Hyposecretion of adrenal cortex hormones can lead to

Correct Answer: A

Rationale: Adrenal cortex hyposecretion (low cortisol/aldosterone) causes Addison's fatigue, low BP, hyperpigmentation from ACTH rise. Diabetes mellitus is pancreatic glucose issue. Cushing's is cortisol excess opposite. Cretinism is neonatal hypothyroidism growth/mental delay. Addison's adrenal failure distinguishes it, key to cortex insufficiency, unlike glucose, excess, or thyroid conditions.

Correct Answer: A

Rationale: Signal transduction transmits hormonal signals via G-proteins (e.g., in glucagon response), converting extracellular messages into intracellular actions (cAMP) core process. Signal conduction is neural, not hormonal electric impulse. Signal targeting isn't a term receptor specificity fits, but not process. Local signaling is paracrine, not G-protein-mediated typically. Transduction's role distinguishes it, critical for hormone effects across membranes, unlike conduction, vague, or local errors.

Correct Answer: B

Rationale: ACTH (adrenocorticotropic hormone) from anterior pituitary stimulates adrenal cortex to release corticosteroids (e.g., cortisol) stress axis. TSH (thyroid-stimulating) targets thyroid, not adrenal. FSH (follicle-stimulating) and LH (luteinizing) regulate gonads, not cortex. ACTH's adrenal control distinguishes it, key to HPA axis and corticosteroid production, unlike thyroid or gonadal hormones.

Correct Answer: D

Rationale: Growth hormone (GH) is the most abundant anterior pituitary hormone, driving growth and metabolism not LH (reproduction), TSH (thyroid), or ACTH (adrenal). Its high output reflects somatotroph prevalence, distinguishing its systemic role, a NEET key point contrasting with less abundant tropic hormones.