Which of the following pairs of endocrine glands is located in the brain?

Correct Answer: D

Rationale: The hypothalamus (forebrain) and pineal (epithalamus) are brain-located endocrine glands; the former regulates via releasing hormones, the latter secretes melatonin for sleep. Thymus (chest), parathyroid (neck), and thyroid (neck) are external. Only hypothalamus, pineal, and pituitary (also brain) fit, but 'hypothalamus and pineal' is the pair. This brain-centric role distinguishes them, key to neuroendocrine integration, contrasting with peripheral glands.

Correct Answer: C

Rationale: Prostaglandins (e.g., PGE2) increase renin secretion from juxtaglomerular cells, boosting RAAS during inflammation or low perfusion. High Na/Cl at macula densa or high arteriole pressure (stretch) suppress renin negative feedback signals adequacy. ADH conserves water, not directly affecting renin. Prostaglandins' stimulatory role distinguishes them, critical for RAAS activation in stress, unlike inhibitory or unrelated factors.

Correct Answer: A

Rationale: Glucagon raises glucose via glycogenolysis without increasing lactate gluconeogenesis (lactate source) is secondary. Insulin uses GLUT2 in liver, not GLUT4 (muscle/adipose). Cortisol boosts gluconeogenesis, not glycogenolysis primarily. Glucagon stimulates insulin short-term, not inhibits. Glucagon's lactate-free glucose rise distinguishes it, key to its hepatic action, unlike transporter, cortisol, or insulin errors.

Correct Answer: A

Rationale: α-adrenergic stimulation (e.g., norepinephrine) inhibits insulin secretion via α2-receptors, reducing glucose uptake in stress. Theophylline enhances insulin by increasing cAMP, not inhibits. Insulin's half-life is ~5-10 minutes, not 30. Somatostatin inhibits insulin, not stimulates. α-adrenergic inhibition distinguishes it, key to sympathetic-glucose balance, unlike cAMP, kinetics, or somatostatin errors.

Correct Answer: D

Rationale: T4 increases cardiovascular β-receptors, enhancing catecholamine sensitivity metabolic/cardiac boost. It's regulated by negative feedback (TSH, TRH). Most T4 binds TBG (~70%), not albumin (~10%). T4 lowers LDL by increasing clearance, not raising it. β-receptor increase distinguishes T4's action, critical for heart response, unlike feedback, transport, or lipid errors.