Endocrine System
Axis logic
Every endocrine axis follows the same pattern: hypothalamic releasing hormone, pituitary trophic hormone, target gland hormone with negative feedback. In primary target-gland failure the trophic hormone is elevated and the target hormone low; in secondary failure both are low. Steroid and thyroid hormones act on intracellular receptors and alter gene transcription; peptide hormones use surface receptors and second messengers.
Glands to master
Thyroid: Hashimoto (anti-TPO, germinal centers, Hurthle cells), Graves (thyroid-stimulating immunoglobulin, exophthalmos, pretibial myxedema), subacute painful thyroiditis (high ESR, self-limited), Riedel fibrosis. Adrenal: Cushing disease suppresses with high-dose dexamethasone, an adrenal adenoma does not; primary hyperaldosteronism shows an elevated aldosterone-to-renin ratio; Addison disease shows hyperpigmentation, hyperkalemia, and hyponatremia; 21-hydroxylase deficiency causes virilization with salt wasting. Calcium: PTH raises calcium and lowers phosphate; PTHrP drives humoral hypercalcemia of malignancy; vitamin D deficiency causes secondary hyperparathyroidism.
Pituitary and pancreas
Prolactinoma presents with galactorrhea and bitemporal hemianopia; dopamine agonists treat it. Acromegaly is confirmed by failure to suppress growth hormone during an oral glucose tolerance test. SIADH is euvolemic hyponatremia with concentrated urine. Type 1 diabetes causes diabetic ketoacidosis with an anion gap and Kussmaul respirations; type 2 with hyperosmolar hyperglycemic state.
Traps
Interpreting a hormone level without its trophic partner. Assuming hypercalcemia always means hyperparathyroidism. Forgetting that total calcium changes with albumin.
Worked rule
Low free T4 with elevated TSH equals primary hypothyroidism; low free T4 with low TSH equals central hypothyroidism.