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Most Frequently Asked Viva Questions - Physiology (Chapter-wise)

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1. General Physiology / Cell Physiology

• What is homeostasis? Give an example of positive and negative feedback.
• What is the resting membrane potential and how is it maintained?
• Explain the Na⁺/K⁺ ATPase pump - its role and why it is electrogenic.
• What is the difference between osmolarity and osmolality?
• Define tonicity. What happens to an RBC placed in hypotonic solution?
• What are the different types of cell transport? Difference between primary and secondary active transport.
• What is the Gibbs-Donnan equilibrium?

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2. Blood / Haematology

• What is the normal composition of blood? What is the PCV (haematocrit)?
• What are the ABO blood groups? Explain the basis of incompatibility reactions.
• What is the Rh factor? What is erythroblastosis fetalis and how does it occur?
• Describe the coagulation cascade. What are the intrinsic and extrinsic pathways?
• What are the functions of the spleen?
• Define ESR. What are the factors that increase and decrease ESR?
• What is the difference between plasma and serum?
• What is haemoglobin? Describe the oxygen-haemoglobin dissociation curve.
• What is the role of vitamin K in coagulation?
• Define anaemia and classify it.

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3. Nerve and Muscle Physiology

• What is an action potential? Describe its phases.
• What is the all-or-none law?
• Define absolute and relative refractory periods.
• What is a synapse? Explain synaptic transmission.
• What is the neuromuscular junction (NMJ)? What happens when acetylcholine is released?
• Explain the sliding filament theory of muscle contraction.
• What is a motor unit? What is recruitment?
• Difference between fast (white) and slow (red) muscle fibres.
• What is rigor mortis and why does it occur?
• What is the difference between twitch, summation, and tetanus?
• What are the types of nerve fibres? Classify based on diameter and conduction velocity.

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4. Cardiovascular Physiology

• Describe the cardiac cycle. What are its phases and duration?
• What are the heart sounds? What causes the first and second heart sounds?
• What is the cardiac output? How is it calculated? What is Fick's principle?
• Define stroke volume and the factors that determine it (preload, afterload, contractility).
• Explain Frank-Starling's law.
• What is the normal ECG? Explain each wave, segment, and interval.
• What is the conducting system of the heart?
• What is blood pressure? Define systolic, diastolic, and pulse pressure.
• Explain the baroreceptor reflex.
• What is the difference between arteries, veins, and capillaries?
• What is venous return and what are the factors that affect it?
• What is the coronary circulation? When does maximum coronary blood flow occur?

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5. Respiratory Physiology

• What are the lung volumes and capacities? Define each.
• What is FRC (Functional Residual Capacity) and what is its significance?
• Explain the oxygen-haemoglobin dissociation curve. What are the factors that cause right and left shift?
• What is the Bohr effect and the Haldane effect?
• What is the V/Q ratio? What happens when V/Q is altered?
• Explain the mechanism of breathing (Boyle's law application).
• What is surfactant? What is its role and what produces it?
• How is CO₂ transported in blood?
• What are the types of hypoxia?
• What is cyanosis? Distinguish central from peripheral cyanosis.
• Explain the Hering-Breuer reflex.

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6. Renal Physiology

• What is GFR (Glomerular Filtration Rate)? What is its normal value and how is it measured?
• What is the juxtaglomerular apparatus (JGA)? Explain tubuloglomerular feedback.
• Describe the counter-current mechanism in the kidney.
• What is the renal threshold for glucose? What is Tm (transport maximum)?
• How does the kidney regulate acid-base balance?
• What is the renin-angiotensin-aldosterone system (RAAS)?
• What is the role of ADH (vasopressin)?
• Define clearance. What is the clearance of inulin, PAH, and creatinine?
• What is the difference between obligatory and facultative water reabsorption?
• What is the diluting and concentrating ability of the kidney?

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7. Gastrointestinal Physiology

• What are the functions of saliva?
• What is swallowing (deglutition)? Name the phases.
• What are the components of gastric juice? What is the role of HCl?
• What is the cephalic, gastric, and intestinal phase of gastric secretion?
• What is the role of bile? What are the constituents of bile?
• What is the enterohepatic circulation?
• Explain the secretin-pancreozymin mechanism.
• What are the movements of the small intestine?
• How are fats absorbed in the gut?
• What is the ileocaecal valve? What is its role?

