Complete Physiology Theory Viva Compilation (MBBS Practical)
GP and Blood were covered in detail earlier. Here are the remaining 8 systems in the same Q&A format.
1. Nerve-Muscle Physiology (NMJ)
Q1. Describe the structure of the neuromuscular junction (NMJ).
The NMJ has three components: the presynaptic motor nerve terminal (containing acetylcholine-filled vesicles), the synaptic cleft, and the postsynaptic motor end plate (muscle membrane with junctional folds bearing nicotinic acetylcholine receptors and acetylcholinesterase enzyme).
Q2. Describe the events of neuromuscular transmission.
Nerve action potential reaches the terminal -> opens voltage-gated Ca2+ channels -> Ca2+ influx triggers ACh vesicle exocytosis -> ACh diffuses across the cleft and binds nicotinic receptors on the end plate -> opens ligand-gated Na+/K+ channels -> produces an End Plate Potential (EPP) -> if EPP reaches threshold, it triggers a propagated muscle action potential -> ACh is then hydrolyzed by acetylcholinesterase, terminating the signal.
Q3. What is the End Plate Potential (EPP)? How does it differ from EPSP?
EPP is the local, graded depolarization produced at the motor end plate by ACh action; it is normally large enough to always exceed threshold (high safety factor), unlike an EPSP in neuron-to-neuron synapses which often requires summation to reach threshold.
Q4. Describe the sliding filament theory of muscle contraction.
Muscle shortening occurs by the myosin (thick filament) cross-bridges attaching to actin (thin filament) and pulling it toward the center of the sarcomere in a ratchet-like cycle, without any change in the length of the filaments themselves - only the overlap between actin and myosin increases, shortening the sarcomere.
Q5. Explain excitation-contraction coupling.
Muscle action potential travels along the T-tubules -> activates dihydropyridine receptors -> triggers ryanodine receptors on the sarcoplasmic reticulum to release Ca2+ -> Ca2+ binds troponin C -> causes tropomyosin to shift, exposing myosin-binding sites on actin -> cross-bridge cycling begins (myosin head uses ATP hydrolysis to attach, pull "power stroke," detach, and reset).
Q6. What are troponin and tropomyosin? Their role?
Both are regulatory proteins on the thin filament. Tropomyosin normally blocks the myosin-binding site on actin. Troponin (subunits C, I, T) is bound to tropomyosin; when Ca2+ binds troponin C, it shifts tropomyosin away, unblocking the site for cross-bridge formation.
Q7. Differentiate isotonic and isometric contraction.
- Isotonic: muscle length changes, tension remains constant (e.g., lifting a weight).
- Isometric: tension develops but muscle length remains unchanged (e.g., pushing against an immovable object).
Q8. Describe the phases of a simple muscle twitch.
- Latent period - electrical events occur, no visible contraction yet
- Contraction phase - muscle shortens/develops tension
- Relaxation phase - muscle returns to resting length
Q9. What is summation and tetanus?
If a second stimulus arrives before the muscle fully relaxes from the first, the twitches summate (wave summation), producing greater tension. With sufficiently high stimulus frequency, individual twitches fuse into a smooth sustained contraction called tetanus (complete tetanus - no relaxation between stimuli; incomplete tetanus - partial relaxation visible).
Q10. What is Treppe (staircase phenomenon)?
A gradual increase in the force of successive twitches when a muscle is stimulated repeatedly at a fixed submaximal frequency after a period of rest, due to increasing availability of intracellular Ca2+ with each successive stimulus.
Q11. Define motor unit. What is innervation ratio?
A motor unit is a single motor neuron together with all the muscle fibers it innervates. Innervation ratio = number of muscle fibers per motor neuron; small in fine-movement muscles (e.g., extraocular muscles - high precision) and large in postural muscles (e.g., gastrocnemius - high force).
Q12. Differentiate Type I and Type II muscle fibers.
- Type I (slow-twitch, red): high myoglobin/mitochondria, oxidative metabolism, fatigue-resistant, used for posture/endurance
- Type II (fast-twitch, white): fewer mitochondria, glycolytic metabolism, fatigue quickly, used for rapid powerful movements
Q13. What is muscle fatigue? Causes?
Fatigue is the decline in force-generating capacity with sustained/repeated activity, due to depletion of ATP/glycogen, accumulation of lactic acid and H+, impaired Ca2+ release, and failure of neuromuscular transmission.
Q14. What is rigor mortis?
Stiffening of muscles after death due to depletion of ATP - cross-bridges attach to actin but cannot detach (detachment requires ATP), leaving the muscle in a fixed, contracted state until proteolysis begins.
Q15. Explain the mechanism of action of neuromuscular blocking drugs.
- Depolarizing (e.g., succinylcholine) - acts as an ACh receptor agonist causing sustained depolarization and receptor desensitization (initial fasciculations then flaccid paralysis).
- Non-depolarizing (e.g., d-tubocurarine, vecuronium) - competitively block ACh from binding nicotinic receptors, preventing end plate depolarization.
Q16. What is Myasthenia Gravis?
