I.

CLIENTS PROFILE

Name: Nurkis Suhaili

Age: 44 years old
Birth Date: September 12, 1971
Address: Atilano Drive, Baliwasan, Zamboanga City
Sex: Female
Status: Married
Occupation: Housewife
Educational Attainment: High School Graduate
Ethnic Group: Tausug
Dialect: Tausug, Tagalog
Religion: Islam
Medical Diagnosis: Stroke
Past History: Hypertension
Present Illness: Stroke

II.

GORDONS ELEVEN FUNCTIONAL HEALTH PATTERN

1. Health Perception Health Management Pattern
The client verbalized her difficulty in doing things since her right
arm cannot be moved after visiting Ciudad Medical Zamboanga last March
2015 where she was diagnosed with Stroke with a blood pressure of
160/100 mmHg. She also said that before having a stroke she used to do
household chores but she had to stop because of her condition. She is
taking medications like Coumadin and Losartan to help with her stroke.
2. Nutritional Metabolic Pattern
The client verbalized that she only eats fish, rice and non-green
leafy vegetables which was advised to her by the physician. She used to
eat green leafy vegetables before her stroke. She usually drinks water and
milk and stopped drinking carbonated drinks and coffee after being
diagnosed with stroke. She feels like she lose weight since she was more
heavier before but she does not know her specific weight.
3. Elimination Pattern
The client verbalized that she defecates after every two days
without any pain and difficulty. She urinates five times a day without any
pain and does not take any medication for bowel movement.
4. Activity Exercise Pattern
The client verbalized that she had sufficient energy before the
stroke and gets easily tired nowadays. She watches television during
her spare time. She does flexion for her right arm and tries to walk
around the house with the use of a cane as a form of exercise. She is
usually visited by a reflexologist to massage her right arm.
Clients perceived ability for the following is:
Feeding
Dressing

0
0

Home Maintenance 3
General Mobility
3

Cooking

Bed Mobility

Toileting

Bathing

Grooming
Shopping

0
3

5. Sleep Rest Pattern

The client sleeps at 8 or 9 in the evening and wakes up at
5:30 in the morning. She does not have any nightmares.

6. Cognitive Perception Pattern

The client verbalized that she has difficulty reading smaller
font sizes but she does not wear a glasses. She has no difficulty in her
hearing and changes in memory.

7. Self-Perception Self-Concept Pattern

The client feels sad that she cannot do a lot of things
inside the house because of her condition.
8. Role Relationship Pattern
The familys structure is a nuclear type with six children,
four boys and two girls, and the parents. They communicate with each
other in Tausug. The breadwinner is the husband and provides sufficient
money for the needs of the family.
9. Sexuality Reproductive Pattern
The client is a female who had her menarche during her
elementary years. She has six children and had no abortions,
10. Coping Stress Tolerance Pattern
The client has problems about her children since some
prefer to be absent which makes her scold them.
11. Value Belief Pattern
The client is following the Islamic religion and considers
her children as the most valuable in life since she wants them to finish
their studies and become successful in the future.

III.

COMPREHENSIVE CASE ANALYSIS

STROKE
A stroke is a "brain attack". It can happen to anyone at any time. It occurs when
blood flow to an area of brain is cut off. When this happens, brain cells are
deprived of oxygen and begin to die. When brain cells die during a stroke,
abilities controlled by that area of the brain such as memory and muscle control
are lost.
How a person is affected by their stroke depends on where the stroke occurs in
the brain and how much the brain is damaged. For example, someone who had a
small stroke may only have minor problems such as temporary weakness of an
arm or leg. People who have larger strokes may be permanently paralyzed on
one side of their body or lose their ability to speak. Some people recover
completely from strokes, but more than 2/3 of survivors will have some type of
disability.

