⚗️ A&P II · Endocrine System

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.

⚗️ Endocrine System

Memory Tricks

Proven Mnemonics & Acronyms — fast to learn, hard to forget.

Hormone Classes
SPAN — Steroids · Peptides · Amines · Non-peptides (eicosanoids)
Lipid-soluble (steroids) enter cells · Water-soluble (peptides/amines) use receptors on surface
Four hormone classes — solubility determines how they work
Hormones are chemical messengers secreted into blood → act on distant target cells. Classification by solubility determines mechanism. Lipid-soluble hormones (steroids and thyroid): cross plasma membrane → bind intracellular receptors → receptor-hormone complex enters nucleus → alters gene transcription → slow but long-lasting effects. Examples: cortisol, estrogen, testosterone, thyroid hormone (T3/T4). Water-soluble hormones (peptides and catecholamines): cannot cross membrane → bind surface receptors → activate second messenger (cAMP, IP3, Ca2+) → rapid but short-lived effects. Examples: insulin, glucagon, ADH, epinephrine, GH. Eicosanoids (prostaglandins, leukotrienes): lipid-derived, local paracrine/autocrine effects. NSAIDs block their synthesis.
Steroids
Lipid-soluble. Cross membrane → nuclear receptor → gene expression. Cortisol, sex hormones, aldosterone.
Peptides
Water-soluble. Surface receptor → second messenger (cAMP). Insulin, GH, ADH, oxytocin.
Amines
From amino acids. Catecholamines (epinephrine, NE) = water-soluble. Thyroid hormones = lipid-soluble.
Second messengers
cAMP (most common), IP3, DAG, Ca2+. Amplify the signal — one hormone → millions of effects.
Pituitary Gland
Anterior = FSH LH ACTH TSH GH PRL · Posterior = ADH + Oxytocin
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
T3 and T4 from iodine + tyrosine · T3 more active · Calcitonin lowers calcium
Triiodothyronine (T3) · Thyroxine (T4) · Calcitonin — three thyroid hormones
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.
BMR effects
↑ metabolic rate → ↑ O₂ consumption, ↑ heat production. Hyperthyroid = hot, sweaty, tachycardic.
Graves' disease
Anti-TSH receptor antibodies → constitutive activation → ↑ T3/T4. Exophthalmos, goiter, tremor.
Calcitonin
C cells → inhibits osteoclasts → ↓ blood Ca2+. Minor in adults. Used therapeutically in hypercalcemia.
Adrenal Gland
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.
Sugar (fasciculata)
Cortisol → ↑ blood glucose, anti-inflammatory, stress response. Controlled by ACTH (CRH → ACTH → cortisol).
Sex (reticularis)
DHEA (weak androgen). Important for female libido and some secondary sex characteristics.
Medulla
Epinephrine (80%) + NE (20%). Fight-or-flight. Pheochromocytoma = tumor → hypertensive crisis.
Cortisol Physiology
Cortisol = stress hormone — raises glucose · suppresses immunity · breaks down muscle
HPA axis: CRH → ACTH → Cortisol → negative feedback
Cortisol — what it does and the HPA axis that controls it
Cortisol is the primary glucocorticoid — released from zona fasciculata in response to ACTH. HPA axis: stress → hypothalamus → CRH → anterior pituitary → ACTH → adrenal cortex → cortisol → negative feedback suppresses CRH and ACTH. Cortisol effects: ↑ blood glucose (gluconeogenesis + glycogen breakdown + ↓ glucose uptake in muscle/fat — diabetogenic), anti-inflammatory (↓ PLA2 → ↓ prostaglandins and leukotrienes, stabilizes mast cells), immunosuppressive (↓ lymphocytes, ↓ antibodies), ↑ protein catabolism (muscle breakdown), ↑ fat mobilization. Permissive effect: sensitizes blood vessels to epinephrine. Cushing's syndrome: excess cortisol → moon face, buffalo hump, central obesity, hypertension, hyperglycemia, immunosuppression, osteoporosis. Addison's disease: adrenal insufficiency → fatigue, hypotension, hyperpigmentation.
HPA axis
CRH (hypothalamus) → ACTH (anterior pituitary) → Cortisol (adrenal cortex) → negative feedback.
Cushing's
