can also compromise the adrenals (amyloid,
sarcoid, and hemochromatosis). In primary failure (loss of
cortisol, maintenance of ACTH) the symptoms will be Test
hypotension, fatigue, N/V of cortisol loss, as well as the
Cortisol Cortisol after 60 minutes
hyperpigmentation and hyperkalemia. Hyperpigmentation is a
result of ACTH production trying to increase cortisol while 1o Failure 2o Failure
hyperkalemia is from deficient aldosterone. In secondary failure,
Prednisone Prednisone Only
no ACTH is produced so hyperpigmentation is absent. Because AND
aldosterone production is intact theres also no hyperkalemia. Its Fludrocortisone
key to make sure its not a primary deficiency so perform a
cosyntropin test (exogenous ACTH administration). Establish a Cortex - Glomerulosa Salt Aldosterone
baseline cortisol in the morning (<3ug = Dz, >18ug = ruled out). Fasiculata Sugar Cortisol
Give the ACTH then reassess in 60 minutes to determine if theres Reticularis Sex Testosterone
any change in cortisol. (3, 3, 3 = ACTH problem = 10 deficiency)
vs (3, 3, 20 = ACTH problem, 2o deficiency). Treat this by giving
the steroids they dont have. Prednisone for all types and
fludrocortisone for primary only (its a synthetic aldo that has its
Medulla Catecholamines
function retained through the RAAS in secondary).

Dz Path/Etiology Presentation Diagnostic Tx

Cushings Iatrogenic Obesity, Diabetes Low Dose Dexa Suppression Stop Steroids
Pituitary Tumor Moon Facies, ACTH levels or
Adrenal Tumor Buffalo Hump High Dose Dexa Suppression Cut out Tumor
Ectopic Tumor CT/MRI Abd/Pelvis/Thorax
Hyperaldo 1o Dz = Tumor Hypertension and HypoK Aldo, Renin, Aldo:Renin Cut out Tumor
(Conns) 2o Dz = Systemic OR Salt Suppression Fix Systemic Dz
Mimickers Refractory HTN CT/MRI
MIBG Scintillography
Pheo Adrenal Tumor Paroxysmal Pain Pressure 24-hr Urinary Metanephrine -Blockade
Palpitations Pallor or -Blockade
Perspiration VMA Urine Adrenalectomy
Adrenal Autoimmune Hypotension Cortisol Level @ 3am 1o = Prednisone (cortisol) and
Insufficiency Infection Fatigue Cosyntropin Test Fludrocortisone
Hemorrhage Anorexia CT/MRI 2o = Prednisone Only
Deposition Disease Nausea/Vomiting
Pituitary Failure Hyperpigmentation


The pituitary is divided into two structures: 1) the Hypothalamic Neural Tissue
adenohypophysis (anterior pituitary), which receives endocrine GnRH TRH CRH GHRH
signals from the hypothalamus 2) the neurohypophysis
(posterior pituitary), which has axon terminals from neurons of
the hypothalamus in it. The pituitarys a small endocrine gland
Anterior Pituitary Posterior Pituitary
that regulates endocrine and metabolic function throughout the
body. There can be problems with overproduction or FSH LH TSH ACTH GH Prolactin Oxytocin
underproduction of just one or all hormones. Because of its
location within the optic chiasm, tumors of the pituitary can 3 Levels of Feed Back and Endocrine Regulation of the Ant Pituitary
present with bitemporal hemianopsia. Well discuss the typical (1) Hypothalamus GnRH TRH CRH GHRH
hyper and hypo secretory disease here. Portal
(2) Pituitary FSH/LH TSH ACTH GH
1) Prolactinoma Systemic
A benign tumor that autonomously secretes Prolactin will cause Circulation
a prolactinemia. Prolactinemia presents differently in men than (3) Target Organ Ovaries Thyroid Adrenals Liver
women. Theyre caught early in women as microadenomas, Metabolic Estrogen T3 Cortisol ILGF
Effect Progesterone T4
because women tend to notice galactorrhea and amenorrhea.
Theres been no time for the tumor to grow; its small and
Ovulation Metabolism Stress Growth
presents without field cuts. In men, who dont lactate or have
periods, theres nothing to tip them off that somethings wrong
(decreased libido may be the only symptom). Thus, the tumor
TRH TRH @ High Doses stimulates
grows. As it becomes a macroadenoma it digs into the optic
chiasm to produce a bitemporal hemianopia. In the case of field TSH PROLACTIN Dopamine Dopamine
cuts its easy to be pretty sure theres a tumor. But in the case of
Normally Antagonists
a microadenoma other causes of prolactinemia must be ruled out. T3/T4 Inhibits Disinhibit
For example, dopamine antagonists (antipsychotics) disinhibit Prolactin Prolactin
Prolactin while TRH (from hypothyroidism) stimulates its F: Microadenoma
production. So, before getting an MRI test, get Prolactin levels Galactorrhea Galactorrhea, Amenorrhea,
and a TSH after looking over their med list. Treat by using Amenorrhea Bitemporal Hemianopsia
dopamine agonists (cabergoline > bromocriptine). Consider
M: Macroadenoma Elevated
surgery only after medical therapy fails; unlike most tumors Field Cuts TSH Hypothyroid
Prolactinomas are very sensitive to medical therapy. Follow
prolactinomas with prolactin levels q3months and an MRI Synthroid
annually until stable. Prolactin
Elevated Else
2) Acromegaly
A benign tumor that autonomously secretes Growth Hormone Prolactinemia
will cause things that can grow to grow. In a child, before the Cancer Cancer
Prolactinoma MRI
closure of the growth plates, that means the long bones - resulting
in gigantism. But in an adult it means the hands, feet, face, and
visceral organs. It also induces gluconeogenesis and causes the
patient to present with glucose intolerance or even frank Big Hands, Face, Feet, Cardiomegaly, DM
diabetes. The thing that kills these patients is the cardiomegaly
and subsequent diastolic heart failure. The diagnosis is made
biochemically. However, GH is pulsatile, and so it cant be used Measure Somatomedin C Normal Dz
(ILGF-1) r/o
to make the diagnosis. Instead, because GH exacts its effects
through the liver via ILGF-1 (somatomedin); the diagnosis Elevated
begins there. A failure to suppress GH levels in a glucose Normal Dz
Glucose Suppression Test
tolerance test (next page) is a finding and should prompt the r/o
confirmatory MRI. The only treatment is surgery. However, Screen Suppress
radiation or medical therapy with octreotide (somatostatin) can GH Tumor
be used for residual tissue to GH production which will ILGF
effects. Extrapituitary Out of our
Ant Pituitary Tumor MRI scope
Octreotide Surgery


3) Cushings Disease
Autonomous secretion of ACTH causes cortisol. This is Insulin bG Normal: Glucose = bG
covered in the adrenal disorders. Load
4) Central Hyperthyroidism Screen: Glucose = bG
GH Cortisol bG Load
An incredibly rare secretion of TSH causes T4/T3. This is
covered in thyroid disorders.
5) Hypopituitarism
Anterior Pituitary
The lack of one or all pituitary hormones can cause some
problems for the body. There are a variety of ways pituitary Liver Gluconeogenesis bG
function can be lost. There are acute losses that usually present as ILFG Frank DM
really sick (coma, hypotension, death) and chronic losses that
result in losing lesser hormones first. Lets start with chronic then Bones Visceral Organs More on Acromegaly
go over some specific syndromes that need to be known about Acromegaly Hepatomegaly, Cardiomegaly
acute diseases. Because the less important hormones are lost first
(FSH and GH before TSH), screening can be done with an Hypopituitarism
insulin stimulation test - the reverse of the glucose suppression Infarction Tumor
test. If hypoglycemia fails to stimulate GH then its Surgery Infiltration
hypopituitarism. Confirm with an MRI and replace deficient Radiation Autoimmune
hormones. If possible, reverse the underlying cause if there is ACUTE CHRONIC
one. TSH = Lethargy, Coma, Death 1st To go
ACTH = Hypotension, Coma, Death FSH LH GH
FSH/LH = Not Felt TSH
Acute loss of function is much worse. Specific syndromes to be ACTH
aware of are Sheehans and Apoplexy. Sheehans is a post- Last to go
partum hypopituitarism after prolonged labor, usually with some
blood loss. The pituitary becomes ischemic and dies. This can Normal: Insulin = bG
GH Cortisol Glucagon
typically be detected by the inability to lactate as the first sign.
Apoplexy is a medical emergency; a pre-existing pituitary tumor Insulin
outgrows its blood supply and bleeds into the pituitary. The Screen: Insulin = bG GH (early disease) Glucagon
Cortisol (late disease)
patient rapidly decompensates with stupor, nuchal rigidity,
headache, nausea and vomiting, etc.
6) Empty Sella Syndrome
This is an incidental finding in a patient who has no endocrine
abnormalities but is found to have an absent pituitary on an
MRI they had for some other reason. If it aint broke, dont fix Meninges fill
it. They have a pituitary - its just not in the sella. Sella Turcica
Normal Empty Sella

Patient Presentation Pathology Dx Tx

Prolactinoma F: Amenorrhea, Galactorrhea, Dopamine 1st: Prolactin Start: Bromocriptine
Vision s, Microadenoma Antagonists Then: TSH/T4 Best: Surgery when
Hypothyroid Best: MRI pregnancy, field cuts,
M: Vision s, Macroadenoma Pituitary Tumor medication failure
Acromegaly Children: Gigantism 1st: Glucose Start: Octreotide
Adults: Big hands, Big Feet, Big GH Suppression Test Best: Surgery
Heart and DM Best: MRI
Hypopituitary Acute: Coma, Lethargy, Hypotension Infection, 1st: Glucose Start: Replace Missing
Chronic: Less important go first Infarction, Surgery, Stimulation Test Hormones
Radiation Best: MRI
Sheehans Post-partum after a long labor Best: Treat underlying
Apoplexy Previous Tumor Bleeds, Stupor Tumor, Infiltration, disease if possible
Nuchal Rigidity, Nausea/Vomiting Autoimmune
Empty Sella Asx Not pathological 1st and Best: MRI : Needs no treatment


Hypoglycemia in a Diabetic
Hypoglycemia in a diabetic can come from a number of causes.
The usual suspects are too little food, too much exercise, and too
much medication. Hypoglycemia is defined as a bG < 70 or
symptoms of hypoglycemia (palpitations, perspiration,
presyncope); its corrected with ingestion of sugar. Severe
hypoglycemia may cause coma, anoxic brain injury, and death.

The most important thing to do is get the sugar up. Do it with an

oral glucose load if the patient is awake, or with IV D50 if the
patient is in a coma. After the event has resolved, assess life-style
and medications to determine exactly what happened and try to
prevent it in the future.

Hypoglycemic events are potentially fatal and should be treated

with significantly more acuity than a high reading.

Hypoglycemia in a Non-Diabetic
Hypoglycemia, a bG < 60 AND symptoms, in a non-diabetic is
usually factitious disorder. Two potential disease states (that are
quite rare) are insulinoma and autoimmune hypoglycemia. To
discover if the patient is doing it to themselves, obtain a C-
peptide, Pro-Insulin, bG, and Secretagogue screen.

Endogenous insulin comes from Pro-insulin, cleaving the C-

peptide portion to result in insulin. Thus, if theres NO rise in C-
peptide, the insulin must be exogenous (self-injecting). Your job
is done if the C-peptide is normal.

Endogenous insulin secretion may be induced by secretagogues

(like sulfonylureas) or produced by insulinomas. The only way
to tell the two apart is to obtain a secretagogue screen. If positive,
theyre ingesting secretagogues - tell them to stop.

Only evaluate for insulinoma if the C-peptide is elevated AND

the secretagogue screen is negative. Perform a 72-hour fast,
retest for all the same things above, and if positive perform the
CT scan or MRI of the abdomen to find + resect the tumor.

If all else fails, consider the option of looking at insulin



Diabetic Ketoacidosis
DKA is a life-threatening emergency of Type I diabetics. There
is plenty of sugar in the blood, but without insulin none of it can
get into the cells. Its as if the patient is starving. The brain
activates ketones from fatty acids, causing both ketosis and
acidosis. Simultaneously, the high levels of sugar in the blood
spill into the urine. With the Tmax of the renal tubules at only
about 180, excess glucose is spilled into the urine. Glucose is a
potent osmotic diuretic; the patient becomes dehydrated.

The patient will present obtunded or in a coma. They will be dry.

Diagnose the condition by finding elevation blood glucose
(Diabetic) ketones in the urine and blood (Keto) and acidosis
on ABG / anion gap on BMP (Acidosis). Mechanism of dehydration in hyperglycemia. Excess
glucose is lost in urine and draws with it water, leading to
The treatment is threefold: Replete Potassium before giving potent diuresis.
Insulin, IV Insulin, and Fluid. Monitor therapy with hourly blood
glucoses and BMPs every 4 hours. If the gap hasnt closed but
the glucose is approaching normal (this value differs per
protocol) switch to D5 NS. As the anion gap resolves (the gap
closes) bridge to subQ insulin long acting and let them eat.

While insulin noncompliance is the most common cause of DKA,

also look for NSTEMI, GI bleeds, and infections as precipitating

Hyperosmolar Hyperglycemic Nonketotic Coma

HHNKC or HHS is the life-threatening emergency of Type II
diabetics. No ketones are made because theres sufficient insulin
to feed the brain. No acidosis occurs because fatty acids arent
accessed. However, the patient will still present with coma
because of profound dehydration. The blood glucoses are often Treatment of DKA. Replete K, give insulin, then give fluids.
much more elevated in HHNKC than in DKA + the diuresis has HHS/HHNKC is the same thing, except no need to follow
gone on longer. This patient needs fluids and IV insulin. anion gap.

Characteristic DKA HHNKC / HHS

Path: Type I, Insulin Dependent Diabetes Mellitus Type II, Non-Insulin Dependent Diabetes Mellitus
Pt: + Diabetic Coma + Diabetic Coma
+ Ketones - Ketones
+ Acidosis - Acidosis
Dx: bG 300-500 bG 800-1000
U/A: + Ketones U/A: - Ketones
ABG: + Acidosis ABG: - Acidosis
BMP: + Gap BMP: - Gap
Tx: Replete K Replete K
IV Fluids Bolus a lot IV Fluids Bolus a lot
IV insulin IV Insulin
Follow the GAP Follow the symptomatic improvement


Insulins Drug Class Use When
Learning insulins for exams is a nightmare. Everything makes Lantus Long Acting Basal insulin qPM
sense if trade names are used. Im going to let YOU learn how Levemir Insulin
to recall generics, because its easier using what we use in real HumaLog Rapid acting Prandial Insulin qAC
life and I want you remembering the medicine first. Its NovoLog Insulin Combo
imperative to learn the difference between their peak onset and HumuLin Medium acting Insulin Idiot Insulin biD
how long they last. All insulins require SubQ injections. Some NovoLin Combo (old school, easy)
hints to help get started. 1) L drugs (Lantus and Levemir) are NPH Rapid Acting Prandial qAC
Long acting and all equivocal (except for how good the meal is Regular Rapid Acting Generally useless
at the drug rep dinner). 2) Log math is more advanced than
drawing a Line, so Log drugs (Humalog Novolog) are used in
more complex ways (qAc) versus the 3) Lin drugs (HumuLin
NovoLin), which as well see are ancient, not great, and useful
for those who dont want to think. Finally, 4) NPH is the rapid IDIOT INSULIN
part of the log combos, while 5) regular insulin is a longer acting
(medium) insulin. 2/3 AM Humulin 70/30
0.5Units/kg Novolin 50/50
Insulin Regimen 1/3 PM
The goal of insulin regimens is to control the blood glucose as
though it were a normal pancreas. That means post prandial
glucose spikes are met by insulin spikes post-prandially. There
is also a certain level of insulin always floating around in the body
its called basal insulin. So to simulate a normal pancreas the BASAL BOLUS
basal-bolus is best. Insulin demand can be approximated by 0.5 1/2 Bolus Lantus/Levemir
Units/kilogram the total amount per day. In the basal bolus 0.5Units/kg
method, is in the night time as Long Acting Insulin (the 1/2 Prandial Novolog/Humalog
basal). The other is divided qAC of short acting insulin (the
bolus). Its important to remember that a blood sugar is affected
by the insulin that precedes it. If the AM Dose is high, increase Breakfast Lunch Dinner Sleep
the nighttime dose. If the bG taken near lunch is high, increase 2hr 2hr 2hr
the breakfast dose. AM PP PP PP
A lot of people try the Idiot Insulin method. Its called (I call it) Wake Log Log Log Levemir
idiot insulin because the same amount of medium acting insulin Lantus
is given regardless of the blood sugar. If patients dont want to
check bG or are afraid of needles, they can use this method. It has CHASING THE SUGAR (DONT EVER DO THIS)
poor basal coverage and poor post prandial coverage, but its
only biD dosing. bG bG bG bG
The worst method is sliding scale insulin where no basal insulin
is given. Rather, a certain amount of short-acting insulin is given
with each accucheck. Bad hospitalists will do this. Since current
Insulin Insulin Insulin Insulin
bG is a product of the last insulin it will create hyperglycemic
peaks and hypoglycemic troughs as the nurse tries to chase
down the bG on your orders. If following another regimen and
Effect Findings
sugars are still high, adjustment of daily doses is appropriate.
Somogyi Effect Too MUCH insulin at night High AM bG
However, if the patient eats a cake or has ridiculous bG one time,
Dawn Phenomena Too LITTLE insulin at night High AM bG
using the sliding scale is a great supplement - but only on top of
Check early AM bG to tell the difference
an existing regimen.

Complications What we do
Nephropathy Microalbumin Screen, ACE-i
Peripheral Foot care, education, educations
Eyes Fundoscopic Exams, Laser
Erectile Nighttime Tumescence, Viagra
Control the Blood Sugars is paramount


This is for those going for the gold. I include it because it was my
first patient in residency. It was also likely my last encounter with

MEN1 Syndrome
Also known as Wermers Syndrome, this is an autosomal
dominant mutation of MEN1 gene that causes hyperplasia or
adenomas of the 3 Ps: Pituitary Adenomas, Parathyroid
Adenomas, and Pancreatic Adenomas. Theres a strong
association with Gastric Ulcers (Zollinger-Ellison syndrome from
the pancreatic adenomas), Hypoglycemia (Insulinoma), and
Hypercalcemia (PTH).


These are essentially the same disease and arent clearly
separated. Both are caused by a mutation in the RET proto-
oncogene. They cause endocrine tumors everywhere except the
3ps. Look for Pheochromocytomas and thyroid adenomas. The
parathyroid gland can also be involved, but isnt classic. Really,
the only difference between 2A and 2B is the presence of
neuronal tumors found in MEN2B.

MEN1 = Pituitary + Pancreas + Parathyroid

MEN2A = Pheochromocytomas + Thyroid + Parathyroid
MEN2B = Pheochromocytomas + Thyroid + Neuronal

Real life vs test

This is rare (~1 in 50,000) youre not going to see it. If theres
a combination of:
- recurrent endocrine neoplasias +
- age <40 +
- family history +
- multiple organ systems affected

Youd suspect something was up and do a mutational analysis

of the MEN1/2 genes.


