PGIMER Entrance Physiology Syllabus

Physiology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Physiology in PGIMER Entrance, not a summary of it.

1. 1

   General, Nerve and Muscle Physiology

   4 topics

   • Body fluid compartments and membrane transport
   • Resting membrane and action potential
   • Neuromuscular junction transmission
   • Skeletal, cardiac and smooth muscle contraction
2. 2

   Cardiovascular and Respiratory Physiology

   5 topics

   • Cardiac cycle and pressure-volume loop
   • ECG genesis and arrhythmia basics
   • Regulation of arterial blood pressure
     • Baroreceptor and chemoreceptor reflexes
     • Renin-angiotensin-aldosterone control
   • Lung volumes, compliance and ventilation-perfusion
   • Oxygen and carbon dioxide transport
3. 3

   Renal, GI and Endocrine Physiology

   4 topics

   • Glomerular filtration and tubular handling
   • Acid-base balance and renal compensation
   • GI secretions and motility regulation
   • Hypothalamo-pituitary axis
     • Thyroid and adrenal hormone regulation
     • Insulin, glucagon and glucose homeostasis
4. 4

   Neurophysiology and Special Senses

   4 topics

   • Sensory and motor pathways
   • Reflexes and posture control
   • Vision, hearing and equilibrium physiology
   • Sleep, EEG and limbic function

Physiology flashcards for PGIMER Entrance

22 of 61 cards from the Physiology deck — real questions with worked answers.

1. What is the approximate distribution of total body water in a 70 kg adult male, and how is it divided between intracellular and extracellular compartments?

   Total body water is about 60% of body weight (~42 L). Intracellular fluid (ICF) is 2/3 (~28 L); extracellular fluid (ECF) is 1/3 (~14 L), of which interstitial fluid is ~11 L and plasma ~3 L.

2. Compare primary active transport and secondary active transport.

   Primary active transport directly uses ATP hydrolysis to move solutes against their gradient (e.g., Na+/K+-ATPase). Secondary active transport uses the energy stored in an ion's electrochemical gradient (established by primary transport) to move another solute, via symport (co-transport) or antiport (counter-transport).

3. How many Na+ and K+ ions does the Na+/K+-ATPase pump per ATP, and in which directions?

   It pumps 3 Na+ out of the cell and 2 K+ into the cell per molecule of ATP hydrolyzed, making it electrogenic (net loss of one positive charge from inside).

4. State the Gibbs-Donnan effect and one of its physiological consequences.

   When a non-diffusible charged ion (e.g., protein anion) is on one side of a semipermeable membrane, it causes asymmetric distribution of diffusible ions to maintain electroneutrality and osmotic equilibrium. Consequence: higher total solute/osmotic pressure on the protein-containing side, contributing to plasma oncotic pressure.

5. What is the typical resting membrane potential of a neuron, and which ion's equilibrium potential is it closest to?

   About -70 mV; it lies closest to the K+ equilibrium potential (~ -90 mV) because the resting membrane is most permeable to K+.

6. Write the Nernst equation for an ion at body temperature (37°C) and give the form for a monovalent cation.

   E_ion = (61/z) × log10([ion]outside/[ion]inside) mV. For a monovalent cation (z = +1): E = 61 × log10([out]/[in]) mV.

7. What does the Goldman-Hodgkin-Katz (GHK) equation account for that the Nernst equation does not?

   The GHK equation calculates membrane potential considering the relative permeabilities and concentrations of multiple ions (Na+, K+, Cl-) simultaneously, whereas the Nernst equation gives the equilibrium potential for a single ion.

8. List the phases of a neuronal action potential and the main ionic event in each.

   1) Depolarization (rising phase): voltage-gated Na+ channels open, Na+ influx. 2) Repolarization (falling phase): Na+ channels inactivate, voltage-gated K+ channels open, K+ efflux. 3) Hyperpolarization (undershoot): K+ channels remain open longer, then close.

9. Distinguish the absolute refractory period from the relative refractory period.

   Absolute refractory period: no stimulus, however strong, can trigger another action potential because Na+ channels are inactivated. Relative refractory period: a stronger-than-normal stimulus can elicit an action potential, occurring during hyperpolarization when some Na+ channels have recovered but K+ permeability is still elevated.

