PGIMER Entrance Physiology Syllabus

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.

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.

State normal durations for the PR interval and QRS complex on ECG.

Normal PR interval is 0.12-0.20 s (120-200 ms); normal QRS duration is less than 0.12 s (under 120 ms, typically 0.06-0.10 s).

Describe the action potential of cardiac SA nodal (pacemaker) cells and what causes the pacemaker potential.

Phase 4 (pacemaker/slow diastolic depolarization) is driven by the funny current (If, Na+ influx) plus T-type Ca2+ current; Phase 0 (upstroke) is due to L-type Ca2+ influx; Phase 3 (repolarization) is due to K+ efflux. There is no stable resting potential or fast Na+ phase.

Explain the mechanism of a reentry arrhythmia.

Reentry occurs when an impulse travels in a circuit with a unidirectional block and an area of slow conduction, allowing the wave to re-excite tissue that has recovered. This requires the impulse circulation time to exceed the refractory period, producing self-sustaining arrhythmias (e.g., AV nodal reentrant tachycardia, atrial flutter).

Write the equation relating mean arterial pressure (MAP) to cardiac output and total peripheral resistance, and estimate MAP from systolic/diastolic pressures.

MAP = Cardiac Output × Total Peripheral Resistance (plus central venous pressure, usually negligible). Estimated MAP = Diastolic Pressure + 1/3 (Systolic - Diastolic) = DBP + 1/3 pulse pressure.

Describe the baroreceptor reflex response to a fall in arterial blood pressure.

Decreased stretch of carotid sinus/aortic arch baroreceptors reduces afferent firing to the medulla, leading to increased sympathetic and decreased parasympathetic outflow, raising heart rate, contractility, and vasoconstriction (and venoconstriction) to restore blood pressure.

Outline how the renin-angiotensin-aldosterone system (RAAS) raises blood pressure.

Low BP/renal perfusion stimulates renin from juxtaglomerular cells; renin converts angiotensinogen to angiotensin I; ACE (lung) converts it to angiotensin II, a potent vasoconstrictor that also stimulates aldosterone (Na+/water retention), ADH, thirst, and sympathetic activity, raising BP and volume.

Define tidal volume, inspiratory reserve volume, residual volume, and vital capacity.

Tidal volume (TV): air per normal breath (~500 mL). Inspiratory reserve volume (IRV): extra air inhaled beyond TV (~3000 mL). Residual volume (RV): air remaining after maximal expiration (~1200 mL). Vital capacity (VC) = IRV + TV + ERV (~4600 mL); the maximum air expelled after maximal inspiration.

Why can't functional residual capacity (FRC) or residual volume be measured by simple spirometry?

Because they include the residual volume, which is air that cannot be exhaled and thus cannot be directly measured by spirometry. They require methods such as helium dilution, nitrogen washout, or body plethysmography.

Define lung compliance and state how it changes in emphysema versus pulmonary fibrosis.

Compliance = change in volume / change in pressure (distensibility of the lung). Emphysema increases compliance (loss of elastic tissue, easy to inflate, hard to deflate); pulmonary fibrosis decreases compliance (stiff lungs).

What is the normal ventilation-perfusion (V/Q) ratio, and how does it differ between lung apex and base when upright?

The overall normal V/Q ratio is about 0.8. At the apex, V/Q is high (~3, more ventilation relative to perfusion); at the base, V/Q is low (~0.6, more perfusion than ventilation).

Explain hypoxic pulmonary vasoconstriction and its purpose.

In the lungs, low alveolar O2 causes local vasoconstriction (opposite to the systemic circulation). This diverts blood from poorly ventilated to well-ventilated alveoli, optimizing ventilation-perfusion matching and gas exchange.

In what forms is oxygen carried in the blood, and what is the approximate O2-carrying capacity of hemoglobin?

O2 is carried bound to hemoglobin (~98%) and dissolved in plasma (~2%). Each gram of hemoglobin binds ~1.34 mL O2; with ~15 g/dL Hb, capacity is ~20 mL O2/dL of blood.

List factors that shift the oxygen-hemoglobin dissociation curve to the right.

A rightward shift (decreased Hb-O2 affinity, easier unloading) is caused by increased CO2/H+ (low pH, Bohr effect), increased temperature, and increased 2,3-bisphosphoglycerate (2,3-BPG). Fetal hemoglobin and CO shift it left.

Describe the three forms in which CO2 is transported in blood and their approximate proportions.