Diagnosing Diabetes Screening and Diagnosing Diabetes
Screening is indicated when there are risk factors such as an Random Glucose
elevated BMI, hypertension, or advanced age. Different screening Normal < 200
tools exist, each with their own advantages. Diabetes > 200
Must have symptoms of diabetes
The random glucose is convenient it can be obtained at any
time without preparation and its a one-time test. The diagnosis is Fasting Glucose
Normal < 100
made if the random glucose is > 200 and there are symptoms of
Prediabetes 100-124
diabetes (polyuria, polydipsia). No repeat confirmatory test is Diabetes > 125
necessary. The random glucose can be affected by acute stress, Must have two readings to confirm
such as illness or steroid use, and does not reflect the long-term
impact on the body. 2-Hour Glucose Tolerance Test
Normal < 140
The fasting glucose is a better screen but requires preparation. Prediabetes 140-199
The patient must have an overnight fast. It also needs a second Diabetes > 200
confirmatory check. A bG > 125 on the fasting check is Indicated when prediabetes is found on fasting
indicative of diabetes. < 100 is normal and between 100-125 is
termed prediabetes or insulin insensitivity. A1c
Normal < 5.7
Prediabetes 5.7-6.4
The oral glucose tolerance test accurately reflects the
Diabetes > 6.5
pathophysiology of diabetes but is time-intensive. The patient has
May miss early disease, do not use in gestational
a fasting check, then consumes an oral glucose load of 75g. Two
hours later the glucose is tested (effectively the post-prandial
glucose). A value of < 140 is normal, 140-199 is prediabetes, and
> 200 is diabetes.

The HgbA1c is the preferred method in the United States because

it reflects the past 3 months of blood glucose and is a more
accurate reflection of whats happened rather than whats going
on in the body immediately (it isnt influenced by stress or
infection like a one-time glucose check is). However, it may miss
early glucose abnormalities and requires 3 months of
hyperglycemia to turn positive (thus its NOT used to screen for
gestational diabetes). A normal A1c is < 5.7. Prediabetes is Type I = Autoimmune Destruction
between 5.7 and 6.4, and diabetes A1c is > 6.5. Usual Juvenile Onset Type I Diabetes
Type I Physiology,
When considering Type I diabetes (even if the onset is in adult Antibodies Positive
age ranges) measurement of autoantibodies are recommended. If Childhood
the patient has rapidly progressive diabetes refractory to oral LADA Late Autoimmune Diabetes in Adults
medications or has a high insulin requirement despite being Type I Physiology,
relatively normal weight, assess GAD65 and IA-2 antibodies. Antibodies Positive
Those who have slowly progressive type II diabetes shouldnt Adult Age
have antibodies checked. Type I should be considered instead Idiopathic Type I just because (rare)
autoimmune destruction and can occur at any age or BMI Type I Physiology,
Antibodies negative
Adult Age
Treating Prediabetes
Early intervention can delay or prevent th onset of diabetes. When
in the pre-diabetic range metformin and lifestyle adjustment
(diet and exercise) are absolutely indicated and can prevent Treatment of Pre-Diabetes
diabetes onset. Diet and Exercise (Start both at the same
Metformin time)


Treatment of Type I Diabetes
Type I diabetics will require life-long insulin therapy. Insulins
are discussed in the subsequent lecture. If they can maintain
adequate glycemic control on multiple injections per day therapy,
they should continue that. If they cant, they should be considered Type Name Mechanism SE
for insulin pumps and/or continuous monitor glucose devices. Biguanides Metformin Insulin sensitivity Diarrhea
Sulfonylurea Glyburide Insulin secretion Hypoglycemia
Treatment of Diabetes Non Insulins Glipizide
Lifestyle is always the first step. TZDs Pioglitazone Insulin Weight Gain
Rosiglitazone Sensitivity
Metformin is the by far the best pharmacologic therapy and is DDP-4-i Sitagliptin DDP-4-i Weight Neutral
(liptins) Saxagliptin
always first line unless contraindicated. Metformin cant be used
GLP-1 Exenatide GLP-1 Weight Loss
in CKD, CHF, or liver disease because of the risk of lactic analogs Liraglutide
acidosis. It should always be held when hospitalized. Meglitinides Repaglinide Insulin Secretion Hypoglycemia
The second-line agent is chosen based on patient preference and SGLT2-i Canagliflozin Block glucose Euglycemic
side effect profile. Dapagliflozin absorption in DKA
The combination of three of more oral agents is NOT Alpha- Acarbose Block intestinal Diarrhea, Gas
SUPERIOR compared to two agents. Failure of two oral agents Glucosidase Miglitol absorption
should prompt insulin. inhibitors

In general, initiation of lifestyle modifications can reduce the A1c Dont ever use SGLT2-inhibitors. Youre giving your type II
by about 1%. Oral agents reduce the A1c by 3%. If the patient has diabetic a medication that has the same mechanism of action
an A1c >9%, insulin should be started. as DKA.

Ongoing Assessment of Diabetes Do What When

Self-monitoring of blood sugar is a means of controlling blood Self-Monitoring of On insulin
glucose for those with insulin. Pre-prandial glucose checks are Blood Glucose
Pre-Prandial Checks On insulin
used for all-comers. Once the pre-prandial glucoses are at goal
Post-Prandial Checks Pre-prandials are controlled by
but the A1c is not, post-prandial glucose checks can be added.
A1c is not
Those patients who do NOT use insulin should NOT use self-
monitoring of blood glucose. A1c Every 3 months

The A1c is assessed every three months for all patients with
prediabetes, diabetes, and insulin-dependent diabetes. The goal
A1c is <7.

Preventative Care in Diabetes Complication Screen Treatment

Diabetes takes the eyes, the kidneys, and the nerves. Long- Retinopathy Retina Exam Laser
standing diabetes and the microvascular changes it brings can Nephropathy Microalb/Crea Ace-inhibitor
lead to amputations, blindness, and dialysis. Diabetic wounds are Neuropathy Monofilament Gabapentin
difficult to heal due to the microvascular damage. Diabetic
wounds form because of the peripheral neuropathy that develops.
So, screening becomes important.

A physician needs to screen for retinopathy every year with a

retinal examination, nephropathy every year with a urinalysis
and microalbumin/creatinine ratio, and neuropathy every year
with a monofilament wire examination.

Patients should be educated to exam their feet periodically for

wounds and to ensure that shoes are not too tight.


The posterior pituitary is actually an extension of the
hypothalamus. Neurons of the hypothalamus produce oxytocin
and ADH, where they are transported to the posterior pituitary for
storage. Deficiency in or excess of Oxytocin causes no disease.
ADH on the other hand has two potential diseases. ADH =
SIADH = Hypo Na from too much water being retained. ADH
= DI = HyperNa from too much water lost. Any acute or chronic
process can disrupt the stalk or neuronal processing, leading to
either condition. Oxytocin
Dz association
1) Diabetes Insipidus
A patient deficient in ADH the kidneys has no signal to retain Too LITTLE: DI
water so they will pee a lot. This leads to them getting thirsty and
drinking a lot. Thus the patient with DI will present with
polydipsia and polyuria. Sounds like regular ol diabetes. The
difference is in the urine; DM has hypertonic urine full of
glucose pulling water with it. DI has hypotonic urine because
even though the patient is becoming dehydrated, the kidneys cant
retain the water. Thus, the first test to get is a U/A looking for
glucose (to rule out diabetes mellitus). If , the decisions
between Nephrogenic ( ADH but broken receptors) and
Central (kidneys work fine - theres just ADH being made).
Do that with a water deprivation test (see to the right). Treat
psychogenic polydipsia with psychotherapy, central diabetes
with desmopressin, and Nephrogenic DI with diuretics. Endogenous Exogenous
Obviously, start with hydration with IVF to correct electrolyte
(Water Deprivation) (Administered)

2) Syndrome of Inappropriate ADH

Central DI
When theres too much ADH the kidneys absorb all the water
there is, leaving behind a urine rich in Na. The patient dilutes
their blood (hyponatremia and hypotonic serum) and ADH ADH
concentrates their urine - the opposite of DI. The ADH came ADH
from the brain (tumor, infection, trauma, or granuloma) or the
lungs (TB, COPD, and Cancer). However, hypothyroid can do
it as well, as TSH simulates ADH at high doses. The patient will
present with hyponatremia. Get a serum Osms (low) and Urine H2 O
Urine Extra ADH-R
Osms (high). The goal should be to treat the underlying disease. H2 O
Urine Osms H2 O
In the meantime, induce a Nephrogenic DI with Demeclocycline
to get rid of the free water. If HypoNa is severe, replace with
hypertonic saline. Urine
Urine Osms

Dz Pt U/A Water Deprivation Test Tx Cause

Diabetes Polydipsia Polyuria Hypertonic Urine N/A Insulin Autoimmune
Mellitus Weight Loss with Glucose Obesity
Central DI Polydipsia Polyuria Hypotonic Corrects with ADH Desmopressin Trauma, Stroke, Tumor
Nocturnal Sx Urine Granulomas
Nephro DI Polydipsia Polyuria Hypotonic Does Correct Diuretics Lithium
Nocturnal Sx Urine Demeclocycline
Psychogenic Polydipsia Polyuria Hypotonic Corrects with Water Stop drinking Psychiatric Disease
Polydipsia Nocturnal Sx Urine Restriction so much water


Thyroid Nodules Pre Test Risk of Malignancy
Thyroid nodules are prevalent; up to 60% of patients have them
and they increase with age. Your job will be to determine is this History Physical
a cancer or not? Radiation to head and neck Fixed, hard, firm
Personal History of Thyroid Nontender Lymph Nodes
The physical exam can be revealing: a fixed, hard nodule with Cancer
nontender lymph nodes is suspicious for malignancy, while a Hoarseness Painless
Age < 20
soft, mobile nodule with pain is suggestive of something else.
Age > 60
Risk factors are listed to the right.

The diagnosis is best made with labs and imaging. There are Tests for Thyroid Nodules
several tools at our disposal.
Test Use
The Fine Needle Aspiration (FNA) is the best test to assess a TSH First test always
thyroid nodule; its a biopsy. However, it should be near the end RAIU If TSH depressed
of the diagnostic tree. U/S Prior to FNA
FNA Best Test
The risk of a functioning nodule (that is, any nodule that secretes
T4) being cancer is quite low. So the first test that should be
obtained after a nodule is discovered is a TSH. If the TSH is low
(which means the nodule is secreting T4), it should be followed
with a RAIU scan. If indeed the nodule lights up hot, this
confirms suspicion of a hyperfunctioning nodule. It can be treated
as hyperthyroidism medications to suppress, radioactive iodine
ablation or surgery to cure. But if the nodule is cold, then the
T4 was coming from somewhere else. Here, the nodule is NOT
hyperfunctioning; it needs to be biopsied with an FNA. Whenever
a biopsy is being considered, an ultrasound should be done first.

The risk of malignancy is much higher if the TSH was high or

normal on that original TSH test. A RAIU isnt indicated as its
unlikely to reveal a hot nodule. Instead, the next step is
ultrasound. If the lesion is small (< 1cm for solid, < 2cm for
cystic) and has non-malignant features, it can be followed with
repeat ultrasound months later. If the lesion is large or has
malignant features, it should be biopsied with the FNA.

Risk of malignancy is dependent both on the size and the risk of FNA results
the nodule and patient. FNA is indicated if a solid hypoechoic
nodule is > 1cm. FNA can be deferred if the nodule is lower risk; FNA Results Action
as an example a 2cm may be the cut-off for a cystic lesion. FNA Malignancy Prompt Surgery
can be prescribed for a smaller lesion if the patient is high risk Benign Repeat U/S 6-12 months
(see risk factors above); as an example a 5mm nodule in someone Inconclusive Repeat FNA immediately
with radiation to the head and neck.

If the FNA shows a malignancy the thyroid must be removed Cancers Need-to-know
(surgery). Deciding between hemi and total thyroidectomy is Papillary Most common thyroid cancer, associated with XRT
beyond the scope of this course. If the FNA reveals benign tissue, Orphan-Annie Nuclei and Psammoma Bodies
then the nodule should be followed with ultrasound and re- Papillary Architecture (FNA), h/o Head and Neck Ca
biopsied if it changes in size. If the FNA is inconclusive, the FNA Positive Prognosis (Slow Growing) Resection
should be repeated. Follicular Tumor difficult to diagnose on biopsy, looks normal
Spreads hematogenously, tx resection & I2 ablation
Medullary C-Cells producing Calcitonin = Hypo-Ca
Part of MEN2a and MEN2b genetics
Anaplastic Found in elderly patients
Grows locally and quickly
Dismal Prognosis correlated with degree of Anaplasia


Before discussing thyroid diseases, lets review some physiology
Hypothalamus 99.9% Bound 0. 1% Free T4
and tests which will help with decision making.
TRH is secreted by the hypothalamus. It stimulates the anterior Thyroid Thyroid Binding
pituitary to make TSH. TSH stimulates the thyroid to make Globulin Bound T4 (inactive)
T4/T3 in a 10:1 ratio. T3 is more potent than T4; T4 is converted T4/T3
into T3 in the periphery to exert its effects. Most of the T4 is
Estrogen: Protein, Total T4, Nrml Free T4
inactive, bound to Thyroglobulin Binding Protein. Only 0.1% Pregnancy
is free and active. Free T4 is tightly regulated and doesnt
change in the absence of thyroid disease. Total T4 changes with Move Heat Cirrhosis: Protein, Total T4, Nrml Free T4
alterations in protein (pregnancy, OCPs, cirrhosis, nephrosis). Nephrosis
The effect of T4/T3 is to metabolism (catabolic and
thermogenic). Tests
TSH Best Screening Test. Hypothyroid, Hyperthyroid
Tests Normal = Euthyroid. Some states can fool you, so
Screen people with a history of thyroid disease and any woman Free T4 Confirms TSH findings
over the age of 50. The best screen is the TSH. If its: low = Free T3 Only if TSH and normal or T4
RAIU Evaluate a 1o Hyperthyroidism. Differentiates between
hyperthyroidism, high = hypothyroidism, normal = euthyroid.
causes of hyperthyroid. May not be necessary with a good
Looking at Free T4 is useful in confirming an atypical screening
TSH because theres a disease associated with every TSH+T4
combination. However, a normal TSH means Euthyroid
(highly sensitive). Do NOT get a Free T4 if TSH is normal;
instead, ignore the Free T4 if TSH is normal. Sick people can get Patient with Thyroid Trouble or Asx Screen
whats called sick euthyroid syndrome (theyre sick, T4 is
wacky but TSH is normal), but theres no need do anything. TSH
Decreased Normal Increased
Free T3 is pretty much useless unless you suspect hyperthyroid
despite a normal T4. Likely r/o Thyroid Likely
Hyperthyroidism Disease Hypothyroidism
Look at the chart to the right. What it says is, the only diseases
that really matter are High TSH + Low T4 and Low TSH + High Free T4 Free T4
T4. Thats primary hypothyroidism and primary

hyperthyroidism. If theres a primary hypothyroidism, simply
give synthroid. Secondary Primary Primary Secondary
Synthroid Levothyroxine Rare
When a hyperthyroid patient is encountered a RAIU scan can
help with a diagnosis. Radiolabeled Iodine is picked up by active Subclinical Subclinical
thyroid tissue which lights up = hot while inactive tissue does Do Nothing Do Nothing
not = cold. Finally, there are antibodies that when present in
some diseases are specific (but theyre not sensitive). While
Diffuse RAIU Scan Uptake
helpful, theyre academic rather than confirmatory.
Thyroid not working
Confirmation is made by FNA Biopsy. More on Biopsying and
RAIUs in the thyroid nodule section. Focal

Graves Diffuse Hot Factitious Thyroiditis

Nodular Functioning
PTU Goiter Adenoma Confront Pt Wait,
Methimazole NSAIDs, BX
Surgery Surgery
Ablation >40
Surgery <40



Hypothyroidism is a product of metabolism secondary to T4.
This causes the patient to slow down. A variety of things slow:
heart (bradycardia), mind (dementia), reflexes ( DTRs), bowel
function (constipation), and metabolism (weight gain).
Hypothyroidism is easier than hyperthyroidism because
regardless of how they got there, theres only one treatment -
Levothyroxine. Screen with TSH (itll be elevated). Confirm Hypothyroid Myxedema coma
with T4 (itll be low) and replace as needed. Dont do any Bradycardia Hypothermia
biopsies or RAIU scans as they are extraneous. Dementia Hypotension
DTRs Altered Mental Status
Iatrogenic Constipation
The most common cause of hypothyroidism is iatrogenic. We Brittle Hair/Nail
treat hyperthyroidism and cancer with ablation or surgery, leaving
the patient without a thyroid. This is why close follow up is
necessary with these patients. Eventually, the circulating T4
diminishes and the patient becomes hypothyroid. When the Iatrogenic
patients TSH begins to rise, exogenous T4 must be substituted
with Levothyroxine. Screen: TSH Hashimotos
Confirm: Free T4
Hashimotos Myxedema Coma
Tx: Synthroid
The most common disease that causes hypothyroidism is
Hashimotos. Its caused by a lymphocytic infiltrate secondary Subclinical
to antibodies (Antithyroid Peroxidase and antithyroglobulin
90% Specific). The only way to definitively diagnose is with a
biopsy, but because Hashimotos is irreversible and the patient
presents with hypothyroidism, just treat the hypothyroid. The
natural course of the disease is a period of transient
Complicated Nonsense. Be able to spot it, give
hyperthyroidism followed by transient hypothyroidism.
Levothyroxine as needed. Thats it.
Myxedema Coma
If the hypothyroid gets really bad, or theres a precipitating event,
everything shuts down. Like thyroid storm this is a medical
emergency. This time its characterized by hypothermia,
hypotension, and coma. Initiate supportive care (IVF, Warming
Blankets) and give high-dose T4. Because peripheral conversion
is impaired, also give straight up T3 if T4 fails or symptoms are
severe from the start.