PATHOPHYSIOLOGY
Cerebral Blood Flow
Normal cerebral blood flow (CBF) is approximately 50-to 60 ml/100g/ Min and
varies in different parts of the brain. In response to ischemia, the cerebral auto
regulatory mechanisms compensate for a reduction in CBF by local
vasodilatation, opening the collaterals, and increasing the extraction of oxygen
and glucose from the blood. However, when the CBF is reduced to below 20
ml/100g/min, an electrical silence ensues and synaptic activity is greatly
diminished in an attempt to preserve energy stores. CBF of less than
10ml/100g/min results in irreversible neuronal injury.
Mechanisms of Neuronal Injury
Formation of microscopic thrombi responsible for impairment of microcirculation
in the cerebral arterioles and capillaries is a complex phenomenon. Formation of
a micro thrombus is triggered by ischemia-induced activation of destructive
vasoactive enzymes that are released by endothelium, leucocytes, platelets and
other neuronal cells. Mechanical plugging by leucocytes, erythrocytes, platlets
and fibrin ensues. At a molecular level, the development of hypoxic- ischemic
neuronal injury is greatly influenced by overreaction of certain eurotransmitters,
primarily glutamate and aspartate. This process called excitotoxicity is triggered
by depletion of cellular energy stores. Glutamate, which is normally stored inside
the synaptic terminals, is cleared from the extracellular space by an energy
dependent process. The greatly increased concentration of glutamate (and
aspartate) in the extracellular space in a depleted energy state results in the
opening of calcium channels associated with N-methy1-D-asapartate (NMDA)
and alpha-amino-3-hydroxy-5-methyl-4-isoxanole propionate (AMPA) receptors.
Persistent membrane depolarization causes influx of calcium, sodium, and
chloride ions and efflux of potassium ions. Intracellular calcium is responsible for
activation of a series of destructive enzymes such as proteases, lipases, and
endonucleases that allow release of cytokines and other mediators, resulting in
the loss of cellular integrity. Inflammatory response to tissue injury is initiated by
the rapid production of many different inflammatory mediators, tumor necrosis
factor being one of the key agents. Leukocyte recruitment to the ischemic areas
occurs as early as thirty minutes after ischemia and reperfusion. In addition to
contributing to mechanical obstruction of microcirculation, the leucocytes also
activate vasoactive substances such as oxygen free radicals, arachidonic acid
metabolites (cytokines), and nitric acid. The cellular effects of these mediators
include vasodilatation, vasoconstriction, increased permeability, increased
platelets aggregation, increased leukocyte adherence to the endothelial wall, and
immune-regulation. Endothelial cells are one of the first cell types to respond to
hypoxia. This response occurs at morphological, biochemical and immunological
levels, causing a variety of physiological and pharmacological effects.
Morphologically, endothelial cells swell and form microvilli at the luminal surface
of the cell. This results in a reduction in the luminal patency of the capillary
vessel. Mechanical plugging by erythrocytes, leukocytes, and platelets ensues.
At a biochemical level, endothelial cells mediate the effects of vasoactive agents
5

such as endothelin peptides, eicosanoids, and smooth muscle relaxant (probably

nitric acid), which in part modulate the vascular tone of the microcirculation.
Activation of endothelial adhesion molecules promotes leukocyte adherence to
the endothelial wall, a key process in the initiation of the inflammatory process.
Ischemic Penumbra (IP)
Within an hour of hypoxic- ischemic insult, there is a core of infarction
surrounded by an oligemic zone called the ischemic penumbra (IP) where
autoregulation is ineffective. The critical time period during which this volume of
brain tissue is at risk is referred to as the window of opportunity since the
neurological deficits created by ischemia can be partly or completely reversed by
reperfusing the ischemic yet viable brain tissue within a critical time period (2 to 4
hours?). IP is characterized by some preservation of energy metabolism because
the CBF in this area is 25% to 50% of normal. Cellular integrity and function are
preserved in this area of limited ischemia for variable periods of time. The
pathophysiology of IP is closely linked to generation of spontaneous waves of
depolarization (SWD). SWD can originate from multiple foci; some from the
ischemic core and others form ischemic foci within the peri-infarct zone
(penumbra). Sustained increases of synaptic glutamate and extracellular
potassium ions are closely associated with the development of SWD. Glutamate
receptor antagonists that block transmembrane calcium flux and prevent
intracellular calcium accumulation are known to suppress SWD. Hypoxic or rapid
depolarizations eventually supervene just before irreversible neuronal death.
Neuronal Death
The two processes by which injured neurons are known to die are coagulation
necrosis and apoptosis. Coagulation necrosis (CN) refers to a process in which
individual cells die among living neighbor cells without eliciting an inflammatory
response. This type of cell death is attributed to the effects of physical, chemical,
or osmotic damage to the plasma membrane. This is in contrast to liquefaction
necrosis, which occurs when cells die, leaving behind a space filled by
inflammatory response or pus. In CN, the cell initially swells then shrinks and
undergoes pyknosis a term used to describe marked nuclear chromatin
condensation. This process evolves over 6 to 12 hours. By 24 hours extensive
chromatolysis occurs resulting in pan-necrosis. Astrocytes swell and fragment,
myelin sheaths degenerate. Irreversible cellular injury as demonstrated by
eosinophilic cytoplasm and shrunken nuclei are seen between 8 to 12 hours after
arterial occlusion (91). The morphology of dying cells in coagulation necrosis is
different than that of cell death due to apoptosis. The term apoptosis is derived
from the study of plant life wherein deciduous trees shed their leaves in the fall.
This is also called programmed cell death, because the leaves are programmed
to die in response to seasonal conditions. Similarly, cerebral neurons are
programmed to die under certain conditions, such as ischemia. During
apoptosis, nuclear damage occurs first. The integrity of the plasma and the
mitochondrial membrane is maintained until late in the process. Ischemia

