Hypersecretion of growth hormone after closure of the epiphyseal cartilage causes:

Correct Answer: A

Rationale: Hypersecretion of growth hormone (GH) post-epiphyseal closure (adulthood) causes acromegaly, enlarging bones (e.g., hands, jaw) without lengthening, due to fused growth plates. Myxedema is hypothyroidism's effect, slowing metabolism. Addison's disease is adrenal insufficiency. Gigantism occurs pre-closure from GH excess, increasing height. Acromegaly's adult-onset bone thickening distinguishes it, key to endocrine pathology, unlike metabolic or pre-pubertal conditions.

Correct Answer: C

Rationale: Negative feedback, like cortisol inhibiting ACTH, works by reducing hypothalamic releasing factor (e.g., CRH) secretion, decreasing pituitary output. Stimulating releasing factors increases pituitary hormones, opposite to feedback. Inhibiting an inhibiting factor (e.g., dopamine for prolactin) raises secretion, not shuts it off. 'All' overcomplicates only releasing factor inhibition fits most (e.g., TSH, ACTH). This mechanism distinguishes it, key to endocrine regulation, unlike stimulatory or mixed effects.

Correct Answer: C

Rationale: Negative feedback in the endocrine system adjusts hormone levels inversely: low T₃ and T₄ (thyroid hormones) signal the pituitary to increase TSH, stimulating thyroid output to restore levels. High T₃/T₄ would decrease TSH, not increase, opposing feedback's corrective nature. Low T₃/T₄ decreasing TSH would worsen deficiency, defying regulation. No effect ignores feedback entirely TSH rises to compensate. This inverse response exemplifies negative feedback, distinguishing it, essential for homeostasis, unlike positive or null reactions.

Correct Answer: B

Rationale: Intracellular hormone receptors, typically in the nucleus or cytoplasm, bind steroid or thyroid hormones, which cross membranes due to lipid solubility. Thyroid hormone (T3/T4) uses such receptors to regulate metabolism. Melatonin, growth hormone, and insulin act via membrane receptors, not intracellular ones. Pesticide binding could mimic or block thyroid hormone, disrupting metabolic balance, distinguishing it as the likely target, critical for endocrine disruption studies.

Correct Answer: C

Rationale: A goiter, thyroid enlargement, often results from excessive colloid (thyroglobulin storage) accumulation, typically from iodine deficiency or TSH overstimulation, impairing hormone synthesis. Pituitary enlargement or growth hormone excess (acromegaly) don't cause goiters, nor does follicle hypertrophy alone. Colloid buildup distinguishes goiter pathology, key to diagnosing thyroid dysfunction.