If the TSH + Normal T4/T3, the patient needs to be followed.
If Ab theyll eventually progress to hypothyroid. If Ab they
might get better. Theres no consensus on when to start treatment,
but generally make the patient happy by treating when
symptoms start and treat everyone with overt hypothyroidism


Hyperthyroidism Thyroid Storm Hyperthyroidism
- Fever - Heat Intolerance
Introduction - Delirium - Diarrhea
- Hypotension - Sweating
Hyperthyroidism is caused by too much T4. It can come either
- Palpitations
from overproduction as in Graves, exogenous intake (factitious - Weight Loss
or struma ovarii), or release as in Thyroiditis. The symptoms are - Afib
metabolism (heat intolerance, diarrhea, sweating, palpitations,
tachycardia, Afib, and Weight Loss). Determining a definitive
diagnosis may require a biopsy, but its usually not necessary. Also
1) Graves RAIU
An autoimmune disease caused by thyroid stimulating T4
Pt: Hyperthyroidism Plus
antibodies that mimic TSH and cause proliferation of cells as - Pretibial Myxedema = Swelling of the Feet
well as production of T4. This causes a diffuse homogeneous - Ophthalmopathy = Proptosis + Exophthalmos
enlargement of the thyroid. Its the most common cause of Dx: TSH, T4, Diffuse RAIU , Anti-Thyroid Ab
hyperthyroidism. Beyond the usual hyperthyroid condition there Tx: Acute: Propranolol to control adrenergic symptoms
can also be pretibial myxedema and ophthalmopathy PTU or Methimazole to quell hyperthyroid
(proptosis and exophthalmos) - both unique to Graves. Its state
Chronic: Radioablation with radioactive iodine
essentially a clinical diagnosis, but thyroid labs will show: TSH, Surgery if Pregnant
T4, and a Diffuse RAIU. Antibodies (80% Sp, Se) can be F/u: Synthroid when hypothyroid, after treatment
checked, but the focus should be on treatment. Control their Steroids/Radiation for Ophthalmopathy, if worsens
symptoms with propranolol. To help them out of a hyperthyroid
state use PTU (safe in pregnancy) or Methimazole. Be careful
not to start these drugs if awaiting RAIU or ablation. These
patients require definitive therapy: Radioactive Iodine Ablation
Normal Thyroiditis Hypothyroid
or Surgery (usually if pregnant, 2nd trimester surgery). Since this
will make them hypothyroid follow up and start synthroid when Stored T4 Hypothyroid
hypothyroid. Finally, the ophthalmopathy may worsen despite
treatment; treat it with steroids or radiation. Acute
2) Thyroiditis
In an inflammatory process, even destructive ones, the first step
is to break open the cells and release stored T4. This causes a Released Increased Depleted Either Resolution or Chronic
transient hyperthyroidism. If the insult is acute T4 T4 T4 State will persist
(infection/trauma) or subacute (subacute thyroiditis) the
thyroid will recover - sometimes with a period of hypothyroidism. Thyroiditis
Rarely does this require intervention. If chronic (Hashimotos), Acute: trauma, infection, drugs Supportive Resolution
destruction wins = persistent hypothyroidism. Because TSH/T4 Subacute: Silent = Lymphocytic, TPO Antibodies Resolution
looks like Graves, differentiate with RAIU (cold inactive thyroid) Painful = Viral Granulomas Supportive
Chronic: Hashimotos NSAIDs Resolution
and ESR/CRP (elevated in Hashimotos only).
Steroids Hypothyroid

3) Toxic Multinodular Goiter or Adenoma

For whatever reason, autonomous nodules referred to as hot
produce T4 without an off switch. Rarely cancer (see workup for
thyroid nodules), nodules can usually be seen on RAIU or felt on
an exam. Because the rest of the thyroid senses too much T4 it
shuts off, so only the toxic nodules light up. Toxic means
Makes T4. Toxic Multinodular Goiter Toxic Adenoma


4) Factitious and 5) Struma Ovarii
If someone thats normal to begin with gets levothyroxine the Exogenous/Factitious
thyroid will shut off ( TSH RAIU). Still, the T4 will remain
high. The only way this can happen is if shes taking it
exogenously (as in Synthroid to lose weight or we dosed a
hypothyroid patient with too much of it) or if theres a tumor RAIU scan
somewhere other than the thyroid (usually a dermoid completely cold T4
cyst/teratoma of the ovary). Use the Sestamibi scan of the ovaries
to r/o tumor then confront her about her factitious disorder. These
two are together because 1 - the RAIU is normal and 2 - on the Struma Ovarii
test both will be woman. RAIU of
the Pelvis
6) Thyroid Storm
When the hyperthyroidism gets out of control its a life
threatening emergency. Its a clinical diagnosis - defined by
someone with hyperthyroidism plus alarm symptoms = fever,
delirium, and hypotension. They have such heat intolerance that IVF
they burn up and such tachycardia that theres hypotension. After Cooling
making the diagnosis start immediate supportive therapy with Blankets
IVF and cooling blankets. To treat, start Propranolol (-
Blockers) to slow the heart down and get the BP back up. Give (1) -Blockers for HR (bring up BP)
PTU or Methimazole to reduce the production of new thyroid
hormone. Finally, steroids will reduce the T4 to T3 conversion.
(2) PTU / Methimazole to T4 production
In storm, Iodide can be given. The thyroid can either pick up
Iodide or make Thyroid Hormone; it preferentially picks up (3) Steroids to T4 to T3 conversion
Iodide. For a temporizing measure, use Iodide to T4. If not fixed
that Iodide will be used to make T4 (Iodide Escape). Thatll
make the patient worse. A single storm is indication for definitive
therapy (removing the thyroid altogether).

Disease Path Patient TSH T4 RAIU Diagnosis Treatment

Graves Autoimmune stimulating Hyperthyroid Anti-TSH-R Antibody Propranolol
antibodies +ophthalmopathy PTU/Methimazole
+Pretibial Myxedema Radioactive Ablation
Thyroiditis Either painful or N/A Bx for Infiltrate NSAIDs
Painless Subacute Lymphocytic +TPO painless transient Anti-Peroxidase Wait
Painful Subacute Granuloma Viral hyperthyroidism that Antibody (TPO) Synthroid if Hypothyroid
Chronic Lymphocytic may persist
Toxic Autonomous Nodules Hyperthyroid with Bx if suspicious for
Goiter Secrete T4 palpable nodules cancer

Factitious Exogenous T4, Oral Hyperthyroid, often Confrontation Stop taking exogenous T4
in a woman
Struma Ovarian tissue Hyperthyroid, always RAIU of the Ovaries, Remove the Cyst
Ovarii Dermoid Cyst in a woman Sestamibi Scan
produces T4
Thyroid Super mega ultra Hyperthyroid Any , Diagnosis Needed IVF, Cooling Blankets,
Storm hypothyroidism CHF no one Just Treat, and treat fast Steroids, Propranolol,
AMS diagnostic PTU, Iodide


muscle bone cord

back pain neurologic


Warning Symptoms


MRI radiation surgery
Alarm Yes
most common
inciting event
symmetric belt-like Sxs
fashion ache Alarm
analgesia exercise
> 30

rule out herniated disk

lightning shooting pain

Yes No
hip flexion movement cough
activity plantar flexion Dorsiflexion


elderly male


elderly patient history of

osteoporosis X-ray

point tenderness vertebral step off


elderly patient
leg and butt pain

pain loss of pain/temperature sensation

MRI surgery corrects

HTN CAD Smoking

anterior spinal artery
spastic paralysis pain and

MRI Surgery

diarrhea constipation GYN

intermittent low back pressure

Age Risk Factors First Best Tx

Neuro [COMA]

Producing unconsciousness - a depression of brain function that
extends beyond executive function - requires significant CNS (1) True Coma
compromise. In each of the conditions were going to discuss the (2) Persistent Vegetative State
(3) Brain Death
patient is mostly unaware and unable to be aroused. The degree
(4) Locked-in Syndrome
of arousal (response to external stimuli, brainstem function)
determines what the diagnosis is. Cerebral function is the most
sophisticated, the most human, and the least required for survival,
so is sacrificed first, meaning that relatively small insults can
induce coma. Brainstem function is vital and can persist despite
the absence of awareness (breathing, sleep/wake cycles), leaving
the patient in a persistent vegetative state. In the absence of
cerebral function and brainstem function theres nothing left -- Brainstem Motor
brain death. Watch out for locked-in syndrome which can look Function
like any of the above, but the person is still fully alive, awake, and
Coma Function
Coma is a state of unconsciousness of depressed cerebral Cerebral Brainstem Heart Motor
function such that there is no response to internal or external Function Function Function Function
stimuli. Literally anything can produce coma: Toxins (EtOH, Normal Aroused
Benzos, Opiates), Electrolytes (all), and Endocrine (Hypothyroid, Coma Depressed
Thiamine) are potential reversible causes. However, to knock out PVS Absent
all arousal there must be significant/catastrophic cerebral damage. Brain Absent Absent
It can occur via hypoxic/ischemic encephalopathy (drowning, Dead
cardiac arrest), trauma (diffuse axonal injury) or brainstem path Locked Aroused
(hemorrhage or infarction). By definition, coma is reversible. Do a
comprehensive workup (CMP, CT scan, LP, EEG), give the
coma cocktail (Thiamine, D 50 , Oxygen, Naloxone), and reverse
underlying causes. A full recovery from comas is possible.
Persistent Vegetative
Persistent Vegetative State Coma State Brain Death
The patient has a flat EEG but opens her eyes or has a positive
caloric test. The patient has no arousal but can move, display pain,
Awake Dead
and have sleep wake cycles. Nonetheless, the personality is gone;
he/shes in a persistent vegetative state. He/she will never recover
and will require tube feeds/institutionalized care for life.

Brain Death
If someone goes down and stays out despite resuscitative efforts,
and attempts at reversal fail you must consider brain death. In brain
death the cerebral EEG shows nothing: theres no arousal, sleep
wake cycle, or drive to breathe (life is ventilatory dependent).
Before confirming brain death rule out intact neural reflexes with a
caloric test (COWS) and a corneal reflex. If theres no response
brain death is in place and the patient should be removed from life
support. Two doctors must confirm death.

Locked-In Syndrome
The pons is the site where both motor and sensory tracts pass. If
theres a basilar artery infarct or central pontine myelinolysis
these tracts are severed. The patient LOOKS LIKE he/shes in a
Persistent Vegetative State but they have full awareness. He/shes
able to communicate via eye movements. Theres no recovery
from this. MRI should confirm the diagnosis; make the patient


Dementia is a combination of memory loss and an alteration of Hypothyroid
cognitive function. Having trouble finding your keys or losing B12 Deficiency
spans of time is insufficient for the diagnosis of dementia. As Pseudodementia
Reversible Frontal Tumor
such, the MMSE was created to assess if there are changes in
attention, concentration, or executive function in addition to Chronic Subdural
memory. Once dementia is established there are a variety of Syphilis
diagnoses. The most important thing to do is rule out all Uremia
reversible causes, or identify a reversible cause and fix it. The Dementia Cirrhosis
possible reversible causes, their history, diagnosis, and treatment
are listed to the right. If no reversible cause is identified,
organic dementia must be entertained, differentiating based on
the history, the time course, and associated symptoms. Organic
Alzheimers Disease (AD)
Normal Pressure Hydrocephalus
This is the most common cause of organic dementia. Linked
with neurofibrillary tangles, neurotic plaques, and amyloid
deposition, a definitive diagnosis is only made on brain biopsy Memory Loss
at autopsy. However, AD has a very classic presentation of an Memory Loss Memory Loss
insidious (slowly progressive) onset dementia taking memory Only Mini Mental and Cognition
Amnesia Dementia
first (short term then long term) sparing social graces until late Status
No Cognitive Attention
in the disease. A CT scan will show diffuse cortical atrophy. Impairment Concentration
There is a link to chromosome 21 (all Down syndrome > 40 Executive Fxn Reversible
years old develop AD). Once reversible causes have been ruled
out treat with cholinesterase inhibitors such as tacrine or
donepezil (Aricept). These will slow progression but dont TSH, B12, RPR, BUN/Cr,
reverse disease. Death usually occurs within 5-10 years; its
often from a secondary cause like pneumonia.
Reversible Organic
Picks Disease Causes Dementia
In contrast to AD, the Personality goes first in Picks disease. Correct Cause Use Hx to Dx
Social graces are lost (violence, hypersexual) but memory Follow MMSE Supportive
remains intact. Whereas AD has diffuse cortical atrophy, Picks
has frontal and hypothalamic degeneration. Diagnosis is Condition Clinical Picture Test Treatment
clinical and theres no treatment. Hypothyroid Weight Gain, Heat Intolerance, TSH Synthroid

CJD B12 Def Megaloblastic Anemia and B12 B12

This disease is caused by an abnormal protein called a prion. Neuro sxs
Subdural Focal Neurologic Deficit, CT Surgery
Prions evade denaturation even with cooking so can be
Hematoma Headache, Trauma
transmitted in infected meat, by eating human brains with the Syphilis Sexually Active, Any Neuro, RPR Penicillin
disease (Kuru, and zombies), or with corneal transplant. While Screen endemic areas
eating infected meat is certainly a scary thought, the most Uremia Renal Failure, Uremic Frost Cr Dialysis
common means of acquiring prion disease is a sporadic Cirrhosis Asterixis, Ascites, NH4 Transplant
mutation. In a patient thats too young to have dementia and Hepatomegaly Lactulose
Pseudo- Depression, Loss of Loved One Psych SSRI
displaying a rapid decline (within a year) of memory, consider
CJD. There may be the associated symptoms of myoclonus.
Treatment is palliative and death occurs in years from infection
but usually months from diagnosis.


Lewy Body Dementia

Lewy Bodies are the pathognomonic finding on biopsy for
Parkinsons. Dementia with Lewy Bodies without the stigmata
of Parkinsons is Lewy Body Dementia. This will present as an
acute onset delirium picture in an elderly male. Difficult to
diagnose, unable to treat, just know it exists.

Multi-Infarct Dementia (Vascular)

When someone has a stroke his/her memory and cognitive
function may become impaired. The problem is a person with Stroke
Alzheimer Disease often has Risk Factors for stroke (HTN,
DM, CVA), but without a focal neurologic deficit the stroke Stroke
may not be diagnosed. However, if a patient has a stroke and
gets abruptly demented or abruptly worse and you can tie the
stroke temporally to the decline in cognitive function, call it
vascular dementia (Multi-Infarct Dementia). An MRI may show
old infracts, but these may be coincidental rather than causative.
If theres a question treat it as Alzheimers but of course control
risk factors for stroke.
Normal Pressure Hydrocephalus
This is both an organic and reversible cause of dementia. In an
elderly patient with an ataxic gait, urinary incontinence, and
dementia, get a CT or MRI to evaluate for hydrocephalus. The Wet (urinary incontinence)
pressures are normal so there are no signs and symptoms of Wobbly (ataxic gait)
its possible to do Weird (Dementia)
serial LPs to take off extra fluid (if it improves its also
diagnostic) and eventually fit them for a VP Shunt. Be carefully
calling cortical atrophy with subsequent volume expansion
Normal Pressure Hydrocephalus (NPH is a specific diagnosis
with specific criteria).

History Location Diagnosis Treatment

Alzheimers Short Term Memory, Diffuse Cortical Atrophy CT Donepezil
Long Term Memory,
then Social Graces,
Chronic & Insidious Dz
Picks Disease Personality 1st Frontal-Temporal CT to r/o None
Memory Later Degeneration Clinical Diagnosis
CJD Myoclonus Diffuse Cortical Atrophy Clinical Diagnosis None
Rapid Decline
Lewy Body Delirium N/A Lewy Bodies on Donepezil maybe
Stain None
Multi-Infarct Acute exacerbation with Anywhere Clinical Correlation Control CVA risk
CVA of dementia with
Normal Ataxic Gait, Urinary Nowhere LPs Dx and Tx Serial LPs, VP Shunt
Pressure Incontinence Dementia


Dizzy is a very vague complaint that needs further
investigation. The first question needs to be what does the
Posterior Fossa Tumor
patient mean: presyncope or vertigo? In presyncope the patient Central Multiple Sclerosis
will complain of blacking out, lightheadedness, or cardiac
symptoms. This is covered in the cardiology lectures. In vertigo
a patient will sense movement where none exists. This will Seizure
present as either the room spinning or being unsteady on Labyrinthitis
his/her feet. Once vertigo is established its critical to Peripheral Meniers
differentiate between central (usually a structural lesion Benign Paroxysmal Positional Vertigo
requiring MRI of the posterior fossa) and peripheral (sparing
the need for costly MRI, focusing more on symptom control).
Lesions that are central are generally chronic and progressive;
they occur in the posterior fossa (i.e. away from ears, sparing Black out, Dizzy Room Spinning
aural symptoms) where the cranial nerves are. This produces Light Headed, Unsteady
cranial nerve deficits. Get an MRI and correct as needed. CP, SOB on Feet
What does
Presyncope Vertigo
Peripheral lesions are essentially in the ear, away from cranial the patient
nerves, but acute with ear symptoms (hearing loss and Cardiac Lectures mean

Posterior Fossa Lesions Acute Chronic

Whether its vertebrobasilar insufficiency or a posterior fossa Neighborhood Signs Neighborhood Signs
tumor, the main problem is a structural lesion compressing on Tinnitus Tinnitus
Hearing Loss Hearing Loss
or eating away at the cerebellum and brainstem. If there are
focal neurologic deficits and vertigo its almost pathognomonic Central Organic
Peripheral Dementia
for a central lesion. Get an MRI. If normal, follow with MRA. Peripheral
Focus on symptom Focus on Imaging
Benign Paroxysmal Positional Vertigo control and specific of posterior fossa
This disease is caused by an otolith within the semicircular maneuvers based with MRI
canals. It moves with head movements and settles randomly on diagnosis
producing vertigo and rotary nystagmus on head movement
thats transient (<1 minutes). This occurs every time the head Disease Onset Duration Diagnosis Treatment
moves (easily reproducible). Sensation can be reproduced by the BPPV With <1 min Dix- Movement
Dix-Hallpike maneuver. Movement Exercises dislodge and Movement, Hallpike Exercise
break up the stone, curing the patient of disease. An Epley Acute, Rotary
Maneuver can be done in the office and is often curative. Reproducible Nystagmus
Menier Without 30 mins Clinical Diuretic and
Meniers Disease Movement, Low Salt
A peripheral cause of vertigo presenting with a triad of vertigo, Acute,
and hearing loss, fullness, or tinnitus thats unrelated to Repetitive
movement. Like BPPV, its acute but the vertigo persists - Labyrinthitis 1-3 weeks after Persistent, Diagnosis of Steroids
lasting ~30 minutes. This also occurs repeatedly, but not every an URI, N/V, sxs may Exclusion
vertigo, occur or
time the head moves, and may be separated by long periods of
deafness and off for
time. Treat with diuretics and low salt diet.
Posterior Chronic and Persistent MRI Surgery
Labyrinthitis/Vestibular Neuritis
Fossa Progressive Steroids
A diagnosis of exclusion. Suspect this disease in a patient with
Lesions CVA control
vertigo, Nausea/Vomiting hearing symptoms for weeks after
a URI (pharyngitis, otitis, sinusitis). Its a diagnosis of exclusion
because pontine strokes and tumors mimic the chronic nature of
vertigo and the URI often goes unnoticed. If diagnosed early
give steroids within 72 hrs. The disease will resolve in months,
but balance and hearing may be compromised for those months.