As bicarbonate (HCO3-) ~70% (via carbonic anhydrase in RBCs with the chloride shift), bound to hemoglobin as carbaminohemoglobin ~23%, and dissolved in plasma ~7%.

Explain the chloride shift (Hamburger phenomenon).

In tissues, CO2 enters RBCs and forms HCO3- via carbonic anhydrase; HCO3- exits into plasma in exchange for Cl- entering the cell to maintain electroneutrality. The process reverses in the lungs.

Write the equation for glomerular filtration rate (GFR) in terms of clearance, and name the ideal marker.

GFR = Clearance of a substance = (Urine concentration × Urine flow rate) / Plasma concentration (Ux·V/Px). The ideal marker is inulin (freely filtered, not reabsorbed, secreted, or metabolized); creatinine clearance is the clinical approximation.

List the forces (Starling forces) governing glomerular filtration and the net direction of each.

Favoring filtration: glomerular capillary hydrostatic pressure (PGC). Opposing filtration: Bowman's capsule hydrostatic pressure (PBS) and glomerular capillary oncotic pressure (πGC). Net filtration pressure = PGC - PBS - πGC.

What is renal autoregulation and name its two mechanisms?

Renal autoregulation keeps GFR and renal blood flow relatively constant despite changes in arterial pressure (~80-180 mmHg). Mechanisms: 1) Myogenic mechanism (afferent arteriole constricts when stretched), 2) Tubuloglomerular feedback (macula densa senses NaCl and adjusts afferent tone via adenosine).

Where in the nephron is most glucose, sodium, and water reabsorbed, and what is the glucose transport maximum significance?

The proximal convoluted tubule reabsorbs ~65% of filtered Na+ and water and essentially all glucose (via SGLT). When plasma glucose exceeds the transport maximum (Tm, ~375 mg/min) and threshold (~180 mg/dL), glucose appears in urine (glucosuria).

How does the loop of Henle establish the medullary concentration gradient (countercurrent multiplier)?

The thick ascending limb actively pumps out NaCl (via NKCC2) but is impermeable to water, diluting tubular fluid and concentrating the interstitium. The descending limb is permeable to water, which leaves passively. This countercurrent arrangement multiplies the gradient up to ~1200 mOsm/L at the medulla.

Give the Henderson-Hasselbalch equation for the bicarbonate buffer system and normal arterial values.

pH = 6.1 + log10([HCO3-] / (0.03 × PCO2)). Normal arterial values: pH 7.35-7.45, HCO3- ~24 mEq/L, PCO2 ~40 mmHg.

Classify the four primary acid-base disorders by pH, PCO2, and HCO3- changes.

Metabolic acidosis: ↓pH, ↓HCO3-. Metabolic alkalosis: ↑pH, ↑HCO3-. Respiratory acidosis: ↓pH, ↑PCO2. Respiratory alkalosis: ↑pH, ↓PCO2. Respiratory disorders are primary PCO2 changes; metabolic are primary HCO3- changes.

How do the kidneys compensate for chronic respiratory acidosis?

The kidneys increase H+ secretion and generate/reabsorb more HCO3- (enhanced NH4+ excretion and titratable acid), raising plasma bicarbonate to buffer the elevated PCO2 and restore pH toward normal over days.

Match the major GI hormones to their main stimulus and action: gastrin, secretin, CCK.

Gastrin (G cells, antrum): stimulated by peptides/distension/vagus; increases gastric acid secretion and mucosal growth. Secretin (S cells, duodenum): stimulated by acid; increases pancreatic/biliary HCO3- and decreases gastric acid. CCK (I cells): stimulated by fat/protein; causes gallbladder contraction, pancreatic enzyme secretion, and slows gastric emptying.

Describe the cellular mechanism of gastric acid (HCl) secretion by parietal cells.

The H+/K+-ATPase (proton pump) on the apical membrane pumps H+ into the lumen in exchange for K+. H+ comes from H2CO3 (via carbonic anhydrase); the generated HCO3- exits the basolateral side in exchange for Cl- ('alkaline tide'), and Cl- enters the lumen to form HCl. Stimulated by ACh, gastrin, and histamine.

What are slow waves (basic electrical rhythm) in GI smooth muscle and what generates them?

Slow waves are spontaneous, rhythmic oscillations in the resting membrane potential that set the maximum frequency of contractions. They are generated by the interstitial cells of Cajal (pacemaker cells) and cause contraction only when they reach threshold and trigger spike potentials.

Compare the regulation of anterior versus posterior pituitary hormone release.