Excess cortisol. Moon face, buffalo hump, striae, central obesity, hypertension, T2DM, osteoporosis.
Addison's
↓ cortisol (and aldosterone). Fatigue, hypotension, hyperpigmentation (↑ ACTH → ↑ MSH).
Diurnal rhythm
Cortisol peaks at 8 AM (wake up), lowest at midnight. Disrupted by shift work and Cushing's.
Pancreatic Hormones
Alpha cells = Glucagon (Goes up) · Beta cells = Insulin (Brings down) · Delta = Somatostatin
Islets of Langerhans — three cell types with opposing glucose effects
Insulin and glucagon — the two opposing hormones that control blood glucose
Islets of Langerhans (1-2% of pancreas): Alpha cells (20%) → glucagon. Beta cells (70%) → insulin. Delta cells (10%) → somatostatin. Insulin: released when blood glucose ↑ (eating). Effects: ↑ glucose uptake by muscle and fat (GLUT4 insertion), ↑ glycogen synthesis (liver and muscle), ↑ protein synthesis, ↑ fat storage, ↓ gluconeogenesis → overall anabolic hormone, lowers blood glucose. Glucagon: released when blood glucose ↓ (fasting). Effects: ↑ glycogenolysis (liver), ↑ gluconeogenesis → raises blood glucose — catabolic. Somatostatin: inhibits both insulin and glucagon. Also inhibits GH and GI secretions. Type 1 DM: beta cells destroyed (autoimmune) → no insulin. Type 2 DM: insulin resistance + relative insulin deficiency.
Insulin
↑ blood glucose → insulin → GLUT4 in muscle/fat → glucose in → glycogen made. Anabolic.
Glucagon
↓ blood glucose → glucagon → liver glycogenolysis + gluconeogenesis → glucose released. Catabolic.
Type 1 DM
Autoimmune destruction of beta cells. No insulin. DKA risk. Requires insulin injections.
Type 2 DM
Insulin resistance → beta cells compensate → eventually fail. Lifestyle + metformin + other drugs.
Calcium Regulation
PTH raises Ca2+ · Calcitonin lowers Ca2+ · Vitamin D absorbs Ca2+ — all three work on bone, kidney, gut
Parathyroid hormone · Calcitonin · Calcitriol — three hormones maintaining blood Ca2+ 8.5–10.5 mg/dL
Calcium homeostasis — three hormones and three target organs
Blood calcium must stay 8.5–10.5 mg/dL — essential for nerve function, muscle contraction, clotting, bone. PTH (parathyroid hormone): from chief cells of 4 parathyroid glands. ↓ Ca2+ → PTH released → bone resorption (osteoclast stimulation), kidney Ca2+ reabsorption (DCT), kidney activates vitamin D (→ gut absorption). Net: ↑ blood Ca2+. Calcitonin: from thyroid C cells. ↑ Ca2+ → calcitonin → inhibits osteoclasts → ↓ blood Ca2+ (minor in adults). Vitamin D (calcitriol): from skin (UV) → liver (25-OH) → kidney (1,25-OH = calcitriol). Stimulates gut Ca2+ absorption (most important effect). Stimulated by PTH. Hypoparathyroidism: ↓ PTH → ↓ Ca2+ → tetany, seizures, positive Chvostek/Trousseau signs. Hyperparathyroidism: ↑ PTH → ↑ Ca2+ → kidney stones, bone pain, constipation.
PTH
↓ Ca2+ → PTH → bone resorption + renal Ca2+ retention + ↑ vitamin D activation → ↑ Ca2+.
Vitamin D
Skin UV → D3 → liver 25-OH → kidney 1,25-OH (calcitriol). Gut Ca2+ absorption. Stimulated by PTH.
Hypocalcemia
↓ Ca2+ → ↑ neuronal excitability → tetany, muscle cramps, Chvostek sign (facial twitch). Seizures.
Hypercalcemia
"Bones, Stones, Groans, Moans" — bone pain, kidney stones, constipation, depression/psychosis.
Growth Hormone
GH → IGF-1 from liver → growth · Released in pulses at night · GHRH stimulates · Somatostatin inhibits
Growth hormone acts via IGF-1 — promotes growth of all tissues, mobilizes fat, raises blood glucose
Growth hormone — how it works, when it's released, and disorders of excess or deficiency
GH (somatotropin) from anterior pituitary somatotrophs — most abundant pituitary hormone. Controlled by: GHRH (↑ GH), somatostatin (↓ GH), sleep (peak release during deep sleep — stage 3/4 NREM), exercise, stress, hypoglycemia all stimulate. Direct effects: ↑ protein synthesis, ↑ fat mobilization (lipolysis), ↑ blood glucose (anti-insulin = diabetogenic). Indirect effects via IGF-1 (insulin-like growth factor 1) from liver: promotes chondrocyte division → linear bone growth (before epiphyseal closure). Deficiency: dwarfism (short stature, proportionate). Excess in childhood: gigantism (tall stature). Excess in adults (after epiphyseal closure): acromegaly — enlarged hands, feet, jaw, tongue, organomegaly. Treated with somatostatin analogs (octreotide) or surgery.