1st New Onset > 50

Fever Progressing Chronic hdche
FND Sudden Onset Crescendo
Chronic Fever + Headache + FND

Patient Presumed Test Tx


Dz Danger History and Laterality Quality Duration Aggravation Dx Treatment PPx

Associated Sxs

uncontrolled synchronous firing of neurons

epilepsy V
tonic clonic
convulsions bowel/bladder incontinence tongue biting
loss of
consciousness post-ictal confusion
No Yes


Status Epilepticus medical

emergency reverse Yes
the underlying cause
control ABCs

seizure must be aborted

IV/IM Benzos
Phenytoin Midazolam Propofol
Phenobarbital draw labs
actively seizing ABCs Abort Idiopathic
Seizure Neoplasm
Valproate Depakote

Carbamazepine Phenytoin
therapeutic levels switch Valproate or Lamotrigine
seize while therapeutic
EEG spike and waves

24hr video monitoring + EEG

Neuro [STROKE]

Stroke is high impact disease; its the 3rd leading Cause of
Death and a leader in lingering morbidity. Not only that, but Etiology Type Examples
its a preventable and largely time-sensitive disease. Ischemic Embolus Afib, Carotid Stenosis
Thrombotic CAD/PVD, Atherosclerosis, HTN
Etiologies Hemorrhagic Hemorrhagic SAH, Intraparenchymal, HTN
Stroke is a brain attack - that is, an ischemic injury to the brain
parenchyma. This can happen in three ways. 1) Emboli may
form on diseased valves, in the left atrial appendage during Afib,
or on a carotid dissection/stenosis. The emboli will then travel to
Region of infarct
a smaller vessel where it gets lodged in the lungs and occludes
flow. 2) Thrombi may form in a vessel. This is the same Carotid
pathogenesis as atherosclerotic plaque in the heart, predisposed
by CAD/PVD/HTN/Atherosclerosis. Of the etiologies, 3)
Region of Infarct
Hemorrhage has the worst prognosis. Both subarachnoid and
intraparenchymal hemorrhage (discussed elsewhere) are L Atria
considered brain bleeds - usually a product of hypertension. In
this case blood does flow, just into the parenchyma. Its an Embolic Stroke Thrombotic Stroke
irritant, decreases perfusion to the distal brain, and is a potential
mass effect. Anterior Circulation

The clinical presentation does not correlate with etiology. The Middle Circulation
tell-tale sign of any stroke is Focal Neurologic Deficit of Acute
Onset. The location of infarct correlates to the defect. Thus a
sudden onset loss of motor, speech, sensation, or level of
consciousness prompts investigation. It becomes important to
revisit arterial supply and vascular distribution. The posterior
circulation is made of the vertebral arteries that come to form
Anterior Circulation = Leg/Foot
the basilar artery. Lesions here cause cerebella dysfunction,
in Mental Status, and blindness. The anterior circulation is
comprised of the anterior and middle cerebral arteries. These Middle Cerebral Artery = Face / Arm / Speech
feed the speech centers, motor strips, and sensory strips. Recall
the homunculus. Posterior Cerebral Artery = Vision
Certain elements of presentation may help beyond simply Pons = Locked In Syndrome
location. For example, the patient with Afib has an increased
likelihood of embolism. Painful neck pulsations and a patient Vertebral = Syncope, Cerebellar
who grabs her neck are indicative of a carotid dissection.
Patients who experienced TIAs (FND < 24hrs) in the past likely Focal Neurologic Deficit
have a thrombotic event. Bleed Bleed
Ischemic CT scan Hemorrhagic
Diagnosis and Workup Neurosurgery
Regardless of presentation, in the acute phase of a stroke Do Nothing ICU, Pray
(within 30 minutes of presentation and within 6 hrs of Sys BP < 150

symptoms) the goal is rapid identification and intervention if The Next Day TEE
possible. The first thing to do is a CT scan without contrast to
rule out hemorrhage. At this point therapeutic intervention is Clot
considered. After the initial presentation (usually on day 2), 2o Prevention
U/S Carotid Embolic Stroke
additional testing may be done. Transesophageal Echo assesses
the cardiac valves, carotid duplex for carotid stenosis, MRI to Heparin Coumadin ASA
<70% or >70% with
Bridge or
look at areas of ischemia (CT scan is not to diagnose CVA, but Sxs Sxs
to rule out hemorrhage), and CT angiogram for blood vessels
of the brain. Do Nothing Carotid

Neuro [STROKE]

Treatment Options
Treatment is broken into the treat right now and secondary Penumbra (can be saved)
prevention. Most strokes occur and its too late - nothing can be Infarct (cannot be saved)
done for them - so preventing the next one becomes crucial.
Aspirin is the mainstay treatment unless the patient gets/has (1)
ASA Allergy, (2) GI Bleed, or (3) Strokes while on ASA. At tPA ASA
that point ASA is switched to clopidogrel. If the strokes Thrombotic / Embolic only Primary med for secondary
embolic from Afib a Heparin to Coumadin Bridge is Never if Brain Bleed Ever prevention
considered, given the patients CHADS2 score. Sxs onset < 3 hrs
if surgery in 21 days
if head trauma
The big to-do for stroke is tPA, the clot buster. It has greatly
Heparin / Coumadin Clopidogrel
restricted use but can actually rescue ischemic tissue and Embolic Stroke Prevention Used when the patient cannot
preserve the penumbra. The risk of transforming an ischemic CHF tolerate ASA or when ASA fails.
stroke into a hemorrhagic one is high so caution must be used. HTN Caution thrombocytopenia
Even if tPA isnt used the stroked brain will die. However, Age > 65
optimally controlling oxygen >95%, tight glucose control 60- DM
100, and Blood Pressure (permissive hypertension) will allow Stroke (worth 2)
the at-risk penumbra to recover.
Test Notes Timing
For future stroke prevention, control dyslipidemia with statins
CT scan Do it at presentation, rule out hemorrhage <30 min
with HDL >40 and LDL <100, control diabetes with Insulin, but is useful to diagnosis CVA until
bG <125 (HgbA1C <7%), continue cardiovascular exercise, and days later
daily ASA. These will decrease the risk of stroke. MRI Visualize areas of ischemia, track 24 hrs
resolution, confirm diagnosis if unsure
In the condition where theres a carotid dissection or carotid U/S Carotid Carotid Visualization to rule out or rule in 2nd Day
stenosis >70% and symptoms, a carotid endarterectomy may be carotid artery stenosis and dissection
performed. TTE TEE Visualize heart valves, especially in Afib, 2nd Day
r/o source of embolism.
If theres Afib perform a Heparin to Coumadin Bridge. Rate Difficult
CTA, MRA Visualize blood vessels, require 2nd Day
control is equivalent cardioversion. Anticoagulation is not angiogram
required if the rhythm is converted, though the tendency is to
leave them in afib with anticoagulation.
Treatment Notes Timing
tPA Rescue ischemic tissue, recover penumbra, One time
only if symptoms start <3 hrs ago. High
risk of hemorrhagic transformation,
Mainstay of acute therapy
Heparin If actively worsening stroke or suspected X6
embolic disease. Bridge to Coumadin for months
embolic stroke only
ASA Mainstay of secondary prevention. Almost Forever
as good as clopidogrel and its cheap.
Clopidogrel ASA Allergy or stroke while on aspirin. Forever
Risk of TTP and Thrombocytopenia

Neuro [TREMOR]

Carpines Agonists



Yes No

<60 >60

Drug Mechanism Indications Side Effects

Disease Rest Moving Other Tx



chronic progressive unknown etiology

asymmetric Upper Motor Neuron Lower Motor
Neuron lesions atrophy
upward Babinski hyper-reflexia

emotional lability weight loss

Spinal X-ray
superoxide dismutase

autoimmune post-synaptic Ach-R.

eyes throat

relieved by rest
intact reflexes Acetylcholine receptor antibodies block the
Anti Ach-R function of acetylcholine on nerve contraction.
Antibody Muscles you use the most fatigue first (Eyes,
Throat) and worsen with repetitive motion.
Pyridostigmine acetyl-
choline concentration
thymoma CT scan of the chest

paraneoplastic syndrome
antibodies presynaptic Calcium channels
proximal muscle
weakness improves with repeated use Antibodies against cancer cells also function
antibodies CT against presynaptic calcium channels. With
scan repetitive use these antibodies are overcome.
EMG Affects muscles that are used the least (the
proximal muscles)
chemotherapy, radiation, or resection


autoimmune disease
ascending paralysis
distally moving proximally diarrhea
flu vaccinations
hyporeflexia paresthesia autonomic dysregulation

LP lots
of proteins very few cells EMG
Nerve Conduction Velocity
IVIG plasmapheresis


autoimmune etiology

demyelinating disease
symptoms separated by time and space

blurry vision diplopia optic

neuritis MRI periventricular
plaques multiple lesions, corpus callosum


LP pleocytosis
oligoclonal IgG evoked potentials

chronic management Interferon-

B1b acute flares steroids
symptomatic relief
Bethanechol Amitriptyline

History Associated Sxs Repeated Diagnosis Tx Path


Differential Diagnosis
Rheumatology is essentially the diagnosis and management of
joint pain. It has quite an extensive differential as it could be the Arthritis
primary complaint or the symptomatology that links all disease. Joint Pain
Unfortunately, many of these diseases have a list of associated Acute Chronic
symptoms that have be memorized in order to ascertain the Timing and
correct diagnosis. However, there are some classifications that Toxicity
can help reduce the potential list of diagnoses. The number of Acute Chronic
joints, pattern, and symmetry of joint pain play a huge role.
Septic Arthritis
Usually monoarticular involvement has to do with a disease of Inflammatory
that joint, indicating an absence of systemic involvement. Its Crystal Deposition
often acute. Polyarticular involvement is associated with Reactive Arthritis Rubor, Dolor,
systemic disease. Lets break it down further. In polyarticular Calor, Tumor
Just 1
disease absence of symmetry means its likely degenerative as Inflammatory Osteoarthritis
it reflects the asymmetry of use. If theres symmetry it indicates
autoimmune. Finally, even paying attention to WHICH joint is Monoarthropathy # of Joints Polyarthropathy
involved can be useful (RA spares the DIP for example). Besides Involved
Indolent Infection Lupus
that, extrarticular manifestations are often unique to a given Rheumatoid Arthritis
diagnosis, though crossover does exist. The important thing is Seronegative
that no one finding is sensitive or specific its the combination Connective Tissue Dz
of symptoms that lets the diagnosis comes to light. Using this Single Joint vs Multiple Joints
algorithm may be useful, but its the memorization that excels in Septic Osteoarthritis, Lupus, Rheumatoid
Crystals Scleroderma, Myositis, Seronegatives
Acute vs Chronic
Septic, Trauma, Osteo, Lupus, Rheumatoid, Scleroderma,
Crystal, Reactive Myositis, Seronegatives
If you see a red, hot, swollen joint, the answer on the test will be Isolated vs Systemic Manifestations
Arthrocentesis. The diagnosis can be made without an Septic Seronegative (IBD)
arthocentesis (history of gout that has a gouty flare), but your Crystal Lupus (Face, CNS, Renal, Heart, Lung)
reflex should be to tap the joint. In a normal joint there should Rheumatoid (Nodules, Serositis)
be a bunch of fluid - thats it. In degenerative disease its the Reactive (Oral + Genital Ulcer)
same; the joint is just degraded (neither normal joint or Degenerative vs Inflammatory
Osteoarthritis Everything Else
degenerative joint conditions should have prompted a tap). On the
other end of the spectrum, a septic joint will be full of pus: white,
opaque, LOTS of cells, LOTS of polys. 50,000 is the number to Normal NonInflammatory Inflammatory Sepsis
remember. If there are more than 50,000 WBCs its septic, Appearance Clear Clear Yellow, White Opaque
regardless. WBC <2 <2 >2, <50 >50
Polys <25% <25% > 50% > 75%
An inflammatory joint will be somewhere in between; itll have Gram/Cx
some cloudy fluid, some cells, and mostly polys. Dz None Osteoarthritis Everything Infectio
Else n
WBC is thousands
The presence of staph tells you septic. If septic and no organism,
be cautious of gonorrhea and get a NAAT or chocolate agar Antibody Interpretation Antibody Interpretation
culture. ANA Sensitive Lupus RO + LA Sjogrens

The presence of crystals clues us in on crystal disease. Histone Specific Drug- CCP Rheumatoid
Inflammatory joint without organisms or crystals means its a Induced Lupus Arthritis
rheumatologic disorder and little else. ds-DNA Specific Lupus + RF Rheumatoid
Renal Involvement Arthritis
Antibodies Smooth Autoimmune Jo Polymyositis
Memorize them. Theres no good way other than repetition. Muscle Hepatitis
Mitochondrial Primary Biliary
Sorry. Theyre mostly non-diagnostic, but theyre another clue. Cirrhosis
Bottom line: there isnt one test, but rather a combination of Centromere Scleroderma Topoisomerase Systemic
findings (including serology) that leads to diagnosis. (CREST) (Scl-70) Scleroderma

Rheumatology [LUPUS]

Introduction BAG OF LUPUS
Lupus is an autoimmune disease mitigated by complement 1) Chronic Inflammatory Disorder, Systemic Consequences
forming complexes. Being autoimmune, it effects women more 2) Joints, CNS, Kidneys, and a Rash
than men and non-whites more than whites. It is one of the Multiarthritic Renal Failure
Change in mental status Malar/Discoid Rash
great imitators and can be challenging to make the diagnosis in
3) ANA is sensitive, not Specific, 1st test
the early stages. 4) ds-DNA Specific, not sensitive,
5) Possible Drug-Induced Lupus with Hydralazine, Procainamide,
Presentation (and diagnosis) INH, and -methyldopa get an Anti-Histone Ab, stop the drug
Theres no confirmatory step or biopsy that seals the diagnosis 6) Treat Arthralgias with NSAIDs
of lupus. Instead, the diagnosis is made with 4 of 11 criteria being Treat Flares with Steroids
Treat life-threatening disease with Cyclophosphamide
met. These 11 criteria can be recalled with either the mnemonic
MD SOAP BRAIN or via the hideous monster. See both to the
The things the patient will care about are going to be the serositis Serositis Blood Malar Rash
(chest pain), arthritis (with a predilection for the large joints), Oral Ulcers Renal Discoid Rash
Arthritis ANA
and the face rashes (malar = butterfly, discoid = disk shaped) or
Photosensitivity Immunologic
the skin rashes (photosensitivity). Neurologic

The things that youll care about are the cerebritis

(encephalopathy, psychosis, obtundation), lupus nephritis
(progressive renal failure), and potentially pulmonary
Certain things just jump out on a test. Libman-Sacks- Cerebritis
Endocarditis (LSE) is essentially pathognomonic for Systemic Malar/Discoid Rash
Oral Ulcers
Lupus Erythematosus (SLE). The malar rash that spares the
ANA, dsDNA, Histone
nasolabial fold and early trimester losses are also suspicious for Anemia, Thrombocytopenia, Leukopenia
lupus. Libman-Sacks Endocarditis
Testing (notice this isnt called diagnosis) Arthralgias Renal Failure
There is no confirmatory step. But certain lab tests can be useful. 2nd Trimester Losses (Hypercoagulability)
The CRP (better than ESR) reflects the disease severity. The
ANA is the gateway antibody it is highly sensitive but specific
for nothing. If positive, look for other antibodies: particularly the
anti-histone (drug-induced lupus), anti-smith (lupus), and ds-
DNA (nephritis).

If the patient is in an acute flare (which may appear septic with

fever), obtain complement levels. If reduced, its likely to be a
flare rather than an infection. Unlike some other autoimmune
diseases such as Multiple Sclerosis, lupus doesnt worsen in
infection it may simply be a flare.

Anemia and thrombocytopenia can be seen but are neither

sensitive nor specific.

If lupus nephritis is suspected a renal biopsy is required before


Rheumatology [LUPUS]

Treatment Treatment When
Hydroxychloroquine for everyone. Period. Everybody who can Hydroxychloroquine Everyone
tolerate the drug gets it. Methotrexate can be used if the drug cant Steroids Flares only
be tolerated, but hydroxychloroquine reduces flares and subdues IV Cyclophosphamide Life-threatening illness
disease. Cerebritis, Nephritis
Mycophenolate Mofetil Oral Cyclophosphamide
Steroids are used only in acute flares. If the disease is severe, or Use after IV
its a first time diagnosis, use steroids. The worse the
presentation, the larger the dose of steroids. GET PEOPLE OFF Methotrexate 2nd line to Hydroxychloroquine
STEROIDS. They cause hypertension, diabetes, avascular
necrosis, and osteopenia. Only use them in flares. NSAIDs Symptom control only
Azathioprine Adjunctive
Life threatening cerebritis or nephritis can be treated with IV Biologics Maybe, not yet approved
Cyclophosphamide. When the acute phase is past,
mycophenolate mofetil orally can be used to continue treatment.

Much like in RA, NSAIDs are saved for the end. Why? Because
they treat symptoms - not the disease. Never use NSAIDs as

Drug-Induced Lupus
There are a lot of drugs with a side effect profile of lupus. The
ones you should recognize for the test (even if not prescribed all
that often) are hydralazine, procainamide, isoniazid, and
alpha-methyldopa. Drug-induced lupus presents with skin and
joint symptoms (rash and joint pain), but will spare the visceral
organs. It doesnt kill you - it just hurts and is annoying. Diagnose
with anti-histone antibodies and stop the drug to reverse the

Lupus Nephritis
This condition can be life threatening. Screen using U/A and
Umicro, specifically screening for hematuria, casts, and
proteinuria. If a diagnosis is necessary this is one of the few times
where a kidney biopsy is the right answer. Treatment is with IV
cyclophosphamide followed by scaling back to PO
Mycophenolate Mofetil.


When someone comes in with a single hot joint with a several
hours duration (acute) there are a few possibilities. Its likely
either a septic joint caused by an infection or a crystal deposition
disease. To determine the diagnosis the history with risk factors
becomes vital. But no matter how clear the story is, you cant miss
a septic joint so always do an arthrocentesis.

1) Septic Arthritis
A septic joint gets infected two ways: direct inoculation by
trauma or by hematogenous spread. It really comes down to: is
it Staph aureus / Nongonococcal or is it Gonococcal? Staph can
get in via trauma (hard to miss the arrow sticking out of the knee) Youre going to tap the joint either way.
or by hematogenous spread (think IVDA / Endocarditis septic
emboli). Gonococcus gets in by hematogenous spread only, so Youll treat empirically based on risk factors.
look for the young sexually active adult with a urethral
discharge and a couple of days of constitutional symptoms who Youll treat for BOTH if you dont get a definitive diagnosis
now has a hot, swollen knee. Tapping the joint will show many on Tap.
polys (>50 WBC 90% Poly). Start empiric antibiotics, then alter
them as the stain, cultures, and sensitivities become available. If
the gram stain is negative do double coverage (ceftriaxone +

2) Gout
Gout is caused by deposition of monosodium urate crystals in
the joint space and exacerbated by hyperuricemia. Too much ACUTE
uric acid happens either because of increased cell turnover NSAIDs inflammation 1st Line, Gastritis, CKD
(production of uric acid secondary to DNA lysis) or by decreased Colchicine inflammation 2nd line, Diarrhea
excretion (usually a result of decreasing renal function). Its Steroids inflammation Last Line
usually caused by decreased excretion. Look for the old man who CHRONIC
drinks alcohol and is on a diuretic (all of these decrease the Allopurinol Xanthine-Oxidase Maintenance, can cause
excretion capacity of the kidney). During an acute flare diagnose Inhibitor acute flare
gout with an arthrocentesis; itll show negatively birefringent Probenecid Uricosurics Maintenance, can cause
needle-shaped crystals. The joint is exquisitely tender so a clear Uric Acid Stones
clinical history is sufficient - especially if podagra (inflammation
of the great toe) is present. Treat acute gouty attacks with
NSAIDs or Colchicine. Colchicine causes diarrhea so is dose-
limited by that side effect. Treat chronic gout with the xanthine-
oxidase inhibitor allopurinol (preferred) or the uricosuric
agent probenecid to keep the uric acid between <6. Starting
treatment may induce an acute gouty attack. Dont stop chronic
therapy during this flare.

Gout can get so bad that renal failure may result. This occurs
during severe bouts that increase the production of uric acid. One
such example is Tumor Lysis Syndrome (where a bulky tumor
as in Leukemia or Lymphoma is blasted by Chemotherapy).
To avoid Tumor Lysis Syndrome, prophylax with vigorous
hydration and pretreat with Allopurinol. If the uric acid levels
have already risen, lessen the burden of uric acid with

If the arthrocentesis shows positively birefringent crystals, its

pseudogout. The pathogenesis is unknown but it can be treated
with NSAIDs and Steroids.