An autoimmune disease with antibodies against postsynaptic nicotinic ACh receptors at the NMJ, reducing effective receptor number and causing muscle weakness and fatigability, classically improving temporarily with anticholinesterase drugs (e.g., neostigmine).
Quick Fire Round
- Neurotransmitter at NMJ: Acetylcholine
- Enzyme that degrades ACh: Acetylcholinesterase
- Functional unit of skeletal muscle: Sarcomere
- Ion triggering cross-bridge cycling: Ca2+
- ATP is required for: cross-bridge detachment (and Ca2+ reuptake into SR)
- Drug that blocks acetylcholinesterase: Neostigmine, Physostigmine
Sources: Guyton and Hall Textbook of Medical Physiology; Costanzo Physiology, 7th Edition
2. Cardiovascular System (CVS)
Q1. Describe the cardiac cycle and its phases.
One cardiac cycle (~0.8 sec at 75 bpm) consists of: Atrial systole -> Isovolumetric ventricular contraction -> Rapid ejection -> Reduced ejection -> Isovolumetric relaxation -> Rapid filling -> Reduced filling (diastasis). Ventricular systole lasts ~0.3 sec, diastole ~0.5 sec.
Q2. What are the ECG waves and their significance?
- P wave - atrial depolarization
- QRS complex - ventricular depolarization
- T wave - ventricular repolarization
- PR interval (0.12-0.20 sec) - AV nodal conduction time
- QT interval - total ventricular activity duration
Q3. Describe the heart sounds and areas of auscultation.
- S1 - closure of AV valves (mitral/tricuspid), marks onset of systole
- S2 - closure of semilunar valves (aortic/pulmonary), marks onset of diastole
- S3 (physiological in children) - rapid ventricular filling
- S4 - atrial contraction against a stiff ventricle (pathological in adults)
Areas: Mitral - 5th ICS midclavicular line; Tricuspid - left lower sternal border; Aortic - 2nd ICS right sternal border; Pulmonary - 2nd ICS left sternal border.
Q4. What determines Cardiac Output? State Frank-Starling's law.
Cardiac Output = Heart Rate x Stroke Volume. Stroke volume depends on preload, afterload, and contractility. Frank-Starling law: within physiological limits, the greater the venous return (preload/end-diastolic volume), the greater the force of ventricular contraction and stroke volume, due to increased length-dependent overlap of actin-myosin filaments.
Q5. Describe the cardiac conduction system.
SA node (pacemaker, in right atrium) -> spreads through atria -> AV node (delays impulse ~0.1 sec, allowing ventricular filling) -> Bundle of His -> left and right bundle branches -> Purkinje fibers -> ventricular myocardium.
Q6. Why is the SA node the natural pacemaker?
It has the fastest rate of spontaneous depolarization (pacemaker potential, due to funny current/If and Ca2+ channels causing gradual depolarization to threshold) compared to AV node or Purkinje fibers, so it sets the rhythm for the entire heart.
Q7. How is arterial blood pressure regulated? Explain the baroreceptor reflex.
BP = Cardiac Output x Total Peripheral Resistance. Baroreceptor reflex: baroreceptors in carotid sinus and aortic arch sense stretch (BP); a rise in BP increases their firing, which via the vasomotor center increases vagal (parasympathetic) tone and decreases sympathetic tone, causing decreased HR, contractility, and vasodilation - lowering BP back toward normal (negative feedback).
Q8. What is the role of the Renin-Angiotensin-Aldosterone System (RAAS) in BP regulation?
Fall in renal perfusion pressure/Na+ triggers renin release from juxtaglomerular cells -> converts angiotensinogen to angiotensin I -> ACE converts it to angiotensin II (potent vasoconstrictor, stimulates aldosterone release from adrenal cortex) -> aldosterone promotes Na+/water retention, increasing blood volume and BP. This is a longer-term regulator compared to the baroreceptor reflex.
Q9. What are Korotkoff sounds? Their phases?
Sounds heard over the brachial artery during BP measurement with a sphygmomanometer, due to turbulent flow. Phase I onset = systolic pressure; Phase V (sound disappearance) = diastolic pressure.
Q10. Explain the Starling forces governing capillary fluid exchange.
Net filtration depends on the balance of: capillary hydrostatic pressure and interstitial oncotic pressure (favor filtration out) versus plasma oncotic pressure and interstitial hydrostatic pressure (favor reabsorption). Net Filtration = Kf[(Pc - Pi) - sigma(pi_c - pi_i)].
Q11. What is Venous Return and what factors affect it?
Venous return is the volume of blood flowing back to the right atrium per minute, aided by the skeletal muscle pump, respiratory pump (negative intrathoracic pressure), venous valves, sympathetic venoconstriction, and gravity effects.
Q12. Describe the jugular venous pulse waves.
- a wave - atrial contraction
- c wave - carotid pulsation/tricuspid bulging during isovolumetric contraction
- v wave - atrial filling against a closed tricuspid valve
- x and y descents - atrial relaxation and tricuspid opening respectively
Q13. What are heart murmurs? Give examples.
Abnormal turbulent-flow sounds heard due to valvular defects (stenosis or regurgitation) or abnormal shunts. E.g., mitral stenosis - mid-diastolic murmur; aortic stenosis - ejection systolic murmur; mitral regurgitation - pansystolic murmur.
