Now I'll compile the full MCQ-based notes from all sources gathered plus core medical knowledge.
π MCQ-Based Physiology Notes β Comprehensive Guide
1. π¬ ELECTROMYOGRAPHY (EMG)
Key Facts for MCQs:
Q1. EMG records electrical activity of muscles via:
- (A) Surface electrodes only
- (B) Needle electrodes only
- (C) Surface or needle electrodes β
- (D) Ultrasound
Q2. A CMAP (Compound Motor Action Potential) represents:
- (A) Summated sensory neuron activity
- (B) Summated electrical activity of muscle cells innervated by a motor nerve β
- (C) Single motor unit potential
- (D) Autonomic nerve conduction
Q3. In nerve conduction studies, SNAP (Compound Sensory Nerve Action Potential) is PRESERVED in lesions:
- (A) Distal to dorsal root ganglia
- (B) Proximal to dorsal root ganglia β
- (C) In peripheral neuropathy
- (D) In Guillain-BarrΓ© syndrome
Q4. Slow repetitive stimulation (2-3 Hz) in EMG depletes:
- (A) Postsynaptic AChRs
- (B) Presynaptic ACh stores β
- (C) Myelin
- (D) CaΒ²βΊ channels
Q5. Decreased SNAP amplitude indicates:
- (A) Demyelination
- (B) Axonal damage β
- (C) NMJ disorder
- (D) Myopathy
Q6. Normal nerve conduction velocity (NCV) in upper limbs is approximately:
- (A) 20β30 m/s
- (B) 35β45 m/s
- (C) 50β70 m/s β
- (D) 80β100 m/s
Source: Neuroanatomy through Clinical Cases 3rd Edition
2. π MYASTHENIA GRAVIS (MG)
Q1. Myasthenia gravis is caused by antibodies against:
- (A) Voltage-gated CaΒ²βΊ channels
- (B) Nicotinic ACh receptors (AChR) β
- (C) Voltage-gated NaβΊ channels
- (D) NMDA receptors
Q2. The main immunogenic region (MIR) targeted in MG is on which subunit of AChR?
- (A) Ξ± subunit β
- (B) Ξ² subunit
- (C) Ξ³ subunit
- (D) Ξ΄ subunit
Q3. Bimodal peak incidence of MG β early onset is associated with:
- (A) Young women with thymic hyperplasia β
- (B) Old men with thymoma
- (C) Children with congenital myasthenic syndrome
- (D) Men with thymoma
Q4. Electrophysiological hallmark of MG:
- (A) Increased amplitude of MEPP
- (B) Decreased amplitude of MEPP with normal quantal frequency β
- (C) Complete abolition of MEPP
- (D) Increased quantal frequency
Q5. First-line pharmacological treatment of MG:
- (A) Atropine
- (B) Pyridostigmine (AChE inhibitor) β
- (C) Succinylcholine
- (D) Neostigmine methylsulfate IV only
Q6. Thymectomy in MG patients with thymoma results in clinical improvement in:
- (A) 25%
- (B) 50%
- (C) ~75% β
- (D) 100%
Q7. MG crisis vs. Cholinergic crisis β cholinergic crisis is caused by:
- (A) Insufficient AChE inhibitor
- (B) Overdose of AChE inhibitor β
- (C) Autoimmune flare
- (D) Thymic hyperplasia
Q8. MG is differentiated from Lambert-Eaton syndrome because in MG:
- (A) Strength improves with repeated activity
- (B) Strength worsens with repeated activity (fatigable weakness) β
- (C) Reflexes are absent
- (D) Autonomic features dominate
Q9. Treatment targeting the immunological attack in MG includes:
- (A) Pyridostigmine
- (B) Plasmapheresis + corticosteroids β
- (C) Atropine
- (D) Calcium gluconate
Source: Medical Physiology (Boron & Boulpaep); Neuroanatomy through Clinical Cases
3. π©Έ LYMPHATIC CIRCULATION
Q1. The largest lymphatic vessel in the body is:
- (A) Right lymphatic duct
- (B) Thoracic duct β
- (C) Cisterna chyli
- (D) Subclavian trunk
Q2. Thoracic duct drains into:
- (A) Right subclavian vein