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8. Endocrine Physiology

• What is the hypothalamo-pituitary axis? Explain with one example (e.g., thyroid axis).
• What are the actions of growth hormone (GH)?
• Describe the actions of insulin. What is the mechanism of insulin secretion?
• What are the effects of glucocorticoids?
• What is the role of ADH and oxytocin?
• Describe the synthesis and actions of thyroid hormones.
• What is the role of parathyroid hormone (PTH)?
• Explain the calcium-phosphorus regulation.
• What are the mineralocorticoids and what do they do?
• What are catecholamines? What are their physiological effects?

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9. Neurophysiology / Central Nervous System

• What is the blood-brain barrier (BBB)? What is its significance?
• What are the functions of the cerebellum?
• Explain the basal ganglia and their role in movement.
• What is the limbic system?
• What are the ascending sensory tracts? Describe the dorsal column-medial lemniscus pathway.
• What is the motor cortex? What is a homunculus?
• What are the pyramidal and extrapyramidal tracts?
• Explain the EEG - what are the different brain waves?
• What is sleep? Distinguish REM from NREM sleep.
• What is the role of the hypothalamus?
• What are the functions of the cerebral cortex?

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10. Autonomic Nervous System (ANS)

• What are the differences between the sympathetic and parasympathetic nervous systems?
• What are adrenergic receptors? Classify them with examples.
• What are cholinergic receptors? Classify muscarinic and nicotinic receptors.
• What is the "fight or flight" response?
• What is the autonomic innervation of the heart?
• What are the neurotransmitters of the ANS?

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11. Reproductive Physiology

• Describe the menstrual cycle (ovarian and uterine cycles).
• What are the functions of testosterone?
• What is spermatogenesis? Where does it occur?
• What is oogenesis?
• What is the role of FSH and LH?
• What are the functions of oestrogen and progesterone?
• What changes occur in pregnancy - physiological adaptations?
• What is the role of hCG?

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12. Special Senses

• Explain the mechanism of vision. What are the roles of rods and cones?
• What is the near response (accommodation reflex)?
• What is the mechanism of hearing?
• What is the Rinne and Weber test based on?
• What is referred pain? Give examples.
• What are the types of receptors? Classify sensory receptors.

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High-Yield Viva Tips

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Physiology Viva Q&A - Complete Chapter-wise Guide

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CHAPTER 1: General Physiology / Cell Physiology

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• Negative feedback (most common): The response opposes the stimulus. Example: Rise in blood glucose → insulin secreted → glucose falls back to normal. Other examples: baroreceptor reflex, temperature regulation.
• Positive feedback (amplifies the stimulus): Example: Childbirth - uterine contraction → oxytocin release → more contraction. Also: blood clotting cascade, action potential depolarization phase.

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1. High K⁺ permeability at rest - K⁺ leaks out down its concentration gradient (intracellular K⁺ is 140 mEq/L vs extracellular 4 mEq/L). K⁺ diffusion alone would give -94 mV (Nernst potential for K⁺).
2. Small Na⁺ permeability - Na⁺ leaks in slightly, raising the potential toward ~-86 mV.
3. Na⁺/K⁺ ATPase pump - pumps 3 Na⁺ out for every 2 K⁺ in, creating a net negative charge of an extra -4 mV, giving a final RMP of approximately -90 mV (Guyton) or -70 mV depending on fibre type.
4. Gibbs-Donnan effect - large negatively charged intracellular proteins cannot cross the membrane.

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• Osmolarity: number of osmoles of solute per litre of solution (mOsm/L)
• Osmolality: number of osmoles of solute per kilogram of solvent (mOsm/kg) - measured in clinical labs, normal plasma = 280-295 mOsm/kg
• Tonicity: the effective osmolality - only considers solutes that cannot cross the cell membrane (effective osmoles). Non-penetrating solutes (like NaCl, mannitol) determine tonicity; penetrating solutes (like urea, alcohol) do not.