Q14. What is Cardiac Index?
Cardiac Output divided by Body Surface Area, used to normalize CO across different body sizes; normal is about 3-3.5 L/min/m2.
Q15. What is Pulse Pressure and Mean Arterial Pressure (MAP)?
Pulse pressure = Systolic BP - Diastolic BP. MAP = Diastolic BP + 1/3(Pulse Pressure), representing the average driving pressure for organ perfusion.
Quick Fire Round
- Normal HR: 60-100 bpm
- Duration of cardiac cycle at 75 bpm: 0.8 sec
- AV nodal delay: ~0.1 sec
- Fastest conducting tissue: Purkinje fibers
- Normal cardiac output: ~5 L/min
- Normal BP: 120/80 mmHg
Sources: Guyton and Hall Textbook of Medical Physiology; Costanzo Physiology, 7th Edition
3. Respiratory System (RS)
Q1. Describe the mechanics of quiet inspiration and expiration.
Quiet inspiration is active: diaphragm and external intercostals contract, increasing thoracic volume, decreasing intrapleural/intrapulmonary pressure below atmospheric, drawing air in. Quiet expiration is passive: elastic recoil of the lungs/chest wall returns the thorax to resting position, increasing pressure and expelling air.
Q2. Define and give normal values of lung volumes and capacities.
- Tidal Volume (TV): ~500 mL
- Inspiratory Reserve Volume (IRV): ~2500-3000 mL
- Expiratory Reserve Volume (ERV): ~1000-1200 mL
- Residual Volume (RV): ~1200 mL
- Vital Capacity (VC) = TV+IRV+ERV: ~4500-4800 mL
- Functional Residual Capacity (FRC) = ERV+RV
- Total Lung Capacity (TLC) = VC+RV: ~6000 mL
Q3. What is FEV1/FVC ratio? Its clinical use?
FEV1 (Forced Expiratory Volume in 1 second) / FVC (Forced Vital Capacity) is normally about 80%. It is reduced in obstructive lung disease (e.g., asthma, COPD - airflow limitation) and normal or increased (with reduced FVC) in restrictive lung disease (e.g., pulmonary fibrosis).
Q4. What is lung compliance? What is surfactant and its role?
Compliance = change in lung volume per unit change in transpulmonary pressure - a measure of lung distensibility. Surfactant (dipalmitoyl phosphatidylcholine), secreted by Type II alveolar cells, reduces alveolar surface tension, preventing alveolar collapse (per Laplace's law) and increasing compliance; its deficiency causes Respiratory Distress Syndrome in preterm infants.
Q5. Describe the oxygen-hemoglobin dissociation curve and factors shifting it.
A sigmoid curve relating O2 saturation of Hb to PO2, reflecting cooperative binding. Right shift (decreased O2 affinity, favors O2 unloading to tissues): increased CO2, H+ (Bohr effect), temperature, 2,3-DPG. Left shift (increased affinity): opposite changes, and HbF/CO poisoning.
Q6. How is CO2 transported in blood?
Mainly as bicarbonate (~70%, via carbonic anhydrase in RBCs: CO2+H2O -> H2CO3 -> H+ + HCO3-), as carbaminohemoglobin bound to globin (~20-23%), and dissolved in plasma (~7%).
Q7. Describe the control of respiration.
The medullary respiratory centers (dorsal and ventral respiratory groups) generate the basic rhythm; the pontine centers (pneumotaxic and apneustic centers) modulate rhythm/depth. Central chemoreceptors (medulla) respond mainly to CSF H+/CO2; peripheral chemoreceptors (carotid and aortic bodies) respond mainly to PO2 (and CO2/H+), providing the main drive during hypoxia.
Q8. Differentiate the types of hypoxia.
- Hypoxic hypoxia - low arterial PO2 (e.g., high altitude, lung disease)
- Anemic hypoxia - reduced O2-carrying capacity (low Hb)
- Stagnant/circulatory hypoxia - reduced blood flow
- Histotoxic hypoxia - tissues unable to use O2 (e.g., cyanide poisoning)
Q9. What is dead space? Types?
Dead space is the volume of inspired air that does not participate in gas exchange. Anatomical dead space (~150 mL, conducting airways) + alveolar dead space (ventilated but not perfused alveoli) = Physiological dead space.
Q10. What is Ventilation-Perfusion (V/Q) ratio?
The ratio of alveolar ventilation to pulmonary blood flow, normally about 0.8. Mismatch (high V/Q = wasted ventilation like dead space; low V/Q = shunt-like effect) impairs gas exchange efficiency and is a key mechanism in many lung diseases.
Q11. What is cyanosis?
A bluish discoloration of skin/mucosa due to increased deoxygenated hemoglobin (>5 g/dL) in blood; classified as central (cardiopulmonary causes, also affects tongue) or peripheral (poor peripheral circulation, tongue spared).
Q12. What is the Hering-Breuer reflex?
A protective reflex where stretch receptors in the lung, activated by over-inflation, send vagal afferents to the medulla to inhibit further inspiration and prevent overdistension.