Follow along with the diagram on the next



Trauma, IVDA, Endocarditis Nafcillin

Gram Stain shows Direct Inoculation
(aka Staph) vs
NOT gram-negative Hematogenous Spread Vancomycin
Gram in clusters
Septic Ceftriaxone
Joint Sexually Active young adult IV or IM
Hematogenous Spread Only DAILY
Gram-negative Gram cocci in chains
>50 WBC Urethritis, Cervicitis then
90% Polys Presumptively
migratory polyarthralgias, Treat Chlamydia
Gram Stain
tenosynovitis and a rash with Doxy x 7d

ONE JOINT PPx IVF + Probenecid + Allopurinol

DISEASE Arthrocentesis Production Tx: Rasburicase

Hot, Swollen, Tender Tumor Lysis Syndrome

Gout Leukemia / Lymphoma
< 50 WBC Negatively Birefringent Chemotherapy
gram stain needle-shaped crystals
Crystals Monosodium Urate NSAIDS
Podagra Tx: Inflammation or Steroids
Crystal Excretion
Deposition EtOH, Diuretics, Aging Diet ( red meat, EtOH)
Tx: Uric Acid Levels Allopurinol better than
Cr, Chronic Kidney Dz
Positively Birefringent between 5-6 Probenecid
Rhomboid shaped crystals
Pseudogout NSAID or Colchicine
Calcium Pyrophosphate
Unknown pathogenesis,
Risk Factors
Arthritis Risk Factors Joint Tap Gram Stain Culture Crystals Treatment
Non-Gonococcal IVDA, Endocarditis, >75 WBC Gram Cocci Staph Nafcillin or Vancomycin
Staph Aureus Direct Trauma, Sepsis 90% Polys in clusters
Gonococcal Unprotected Sex, >75 WBC Gram Cocci in Gonococcus Daily IV or IM
Urethritis, Discharge, 90% Polys chains Ceftriaxone
Gout Levels of uric acid 5-50 Urate Crystals NSAIDs or Colchicine
old man on EtoH + negatively birefringent Steroids
Diuretics, Podagra Needle Shaped Allopurinol maintenance
Probenecid maintenance
Pseudogout Calcium 5-50 Pyrophosphate Crystals NSAIDs or Colchicine
Pathogenesis Unknown Positively Birefringent Steroids
Rhomboid Shaped


Scleroderma Sclerodactyly
Scleroderma is an autoimmune disease resulting in 1) collagen
replacing smooth muscle and 2) wide-spread extraneous Restrictive Esophageal dysmotility
Pericarditis (really bad GERD)
collagen deposition. The typical patient has skin tightness in the
hands and face and may suffer some GERD or Raynauds. In
reality, there are two types of scleroderma: CREST and Systemic
Sclerosis. CREST is a limited disease that spares the heart and Renal Failure and
kidneys but has Skin and GI effects. On the other hand, systemic Renovascular HTN Sclerodactyly
sclerosis is a diffuse disease affecting the trunk with cardiac
(restrictive cardiomyopathy) and Renal (renovascular
hypertension) effects. Scleroderma is mainly a clinical diagnosis
but antibodies may aid getting there. Anti-Scl-70 (topoisomerase CREST: Systemic Sclerosis
I) is positive in systemic disease while anti-centromere is Calcinosis CREST +
positive in CREST. Theres also no treatment for the disease Raynauds Renal
itself. Instead, treat the symptoms. Use Calcium Channel Esophageal Dysmotility Heart
Blockers for Raynauds, Penicillamine for skin changes, Sclerodactyly
steroids for acute flares, and aggressive treatment of Telangiectasia
hypertension with ACE-inhibitors. Collagen in the renal
arterioles prevents dilation and constrict. This creates a prerenal Anti-Centromere Anti-Scl-70
picture by activating the renin-angiotensin-aldosterone axis, PAH ILD
which exacerbates the hypertension.

Sjogrens syndrome
An inflammatory condition of exocrine glands due to Dry Eyes
lymphoplasmacytic infiltration. It can exist on its own
(primary) or be part of another Rheumatologic disorder Parotid Glands
(secondary). Its easy to spot: Dry Eyes (Keratoconjunctivitis), Dry Mouth
Dry Mouth (Xerostomia), and bilateral parotid enlargement.
Its a clinical diagnosis assisted by antibodies (Ro or La which
are specific but not sensitive) and tear production testing
(Schirmer test). Theres no treatment so focus on symptom Heliotrope Rash
control (artificial tears / saliva).
Myocarditis Gottrons Papules
Polymyositis / Dermatomyositis / Inclusion Body Myositis
These three inflammatory myopathies are lumped together
because their presentation, diagnosis, and treatment are all the Diaphragmatic
same (well, except IBM, which has no treatment). The underlying Weakness
pathogenesis (T cell / Immune Complex / T cell respectively)
results in the presentation of painless proximal muscle Inflammatory
weakness (difficulty in rising out of a chair but intact grip Myopathy
strength) occurring slowly over time. There may be systemic
involvement. The way it comes to light is usually the
dermatologic signs: 1) erythematous rash on sun-exposed areas Scleroderma Sjogrens DM/PM/IBM
(photosensitivity), 2) Heliotrope rash, a purple discoloration Pt Female, Thickened Skin Female Proximal Muscle
around the eyes with periorbital edema, and 3) Gottrons on fingers, GERD, Dry eyes weakness, tender,
Papules (pathognomonic), which are scaly areas symmetrically Reynauds Dry mouth Heliotrope rash,
over major joints (wrists, elbows, knees, ankles). The first test is Bi Parotitis Gottrons Papules
always EMG to determine if its a nerve conduction issue (MS, F: DM +PM, M: IBM
Ab Scl-70 = Diffuse Ro Jo
for example) versus muscular damage. A muscle biopsy is done
Centromere = CREST La Mi
to definitively diagnose and separates one disease from the other. Dx - Schirmer EMG
Other tests may help. The CK will be elevated (muscular Tear Production Bx
damage) and Anti-Jo or Anti-Mi antibodies may be present. The MRI / CT (Cancer)
goal is to check for occult malignancy (as these are often a Tx Penicillamine Symptom Relief Check for Malignancy
paraneoplastic syndrome) and treatment is with high-dose CCB
steroids. Steroids High Dose Steroids


Introduction BONUS POINTS: Feltys syndrome
Rheumatoid Arthritis is an autoimmune disorder. The Rheumatoid Arthritis + Neutropenia + Splenomegaly = Feltys
pathology is a result of pannus formation at the joint, which
leads to erosions and bony destruction. We dont know why it if you see RA + Splenomegaly think Neutropenia
happens, but we know how to spot it and what to do about it. if you se RA + Neutropenia think Splenomegaly

Presentation BONUS POINTS: Cervical X-ray

Classically therell be Prolonged morning stiffness affecting If a patient with RA is going into surgery for any reason a
many small joints (3 or more, usually in the hands), thats cervical film should be done since rheumatoid arthritis
symmetric; vignettes will often use an older woman. affects the cervical spine and the cervical spine only.

Morning Stiffness + The Spine might come up. The reaction Spine Involvement except C1 + C2
is to go for Ankylosing Spondylitis. If it involves the lower back
its ank spond. If it involves the neck (C1, C2) its RA.

Diagnosis Clinical Criteria

Symmetrical Arthritis, often of the hands, Sparing DIP
There are a number of clinical criteria available to diagnose
Morning Stiffness for > 60 minutes, improves with use
rheumatoid arthritis. Theyre not all needed, but some common Multiple Joint Involvement ( > 3)
findings are almost always present on a vignette. The old wait 6 Radiographic Destruction of Joints (erosions)
weeks, is now out; RA can be diagnosed right off the bat. + Rheumatoid Factor or + Anti CCP
Rheumatoid Nodules
Serology. Either the Rheumatoid Factor (cheap, sensitive) or the
Anti-CCP (expensive, specific) can be used. If either is positive
it counts for serology. Nobody Should Have Rheumatoid Symptoms 3 times (X)
N: Nodules
Joints. There must be symmetric arthritis that involves more S: Symmetric
than three joints and spares the DIPs. Both the number of joints H: Hands
involved and the symmetry are crucial. Look for small joints like R: RF or CCP
hands, feet, and wrists. S: Stiffness
3: 3 or more joints
Radiology. An X-ray can be used to assess for periarticular X: X-ray findings of erosions
osteopenia and marginal bony erosions. These findings will
also be symmetric. The x-ray can also identify regular old arthritis Be Careful
if osteophytes are seen. In life, you can have Rheumatoid Arthritis with negative RF
and negative Anti-CCP, or no Rheumatoid Arthritis with
Nodules. Biopsy of a Rheumatoid Nodule will reveal cholesterol positive RF and positive Anti-CCP. On a test its always
deposits. This finding rules out another potential deposition black and white: if positive, then disease, if negative, then
disease. These are pathognomonic. no disease.

Get these patients on disease modifying agents as soon as
possible. Start the treatment of RA with DMARDs as soon as NSAIDs + DMARDS + Biologics . Steroids
possible. Methotrexate is first line for RA. Leflunomide can be (Sxs) (everyone) (severe) (flares)
used if methotrexate cant be. Hydroxychloroquine and
Sulfasalazine have long-acting effects that may be used together Treatment
with methotrexate to avoid biologic therapy (doubling up is ok). DMARD Methotrexate (1st line)
Leflunomide (2nd line)
Hydroxychloroquine is also appropriate for non-erosive mild
Hydroxychloroquine (pregnancy)
disease and during pregnancy. The goal is treat-to-target Sulfasalazine (additive)
(disease remission). If DMARDs fail add biologics. Before Anti-TNF Etanercept
starting biologics a TB screen and vaccines must be given as they Infliximab
significantly compromise immune function. Corticosteroids Rituximab
should be avoided - except during life threatening flares - to Glucocorticoid Flares, get off this as soon as
reduce long-term systemic side effects. NSAIDs can be used to possible
NSAIDs Supplemental only,
control symptoms and are adjunctive therapy. NEVER use


This group of diseases are unique in that they show a predilection HLA-B27 doesnt help - DONT order it.
for the spine, particularly the sacroiliac joints, and have a higher UNLESS you have a clear diagnosis of ankylosing
incidence in men (much unlike the majority of rheumatologic spondylitis despite negative films (x-ray and MRI)
diseases). Theres a correlation to HLA-B27 but it isnt useful for
diagnosis. These patients are seronegative: they have no RF, RF, CCP, ANA dont help - DONT order them.
CCP, or ANA reactive antibodies. What separates them from each
other is their extra-articular involvement and links to other
inflammatory conditions.

1) Ankylosing Spondylitis 32 year old man with lumbar stiffness in the morning who
Ankylosing spondylitis is the most commonly tested seronegative gets an x-ray showing any positive finding of the lumbar
arthropathy. It occurs in men in their 20s and 30s. They will have spine. The vignette should NOT include something about
lower back pain with morning stiffness that improves with use. diarrhea.
Its caused by sacroiliitis with fusion of the sacral joints and
calcification of tendons, which produces the bamboo spine on X- Start him on NSAIDs and escalate to Methotrexate.
ray. Other tendons can calcify as well - especially the Achilles Monoclonal antibodies CAN be used to treat the pain (unlike
tendon. It can be associated with inflammatory bowel disease all other seronegatives).
(distracting towards enteropathic) but its course is different. The
treatment is based on severity and presence of axial vs peripheral TNF-Alpha-Inhibitors
joint involvement. Therapy generally starts with NSAIDs, Etanercept
escalates to Methotrexate, and if all else fails moves to Infliximab
monoclonal antibodies (TNF-alpha inhibitors) like Etanercept. Adalimumab

2) Reactive Arthritis
People with HLA-B27 who also get nongonococcal urethritis Gonococcal Urethritis = Septic Arthritis (one joint)
(usually Chlamydia) will react and develop an asymmetric
bilateral arthritis of the lower back and hands as well as a Non-Gonococcal Urethritis + Arthritis = Reactive Arthritis
conjunctivitis. Treating the underlying infection will prevent this (back and hands)
acute disease from transforming into chronic. Treat the
Chlamydia with doxycycline and arthritis with NSAIDs. Urethritis + Arthritis + Uveitis = Reiters Syndrome

3) Psoriatic Arthritis
Psoriasis + Arthritis is psoriatic arthritis. The main joint involved NSAIDs: Mild arthritis and no / meh skin findings
will be in the hands. Its a symmetric PIP and DIP arthritis with Methotrexate: Severe arthritis and real skin findings
erosive pitting of the nails. The arthritis may precede the TNF-a Inhibitors: Nonresponsive to Methotrexate
psoriatic plaques (making the diagnosis difficult). The goal is
symptom control with NSAIDs if theres mild arthritis and NO Steroids: no... Steroids bad and lead to flare of psoriasis
skin disease. Use Methotrexate if its severe or there are skin
findings, Anti-TNF if Methotrexate resistant.

4) Enteropathic / IBD-Associated
While ankylosing spondylitis is associated with, but independent
of IBDs course, this disease directly correlates with IBD. See how this is different from Ankylosing Spondylitis?
Treating the IBD fixes the arthritis. The arthritis is symmetric Treating IBD makes this better. Treating IBS in AS does not.
and bilateral, non-deforming, peripheral (fingers), and
migratory. It also involves the lower back. The person will have
some history of diarrhea to tell you they have IBD.
Disease Presentation Diagnosis Extraarticular Treatment
Ankylosing Back Pain + Morning Stiffness Bamboo spine IBD but independent of NSAIDs
Spondylitis relieved by exercise on X-ray IBD course Steroids
(Sacroiliitis) Anti-TNF
Reactive Nongonococcal Urethritis Nongonococcal Doxycycline
Arthritis Conjunctivitis PCR/DNA Chlamydia Urethritis and
Asymmetric Bilateral Arthritis (usually Chlamydia) NSAIDs
Psoriatic Psoriatic Patches Psoriasis UV light
Arthritis Erosive pitting of nails Arthritis may appear NSAID (no skin)
MCP, DIP, PIP Arthritis first Methotrexate (skin)
Enteropathic Non-deforming, migratory, IBD and dependent of Tx IBD with ASA
Arthritis asymmetric Bilateral Arthritis IBD course compounds
In a patient with IBD (mesalamine)
Rheumatology [VASCULITIS]

Vasculitides are a bit peculiar. Theyre often a diagnosis of
exclusion as theyre considered only after other diseases have
been ruled out. Lets focus on the few test associations for classic

Giant Cell Arteritis
Also called temporal arteritis, this is the most common primary Polyarteritis Nodosa
vasculitis. It effects the arteries of the external carotid (the PAN is associated with Hepatitis B but can exist on its own. Its
temporal artery and ophthalmologic artery). The classic tough to diagnose because it affects so many organs. When
presentation is age > 50 person with unilateral temporal vasculitis in multiple organs at the same time without a
headache and a tender swollen temporal artery. Another common vascular distribution is seen, think PAN. In the
pattern could be visual changes or jaw claudication. This is an kidneys it causes a non-glomuerlonephritis vasculitis (renal
intensely inflammatory disorder, so systemic symptoms may be failure). In the gut is causes mesenteriC vasculitis (mesenteric
present (elevated ESR, weight loss, low-grade fever, and ischemia). In the nervous system it causes an asymmetric painful
malaise). GIVE STEROIDS FIRST. Even though the diagnosis motor and sensory neuropathy (mononeuritis multiplex). In the
is definitely made with a biopsy, the risk for blindness is too skin it causes purpura and painful nodules. What will probably
great; treatment should precede the diagnostic step. happen is that you will go hunting for ONE problem and do some
vascular imaging like an angiogram. That angiogram will reveal
Polymyalgia Rheumatica aneurysms and stenosis in medium-sized vessels. Treatment is
While this is actually not a vasculitis its so commonly associated aggressive. Start with high-dose steroids and
with Giant Cell Arteritis that its discussed here. PMR presents cyclophosphamide. Treat Hep B.
with symmetric pain and stiffness in the shoulder, neck, and
hips. Itll present as a proximal muscle weakness similar in Kawasaki Disease
pattern to the idiopathic inflammatory myopathies but with a This is as Asian Childhood Disease (look for infants and
normal CK (the ESR and systemic signs of inflammation are children, most commonly Asian boys). The buzz phrase is
present). This disease requires no diagnostic step, though an strawberry-like tongue. Also look for the trunCal rash with a
angiogram could rule out other diseases. It responds well to paLmar and plantar erythema with desquamation. This can
steroids. cause vasculitis of the coronary arteries leading to myocardial
infarction in a child. Treatment is with IVIG and Aspirin (even
Takayasu Arteritis though youre not supposed to give kids aspirin).
This disease is super rare and has the same pathology as GCA,
but instead of the distal arteries it impacts the vessels of the aorta
and its major branches (subclavian, renal, femoral). There are
systemic signs (ESR, weight loss, fever), but what youre keying
in on is the absent pulses in large vessels (brachial, femora,
carotid). Look for a young person (< 40 years old) who has

systemic inflammation and large vessel impairment. An
angiogram will make the diagnosis. Treat with high dose SMALL VESSEL COMPLEX MEDIATED
Think of cryoglobulinemia when theres palpable purpura and
SMALL VESSEL ANCA RELATED Hepatitis C. Assess for cryoglobulins in the serum. Other clues
may be a positive RF, elevated ESR, and decreased compliment.
Granulomatosis with Polyangiitis (Wegners) Treatment can be with steroids, cyclophosphamide, rituximab,
Most common ANCA associated vasculitis. GPA is usually c- and plasmapheresis (in increasing order of severity).
ANCA positive. Look for renal + lung + nasal. This is usually
seen on the test as hematuria and hemoptysis but also with HenochSchnlein purpura
nasal involvement. A biopsy of affected tissue is required for HSP is suspected when theres palpable purpura and
treatment; it will show vasculitis and necrotizing granulomas. abdominal pain or abdominal bleeding. The kidneys can
Treatment is aggressive: steroids and cyclophosphamide. Other be involved. The diagnosis is made by biopsying the
DMARDs can be used as maintenance therapy. effected tissue (usually the skin) to reveal a leukocytoclastic
vasculitis. For treatment, steroids are the main option.

Dermatology [ALOPECIA]

Alopecia Areata
A systemic autoimmune disorder against hair follicles. FACTT M
Ranging from small patches to total body hair loss, its a Fungus (Tinea Capitis)
poorly understood disease. Because its primarily cosmetic, Areata (Alopecia Areata)
without alternatively associated disease, its more about clinical Chemo
diagnosis than management. Traction Alopecia
Traction Alopecia
Permanent scarring resulting in permanent alopecia thats Male Pattern Baldness
secondary to keeping the hair pulled tightly (extreme braiding)
that puts excessive traction on the root. This is preventable but
irreversible once it occurs.

Male Pattern Baldness

A cosmetic issue whereby 5-DHT strangles hair follicles
causing hair loss starting at the crown and working its way
around to the front of the head. Treat with Minoxidil topical
and Systemic Finesteride.

Trichotillomania is a psychiatric disease labeled under anxiety
or OCD. It presents as patchy alopecia with hair at different
lengths. Tell the girl to stop and do behavioral therapy to treat
the anxiety.

Sometimes the hair falls out. Chemotherapy targets rapidly
dividing cells. This means the cancer (yay!) but also the gut
(diarrhea), bone marrow (anemia, infection), and hair. Hair loss
is expected, anticipated, and without treatment.

Tinea Capitis
Tinea Capitis is a fungal infection that causes patchy alopecia
on the head. All of the hairs will be lost at the same time, so all
hairs in the affected region are gone or are regrowing at the
same length. A KOH prep must be gotten to visualize the
infection. Treat with topical and oral antifungals; failure to do so
will result in permanent hair loss.


Disease Age Mucosa Blisters Target Dx IF Tx


symmetric irregular ABCDE
Border mixed Color large Diameter Evolving A

melanoma wide excisional biopsy

ugly looking mole Is it Cancer?

large brown greasy
looking crusted stuck on old

premalignant erythematous with a

sandpaper-like yellow to brown scale. squamous cell

Primary prevention


always on the lower lip

surgical excision


went away on its

HHV-8 Immunosuppression AIDS


Anaphylaxis = shortness of breath and hypotension with

exposure to allergen. Give epinephrine. Follow with
systemic steroids, H1 blocker and H2 blocker.