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CHAPTER 2: Blood / Haematology

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• Normal P50 (pO₂ at 50% saturation) = 26-27 mmHg
• At pO₂ of 100 mmHg (lungs): Hb is ~97-98% saturated
• At pO₂ of 40 mmHg (tissues): Hb releases O₂

• ↑ Temperature
• ↑ pCO₂ (Bohr effect)
• ↑ [H⁺] (↓ pH) - Bohr effect
• ↑ 2,3-DPG (in chronic anaemia, high altitude)

• ↓ Temperature
• ↓ CO₂
• ↑ pH (alkalosis)
• Fetal Hb (HbF) - has γ chains instead of β, binds 2,3-DPG less
• CO poisoning (HbCO)
• Methaemoglobin

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• Extrinsic pathway: Tissue injury → tissue factor (Factor III) + Factor VII → activates Factor X. Tested by PT (prothrombin time).
• Intrinsic pathway: Contact with collagen → activation of Factor XII → XI → IX → VIII → activates Factor X. Tested by aPTT.
• Common pathway: Factor X + Factor V → prothrombinase → prothrombin → thrombin → fibrinogen → fibrin → stabilised by Factor XIII.
• Vitamin K is required for synthesis of Factors II, VII, IX, X (and proteins C and S). Warfarin inhibits vitamin K-dependent clotting factor synthesis.

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CHAPTER 3: Nerve & Muscle Physiology

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1. Resting state (-70 mV): Na⁺ channels closed (deactivated), K⁺ channels closed.
2. Depolarisation: Stimulus reaches threshold (~-55 mV). Voltage-gated Na⁺ channels open rapidly → Na⁺ rushes in → membrane potential rises to about +30 to +40 mV (overshoot).
3. Repolarisation: Na⁺ channels inactivate; voltage-gated K⁺ channels open slowly → K⁺ rushes out → potential returns toward resting.
4. After-hyperpolarisation (undershoot): K⁺ channels stay open slightly too long → membrane goes more negative than resting (-80 mV) briefly.
5. Return to rest: K⁺ channels close; Na⁺/K⁺ pump restores ion gradients.

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• Absolute refractory period (ARP): No stimulus of any strength can trigger another action potential. Corresponds to the period when Na⁺ channels are in the inactivated state (cannot be opened). Lasts ~1 ms.
• Relative refractory period (RRP): Only a supra-threshold stimulus can fire another AP. Corresponds to after-hyperpolarisation when K⁺ channels are still open. The cell is more negative than resting, so a stronger-than-normal stimulus is needed.

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1. Nerve impulse → ACh at NMJ → end-plate potential → AP along sarcolemma → down T-tubules.
2. Ca²⁺ released from sarcoplasmic reticulum.
3. Ca²⁺ binds troponin C → conformational change in troponin-tropomyosin complex → tropomyosin moves to expose myosin-binding sites on actin.
4. Myosin head (with ATP already bound) binds actin → forms cross-bridge.
5. ATP hydrolysis → power stroke: myosin head pivots, pulling actin toward M-line (sarcomere shortens).
6. New ATP binds myosin head → detachment from actin.
7. Cycle repeats. In rigor mortis, no ATP is available → cross-bridges locked permanently.

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1. AP reaches motor nerve terminal.
2. Ca²⁺ enters via voltage-gated Ca²⁺ channels.
3. Acetylcholine (ACh) released by exocytosis from vesicles.
4. ACh binds nicotinic ACh receptors (nAChR) on motor end plate → ligand-gated Na⁺/K⁺ channels open → end-plate potential (EPP).
5. EPP triggers AP in muscle → contraction.
6. ACh broken down by acetylcholinesterase → choline recycled.

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CHAPTER 4: Cardiovascular Physiology

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• EDV (end-diastolic volume) = ~120 mL
• ESV (end-systolic volume) = ~50 mL
• Stroke volume = EDV - ESV = ~70 mL
• Ejection fraction = SV/EDV = ~60%

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• S1 ("lub"): Caused by closure of mitral and tricuspid (AV) valves at the beginning of ventricular systole. Heard best at cardiac apex.
• S2 ("dub"): Caused by closure of aortic and pulmonary (semilunar) valves at the end of ventricular systole. Heard best at base.
• S3 (ventricular gallop): Heard in early diastole during rapid filling. Normal in children; pathological in adults - suggests ventricular failure (↑ EDV).
• S4 (atrial gallop): Heard in late diastole during atrial contraction. Suggests stiff ventricle (e.g., hypertension, hypertrophic cardiomyopathy).

