The relatively constant internal environment of the body is maintained by

Correct Answer: C

Rationale: Homeostasis maintains the body's stable internal environment (e.g., temperature, glucose) via mechanisms like negative feedback, not feedback itself or metabolism (energy processes). Positive feedback amplifies changes. Homeostasis's stabilizing role distinguishes it, key to physiological balance, integrating endocrine and nervous systems.

Correct Answer: B

Rationale: The pineal gland, at 5-8 mm in the brain's epithalamus, is the smallest endocrine gland, producing melatonin for sleep regulation. The pituitary (larger, pea-sized) controls other glands, parotid (salivary) and Ebner's (tongue) are exocrine not endocrine. Pineal's diminutive size and endocrine role distinguish it, vital for circadian rhythms, contrasting with larger or ducted glands.

Correct Answer: D

Rationale: Parathyroid hormone (PTH) deficiency (hypoparathyroidism) reduces blood calcium by decreasing bone resorption and kidney reabsorption, leading to neuromuscular hyperexcitability tetany, cramps due to low Ca²⁺ destabilizing nerve membranes. PO₄ rises, not falls, as PTH normally increases its excretion. Kidney stones occur with high calcium (hyperparathyroidism), not low. It's not self-limiting chronic without treatment (e.g., calcium supplements). Hyperexcitability reflects calcium's role in nerve stability, distinguishing it as PTH's key deficit effect, critical for neuromuscular function, unlike phosphate, stones, or transient illness.

Correct Answer: D

Rationale: Angiotensin II stimulates ADH (vasopressin) release from the posterior pituitary, enhancing water retention to raise blood volume in hypovolemia. Alcohol inhibits ADH, causing diuresis. Carbamazepine can increase ADH (SIADH risk), but isn't primary. High ECF volume suppresses ADH via stretch receptors. Angiotensin II's role distinguishes it, key to RAAS-ADH synergy, unlike inhibitory or secondary triggers.

Correct Answer: D

Rationale: GLUT2 in β-cells allows glucose entry, triggering insulin release via metabolism and Ca²⁺ high capacity, low affinity fits pancreas. Insulin inhibits ketogenesis, not increases release. It's from β-cells, not A (alpha, glucagon). cAMP (e.g., glucagon) doesn't drive insulin glucose metabolism does. GLUT2's role distinguishes it, critical for insulin secretion, unlike ketone, cell, or signaling errors.