- (B) Junction of left subclavian and left internal jugular vein β
- (C) Superior vena cava
- (D) Azygos vein
Q3. Lymph capillaries are permeable to large molecules because they have:
- (A) Tight junctions
- (B) Fenestrations
- (C) Overlapping endothelial cells with no basement membrane (anchoring filaments) β
- (D) Gap junctions
Q4. The main driving force for lymph flow is:
- (A) Cardiac output
- (B) Skeletal muscle contractions + respiratory movements + intrinsic lymphatic vessel contraction β
- (C) Osmotic pressure
- (D) Gravity alone
Q5. Edema in lymphatic obstruction is called:
- (A) Lymphedema β
- (B) Pitting edema
- (C) Anasarca
- (D) Hydrothorax
Q6. Lymph from the lower extremities first passes through:
- (A) Inguinal lymph nodes β
- (B) Axillary nodes
- (C) Mesenteric nodes
- (D) Thoracic duct directly
Q7. Chyle is lymph rich in fat absorbed from:
- (A) Stomach
- (B) Small intestine via lacteals β
- (C) Colon
- (D) Liver
Q8. Lymph does NOT contain:
- (A) Lymphocytes
- (B) Proteins
- (C) RBCs (under normal conditions) β
- (D) Lipids
4. πͺ COMPARISON: SKELETAL vs. CARDIAC vs. SMOOTH MUSCLE
| Feature | Skeletal | Cardiac | Smooth |
|---|
| Nuclei | Multinucleate | Single (central) | Single (central) |
| Striations | Yes | Yes | No |
| Control | Voluntary | Involuntary | Involuntary |
| T-tubules | Wide, at A-I junction | Narrow, at Z-disc | Absent/rudimentary |
| Intercalated discs | No | Yes | No |
| SR development | Extensive | Less developed | Poorly developed |
| Pacemaker | None | SA node (intrinsic) | Some (interstitial cells) |
| CaΒ²βΊ source | Mainly SR | SR + extracellular | Mainly extracellular |
| CaΒ²βΊ mediator | Troponin | Troponin | Calmodulin-MLCK |
| Action potential | All-or-none | Plateau (phase 2) | Slow, graded |
| Fatigue | Yes | No | No |
| Regeneration | Limited (satellite cells) | None | Yes |
| Length of fiber | Long (few cm) | Short, branched | Short, spindle |
Q1. Cardiac muscle is unique because it has:
- (A) Intercalated discs with gap junctions β
- (B) Multiple nuclei
- (C) No T-tubules
- (D) Voluntary control
Q2. CaΒ²βΊ in smooth muscle acts through:
- (A) Troponin-C
- (B) Calmodulin β MLCK (myosin light chain kinase) β
- (C) Troponin-I
- (D) Actin directly
Q3. The refractory period of cardiac muscle is:
- (A) Very short (allows tetanus)
- (B) Long (prevents tetanic contraction) β
- (C) Same as skeletal muscle
- (D) Absent
Q4. Smooth muscle contraction involves phosphorylation of:
- (A) Actin
- (B) Myosin light chain β
- (C) Troponin
- (D) Tropomyosin
Q5. T-tubules in skeletal muscle are located at:
- (A) M-line
- (B) A-I junction (junction of A and I bands) β
- (C) Z-disc
- (D) H-zone
5. π PERIODIC BREATHING & DROWNING
Periodic Breathing:
Q1. Cheyne-Stokes breathing is characterized by:
- (A) Rapid regular breathing
- (B) Waxing and waning tidal volume with apneic episodes β
- (C) Deep, slow regular breathing
- (D) Inspiratory stridor
Q2. Commonest cause of Cheyne-Stokes breathing:
- (A) Left heart failure (increased circulation time) β
- (B) Right heart failure
- (C) Pulmonary embolism
- (D) Asthma
Q3. The underlying mechanism of Cheyne-Stokes breathing is:
- (A) Increased controller gain + increased circulation time β oscillation of COβ around the apnea threshold β
- (B) Peripheral chemoreceptor failure
- (C) Brainstem infarct