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• ↑ baroreceptor firing → medullary cardiovascular centre → ↑ parasympathetic tone (vagus) + ↓ sympathetic tone → ↓ HR, ↓ contractility, vasodilation → BP falls back toward normal.

• ↓ baroreceptor firing → ↓ vagal tone + ↑ sympathetic → ↑ HR, ↑ contractility, vasoconstriction, venoconstriction → BP restored.

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CHAPTER 5: Respiratory Physiology

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• Bohr effect: Rise in CO₂ (or fall in pH) causes a right shift of the O₂-Hb dissociation curve → Hb releases more O₂. CO₂ produced in metabolically active tissues promotes O₂ unloading. Mechanism: CO₂ reacts with Hb → carbaminohaemoglobin and H⁺ ions → H⁺ binds Hb → reduces O₂ affinity.
• Haldane effect: Oxygenation of Hb in the lungs promotes release of CO₂ from Hb (deoxygenated Hb binds CO₂ better than oxygenated Hb). This facilitates CO₂ transport from tissues.

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• Prevents alveolar collapse (atelectasis) at the end of expiration.
• Reduces the work of breathing.
• By reducing surface tension more in small alveoli (where it is more concentrated), it equalises pressure between alveoli of different sizes (prevents large alveoli from expanding at the expense of small ones).

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CHAPTER 6: Renal Physiology

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1. Freely filtered at the glomerulus
2. Not secreted or reabsorbed by tubules
3. Not metabolised

• GFR = (Urine inulin × Urine flow rate) / Plasma inulin = 125 mL/min
• Inulin is a plant polysaccharide given IV

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• Descending limb: Permeable to water (not solute) → water leaves → tubular fluid becomes concentrated.
• Ascending limb (thick): Actively transports NaCl out (NKCC2 co-transporter) but impermeable to water → tubular fluid becomes dilute, interstitium becomes hypertonic.
• Net effect: creates a hyperosmotic medullary interstitium (up to 1200 mOsm/kg at papilla).

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1. Renin released from juxtaglomerular cells of the kidney in response to: ↓ renal perfusion pressure, ↓ NaCl at macula densa, or sympathetic stimulation (β₁).
2. Renin cleaves angiotensinogen (liver) → Angiotensin I.
3. ACE (lung mainly) converts Angiotensin I → Angiotensin II.
4. Angiotensin II actions:
   • Vasoconstriction (AT1 receptors) → ↑ BP
   • Stimulates aldosterone from adrenal cortex (zona glomerulosa) → ↑ Na⁺ reabsorption + K⁺ excretion in collecting duct
   • Stimulates ADH secretion
   • ↑ Thirst
   • Cardiac and vascular hypertrophy (long term)

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CHAPTER 7: Gastrointestinal Physiology

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1. Cephalic phase (~30% of secretion): Stimulated by sight, smell, taste, thought of food → vagus nerve (CN X) → ACh → stimulates parietal cells directly + stimulates G-cells to release gastrin.
2. Gastric phase (~60%): Food in stomach → stomach distension (vagal reflexes) + peptides/amino acids stimulate G-cells in antrum → gastrin released → stimulates parietal cells → HCl. Also H-cells release histamine → H₂ receptors on parietal cells.
3. Intestinal phase (~10%): Chyme in small intestine → initial stimulation (small). Then, acidic chyme and fat → secretin and CCK released → inhibit gastric secretion (enterogastric reflex = negative feedback).

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1. Emulsification of fats - bile salts reduce large fat globules to small droplets, increasing surface area for lipase action.
2. Absorption of fat-soluble vitamins (A, D, E, K) and fat digestion products.
3. Excretion route for bilirubin, cholesterol, drugs, heavy metals.
4. Neutralises gastric acid in duodenum.

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CHAPTER 8: Endocrine Physiology

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1. Hypothalamus secretes TRH (thyrotropin-releasing hormone) → anterior pituitary.
2. Pituitary secretes TSH (thyroid-stimulating hormone) → thyroid gland.
3. Thyroid secretes T3 (tri-iodothyronine) and T4 (thyroxine).
4. T3/T4 inhibit both hypothalamus and pituitary (negative feedback) → system self-regulates.