Anterior pituitary: glandular tissue regulated by hypothalamic releasing/inhibiting hormones delivered via the hypophyseal portal system. Posterior pituitary: neural tissue storing ADH and oxytocin synthesized in hypothalamic (supraoptic and paraventricular) neurons and released directly into blood upon neural stimulation.

Describe the hypothalamo-pituitary-thyroid axis and its negative feedback.

Hypothalamic TRH stimulates anterior pituitary TSH, which stimulates the thyroid to release T3/T4. Circulating T3/T4 exert negative feedback on both the pituitary (TSH) and hypothalamus (TRH) to maintain homeostasis.

Compare the dorsal column-medial lemniscus pathway with the anterolateral (spinothalamic) pathway.

Dorsal column-medial lemniscus carries fine touch, vibration, and proprioception; fibers ascend ipsilaterally and decussate in the medulla. Anterolateral/spinothalamic carries pain and temperature; fibers cross within 1-2 segments in the spinal cord and ascend contralaterally. Both relay in the thalamus (VPL).

Describe the corticospinal tract: origin, decussation, and function.

It originates from the motor cortex, descends through the internal capsule and brainstem; ~85-90% of fibers decussate at the medullary pyramids (lateral corticospinal tract) controlling distal limb voluntary movement, while the rest descend ipsilaterally (anterior corticospinal tract) for axial/proximal muscles.

Describe the components and pathway of the monosynaptic stretch (myotatic) reflex.

Stretch activates the muscle spindle (Ia afferent), which synapses directly on alpha motor neurons in the spinal cord, causing contraction of the same muscle, with reciprocal inhibition of antagonists. It is monosynaptic, ipsilateral (e.g., the knee-jerk reflex).

Contrast the roles of muscle spindles and Golgi tendon organs.

Muscle spindles lie in parallel with muscle fibers and detect muscle length and rate of change (stretch), driving the stretch reflex. Golgi tendon organs lie in series within tendons and detect muscle tension/force, mediating the inverse myotatic reflex (autogenic inhibition) to prevent excessive force.

Describe the phototransduction cascade in rod photoreceptors and the effect of light.

Light isomerizes 11-cis-retinal to all-trans, activating rhodopsin → transducin → phosphodiesterase, which breaks down cGMP. Falling cGMP closes cation (Na+) channels, hyperpolarizing the rod and decreasing glutamate release. Thus light hyperpolarizes photoreceptors (the opposite of most receptors).

Compare rods and cones.

Rods: high sensitivity, used in dim light (scotopic), no color vision, more numerous, concentrated in periphery, contain rhodopsin. Cones: lower sensitivity, function in bright light (photopic), provide color vision (3 types) and high acuity, concentrated in the fovea.

Explain how the cochlea performs frequency (pitch) discrimination.

Via tonotopic organization of the basilar membrane: the base (stiff, narrow) responds best to high frequencies, and the apex (wide, floppy) responds to low frequencies (place principle). Sound vibrations create a traveling wave peaking at a frequency-specific location, stimulating the corresponding hair cells.

How do the semicircular canals and otolith organs differ in what they detect?

Semicircular canals detect angular (rotational) acceleration of the head via endolymph movement bending the cupula. Otolith organs (utricle and saccule) detect linear acceleration and head position relative to gravity via otoliths displacing the otolithic membrane over hair cells.

Describe the EEG waveforms by frequency and associated states: alpha, beta, theta, delta.

Beta (>13 Hz): alert, active mental concentration. Alpha (8-13 Hz): awake, relaxed, eyes closed. Theta (4-7 Hz): drowsiness, light sleep, children. Delta (<4 Hz): deep (slow-wave) sleep, large amplitude.

Contrast NREM (slow-wave) sleep and REM sleep.

NREM: progressively slower EEG (delta in deep stages), decreased HR/BP/metabolism, little dreaming, 'restful' sleep. REM: low-voltage fast (desynchronized, beta-like) EEG resembling wakefulness, rapid eye movements, skeletal muscle atonia, vivid dreaming, irregular autonomic activity ('paradoxical sleep').

What is the role of the limbic system, and name its key structures (Papez circuit)?

The limbic system governs emotion, motivation, and memory formation. Key structures include the hippocampus (memory), amygdala (fear/emotion), hypothalamus, cingulate gyrus, fornix, and mammillary bodies. The Papez circuit links the hippocampus → fornix → mammillary bodies → anterior thalamus → cingulate → back to hippocampus.