EMG, Myasthenia gravis, Lymphatic circulation, Comparison of skeletal, cardiac & smooth muscle, periodic breathing & drowning, physiology deep sea diving & applied, pineal gland& thymus physiolog diabetes mellitus, sex determination & differentiation, puberty & applied, infertility causes & role of IV in infertility, physiology of menopause. Give important point for the above for mcq exam take data from gyton and ganong
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📋 HIGH-YIELD MCQ NOTES — PHYSIOLOGY
Sources: Guyton & Hall Textbook of Medical Physiology | Ganong's Review of Medical Physiology (26th ed.)
1. ELECTROMYOGRAPHY (EMG)
| Key Point | Detail |
|---|---|
| Normal EMG | At rest → electrical silence; minimal insertion activity only |
| Motor unit potential | Amplitude 0.1–3 mV; duration 5–15 ms |
| Fibrillation potentials | Spontaneous, small (1–2 mV) — seen in denervation (LMN lesion) |
| Fasciculation | Spontaneous firing of whole motor unit — seen in ALS/LMN disease |
| Myopathy pattern | Short-duration, low-amplitude, polyphasic potentials; early recruitment |
| Neuropathy pattern | Large-amplitude, long-duration potentials; reduced recruitment |
| Repetitive nerve stimulation (RNS) | In MG → decremental response at 3 Hz stimulation (>10% decrement = abnormal) |
| Single-fiber EMG | Most sensitive test for NMJ disorders; measures jitter (increased in MG) |
| Conduction velocity | Motor NCV: 50–70 m/s (myelinated fibers); reduced in demyelination |
| CMAP | Compound muscle action potential — reduced amplitude in axonal neuropathy |
2. MYASTHENIA GRAVIS (MG)
(Guyton Medical Physiology & Bradley/Daroff Neurology)
Epidemiology & Pathology
- Incidence: 25–125 per million; bimodal — 20s (women) and 60s (men)
- Autoimmune disease: antibodies against nicotinic AChR (α-subunit, MIR = Main Immunogenic Region)
- Early-onset (women): associated with thymic hyperplasia
- Late-onset (men): associated with thymoma (visible on CXR)
Pathophysiology
- Antibodies → activate complement → destroy postjunctional folds → ↓ AChR surface density
- MEPP (miniature end-plate potential) amplitude is decreased (frequency is normal) ← classic EMG finding
- Reduced AChR → reduced EPP → failure to reach threshold → muscle weakness
Clinical Features
- Fluctuating weakness, worse at end of day / after exertion (fatigability)
- Two forms: Ocular (only extraocular muscles) | Generalized (all skeletal muscles)
- Ptosis, diplopia, dysphagia, respiratory failure in severe cases
Treatment
| Treatment | Mechanism |
|---|---|
| Pyridostigmine | AChE inhibitor (most widely used) — ↑ ACh in synapse |
| Corticosteroids/Immunosuppressants | Reduce antibody production |
| Plasmapheresis | Remove circulating anti-AChR antibodies |
| Thymectomy | 75% improvement if thymoma present |
| Caution | Overdose of AChE inhibitors → cholinergic crisis (prolonged depolarization, Na⁺ channel inactivation) |
MCQ Traps:
- Tensilon (edrophonium) test → improves weakness in MG (short-acting AChEI)
- Lambert-Eaton syndrome: antibodies against pre-synaptic voltage-gated Ca²⁺ channels; incremental response on RNS (≥50 Hz); associated with small cell lung cancer
- MG: decremental; Lambert-Eaton: incremental (on high-frequency RNS)
3. LYMPHATIC CIRCULATION
(Ganong, Chapter 31)
Key Facts
- Normal 24-hour lymph flow = 2–4 L
- Fluid efflux > influx across capillaries → excess enters lymphatics → returns to blood
- Two types of lymphatic vessels:
- Initial lymphatics — no valves, no smooth muscle; fluid enters via loose endothelial junctions; massaged by muscle/arteriolar contractions