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1. Glucose enters β cell via GLUT2 → glycolysis → ↑ ATP/ADP ratio.
2. ATP closes ATP-sensitive K⁺ channels → membrane depolarises.
3. Voltage-gated Ca²⁺ channels open → Ca²⁺ influx → exocytosis of insulin granules. (Sulphonylureas act by blocking K-ATP channels)

• Glucose: ↑ uptake into muscle and adipose (via GLUT4), ↑ glycogenesis, ↑ glycolysis, ↓ gluconeogenesis
• Protein: ↑ amino acid uptake, ↑ protein synthesis
• Fat: ↑ lipogenesis, ↓ lipolysis
• K⁺: ↑ cellular uptake of K⁺ (clinically used in hyperkalaemia)

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• Metabolic: ↑ gluconeogenesis (raises blood glucose), ↑ protein catabolism, ↑ lipolysis + fat redistribution (central obesity, moon face, buffalo hump in Cushing's).
• Anti-inflammatory: Suppresses phospholipase A₂ (via lipocortin), ↓ prostaglandins, ↓ cytokines, ↓ histamine, stabilises mast cells.
• Immunosuppressive: ↓ lymphocytes, ↓ eosinophils, ↑ neutrophils.
• Cardiovascular: Maintains vascular responsiveness to catecholamines.
• Renal: Weak mineralocorticoid effect (Na⁺ retention).
• Bone: Inhibits osteoblasts → osteoporosis with long-term use.
• CNS: Mood effects (euphoria or depression).

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CHAPTER 9: Neurophysiology / CNS

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• Tight junctions between cerebral capillary endothelial cells (unlike fenestrated capillaries elsewhere).
• Astrocyte foot processes surrounding capillaries.
• Pericytes.

• Lipid-soluble substances freely (O₂, CO₂, ethanol, most general anaesthetics, steroids)
• Small uncharged molecules
• Glucose via GLUT1 transporter
• Amino acids via specific transporters
• Does NOT pass: large molecules, polar/charged molecules, most antibiotics (except with inflammation), proteins

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1. Coordination of voluntary movement - smooth, precise, sequenced muscle activity.
2. Maintenance of posture and balance (vestibulo-cerebellar - flocculonodular lobe).
3. Regulation of muscle tone.
4. Motor learning - learning new motor skills (e.g., riding a bicycle).
5. Timing of movements - acts as a timing device.

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CHAPTER 10: Autonomic Nervous System (ANS)

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CHAPTER 11: Reproductive Physiology

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• Follicular phase (Day 1-14): FSH → follicle maturation → ↑ oestrogen → LH surge (Day 14) → ovulation.
• Luteal phase (Day 15-28): Ruptured follicle → corpus luteum → secretes progesterone + oestrogen → if no fertilisation, corpus luteum degenerates → progesterone falls → menstruation.

• Menstrual phase (Day 1-5): Endometrium shed.
• Proliferative phase (Day 6-14): Oestrogen → endometrial thickening, gland growth.
• Secretory phase (Day 15-28): Progesterone → glands become secretory, spiral arteries develop (prepares for implantation).

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CHAPTER 12: Special Senses / Sensory Physiology

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1. Light → 11-cis-retinal → all-trans-retinal (isomerisation).
2. All-trans-retinal activates rhodopsin → activates G-protein transducin → activates phosphodiesterase (PDE).
3. PDE hydrolyses cGMP → cGMP levels fall → cGMP-gated Na⁺ channels close → cell hyperpolarises (rods/cones are depolarised in dark, hyperpolarise in light).
4. ↓ Glutamate release → signals ON/OFF bipolar cells → ganglion cells → optic nerve.

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1. Accommodation: Ciliary muscle contracts → zonule fibres relax → lens becomes more convex → ↑ refractive power → near object focused on retina. Controlled by parasympathetic fibres (CN III).
2. Pupil constriction (miosis): Reduces spherical aberration, ↑ depth of focus.
3. Convergence: Both eyes turn medially (medial recti contract) so both eyes focus on near object.

