Chemical signaling that affects neighboring cells is called

Correct Answer: B

Rationale: Paracrine signaling involves chemicals (e.g., prostaglandins) affecting nearby cells, like histamine in inflammation acting locally without entering blood. Autocrine signaling targets the secreting cell itself (e.g., cancer cells self-stimulating). Endocrine signaling uses blood to reach distant cells (e.g., insulin from pancreas). 'Neuron' isn't a signaling type neurons use neurotransmitters, often paracrine-like at synapses, but it's distinct. Paracrine's local effect distinguishes it, critical for short-range coordination, unlike self, systemic, or neural mechanisms.

Correct Answer: D

Rationale: Goiter, thyroid enlargement, stems from multiple causes: iodine deficiency impairs T3/T4 synthesis, increasing TSH and colloid; genetic abnormalities (e.g., enzyme defects) disrupt hormone production; anti-thyroid drugs (e.g., propylthiouracil) block synthesis, prompting hypertrophy. 'All' encompasses these, distinguishing goiter's multifactorial etiology, key to diagnosis, contrasting with single-cause disorders.

Correct Answer: D

Rationale: The thyroid gland sits at the throat's base, below the Adam's apple, secreting T3/T4 for metabolism and calcitonin for calcium. The pituitary, at the brain's base, controls other glands. The pineal, in the brain's midline, releases melatonin. The hypothalamus, above the pituitary, regulates it, not at the throat. Thyroid's neck location and metabolic role distinguish it, key to its anatomical and functional identity, unlike brain-based glands.

Correct Answer: C

Rationale: The pancreas is both endocrine (islets secrete insulin/glucagon into blood) and exocrine (acini release digestive enzymes via ducts). Thyroid (T3/T4) and thymus (thymosin) are purely endocrine, lacking ducts. Pituitary (e.g., GH) is endocrine-only, no exocrine function. Pancreas' dual role distinguishes it, essential for metabolic and digestive integration, unlike single-function glands.

Correct Answer: A

Rationale: Glucagon accelerates glycogenolysis, converting liver glycogen to glucose to raise blood levels, countering insulin. Slowing gluconeogenesis (glucose from lactic acid) opposes glucagon's role it promotes it. Decreasing glycogen conversion is insulin's job. Protein synthesis isn't glucagon-driven GH or insulin-like factors handle that. Glycogenolysis acceleration distinguishes glucagon, key to fasting glucose supply, unlike inhibitory or anabolic actions.