Calcium levels in the blood are increased by:

Correct Answer: D

Rationale: Parathyroid hormone (PTH) from parathyroids raises blood calcium by mobilizing it from bones, enhancing kidney reabsorption, and boosting intestinal uptake via vitamin D. Calcitonin, from thyroid C-cells, lowers calcium, depositing it in bones. Heparin (anticoagulant) and dicumarol (similar) affect clotting, not calcium. PTH's calcium-elevating role distinguishes it, essential for homeostasis, unlike bone-depositing or unrelated agents.

Correct Answer: A

Rationale: Untreated iodine-deficiency goiter raises TSH secretion low iodine cuts thyroxine (Tâ‚„), prompting pituitary TSH increase to stimulate the thyroid, enlarging it. Thyroxine drops, not rises, due to iodine lack. Temperature and metabolic rate fall (hypothyroidism), not rise, from low Tâ‚„. TSH's compensatory surge distinguishes it, key to goiter's feedback loop, unlike reduced thyroid output or metabolic effects.

Correct Answer: C

Rationale: Low growth hormone (GH) in adults isn't abnormal GH peaks in youth for growth, declining naturally post-epiphyseal closure, with minimal adult roles (metabolism, muscle maintenance). Bone abnormalities (e.g., acromegaly) stem from GH excess, not deficit. Growth spurts require high GH pre-closure, impossible in adults. Health concerns (e.g., fatigue) may arise, but low GH is typical, not alarming. Its normal adult decline distinguishes it, key to age-related endocrine shifts, unlike excess or juvenile effects.

Correct Answer: B

Rationale: The hypothalamus connects to the posterior pituitary via nerve axons in the hypothalamohypophyseal tract. These axons transport antidiuretic hormone (ADH) and oxytocin, synthesized in hypothalamic neurons, for release. Blood vessels link the anterior pituitary, not posterior, while cartilage and bone are structural, not functional connectors. This axonal bridge distinguishes posterior pituitary control, key to neurohormone secretion in fluid and reproductive regulation.

Correct Answer: B

Rationale: Hyperparathyroidism, excess PTH, overstimulates osteoclasts, weakening bones and risking fractures by elevating blood calcium. Bone deposition decreases, and convulsions may occur from hypocalcemia (opposite condition), not hypercalcemia. 'All' is incorrect. Fractures distinguish this pathology, key to diagnosing skeletal effects of prolonged PTH elevation, contrasting with deposition or neurological symptoms.