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Quick-Reference Viva Answer Framework

Define → Normal value/anatomy → Mechanism (steps) → Factors affecting → Clinical significance

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Physiology Viva Q&A — Simple & Easy to Remember

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1. GENERAL PHYSIOLOGY

Keeping the body's internal environment stable (temperature, pH, glucose, etc.).

• Negative feedback = corrects the change (e.g., high glucose → insulin → glucose falls) ✅ most common
• Positive feedback = amplifies the change (e.g., childbirth contractions get stronger and stronger)

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The charge inside a cell at rest = -70 mV (inside is negative)

• Because K⁺ leaks OUT of the cell
• Na⁺/K⁺ pump pushes 3 Na⁺ out, 2 K⁺ in → makes inside more negative
• Think: cell is like a battery, negative inside

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It pumps 3 positive charges out but only 2 in → net loss of positive charge from inside → makes inside more negative

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2. BLOOD

S-shaped curve. Shows how much O₂ haemoglobin carries at different oxygen levels.

• Right shift = Hb releases more O₂ (good for tissues)
  • Causes: ↑CO₂, ↑temperature, ↑acid (↓pH), ↑2,3-DPG
  • "HOT ACID" = Right shift
• Left shift = Hb holds O₂ tightly (bad for release)
  • Causes: ↓CO₂, ↓temp, ↑pH, fetal Hb, CO poisoning

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Group	Antigen on RBC	Antibody in plasma
A	A	Anti-B
B	B	Anti-A
AB	A+B	None (universal recipient)
O	None	Anti-A + Anti-B (universal donor)
Rule: If antigen is absent → antibody is present

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• Rh-negative mother + Rh-positive baby
• Mother makes anti-D antibodies after 1st delivery
• In 2nd pregnancy → antibodies cross placenta → destroy baby's RBCs
• Prevented by anti-D injection (Rhogam) within 72 hrs of delivery

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Rate at which RBCs settle in 1 hour

• Normal: 0-15 mm/hr (male), 0-20 mm/hr (female)
• ↑ in: infection, inflammation, pregnancy, anaemia
• ↓ in: polycythaemia, sickle cell disease

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3. NERVE & MUSCLE

A sudden reversal of membrane charge in a nerve/muscle cell.

Steps (simple):

1. Stimulus → membrane reaches threshold (-55 mV)
2. Na⁺ channels open → Na⁺ rushes IN → inside becomes positive (depolarisation)
3. Na⁺ channels close, K⁺ channels open → K⁺ rushes OUT → inside becomes negative again (repolarisation)
4. Brief hyperpolarisation (undershoot) → returns to -70 mV

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• Absolute = No stimulus can fire another AP (Na⁺ channels locked/inactivated) → ~1 ms
• Relative = Only a VERY strong stimulus can fire an AP (cell is hyperpolarised)
• Ensures nerve fires in ONE direction only

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Muscle shortens because thin filaments (actin) slide over thick filaments (myosin) — filaments themselves don't shorten.

Simple steps:

1. Nerve signal → Ca²⁺ released from sarcoplasmic reticulum
2. Ca²⁺ binds troponin → moves tropomyosin → exposes binding sites on actin
3. Myosin head attaches to actin → power stroke (uses ATP) → actin slides inward
4. Sarcomere shortens → muscle contracts

• A-band stays same length; I-band and H-zone shorten

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Where nerve meets muscle.

1. Nerve impulse → Ca²⁺ enters nerve terminal
2. ACh released → binds nicotinic receptors on muscle
3. Na⁺/K⁺ channels open → muscle depolarises → contracts
4. ACh broken down by acetylcholinesterase

• Myasthenia gravis = antibodies destroy ACh receptors → weakness

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4. CARDIOVASCULAR

One heartbeat = 0.8 sec (at 75 bpm)

Phase	What happens
Atrial systole	Atria contract, fill ventricles
Isovolumetric contraction	Ventricles contract, all valves CLOSED, pressure builds
Ejection	Aortic/pulmonary valves OPEN, blood pumped out
Isovolumetric relaxation	Ventricles relax, all valves CLOSED again
Ventricular filling	Mitral/tricuspid OPEN, ventricles fill passively

• Stroke volume = EDV - ESV = 120 - 50 = 70 mL
• Ejection fraction = ~60%

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• S1 ("lub") = AV valves (mitral + tricuspid) CLOSE → start of systole
• S2 ("dub") = Semilunar valves (aortic + pulmonary) CLOSE → end of systole
• S3 = Ventricle filling too fast → heart failure in adults
• S4 = Stiff ventricle → atrial contraction against stiff wall

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"The more the heart is stretched, the harder it contracts"

• More blood in → ventricle stretches more → stronger beat → more blood out
• Ensures left and right output stays equal
• Mechanism: more stretch = better actin-myosin overlap = more cross-bridges = stronger contraction

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Baroreceptors in carotid sinus + aortic arch detect blood pressure changes.

