Memory tricks for hormones and how they control the body
Hormone classes, feedback loops, the pituitary and hypothalamus, thyroid, adrenal glands, pancreas, and key endocrine disorders — these memory tricks unite the anatomy of every endocrine gland with the physiology of the hormones each one produces.
Anterior pituitary hormones made there · Posterior pituitary stores hypothalamic hormones
The pituitary gland — anterior vs posterior and the hormones each releases
Anterior pituitary (adenohypophysis): controlled by hypothalamic releasing and inhibiting hormones via portal blood. Makes and releases: FSH (follicle stimulating), LH (luteinizing), ACTH (adrenocorticotropic), TSH (thyroid stimulating), GH (growth hormone), PRL (prolactin). Mnemonic: FLAT PiG. Posterior pituitary (neurohypophysis): does NOT make hormones — stores and releases hormones made by hypothalamic neurons. ADH (vasopressin) — released in response to ↑ osmolarity or ↓ BP → water retention. Oxytocin — released during labor (Ferguson reflex) and breastfeeding (milk letdown). Hypothalamus is the master controller — receives input from brain, releases regulatory hormones to control anterior pituitary, directly makes ADH and oxytocin.
FLAT PiG
FSH · LH · ACTH · TSH · Prolactin · GH — the six anterior pituitary hormones.
Tropic hormones
FSH, LH, ACTH, TSH — stimulate other endocrine glands. "Tropic" = turning toward a target.
GH
Growth hormone — stimulates IGF-1 from liver. Promotes growth, protein synthesis, fat mobilization.
Posterior pituitary
Stores/releases ADH (water retention) and oxytocin (labor, milk letdown). Made in hypothalamus.
Thyroid hormones — synthesis, function, and clinical disorders
Thyroid gland: two lobes connected by isthmus — largest pure endocrine gland. Follicular cells produce T3 (3 iodine atoms) and T4 (4 iodine atoms) from thyroglobulin + iodine. T4 is prohormone — converted to active T3 in peripheral tissues (by deiodinase). Effects: ↑ basal metabolic rate, ↑ heart rate and output, essential for normal brain development (deficiency in infancy = cretinism), promote bone growth and maturation, permissive for GH effects. TSH from pituitary controls production. Parafollicular (C cells) produce calcitonin: ↑ Ca2+ → calcitonin released → inhibits osteoclasts → ↓ blood Ca2+ (minor role in adults, more in children). Hypothyroidism: ↓ T3/T4, myxedema, weight gain, cold intolerance. Hyperthyroidism: ↑ T3/T4, Graves' disease (anti-TSH receptor antibodies).
T4 → T3
T4 is prohormone. Peripheral deiodinase converts to active T3. Ratio ~4:1 released, T3 more potent.
Cortex = GFR zones · Medulla = Epinephrine and NE · Salt Sugar Sex from outside in
Zona glomerulosa (aldosterone) · Zona fasciculata (cortisol) · Zona reticularis (androgens)
The adrenal gland — cortex layers and medulla, anatomy drives function
Adrenal glands sit atop kidneys. Two distinct regions with different embryological origins and functions. Adrenal cortex (3 zones from outside in — "Salt, Sugar, Sex"): Zona glomerulosa → aldosterone (mineralocorticoid — Na+ retention, K+ excretion, ↑ BP). Zona fasciculata → cortisol (glucocorticoid — stress response, anti-inflammatory, ↑ blood glucose). Zona reticularis → androgens (DHEA — weak sex hormones, important in females). All controlled by ACTH (except aldosterone — controlled by RAAS and K+). Adrenal medulla: modified sympathetic ganglion — chromaffin cells secrete epinephrine (80%) and NE (20%) in response to sympathetic stimulation. Part of fight-or-flight. Pheochromocytoma: catecholamine-secreting tumor → episodic hypertension, headache, sweating.
Salt (glomerulosa)
Aldosterone → Na+ in, K+ out, ↑ BP. Controlled by RAAS and K+, not ACTH.
Four additional endocrine tissues — location and primary hormone
Other endocrine organs — each produces hormones essential to specific body functions
Pineal gland: in brain — produces melatonin (from serotonin, dark triggers release). Controls circadian rhythm and sleep-wake cycle. ↑ at night, ↓ in light. Jet lag = circadian disruption. Thymus: in mediastinum — produces thymosin → T cell maturation and immune function. Most active in childhood, atrophies after puberty. Gonads (ovaries and testes): estrogen and progesterone (ovaries), testosterone (testes) — secondary sex characteristics, gametogenesis, reproductive function. See Reproductive Physiology for details. Heart (atria): produces ANP (atrial natriuretic peptide) when atrial walls are stretched (high blood volume) → promotes Na+ and water excretion → ↓ blood volume and pressure. Opposes RAAS. Adipose tissue: produces leptin (↑ fat stores → leptin → suppresses appetite → energy balance) and adiponectin (↑ insulin sensitivity).
Q: What does the anterior pituitary produce and what controls each hormone?
A: GH (growth hormone): released by GHRH, inhibited by somatostatin → stimulates IGF-1 from liver → growth, protein synthesis, lipolysis, anti-insulin. FSH and LH: released by GnRH → regulate gonads. TSH: released by TRH → stimulates thyroid hormone synthesis. ACTH: released by CRH → stimulates cortisol from adrenal cortex. Prolactin: tonically inhibited by dopamine (DA) → lactation. MSH: melanocyte stimulating hormone. Mnemonic: GH FSH LH TSH ACTH Prolactin = 'Great Follicles Lust To Act Promiscuously'. Posterior pituitary: ADH (made in hypothalamus, stored/released from posterior pituitary) and oxytocin.
Q: Describe the thyroid hormone synthesis and what happens in hypo vs hyperthyroidism.
A: Synthesis: TSH stimulates thyroid → iodide uptake → oxidation to iodine (TPO enzyme) → organification onto tyrosine residues of thyroglobulin → MIT and DIT → coupled to form T3 (MIT+DIT) and T4 (DIT+DIT) → stored as colloid → released. T4 is prohormone; T3 is active (10x more potent). Peripheral conversion T4→T3 by deiodinases. Hypothyroidism: low T3/T4, high TSH. Symptoms: fatigue, cold intolerance, weight gain, bradycardia, constipation, dry skin, myxedema, elevated cholesterol. Hyperthyroidism: high T3/T4, low TSH. Symptoms: heat intolerance, weight loss, tachycardia, diarrhea, tremor, exophthalmos (Graves). Graves disease: TSI antibodies mimic TSH. Hashimoto: autoimmune destruction → hypothyroidism.
Q: What does cortisol do and what is Cushing vs Addison disease?