Endocrine Physiology MCQ

Endocrine physiology drives the dental medical history. Insulin and sulfonylureas bring chair-side hypoglycemia risk. Chronic corticosteroids suppress the adrenal axis and can produce adrenal crisis under severe stress. Hyperthyroidism (with epinephrine), hypothyroidism (with sedatives), hyperparathyroidism (with jaw lesions), and pheochromocytoma (with vasoconstrictors) all change the chair-side plan. The hormones run on tight feedback loops, and the dentist's job is to recognize the pattern before it becomes an emergency.

Hypothalamic-Pituitary Axis

• The hypothalamus releases releasing hormones (CRH, TRH, GHRH, GnRH) and inhibiting factors (somatostatin, dopamine) into the hypophyseal portal system to control the ANTERIOR pituitary.
• The anterior pituitary secretes ACTH (drives cortisol), TSH (drives thyroid hormone), GH (drives IGF-1 from liver), prolactin (under tonic dopamine inhibition), LH and FSH (drive gonads).
• The POSTERIOR pituitary is a direct extension of the hypothalamus; it stores and releases ADH (vasopressin; from supraoptic nuclei) and oxytocin (from paraventricular nuclei).
• Most axes use NEGATIVE FEEDBACK from the end-organ hormone back to hypothalamus and pituitary; the cortisol-ACTH-CRH loop is the textbook example used to explain HPA suppression with chronic steroids.

Thyroid and Parathyroid

• The thyroid follicular cells take up iodide, organify it on thyroglobulin, and secrete T4 (mostly) and T3 (smaller amount); peripheral conversion of T4 to T3 by deiodinases produces most active T3.
• Hyperthyroidism (Graves disease is the autoimmune classic) produces tachycardia, heat intolerance, weight loss, tremor, and warm moist skin; THYROID STORM is the dental emergency, with hyperthermia, severe tachycardia, and altered mental status; epinephrine is avoided in uncontrolled hyperthyroidism.
• Hypothyroidism produces fatigue, cold intolerance, bradycardia, weight gain, and dry skin; MYXEDEMA COMA is the severe form (hypothermia, hypoventilation, altered mental status); sedatives can precipitate it.
• Parathyroid chief cells secrete PTH in response to low ionized Ca2+; PTH raises Ca2+ (bone resorption via osteoclast activation, renal Ca2+ reabsorption and PO4 wasting, and activation of vitamin D to increase intestinal Ca2+ absorption). HYPERPARATHYROIDISM produces dental findings: brown tumors (giant-cell lesions), loss of lamina dura, ground-glass appearance, and 'pepper-pot' skull.

Adrenal Cortex and Medulla

• Adrenal cortex (mnemonic: GFR / salt-sugar-sex) has three zones: glomerulosa (aldosterone), fasciculata (cortisol), reticularis (androgens DHEA/DHEA-S).
• Cortisol is glucocorticoid (glucose mobilization, anti-inflammatory) under CRH-ACTH control with negative feedback; chronic exogenous corticosteroids suppress the HPA axis (typically >5 mg prednisone/day for >3 weeks), risking adrenal crisis under severe stress.
• Aldosterone is mineralocorticoid (Na+ reabsorption, K+ excretion in the cortical collecting duct) under RAAS control (renin → angiotensin I → angiotensin II → aldosterone); ACE inhibitors block this axis and can cause hyperkalemia.
• Adrenal medulla is sympathetic ganglion analog: chromaffin cells secrete epinephrine (~80%) and norepinephrine (~20%) into circulation. PHEOCHROMOCYTOMA is a catecholamine-secreting tumor causing severe hypertension; exogenous epinephrine can precipitate a hypertensive crisis.

Pancreas: Insulin and Glucagon

• Pancreatic islet of Langerhans: β cells secrete insulin in response to glucose; α cells secrete glucagon when glucose falls; δ cells secrete somatostatin (inhibits both).
• Insulin shifts glucose into muscle and adipose (GLUT4 translocation), promotes glycogenesis, lipogenesis, and protein synthesis, and lowers serum K+; glucagon raises hepatic glucose output (glycogenolysis, gluconeogenesis).
• Type 1 diabetes is autoimmune β-cell destruction (insulin-deficient); type 2 diabetes is insulin resistance with progressive β-cell exhaustion; both produce hyperglycemia with secondary microvascular and macrovascular complications.
• Chair-side hypoglycemia is the dental emergency: sulfonylureas and insulin can drop glucose; symptoms include diaphoresis, tremor, confusion, and tachycardia (early adrenergic) progressing to seizure and coma (neuroglycopenic). Oral glucose first; intramuscular glucagon (or IV dextrose) for unable-to-swallow patients.

Growth Hormone, ADH, and Other Hormones

• GH from the anterior pituitary acts directly on tissues and indirectly via IGF-1 from the liver; excess GH in adults (acromegaly) produces macroglossia, spaced teeth, prognathic mandible, and enlarged hands/feet; GH excess in children produces gigantism.
• ADH (vasopressin) from the posterior pituitary raises water permeability in the renal collecting duct (via V2 receptors and aquaporin-2 insertion); ADH excess (SIADH) produces dilutional hyponatremia; ADH deficiency or renal resistance (diabetes insipidus) produces dilute urine and hypernatremia.
• Calcitonin from thyroid C cells LOWERS Ca2+ (inhibits osteoclasts); it is less important than PTH in normal calcium homeostasis but is used as a tumor marker for medullary thyroid carcinoma.
• Other relevant hormones include sex steroids (estrogen and androgens affect bone density and oral mucosa), and the gut hormones the diabetes drugs target (GLP-1 agonists like semaglutide delay gastric emptying and carry aspiration risk under deep sedation).