PY8.1-7 | Endocrine Physiology — Summary & Reflection

REFLECT

Return to Kavya's case (Graves' disease: TSH < 0.01, free T4 = 4.8 ng/dL, diffuse radioiodine uptake):

1. Draw the HPT axis (hypothalamus → pituitary → thyroid → T4 → feedback). Mark where the block is in Graves' disease. Why is TSH so low if the thyroid is overactive?

1. Kavya is started on carbimazole. On follow-up 6 weeks later, her free T4 has normalised but her TSH is still undetectable. Her doctor says 'This is normal — wait longer.' Explain why TSH takes longer to recover than T4.

1. A second patient (60-year-old man) has hypercalcaemia (Ca²⁺ = 12.4 mg/dL) with elevated PTH and a renal calculus. What is the diagnosis? Trace the mechanism: how does excess PTH cause hypercalcaemia, phosphaturia, and renal stones?

1. Compare: why does insulin lower blood K⁺ (useful in hyperkalaemia) and why does DKA cause hyperkalaemia at presentation followed by hypokalaemia during treatment? (This integrates endocrine + renal physiology.)

KEY TAKEAWAYS

• HPT axis: Hypothalamic hormones (portal blood) → anterior pituitary hormones → target organ hormones. All regulated by negative feedback. TSH is the most sensitive thyroid test.
• Posterior pituitary: ADH (supraoptic nucleus) — osmolality/volume regulated; oxytocin (paraventricular nucleus) — labour and milk ejection.
• Thyroid: T4 is prohormone; T3 is active. Synthesis requires iodine + TPO. ↑ BMR, HR, CNS development. TSH ↓ in hyperthyroidism; ↑ in hypothyroidism.
• Adrenal cortex zones (GFR mnemonic): Glomerulosa → aldosterone (RAAS/K⁺); Fasciculata → cortisol (ACTH); Reticularis → androgens. Medulla → catecholamines (stress response).
• Glucose homeostasis: Insulin (anabolic) — GLUT4, glycogen, fat storage, K⁺ entry. Glucagon (catabolic) — glycogenolysis, gluconeogenesis, lipolysis. T1DM = absolute deficiency → DKA; T2DM = resistance then deficiency → HHS.
• Calcium: PTH (chief cells) — raises Ca²⁺ via bone, kidney, Vit D. Vitamin D (activated in kidney by PTH) — gut absorption. Calcitonin (minor in humans). Hypocalcaemia → tetany (Trousseau, Chvostek). Hypercalcaemia → bones, stones, moans, groans.
• GH: Released in sleep and hypoglycaemia; IGF-1 mediates growth; direct anti-insulin effects. Excess in children = gigantism; in adults = acromegaly.
• Function tests: Stimulation test = test for suspected deficiency; suppression test = test for suspected excess.