• BP rises → baroreceptors fire more → brain reduces heart rate + dilates vessels → BP falls
• BP falls → baroreceptors fire less → brain increases heart rate + constricts vessels → BP rises
• It's the body's instant BP controller (works in seconds)

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5. RESPIRATORY

Name	Simple meaning	Value
Tidal Volume (TV)	Normal breath	500 mL
IRV	Extra air you can breathe IN	3000 mL
ERV	Extra air you can breathe OUT	1100 mL
RV	Air always left in lungs (can't breathe out)	1200 mL
FRC	Air left after normal breath out (ERV+RV)	2300 mL
VC	Maximum breath in + out (TV+IRV+ERV)	4600 mL
TLC	Total capacity (VC+RV)	5800 mL
⚠️ RV and FRC cannot be measured by spirometry

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• Bohr effect: More CO₂ in tissues → Hb releases more O₂ → O₂ delivered to active tissues ✅
• Haldane effect: When Hb picks up O₂ in lungs → Hb releases CO₂ → CO₂ cleared ✅
• Together: O₂ and CO₂ swap efficiently at tissues AND lungs

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• Made by Type II pneumocytes
• Reduces surface tension in alveoli → prevents alveolar collapse
• Without it → lungs collapse like a wet balloon
• RDS in premature babies = no surfactant → treat with exogenous surfactant

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Type	Simple cause	Example
Hypoxic	Not enough O₂ in air/lungs	High altitude, pneumonia
Anaemic	Not enough Hb to carry O₂	Anaemia, CO poisoning
Stagnant	Blood not flowing enough	Heart failure, shock
Histotoxic	Cells can't use O₂	Cyanide poisoning

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6. RENAL

Volume of blood filtered by kidneys per minute = 125 mL/min (180 L/day!)

• Measured by inulin clearance (gold standard) or creatinine clearance
• Formula: GFR = (Urine conc × Urine flow) / Plasma conc
• Clinically: ↑ creatinine in blood = ↓ GFR = kidney struggling

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How kidneys make concentrated urine:

1. Loop of Henle creates a salt gradient in kidney medulla (very salty deep inside)
2. When collecting duct passes through this salty area + ADH is present → water pulled out → urine becomes concentrated
3. Without ADH → water stays in → dilute urine (diabetes insipidus)

• Think: Loop builds the gradient, ADH uses it

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The kidney's way of raising blood pressure when it falls:

1. Low BP → kidney releases Renin
2. Renin → Angiotensinogen → Angiotensin I → (ACE in lungs) → Angiotensin II
3. Angiotensin II:
   • Constricts blood vessels (↑ BP)
   • Tells adrenal gland to release Aldosterone → kidneys retain Na⁺ and water → ↑ BP

• ACE inhibitors (enalapril) block step 2 → used to treat hypertension

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7. GASTROINTESTINAL

Phase	Trigger	% of secretion
Cephalic	Sight/smell/thought of food → vagus nerve	30%
Gastric	Food in stomach → distension + gastrin	60%
Intestinal	Chyme in small intestine	10% (then inhibits acid)

• Gastrin → stimulates parietal cells → HCl
• Omeprazole (PPI) blocks the final HCl pump

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• Made in liver, stored in gallbladder, released when fat enters duodenum (triggered by CCK)
• Emulsifies fat = breaks big fat globules into tiny droplets so lipase can digest them
• Also excretes bilirubin, cholesterol
• 95% of bile salts recycled via enterohepatic circulation (ileum → portal vein → liver)

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8. ENDOCRINE

Hypothalamus → TRH → Pituitary → TSH → Thyroid → T3/T4 T3/T4 → negative feedback on hypothalamus + pituitary

