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PY12.1-10 | Integrated Physiology — Gate Quiz
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During vigorous exercise, cardiac output increases from 5 L/min to 20 L/min. The primary mechanisms responsible are:
Correct! During exercise: (1) ↑HR via sympathetic activation + vagal withdrawal (primary factor: HR from 72 → 180 bpm); (2) ↑SV via Frank-Starling (increased venous return from muscle pump, respiratory pump, venoconstriction) + ↑contractility (sympathetic β₁). CO can reach 20–25 L/min in trained athletes (40 L/min in elite athletes).
Key concept: Exercise cardiovascular responses — ↑HR (most important factor), ↑SV (Frank-Starling + ↑contractility), ↑CO; ↓SVR in exercising muscles (metabolic vasodilation: CO₂, K⁺, adenosine, NO); ↑SBP (moderate), ↓DBP (↓SVR); ↑O₂ consumption (from 250 mL/min to >3 L/min in athletes); ↑venous return (muscle pump, respiratory pump, venoconstriction). Fick principle: VO₂ = CO × (CaO₂ - CvO₂).
Incorrect. The 4-fold increase in CO during exercise is achieved by: ↑HR (sympathetic + vagal withdrawal) + ↑SV (↑venous return via Frank-Starling + ↑contractility).
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In fever, the thermoregulatory set point in the hypothalamus is raised. The final mediator of this set point increase is:
Correct! Exogenous pyrogens (LPS, viruses) → macrophages release endogenous pyrogens (IL-1β, IL-6, TNF-α) → act on hypothalamic endothelial cells and OVLT (organum vasculosum of the lamina terminalis, a circumventricular organ without BBB) → ↑COX-2 → ↑PGE₂ → acts on EP3 receptors in the preoptic area → raises thermoregulatory set point.
Key concept: Fever pathway — Pyrogen (LPS/virus) → macrophage → IL-1β + IL-6 + TNF-α (endogenous pyrogens) → cross BBB at OVLT → COX-2 in hypothalamic endothelium → PGE₂ → raises set point in preoptic area → effectors: ↑heat production (shivering, ↑metabolism), ↓heat loss (vasoconstriction) until body temperature reaches new set point. Antipyretics: NSAIDs/paracetamol block COX → ↓PGE₂ → lowers set point. Salicylates in children: Reye's syndrome risk.
Incorrect. The final mediator of fever is PGE₂ (prostaglandin E₂) produced by COX-2 in the hypothalamus. This is why NSAIDs (COX inhibitors) and paracetamol reduce fever — they block PGE₂ synthesis.
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A trekker ascends rapidly to 4500m (Ladakh). She develops headache, nausea, and fatigue (acute mountain sickness). The primary cause of hypoxia at altitude is:
Correct! At high altitude, the fractional concentration of O₂ (21%) is UNCHANGED but barometric pressure falls (at 4500m, Patm ≈ 430 mmHg vs 760 mmHg at sea level). Therefore PO₂ = 0.21 × (430 - 47) ≈ 80 mmHg (vs 149 mmHg at sea level) → reduced alveolar PO₂ → reduced PaO₂ → reduced SaO₂ → tissue hypoxia.
Key concept: Altitude hypoxia — PAO₂ = FiO₂ × (Patm - PH₂O) - PaCO₂/RQ. Acclimatisation (days to weeks): immediate ↑ventilation (respiratory alkalosis, ↑2,3-DPG); Renal compensation (↑bicarb excretion); ↑EPO → polycythaemia (days-weeks); ↑capillary density. AMS treated with: descent, O₂, acetazolamide (promotes HCO₃⁻ excretion), dexamethasone. High-altitude pulmonary oedema (HAPE) and cerebral oedema (HACE) are life-threatening complications.
Incorrect. At altitude, O₂ percentage remains 21% but barometric pressure falls → reduced partial pressure of O₂ → reduced alveolar PO₂ → hypoxia. Acclimatisation: ↑ventilation (hyperventilation, respiratory alkalosis), ↑2,3-DPG, polycythaemia (↑EPO), ↑capillary density.
