Which gland secretes adrenaline?

Correct Answer: B

Rationale: Adrenaline (epinephrine) is secreted by the adrenal glands' medulla, atop the kidneys, triggering the fight-or-flight response by elevating heart rate and glucose availability. The thyroid produces thyroxine for metabolism, the pineal melatonin for sleep neither secrete adrenaline. 'More than one' is invalid as adrenaline is adrenal-specific. This gland's role in acute stress responses distinguishes it, key to survival mechanisms, contrasting with metabolic or circadian regulators.

Correct Answer: C

Rationale: Angiotensinogen, synthesized by the liver, is cleaved by kidney-derived renin to angiotensin I, driving blood pressure regulation via angiotensin II. Prorenin is largely inactive, not 50% active. Propranolol (β-blocker) reduces renin by blocking sympathetic stimulation, not increasing it. Angiotensin I is inactive, not a vasodilator angiotensin II vasoconstricts. Liver synthesis distinguishes angiotensinogen's role, essential for RAAS activation, unlike precursor activity, drug effects, or vasodilation errors.

Correct Answer: C

Rationale: Thyroxine-binding globulin (TBG) binds most circulating T4 (~70%), stabilizing it in plasma for transport high affinity defines it. Prealbumin (transthyretin) binds less (~15-20%). 'Tramothynetim' is a typo, likely irrelevant. A2 globulin isn't a thyroid binder albumin binds some (~10%). TBG's dominance distinguishes it, critical for T4's bioavailability, unlike minor or erroneous binders.

Correct Answer: C

Rationale: ANP inhibits ADH secretion, promoting diuresis to lower volume/BP, countering ADH's water retention. It reduces BP, not increases, via vasodilation/natriuresis. Dopamine responsiveness isn't ANP-mediated ANP acts via cGMP. ANPR-A (active) has higher affinity than ANPR-C (clearance). ADH inhibition distinguishes ANP's role, key to fluid regulation, unlike BP, dopamine, or receptor claims.

Correct Answer: D

Rationale: Bacterial toxins (e.g., LPS) act on the organum vasculosum lamina terminalis (OVLT), releasing pyrogens (IL-1) to raise hypothalamic setpoint, causing fever immune-thermoregulation link. Sweat vaporization is ~20-30% heat loss (radiation dominates). TSH rises in chronic cold, not acutely significant. Anterior hypothalamus cools posterior triggers shivering. OVLT mediation distinguishes fever, key to infection response, unlike sweat, thyroid, or regional errors.