a deficiency of parathyroid hormone is likely to lead to

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: 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.

Correct Answer: D

Rationale: Glucocorticoids (e.g., cortisol) promote gluconeogenesis, support myocardial contractility (via catecholamine sensitivity), and inhibit glucose uptake (insulin resistance), but don't decrease vascular resistance they maintain or increase it via permissive effects on angiotensin II/vasopressors. Decreased resistance aligns with ANP/vasodilators, not cortisol. Vascular support distinguishes glucocorticoid action, critical for stress response, unlike metabolic or cardiac roles.

Correct Answer: A

Rationale: Insulin increases amino acid uptake into cells, promoting protein synthesis anabolic role. It enhances K⁺ uptake (with glucose), not reduces key in hyperkalemia treatment. Absorption varies by injection site (e.g., abdomen faster than thigh). It inhibits protein catabolism, not increases. Amino acid uptake distinguishes insulin's growth function, critical for metabolism, unlike K⁺, pharmacokinetics, or catabolic claims.

Correct Answer: D

Rationale: Down-regulation occurs when excessive hormone levels reduce target-cell receptor numbers, preventing overstimulation a negative feedback mechanism. 'Receptor recognition' isn't a process, 'sensory adaptation' applies to nerves, and 'paracrine regulation' involves local signaling not receptor adjustment. Though option D isn't listed, context and endocrine principles confirm 'down-regulation' as standard terminology (likely missing due to OCR cutoff). This adaptive response distinguishes endocrine self-regulation, vital for homeostasis, contrasting with static or unrelated mechanisms.