activates latent suicide proteins in the nuclei, which starts an autolytic process
resulting in cell death. This autolytic process is mediated by DNA cleavage.
Apoptotic mechanisms begin within 1 hour after ischemic injury whereas CN
begins by 6 hours after arterial occlusion. This observation has an important
bearing on future directions of research. The manner by which apoptosis evolves
is a focus of much research, because, hypothetically, neuronal death can be
prevented by modifying the process of DNA cleavage that seems to be
responsible for apoptosis.
Ischemic Stroke
The three main mechanisms causing ischemic strokes are: (a) thrombosis, (2)
embolism and (3) global ischemia (hypotensive) stroke. All ischemic strokes do
not neatly fall into these categories and the list of entities responsible for unusual
stroke syndromes is very long. However, strokes caused by vasospasm
(migraine, following SAH, hypertensive encephalopathy) and some form of
arteritis stand out among the more infrequent causes
of stroke. Thrombosis Atherosclerosis is the most common pathological feature
of vascular obstruction resulting in thrombotic stroke. Atherosclerotic plaques can
undergo pathological changes such as ulcerations, thrombosis, calcifications,
and intra-plaque hemorrhage. The susceptibility of the plaque to disrupt, fracture
or disrupt or ulcerate depends on the structure of the plaque, and its composition
and consistency. Disruption of endothelium that can occur in the setting of any of
these pathological changes initiates a complicated process that activates many
destructive vasoactive enzymes. Platelet adherence and aggregation to the
vascular wall follow, forming small nidi of platelets and fibrin. Leucocytes that are
present at the site within 1 hour of the ictus mediate an inflammatory response.
In addition to atherosclerosis, other pathological conditions that cause thrombotic
occlusion of a vessel include clot formation due to hypercoagulable state,
fibromuscular dysplasia, arteritis (Giant cell and Takayasu), and dissection of a
vessel wall. In contrast to the occlusion of large atherosclerotic vessels, lacunar
infarcts occur as a result of occlusion of deep penetrating arteries that are 100 to
400 mm in diameter and originate for the cerebral arteries. The putamen and
pallidum, followed by pons, thalamus, caudate nucleus, and internal capsule are
the most frequently affected sites. The size of a lacunar infarct is only about 20
mm in diameter. The incidence of lacunar infarcts is 10% to 30% of all strokes
depending on race and preexisting hypertension and diabetes mellitus. The small
arteriole, most frequently as a result of chronic hypertension lengthens, becomes
tortuous and develops subintimal dissections and micro-aneurysms rendering the
arteriole susceptible to occlusion from micro-thrombi. Fibrin deposition resulting
in lipohyalinosis is considered to be the underlying pathological mechanism.

 Embolism
Embolic stroke (ES) can result from embolization of an artery in the central
circulation from a variety of sources. Besides clot, fibrin, and pieces of
atheromatous plaque, materials known to embolize into the central circulation
include fat, air, tumor or metastasis, bacterial clumps, and foreign bodies.
Superficial branches of cerebral and cerebellar arteries are the most frequent
targets of emboli. Most emboli lodge in the middle cerebral artery distribution
because 80% of the blood carried by the large neck arteries flow through the
middle cerebral arteries. The two most common sources of emboli are: the
leftsided cardiac chambers and large arteries, (e.g. artery to artery emboli that
result from detachment of a thrombus from the internal carotid artery at the site of
an ulcerated plaque). The neurological outcome from an ES depends not only on
the occluded vascular territory but also on the ability of the embolus to cause
vasospasm by acting as a vascular irritant. The vasospasm can occur in the
vascular segment where the embolus lodges or can involve the entire arterial
tree. Vasospasm tends to occur in younger patients, probably because the
vessels are more pliable and less atherosclerotic. Many embolic strokes become
hemorrhagic causing hemorrhagic infarction (HI). Hemorrhagic infarct (used
here synonymously with hemorrhagic transformation of an ischemic infarct) is an
ischemic infarct in which bleeding develops within the necrotizing cerebral tissue.
The pathogenesis of hemorrhagic transformation of a pale infarct is a complex
phenomenon. The two common explanations that are advanced to explain the
pathogenesis of HI in embolic strokes are: (1) Hemorrhagic transformation
occurs because ischemic tissue is often reperfused when the embolus lyses
spontaneously and blood flow is restored to a previously ischemic area. An initial
vascular obstruction is likely to occur at a bifurcation of a major vessel. The
occlusion may obstruct one or both of the branches, producing ischemia of the
distal tissue. Blood vessels as well as brain tissue are rendered fragile and
injured. When the occluding embolus either lyses spontaneously or breaks apart
and migrates distally, CBF is restored to the injured or ischemic icrocirculation.
This can result in a hemorrhagic or red infarct in what had previously been a
bloodless field. The areas that continue to be poorly perfused are referred to as
pale or anemic infarcts. (2) Hemorrhagic transformation is also known to occur
with persistent occlusion of the parent artery proximally, indicating that
hemorrhagic transformation is not always associated with migration of embolic
material. HI on the periphery of infarcts in presence of persistent arterial
occlusion is caused by reperfusion from leptomeningeal vessels that provide
collateral circulation. In patients with ES, it is not unusual to see HI side-by-side
with ischemic infarction. The three main factors associated with red infarcts or
hemorrhagic infarctions include the size of the infarct, richness of collateral
circulation, and the use of anticoagulants and interventional therapy with
thrombolytic agents. Large cerebral infarctions are associated with a higher
incidence of hemorrhagic transformation. Hypertension is not considered to
be an independent risk factor for hemorrhagic transformation of an ischemic
infarct.

