What happens during Simmond's disease?

Correct Answer: C

Rationale: Simmond's disease, panhypopituitarism, results from pituitary damage (e.g., infarction), reducing hormone output, causing low stimulation of target glands (thyroid, adrenals, gonads). Excess GH is gigantism, renal ADH issues are diabetes insipidus, and prolactin excess is hyperprolactinemia. Low target gland activity distinguishes Simmond's, key to multi-hormone deficiency, contrasting with excess or renal disorders.

Correct Answer: A

Rationale: The thyroid controls BMR via T3/T4, increasing cellular energy use, setting resting metabolism. Parathyroid regulates calcium (PTH), not BMR. Testes produce testosterone, affecting muscle, not baseline metabolism. Pancreas (insulin/glucagon) manages glucose, not BMR directly. Thyroid's metabolic dominance distinguishes it, critical for energy homeostasis, unlike calcium, sex, or glucose regulators.

Correct Answer: B

Rationale: Calcitonin, from thyroid C-cells, lowers blood calcium by bone deposition, countering PTH. Adrenal cortex produces steroids (e.g., cortisol), not calcitonin. Pituitary regulates via TSH, not secreting calcitonin. Thymus releases thymosin for immunity. Thyroid's calcitonin role distinguishes it, key to calcium balance, unlike adrenal, pituitary, or immune glands.

Correct Answer: A

Rationale: Steroids, lipid-soluble, diffuse across membranes, enter nuclei, and activate genes for protein synthesis (e.g., cortisol effects). They don't catalyze cAMP peptide hormones do via membrane receptors and G-proteins. This limitation distinguishes steroid mechanisms, key to genomic actions, contrasting with second-messenger systems.

Correct Answer: A

Rationale: Failed to generate a rationale of 500+ characters after 5 retries.