- Collecting lymphatics — have valves + smooth muscle; contract peristaltically (principal propulsive force)
Factors aiding lymph flow:
- Peristaltic contractions of collecting lymphatics ← most important
- Skeletal muscle contractions
- Negative intrathoracic pressure during inspiration
- Venous suction at lymphatic termination points
Protein transport:
- 25–50% of total circulating plasma protein is returned via lymphatics per day
- Lipids from intestine absorbed as chylomicrons via lacteals (intestinal lymphatics)
Interstitial Fluid Volume determinants:
- Capillary hydrostatic pressure, oncotic pressure, capillary filtration coefficient, lymph flow, precapillary:postcapillary resistance ratio
- Edema = excess interstitial fluid accumulation
- Precapillary constriction → ↓ filtration; Postcapillary constriction → ↑ filtration (↑ edema risk)
MCQ Traps:
- Lymph from left half of body + intestines → thoracic duct → left subclavian vein
- Right lymphatic duct drains right upper body
- Protein content of liver lymph is highest (~6 g/dL)
4. COMPARISON: SKELETAL vs. CARDIAC vs. SMOOTH MUSCLE
(Guyton & Ganong)
| Feature | Skeletal | Cardiac | Smooth |
|---|---|---|---|
| Striation | Yes | Yes | No |
| Nuclei | Multiple, peripheral | 1–2, central | Single, central |
| Control | Voluntary | Involuntary | Involuntary |
| AP duration | 1–2 ms | 200–300 ms | Longer, variable |
| Refractory period | Short | Long (prevents tetanus) | Short |
| Tetanus possible | Yes | No (long ARP) | Yes |
| Pacemaker | No | Yes (SA node) | Yes (some cells) |
| T-tubules | Present (at A-I junction) | Present (at Z-disc) | Absent or rudimentary |
| SR development | Well-developed | Moderate | Poorly developed |
| Extracellular Ca²⁺ dependence | Low | High (plateau phase) | High |
| Calmodulin-MLCK pathway | No | No | Yes |
| Troponin system | Yes | Yes | No (uses calmodulin) |
| Length-tension | Yes | Yes (Frank-Starling) | Yes |
| Innervation | Single NMJ | Autonomic + intrinsic | Autonomic |
| Gap junctions | No | Yes (intercalated discs) | Yes |
| Regeneration | Yes (satellite cells) | Minimal | Yes |
MCQ Traps:
- Smooth muscle contraction: Ca²⁺ + calmodulin → activates MLCK → phosphorylates myosin light chain
- Cardiac muscle cannot tetanize because ARP = duration of systole
- Cardiac: Ca²⁺ enters through L-type Ca²⁺ channels → triggers Ca²⁺-induced Ca²⁺ release (CICR) from SR (ryanodine receptor)
5. PERIODIC BREATHING & DROWNING
(Guyton & Hall)
Cheyne-Stokes Breathing (Periodic Breathing)
- Pattern: crescendo-decrescendo breathing → apnea → repeat
- Mechanism: oscillation of CO₂ around the apneic threshold due to:
- Delayed feedback from lung to chemoreceptors (long circulation time)
- Increased sensitivity/gain of respiratory center
- Most common cause: heart failure (prolonged circulation time) and CNS lesions
- Also seen at high altitude (hypoxia lowers CO₂ threshold)
- Apnea occurs when CO₂ falls below apneic threshold
Other Abnormal Breathing Patterns:
| Pattern | Cause |
|---|---|
| Biot's breathing | Irregular, with periods of apnea → damage to pons/medulla |
| Kussmaul breathing | Deep, rapid, regular → metabolic acidosis (DKA) |
| Apneustic breathing | Prolonged inspiration — pontine damage |
| Ataxic breathing | Completely irregular — medullary damage |
Drowning / Near-Drowning:
- Dry drowning (~10–15%): reflex laryngospasm → asphyxia without water aspiration
- Wet drowning (~85%): aspiration of water
- Freshwater: hypotonic → absorbed into blood → hemodilution, hemolysis, hypervolemia, ↑K⁺, hyponatremia, VF