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A scuba diver ascending rapidly from deep water develops joint pain, skin mottling, and neurological symptoms (decompression sickness). The mechanism is:
Correct! Henry's Law: gas dissolved in liquid is proportional to partial pressure. At depth, ↑pressure → ↑N₂ dissolved in tissues. Rapid ascent → ↓pressure → N₂ comes out of solution as bubbles → "the bends" (decompression sickness). Bubbles in joints (pain), skin (pruritus, Marbling), spinal cord (neurological), lungs (chokes). Treat: recompression in hyperbaric chamber.
Key concept: Diving physiology — Henry's Law: [gas] ∝ partial pressure. Decompression sickness: N₂ bubbles in tissues → joint pain ("bends"), skin, spinal cord, lungs. Treatment: hyperbaric O₂ (recompression dissolves bubbles, O₂ replaces N₂). O₂ toxicity: CNS (>1.6 atm PO₂) → seizures; pulmonary (>0.5 atm, chronic) → fibrosing alveolitis. Nitrogen narcosis ("raptures of the deep"): N₂ at high pressure has anaesthetic effect.
Incorrect. Decompression sickness = Henry's Law: dissolved N₂ at high pressure precipitates as bubbles on rapid decompression. Prevention: slow ascent with decompression stops; N₂ replaced by He (helium, less soluble) in deep diving.
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The master circadian clock of the body is located in:
Correct! The suprachiasmatic nucleus (SCN) of the hypothalamus is the master circadian pacemaker. It receives direct photic (light) input via the retinohypothalamic tract (intrinsically photosensitive retinal ganglion cells containing melanopsin). The SCN generates ~24-hour rhythms and synchronises peripheral clocks throughout the body via neural and hormonal signals (including melatonin via the pineal gland).
Key concept: Circadian rhythm control — SCN (hypothalamus): master clock; Light → retina → retinohypothalamic tract → SCN → suprachiasmatic nucleus → pineal gland → ↓melatonin (light) or ↑melatonin (dark) → circadian output. Molecular clock: CLOCK/BMAL1 → Per/Cry → negative feedback loop (~24h period). Jet lag: SCN resynchronisation with new light cycle (takes ~1 day per time zone). Melatonin (from pineal): darkness signal, used to treat jet lag/insomnia.
Incorrect. The master circadian clock is the suprachiasmatic nucleus (SCN) of the hypothalamus — it controls circadian rhythms via light input (retinohypothalamic tract) and melatonin output (via the pineal gland).
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A medical student presenting for a high-stakes examination develops increased heart rate, dry mouth, and heightened alertness. The primary neuroendocrine axis responsible is:
Correct! The acute stress response (immediate, seconds to minutes) is mediated by the sympathetic-adrenal axis: sympathetic activation + adrenal medulla adrenaline release → tachycardia, bronchodilation, dry mouth (↓salivation), pupil dilation, ↑alertness. The HPA axis (cortisol) is the sustained stress response (minutes to hours).
Key concept: Stress response — Immediate (seconds): sympathetic nervous system → NE from nerve terminals + adrenaline from adrenal medulla → fight/flight; Intermediate (minutes-hours): HPA axis → CRH → ACTH → cortisol → ↑gluconeogenesis, ↑lipolysis, anti-inflammatory, immunosuppression; Chronic: high cortisol → metabolic syndrome, immunosuppression, hippocampal damage, HPA dysregulation. Allostatic load = cumulative burden of chronic stress.
Incorrect. Immediate stress symptoms (tachycardia, dry mouth, alertness) are due to the sympathetic-adrenal axis (catecholamines released in seconds). The HPA axis (cortisol) mediates the sustained/prolonged stress response.
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Which of the following is a normal physiological change associated with ageing?
Correct! Normal physiological decline with ageing: GFR falls by ~1 mL/min/year after age 40; FEV₁ falls by ~30 mL/year after age 25; maximum heart rate = 220 - age; bone mineral density decreases (especially after menopause). These changes are predictable and form the basis of age-related disease risk calculations (e.g., Cockcroft-Gault equation for GFR).