IGF-1
Liver makes IGF-1 in response to GH. Promotes chondrocyte proliferation → linear bone growth.
Sleep and GH
GH peaks during deep NREM sleep (stages 3-4). "Children grow while they sleep" is physiologically true.
Gigantism
GH excess before epiphyseal closure → very tall. Rare pituitary adenoma.
Acromegaly
GH excess after closure → hands, feet, jaw, nose enlarge. Carpal tunnel, T2DM, cardiovascular disease.
Other Key Endocrine Glands
Pineal → melatonin · Thymus → thymosin · Gonads → sex hormones · Heart → ANP
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).
Melatonin
Darkness → ↑ melatonin. Light → ↓ melatonin. Controls sleep onset. Supplement for jet lag.
ANP
↑ atrial stretch → ANP → Na+ and water excretion → ↓ BP. Opposes RAAS. Heart failure → high ANP.
Leptin
Satiety hormone from adipose. ↑ fat → ↑ leptin → ↓ appetite. Leptin resistance in obesity.
Thymosin
Promotes T cell maturation. DiGeorge syndrome (no thymus) → severely impaired T cell immunity.
🎓 Common Exam Questions
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?
A: Cortisol (glucocorticoid from adrenal zona fasciculata): released by ACTH. Actions: increases blood glucose (gluconeogenesis, inhibits insulin), anti-inflammatory (inhibits phospholipase A2, reduces cytokines), immunosuppressive, protein catabolism, lipolysis, maintains blood pressure (upregulates adrenergic receptors). Cushing syndrome (excess cortisol): central obesity (moon face, buffalo hump), hypertension, hyperglycemia, striae, osteoporosis, immunosuppression, hypokalemia. Causes: exogenous steroids (most common), pituitary adenoma (Cushing disease), adrenal adenoma, ectopic ACTH. Addison disease (cortisol deficiency): fatigue, weight loss, hypotension, hyperpigmentation (elevated ACTH stimulates MSH receptors), hyponatremia, hyperkalemia, hypoglycemia. Adrenal crisis: acute life-threatening → IV hydrocortisone immediately.
Q: How is blood calcium regulated and what are hypo vs hypercalcemia causes?
A: Normal Ca2+: 8.5-10.5 mg/dL. Three hormones: PTH (parathyroid): low Ca2+ → PTH↑ → increases Ca2+ by bone resorption, renal reabsorption, and activating vitamin D (1,25-OH2D3) which increases intestinal absorption. Calcitonin (thyroid C cells): high Ca2+ → calcitonin↑ → inhibits osteoclasts → lowers Ca2+. Vitamin D: increases intestinal Ca2+ and phosphate absorption. Hypercalcemia (bones, stones, groans, moans): hyperparathyroidism (most common outpatient), malignancy (PTHrP or bone mets, most common inpatient), vitamin D toxicity, sarcoidosis. Hypocalcemia: hypoparathyroidism (post-thyroidectomy), vitamin D deficiency, hypomagnesemia (Mg needed for PTH secretion). Signs: Chvostek (facial tap → facial twitch), Trousseau (BP cuff → carpopedal spasm).
Q: What is the difference between type 1 and type 2 diabetes mellitus?
A: Type 1 DM: autoimmune destruction of beta cells → absolute insulin deficiency. Onset: young, thin. Prone to DKA (no insulin → lipolysis → ketone production). C-peptide absent. Requires insulin. Type 2 DM: insulin resistance + relative insulin deficiency. Onset: older, obese. Prone to HHNS (hyperosmolar hyperglycemic nonketotic state) not DKA (some insulin prevents ketosis). C-peptide present. Treatment: metformin first (decreases hepatic glucose output), then add agents. DKA triad: hyperglycemia + metabolic acidosis + ketonemia. Treatment: insulin drip, IV fluids, K+ replacement (insulin drives K+ into cells → watch for hypokalemia). HHNS: extreme hyperglycemia (>600), hyperosmolarity, no ketones, altered consciousness. Treatment: aggressive fluid replacement.