Quick Fire Round
- Normal respiratory rate: 12-16/min
- Normal PO2 (arterial): 95-100 mmHg
- Normal PCO2 (arterial): 40 mmHg
- P50 of Hb-O2 curve: ~26-27 mmHg
- Site of surfactant production: Type II pneumocytes
- Primary drive for ventilation at rest: arterial/CSF CO2 (via central chemoreceptors)
Sources: Guyton and Hall Textbook of Medical Physiology; Costanzo Physiology, 7th Edition
4. Central Nervous System (CNS)
Q1. What are the components of a reflex arc?
Receptor -> afferent (sensory) neuron -> integrating center (CNS, may involve interneurons) -> efferent (motor) neuron -> effector (muscle/gland). Simplest reflex (monosynaptic, e.g., knee jerk) has only one synapse between afferent and efferent neuron.
Q2. Explain the stretch reflex (knee jerk / deep tendon reflex).
Tapping the patellar tendon stretches the quadriceps muscle -> activates muscle spindle (Ia afferents) -> monosynaptic excitatory connection in the spinal cord directly activates the alpha motor neuron of the same muscle -> causes reflex contraction (extension at the knee). It is used clinically to assess the integrity of a specific spinal segment.
Q3. Classify sensory receptors.
By stimulus type: mechanoreceptors, thermoreceptors, chemoreceptors, photoreceptors, nociceptors. By adaptation: rapidly adapting (phasic, e.g., Pacinian corpuscle) vs slowly adapting (tonic, e.g., Merkel discs).
Q4. Differentiate the Dorsal Column-Medial Lemniscus pathway and Spinothalamic tract.
- DCML: carries fine touch, vibration, proprioception; ascends ipsilaterally in the dorsal column, decussates in the medulla (at the level of the nucleus gracilis/cuneatus), then goes to thalamus and cortex.
- Spinothalamic tract: carries pain and temperature; fibers decussate at/near the level of entry into the spinal cord, then ascend contralaterally to the thalamus.
Q5. What is the corticospinal tract? Where does it decussate?
The main descending motor pathway for voluntary movement, originating from the motor cortex, decussating at the level of the medullary pyramids (lateral corticospinal tract - most fibers, controls limb movement) with a smaller uncrossed ventral corticospinal tract.
Q6. Differentiate Upper Motor Neuron (UMN) and Lower Motor Neuron (LMN) lesions.
- UMN lesion: spastic paralysis, hyperreflexia, Babinski sign positive, no muscle wasting/fasciculations, clasp-knife rigidity
- LMN lesion: flaccid paralysis, hyporeflexia/areflexia, muscle wasting and fasciculations present, Babinski absent
Q7. What are the functions of the cerebellum?
Coordination of voluntary movement, maintenance of posture and balance, regulation of muscle tone, and motor learning. Lesions cause ataxia, intention tremor, dysmetria, nystagmus, and dysdiadochokinesia - typically without weakness or sensory loss.
Q8. What is the role of the basal ganglia? What is Parkinson's disease?
Basal ganglia (caudate, putamen, globus pallidus, substantia nigra, subthalamic nucleus) regulate the initiation and smoothness of voluntary movement and inhibit unwanted movement. Parkinson's disease results from degeneration of dopaminergic neurons in the substantia nigra, causing resting tremor, rigidity, bradykinesia, and postural instability.
Q9. What are EEG waves? Name them with frequency and typical occurrence.
- Alpha (8-13 Hz) - awake, relaxed, eyes closed
- Beta (>13 Hz) - alert, active mental concentration
- Theta (4-7 Hz) - drowsiness, children, light sleep
- Delta (<4 Hz) - deep (slow-wave) sleep
Q10. Describe the stages of sleep.
NREM sleep (stages N1-N3, progressively deeper, with delta waves dominant in N3/slow wave sleep) alternating with REM sleep (rapid eye movements, vivid dreaming, EEG resembles wakefulness, and skeletal muscle atonia), cycling about every 90 minutes through the night.
Q11. Differentiate sympathetic and parasympathetic nervous systems.
- Sympathetic: thoracolumbar outflow, short preganglionic/long postganglionic fibers, neurotransmitter norepinephrine at postganglionic synapse (except sweat glands - ACh), "fight or flight" - increases HR/BP, bronchodilation, pupil dilation
- Parasympathetic: craniosacral outflow, long preganglionic/short postganglionic fibers, neurotransmitter acetylcholine throughout, "rest and digest" - decreases HR, increases GI motility/secretion, pupil constriction
Q12. Name the major neurotransmitters and their general roles.
Acetylcholine (NMJ, autonomic, CNS - memory), Norepinephrine/Epinephrine (sympathetic, arousal), Dopamine (reward, motor control - basal ganglia), Serotonin (mood, sleep), GABA and Glycine (main inhibitory), Glutamate (main excitatory in CNS).
Q13. Differentiate electrical and chemical synapses.