 Global Ischemic or Hypotensive Stroke

Profound reduction in systemic blood pressure due to any reason is responsible
for hypotensive stroke. Some neurons are more susceptible to ischemia than
others. These include the pyramidal cell layer of the hippocampus and the
Purkinje cell layer of the cerebellar cortex. Cerebral gray matter is also
particularly vulnerable. Abundance of glutamate in these neurons renders them
more susceptible to global ischemia. Global ischemia causes the greatest
damage to areas between the territories of the major cerebral and cerebellar
arteries known as the boundary zone or watershed area. The parietaltemporal-occipital triangle at the junction of the anterior, middle, and posterior
cerebral arteries is most commonly affected. Watershed infarction in this area
causes a clinical syndrome consisting of paralysis and sensory loss redominantly
involving the arm; the face is not affected and speech is spared. Watershed
infarcts make up approximately 10% of all ischemic strokes and almost 40% of
these occur in patients with carotid stenosis or occlusion.

RISK FACTORS
Many common medical conditions can increase your risk for stroke. Work with
your health care team to control your risk.
Previous Stroke or Transient Ischemic Attack
If you have already had a stroke or a transient ischemic attack (TIA), also known
as a "mini-stroke," your chances of having another stroke are higher.
High Blood Pressure
High blood pressure is a major risk factor for stroke. It occurs when the pressure
of the blood in your arteries and other blood vessels is too high.
There are often no symptoms to signal high blood pressure. Lowering blood
pressure by changes in lifestyle or by medication can reduce your risk for stroke.
High Cholesterol
Cholesterol is a waxy, fat-like substance made by the liver or found in certain
foods. Your liver makes enough for your bodys needs, but we often get more
cholesterol from the foods we eat. If we take in more cholesterol than the body
can use, the extra cholesterol can build up in the arteries, including those of the
brain. This can lead to narrowing of the arteries, stroke, and other problems.
A blood test can detect of the amount of cholesterol and triglycerides (a related
kind of fat) in your blood.
Heart Disease
Common heart disorders can increase your risk for stroke. For example,
coronary artery disease increases your risk for stroke because plaque builds up
in the arteries and blocks the flow of oxygen-rich blood to the brain. Other heart
conditions, such as heart valve defects, irregular heartbeat (including atrial
fibrillation), and enlarged heart chambers, can cause blood clots that may break
loose and cause a stroke.
Diabetes
Diabetes mellitus also increases the risk for stroke. Your body needs glucose
(sugar) for energy. Insulin is a hormone made in the pancreas that helps move
glucose from the food you eat to your body's cells. If you have diabetes, your
body doesnt make enough insulin, cant use its own insulin as well as it should,
or both.

10

Diabetes causes sugars to build up in the blood. Talk to your doctor about ways
to manage diabetes and control other risk factors.
Sickle Cell Disease
Sickle cell disease is a blood disorder associated with ischemic stroke that
mainly affects black and Hispanic children. The disease causes some red blood
cells to form an abnormal sickle shape. A stroke can happen if sickle cells get
stuck in a blood vessel and block the flow of blood to the brain.
Unhealthy Diet
Diets high in saturated fats, trans fat, and cholesterol have been linked to stroke
and related conditions, such as heart disease. Also, too much salt (sodium) in the
diet can raise blood pressure levels.
Physical Inactivity
Not getting enough physical activity can increase the chances of having other
risk factors for stroke, including obesity, high blood pressure, high cholesterol,
and diabetes. Regular physical activity can lower your risk for stroke.
Obesity
Obesity is excess body fat. Obesity is linked to higher "bad" cholesterol and
triglyceride levels and to lower "good" cholesterol levels. In addition to heart
disease, obesity can also lead to high blood pressure and diabetes.
Too Much Alcohol
Drinking too much alcohol can raise blood pressure levels and the risk for stroke.
It also increases levels of triglycerides, a form of fat in your blood, which can
harden your arteries.

