The alpha cells of the pancreas secrete:

Correct Answer: C

Rationale: Alpha cells in the pancreatic islets secrete glucagon, raising blood glucose by promoting glycogenolysis and gluconeogenesis, countering beta cells' insulin, which lowers it. Enzymes come from exocrine pancreas acinar cells, not endocrine alpha cells. 'None' ignores glucagon's role. Glucagon's glucose-mobilizing action distinguishes it, essential for metabolic balance, unlike insulin's storage or exocrine functions.

Correct Answer: D

Rationale: Glucocorticoids' truths: cortisol is the primary human glucocorticoid, managing stress and glucose; they're secreted by the adrenal cortex's zona fasciculata, regulated by ACTH; in Addison's disease (adrenal insufficiency), their secretion drops, causing metabolic issues. All statements hold cortisol's dominance, fasciculata origin, and Addison's reduction align with physiology. No single statement trumps; their collective accuracy distinguishes them, key to adrenal function understanding.

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.