A client in the endocrine clinic has a low T-lymphocyte count. The nurse is aware that which of the following endocrine glands plays a role in the development of T-lymphocytes?

Correct Answer: C

Rationale: The thymus, an endocrine gland, secretes thymosin to mature T-lymphocytes, critical for immunity, peaking in youth and shrinking with age. Thyroid regulates metabolism via thyroxine, not immunity. Pituitary controls other glands (e.g., via ACTH), not T-cell development. Pancreas manages glucose (insulin/glucagon), not lymphocytes. Thymus' role in T-cell maturation distinguishes it, essential for adaptive immunity, unlike metabolic or regulatory glands.

Correct Answer: A

Rationale: Chromaffin cells in the adrenal medulla secrete catecholamines (epinephrine, norepinephrine) for fight-or-flight responses, derived from neural crest cells. Neuroglial cells support neurons, follicle cells are thyroid-specific, and oxyphil cells are in parathyroids. Chromaffin cells' neuroendocrine role distinguishes them, key to rapid stress responses, contrasting with supportive or other glandular cells.

Correct Answer: B

Rationale: Insulin lowers blood glucose by binding receptors, triggering GLUT4 transporters to move to cell membranes, enhancing uptake. It doesn't transport glucose, breaks glycogen (glucagon does), or act renally (reabsorption is passive). Facilitating transporter movement distinguishes insulin's mechanism, key to glucose regulation, contrasting with glycogenolysis or renal roles.

Correct Answer: C

Rationale: Neural stimuli, like stress from a car accident, activate the adrenal medulla via sympathetic nerves, releasing epinephrine for pupil dilation, heart rate increase, and rapid breathing classic fight-or-flight. Humoral stimuli respond to blood changes (e.g., PTH to low Ca²⁺). Hormonal stimuli involve hormones triggering others (e.g., TSH for thyroid). Positive feedback amplifies (e.g., oxytocin in labor), not acute stress. Neural triggering distinguishes this rapid endocrine response, key to sympathetic-endocrine integration, unlike blood-based or cascading stimuli.

Correct Answer: B

Rationale: Primary hyperaldosteronism (Conn's syndrome) involves excessive aldosterone from the adrenal cortex's zona glomerulosa, raising blood pressure via sodium retention and volume expansion. The pancreas regulates glucose (insulin/glucagon), not BP directly. The thymus produces thymosin for immunity, not hypertension-related hormones. The adrenal medulla secretes epinephrine/norepinephrine, causing acute BP spikes, not chronic aldosterone-driven hypertension. Adrenal cortex's aldosterone excess distinguishes it, key to this pathology, unlike metabolic, immune, or catecholamine sources.