Women should have no more than 1 drink a day.

Men should have no more than 2 drinks a day.

Tobacco Use
Tobacco use increases the risk for stroke. Cigarette smoking can damage the
heart and blood vessels, which increases your risk for stroke. Also, nicotine
raises blood pressure, and carbon monoxide reduces the amount of oxygen that
your blood can carry. Exposure to other peoples secondhand smoke can
increase the risk for stroke even for nonsmokers.

11

 Genetics and Family History

When members of a family pass traits from one generation to another through
genes, that process is called heredity.
Genetic factors likely play some role in high blood pressure, stroke, and other
related conditions. Several genetic disorders can cause a stroke, including sickle
cell disease. It also is likely that people with a family history of stroke share
common environments and other potential factors that increase their risk.
The risk for stroke can increase even more when heredity combines with
unhealthy lifestyle choices, such as smoking cigarettes and eating an unhealthy
diet.
Find out more about genetics and disease on CDCs Office of Public Health
Genomics Web site.
Family health history is a record of the diseases and health conditions that occur
in your family. Family health history is a useful tool for understanding health risks
and preventing disease. To help people collect and organize their family history
information, CDCs Office of Public Health Genomics collaborated with the U.S.
Surgeon General and other federal agencies to develop a Web-based tool called
"My Family Health Portrait."
Other Characteristics
Both men and women can have a stroke. Some other characteristics that you
cannot control, like your age, sex, and race or ethnicity, can affect your risk for
stroke:

Age. Age is the single most important risk factor for stroke. The older you
are, the more likely you are to have a stroke. The chance of having a
stroke about doubles every 10 years after age 55. Although stroke is
common among the elderly, many people younger than 65 years also
have strokes.

Sex. Stroke is more common in men than in women for most age groups.
But women of all ages are more likely to die from stroke than are men.
Pregnancy and use of birth control pills pose special stroke risks for
women.

Race or ethnicity. Blacks, Hispanics, American Indians, and Alaska

Natives have a greater chance of having a stroke than do non-Hispanic
whites or Asians. The risk of having a first stroke is nearly twice as high for

12

blacks than for whites. Blacks are also more likely to die from stroke than
are whites.

SIGNS AND SYMPTOMS

Sudden numbness or weakness in the face, arm, or leg, especially on one
side of the body.
Sudden confusion, trouble speaking, or difficulty understanding speech.
Sudden trouble seeing in one or both eyes.
Sudden trouble walking, dizziness, loss of balance, or lack of coordination.
Sudden severe headache with no known cause.
DIAGNOSTIC EXAMS AND PROCEDURES
Tests that View the Brain, Skull, or Spinal Cord
CT scan (CAT Scan, Computed axial tomography)
A CT scan uses X-rays to produce a 3-dimensional image of your head. A CT
scan can be used to diagnose ischemic stroke, hemorrhagic stroke, and other
problems of the brain and brain stem.
MRI scan (Magnetic resonance imaging, MR)
An MRI uses magnetic fields to produce a 3-dimensional image of your head.
The MR scan shows the brain and spinal cord in more detail than CT. MR can be
used to diagnose ischemic stroke, hemorrhagic stroke, and other problems
involving the brain, brain stem, and spinal cord.
Tests that View the Blood Vessels that Supply the Brain
Carotid Doppler (Carotid duplex, Carotid ultrasound)
Painless ultrasound waves are used to take a picture of the carotid arteries in
your neck, and to show the blood flowing to your brain. This test can show if
your carotid artery is narrowed by arteriosclerosis (cholesterol deposition).
Transcranial Doppler (TCD)

13

Ultrasound waves are used to measure blood flow in some of the arteries in
your brain.
MRA (Magnetic resonance angiogram)
This is a special type of MRI scan which can be used to see the blood vessels
in your neck or brain.