Key concept: Ageing physiology — Renal: GFR ↓1 mL/min/year after 40 (creatinine may appear normal due to ↓muscle mass); Respiratory: FEV₁ ↓25–30 mL/year, ↑RV (air trapping), ↓VC; Cardiovascular: ↓maximum HR (220-age), ↓CO reserve, ↑arterial stiffness (↑SBP), ↓diastolic compliance; Musculoskeletal: sarcopenia, osteoporosis; CNS: ↓processing speed, ↓neurogenesis; Endocrine: ↓GH/IGF-1, insulin resistance. Not: dementia (pathological, not normal ageing).
Incorrect. Normal ageing causes progressive decline in GFR (renal ageing), FEV₁ (respiratory ageing), maximum HR, and bone mineral density. These declines affect drug dosing, exercise capacity, and disease risk in the elderly.
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In kwashiorkor (protein malnutrition) in Indian children, the gross oedema is caused primarily by:
Correct! Kwashiorkor (protein malnutrition): inadequate protein intake → reduced hepatic albumin synthesis → hypoalbuminaemia → reduced plasma oncotic pressure (πc falls) → Starling forces shift: less fluid reabsorbed into capillaries + more filtered → gross oedema (characteristically oedematous malnutrition — "moon face," pedal oedema, ascites).
Key concept: PEM in India — Marasmus: severe calorie + protein deficiency → wasting, stunting, NO oedema (low plasma albumin preserved by catabolism); Kwashiorkor: protein deficiency (adequate calories) → hypoalbuminaemia → oedema ("sugar baby"), fatty liver, skin changes (flaky paint, hypopigmentation), apathy. MUAC (mid-upper arm circumference) <11.5 cm = SAM. Treatment: F-75 (stabilisation) → F-100 (rehabilitation) WHO protocol.
Incorrect. Kwashiorkor oedema is due to hypoalbuminaemia → ↓plasma oncotic pressure → fluid shift from capillaries to interstitium (Starling forces). Marasmus (calorie deficiency) does not typically cause oedema because protein stores are relatively preserved.
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Leptin, produced by adipose tissue, communicates nutritional status to the brain. In obesity, leptin levels are typically:
Correct! In obesity, adipose tissue mass is increased → ↑leptin production (high serum leptin). However, hypothalamic leptin receptors become resistant (similar to insulin resistance) → the "satiety" signal is not perceived → continued hunger and reduced energy expenditure despite high leptin levels. This leptin resistance is a key mechanism perpetuating obesity.
Key concept: Leptin (adipokine, 16 kDa protein): produced by white adipose tissue in proportion to fat mass; acts on hypothalamic arcuate nucleus (leptin receptors on POMC/CART neurons) → ↑satiety + ↑energy expenditure; leptin deficiency (rare, congenital): severe obesity (treatable with leptin injections). Leptin resistance in common obesity: downstream signalling failure (SOCS3 upregulation, ER stress). Ghrelin (stomach): hunger hormone (opposite of leptin) — rises before meals.
Incorrect. Obese individuals have HIGH circulating leptin (from excess adipose tissue) but are LEPTIN RESISTANT — hypothalamic receptors don't respond normally. This paradox (high leptin + obesity) is analogous to insulin resistance in T2DM.
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A patient finds that rubbing the site of a painful injury temporarily reduces the pain. This is best explained by:
Correct! Gate control theory (Melzack and Wall, 1965): Stimulation of large myelinated Aβ fibres (touch/vibration) activates inhibitory interneurons (using enkephalins) in the substantia gelatinosa of the dorsal horn → inhibit C fibre/Aδ nociceptive transmission → "gate closed" → reduced pain perception. This explains rubbing, TENS (transcutaneous electrical nerve stimulation), and acupuncture mechanisms.
Key concept: Pain modulation — Gate control (spinal): Aβ fibres activate inhibitory interneurons → close gate for C/Aδ nociception. Descending modulation (brain): PAG (periaqueductal grey) → raphe nuclei (5-HT) + locus coeruleus (NE) → dorsal horn inhibitory interneurons → pain suppression. Endogenous opioids (β-endorphin, enkephalin, dynorphin) → μ, δ, κ opioid receptors → ↓nociceptor sensitivity + ↓NT release. TENS uses this gate control principle (Aβ stimulation).
Incorrect. Gate control theory: Aβ (touch) fibre activation → inhibitory interneurons in dorsal horn → reduced C fibre pain transmission. The "gate" closes, reducing pain perception. This is the physiological basis of TENS therapy.
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