BULLETS USMLE PHYSIOLOGY

Red = important

Orange Think! Green= Pharma Blue= Graphics Firecracker

Kaplan/ First Aid hints

Violet =

Starling Forces
The osmolarity of the body is about x2 the {} of Na nM 150 = 300 mosmol
Nernst Formula

SKELETAL

Californians Like Girls in String Bikinis ( Corneum, Lucid, Granulosum, Spinosum, Basalis)
Skeletal, Smooth, Cardiac Muscle
Depolarization

VI.- CARDIAC CYCLE AND VALVULAR HEART DISEASE

VII.- RESPIRATION

RESPIRATORY

ENDOCRINOLOGY
I

X.- Male Reproductive System

Overall Control of Adult Male Hormonal Secretion

Hormonal Control of Testicular Function

o GnRH synthesized in preoptic region of hypothalamus.
o Pituitary produces pulsatile release of LH and FSH (glycoproteins)
o Leydig cells + LH = activates conversion of chol into pregnolone = testosterone
Testosterone is negative feedback for LH
5-reductase + Testosterone = DiHydroTestosterone (powerfull stuff)

Confers secondary sexual characteristics. Sperm formation.

Can create baldness, BPH ( finasteride is a blocker of 5-reductase)

Attached to estrogen-testoteron binding globuline.

o Sertoli cell + Testosterone = creates sperm growth factors and promotes protein
synthesis
Aromatase transforms testosterone into estrogen = estradiol is secreted
2/3 of estradiol is created in gonads. 1/3 is created in adipose tissue.
inhibin for FSH negative feedback.
Age Related Changes in LH and Testosterone Secretion

Fetal Life: Normal male development requires testosterone, DHT and Mullerian inhibiting
factor.
o hCG + LH = Leydig cells = testosterone = Wolffian ducts=(epididymis, vas
deferentia, seminal vesicles)
o Testosterone + 5-reductase = DHT = urogenital sinus and genital organs
= scrotum, penis, prostate
o Sertoli cells + MIH =Absence of female internal structures
Dependence of Spermatogenesis on Lower Temperatures of the Scrotum

Effect on Fertility: Spermatogenesis ceases at temperatures typical of abdomen. The

scrotum provides 4C less of body temp for spermatoegenesis. Elevation and descent of
testes given by cremasteric muscles.

Effects on FSH and LH: In cryptorchid testes high temp prevents adequate
spermatogenesis. Thus there is no proper creation of inhibins and in response FSH is
elevated. Testosterone production goes down, thus elevated LH
Erection, Emission, Ejaculation

Erection: Parasympathetic

Emission: Sympathetic

Ejaculation: Sympathetic
Gonadal Function in the Male

Testosterone deficiency:
o 2-3 month of gestation : Genitalia ambiguity
o 3rd trimester: Testicular descent abnormalities and micropenis
o Pubertal: poor secondary characteristics
o Postpuberal: decreased libido, erectile dysfunction, low energy, decreased facial or
body hair.

Causes of hypogonadism:
o Noonan Syndrome: Low FSH & LH
o Klinefelter Syndrome: High FSH & LH : tall
o Kallmans Syndrome : Hypothalamic disorders: anosmia
o Gonadal/ sex steroid synthesis failure
o
Prostate Cancer? Tx: Complete androgen block ( flutamide and THEN GnRH agonists)

XI.- Female Reproductive System

The Menstrual Cycle

Theca cell + LH = it creates androgen (same machinery as adrenal Reticularis)

Granulosa cell + FSH + Aromatase = Estrogen and inhibins (FSH is inhibited to prevent
further follicle maturation)
o Estrogen is inhibitory in pituitarys FSH & LH secretion, until a certain
point where concentration is high and magically turns to be excitatory
(positive feedback).

Phases:
o Follicular: Variable: Estrogen, endometrial lining.
LH surge= ovulation
The length of the menstrual cycle minus 14 days is the ovulation
day
o Luteal: Fixed at 14 days, progesterone, secretions in the endometrium lining,
increased temp.