Dz Pt Tx Bx

Piebaldism is inadequate melanocyte migration with a

white forelock on the scalp)

Albinism is inadequate tyrosinase activity, total

depigmentation in all surfaces

PK is a deficiency in phenylalanine hydroxylase, causing a

relative deficiency of tyrosine. Screened for at birth.
Mental retardation, seizures follow if not for a special diet

Shagreen patches (elevated fleshy collagen plaques)

Adenoma Sebaceum (hyperplastic blood vessels)

Dz Patient Diagnosis Biopsy Treatment Path Risk Factors


fungal infection

hair scalp and eyebrows


HIV infection cradle cap

symmetric, well-demarcated
silvery scales bleed when picked
Nail pitting
UV light
Topical steroids

flat, oval, salmon-colored macule

herald patch
several salmon-colored scaling lesions
trailing scale
spare the palms and soles


intensely pruritic pink purple

papules reticulated network of fine
white lines

Topical steroids

drug eruption
Pediatrics [ALLERGIES]

H1 Blockers (Allergies) H2 Blockers (GERD)

seasonal dander pollen
rhinorrhea salute,
nasal crease

allergic shiners

Skin test)

Intranasal corticosteroids

bee stings foods pollen Urticaria Anaphylaxis

raised blanching wheal

no anaphylaxis
hypotension dyspnea wheezing 1:1000
IM epi

avoid triggers
skin testing

rash antigen triggers.

eczema asthma seasonal
allergies -
young kids face new food
flexor surfaces
pruritic - excoriations potential
lichenification adulthood Topical corticosteroids
non-drying soaps

early C1 esterase deficiency,
Ace-inhibitor .

This is a duplicate from the surgery videos. Use this

only for shelf study and not for Step study. Go to the
Surgery videos if step studying.

See peds. GI Bleeds for more details

See peds, Constipation for more details

Se peds, vomiting for more details

See peds, vomiting for more details

See peds, constipation for more details

See peds, GI bleed for more details


URI Bugs

respiratory bugs Unilateral ear

no pain with pinna
pneumatic insufflation tense immobile Ear Pain
membrane bulging red angry membrane loss of
light reflex
amoxicillin azithromycin
amoxicillin and
clavulanate. Rhinorrhea
mastoid inner ear
brain tubes

unilateral ear pain Throat
pain on palpation of pinna

Staph aureus Bloody
angry erythematous canal Nose

nose sinuses
Purulent bilateral nasal discharge viral wait bacterial amoxicillin

sinus tenderness facial tap

not necessary air-fluid levels opacification

> 10 days
presume bacterial infection
amoxicillin azithromycin

large droplets rhinorrhea congestion
low-grade fever Nasopharyngeal
washes with culture
not do anything
< 7 days AND no cough

throat pain on swallowing Calculating the Centor score

Centor Criteria
Rapid Strep Test specific
not sensitive culture

Interpreting the Score

foul-smelling unilateral ear
throat Site Retrieval
infection treated


unilateral scratching buzzing

lidocaine never light

digital trauma Anterior Epistaxis You Treat

unilateral <30 minutes - Nose picking
forward - Dry Air

anatomical foreign Posterior Epistaxis ENT Treats

humidified air ablation - Look for HTN
- Look for CHF
Posterior epistaxis packing

cystic fibrosis

intranasal steroids surgically remove

anatomically stenosed
blue at rest
pink up with crying
snore catheter will
fail to pass fiber-optic scope


Pediatrics [GI BLEEDS]

Premature Disease How to look for it

premature baby bloody diarrhea

x-ray babygram pneumatosis intestinalis

NPO immediately TPN IV antibiotics

no improvement conditions worsen

tear in the anal mucosa

abrupt onset colicky abdominal pain

knee-chest position vomiting

currant jelly
diarrhea sausage-shaped mass

air enema diagnose and treat

GI bleeding child FOBT

hematochezia painless rule of 2s


melena babies
maternal blood children own

history of epistaxis Apt Test




Unconjugated Conjugated




Breast Milk (Lack of) Breast Feeding


cortical blindness
development This is a duplicate note-set from Surgery. The questions,
the notes, and the video are identical for Peds-Ophtho and

reflection of light comes from

separate locations on each eye

resolve spontaneously

red light reflex pure white retina

can be seen
Resect Avoid radiation


milky white

galactokinase deficiency Fix


Premature neonates
laser ablation
intraventricular hemorrhage,
bronchopulmonary dysplasia necrotizing enterocolitis

Type Timing Purulent Problems Treatment

screen and treat 24 hrs

Day 2-5 Topical

silver nitrate drops erythromycin
prophylaxis chemical
conjunctivitis blindness Silver Nitrate
Gonorrhea 2-5 days purulent Day 7-12 Oral + Topical
bilateral topical erythromycin Erythromycin
Chlamydia day 7-14 mucopurulent unilateral
topical PLUS oral erythromycin pneumonia PPX
Pediatrics [ORTHOPEDICS]

This is a reproduction of the surgery content in the

pediatrics section, should you be viewing only pediatrics

Dx Age Patient Dx Tx

Dx Patient Sxs Dx Tx
Pediatrics [CT SURGERY]

This is a duplication from the surgery videos, in

case you are studying pediatrics only.

Left to Right Shunts

Pediatrics [CT SURGERY]

Right to Left Shunts

The others are rare. Things like Truncus Arteriosus,

Tricuspid Atresia, and Total Anomalous Pulmonary
Venous Return are almost never seen. Review Step 1 notes
for clarity or to impress your attending

Scabies Lice Pinworm

Skin Osteomyelitis

Septic Joints


Meningitis Babies Adolescent


Viral Meningitis

Petechial Rash

Disease Bug Prodrome Rash Other



Disease Trauma Symptoms CT Treatment

Head Trauma Prevention


Drowning Prevention


Front Back
Pediatrics [SEIZURES]
Pediatrics [LOWER AIRWAY]

Don't be tricked into choosing parainfluenza

Pediatrics [LOWER AIRWAY]

Pseudomonas in teens and adults

Staph aureus in neonates and children.

Disease Patient 1st Test Best Test Treatment Prophylaxis


Stridor inspiratory wheeze

partial obstruction
trachea larynx

visual inspection
chest X-ray


viral prodrome week

barking seal-like cough
inspiratory stridor

AP Film clear
lungs steeple sign

dont be tricked into choosing RSV (that's Bronchiolitis -

respiratory impairment call it RSV Bronchiolitis)
racemic epinephrine

extremely rare Hib

Vaccine 3-7
years bacterial
no prodrome high
fever rapid onset
tripoding drooling
AP film thumb print sign,

straight to the OR intubation



drooling fever

supine limited neck

mobility hot potato voice
unilateral cervical lymphadenopathy
X-rays lateral
expansion of soft tissue

abscess incision and drainage


Adult patients with tracheostomies can get tracheitis easily.

It looks like a pneumonia, only there is no consolidation on
X-ray. These patients are treated with Pip/Tazo for gram
same age range postiive, gram negative, and anerobic coverage. Very
prodrome subglottic narrowing on AP different in an adult, and one of the bread-and-butter ENT
infections (ENT puts the trache in and manages these
Staph Aureus patients in the outpatient setting)
failure to respond
does not improve incredibly rare

tracheal culture, visualize

pus treat with antibiotics

hot potato voice 10

years old
abscess be een

incision and drainage


Disease Patient Bug Racemic Epi Diagnosis Treatment

barking cough Parainfluenza Improves Steeple Sign

Racemic Epi
Drooling Thumb Print Sign Secure Airway in
Operating Room

Direct Visualization
Soft tissue >50% of Incision &
Drooling vertebra on lateral drainage and
neck film
Steeple Sign

Incision &
Drooling Drainage and

This is duplicated in both pediatrics and surgery


Test Why

Vaccine Comments

Vaccine Comments

Disease Comments
Pediatrics [VOMITING]

spit up
volume non-projectile formula colored

anatomic -

Green vomit

total obstruction
first feed x-ray babygram
gas patterns
Double-Bubble + No Distal Air = Duodenal Atresia
fails to recanalize Surgery
polyhydramnios Downs
double-bubble sign no distal air
Double-Bubble + No Distal Air = Annular Pancreas
double-bubble without distal air Surgery

Double-Bubble + Normal Gas = Malrotation

bilious vomiting double-bubble Emergency Surgery
sign normal gas patterns

barium enema
upper GI series
immediate surgery

double-bubble or triple bubble multiple-air Double-Bubble + Air Fluid Levels = Intestinal Atresia
fluid levels cocaine Tell mom to stop cocaine
vascular accident Surgically remove

Boy with olive-shaped mass, projectile vomiting

projectile vomiting Ultrasound = Donut
olive-shaped mass peristaltic waves Surgery = Myomectomy
CMP hypochloremic hypokalemic metabolic
alkalosis IVF
Ultrasound donut sign
Psychiatry [ADDICTION]




Acute EtOH Intoxication

Psychiatry [ADDICTION]

Drug Intoxication Withdrawal Drug / Antidote


Anxiety is a diffuse response without a precise feeling involving
worry, fear, and hyper-vigilance, coupled with the physical
symptoms of anxiety: palpations, perspiration, and dyspnea.
Everyone has felt the sinking feeling in the pit of their stomach
before opening a letter about their Step 1 grade or a phone call
from the parents at 2 AM bearing bad news. This is what
anxietys all about. Some anxiety is provoked by triggers
(places and things), but it can also be in a constant state.

1) Generalized Anxiety Disorder

Patients who have constant anxiety about almost everything in
life will spend a lot of time worrying and worrying about
worrying. If patients have anxiety on most days of > 6 months
and have > 3 somatic symptoms they meet criteria for GAD.
Somatic symptoms manifest as restlessness, irritability, trouble
concentrating, sleep changes, etc. If diagnosed, psychotherapy
is paramount. To let them get control of their lives use benzos
for immediate relief and SSRI / Buspirone for long term

2) Obsessive-Compulsive
Patients have persistent, intrusive, unwanted thoughts (the
obsessions) that provoke anxiety. The only way to relieve these
obsessions is by performing repeated behaviors (the
compulsions) that neutralize the anxiety. The patient is
painfully aware of the actions/thoughts and how irrational
they are. Theyll even seek help. Two obsessions are common:
contamination and safety - leading to excessive cleaning or
door/window/lock checking. These patients will need intense
desensitization therapy, but the mainstay is SSRI. Once stable a
therapist can produce the obsession in reality, preventing the
compulsion while controlling anxiety with drugs.

3) Panic Disorders
Patients will experience Panic Attacks (PANICS) that come
without provocation, i.e. out of the blue. Panic Attacks can
resemble a medical disease (MI, Asthma) and should be ruled Palpitations / Paresthesias
out if its the first attack. Because patients get random attacks Abdominal Distress (Pain, Diarrhea)
they may also fear having them in public; look for panic Nausea
attacks + Agoraphobia. Onset is usually in females in their 20s. Intense fear of dying
In particular, look for thyroid and drugs. Once a panic disorder Chest pain or tightness
is diagnosed three things can be done. 1Abort the attack with Shortness of breath
benzos but because of their addictive potential, dont prescribe
them long-term. 2SSRIs are a better long term choice and are
more effective than cognitive behavior therapy. 3Cognitive
Behavioral Therapy should be started as well.

4) Phobias
Specific phobias are irrational and exaggerated fear of an
object or situation. They produce anxiety and avoidance of the
stimulus. Theyre generally considered to be learned responses.
There was some negative experience that the brain extrapolated
to involve the target stimulus. If your family gets eaten by a lion
it would be wise to avoid all things with paws, whiskers, claws,
or fur. And so, the person who fears all lions will live. Phobia is
an irrational exaggeration of the normal response - the same
person now fears housecats. Cute, snuggly and purring, they
pose no threat. This is a cat phobia.


(i) Social Phobias

The situation is often one where potential embarrassment
could occur (public urination, public speaking) or a fear of Reclusive person who does not like going to parties
crowds + outdoors (agoraphobia). While Cognitive becomes so fearful he/she never leaves his/her house.
Behavioral Therapy is the best therapy, remember that Beta-
Blockers are used for Performance Anxiety (stage fright).

(ii) Specific Phobias

Its common to hear of people afraid of heights, spiders, or
flying. The fear comes from somewhere. Because its learned
we try to learn serenity in the place of anxiety. This is done in
two ways via CBT. Systemic Desensitization involves stages Fear of clowns
of anxiety provoking situations, each of which are conquered
sequentially. The other is flooding: overwhelming the patient
with a major stimulus while engaging in anxiety-reducing
behaviors or under medication. SD is generally more effective
but takes longer.

5) Post Traumatic Stress Disorder

This requires a life-threatening event (rape, combat, child
abuse) or simply witnessing something terrible (9/11, Murder,
etc). The patient will present with the classic four symptoms:
re-experiencing event (flashbacks or night mares),
anhedonia, 3increased arousal (startle reflex, hyper- Witnessing or surviving a rape, murder, or war with
vigilance), and 4avoidance of the stimulus. Its often linked to a flashbacks, avoidance, and chronic anxiety, the event
location or specific details of the event. Not all four symptoms plaguing your waking mind and your dreams
need to be present but all four often are. The closer to the
stressor the treatment gets started the better the prognosis.
Pharmacotherapy is generally ineffective, but attacks are
controlled with benzos. Therapy is focused at psychotherapy
and support groups. If symptoms have been only for <1 month
we call it Acute Distress Disorder. Initiate psychotherapy
before it becomes PTSD, > 1 month of symptoms.

Disorder Symptoms Pharmacotherapy Preferred Treatment

Generalized Worrying about every little thing for most days in Benzos immediate abortion Medications
Anxiety > 6 months with > 3 somatic sxs SSRI Long Term (and CBT)
Obsessive Obsessions (thoughts) provoke anxiety SSRI Medications
Compulsive Compulsions (actions) reduce anxiety (and CBT)
Disorder Egodystonic both the thoughts and actions
Panic Disorder Random, unprovoked panic attacks Benzos immediate abortion Medications
+ Agoraphobia PANICS SSRI Long Term (and CBT)
Performance Anxiety in public speaking or performance Beta-Blockers Meds
Social Anxiety in social situations Benzos
Specific Unreasonable fear of a specific object of Not Drugs Systemic Desensitization
situation (and flooding)
Post Traumatic Stress Follows life-threatening event or witness Benzos + SSRI Support Group and
Disorder Avoidance of stimuli psychotherapy
Arousal (hyper vigilance, startle reflex) (and SSRI)
Re-experiencing (flashbacks, nightmares)
Acute Distress Disorder PTSD for < 1 month N/A Psychotherapy






ii. Delusional Disorder




Movie Reference: Sybil

Movie Reference: Shutter Island

Movie Reference: The Long Kiss Goodnight


Discussion of eating disorders is typically centered on girls
dealing with either anorexia or bulimia. When considering
which disease the girl is suffering from, looking at body weight
and what thing(s) causes her distress (being fat or doing binge
+ purge) is most important. All other facets can be similar
between diseases so use those two to differentiate. Note that
males can and do suffer from these diseases but its likely
females will be in the questions.

Anorexia Nervosa
Anorexias typically the eating disorder of the underweight
female with a body dysmorphic disorder (she perceives
herself as fat). The classic patient will restrict (starving herself
by hiding food or eating alone), though anorexics can also binge
and purge. These girls are sick. Theyre usually <85% Ideal
Body Weight but have a fear of weight gain. Theyll have an
appearance of hypothyroid (except that they are thin) with
lanugo, bradycardia, lethargy, hypotension, and cold
intolerance. Treatment requires intense psychotherapy. In the
meantime, these girls require hospitalization for nutrient
support; managed meals, gastric tube, IV nutrition, etc. If these
girls can be caught before <85% IBW, therapy and meds can be
started without hospitalization or forced meals. Regardless, they
need to be closely monitored.

Bulimia Nervosa
Bulimics are usually normal weight or overweight, but unlike
the anorexic the bulimic is ashamed of her actions - shes
primarily worried about actions rather than body image.
Bulimics will engage in binge eating then compensate by
purging (vomiting or laxative use) or fasting. Because they
stick a finger down their own throats, theyll have dental
enamel erosion from the vomit, enlarged parotid glands, and
scars on dorsal surface of hands. These girls want help.
Psychotherapy focuses on behavior modification and weight
loss. Antidepressants are usually effective but its essential to
avoid bupropion to avoid seizures.

Dz Body Image Method Weight Treatment

Anorexia Disturbed by body image Usually restrict <85% Ideal Body Weight Forced Feeding
but fear weight gain May binge and purge Bradycardia, Hypotension, Antidepressants
active body dysmorphic disorder Cold Intolerance, Lethargy Psychotherapy
Do not think they have a problem Hospitalization
Bulimia Disturbed by body image Usually binge and purge Psychotherapy
but know they have a problem May restrict Parotid Swelling Antidepressants
Dental Erosion Avoid Seizures!
Dorsal Hand Scarring


Impulses are anxiety-decreasing actions that are generally
egosyntonic. Theres a link between impulsivity and low serotonin
levels. It makes sense then that impulses can be controlled with

Intermittent Explosive Disorder

Theres an inappropriate violent act in response to a stressor. The
Driver gets cut off. Rather than yelling at the steering wheel
response is out of proportion to the stressor. It involves violence
person chases down the driver, drags him into the street, and
towards people or property. After the act, the patient is calm,
shoots him.
relaxed, and without remorse. Because theres violence its more
frequently seen in men. The symptoms tend to lessen with age.
Until then, treat the patient with SSRIs; mood stabilizers are also
handy. Always involve group therapy oriented at self-reflection.

Patients set fire to things for pleasure or anxiety reduction. These
patients have a fascination with fires and burning - they may even The prisoner was arrested for masturbating after lighting his
be sexually aroused by fire. Theres generally no successful neighbors shed on fire.
therapy and incarceration may be required. You must rule out
Arson, setting fire for monetary gain, and NOT for anxiety of The construction worker, late on the payments for his
pleasure. Thats legal, but important. mortgage, burns his house down to get the insurance.

A patient has an impulse to steal. The disorder usually has an object
or environment of interest, that when identified, causes an Every time the girl visits a restaurant, she becomes intensely
increased anxiety. Only the theft of the object will reduce anxious at the sight of a fork. The anxiety is relieved only by
anxiety. A useful test question is the link between this disease in stealing the fork.
women with Bulimia + OCD. Pharmacology is targeted at SSRIs,
but Cognitive Behavioral Therapy is critical as it can train
relaxation techniques. Instead of stealing, reduce anxiety in another
way. People who commit multiple petty thefts are not kleptos -
kleptos usually steal the same thing over and over.

Patients pull out their hair to reduce anxiety. If a patient has
alopecia we generally dont think of psych. But if the hairs in The 23 year old female with patches of her hair missing
different lengths (vs a patchy alopecia) then its strongly presents with a small bowel obstruction
suggestive of trichotillomania vs medical disease. Take steps to rule
out hair loss disease (fungus in particular). If she presents with a
small bowel obstruction as well, think of a trichobezoar (a hair

Intermittent Violent or Destructive Act out Men SSRIs Group Therapy
Explosive Disorder of proportion with stressor
Pyromania Sets fire for pleasure / Anxiety Men None Incarceration
Arson Sets fire for money (or Reaction Formation)
Kleptomania Steals to reduce anxiety Women CBT SSRI
Trichotillomania Pulls out hair, may eat hair Women CBT SSRI

Psychiatry [MOOD DISORDERS ]



Mild versions of disease cause no decreased functioning.