Cerebral arteriogram (Cerebral angiogram, Digital subtraction angiography,

[DSA])
A catheter is inserted in an artery in your arm or leg, and a special dye is injected
into the blood vessels leading to your brain. X-ray images show any
abnormalities of the blood vessels, including narrowing, blockage, or
malformations (such as aneurysms or arterio-venous malformations). Cerebral
arteriogram is a more difficult test than carotid doppler or MRA, but the results
are the most accurate.
Tests that View the Heart or Check its Function
Echocardiogram (2-d echo, Cardiac echo, TTE, TEE)
Painless ultrasound waves are used to take a picture of your heart and the
circulating blood. The ultrasound probe may be placed on your chest (transthoracic echocardiogram, TTE) or deep in your throat (trans-esophageal
echocardiogram, TEE).
Electrocardiogram (EKG, ECG)
This is a standard test to show the pattern of electrical activity in your heart.
3-10 electrical leads are attached to your chest, arms and legs. Sometimes
the EKG is recorded continuously over days, with the signals sent to a
portable recorder (Holter monitor) or by radio to a hospital monitoring station
(telemetry).
Routine Screening Tests
Chest x-ray (CXR)
An x-ray of the heart and lungs is a standard test for patients with acute
medical problems. Abnormalities may alert your doctor to important problems
such as pneumonia or heart failure.

14

 Urinalysis (UA)
A urine sample is often obtained to screen for bladder infection or kidney
problems. If infection is suggested, a urine culture test may be required.
Pulse oximetry (Blood oxygen)
This painless test is sometimes done in the emergency room or hospital to
determine if your blood is receiving enough oxygen from the lungs. A small
probe with a red light is usually attached to one finger.
Other Neurologic Tests
Electroencephalogram (EEG)
The EEG measures your brain waves through several electrical leads
painlessly attached to your head. EEG is not routinely used for stroke
diagnosis, but would be ordered if your doctor thinks that you may have had a
seizure.
Lumbar puncture (LP, spinal tap)
A needle is inserted in your lower back to obtain a sample of the fluid
(cerebrospinal fluid, CSF) which surrounds your brain and spinal cord. LP is
not routinely used for diagnosis of ischemic stroke. However, LP is often
required if subarachnoid haemorrhage (bleeding from a cerebral aneurysm) is
suspected. LP may also be needed if your doctor suspects a nervous system
infection (such as meningitis) or inflammation.
Electromyogram / Nerve conduction test (EMG / NCV)
This test records the electrical activity of the nerves and muscles. EMG is not
used for stroke diagnosis, but might be needed if your doctor suspects a
problem with the nerves in your arms or legs.
Brain biopsy
This is a surgical procedure in which a small piece of the brain is removed for
microscopic examination. Biopsy is used to diagnose lesions (such as
tumors) which cannot be identified by CT or MRI scan. It is very rarely used
for stroke diagnosis, often only when cerebral vasculitis is suspected.

15

TREATMENT
Drug Treatment
There is only one Food & Drug Administration (FDA) approved drug treatment for
acute ischemic stroke. Tissue plasminogen activator (tPA) is given via
intravenous therapy (IV) and works by dissolving the clot and improving blood
flow to the part of the brain being deprived of blood flow. tPA should be given
within three hours (and up to 4.5 hours in certain eligible patients)of the time
symptoms first started.
Mechanical Devices
Some ischemic strokes are treated with small mechanical devices that remove or
break up blood clots. If clot-busting drugs are ruled out, another option one of the
many FDA approved mechanical devices. A surgeon inserts a small mechanical
device into the blocked artery using a thin tube. Once inside, the tool traps the
clot, and either breaks it up or the surgeon pulls it out of the brain, reopening the
blocked blood vessel in the process.
A hemorrhagic stroke (sometimes called a bleed) occurs if an artery in your brain
leaks blood or ruptures (breaks open). The first steps in treating a hemorrhagic
stroke are to find the cause of bleeding in the brain and then control it. Some of
the options for treatments include surgical clips or coils inserted in aneurisms
(weaknesses in the blood vessel wall), controlling high blood pressure, and
surgery to remove the bleeding vessel and blood that has spilled into the brain.
Medical advances have greatly improved survival rates and recovery from stroke
during the last decade. Your chances of survival and recovery outcomes are
even better if the stroke is identified and treated immediately.

16

DRUG STUDY
COUMADIN
Generic Name:
Warfarin
Sodium
Brand Name:
Apo-Warfarin
(CAN)
Coumadin
Gen-Warfarin
(CAN)
Jantoven

Dosage / Frequency /
Route:
2-5 mg PO daily

Indication:
Venous thrombosis
and its extension,
treatment and
prophylaxis
Treatment of
thromboembolic
complications of
Classification:
atrial fibrillation with
Coumarin
embolization, and
Derivative
cardiac valve
Oral
replacement
Anticoagulant PE treatment and
prophylaxis
Prophylaxis of
Mechanism of
system embolization
Action:
after acute MI
Interferes with
the hepatic
Contraindication:
synthesis of
Allergy to warfarin;
vitamin kSBE; haemorrhagic
dependent
disorders; TB;
clotting
hepatic diseases; GI
factors

