DNB CET 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 DNB CET, not a summary of it.

1. 1

   General, Nerve and Muscle Physiology

   4 topics

   • Cell membrane transport and resting membrane potential
   • Action potential generation and propagation
   • Neuromuscular transmission and excitation-contraction coupling
   • Skeletal, cardiac and smooth muscle mechanics
2. 2

   Cardiovascular and Respiratory Physiology

   3 topics

   • Cardiac Cycle and Output
     • Pressure-volume loops and Wiggers diagram
     • Determinants of stroke volume and ejection fraction
     • Baroreceptor and chemoreceptor reflexes
   • Respiratory Mechanics and Gas Exchange
     • Lung volumes, capacities and compliance
     • Oxygen-hemoglobin dissociation curve shifts
     • Ventilation-perfusion ratio and hypoxia types
   • Hemodynamics and Microcirculation
     • Blood pressure regulation and Poiseuille relationships
     • Capillary exchange and Starling forces
     • Regional and coronary circulation
3. 3

   Renal, GI and Endocrine Physiology

   5 topics

   • Glomerular filtration, clearance and tubular handling
   • Acid-base balance and renal compensation
   • GI secretions, motility and absorption
   • Hypothalamo-pituitary axis and hormone feedback
   • Thyroid, adrenal and pancreatic hormone actions
4. 4

   Neurophysiology and Special Senses

   5 topics

   • Synaptic transmission and reflex arcs
   • Visual pathway and photoreceptor physiology
   • Auditory and vestibular transduction
   • Autonomic nervous system organization
   • Sleep, EEG and higher cortical functions

Physiology flashcards for DNB CET

22 of 71 cards from the Physiology deck — real questions with worked answers.

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

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

2. State the Nernst equation for an ion at 37°C (using log base 10) and what it calculates.

   E_ion = (61/z) × log([ion]outside/[ion]inside) in mV. It calculates the equilibrium potential at which the electrochemical gradient for that ion is zero.

3. Differentiate primary active transport from secondary active transport, with an example of each.

   Primary active transport uses ATP directly to move ions against a gradient (e.g., Na+/K+-ATPase). Secondary active transport uses the energy stored in an ion gradient (created by primary transport) to drive another solute (e.g., Na+/glucose SGLT cotransport).

4. What ions does the Na+/K+-ATPase move and in what stoichiometry per ATP?

   It pumps 3 Na+ out of the cell and 2 K+ into the cell per ATP hydrolyzed, making it electrogenic.

5. List the phases of a typical neuronal action potential and the main ion movement in each.

   Depolarization: Na+ influx (voltage-gated Na+ channels open). Repolarization: Na+ channels inactivate and voltage-gated K+ channels open (K+ efflux). Hyperpolarization (after-potential): continued K+ efflux before channels close.

6. Define the absolute and relative refractory periods of an action potential.

   Absolute refractory period: no stimulus can trigger a second AP because Na+ channels are inactivated. Relative refractory period: a stronger-than-normal stimulus can trigger an AP, occurring during hyperpolarization when some Na+ channels have recovered.

7. What is saltatory conduction and why does it increase conduction velocity?

   In myelinated axons, the action potential jumps from one node of Ranvier to the next because myelin insulates internodal segments. This speeds conduction and conserves energy since depolarization only occurs at nodes.

8. Name two factors that increase the conduction velocity of an axon.

   Larger axon diameter (lower internal resistance) and myelination (saltatory conduction). Higher temperature also increases velocity.

9. Describe the sequence of events in neuromuscular transmission at the motor end plate.

   AP reaches axon terminal -> voltage-gated Ca2+ channels open -> Ca2+ influx -> ACh vesicles fuse and release ACh -> ACh binds nicotinic receptors on the motor end plate -> end-plate potential -> threshold reached -> muscle AP. ACh is broken down by acetylcholinesterase.

10. Explain excitation-contraction coupling in skeletal muscle.

    Muscle AP travels down T-tubules -> activates dihydropyridine (DHP) receptors -> mechanically opens ryanodine receptors on the sarcoplasmic reticulum -> Ca2+ released -> Ca2+ binds troponin C -> tropomyosin moves, exposing actin binding sites -> cross-bridge cycling and contraction.

11. What is the role of troponin C and tropomyosin in muscle contraction?

    Tropomyosin blocks myosin-binding sites on actin at rest. Ca2+ binds troponin C, causing a conformational change that moves tropomyosin aside, allowing myosin heads to bind actin and generate force.

12. Compare the source of activator Ca2+ in skeletal versus cardiac muscle.

    Skeletal muscle: Ca2+ comes almost entirely from the sarcoplasmic reticulum (no need for extracellular Ca2+). Cardiac muscle: requires extracellular Ca2+ entry that triggers Ca2+-induced Ca2+ release from the SR.

13. How does smooth muscle contraction differ from skeletal muscle at the molecular level?

    Smooth muscle lacks troponin; Ca2+ binds calmodulin, which activates myosin light-chain kinase (MLCK) to phosphorylate myosin, enabling cross-bridge cycling. It is slower, uses less ATP, and can sustain tone (latch state).

14. What is the length-tension relationship in skeletal muscle?

    Active tension is maximal at optimal sarcomere length (~2.0-2.2 µm) where actin-myosin overlap is ideal. Tension falls at shorter lengths (filament overlap interference) and longer lengths (reduced cross-bridge overlap).

15. List the phases of the cardiac cycle in order.

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

16. Define cardiac output and give its formula and normal value.

    Cardiac output = Stroke volume × Heart rate. Normal resting value is about 5 L/min (e.g., 70 mL × 70 bpm).

17. State the Frank-Starling law of the heart.

    Within physiological limits, the force of ventricular contraction (stroke volume) increases with increased end-diastolic volume (preload), because greater stretch of myocardial fibers increases contractile force.

18. Define preload and afterload.

    Preload is the ventricular wall tension/stretch at the end of diastole (related to end-diastolic volume/venous return). Afterload is the resistance/pressure the ventricle must overcome to eject blood (related to aortic pressure/systemic vascular resistance).

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

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

20. Define ejection fraction and give its normal value.

    Ejection fraction = Stroke volume / End-diastolic volume × 100. Normal is about 55-70%.

21. Define tidal volume, residual volume, and functional residual capacity.

    Tidal volume (~500 mL): air moved in/out per normal breath. Residual volume (~1200 mL): air remaining after maximal expiration. Functional residual capacity = expiratory reserve volume + residual volume (~2400 mL): air remaining after normal expiration.

22. Why can't residual volume and functional residual capacity be measured by simple spirometry?

    Spirometry only measures air that is moved in and out of the lungs. Residual volume (and any capacity that includes it) represents air that cannot be exhaled, so it must be measured by helium dilution, nitrogen washout, or body plethysmography.

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