Think: would I hospitalize this patient? If no, likely a mild
version depression - Dysthymia.
Psychiatry [MOOD DISORDERS ]

Grief Depression

Baby Blues Post-Partum Post-Partum

Depression Psychosis

PD Description Defense Examples How to Handle Them

Psychiatry [PSYCH PHARM]

Anti-Depressant RULES


Mood Stabilizers

Psychiatry [PSYCH PHARM]




Unique to itself

Extrapyramidal Side Effects

Choosing the Right Drug


1) Sleep Apnea
When the obese, hypertensive middle-aged man comes in Tired All the Time
complaining of daytime somnolence, ask the roommate if they
snore. If he does, send him for a sleep study (poly-
somnography) to determine the number of disturbances, Yes
OSA Snoring, Obese,
awakenings, and apnea spells. These people need to lose weight
and get CPAP at night to keep the airways open. Avoid PHT Polysomnography
and Cor Pulmonale. Its possible to have central sleep apnea CPAP No
in a thin person - treat with BiPAP with backup vents. Weight Loss
2) Narcolepsy Refreshing Sleep Attacks
Theres excessive daytime somnolence plagued by sleep Paralysis Yes Narcolepsy
attacks. Since REM latency is decreased the patients wake up Hypnagogic Scheduled Naps
refreshed. AS they fall asleep they lose all muscle tone Hypnopompic Stimulants
(cataplexy) and may be paralyzed upon waking. These events
are usually triggered by large sounds and emotional stressors.
While commonly associated with narcolepsy, both hypnaGOgic Insomnia
(when GOing to sleep) and hypnopompic hallucinations (on
waking up) can be experienced by anyone. People are going to >6 <6
Normal Sleep # of hours slept Insomnia
nap so its best to schedule naps and use stimulants to keep
them awake (amphetamines). Adjust 1) Sleep Hygiene
Sleep Schedule Recent - Avoid Stimulants
Travel - Sleep Schedule
3) Insomnia
A patient complaining of not sleeping enough or having Jet Lag - Sex + Sleep
Sleep Deprivation Reset - Phototherapy
troubling falling asleep has trouble with his/her sleep hygiene
Phototherapy - Routine
or an underlying psychiatric disorder producing insomnia. In - Avoid exercise, meals,
either case, the goal is long-term therapy to treat the underlying fluid, and naps
disease. Pharmacotherapy, when used, should be with short 2) Tx Underlying Dz
term sleep aids (benzos like Zaleplon/Zolpidem, Trazodone, or 3) Short-Term Benzos
even diphenhydramine compounds). Be aware of potential
dependence and adjust accordingly. The first step is to determine
the number of hours of sleep; if a patient sleeps 6-8 hrs just
adjust sleep time or investigate for OSA. If sleeping too little,
go after sleep hygiene. Avoid stimulants (caffeine, cocaine)
five hours before sleep, establish a sleep schedule
(programming the brain to sleep at a certain time), use
phototherapy (lights out = sleep), use the bed for sex and sleep
(dont read, watch TV, etc in bed), avoid exercise, large meals,
and fluid before sleep and avoid naps during the day (to ensure
being tired at bed time).

Psychiatry [SLEEP 1 - PARASOMNIA]

Stage EEG

Neuro Effect Drugs

Nightmares Night Terrors

Gynecology [ADNEXAL MASS]

Introduction Premenstrual Reproductive Postmenopausal

Much like vaginal bleeding, the most common and most
dangerous cause of adnexal masses changes based on the age. In Ovarian Cancer 11 Physiologic 51 Ovarian Cancer
the premenarchal group think cancer (germ cell). In the post GERM CELL Simple Cysts EPITHELIAL
menopausal group think cancer (epithelial). In the or
reproductive age group, where physiologic (simple) cysts can
occur, and where cycles, pregnancy, and infections occur, a Complex Cyst
more expansive differential exists. Regardless, all age groups
need a sonogram (ultrasound) if a mass is felt. Itll help us
distinguish a simple (smooth, small, like a balloon) versus a
complex (loculated, lobulated, large) cyst. The simple cyst
needs watchful management while a complex cyst requires Simple Cyst Complex Cyst
additional workup. Teratoma PID Abscess
Ectopic Torsion
Simple Cyst Endometrioma Cancer
A simple cyst represents a follicle of the corpus luteum thats
become fluid filled. It looks like a mass but is physiologic, not
pathologic. Itll present as an asymptomatic adnexal mass. The
ultrasound will show a simple cyst: smooth, continuous, and
small. Because follicles grow in response to FSH/LH, if we turn
off the axis with OCPs x 2 months the cyst should resolve on
its own. Resolution must always occur within 2 months, else its
designated complex regardless of appearance. If theres no
resolution, or the cyst occurred while she was already on
OCPs, or if its large (>7cm), its automatically a complex cyst Single, Fluid Filled, Loculated, Lobulated
and requires a CT scan. Homogenous Multiple Spaces

Complex Cyst Resolves in 2 months Resolution

A complex cyst can be anything. Often a mass is the <7cm > 7cm
presenting complaint. Lets use this opportunity to discuss some OCP at onset OCP at onset
topics that are pathologic and present as a mass.

Teratoma / Dermoid Cyst

The teratoma is a benign (in girls) germ cell tumor of the
ovary. Since its germ cell expect the patient to be young (<20).
Ovary Ovary
Shell complain of weight gain or increased abdominal girth.
The ultrasound will show a complex cyst which is often
enormous. Due to the weight its likely to cause the ovary to
twist about its vascular supply; its a risk factor for torsion.
Since its complex it must be removed. Cystectomy without
oophorectomy is the treatment of choice. Because its benign,
the patient is young, the chance for recurrence on the
contralateral side is high, and we dont want to put her into
menopause early we spare the ovary. Cyst (can be enormous)

Ectopic Pregnancy
A complex cyst may simply be an ectopic pregnancy. In a
patient with a history of salpingitis where inflammation may
have created a stricture, fertilized eggs cannot pass. Ectopics
most commonly occur in the ampulla. This is a botched
pregnancy. The patient will present with amenorrhea
(pregnant), lower abdominal pain (as the cyst grows), and
vaginal spotting. The ultrasound will Risk of Ectopic: 1%
Risk with previous ectopic: 15%
Risk with previous ectopic with salpingostomy: 15%
Risk with previous ectopic with salpingectomy: 15%

Gynecology [ADNEXAL MASS]

show a complex cyst and absent uterus. An elevation of the B-

HCG quant confirms ectopic. If there isnt a rupture a
salpingostomy is performed. If there is a rupture perform a
salpingectomy. In very select patients where the diagnosis is
made very early (<3.5cm and HCG<8000) and the patient is not
on Folate, methotrexate can be used. The risk of ectopic
pregnancy is about 1% in the general population. The risk with
previous ectopic, previous ectopic with ostomy, and previous
ectopic with gectomy are all 15%. This is discussed in greater
detail in the Obstetrics section. Retrograde Ectopic
Endometrioma / Endometriosis / Chocolate Cyst
Retrograde menses (presumed, unknown true cause) leaves
estrogen-sensitive endometrial tissue outside of the uterus. This
produces proliferation and hemorrhage with each cycle, leading
to many problems: dysmenorrhea, dyspareunia, and
infertility. A sonogram will show a complex cyst. It may be
anywhere: on the uterus, ovary, or even distant in the peritoneal
cavity. This often takes time to diagnose - as in weeks to
months. While a diagnostic scope with laser ablation (i.e.
laparoscopic exploratory laparotomy) is both diagnostically Anterograde Normal endothelial
superior and curative, its invasive. Usually, the goals to 1) turn Normal proliferation
off the axis with OCPs, continuous Leuprolide, or Progesterone
2) see symptomatic improvement 3) and only then go in for
surgery when suspicion is high enough.

Torsion of the Ovary

This wont be a diagnostic mystery as its a surgical emergency.
The suspensory ligament acts as a hinge that the ovary spins
around, cutting off its own vascular supply. Often, its the
weight of the cyst that causes torsion. There will be a severe
and sudden onset abdominal pain that was not provoked by any
inciting event. The sonogram will show a cyst, but cant tell if
the ovary is necrotic or not. The patient must be brought to the
OR immediately so the ovary can be untwisted. If the ovary
pinks up simply remove the cyst only. If the ovary is necrotic
remove the cyst and ovary.

Tubo-ovarian Abscess
This is discussed in gyn infections. Essentially - repeated acute
PID (Gc/Chla) causes inflammation and allows the vaginal
flora to access the uterus, tubes, and ovary. One consequence is
abscess. The patient will present with a fever, leukocytosis, and
an adnexal mass. The sonogram will show said abscess. Treat it
with antibiotics x 72 hrs and continue if theres improvement.
If not, the abscess needs to be drained. Indications to go to
emergent surgery for TOA is if the patient is very ill or if its
very large. TOA is one of the few abscess conditions that does
not require emergent drainage.

Ovarian Cancer
Any complex cyst can be cancer. Please see the Ovarian Cancer
section for details.

Gynecology [INTRO TO CANCER]

Mortality Incidence Incidence Mortality

GYN GYN Women Women

Locale Etiology Precancer Cancer Symptoms Screen


Human Papilloma Virus

sexually active females

Carcinoma In Situ
16 18 30s
6 11

screened Pap Smears

HPV 16,18,30 Dysplasia/CIS Squamous Cell

mass biopsy
clinically staged

CT scan

pap q3y 21 years old

abnormal pap reflexive colposcopy

biopsy endocervical curettage Ecto Endo
local destruction
Ecto Endo
ASCUS Anything but ASCUS
cone biopsy or a normal pap
repeat the pap q3month


Mets Negative

Precancer Cancer

Infections in a female can be either of the vagina or the cervix. Discharge Micro pH Abx
Candida Sticky white, Pseudohyphae 4 Anti-Fungals
Vaginal Infections adherent to (KOH prep) normal topical then
Patients with a vaginal infection come down to three diseases: wall oral
Candida, Gardnerella, and Trichomonas. The patient presentation Gardnerella Fishy odor, Clue Cells >5 Metronidazole
(Bacterial KOH, whiff (saline prep) Basic
is very nonspecific but involves pruritus, odor, and discharge.
Vaginosis) test
Nothing is very sensitive or specific from patient history so
Trich Yellow- Motile >5 Metronidazole
always do a pelvic exam and run some tests before treating. Green and Flagellated Basic Both partners!
Though its the best test, a culture often isnt necessary. Frothy (saline prep)
However do these in order: speculum exam, microscopic exam,
and then antibiotics. The microscopic exam should be of the
cervical mucous. There should be two samples on one slide - one
with normal saline the other with KOH.

Cervical Infections Speculum Wet Mount Cx Abx

Cervical infections come in three varieties: cervicitis, acute PID Exam
and chronic PID. All involve cervical motion tenderness. The
pathogenesis, organisms, and physical findings separate the
Only use a culture when your speculum and
1) Cervicitis Wet Mount/KOH are negative, otherwise, just
Cervicitis is essentially the same thing as a vaginal infection - treat by what you see!
including the same bugs. The difference is therell be cervical
motion tenderness, cervical discharge, but in the absence of
PID symptoms. Do a wet mount as well as a
Gonorrhea/Chlamydia PCR + treat accordingly.

2) Acute Pelvic Inflammatory Disease

Acute PID is essentially cervicitis plus. The distinction often Acute PID Chronic PID
isnt necessary except on a Board exam. Acute PID is caused by Cervicitis Tubo-Ovarian
gonorrhea or Chlamydia. There will be cervical motion + Abscess
tenderness and coital pain with cervical discharge. Essentially Salpingitis
assume the diagnosis by history and physical; treat with
antibiotics while Gc/Chla PCR is pending. Treat Gonorrhea with Ceftriaxone Amp-Gent x 72 H
ceftriaxone IM x 1 and Chlamydia with Doxy po x 14 days (Gonorrhea) Clinda or MTZ
(azithromycin can also be used). These are STDs, and because Doxycycline x 14 days I&D if no improvement
chronic PID (ectopic, tubo-ovarian abscess, infertility, and (Chlamydia)
chronic pain) is possible she should be educated towards safe sex
practice. Ampicillin Gentamycin
3) Chronic PID Tubo ovarian abscess
After repeated trauma to the cervix from Acute PID, vaginal
organisms are able to penetrate the mucosal barrier and get into
the should-be-sterile uterus. They create an ascending infection
with or without abscess. Chronic PID will present with chronic
abdominal pain and a pelvic mass. There will be cervical
motion tenderness and adnexal tenderness. Often theres fever.
Initially, assume theres no abscess and treat with Amp-Gen and
Metronidazole. This can be continued if theres improvement. If
Acute PID / Cervicitis Ceftriaxone
there isnt its time to investigate for an abscess. Use ultrasound
Gonorrhea and
or CT scan. An abscess can be drained percutaneously or with a
Chlamydia Doxycycline
colpotomy. If peritonitis, perform ex-lap (best
diagnosis/treatment for abscess).

Normal Vaginal Flora


Stress Incontinence
With multiple or large births the cardinal ligament gets bladder Abdominal pressure ( ) is
stretched. This weakens the pelvic floor and the bladder falls translated to both sphincter and
into the vagina - a high-grade cystocele. Basically, the sphincter bladder
of the bladder falls into the vagina, while most of the bladder
remains in the abdomen. In a normal patient abdominal pressure
is translated to both the bladder and the sphincter; the patient has
to relax the sphincter to void. In a cystocele, as abdominal
pressure increases its translated to the bladder but not the
sphincter. Thus, theres loss of urine with any increase in
abdominal pressure (cough, sneeze, tennis) but no loss any
Abdominal pressure ( ) is
other time. The diagnosis is made clinically: cystocele can be
translated to bladder only
seen on exam (physical) and there will be a rotation of the causing leak
urethra by more than 30o on the Q-Tip Test. No additional
testings required. Treatment begins with attempts to strengthen
the pelvic floor using pessaries and will eventually require
surgery (Burch, MMK, or anterior vaginal repair).
Normal Pressure-Volume Cystometry
This is the only form of urinary incontinence that is unique to Notice that pressure increases naturally
women. All others can be found in both men and women. as volume increases

Motor Urge or Hypertonic
The normal bladder fills with urine. At around 250cc theres the
urge to void. 500cc plus and it begins to hurt. The bladder does
not contract until the patient relaxes the sphincter and chooses to
void. In motor urge incontinence there are random detrusor
muscle contractions that occur at any time, randomly, and at all Volume
volumes. The patient can sense (urge) the contraction (motor)
and will have involuntary loss of urine day and night with Motor Urge Cystometry
frequent, insuppressible urges. The diagnosis can often be Spastic contractions at all
made clinically though cystometry will demonstrate volumes, low and high.
contractions at all volumes. All other testing (urinalysis, urine
culture, physical exam) are normal. Quell these contractions
with antispasmodics such as Solifenacin or other anti-
muscarinic drugs such as oxybutynin or propantheline.

Overflow or Hypotonic
Lesions of the spine or nerves of any kind (trauma, diabetic
neuropathy, multiple sclerosis) can induce overflow
incontinence. The patient loses sensory feedback indicating
fullness, and cant sense the urge to void. The patient may lose
the motor outputs that initiate bladder contractions, even if the
sensation of fullness is intact. Either way, the bladder gets
massively distended - filled with urine. Eventually, the intrinsic
Overflow Cystometry
stretch of the bladder muscles contracts against massive
No contractions occur, urine
pressure. A small amount of urine dribbles out, decreasing the leaks only at high volumes, at
pressure to just under critical. As the kidneys filter more urine very high pressures
the volume slightly increases to just over the critical pressure -
more urine leaks. Then theres a constant balance of just too



much and just under enough where the patient has

involuntary loss of urine day and night without the urge or
ability to void. Additionally, the bladder never empties.
Physical exam, urinalysis, and urine culture are normal.
Cystometry demonstrates absent detrusor contractions and an
always full bladder. To treat the condition we either need to
induce contractions with bithanechol with timed voids or use
regular and scheduled catheterization to relieve the pressure.
Some patients may have permanent foley or suprapubic
catheters in place.

Irritative Bladder
Some kind of inflammation (stones, infection, tumor) irritates
the lining of the bladder and produces contractions. Unlike
hypertonic, theyre suppressible. The patient will present with
the typical symptoms of urinary inflammation (i.e. a UTI):
urgency, frequency, and dysuria. A urinalysis will show
WBC. If leukocyte esterase, nitrates, or bacteria are seen its
infectious and a culture will speciate the organisms. If not,
cytology will help confirm or reject cancer. The medicine
section has lectures dedicated to UTI, Kidney Stones, and
cancer. Essentially, infection gets antibiotics, stones get
passed, lithotripsy or nephrostomy depending on their size,
and cancers need surgery. Be able to recognize the symptoms
of irritative bladder in OB/GYN and know that no cystometry is
needed; U/A and Urine culture are sufficient for the diagnosis.

Fistulas are epithelialized connections between one organ and
another. One such fistula can be from the bladder to any other
organ such as the vagina, rectum, or skin. Fistulas are caused by
inflammatory disease (such as Crohns) or with radiation
exposure (as in cancer treatment). Theres a permanent
connection without valve or sphincter between the bladder and
the connected organ. Thus theres a constant and continuous
leak of urine day and night. The dye tampon test can be used to
determine if theres a fistula or not. Dye injected into the bladder
will appear on a tampon in the vagina or rectum (or visually
seen leaking from the skin) indicating the fistulous tract.
Surgical repair is curative - a LIFT procedure, a fistulotomy.

Path Urine Nocturnal Patient Diagnosis Treatment

Stress Big babies Cough, Sneeze, No Cystocele Q-Tip Test Pessary
Incontinence Multiple Births Tennis Surgery
Motor Urge Detrusor Random Yes Insuppressible urges Cystometry Anti-Ach
Hypertonic Instability Day and Night medications
Overflow Spinal Lesions Dribble, Yes Involuntary loss, bladder Cystometry Bethanecol
Hypotonic Neuro dysfxn Day and Night never empties
Irritative Stones, Cancer U/F/D No Urgency, Frequency, Urinalysis Antibiotics
Bladder Infection, Dysuria Urine Culture Surgery
Fistula Radiation, Constant Leak Yes Constant leak Tampon Test Surgery,
Cancer, Crohn Fistulotomy

Gynecology [INFERTILITY]

inability to conceive after 1 year

Erectile Dysfunction
Erectile dysfunction night time tumescence Path:
psychological Dx:

Semen Analysis
sufficient number Insufficient, Dysfunctional Semen
sufficiently motile Path:
of conception
Gynecology [INFERTILITY]

Inhospitable Mucous
hostile mucous Path:

6cm smush test


fern sign sperm

Ovulation Issues
estrogen Pt:


1o rise of basal Tx:

endometrial biopsy
Anatomic Issues
progesterone level Path:

anovulatory Pt:
clomiphene pergonal

Hysterosalpingogram Endometriosis

diagnostic scope with laser ablation Idiopathic

unexplained fertility




Gynecology [MENOPAUSE]

Perimenopause menopausal

Premature ovarian failure

<40 What You Care About What You Do

bleeding cycles stop

Vaginal atrophy

estrogen creams

Hot Flashes

SSRIs venlafaxine
HRT endometrial cancer

Vit D3 + Calcium
Dexa scans



should not be
elevated FSH
Gynecology [MOLES]

Moles (aka Gestational Trophoblastic Disease)

Moles are not cancerous, but they are potentially premalignant
as choriocarcinoma may arise from Moles. Lets discuss the
precancer before getting to the cancer.

A complete mole is complete. Its a product of normal

fertilization, has a completely normal number of
chromosomes (46), and is completely molar; there are no fetal
parts. Its a product of a broken egg. One single sperm gets
inside one single egg, but that egg has no nucleus, so the sperm
spontaneously doubles its chromosomes. Though normal in the
number of chromosomes, it isnt normal in chromosome
complement; all the genetic material is of the sperm.

An incomplete mole is incompletely molar in that it contains Complete Mole Incomplete Mole
some fetal parts, doesnt have the normal number of
chromosomes (69), and is a product of two separate sperm Each letter represents 23 chromosome, S: Sperm, E: Egg
fertilizing one normal egg. Aside from the differences in
fertilization, genetic content, and presence of fetal parts, all
moles present the same way.

