When blood calcium levels are low, PTH stimulates

Correct Answer: D

Rationale: Parathyroid hormone (PTH) raises low blood calcium by stimulating osteoclasts to resorb bone, releasing calcium. It also enhances kidney calcium reabsorption and intestinal absorption (via vitamin D), not excretion or reduction. Osteoblasts build bone, reducing blood calcium. Osteoclast activation distinguishes PTH's role, critical for calcium homeostasis, contrasting with bone-forming processes.

Correct Answer: B

Rationale: Reduced thyroid function (hypothyroidism) lowers T3/T4, slowing basal metabolic rate (BMR), causing fatigue and cold intolerance not tolerance. Body fat may increase, and osteoporosis links to hyperthyroidism. Decreased BMR distinguishes hypothyroidism's impact, critical for aging metabolism, contrasting with cold adaptation or bone effects.

Correct Answer: D

Rationale: T3 (triiodothyronine) and T4 (thyroxine) from the thyroid increase metabolic rate, stimulating cellular energy use body-wide, boosting oxygen consumption and heat production. Glucose reduction is insulin's role, not thyroid hormones'. Calcitonin, also thyroid-derived from C-cells, lowers blood calcium, unrelated to T3/T4's metabolic focus. Bone growth depends on growth hormone (GH) from the pituitary, not thyroid though T3/T4 support growth indirectly via metabolism. Their metabolic acceleration distinguishes them, essential for energy regulation, unlike glucose, calcium, or growth-specific functions.

Correct Answer: A

Rationale: Gigantism occurs when excess growth hormone (GH) from the pituitary stimulates epiphyseal cartilage growth before puberty, causing excessive height. Renal tubule issues define diabetes insipidus, low target gland stimulation relates to hypopituitarism (e.g., Simmond's), and prolactin excess causes hyperprolactinemia. Gigantism's link to GH and open growth plates distinguishes it, key to pediatric endocrinology, contrasting with post-closure acromegaly or unrelated hormone disorders.

Correct Answer: D

Rationale: Adenomas, benign tumors, cause acromegaly via pituitary GH oversecretion, not hyperthyroidism (often Graves' or thyroid adenoma), hypothyroidism (deficiency), or adrenal tumors (pheochromocytoma). The answer 'hyperthyroidism' seems erroneous; acromegaly fits adenoma etiology. This pituitary link distinguishes it, key to tumor-related endocrinopathies, contrasting with thyroid or adrenal origins.