- Saltwater: hypertonic → draws fluid from blood into alveoli → hemoconcentration, hypovolemia, pulmonary edema
- Secondary drowning: delayed pulmonary edema hours after apparent recovery
- Key MCQ: Both types cause hypoxia; freshwater causes electrolyte disturbances more severely
6. PHYSIOLOGY OF DEEP SEA DIVING (APPLIED)
(Guyton & Hall)
Pressure & Gas Laws:
- 1 atm = 760 mmHg = pressure at sea surface
- For every 10 m of seawater descent → +1 atm pressure
- At 30 m depth = 4 atm absolute pressure
Nitrogen Narcosis ("Rapture of the Deep"):
- Increased PN₂ at depth → narcotic effect (similar to alcohol/anesthetics)
- Begins at ~4 atm (30 m); serious at 6–10 atm
- Mechanism: ↑N₂ dissolves in neuronal membranes → depresses CNS
Oxygen Toxicity:
- High PO₂ (>2 atm) → pulmonary and CNS toxicity
- CNS O₂ toxicity: seizures, visual disturbances ← with pure O₂ diving at depth
- Pulmonary O₂ toxicity: inflammation, edema (with prolonged exposure)
Decompression Sickness ("The Bends"):
- Rapid ascent → dissolved N₂ bubbles form in blood/tissues
- Symptoms: joint pain (bends), pruritus (skin bends), dyspnea (chokes), neurological deficits
- Treatment: recompression in hyperbaric chamber, then slow decompression
- Prevention: staged decompression with stops at specified depths
High-Pressure Nervous Syndrome:
- Deep helium dives (>150 m) → tremors, nausea, psychosis
- He replaces N₂ (no narcosis) but pressure itself causes HPNS
CO₂ Retention in Divers:
- Breath-hold diving → progressive hypoxia (shallow water blackout) due to ↓PO₂ on ascent
7. PINEAL GLAND PHYSIOLOGY
(Guyton & Ganong)
Key Facts:
- Located in epithalamus (roof of 3rd ventricle)
- Principal secretion: Melatonin (from serotonin, via HIOMT enzyme)
- Melatonin synthesis controlled by: light (via retino-hypothalamic-pineal pathway)
- Light → inhibits melatonin; Darkness → stimulates melatonin
- Innervation: Superior cervical ganglion (sympathetic; norepinephrine)
- Peak melatonin: 2–4 AM
Functions of Melatonin:
- Regulates circadian rhythm (biological clock)
- Entrains the SCN (suprachiasmatic nucleus) — "zeitgeber"
- Antigonadotrophic: inhibits LH/FSH release → inhibits reproduction (seasonal breeders)
- Antioxidant properties
- Promotes sleep
- Inhibits GnRH release
MCQ Key Points:
- Calcification of pineal (pineal sand) → visible on X-ray; useful as midline marker
- Pinealoma in children → precocious puberty (removes melatonin inhibition of GnRH)
- Hypofunction → delayed puberty is NOT typical; precocious puberty if tumor destroys pineal
- Melatonin receptor: MT1 and MT2 (GPCRs); couple to Gi → ↓cAMP
8. THYMUS PHYSIOLOGY
(Guyton & Ganong)
Key Facts:
- Bilobed organ in superior mediastinum; derived from 3rd pharyngeal pouch
- Maximum size at puberty → then involutes
- Site of T-lymphocyte maturation
Thymic Hormones:
| Hormone | Action |
|---|---|
| Thymosin | Promotes T-cell differentiation |
| Thymopoietin | Induces T-cell differentiation; inhibits NMJ transmission |
| Thymulin (thymic serum factor) | Promotes expression of T-cell markers |
| Thymic humoral factor | General T-cell stimulation |
Thymic Education (T-cell maturation):
- Positive selection: T-cells that recognize self-MHC are selected (in cortex)
- Negative selection: T-cells with high affinity for self-antigens are deleted → prevents autoimmunity (in medulla)
- Surviving T-cells: ~5% of those entering
MCQ Traps:
- DiGeorge syndrome = absence of thymus (3rd/4th pharyngeal pouch) → no T-cells → cell-mediated immunity deficiency
- MG is associated with thymic abnormalities (thymoma or hyperplasia)