Side Effects:
Dermatologic:
Alopecia, urticaria,
dermatitis
GI: Nausea, vomiting,
anorexia, abdominal
cramping, diarrhea,
retroperitoneal
hematoma, hepatitis,
jaundice, mouth ulcers
GU: Priapism,
nephropathy, redorange urine
Hematologic:
Granulocytosis,
leukopenia,
eosinophilia, petechial
and purpura, bleeding
from mucous
membranes,
hemorrhagic infarction,
vasculitis, skin
necrosis, adrenal
hemorrhage and
resultant adrenal
insufficiency,
compressive

Nursing
Responsibilities:
Genetic
testing can
help to
determine
reasonable
dosage
Advise
patient to use
contraceptive
s
Monitor PT
ratio or INR
regularly to
adjust
dosage.
Administer IV
form to
patients
stabilized on
Coumadin
who are not
able to take
oral drug.
Do not
change brand
17

(factors IIprothrombin,
VII, IX and X),
resulting in
their eventual
depletion and
prolongation
of clotting
times.

ulcers; renal
disease; indwelling
catheters; spinal
puncture; aneurysm;
diabetes; visceral
carcinoma;
uncontrolled
hypertension;
severe trauma;
threatened abortion;
menometorrhagia;
pregnancy;
lactation.

neuropathy secondary
to hemorrhage near a
nerve.
Other: Fever, purple
toes syndrome

names once
stabilized.

Adverse Effects:
Hemorrhage (GI or
Urinary Tract bleeding)

DRUG STUDY
LOSARTAN
Generic Name:
Losartan Potassium
Brand Name:
Cozaar
Classification:
Antihypertensive
ARB
Mechanism of Action:
Selectively blocks the
binding of angiotensin II
to specific tissue
receptors found in the
vascular smooth muscle
and adrenal gland; this
action blocks the
vasoconstriction effect
of the renin-angiotensin
system as well as the

Dosage / Frequency Side Effects:

/ Route:
CNS:
50 mg PO daily
Headache,
dizziness,
syncope,
Indication:
insomnia
Treatment of
CV:
hypertension,
Hypotension
alone or in

Dermatologic:
combination with
Rash,
other
urticarial,
antihypertensive
pruritus,
Treatment of
alopecia, dry
diabetic
skin
nephropathy

GI: Diarrhea,
with an elevated
abdominal
serum creatinine
pain, nausea,
and proteinuria
constipation,
in patients with
dry mouth
type 2 diabetes
Respiratory:
and a history of
URI
hypertension

Nursing
Responsibilities:
Administer without
regard to meals.
Monitor patient
closely in any
situation that may
lead to a decrease
in BP secondary to
reduction in fluid
volume excessive
perspiration,
dehydration,
vomiting, and
diarrhea
excessive
hypotension can
occur.

18

release of aldosterone
leading to decreased
BP.

Reduction of the
risk of stroke in
patients with
hypertension
and left
ventricular
hypertrophy

symptoms,
cough, sinus
disorders
Other: Back
pain, fever,
gout, muscle
weakness

Contraindication:
Hypersensitivity
to Losartan
Pregnancy
Lactation

DIET
A healthy diet to help prevent a stroke should include:

Limit fat intake to no more than 30% of your total calories.

Eat quality fats:

Use virgin olive oil and other unsaturated, low-cholesterol fats.
10% to 15% of your total calories should be in the form of
monounsaturated fatty acids (e.g. olive oil, canola oil, and
peanut oil).

Talk to your doctor about vitamin D supplements.

Eat foods that are rich in omega-3 fatty acids:

Omega-3's are present in salmon, tuna, and mackerel.
Walnuts and flax seed are also rich in omega3's.
If you don't like fish, your local pharmacy has omega-3
supplements in capsule form.
19

Eat less than 300 milligrams of dietary cholesterol a day.

Reduce salt in your diet to no more than 3 grams per day. You doctor may
lower this recommendation to no more than 2 grams if you have high blood
pressure or congestive heart failure.

Eat plenty of fresh fruit and vegetables.

Eat more complex carbohydrates, such as starch and fiber. Whole grains and
brown rice are good fiber sources. Other sources include:

Fruits
Vegetables
Bran
Barley
Oats
Legumes

Limit iron intake:

Too much iron can increase atherosclerosis.

Avoid fad diets:

Eat a well-rounded diet instead.

Check with your doctor about supplementing your diet with B vitamins. Some
people may benefit from these supplements.