A mole grows faster, produces more B-HCG, and looks different

than a normal pregnancy on exam and ultrasound. That being
said, there are a couple of ways it can present. If the B-HCG is
Persistence of B-HCG
super high, much higher than for dates, or theres a size-date
suggests chorio
discrepancy (that is, its growing too fast), thats a sign of a
molar pregnancy. Because the B-HCG is elevated so high and
B-HCG looks like TSH, the patient may present with
hyperthyroidism. But B-HCG also causes morning sickness,
presenting with nausea and vomiting in the first trimester. Too
much B-HCG causes Hyperemesis Gravidarum - a severe,
dehydrating morning sickness or one that lasts beyond the first Normal return to baseline
trimester. A pelvic exam may demonstrate a grape-like mass in
the vagina. Finally, that grape-like mass looks like a snowstorm
on an ultrasound, which is how its diagnosed. Its not normal;
the only way to get rid of it is to cut it out with suction

Track the HCG weekly to assure it was all gotten. It should

decline linearly. Put her on OCPs to prevent pregnancy; if she
gets pregnant its impossible to sure if its a molar or regular

Any pregnancy, molar or regular, can result in a cancer:
Choriocarcinoma. Its a cancer of gestational contents. After a
miscarriage, normal delivery, or molar pregnancy, if theres
elevation of the B-HCG or its symptoms (listed above), suspect
chorio. Diagnose it with an ultrasound first, cut it out with a
curettage, and stage it with a CT scan. The treatment is with
Methotrexate. More severe forms can be treated with the
addition of Actinomycin D (dactinomycin) and


Ovarian cancer is the leading cause of reproductive aged Germ Cell
- Dysgerminoma LDH, Chemo Presents in Stage I
cancer death. This is because theres no good screening tool Pre-menopausal
- Endodermal Sinus AFP
for ovarian cancer; it often presents as Stage III or worse when Markers as to the left
- Choriocarcinoma B-HCG
trying to screen. Because its in the pelvis there are no structures - Teratoma or Struma Ovarii Unilateral Oophorectomy
to bump against and plenty of room to grow before becoming Chemo
symptomatic. However, it isnt as simple as ovarian cancer;
there are many subtypes. You need to be able to visualize the
cross-section of an ovary, know which tumors come from which
type of cell, and recognize the presentation of each. Stromal Tumors
- Sertoli-Leydig Testosterone
Epithelial Ovarian Cancer - Granulosa-Theca Estrogen
When we talk about the highest mortality and late presentation,
what we really mean is epithelial ovarian cancer. With
repeated trauma of ovulation comes inflammation.
Inflammation leads to cancer. The more ovulations, the higher
the risk. Therefore, its not surprising this shows up in an older Epithelial
- Serous Cystadenocarcinoma
(post-menopausal) patient. Likewise, states that increase
- Mucinous Cystadenocarcinoma
ovulations (low parity, delayed child bearing, early - Endometroid Cystadenocarcinoma
menarche) increase risk. Other risk is genetic (HNPCC, - Brenner tumor
BRCA1 > BRCA2), while having children and 5 year OCP is
protective. Epithelial cancer spreads by peritoneal seeding and
remains asymptomatic until its too late, presenting with renal
Presents in Stage III
failure, small bowel obstruction, and ascites. An ultrasound Post-menopausal
or CT scan confirms diagnosis and stages the cancer, while CA-125
remission can be tracked with CA-125 levels. Since its often Transvaginal Ultrasound
Stage III, the only option is debulking surgery (TVH+BSO) TVH+BSO Paclitaxel
followed by chemo with a platinum-based drug such as
paclitaxel. For women at super-high risk (BRCA1 ) screening
can be done with annual Ca-125 and transvaginal ultrasound. Adnexal Mass
After shes done having kids a prophylactic BSO @ 35 will
prevent the need for screening. Screening the general population
doesnt work since it detects cancer at Stage III or worse. Transvaginal
Germ Cell Cancer
Unlike the malignant epithelial cancer that occurs in post- Smooth Balloon Cystic
Small Multiple Echoes
menopausal women, germ cell tumors occur in teenage
reproductive girls and are often benign. These tumors usually
get big before they get dangerous and are often found at Stage I. Simply Cyst Complex
A mass may be palpated then confirmed on transvaginal Cyst
ultrasound. Just as in testicular cancer, there are multiple types,
with each followed by a given tumor marker. In girls a
teratoma is usually benign, and the chemoreceptive cancer is Age, Biopsy
Dysgerminoma. Because theyre usually benign, Stage I, and
present in a young girl, treatment is conservative (unilateral
oophorectomy) because we want her to grow and have kids!
Germ Epithelial
Cell Cell

Unilateral Aggressive
Oophorectomy TVH + BSO


ovarian arteries
uterine arteries

joins the renal vein on the left

the vena cava directly on the right

ligament of the ovary

Ovarian Torsion

common iliac external

iliacs femoral arteries

internal iliacs
uterine arteries

Management of Post-Partum Hemorrhage


Suspensory ligament of the ovary

Uterosacral Ligament


Cardinal Ligament of the Uterus

Uterine Prolapse

Pelvic Floor Relaxation


Introduction Visual Ultrasound

For a girl whos never had a period both her anatomy and the Axis Anatomy
axis must be investigated. The diseases can be differentiated Breast Uterus Disease Diagnosis
based on the table to the right. Lets review embryology as we Imperforate Hymen Visual Inspection
highlight the 4 major need-to-know diseases for the shelf / step. Anorexia/Weight Loss History
Pregnant before period UPT / B-HCG
Mullerian Agenesis Mullerian Agenesis Testosterone and
The Mullerian ducts create the tubes, uterus, and the upper Testicular Feminization Karyotype
third of the vagina. If they fail to form the girl will still be Cranipharyngioma
genetically XX (female), so will have normal primary and Kallmann
normal secondary sex characteristics (the ovaries are working Turner
great), but shell have no uterus. She can never have children Enzymatic deficiency N/A
and will never bleed. However, to increase satisfaction with sex beyond our scope
elevate the vagina to increase the length. This is considered a
Breast Uterus disease. This is differentiated from
testicular feminization based on the karyotype (XX) and (X,O), Turner
testosterone level (normal).
(X,X) Ovaries E+P Breasts
Testicular Feminization
A male genotype expresses mullerian inhibitory factor as well
(X,Y) Mullerian Vulva/Vagina/Clitoris
as testosterone. In this disease testosterone is made fine, but
MIF Ducts
theres an insensitvity to testosterone by the body. Thus,
despite having testes, the primary and secondary sex Mullerian MIF = Uterus,
characteristics are as if there was no testosterone - she appears Agenesis Tubes, Vagina
totally female. MIF works perfectly and inhibits the mullerian
ducts (see above). Shell never have children or ever bleed. Its Uterus (X,Y) Testes Testosterone = Penis, Scrotum
also imperative to elevate the vagina in this patient we did in Testicular Feminization
mullerian agenesis. Theres also the issue of the testes perform Testes = No Ovaries
an orchiectomy to prevent testicular cancer. Do this after age
20 (i.e. after puberty) to allow her to develop normally. This is
considered a Breast Uterus disease. This is differentiated
from Mullerian Agenesis by the karyotype (XY) and
testosterone level (elevated). Normal Axis Kallmans Turners

Turner Syndrome
Hypothalamus Hypothalamus Hypothalamus
A genetic abnormality (X,O) that causes the production of
E+P GnRH ? ? GnRH
streak ovaries. Patients are female with intact primary sex
characteristics and mullerian structures ( uterus). But, in Ant Pit Ant Pit Ant Pit
the absence of estrogen shell never develop secondary sex
characteristics. Shell also have a broad, shield-shaped chest
with wide spaced nipples and a webbed neck. Lacking both Ovary Ovary Ovary
Estrogen and Progesterone, treat by giving them what they dont E+P ? ?
have (estrogen and progesterone) to induce puberty. Also
investigate for cardiac abnormalities with an Echo Endometrium Endometrium Endometrium
(transposition). In this disease, the FSH and LH will be high as
1. Kallmann: Absent hypothalamus cant drive any endocrine
the normal pituitary tries to drive the production of estrogen and
function, so FSH and LH are low.
progesterone. Karyotype confirms.
2. Turner: Absent ovaries cant make E+P, so no signal to turn
Craniopharyngioma and Kallmann Syndrome off FSH and LH is present
Lesions of the hypothalamus will cause the entire axis to shut
down. GnRH is low, FSH/LH are low, and estrogen and All girls should develop menarche by age 16
progesterone are low. The anatomy is fine and intact (shes
All girls should develop secondary sex char by age 14
female on the outside as well as inside), but the absence of
Girls who have not met age get reassurance
endocrine effects leaves the girl without secondary sex
Girls who have not met milestones by age, get worked up
characteristics. Kallmann syndrome is a defunct hypothalamus
despite a normal FSH and LH. Anosmia and Primary
amenorrhea gives the diagnosis away.


If a woman is within her reproductive age and was having Disease State Test Treatment
periods that have since stopped for > 6 months shes said to 1. Pregnancy UPT Prenatal Care
have secondary amenorrhea. Most OBs wont wait 6 months to 2. Thyroid TSH Levothyroxine
decide if shes pregnant so diagnostic intervention can begin 3. Prolactin Prolactin Surgery or
after just 2 cycles, even 1 for UPT. In general, the workup
4. Medications Prolactin Switch or D/C
begins with the three most common causes (pregnancy,
thyroid, and prolactin) then proceeds in reverse order of how the
HP axis is set up; beginning with the endometrium, then the
ovary, then the anterior pituitary with the hypothalamus as the Hypothalamus 5. Diagnosis of Exclusion
diagnosis of exclusion. The chart and diagram to the right give
an overview of the topics discussed and the order in which they
should be investigated. The next page has an algorithm that can Ant Pit 4. MRI
be used to work up a patient with secondary amenorrhea.

Pregnancy Ovary 3. FSH/LH and U/S

The most common cause of 2o amenorrhea is pregnancy. Get a
UPT to rule out pregnancy in every patient every time. There is Endometrium 2. Estrogen and Progesterone
a section called OB for this condition. 1. Progestin Challenge

Thyroid Disease See the correlation to the algorithm on the next page
While both hyper and hypo thyroidism can cause absence of
bleeding or too much bleeding, its usually
Hypothyroid that causes thereby inhibiting GnRH
that leads to the amenorrhea. During the first visit we screen
with a TSH alongside the UPT. If the TSH is elevated she needs
synthroid (see medicine, endo).
TRH Hypothalamus GnRH
Pituitary Tumor (Prolactinoma)
While a tumor of the anterior pituitary can either cause crush
Ant Pituitary Prolactin Dopamine Dopa
syndrome ( ), bleed (apoplexy), or die
(Sheehans), its more likely that an otherwhise healthy woman Antag
would develop amenorrhea from a tumor that produces Ovary LH
prolactin erroneously (the first free would make her much T4
sicker than just stopped bleeding). Just as in thyroid disease,
elevated prolactin will inhibit the axis and turn off her cycle. It Endometrium
doesnt matter how you get prolactin; if you have theres too
much it messes with the axis. Sucpect prolactinoma if
galactorrhea and amenorrhea. Screen her prolactin level and Means inhibits
get an MRI if its elevated. The options are bromocriptine if Means stimulates
small or surgery if large or desires pregnancy. See medicine,
endo. Red

Anything that inhibits dopamine (aka Prolactin-Inhibiting
Factor) will disinhibit prolactin. Unrestrained prolactin acts
just like a prolactinoma (i.e. prolactinemia), presenting with
galactorrhea and amenorrhea. Switch medications (typically
a typical for an atypical antipsychotic) or add bromocriptine. If
its the medication that could be the culprit theres no need for
an MRI if youve found prolactinemia!


If menopause occurs in a woman <40 years old its pathologic. 2o Amenorrhea
Unfortunately, nothing can be done for her. Menopause is
menopause and there are no more cycles for her. The typical
findings of menopause will be present ( and ) and
absent follicles on ultrasound. Prolactin

Savage Syndrome = Resistant Ovary Syndrome

This is effectively menopause. Its caused by an FSH-R
insensitivity. The FSH and LH will be elevated trying to induce
ovulation (just like in menopause) but nothing will happen. An Prolactinemia Thyroid Pregnant
ultrasound will show many follicles (shes NOT in menopause Levothyroxine Prenatal Care
yet). Try giving HRT to achieve pregnancy but this is
generally considered menopausal; theres no treatment or MRI
procedure to be done. Progestin
Drugs Challenge
Ashermans Syndrome
Scarring and fibrosis of the endometrium prevents the Prolactinoma
endometrium from developing properly, and, if nothing grows,
nothing can slough off. Its an unresponsive endometrium.
Shes hormonally intact (FSH and LH induce estrogen, ? Anovulation
ovulation, and progesterone), but she is anatomically deficient.
PCOS workup
This is a product of vigorous D+C (and is a complication of
Estrogen and
elective abortions). It can also be done on purpose with
endometrial ablation to help patients with menometrorrhagia
who are no longer interested in pregnancy. Dont forget to check
their surgical history!

There isnt a test for the hypothalamus; its diagnosis by Endometrial
Dysfxn ?
exclusion. All endocrine function begins there. While its
determined by exclusion something can likely be elicited from Supportive
the history thatd allow for reassurance if TSH, UPT, and
Prolactin are negative. If the woman has experienced anorexia
or extreme weight loss / exercise, that might induce
amenorrhea. Emotional stress might have her miss a single cycle FSH, LH
Ovaries Ovaries
(bringing her in to check for pregnancy), but it shouldnt cause and Ratio
prolonged cycle loss.

Algorithm: Ultrasound MRI Brain

1. Is it the common stuff?
(UPT, TSH, Prolactin, Meds)
2. Is the endometrium ready to bleed?
(Progestin Challenge)
3. Is the endometrium capable of bleeding?
(Estrogen and Progesterone)
Menopause Resistant Pituitary Hypothalamus
4. Is there a signal coming from the
pituitary? (FSH and LH) Symptom Relief Bromocriptine Weight Gain
5a. Is there a problem with the anterior Symptom Relief Surgery Emotional Stress
pituitary? (MRI)
5b. Are there follicles? (U/S)
6. All has been negative - Hypothalamus


>1500 <1500

Does Not Double Doubles

No heart tones
Zygote < 3cm
+ Ruptured HCG < 8000
No Folate
- Ruptured

Systemic Causes and Coagulopathy

Not relevant to this discussion of Anatomy, DUB, and PCOS, but
important to mention none-the-less - uterine bleeding may have
nothing to do with an abnormal uterus at all. If the woman has
normal cycles but some other reason to bleed, she may bleed too
much or too often. These include coagulopathies,
thrombocytopenia, von Willebrand, liver, or renal diseases. Well
stay focused on the uterus for this discussion.

Structural Abnormalities
Structural lesions are a common cause of uterine bleeding. Of
them, Fibroids are by far the most common. While theres much
to know about each disease, focus on three: adenomyosis,
fibroids, and polyps.

Leiomyoma, better known as fibroids, are benign growths of the
myometrium. Theyre estrogen-responsive and non-malignant.
The patient may present as an asymptomatic mass on physical
exam, they may bleed and cause anemia, they may cause
infertility (implantation compromised), or they may present with
pain. Make the diagnosis first with transvaginal ultrasound.
The best radiographic test is an MRI, though routine cases dont
require an MRI. DONT biopsy fibroids. Treatment is dependent
on what mom wants. If mom wants children, a myomectomy is
performed (scoop out the fibroid). If she doesnt, then perform a
total abdominal hysterectomy. If the fibroid is too large for
surgery, give leuprolide (continuous) until the fibroids shrink,
then go to surgery.

Adenomyosis is a symmetrical smoothed uterus thats filled
with normal uterine tissue; generally stromal and glandular
epithelium. The classic form of adenomyosis, diffuse
adenomyosis, is the one most often tested. The physical exam will Focal Adenomyosis and Leiomyoma are essentially
reveal an enlarged smooth uterus. The diagnostic test and indistinguishable except on pathology of surgical specimens.
treatment are essentially identical to Fibroids, the goal being
reduction in bleeding and pain. The only difference is that they
dont have a layer of connective tissue that easily defines the
plane of adenomyosis (unlike fibroids, which does), making
residual disease the cause of most treatment failure.

These structural causes of vaginal bleeding do not present with an
abnormal physical exam. They present very similarly to
Adenomyosis and Leiomyomas, but have a normal exam.
Diagnostic tools involve the transvaginal ultrasound, saline
infusion sonography, and hysteroscopy. Polyps should be
surgically excised (DONT treat with NSAIDs, OCPs) via
hysteroscopic polypectomy.


Dysfunctional Uterine Bleeding

This is the diagnosis of exclusion. Once all organic causes have
been ruled out, the woman can be diagnosed with DUB. Most of Ovulatory DUB is a thing, but is rare. Dont learn about it
DUB is caused by anovulation. If ovulation doesnt occur,
progesterone isnt produced, and the proliferative endometrium
continues to grow until it outgrows its blood supply. Endometrial
vessels become markedly dilated and unstable. Since theyre
dilated (prostaglandin effect), the bleeding can be severe.

Abnormal periods - whether meno, metro, or menometrorrhagia -

are normal near menarche and menopause.

Even if there isnt diagnosed DUB, if there is life-threatening

bleeding use IV estrogen (and taper to OCPs). If the bleeding
continues despite estrogen, surgical ligation or embolization of
arteries may be required. Ultimately, a hysterectomy is curative.

For most cases of DUB, treatment centers on NSAIDs and OCPs.

NSAIDs is a bit of a weird one because generally you should
consider NSAIDs to worsen bleeding by inhibiting platelets. And
yet, NSAIDs can adequately treat DUB - especially if started at
the onset of menses. For more chronic control, OCPs are the drug
of choice. They provide contraception, reduction in
dysmenorrhea, and control bleeding. There are also procedures
that can control bleeding such as endometrial ablation or Levonorgestrel-releasing intrauterine system (Mirena) is
elective TAH (even if the bleeding isnt severe). essentially equivocal to OCPs in all ways.

Polycystic Ovarian Syndrome

One particular cause of anovulation is PCOS, whereby the ovary
is replaced by thousands of atretic follicles. These follicles cant
produce progesterone, so they produce large amounts of estrogen.
Thats then converted to testosterone, which makes these women
hirsute. Look for the woman who is fat and hairy, maybe with
a deep voice, who has irregular menses and trouble getting
pregnant. This is an endocrine diagnosis; an ultrasound ISNT
required. Even still, often the test will show an ovarian
ultrasound with lots of little black circles, representing cysts. To
make the diagnosis, instead use the LH/FSH > 3, and make a
metabolic diagnosis of diabetes (with the 2-hour glucose
tolerance test) and dyslipidemia. Levels of testosterone
(elevated in PCOS) and DHEAS (normal in PCOS) arent
necessary if theres no evidence of virilization, but are often
obtained to rule out other causes of hirsutism.

Once diagnosed, the mainstay of therapy is OCPs to reset the axis

and to reduce anovulation. Metformin treats the diabetes but also
reduces circulating androgens, making the effects of PCOS less
severe. You may also see patients on Spironolactone for its
androgen-receptor antagonism, further reducing the symptoms of
hirsutism. Finally, if the woman wants to become pregnant,
facilitation with clomiphene or pergonal can induce ovulation.
The risk is multiple pregnancies.


reproductive aged females

21-35 days Premenstrual Reproductive Postmenopausal

metrorrhagia premenarchal

premenarchal foreign bodies

sexual abuse speculum Development Normal Age
exam under anesthesia

post menopausal cancer

endometrial sampling

reproductive aged female


fusion of the growth plates

8 years old
Wrist X-ray
stimulation test central precocious
puberty MRI

constitutional continuous

ultrasound ovaries adrenals

estradiol DHEAS
17-OH-Progesterone Resect tumors
corticosteroids cysts alone.
+ -

Cancer Lesion Diagnosis Symptoms Treatment


Hirsute Virilization

fat and hairy

Ovaries Adrenals