- Thymopoietin → inhibits NMJ → tested in context of MG
9. DIABETES MELLITUS
(Guyton & Hall, Chapter 79)
Islet Cell Types:
- β cells (60%): insulin + amylin (center of islet)
- α cells (25%): glucagon
- δ cells (10%): somatostatin (inhibits both insulin and glucagon)
- PP cells: pancreatic polypeptide
Insulin: Structure & Secretion
- 51 amino acids; two chains (A: 21 AA, B: 30 AA) connected by disulfide bonds
- Precursor: Preproinsulin → Proinsulin → Insulin + C-peptide
- C-peptide has no known function but is used as marker of endogenous insulin secretion
- t½ = ~6 min; degraded by liver (first-pass ~50%), kidney, muscle
- GLUT-2 transporter in β-cells (glucose sensor; high Km)
Stimulus for Insulin Secretion:
- Primary: blood glucose ↑ (>100 mg/dL begins; strong at >150 mg/dL)
- Amino acids: arginine, leucine (especially after protein meal)
- GLP-1, GIP (incretins) → amplify insulin secretion (basis of DPP-4 inhibitors, GLP-1 agonists)
- ACh (vagal stimulation), β-adrenergic stimulation ↑ insulin
- α-adrenergic stimulation (epinephrine) → inhibits insulin
- Somatostatin → inhibits insulin and glucagon
- Sulfonylureas: close K_ATP channels → depolarization → Ca²⁺ entry → insulin release
Insulin Effects:
| Target | Effect |
|---|---|
| Muscle | ↑ glucose transport (GLUT-4); ↑ glycogen synthesis |
| Liver | ↑ glycogen synthesis; ↑ glycolysis; ↓ gluconeogenesis; ↓ glycogenolysis |
| Adipose | ↑ lipogenesis; ↓ lipolysis |
| General | ↑ protein synthesis; ↓ proteolysis; anabolic |
| K⁺ | ↑ cellular K⁺ uptake (used in hyperkalemia treatment) |
- Insulin increases rate of glucose transport into resting muscle cells at least 15-fold
- Liver glycogen can reach 5–6% of liver mass with insulin
Types of Diabetes:
| Feature | Type 1 (IDDM) | Type 2 (NIDDM) |
|---|---|---|
| Mechanism | Autoimmune β-cell destruction | Insulin resistance + β-cell dysfunction |
| Insulin | Absent | Present (↑ early, ↓ late) |
| Age | Usually <30 | Usually >40 |
| Body type | Lean | Obese |
| HLA association | DR3, DR4 | Weaker association |
| Prone to | DKA | HONK (hyperosmolar non-ketotic coma) |
| Treatment | Insulin (mandatory) | Diet, OHAs, ± insulin |
DKA vs. HONK:
| DKA | HONK | |
|---|---|---|
| Blood glucose | 250–600 mg/dL | >600 mg/dL |
| Ketosis | Yes | No/minimal |
| pH | <7.3 | Normal/near normal |
| Osmolality | Mildly elevated | Very high (>320 mOsm) |
| Type | Type 1 DM | Type 2 DM (elderly) |
Glucagon:
- Secreted by α-cells; 29 AA peptide
- Actions: ↑ glycogenolysis, ↑ gluconeogenesis, ↑ ketogenesis, ↑ lipolysis
- Stimulated by: hypoglycemia, amino acids (protein meal), exercise, stress
- Inhibited by: hyperglycemia, insulin, somatostatin
Amylin (IAPP):
- Co-secreted with insulin; inhibits insulin secretion
- Delays gastric emptying; suppresses glucagon; promotes satiety
- Analogue: Pramlintide (used in DM management)
10. SEX DETERMINATION & DIFFERENTIATION
(Guyton & Hall)
Sex Determination:
- Genetic sex: XX (female), XY (male) determined at fertilization
- SRY gene (sex-determining region on Y chromosome) → triggers testicular development
- SRY → SOX9 → Sertoli cells → AMH (Anti-Müllerian Hormone) + testosterone
Gonadal Differentiation:
- Default pathway = Female (ovarian differentiation occurs in absence of SRY/testosterone)
- Undifferentiated gonad has both Wolffian and Müllerian ducts
Ductal Development:
| Structure | Male Development | Female Development |
|---|---|---|
| Wolffian ducts | → Epididymis, vas deferens, seminal vesicles (need testosterone) | Regress |