- Electrical: via gap junctions, very fast, bidirectional, no synaptic delay (e.g., cardiac muscle, some neurons)
- Chemical: via neurotransmitter release, unidirectional, has synaptic delay (~0.5 ms), can be excitatory (EPSP) or inhibitory (IPSP)
Quick Fire Round
- Monosynaptic reflex example: Knee jerk (stretch reflex)
- Decussation site of corticospinal tract: Medullary pyramids
- Positive sign in UMN lesion: Babinski sign
- Main inhibitory neurotransmitter: GABA
- Main excitatory neurotransmitter: Glutamate
- Neurotransmitter deficient in Parkinson's disease: Dopamine
Sources: Guyton and Hall Textbook of Medical Physiology; Ganong's Review of Medical Physiology
5. Gastrointestinal System (GIT)
Q1. Describe the composition and functions of saliva.
Saliva is hypotonic, secreted by parotid (serous), submandibular, and sublingual (mixed) glands; contains salivary amylase (starch digestion), lysozyme and IgA (antibacterial), mucin (lubrication), and bicarbonate (buffering). Regulated by autonomic nerves (both sympathetic and parasympathetic stimulate secretion; parasympathetic produces more watery secretion).
Q2. Describe gastric secretion - components and cells.
Gastric glands contain: Parietal cells (HCl and intrinsic factor), Chief cells (pepsinogen), G cells (gastrin, in antrum), Mucous neck cells (mucus/bicarbonate protection), ECL cells (histamine).
Q3. Describe the phases of gastric secretion.
- Cephalic phase (~30%): triggered by sight/smell/taste of food, mediated via vagus
- Gastric phase (~60%): food distension and peptides in stomach stimulate gastrin release and local reflexes
- Intestinal phase (~10%): initially stimulatory (duodenal distension), later inhibitory (via secretin, GIP, and the enterogastric reflex) as chyme enters the duodenum.
Q4. What is Intrinsic Factor and its importance?
A glycoprotein secreted by gastric parietal cells that binds Vitamin B12, essential for its absorption in the terminal ileum. Loss of parietal cells (e.g., autoimmune gastritis) causes B12 deficiency and pernicious anemia.
Q5. Describe the actions of Gastrin, Secretin, and CCK.
- Gastrin (from G cells): stimulates HCl secretion, gastric motility
- Secretin (from S cells, released by acid in duodenum): stimulates pancreatic bicarbonate secretion, inhibits gastric acid secretion
- CCK (Cholecystokinin, released by fat/protein in duodenum): stimulates gallbladder contraction, pancreatic enzyme secretion, and inhibits gastric emptying
Q6. Describe pancreatic exocrine secretion.
Acinar cells secrete digestive enzymes (trypsinogen, chymotrypsinogen, lipase, amylase - activated in the duodenum), while duct cells secrete bicarbonate-rich fluid to neutralize gastric acid, stimulated mainly by secretin (aqueous/bicarbonate component) and CCK (enzymatic component).
Q7. Describe bile secretion and enterohepatic circulation.
Bile (containing bile salts, bilirubin, cholesterol, phospholipids) is secreted by hepatocytes, concentrated/stored in the gallbladder, released into the duodenum upon CCK stimulation to emulsify fats. About 95% of bile salts are reabsorbed in the terminal ileum and recycled back to the liver - the enterohepatic circulation.
Q8. How are carbohydrates, proteins, and fats digested and absorbed?
- Carbohydrates: salivary/pancreatic amylase break starch to disaccharides; brush border enzymes (maltase, sucrase, lactase) yield monosaccharides absorbed via SGLT1 (glucose/galactose, with Na+) and GLUT5 (fructose).
- Proteins: pepsin (stomach) and pancreatic proteases (trypsin, chymotrypsin) break proteins to peptides/amino acids, absorbed via Na+-dependent cotransporters.
- Fats: emulsified by bile salts, digested by pancreatic lipase to monoglycerides/fatty acids, packaged into micelles, absorbed into enterocytes, and re-esterified into chylomicrons for lymphatic transport.
Q9. Describe GI motility - peristalsis and MMC.
Peristalsis: coordinated wave of circular muscle contraction behind and relaxation ahead of a bolus, propelling content aborally, coordinated by the myenteric plexus. Migrating Motor Complex (MMC): strong peristaltic waves occurring during fasting (interdigestive period) that sweep the small intestine clean of residual content and bacteria.
Q10. Describe the defecation reflex.
Distension of the rectum by feces stimulates stretch receptors -> triggers the intrinsic (myenteric) defecation reflex causing relaxation of the internal anal sphincter -> also relayed via parasympathetic (pelvic nerve) reflex to the sacral spinal cord for a stronger response, with voluntary control of the external anal sphincter (striated muscle, under conscious control).
Q11. What are the major functions of the liver?
Metabolism of carbohydrates/proteins/fats, synthesis of plasma proteins (albumin, clotting factors), detoxification/drug metabolism, bile secretion, storage (glycogen, vitamins, iron), bilirubin conjugation and excretion, and immune functions (Kupffer cells).
Q12. What is jaundice? Classify it.
Jaundice is yellowish discoloration of skin/sclera due to increased bilirubin.
