All answers verified against physiology references (Guyton, Ganong, Costanzo).
Answer Key — Physiology Paper I (Set D), Q11–20
11. (A) Decreased muscle tone
Microgravity removes the constant antigravity muscular workload, causing disuse atrophy and loss of muscle tone/mass (and bone density) — the hallmark deconditioning effect seen on return to Earth. Cardiovascular deconditioning actually reduces effective plasma volume/orthostatic tolerance, so (B) and (C) are wrong; increased diuresis (D) occurs early during the flight's fluid shift, not on return.
12. (B) B cells
Reduced immunoglobulins + no response to a protein vaccine (tetanus toxoid) but normal delayed-type hypersensitivity (intact T-cell/cell-mediated immunity) points to a pure humoral (antibody) defect — a B-cell lineage disorder (e.g., X-linked agammaglobulinemia).
13. (D) Used as a source of energy for the transport of other ions
Confirmed in the library: the transmembrane Na⁺ gradient (built by Na⁺/K⁺-ATPase) provides the driving force for secondary active transport of glucose, amino acids, H⁺, Ca²⁺, etc. (Brenner & Rector's The Kidney; Guyton). It is not a Donnan-equilibrium product, doesn't change appreciably with a single action potential, and contributes little to resting membrane potential (which is dominated by K⁺ conductance).
14. (B) Secretin
Acidification of the duodenal lumen to pH ≤ 4.5 (here pH 3.0) is the classic physiologic trigger for secretin release from S cells, which then stimulates pancreatic HCO₃⁻ secretion.
15. (C) Interstitial hydrostatic pressure
Normal interstitial (tissue) fluid hydrostatic pressure is slightly subatmospheric (negative) in most tissues, including the lower limb, maintained by continuous lymphatic drainage (Guyton).
16. (D) Delayed closing of the pulmonary valve
Inspiration increases venous return to the right heart and pulmonary vascular capacitance, prolonging RV ejection and delaying P2 relative to A2 — producing physiologic splitting of S2.
17. (A) Actin to β-dystroglycan
Dystrophin's N-terminus binds cytoskeletal actin and its C-terminus binds β-dystroglycan, linking the actin cytoskeleton through the dystrophin-glycoprotein complex (β-dystroglycan → α-dystroglycan → laminin) to the extracellular matrix, stabilizing the sarcolemma during contraction.
18. (A) Calmodulin
Per Guyton/Ganong: in smooth muscle, Ca²⁺-calmodulin directly activates myosin light-chain kinase to trigger contraction (smooth muscle lacks troponin). In striated (skeletal) muscle, the same Ca²⁺-calmodulin-MLCK pathway phosphorylates myosin light chains as a modulatory mechanism (contributing to post-tetanic potentiation), even though troponin C is the primary trigger there. Troponin is striated-only; tropomyosin's regulatory role differs mechanistically between the two; actin is structural rather than a regulatory "contraction protein" in this sense.
19. (B) Lung compliance
Surfactant lowers alveolar surface tension, which increases lung compliance (easier alveolar expansion, better recruitment) and thereby improves oxygenation and shunt fraction — it decreases surface tension and work of breathing, so those options are the opposite of what surfactant "increases."
20. (C) 5, 2, 3, 1, 4
Rising room CO₂ → increased alveolar PCO₂ (5) → increased arterial PCO₂ (2) → CO₂ diffuses into CSF, increasing CSF PCO₂ (3) → CSF carbonic acid formation lowers CSF pH (1) → H⁺ stimulates central (medullary) chemoreceptors (4) → increased minute ventilation.
Quick reference table
| Q | Answer |
|---|
| 11 | A |
| 12 | B |
| 13 | D |
| 14 | B |
| 15 | C |
| 16 | D |
| 17 | A |
| 18 | A |
| 19 | B |
| 20 | C |