| Müllerian ducts | Regress (need AMH from Sertoli cells) | → Fallopian tubes, uterus, upper vagina |
| Urogenital sinus | → Prostate, urethra | → Lower vagina, urethra |
| External genitalia | → Penis, scrotum (need DHT via 5α-reductase) | → Clitoris, labia |
Key Hormones:
- AMH: from Sertoli cells → causes regression of Müllerian ducts
- Testosterone: from Leydig cells (LH-stimulated) → maintains Wolffian ducts
- DHT: 5α-reduction of testosterone → masculinizes external genitalia
- Without testosterone → female external genitalia (default)
Disorders of Sex Development (MCQ favorites):
| Disorder | Cause | Phenotype |
|---|---|---|
| Congenital Adrenal Hyperplasia (CAH) | 21-hydroxylase deficiency; excess androgens | 46XX female → virilized external genitalia |
| Androgen Insensitivity Syndrome (AIS) | Androgen receptor defect in 46XY | Female phenotype (complete AIS = testicular feminization) |
| 5α-reductase deficiency | Can't convert T→DHT | 46XY: ambiguous at birth, masculinizes at puberty |
| Turner syndrome | 45XO | Short, female phenotype, streak ovaries, no puberty |
| Klinefelter syndrome | 47XXY | Male phenotype, small testes, gynecomastia, infertile |
11. PUBERTY (Applied)
(Guyton & Hall)
Definition: Period of sexual maturation enabling reproduction
Trigger: Maturation of GnRH pulse generator in hypothalamus → ↑ LH/FSH → gonadal activation
Sequence of pubertal events:
Girls (average age 8–13 years):
- Thelarche (breast development) — first sign; begins ~10–11 years
- Pubarche (pubic hair)
- Growth spurt — peaks ~12 years
- Menarche (first menstruation) — ~12–13 years; last major event
Boys (average age 9–14 years):
- Testicular enlargement — first sign (testicular volume >4 mL)
- Pubic hair, penile growth
- Growth spurt — peaks ~14 years (later than girls)
- Voice changes, axillary hair, acne
Hormonal Changes at Puberty:
- ↑ GnRH pulsatility → ↑ LH, FSH
- ↑ Gonadal steroids → secondary sex characteristics
- ↑ GH + IGF-1 → growth spurt
- Estrogen in girls → epiphyseal fusion (ends growth); androgens in boys (same)
Adrenarche: ↑ adrenal androgens (DHEA, DHEAS) — pubic/axillary hair; occurs before gonadarche
Precocious Puberty:
| Type | Definition | Cause |
|---|---|---|
| Central (GnRH-dependent) | Puberty <8 (girls), <9 (boys) | Hypothalamic hamartoma, CNS tumor, idiopathic |
| Peripheral (GnRH-independent) | Sex steroids without GnRH activation | CAH, adrenal tumor, McCune-Albright, Leydig cell tumor |
- Treatment: GnRH agonist (continuous → desensitization of pituitary → ↓ LH/FSH)
Delayed Puberty:
- No breast development by 13 (girls), no testicular enlargement by 14 (boys)
- Causes: Constitutional delay (most common), hypogonadotropic (Kallmann's: GnRH deficiency + anosmia), hypergonadotropic (Turner's, Klinefelter's)
12. INFERTILITY — CAUSES & ROLE OF IVF
(Guyton & Hall)
Definition: Inability to conceive after 12 months of regular unprotected intercourse (6 months if >35 years)
Male Infertility Causes:
| Category | Examples |
|---|---|
| Pretesticular | Hypogonadotropic hypogonadism (Kallmann's, hyperprolactinemia) |
| Testicular | Klinefelter's (47XXY), varicocele, cryptorchidism, orchitis (mumps), chemotherapy |
| Post-testicular | Obstructive azoospermia (vas deferens blockage, CF), retrograde ejaculation |
| Spermatogenesis | Oligospermia (<15 million/mL), asthenospermia (poor motility), teratospermia |
Semen Analysis (WHO normals):
- Volume: ≥1.5 mL
- Sperm concentration: ≥16 million/mL
- Total motility: ≥42%
- Progressive motility: ≥30%
- Morphology: ≥4% normal forms (Kruger strict criteria)
Female Infertility Causes:
| Category | Examples |