- Pre-hepatic (hemolytic): excess unconjugated bilirubin from increased RBC breakdown
- Hepatic: impaired hepatocyte conjugation/uptake (e.g., hepatitis)
- Post-hepatic (obstructive): impaired excretion of conjugated bilirubin (e.g., gallstones, tumor)
Quick Fire Round
- Enzyme activating pepsinogen: HCl
- Cell secreting HCl: Parietal cell
- Hormone stimulating gallbladder contraction: CCK
- Site of B12 absorption: Terminal ileum
- Main site of iron absorption: Duodenum
- Enzyme deficient in lactose intolerance: Lactase
Sources: Guyton and Hall Textbook of Medical Physiology; Ganong's Review of Medical Physiology
6. Endocrine System
Q1. What are the general mechanisms of hormone action?
- Peptide/protein hormones and catecholamines: bind cell-surface receptors, act via second messengers (cAMP, IP3/DAG, Ca2+)
- Steroid and thyroid hormones: lipophilic, cross the cell membrane, bind intracellular/nuclear receptors, directly alter gene transcription
Q2. Describe the hypothalamo-pituitary axis.
The hypothalamus secretes releasing/inhibiting hormones (e.g., TRH, CRH, GnRH, GHRH, somatostatin, dopamine) into the hypophyseal portal system, regulating anterior pituitary hormone secretion. The posterior pituitary stores and releases hormones (ADH, oxytocin) synthesized in the hypothalamus and transported via the hypothalamo-hypophyseal tract.
Q3. List the anterior pituitary hormones and their actions.
GH (growth, metabolism), TSH (stimulates thyroid), ACTH (stimulates adrenal cortex/cortisol), FSH and LH (gonadal function), Prolactin (lactation).
Q4. Describe ADH (Vasopressin) - source, action, regulation.
Synthesized in the hypothalamus (supraoptic nucleus mainly), released from the posterior pituitary. Acts on renal collecting duct V2 receptors to increase water reabsorption (via aquaporin-2 insertion), concentrating urine. Released in response to increased plasma osmolality (sensed by hypothalamic osmoreceptors) or decreased blood volume/pressure.
Q5. Describe thyroid hormone synthesis and regulation.
Iodide trapping -> oxidation and organification onto tyrosine residues of thyroglobulin -> coupling to form T3/T4 -> stored in follicular colloid -> released into circulation upon TSH stimulation. Regulated by the Hypothalamus (TRH) -> Pituitary (TSH) -> Thyroid (T3/T4) axis with negative feedback of T3/T4 on TRH and TSH.
Q6. Differentiate hypothyroidism and hyperthyroidism.
- Hypothyroidism: weight gain, cold intolerance, bradycardia, lethargy, myxedema, constipation
- Hyperthyroidism: weight loss, heat intolerance, tachycardia, tremor, increased appetite, exophthalmos (in Graves disease)
Q7. What are the hormones of the adrenal cortex and their regulation?
- Cortisol (zona fasciculata) - regulated by ACTH via HPA axis; increases blood glucose (gluconeogenesis), has anti-inflammatory/immunosuppressive effects, stress response
- Aldosterone (zona glomerulosa) - regulated mainly by the renin-angiotensin system and plasma K+; promotes Na+ reabsorption and K+ secretion in the distal nephron
- Androgens (zona reticularis)
Q8. What hormones does the adrenal medulla secrete?
Epinephrine (mainly) and norepinephrine, released in response to sympathetic stimulation (stress, "fight or flight") - increase heart rate, blood pressure, blood glucose, and bronchodilation.
Q9. Describe insulin action and regulation.
Secreted by pancreatic beta cells in response to rising blood glucose. Promotes glucose uptake into cells (via GLUT4 translocation in muscle/adipose), glycogenesis, lipogenesis, and protein synthesis; lowers blood glucose. Glucagon (from alpha cells) has opposing actions - stimulates glycogenolysis and gluconeogenesis, raising blood glucose.
Q10. What is Diabetes Mellitus? Differentiate Type 1 and Type 2.
A metabolic disorder of chronic hyperglycemia.
- Type 1: autoimmune destruction of beta cells, absolute insulin deficiency, typically younger onset, requires insulin
- Type 2: insulin resistance with relative insulin deficiency, typically older/obesity-associated, managed initially with lifestyle/oral agents
Q11. Describe calcium homeostasis - PTH, Calcitonin, Vitamin D.
- PTH (parathyroid glands, released when serum Ca2+ falls): increases bone resorption, renal Ca2+ reabsorption/phosphate excretion, and activates vitamin D
- Calcitonin (thyroid C cells, released when serum Ca2+ rises): inhibits osteoclast activity, lowers serum calcium (minor role in humans)
- Vitamin D (calcitriol): increases intestinal absorption of calcium and phosphate
Quick Fire Round
- Only lipid-soluble hormones acting via nuclear receptors: Steroid and thyroid hormones
- Hormone regulating milk let-down: Oxytocin
- Hormone deficient in Type 1 DM: Insulin
- Site of aldosterone action: Distal tubule/collecting duct
- Hormone raising blood glucose besides glucagon: Cortisol, epinephrine, GH
- Master gland: Pituitary (itself controlled by the hypothalamus)
Sources: Guyton and Hall Textbook of Medical Physiology; Ganong's Review of Medical Physiology
7. Excretory / Renal System
Q1. Describe the structure of the nephron.
