A client with a history of hypertension is admitted due to primary hyperaldosteronism. This diagnosis indicates that the client's hypertension is caused by excessive hormone secretion from which gland?

Correct Answer: B

Rationale: Primary hyperaldosteronism (Conn's syndrome) involves excessive aldosterone from the adrenal cortex's zona glomerulosa, raising blood pressure via sodium retention and volume expansion. The pancreas regulates glucose (insulin/glucagon), not BP directly. The thymus produces thymosin for immunity, not hypertension-related hormones. The adrenal medulla secretes epinephrine/norepinephrine, causing acute BP spikes, not chronic aldosterone-driven hypertension. Adrenal cortex's aldosterone excess distinguishes it, key to this pathology, unlike metabolic, immune, or catecholamine sources.

Correct Answer: B

Rationale: Adrenal glands rest atop the kidneys, secreting cortisol, aldosterone, and epinephrine for stress, electrolyte balance, and fight-or-flight. The pituitary, brain-based, oversees hormones. The pancreas, abdominal, manages glucose. Ovaries, pelvic in females, produce sex hormones, not above kidneys. Adrenals' suprarenal position and diverse outputs distinguish them, essential for adrenal-renal interactions, unlike distant or unrelated glands.

Correct Answer: D

Rationale: ADH (antidiuretic hormone) is stored and released by the posterior pituitary, synthesized in the hypothalamus, regulating water balance. FSH, LH, and ACTH (follicle-stimulating, luteinizing, adrenocorticotropic hormones) are anterior pituitary products, driving reproduction and adrenal function. Posterior pituitary doesn't synthesize ADH's hypothalamic origin and storage role distinguish it, key to neurohypophyseal function, unlike anterior glandular outputs.

Correct Answer: A

Rationale: Negative feedback regulates most hormones (e.g., cortisol inhibits ACTH), reducing secretion when levels suffice, maintaining homeostasis. Positive feedback (e.g., oxytocin in labor) amplifies, rare in endocrine control. Hormone-receptor complexes mediate effects, not regulation. Hormone-gene complexes influence steroid action, not feedback. Negative feedback's inhibitory loop distinguishes it, critical for stability, unlike amplifying or mechanistic options.

Correct Answer: B

Rationale: Hormone binding alters membrane permeability (e.g., ion channels), activates/inactivates enzymes (e.g., cAMP pathways), and stimulates mitosis (e.g., growth hormone) all typical. Cellular mutations, DNA damage events, aren't standard hormone effects. This absence distinguishes normal signaling, critical for physiological responses, contrasting with pathological changes.