Menstruation: passive phenomena (corpus lutheum not rescued = drop in

progesterone & estrogen)
o Conception at day 15, implant at day 20, hCG production of trophoblas at day 25.
Corpous lutheum rescue and progesterone and estrogen continuous production.

The surge of LH creates ovulation. (and receptors for LH appear everwhere)= broken fallicle
breaks into corpus luteum = progesterone & estrogen = FH n LH inhibition

Corpos luteum involution after 2 weeks= decreases prog & estrogen FSH & LH

Progesterone: Makes cervical mucus thick. Causes endometrium secretions. Increases temp
and appetite.

As long as estrogen levels are still rising, ovulation hasnt happened. ( It happens at peal
levels)
Female Sex Steroid Metabolism and Excretion

Potency : Estradiol>estrone>estriol
Menstrual Irregularities

Amenorrhea: Lack of menstruation bleeding:

o Exclude pregnancy, prolactin, starvation.
o 1 Hypothyroidism ( increased TRH increases prolactin= FSH n LH inhibition)
o Pituitary tumor (prolactinoma)
o Polycystic ovary

Polycystic Ovary Syndrome

o Enlarged ovaries = high andorgens = follicle disruptions
o Infertility, hirsutism, obesity, insulin resistance, amenorrhea/oligomenorrhea
o Polycystic Ovarian Syndrome

Hirsutism
o Increased adrenal androgen concentrations
o Abnormal hair growth
o Virilization (breast atrophy, clitorimegaly, muscle bulk)
o Tx: dexamethasone shuts of ACTH = feedback inhibition. Spironolactone is antiandrogen
Pregnancy

Ovum Pick up and Fertilization

Implantation

Hormonal Maintenance of Uterine Endometrium

o The trophoblast has to implant and create hCG to rescue the corpus luteum to keep
up the production of progesterone ( this for the 1 Trimester)
o During 2 and 3 Trimester the placenta is mature enough to produce
progesterone and estrogen.
o The mother uses the fetal adrenals to produce DHEA to maintain hormonal
requirements.

Peripheral Effects of Hormonal Changes

o Elevated estrogen = elevated prolactin
o hPL ( human placental lactogen)= works a bit like GH ( lipolysis and ketogenesis,
maternal glucose uptake). During 2 trimester it creates extra insulin resistance.
May cause pregnancy diabetes.

Maternal Compensatory Changes of Pregnancy

o Cardiovascular: 50% in plasma volume. CO, TPR, GFR, Renal threshold =
glucose spill.
o Endocrine: Pituitary enlarges 1/3.
Sheehan Syndrome: Pituitary infraction ( most common sign is lack of
lactation)
Estrogen increases renin-AT-Ald system = fluid retention
o Parturition:
Oxcytocin doesnt initiate contractions of labor onset but does help the
contraction of the uterus after the fetal expulsion.
Oxytocin increase prostaglandine synthesis and these increase
contractions.
Lactation

Estrogen causes mammary tissue growth. Prolactin stimulate maximum growth

High estrogen levels prevent the active secretion of milk

After parturition happens, estrogen level drops = milk flows.

Baby suckling stimulates release of oxytocin which create milk

Baby suckling stimulates the decrease of dopamine = prolactin stops being inhibited and
increases = milk flow = decreased GnRH = decreased FSH, LH release = non ovulation.
(less fertile but NOT infertile)
o

How does hyperaldosteronism cause hypocalcemia?

Can you describe how insulin decreases blood levels of amino acids?
How does thyroid hormone affect metabolism?

During pregnancy, which of the following statements regarding thyroid hormone is true?

ASerum TBG concentrations are decreased

BFree T4 and T3 concentrations are elevated

CTotal T4 and T3 concentrations are elevated

DTotal T4 and T3 concentrations are decreased

EFree T4 is elevated while free T3 is decreased

What are Orphan Annie eye nuclear inclusions? What are Psammoma bodies?