Each nephron consists of a renal corpuscle (glomerulus + Bowman's capsule) and a renal tubule (proximal convoluted tubule, loop of Henle - descending and ascending limbs, distal convoluted tubule, connecting to the collecting duct). Cortical nephrons have short loops; juxtamedullary nephrons have long loops important for urine concentration.
Q2. What is Glomerular Filtration Rate (GFR)? Normal value and determinants?
GFR is the volume of plasma filtered by the glomeruli per minute; normal is about 125 mL/min (~180 L/day). Determined by the net filtration pressure (glomerular capillary hydrostatic pressure favoring filtration, opposed by capsular hydrostatic pressure and plasma oncotic pressure) and the filtration coefficient (Kf, surface area x permeability).
Q3. What is renal clearance? How is creatinine clearance used to estimate GFR?
Clearance of a substance = volume of plasma cleared of that substance per unit time = (Urine concentration x Urine flow rate)/Plasma concentration. Creatinine is freely filtered and not significantly reabsorbed/secreted, so its clearance approximates GFR and is used clinically as a marker of renal function (inulin clearance is the gold standard experimentally).
Q4. Describe tubular reabsorption in the proximal convoluted tubule (PCT).
The PCT reabsorbs about 65% of filtered Na+/water (isosmotic reabsorption), essentially all filtered glucose and amino acids (via Na+-dependent cotransport, e.g., SGLT2), and most bicarbonate (via Na+-H+ exchange and carbonic anhydrase).
Q5. Explain the countercurrent mechanism of urine concentration.
The loop of Henle acts as a countercurrent multiplier: the thick ascending limb actively pumps out NaCl (impermeable to water), progressively diluting tubular fluid while creating a hyperosmotic medullary interstitium; the descending limb is water-permeable but not solute-permeable. This gradient (increasing osmolality from cortex to inner medulla, up to ~1200 mOsm/L) is used by the collecting duct (under ADH influence) to reabsorb water and concentrate urine. Vasa recta act as countercurrent exchangers to preserve this gradient.
Q6. What is the role of ADH in urine concentration?
ADH acts on V2 receptors of the collecting duct principal cells, inserting aquaporin-2 water channels into the luminal membrane, increasing water permeability and reabsorption, producing concentrated urine. In its absence (diabetes insipidus), the collecting duct remains impermeable to water, producing large volumes of dilute urine.
Q7. Describe the Renin-Angiotensin-Aldosterone System (RAAS) as it relates to the kidney.
Decreased renal perfusion/Na+ delivery to the macula densa triggers renin release from juxtaglomerular cells -> generates Angiotensin II (vasoconstrictor, stimulates aldosterone) -> aldosterone acts on the distal nephron to increase Na+ reabsorption (and K+/H+ secretion), helping restore blood volume and pressure.
Q8. How does the kidney regulate acid-base balance?
The kidney reabsorbs filtered bicarbonate (mainly in PCT), and generates new bicarbonate by excreting titratable acid (as H2PO4-) and ammonium (NH4+, from glutamine metabolism in PCT cells), which is the major mechanism for excreting the daily fixed acid load and regenerating bicarbonate consumed in buffering.
Q9. Describe the micturition reflex.
Bladder distension (>300-400 mL) stimulates stretch receptors -> afferents to the sacral spinal cord (S2-S4) -> parasympathetic efferents (pelvic nerve) cause detrusor contraction and internal sphincter relaxation, while voluntary relaxation of the external urethral sphincter (pudendal nerve, under cortical control) permits voiding.
Q10. What is the normal composition of urine and what are its abnormal constituents?
Normal urine contains water, urea, creatinine, uric acid, electrolytes (Na+, K+, Cl-), with no (or trace) glucose, protein, blood, ketones, or bilirubin. Proteinuria suggests glomerular damage; glucosuria suggests hyperglycemia exceeding the renal threshold (~180 mg/dL) or tubular defects; hematuria suggests bleeding anywhere in the urinary tract.
Q11. What are common renal function tests?
Blood urea, serum creatinine, creatinine clearance/eGFR, urine routine examination (protein, glucose, microscopy), specific gravity, and electrolyte panel.
Quick Fire Round
- Normal GFR: ~125 mL/min
- Gold standard marker for GFR: Inulin
- Clinically used marker for GFR: Creatinine
- Site of maximum Na+/water reabsorption: Proximal convoluted tubule (~65%)
- Hormone acting on collecting duct for water reabsorption: ADH
- Site of action of aldosterone: Distal tubule/collecting duct
- Countercurrent multiplier structure: Loop of Henle
Sources: Guyton and Hall Textbook of Medical Physiology; Costanzo Physiology, 7th Edition
8. Special Senses
Q1. Describe accommodation and the common refractive errors.
Accommodation is the eye's ability to increase lens curvature (via ciliary muscle contraction, relaxing the suspensory ligaments) to focus near objects onto the retina.
- Myopia (near-sightedness): image focuses in front of retina (eyeball too long/lens too strong); corrected with concave (diverging) lens
- Hypermetropia (far-sightedness): image focuses behind retina; corrected with convex (converging) lens
- Astigmatism: unequal curvature of the cornea/lens in different meridians, corrected with a cylindrical lens
Q2. Describe the visual pathway.
