Estrogens and progesterone are produced by:

Correct Answer: B

Rationale: Ovaries produce estrogens and progesterone, driving female reproductive cycles and traits. Testes produce testosterone, adrenals minor sex hormones, and hypothalamus GnRH not estrogens/progesterone. Ovarian production distinguishes these hormones' source, essential for female endocrinology, contrasting with male or regulatory glands.

Correct Answer: C

Rationale: Hypothalamic releasing hormones (e.g., TRH, GnRH) target anterior pituitary cells, stimulating hormone release (e.g., TSH, FSH). Thyroid responds to TSH, hypothalamus produces, posterior pituitary stores ADH/oxytocin. Anterior pituitary targeting distinguishes this axis, vital for endocrine regulation, contrasting with storage or effector glands.

Correct Answer: D

Rationale: The hypothalamus (forebrain) and pineal (epithalamus) are brain-located endocrine glands; the former regulates via releasing hormones, the latter secretes melatonin for sleep. Thymus (chest), parathyroid (neck), and thyroid (neck) are external. Only hypothalamus, pineal, and pituitary (also brain) fit, but 'hypothalamus and pineal' is the pair. This brain-centric role distinguishes them, key to neuroendocrine integration, contrasting with peripheral glands.

Correct Answer: D

Rationale: The pituitary gland, dubbed the 'master gland,' controls other endocrine glands (e.g., thyroid via TSH, adrenals via ACTH) through tropic hormones. Thyroid regulates metabolism, pineal sleep, adrenals stress not others. Pituitary's anterior/posterior lobes orchestrate this, distinguishing its hierarchical role, vital for endocrine harmony, contrasting with effector glands.

Correct Answer: C

Rationale: Prostaglandins (e.g., PGE2) increase renin secretion from juxtaglomerular cells, boosting RAAS during inflammation or low perfusion. High Na/Cl at macula densa or high arteriole pressure (stretch) suppress renin negative feedback signals adequacy. ADH conserves water, not directly affecting renin. Prostaglandins' stimulatory role distinguishes them, critical for RAAS activation in stress, unlike inhibitory or unrelated factors.