- (D) Hyperthyroidism
Q4. Biot's breathing (ataxic breathing) is seen in:
- (A) Cheyne-Stokes
- (B) Medullary compression (meningitis, raised ICP) β
- (C) Metabolic acidosis
- (D) Anxiety
Q5. Kussmaul breathing (deep, rapid) is caused by:
- (A) Metabolic acidosis (diabetic ketoacidosis) β
- (B) Respiratory alkalosis
- (C) Opioid overdose
- (D) Cervical cord lesion
Drowning:
Q6. "Dry drowning" occurs due to:
- (A) Massive water aspiration
- (B) Laryngospasm preventing water aspiration β
- (C) Cardiac arrest first
- (D) Pulmonary edema
Q7. In wet drowning (fresh water), the major pathophysiology is:
- (A) Hemodilution β hemolysis β hyperkalemia β ventricular fibrillation β
- (B) Hemoconcentration
- (C) Hypokalemia
- (D) Metabolic alkalosis
Q8. In seawater drowning (hypertonic):
- (A) Water moves from blood into alveoli β hemoconcentration β pulmonary edema β
- (B) Hemolysis occurs
- (C) Hyponatremia
- (D) Hypervolemia
Q9. "Secondary drowning" (near-drowning syndrome) is characterized by:
- (A) Immediate death
- (B) Delayed pulmonary edema/ARDS hours after rescue β
- (C) Bradycardia only
- (D) Metabolic alkalosis
6. π€Ώ DEEP SEA DIVING β PHYSIOLOGY & APPLIED
Q1. As depth increases by 10 meters of sea water, pressure increases by:
- (A) 0.5 atm
- (B) 1 atm β
- (C) 2 atm
- (D) 5 atm
Q2. Nitrogen narcosis is also called:
- (A) Oxygen toxicity
- (B) "Rapture of the deep" β narcotic effect of Nβ under high pressure β
- (C) Decompression sickness
- (D) COβ retention
Q3. Decompression sickness ("The Bends") results from:
- (A) COβ bubble formation
- (B) Nitrogen bubble formation in tissues on rapid ascent β
- (C) Oβ toxicity
- (D) Hypercapnia
Q4. Treatment of decompression sickness is:
- (A) Hyperbaric oxygen therapy (recompression) β
- (B) Diuretics
- (C) Vasodilators
- (D) Mechanical ventilation
Q5. Oxygen toxicity at high partial pressures affects primarily:
- (A) Kidneys
- (B) CNS (Grand mal seizures β Paul Bert effect) and lungs (Lorrain Smith effect) β
- (C) Liver
- (D) Heart
Q6. Helium is substituted for nitrogen in deep diving mixtures because:
- (A) Low solubility in blood, low narcotic effect, low density β
- (B) It provides more Oβ
- (C) It prevents hypercapnia
- (D) It has high solubility
Q7. Henry's Law states that at constant temperature:
- (A) Volume of gas is inversely proportional to pressure
- (B) Amount of gas dissolved in liquid is proportional to its partial pressure β
- (C) Volume is directly proportional to temperature
- (D) Pressure Γ volume = constant
Q8. "Squeeze" injury in diving affects:
- (A) Only the eyes
- (B) Air-filled body spaces (sinuses, ears, lungs) due to unequal pressure β
- (C) Only skin
- (D) Only joints
Q9. High Pressure Nervous Syndrome (HPNS) occurs at depths:
- (A) >10 m
- (B) >30 m
- (C) >150β200 m β
- (D) >50 m
Q10. The diving reflex includes:
- (A) Bradycardia + peripheral vasoconstriction + blood shift to core β
- (B) Tachycardia
- (C) Vasodilation
- (D) Bronchodilation
7. π PINEAL GLAND PHYSIOLOGY
Q1. Main hormone secreted by the pineal gland:
- (A) Serotonin
- (B) Melatonin β
- (C) Dopamine
- (D) TSH
Q2. Main cell type of the pineal gland:
- (A) Pinealocyte β
- (B) Astrocyte
- (C) Chromaffin cell
- (D) Pituicyte
Q3. Melatonin secretion is HIGHEST at:
- (A) Noon
- (B) 6 PM
- (C) 2β4 AM β
- (D) 8 AM