10. What is the neurotransmitter at the neuromuscular junction, and which receptor type does it act on?

    Acetylcholine (ACh), acting on nicotinic acetylcholine receptors (a ligand-gated cation channel) on the motor end plate.

11. Describe the sequence of events at the neuromuscular junction from nerve action potential to muscle contraction.

    Nerve AP opens voltage-gated Ca2+ channels at the terminal; Ca2+ influx triggers ACh release; ACh binds nicotinic receptors causing Na+ influx and end-plate potential; this depolarizes the sarcolemma to threshold, generating a muscle AP that spreads along T-tubules to trigger Ca2+ release and contraction.

12. Compare the mechanisms of myasthenia gravis and Lambert-Eaton myasthenic syndrome.

    Myasthenia gravis: autoantibodies against postsynaptic nicotinic ACh receptors; weakness worsens with activity. Lambert-Eaton: autoantibodies against presynaptic voltage-gated Ca2+ channels, reducing ACh release; strength improves with repeated activity (facilitation).

13. Describe the cross-bridge cycle of skeletal muscle contraction.

    1) ATP binds myosin, detaching it from actin. 2) ATP hydrolysis cocks the myosin head. 3) Head binds actin forming a cross-bridge. 4) Pi release triggers the power stroke, sliding actin past myosin. 5) ADP released; new ATP binds to detach. Repeats while Ca2+ is present.

14. How does Ca2+ initiate skeletal muscle contraction at the molecular level?

    Ca2+ binds troponin C, causing a conformational change that moves tropomyosin away from the myosin-binding sites on actin, allowing cross-bridge formation.

15. Compare excitation-contraction coupling in skeletal versus cardiac muscle.

    Skeletal: depolarization of T-tubule directly activates dihydropyridine receptors mechanically coupled to ryanodine receptors, releasing SR Ca2+ (no extracellular Ca2+ needed). Cardiac: Ca2+ influx through L-type channels triggers further SR Ca2+ release (calcium-induced calcium release), so extracellular Ca2+ is essential.

16. Compare smooth muscle contraction regulation with skeletal muscle.

    Smooth muscle: Ca2+ binds calmodulin, activating myosin light-chain kinase (MLCK) which phosphorylates myosin to allow cross-bridging; relaxation by myosin light-chain phosphatase. It lacks troponin. Skeletal muscle uses the troponin-tropomyosin (thin-filament) regulatory system.

17. Define a motor unit and explain the size principle of recruitment.

    A motor unit is a single motor neuron and all the muscle fibers it innervates. The size principle states that smaller (low-threshold) motor units are recruited first for fine/weak contractions, and larger units are recruited progressively as more force is needed.

18. Name the phases of the cardiac cycle in order, beginning with atrial systole.

    1) Atrial systole, 2) Isovolumetric (isovolumic) ventricular contraction, 3) Rapid ventricular ejection, 4) Reduced ejection, 5) Isovolumetric ventricular relaxation, 6) Rapid filling, 7) Reduced filling (diastasis).

19. On the ventricular pressure-volume loop, what do the four corners/segments represent?

    The loop runs counterclockwise: 1) Isovolumetric contraction (vertical rise after mitral valve closes), 2) Ejection (volume falls after aortic valve opens), 3) Isovolumetric relaxation (vertical fall after aortic valve closes), 4) Filling (volume rises after mitral valve opens).

20. Define stroke volume, ejection fraction, and give normal values.

    Stroke volume = end-diastolic volume - end-systolic volume (~70 mL). Ejection fraction = stroke volume / end-diastolic volume × 100 (normal ~55-70%).

21. What causes the first (S1) and second (S2) heart sounds?

    S1 is produced by closure of the atrioventricular (mitral and tricuspid) valves at the start of ventricular systole. S2 is produced by closure of the semilunar (aortic and pulmonary) valves at the end of systole.

22. What do the P wave, QRS complex, and T wave of the ECG represent?

    P wave = atrial depolarization; QRS complex = ventricular depolarization (atrial repolarization is hidden within it); T wave = ventricular repolarization.

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