|---|---|
| Ovulatory | PCOS (most common), hypothyroidism, hyperprolactinemia, POI, hypothalamic amenorrhea |
| Tubal/Peritoneal | PID, endometriosis, previous ectopic pregnancy |
| Uterine | Fibroids (submucous), Asherman's syndrome (intrauterine adhesions), congenital anomalies |
| Cervical | Hostile cervical mucus, cervical stenosis |
PCOS (Most common cause of female infertility):
- Diagnostic criteria (Rotterdam): 2 of 3 — oligo/anovulation + clinical/biochemical hyperandrogenism + polycystic ovaries on USS
- ↑ LH:FSH ratio (>2:1); ↑ LH → ↑ androgens from thecal cells
- Insulin resistance common; associated with obesity
Role of IVF (In Vitro Fertilization):
Steps of IVF:
- Ovarian stimulation: gonadotrophins (FSH ± LH) → multiple follicle development; GnRH agonist/antagonist to prevent premature LH surge
- Oocyte retrieval: transvaginal ultrasound-guided follicle aspiration (34–36 h after hCG trigger)
- Fertilization: conventional insemination or ICSI (intracytoplasmic sperm injection — for severe male factor)
- Embryo culture: 2–5 days (to blastocyst stage for better selection)
- Embryo transfer: usually day 3 or day 5 (blastocyst); fresh or frozen
- Luteal support: progesterone supplementation
Indications for IVF:
- Tubal factor (blocked tubes)
- Severe male factor (ICSI)
- Failed ovulation induction/IUI
- Endometriosis
- Unexplained infertility
- Age-related infertility (with egg freezing)
MCQ Traps:
- OHSS (Ovarian Hyperstimulation Syndrome): complication of stimulation; high E2, ascites, risk of thrombosis; prevented by GnRH antagonist + agonist trigger
- hCG used to trigger ovulation (mimics LH surge)
- Clomiphene citrate: anti-estrogen → ↑ GnRH pulsatility → ↑ FSH/LH → ovulation induction (first-line for PCOS)
13. PHYSIOLOGY OF MENOPAUSE
(Guyton & Hall)
Definition: Permanent cessation of menstruation; cessation for ≥12 consecutive months
- Average age: 51 years (range 45–55)
- Perimenopause: 2–8 years before; irregular cycles, fluctuating hormones
Pathophysiology:
- Progressive depletion of ovarian follicles → ↓ estrogen and progesterone
- Loss of negative feedback → ↑↑ FSH (most sensitive marker; FSH >40 IU/L)
- ↑ LH also, but FSH rises more
- ↓ Inhibin B (from granulosa cells) → first hormonal change in perimenopause
Hormonal Milieu of Menopause:
| Hormone | Change |
|---|---|
| Estradiol (E2) | ↓↓ (major source lost) |
| Estrone (E1) | Becomes dominant estrogen (from peripheral aromatization of androstenedione in fat) |
| FSH | ↑↑↑ |
| LH | ↑↑ |
| GnRH | ↑ |
| Inhibin B | ↓↓ |
| Progesterone | ↓↓ |
| Androgens | ↓ (but less than estrogen) |
Symptoms:
| Category | Symptoms |
|---|---|
| Vasomotor | Hot flushes, night sweats (most characteristic; due to ↑ norepinephrine, altered thermoregulatory set-point) |
| Genitourinary | Vaginal dryness, dyspareunia, urinary frequency (GSM — genitourinary syndrome of menopause) |
| Psychological | Mood changes, irritability, sleep disturbance, difficulty concentrating |
| Skeletal | Osteoporosis — ↑ bone resorption (↑ RANKL activity, loss of estrogen protective effect) |
| Cardiovascular | ↑ LDL, ↓ HDL, ↑ CVD risk |
Hot Flush Mechanism:
- ↑ NE + serotonin changes → ↓ thermoregulatory setpoint → heat dissipation response
Hormone Replacement Therapy (HRT):
- Combined (E+P) for women with uterus; estrogen-only for hysterectomy
- Benefits: Vasomotor symptoms, osteoporosis, GSM, mood
- Risks: Breast cancer (with combined HRT >5 years), VTE, stroke
- Window of opportunity hypothesis: HRT started <10 years of menopause → cardioprotective