• Hypothyroidism → ↓T3/T4 → ↑TSH → goitre
• Hyperthyroidism → ↑T3/T4 → ↓TSH

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How it's released (simple): Glucose enters β cell → ATP increases → K⁺ channel closes → cell depolarises → Ca²⁺ enters → insulin released (Sulphonylureas work here — they close the K⁺ channel)

What insulin does:

• Pushes glucose INTO cells (muscle, fat) — lowers blood glucose
• Builds glycogen, protein, fat
• The only hormone that lowers blood sugar
• Also drives K⁺ into cells (useful in hyperkalaemia treatment)

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The "stress hormone" from adrenal cortex:

• Raises blood sugar (breaks down protein + fat to make glucose)
• Anti-inflammatory (used as medicine — prednisolone)
• Immunosuppressive (↓ lymphocytes)
• Long-term excess → Cushing's syndrome (moon face, central obesity, easy bruising, osteoporosis)

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9. NEUROPHYSIOLOGY

A tight seal between blood vessels and brain tissue that protects the brain.

• Formed by: tight junctions in brain capillaries + astrocyte foot processes
• Lets through: O₂, CO₂, glucose (via transporter), lipid-soluble drugs (alcohol, anaesthetics, steroids)
• Blocks: bacteria, toxins, most drugs, large molecules
• Inflamed in meningitis → becomes more permeable

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The brain's "auto-correct" for movement:

1. Coordinates smooth voluntary movements
2. Maintains balance and posture
3. Regulates muscle tone
4. Motor learning (learning to ride a bike)

• Damage → ATAXIA (unsteady gait), intention tremor, slurred speech, nystagmus
• Cerebellar signs are IPSILATERAL (same side as lesion)

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Feature	NREM	REM
EEG	Slow waves	Fast (like awake)
Eye movement	None	Rapid eye movements
Muscle tone	Reduced	Completely absent (paralysed!)
Dreaming	Rare	Vivid dreams
Growth hormone	Released in deep NREM	—
Memory	Declarative (facts)	Procedural (skills)

• Cycle alternates every ~90 minutes; 4-5 cycles per night

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10. AUTONOMIC NERVOUS SYSTEM

Feature	Sympathetic	Parasympathetic
Role	Fight or Flight	Rest and Digest
Origin	T1-L2 (thoracolumbar)	CN III, VII, IX, X + S2-4
Neurotransmitter	Noradrenaline	Acetylcholine
Heart	↑ rate	↓ rate
Bronchi	Dilate (open)	Constrict
Pupil	Dilate	Constrict
Gut	Slow down	Speed up

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• α1 = blood vessel walls → vasoconstriction
• α2 = nerve endings → reduces its own NA release (auto-brake)
• β1 = heart → faster + stronger beat; kidney → releases renin
• β2 = bronchi, uterus, blood vessels → relaxation (salbutamol = β2 agonist)
• β3 = fat → breaks down fat

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11. REPRODUCTIVE PHYSIOLOGY

Day 1-14: Follicular phase FSH → follicle grows → makes oestrogen → endometrium thickens Oestrogen peaks → LH surge → ovulation on Day 14

Day 15-28: Luteal phase Empty follicle → corpus luteum → makes progesterone Progesterone → endometrium becomes secretory (ready for implantation) No pregnancy → corpus luteum dies → progesterone drops → menstruation

If pregnant → hCG from embryo keeps corpus luteum alive

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12. SPECIAL SENSES

	Rods	Cones
Location	Peripheral retina	Macula/Fovea (centre)
Function	Night/dim vision	Day/colour vision
Colours	Black and white only	3 types: Red, Green, Blue
Pigment	Rhodopsin	Photopsin
Acuity	Low	High

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When you look at something close, 3 things happen TOGETHER:

1. Lens bulges (thickens) → more powerful → focuses near object
2. Pupil constricts → sharper image
3. Eyes converge (turn inward) → both eyes on same object All controlled by CN III (parasympathetic). Blocked by atropine.

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✅ Golden Viva Tip

For every answer, say: Definition → Normal value → Mechanism → Clinical link Example for GFR:

• "GFR is the volume filtered per minute — 125 mL/min — measured by inulin clearance — clinically, creatinine is used — falls in CKD."