Q4. Pathway for light suppression of melatonin: retina β
- (A) Suprachiasmatic nucleus β intermediolateral cell column β superior cervical ganglion β pinealocyte β
- (B) Retina β hypothalamus β pituitary β pineal
- (C) Retina β thalamus β pineal directly
- (D) Retina β optic cortex β pineal
Q5. In darkness, norepinephrine released onto pinealocytes:
- (A) Stimulates melatonin synthesis and release β
- (B) Inhibits melatonin
- (C) Stimulates serotonin release only
- (D) Has no effect
Q6. Clinical application of melatonin β calcification of pineal gland ("brain sand") is useful for:
- (A) Detecting midline shift on X-ray/CT (radiological landmark) β
- (B) Diagnosing diabetes
- (C) Measuring ICP
- (D) Diagnosing MG
Q7. Pineal tumors are associated with:
- (A) Excess melatonin
- (B) Loss of melatonin secretion; precocious puberty (germinoma destroying gland) β
- (C) Hypothyroidism
- (D) Acromegaly
8. π¦ THYMUS PHYSIOLOGY
Q1. The thymus is the site of maturation for:
- (A) B lymphocytes
- (B) T lymphocytes β
- (C) NK cells
- (D) Macrophages
Q2. Thymic hormone responsible for T-cell maturation:
- (A) Thyroxine
- (B) Thymosin (thymopoietin, thymulin) β
- (C) Thyroglobulin
- (D) PTH
Q3. The thymus is LARGEST at:
- (A) Birth
- (B) Puberty β
- (C) Middle age
- (D) Old age
Q4. After puberty, the thymus undergoes:
- (A) Involution (replaced by fat and fibrous tissue) β
- (B) Hyperplasia
- (C) Malignant transformation
- (D) Enlargement
Q5. In DiGeorge syndrome, absence of thymus leads to:
- (A) B-cell deficiency
- (B) T-cell deficiency β recurrent infections with intracellular pathogens β
- (C) NK cell deficiency
- (D) Complement deficiency
Q6. Thymic selection processes:
- (A) Positive selection (cortex) + Negative selection (medulla) β self-tolerant T cells β
- (B) Only positive selection
- (C) Only negative selection
- (D) Random selection
Q7. MHC restriction of T cells is established during:
- (A) Positive selection in thymic cortex β
- (B) Negative selection
- (C) Peripheral activation
- (D) Bone marrow development
9. π¬ DIABETES MELLITUS
Q1. Beta cells of islets of Langerhans constitute approximately ___% of islet cells:
- (A) 25%
- (B) 60% β
- (C) 10%
- (D) 80%
Q2. Alpha cells secrete:
- (A) Insulin
- (B) Glucagon β
- (C) Somatostatin
- (D) Amylin
Q3. Hormone that inhibits both insulin AND glucagon secretion:
- (A) Amylin
- (B) GIP
- (C) Somatostatin (from delta cells) β
- (D) Pancreatic polypeptide
Q4. Type 1 DM is characterized by:
- (A) Autoimmune destruction of beta cells β absolute insulin deficiency β
- (B) Insulin resistance
- (C) Gestational hormones
- (D) MODY gene mutations
Q5. HbA1c reflects blood glucose over:
- (A) 1 week
- (B) 1 month
- (C) 2β3 months β
- (D) 6 months
Q6. In DKA (Diabetic Ketoacidosis), breathing pattern is:
- (A) Cheyne-Stokes
- (B) Kussmaul (deep, labored) β
- (C) Biot's
- (D) Apneusis
Q7. Diagnostic criterion for DM (fasting plasma glucose):
- (A) β₯100 mg/dL
- (B) β₯126 mg/dL on two occasions β
- (C) β₯110 mg/dL
- (D) β₯200 mg/dL fasting
Q8. GLUT-2 is the glucose transporter in:
- (A) Brain
- (B) Muscle
- (C) Pancreatic beta cells and liver β
- (D) RBCs
Q9. Insulin promotes all EXCEPT:
- (A) Glycogenesis
- (B) Lipogenesis
- (C) Protein synthesis
- (D) Glycogenolysis β
(insulin inhibits glycogenolysis)
Q10. Amylin (co-secreted with insulin) functions by:
- (A) Stimulating glucagon
- (B) Inhibiting insulin secretion, slowing gastric emptying β
- (C) Increasing appetite
- (D) Promoting glycogenolysis
Source: Guyton and Hall Textbook of Medical Physiology
10. 𧬠SEX DETERMINATION & DIFFERENTIATION
Q1. Sex determination is primarily decided by:
- (A) Testosterone at conception
- (B) Presence or absence of Y chromosome (SRY gene) β
- (C) Maternal hormones
- (D) Gonadotropins
Q2. SRY gene on Y chromosome encodes:
- (A) Testis-determining factor (TDF) β
- (B) Anti-MΓΌllerian hormone
- (C) Testosterone
- (D) LH receptor
Q3. Without SRY gene, the undifferentiated gonad develops into:
- (A) Testis
- (B) Ovary β
- (C) Neither
- (D) Adrenal cortex
Q4. MΓΌllerian-inhibiting factor (AMH) is produced by:
- (A) Sertoli cells of testis β
- (B) Leydig cells
- (C) Granulosa cells
- (D) Theca cells
Q5. In females, the Wolffian duct degenerates because:
- (A) Absence of testosterone β
- (B) Estrogen actively degrades it
- (C) AMH destroys it
- (D) Progesterone degrades it
Q6. Congenital Adrenal Hyperplasia (CAH) virilizes females because of excess:
- (A) Estrogen
- (B) Androgens (17-hydroxyprogesterone β androstenedione) β
- (C) Cortisol
- (D) AMH
Q7. 5Ξ±-reductase deficiency causes:
- (A) Ambiguous genitalia at birth β virilization at puberty in 46,XY males (DHT deficiency) β
- (B) Complete feminization
- (C) Infertility in females
- (D) No phenotypic change
Q8. Androgen Insensitivity Syndrome (AIS) β complete form presents as:
- (A) 46,XY female phenotype with absent uterus, blind vagina, testes β
- (B) 46,XX male
- (C) Turner's syndrome
- (D) Klinefelter's
11. π§ PUBERTY & APPLIED
Q1. The first sign of puberty in girls is:
- (A) Menarche
- (B) Thelarche (breast development β budding) β
- (C) Pubic hair
- (D) Growth spurt
Q2. The first sign of puberty in boys is:
- (A) Testicular enlargement (>4 mL or >2.5 cm length) β
- (B) Pubic hair
- (C) Voice change
- (D) Growth spurt
Q3. Average age of menarche in girls (in developed countries):
- (A) 10 years
- (B) 12β13 years β
- (C) 15 years
- (D) 16 years
Q4. GnRH pulse frequency is critical β high-frequency pulses favor secretion of:
- (A) FSH
- (B) LH β
- (C) Both equally
- (D) Inhibin
Q5. Precocious puberty (central/GnRH-dependent) is caused by:
- (A) Adrenal tumor
- (B) Ovarian cyst
- (C) Early activation of hypothalamic-pituitary-gonadal axis β
- (D) CAH
Q6. Delayed puberty in boys is defined as no secondary sex characteristics by age:
- (A) 12
- (B) 13
- (C) 14 β
- (D) 16
Q7. Leptin's role in puberty:
- (A) Acts as a permissive signal β adequate fat mass triggers GnRH pulse generator β
- (B) Inhibits GnRH
- (C) Directly stimulates gonads
- (D) No role in puberty
Q8. Kallmann syndrome presents with:
- (A) Hypogonadotropic hypogonadism + anosmia (absent olfactory bulb) β
- (B) Hypergonadotropic hypogonadism
- (C) Normal puberty + anosmia
- (D) Precocious puberty
12. π₯ INFERTILITY β CAUSES & ROLE OF IVF
Q1. Infertility is defined as failure to conceive after:
- (A) 6 months
- (B) 1 year of regular unprotected intercourse β
- (C) 2 years
- (D) 3 years
Q2. Most common cause of female infertility:
- (A) Uterine fibroids
- (B) Ovulatory disorders (PCOS most common) β
- (C) Tubal factor
- (D) Cervical factor
Q3. Normal semen analysis (WHO 2021) β minimum sperm concentration:
- (A) 16 million/mL β
(revised from 15 million)
- (B) 20 million/mL
- (C) 5 million/mL
- (D) 40 million/mL
Q4. Oligozoospermia is sperm count <:
- (A) 16 million/mL β
- (B) 20 million/mL
- (C) 5 million/mL
- (D) 40 million/mL
Q5. In IVF, ovulation induction is typically achieved with:
- (A) GnRH alone
- (B) Gonadotropins (FSH/hMG) with or without GnRH agonist/antagonist suppression β
- (C) Clomiphene only
- (D) Progesterone
Q6. In IVF, oocyte retrieval is performed:
- (A) At ovulation spontaneously
- (B) ~36 hours after hCG trigger, transvaginally under ultrasound guidance β
- (C) 72 hours after LH surge
- (D) Laparoscopically always
Q7. ICSI (Intracytoplasmic Sperm Injection) is specifically indicated for:
- (A) Tubal factor
- (B) Severe male factor infertility (low count, motility, or morphology) β
- (C) Endometriosis only
- (D) Recurrent miscarriage
Q8. Asherman's syndrome causes infertility through:
- (A) Tubal occlusion
- (B) Intrauterine adhesions (synechiae) preventing implantation β
- (C) Anovulation
- (D) Cervical stenosis only
Q9. Antisperm antibodies cause infertility by:
- (A) Impairing sperm motility, penetration of cervical mucus, and fertilization β
- (B) Destroying ova
- (C) Blocking tubal transport of embryo
- (D) Preventing implantation
Q10. First successful IVF baby was born in:
- (A) 1973
- (B) 1978 β
(Louise Brown β Steptoe & Edwards)
- (C) 1985
- (D) 1990
13. πΈ PHYSIOLOGY OF MENOPAUSE
Q1. Average age of natural menopause:
- (A) 40β42 years
- (B) 45β47 years
- (C) 48β52 years (average ~51) β
- (D) 55β60 years
Q2. Premature ovarian insufficiency (POI) is menopause before age:
- (A) 40 years β
- (B) 45 years
- (C) 50 years
- (D) 35 years
Q3. FSH levels in menopause:
- (A) Decreased
- (B) Normal
- (C) Markedly elevated (>40 IU/L on two occasions 4 weeks apart) β
- (D) Fluctuating only
Q4. Primary estrogen in postmenopausal women is:
- (A) Estradiol (E2)
- (B) Estrone (E1) β from peripheral conversion of androstenedione in adipose β
- (C) Estriol (E3)
- (D) Ethinyl estradiol
Q5. "Hot flashes" in menopause are due to:
- (A) Excess progesterone
- (B) Estrogen withdrawal β thermoregulatory instability (lowered thermostat set-point) β
- (C) LH excess directly
- (D) Cortisol changes
Q6. Long-term consequence of estrogen deficiency in menopause:
- (A) Hypertension alone
- (B) Osteoporosis (bone resorption > formation) β
- (C) Hypoglycemia
- (D) Hypothyroidism
Q7. Genitourinary syndrome of menopause (GSM) includes:
- (A) Vaginal dryness, dyspareunia, urinary urgency, recurrent UTIs β
- (B) Hot flashes only
- (C) Mood changes only
- (D) Only bone changes
Q8. Hormone Replacement Therapy (HRT) is contraindicated in:
- (A) Estrogen-receptor positive breast cancer, thromboembolic disease, undiagnosed vaginal bleeding β
- (B) Osteoporosis
- (C) Vasomotor symptoms
- (D) Coronary heart disease in young women (not a contraindication per current guidelines)
Q9. After menopause, FSH:LH ratio is:
- (A) LH > FSH
- (B) FSH > LH β
- (C) Equal
- (D) Both suppressed
Q10. The "menopausal triad":
- (A) Vasomotor symptoms + Urogenital atrophy + Osteoporosis β
- (B) Weight gain + Depression + Acne
- (C) Hirsutism + Infertility + Anovulation
- (D) Polyuria + Polydipsia + Polyphagia
---You've run out of free credits. Sign up for a free account to continue using Orris.