Premature Ovarian Insufficiency (POI):
- Menopause <40 years
- Causes: Turner's, autoimmune, chemotherapy, FMR1 premutation
- FSH >25 IU/L on two occasions 4 weeks apart
MCQ Traps:
- First change in perimenopause: ↑ FSH (due to ↓ inhibin B)
- Principal estrogen after menopause: estrone (E1), not estradiol (E2)
- Commonest presenting symptom: hot flushes
- Osteoporosis marker: ↑ serum/urine CTX (collagen cross-links); DEXA T-score ≤ −2.5
- Karyotype in Turner's: 45XO → premature menopause + short stature
🔑 QUICK RECALL TABLE — MCQ FAVORITES
| Topic | Most Tested MCQ Point |
|---|---|
| MG | Anti-AChR antibodies; decremental RNS; pyridostigmine treatment |
| Lambert-Eaton | Anti-VGCC antibodies; incremental RNS; SCLC association |
| EMG denervation | Fibrillation potentials + positive sharp waves |
| Lymph flow | 2–4 L/day; principal force = peristalsis of collecting lymphatics |
| Smooth muscle | Calmodulin-MLCK pathway (no troponin) |
| Cardiac muscle | Cannot tetanize; CICR from SR; gap junctions in intercalated discs |
| Cheyne-Stokes | Heart failure; CO₂ oscillates around apneic threshold |
| Dry drowning | Laryngospasm (~15%) |
| Freshwater drowning | Hemodilution, hemolysis, VF |
| Decompression sickness | N₂ bubbles; treat with hyperbaric O₂ |
| Melatonin | Peaks 2–4 AM; light inhibits; promotes sleep + circadian rhythm |
| Pinealoma (child) | Destroys pineal → precocious puberty |
| Thymus | T-cell maturation; max size at puberty; 3rd pharyngeal pouch |
| Diabetes islets | β60%, α25%, δ10% |
| Insulin t½ | ~6 min; degraded by liver (50%) |
| SRY gene | On Y chromosome; triggers testes formation |
| Default sex | Female (in absence of SRY/androgens) |
| AMH | From Sertoli cells; regresses Müllerian ducts |
| DHT | From testosterone via 5α-reductase; masculinizes external genitalia |
| Thelarche | First sign of puberty in girls |
| Testicular enlargement | First sign of puberty in boys |
| PCOS | Most common female infertility; ↑ LH:FSH; Rotterdam criteria |
| IVF trigger | hCG (mimics LH surge); 34–36 h before retrieval |
| Menopause age | ~51 years; FSH >40 IU/L |
| Post-menopausal estrogen | Estrone (E1) from peripheral aromatization |
| First perimenopausal change | ↑ FSH (from ↓ inhibin B) |
*Sources: Guyton & Hall Textbook of Medical Physiology (14th ed.); Ganong's Review of Medical Physiology (26th ed.); Medical Physiology (Boron & Boulpaep / Elsevier)*All 13 topics have been covered. Here's a summary of what's included and key exam strategy tips:
How to Use These Notes for MCQs
Highest-yield topics based on exam frequency:
- MG — Know: anti-AChR antibodies, decremental RNS, pyridostigmine, thymectomy, distinction from Lambert-Eaton
- Diabetes — Islet cell proportions, insulin actions on liver/muscle/fat, DKA vs. HONK, C-peptide significance
- Menopause — FSH rises first, estrone dominates post-menopause, hot flush mechanism
- Sex differentiation — Default = female, AMH role, 5α-reductase, AIS, CAH
- IVF — Steps, ICSI indication, OHSS complication, luteal support
- Lymphatics — 2–4 L/day, principal propulsive force = peristalsis, 25–50% plasma protein recycled
- Muscle comparison — Calmodulin in smooth muscle; no tetanus in cardiac; T-tubule differences
- Drowning — Dry vs. wet; freshwater (VF, hemolysis) vs. saltwater (hemoconcentration)
- Deep sea diving — Decompression sickness (N₂ bubbles, hyperbaric O₂ treatment), nitrogen narcosis, O₂ toxicity
- Puberty — Thelarche first in girls; testicular enlargement first in boys; GnRH agonist for precocious puberty
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