The pancreas

Correct Answer: D

Rationale: Pancreas secretes trypsinogen, an inactive enzyme, activated to trypsin in the gut, not directly activating phospholipase A₂ trypsin cleaves proteins, indirectly aiding lipid digestion. It resembles salivary glands (mixed endocrine-exocrine). Enzymes are in acinar zymogen granules, not α-cells (glucagon). It secretes ~1-1.5 L pancreatic juice daily, not 500 mL. Trypsinogen's role distinguishes pancreatic exocrine function, key to digestion, unlike structural, cellular, or volume errors.

Correct Answer: C

Rationale: Thyroid hormones (T3/T4) boost Na/K ATPase (metabolism), nitrogen excretion (catabolism), and α-myosin chains (cardiac efficiency), but don't directly increase catecholamine levels they sensitize tissues to them via β-receptors. Catecholamine production is adrenal, not thyroid-driven. Exclusion of catecholamine increase distinguishes it, key to thyroid's calorigenic scope, unlike metabolic or cardiac effects.

Correct Answer: D

Rationale: High plasma Ca²⁺ reduces 1,25-dihydroxycholecalciferol (active vitamin D) via feedback, inhibiting renal 1α-hydroxylase balances absorption. ~99% filtered Ca is reabsorbed, not 60%. GIT Ca absorption is active (vitamin D-dependent), not mainly passive. Ca binding is proportional to protein levels (e.g., albumin), not inverse. Vitamin D reduction distinguishes it, key to Ca homeostasis, unlike reabsorption, absorption, or binding errors.

Correct Answer: B

Rationale: Somatostatin inhibits insulin secretion from β-cells, reducing glucose uptake regulatory role. Insulin promotes protein synthesis, not catabolism anabolic. Phenytoin doesn't notably stimulate insulin glucose metabolism does. Insulin increases K⁺ uptake with glucose, not decreases. Somatostatin's inhibition distinguishes it, key to pancreatic regulation, unlike anabolic, drug, or K⁺ errors.

Correct Answer: B

Rationale: Adrenocorticotropic hormone (ACTH) from the anterior pituitary stimulates cortisol secretion from the adrenal cortex, key to stress response not LH, prolactin, IGFs (GH mediators), or MSH. ACTH's role in the HPA axis distinguishes it, critical for glucocorticoid regulation, contrasting with unrelated hormones.