NURSING CARE PLAN

Subjective &
Objective
Cues with
Nursing
Diagnosis
Subjective
Cue:
Dih na aku
makahinnang
marayaw bya
tagna. As
verbalized

Objectives of
Care

Nursing
Interventions

At the end of
30 minutes
nursing
intervention,
the patient will
be able to:

At the end of
30 minutes
nursing
intervention,
the patient will
be able to:

Rationale

Evaluation

The client
was able to
perform
tasks within
her
capabilities.
To
20


Objective Cue:
Fleeting
Eye
Contact
Low Tone

of Voice
Nursing
Diagnosis:
Ineffective role
performance
related to
health
condition

Recognize
capabilities
in role
performanc

e
Maintain a
sense of
purpose
Preserve
connection
s with
other
people

Assess
clients
knowledge
of illness
Encourage
client to
express
thoughts or
feelings
Provide
opportuniti
es for
client to
make
decisions.
Educate
client and
family
members
about
rendering
roles.
Encourage
client to
continue to
fulfil life
roles within
the
constraints
.

establish
baseline
data
To
identify
life
affects of
altered
role
performa
nce
To show
respect
for
clients
decisionmaking.
To
promote
optimal
functionin
g.

To
maintain
a sense
of
purpose
and
preserve
connectio
ns with
other
people.

21

COMPLICATIONS
Complications of a right hemisphere stroke:
Left hemiplegia
Spatial problems
Perception problems
Impaired judgment
Behaviour problems
Short-term memory problems
Complications of a left hemisphere stroke:
Right hemiplegia
Aphasia
Speech problems
Language problems
Slowness
Cautious behaviour
Short-term memory problems
Complications of a cerebellar stroke
Abnormal head reflexes
Abnormal torso reflexes
Coordination problems
Balance problems
Dizziness
22

 Nausea
Vomiting
Complications of a brain stem stroke
One-sided paralysis
Two-sided paralysis
Breathing difficulty
Blood pressure problems
Heart problems
Eye movement problems
Hearing problems
Speech problems
Swallowing problems

HEALTH TEACHING PLAN

Health Teaching Plan
Subject Matter: Stroke
Time Allotment: 15 Minutes
General Objective: Restore an active lifestyle
Learning
Content
Objectives

Strategy

Evaluation

23

At the end
of 15
minutes
health
teaching,
the client
will be able
to:

Stroke occurs when the

blood supply to parts of the
brain is interrupted or
severely reduced,
depriving brain tissue of

oxygen and nutrients.

Stroke may be caused by

a blocked artery (ischemic
stroke) or leaking/bursting
of a blood vessel
(haemorrhagic stroke).
Some experience a
temporary disruption of
blood flow to the brain
(transient ischemic attack).

1. Define
Stroke

2. Enumer
ate
Causes

3. Enumer
ate
Signs
and
Sympto
ms

4. Identify
Complic
ations

Trouble with speaking

and understanding
Paralysis/numbness of
face, arm, or leg
trouble in seeing in one
or both eyes
headache
trouble with walking

Paralysis/loss of
muscle movement
difficulty talking or
swallowing
memory loss/thinking
difficulties
emotional problems
pain

Lecture
Discuss
ion
Student
Nurse
and
Client
Interacti
on
Questio
n and
Answer
for
underst
anding
the
subject
matter

Direct
Questioning
1. Can you
define to
me what
stroke
means?
2. Can you
enumerate
some
causes?
3. Can you tell
me some of
the signs
and
symptoms
of stroke?
4. Can you
enumerate
some
complicatio
ns?
5. Do you
know what
the
preventive
measures
are?
6. Enumerate
some
preventive
measures
you know.

24

 changes in behavior

5. Identify
SelfManage
ment

6. Identify
Preventi
ve
Measur
es

Do not be hard on
yourself
get out of the house
even if it is hard
join a support group
let friends and family
know what you need
know that you are not
alone

Control high blood

pressure
lowering the amount of
cholesterol and
saturated fat in diet
quit smoking
control diabetes
maintain a healthy
weight
eating a diet rich in
fruits and vegetables
exercising regularly
avoiding illicit drugs

25

REFERENCE
http://www.stroke.org/understand-stroke/what-stroke
https://www.uic.edu/com/ferne/pdf/pathophys0501.pdf
http://www.cdc.gov/stroke/conditions.htm
http://www.cdc.gov/stroke/behavior.htm
http://www.cdc.gov/stroke/family_history.htm
http://www.cdc.gov/stroke/signs_symptoms.htm
http://www.strokecenter.org/patients/stroke-diagnosis/lab-tests-and-procedures/
http://www.stroke.org/we-can-help/survivors/just-experienced-stroke/stroketreatments
http://www.freemd.com/stroke/prevention-diet.htm
http://www.rightdiagnosis.com/s/stroke/complic.htm
Lipincotts Drug Handbook (2013)
Spark and Taylors Nursing Diagnosis Pocket Guide

26