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Answer

Colloid: central space in follicle where thyroid hormone is stored as a component of thyroglobulin
Papillary thyroid cancer: common in women, particularly in their 20s or 30s, and in patients with prior
neck radiation
Thyroglobulin is a marker for well differentiated papillary thyroid cancer
Look for characteristic Orphan Annie eye nuclear inclusions (nuclei with uniform staining, which appear
empty), and psammoma bodies (round concentric collection of calcium) on light microscopy.

Treatment of hyperthyroidism:

1) -blocker to control symptoms of SNS tone

2) Thioamide e.g., PTU (propylthiouracil), methimazole:

- May induce remission by blocking new thyroid hormone production via inhibition of the organification and
coupling steps of thyroid hormone synthesis.
- PTU (not methimazole) also inhibits peripheral conversion of T4 to T3.
3) High-dose iodine blocks release of T4 and T3 into the circulation
4) High-dose radioactive iodine 131I (versus the 123I used in imaging studies) becomes concentrated in
the thyroid gland ablation of thyroid function

atients with Hashimoto thyroiditis are at increased risk of developing other autoimmune diseases can you give 4
examples?

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Answer

Clinical presentation:
Nontender thyroid, which often becomes diffusely enlarged insidious development of hypothyroidism,
most commonly in women age 30-50
Presents with all other signs of hypothyroidism.
Risk of developing other autoimmune diseases, for example:
- DM 1 (Type 1 Diabetes Mellitus)
- SLE (Systemic Lupus Erythematosus)
- SS (Sjgrens syndrome)
- MG (Myasthenia Gravis)
Risk of primary thyroid lymphoma:
- B-cell non-Hodgkin lymphomas, especially extranodal marginal zone lymphomas ofMALT (mucosa-associated
lymphoid tissue) type
Treatment: levothyroxine

What is the key GI symptom associated with hypothyroidism?

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Answer

Signs and symptoms can be organized by system:

Metabolic:
- BMR (basal metabolic rate); O2 consumption RR
- Positive nitrogen balance (anabolic) weight gain
- Heat production sweating and cold intolerance
- Growth retardation

Cardiovascular:
- Peripheral vasoconstriction to maintain body heat cool, pale, dry skin
- Synthesis of cardiac 1 receptors
- HR (bradycardia)
- contractility SV (stroke volume) PP (pulse pressure)
- HR and SV CO (cardiac output) exercise capacity, shortness of breath
- Blunted EKG voltages
- Accelerated atherogenesis: Total cholesterol, LDL
Central Nervous System:
- Slow DTRs with prolonged relaxation phase
- Fatigue
- Lethargy
- Mental slowness
- Mental retardation (perinatal)
Dermatologic:
- Coarse, brittle hair/nails
- Yellow/orange skin
- Myxedema (non-pitting edema due to interstitial accumulation of osmotically active mucopolysaccharides) of
the hands, face, periorbital region.
Gastrointestinal:
- GI motility constipation
Musculoskeletal:
- Carpal tunnel syndrome
Endocrine:
- Hyperprolactinemia (if primary or secondary hypothyroidism): T3, T4 TRH prolactin

Can you name some of the presenting S/Sx of congenital hypothyroidism? (Try to name 8)

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Answer

Congenital hypothyroidism is most commonly caused by thyroid dysgenesis due to thyroid

aplasia/hypoplasia/ectopy. Congenital hypothyroidism may present with:
1) hoarse cry, weak cough, slow respiratory effort
2) abdominal distention (protuberant abdomen), potbelly with umbilical hernia
3) prolonged neonatal (physiologic) jaundice
4) poor feeding, neonatal hypotonia
5) macroglossia (protruding tongue)
6) enlarged fontanelles, delayed dentition, retarded bone age
7) coarse facial features, widely set eyes, broad flat nose, dry skin with scarce lanugo, pale body
with mottled cool extremities
8) S/Sx of hypothyroidismeg, constipation, somnolence