Retina -> optic nerve -> optic chiasma (nasal fibers from each eye decussate) -> optic tract -> lateral geniculate body of thalamus -> optic radiation -> primary visual cortex (occipital lobe, area 17/V1).
Q3. Differentiate rods and cones.
- Rods: more numerous, high sensitivity (scotopic/dim light vision), contain rhodopsin, no color discrimination, concentrated in periphery
- Cones: less numerous, lower sensitivity (photopic/bright light and color vision), three types (red/green/blue sensitive photopigments), concentrated at the fovea for high visual acuity
Q4. Briefly explain phototransduction.
Light causes photoisomerization of retinal (11-cis to all-trans) within the photopigment, activating transducin, which activates phosphodiesterase, reducing cGMP levels, closing Na+ channels, and hyperpolarizing the photoreceptor - this is a unique example of a sensory receptor that hyperpolarizes with its stimulus (light) rather than depolarizing.
Q5. What is the Young-Helmholtz trichromatic theory of color vision?
Color perception is based on the differential stimulation of three types of cones, each maximally sensitive to a different wavelength (blue ~420 nm, green ~530 nm, red ~560 nm); the brain interprets the ratio of stimulation among the three to perceive the full color spectrum.
Q6. Describe the structure of the cochlea and organ of Corti.
The cochlea is a coiled, fluid-filled tube with three compartments (scala vestibuli, scala media/cochlear duct, scala tympani) separated by Reissner's and basilar membranes. The organ of Corti, sitting on the basilar membrane, contains hair cells (inner - primary sensory transducers; outer - amplify sound) whose stereocilia are embedded in the tectorial membrane.
Q7. Explain the mechanism of hearing (traveling wave theory - Bekesy).
Sound vibrations transmitted via the ossicles to the oval window set up a traveling wave along the basilar membrane; high-frequency sounds cause maximal displacement near the base (stiffer, narrower), while low-frequency sounds cause maximal displacement near the apex (more flexible, wider) - this tonotopic organization allows frequency discrimination.
Q8. Describe the auditory pathway.
Hair cells -> cochlear nerve (CN VIII) -> cochlear nuclei -> superior olivary nucleus (binaural processing for sound localization) -> lateral lemniscus -> inferior colliculus -> medial geniculate body (thalamus) -> auditory cortex (temporal lobe).
Q9. Differentiate conductive and sensorineural deafness. Describe the Rinne and Weber tests.
- Conductive deafness: problem in outer/middle ear (e.g., wax, otitis media, ossicular fixation)
- Sensorineural deafness: problem in cochlea or auditory nerve/pathway
- Rinne test: compares air conduction (AC) to bone conduction (BC); normally AC > BC (Rinne positive). In conductive deafness, BC > AC (Rinne negative); in sensorineural deafness, AC > BC but both reduced (Rinne positive but overall reduced hearing).
- Weber test: tuning fork on the vertex/forehead; sound lateralizes to the affected ear in conductive deafness, and to the normal (better) ear in sensorineural deafness.
Q10. Describe the basic taste modalities and pathway.
Five basic tastes: sweet, salty, sour, bitter, umami - detected by taste receptor cells in taste buds (on fungiform, foliate, circumvallate papillae). Pathway: anterior 2/3 of tongue via facial nerve (chorda tympani, CN VII), posterior 1/3 via glossopharyngeal nerve (CN IX), epiglottis/pharynx via vagus (CN X) -> nucleus tractus solitarius -> thalamus -> gustatory cortex.
Q11. Describe olfaction basics.
Olfactory receptor neurons in the nasal mucosa (olfactory epithelium) bind odorant molecules via specific G-protein coupled receptors, generating action potentials that travel via the olfactory nerve (CN I) through the cribriform plate to the olfactory bulb, then to the olfactory cortex - notably bypassing the thalamus, unlike other sensory pathways (thalamic relay occurs later for conscious perception).
Q12. Describe the vestibular apparatus and its role in balance.
The vestibular apparatus (semicircular canals, utricle, saccule) detects head movement and position. Semicircular canals detect angular/rotational acceleration (via endolymph movement bending hair cell cilia in the ampulla). Utricle and saccule (otolith organs, containing otoconia) detect linear acceleration and static head position relative to gravity.
Quick Fire Round
- Photopigment in rods: Rhodopsin
- Area of sharpest vision: Fovea centralis
- Nerve for anterior 2/3 tongue taste: Facial nerve (chorda tympani)
- Test lateralizing to bad ear: Conductive deafness (Weber test)
- Structure detecting angular acceleration: Semicircular canals
- Structure detecting linear acceleration: Utricle and saccule
Sources: Guyton and Hall Textbook of Medical Physiology; Ganong's Review of Medical Physiology
That completes all 10 lessons: General Physiology, Blood, Nerve-Muscle (NMJ), CVS, RS, CNS, GIT, Endocrine, Excretion, and Special Senses - the full set typically asked at the theory viva station of the MBBS Physiology practical exam. If you want, I can turn this whole compiled set into a downloadable PDF/Word document for easier revision.