⚗️ Anatomy · Endocrine System

Memory tricks for glands and hormones

The endocrine system controls growth, metabolism, reproduction, and stress response through chemical messengers. These memory tricks help you link each gland to its hormones and understand what happens when things go wrong.

⚗️ Endocrine System

Memory Tricks

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

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Major Endocrine Glands
HOPAT PAT — Hypothalamus · Pituitary · Pineal · Adrenal · Thyroid · Parathyroid · Pancreas · Thymus · Gonads
Nine major endocrine glands and their locations
All major endocrine glands — where each one is located
Hypothalamus (brain base) — master controller, releases releasing/inhibiting hormones. Pituitary (sella turcica of sphenoid) — master gland, two lobes. Pineal (brain) — melatonin, circadian rhythm. Adrenal (atop kidneys) — cortex and medulla. Thyroid (anterior neck) — metabolism. Parathyroid (posterior thyroid, 4 glands) — calcium. Pancreas (retroperitoneal) — blood sugar. Thymus (mediastinum) — T-cell maturation. Gonads (testes/ovaries) — sex hormones.
Hypothalamus
Brain base — releasing/inhibiting hormones control anterior pituitary.
Pituitary
Anterior (hormone producing) + posterior (hormone storing/releasing).
Adrenal
Cortex = steroids (cortisol, aldosterone). Medulla = catecholamines (epinephrine).
Parathyroid
4 small glands on posterior thyroid — PTH raises blood calcium.
Pancreas
Islets of Langerhans — alpha (glucagon) + beta (insulin) cells.
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🃏 Major Endocrine Glands
Major endocrine glands — HOPAT PAT
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🃏 Answer
HOPAT PAT — Hypothalamus · Pituitary · Pineal · Adrenal · Thyroid · Parathyroid · Pancreas · Thymus · Gonads
HypothalamusBrain base — releasing/inhibiting hormones control anterior pituitary.
PituitaryAnterior (hormone producing) + posterior (hormone storing/releasing).
AdrenalCortex = steroids (cortisol, aldosterone). Medulla = catecholamines (epinephrine).
Parathyroid4 small glands on posterior thyroid — PTH raises blood calcium.
PancreasIslets of Langerhans — alpha (glucagon) + beta (insulin) cells.
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Anterior Pituitary Hormones
FLAT PiG — FSH · LH · ACTH · TSH · Prolactin · GH
Six anterior pituitary hormones
All six anterior pituitary hormones — what each targets
FSH (follicle stimulating hormone): follicle development and spermatogenesis. LH (luteinizing hormone): ovulation and testosterone production. ACTH (adrenocorticotropic hormone): stimulates adrenal cortex to produce cortisol. TSH (thyroid stimulating hormone): stimulates thyroid to produce T3/T4. Prolactin: milk production. GH (growth hormone): stimulates growth and IGF-1 production. The posterior pituitary stores and releases ADH and oxytocin — but does NOT produce them (they are made in the hypothalamus).
FSH
Follicle development (F) + spermatogenesis (M). From anterior pituitary.
LH
Ovulation trigger (F) + testosterone (M). Surge at day 14 of cycle.
ACTH
Stimulates adrenal cortex → cortisol. Elevated in Cushing's disease.
TSH
Stimulates thyroid → T3/T4. High TSH = hypothyroidism (thyroid not responding).
GH
Growth + IGF-1. Excess in adults = acromegaly. Deficiency = dwarfism.
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🃏 Anterior Pituitary Hormones
Anterior pituitary hormones — what is FLAT PiG?
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🃏 Answer
FLAT PiG — FSH · LH · ACTH · TSH · Prolactin · GH
FSHFollicle development (F) + spermatogenesis (M). From anterior pituitary.
LHOvulation trigger (F) + testosterone (M). Surge at day 14 of cycle.
ACTHStimulates adrenal cortex → cortisol. Elevated in Cushing's disease.
TSHStimulates thyroid → T3/T4. High TSH = hypothyroidism (thyroid not responding).
GHGrowth + IGF-1. Excess in adults = acromegaly. Deficiency = dwarfism.
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Thyroid Hormones
T3 T4 — Triiodothyronine · Thyroxine · need Iodine
T3 = active form · T4 = storage form · Calcitonin lowers calcium
Three thyroid hormones — and why iodine deficiency matters
T4 (thyroxine) is the main secreted hormone — converted to T3 (triiodothyronine) in peripheral tissues. T3 is 3-4× more potent. Both require iodine — deficiency causes goiter (enlarged thyroid). Calcitonin is produced by parafollicular C cells — lowers blood calcium by inhibiting osteoclasts. Hypothyroidism: low metabolism, weight gain, cold intolerance, fatigue, constipation. Hyperthyroidism: high metabolism, weight loss, heat intolerance, tachycardia, exophthalmos (in Graves' disease).
T4
Thyroxine — main secreted form. Converted to T3 in tissues. Longer half-life.
T3
Triiodothyronine — active form. 3-4× more potent than T4.
Calcitonin
C cells — lowers calcium by inhibiting osteoclasts. Opposite of PTH.
Hypothyroid
Weight gain, cold, fatigue, constipation, slow HR. High TSH, low T4.
Hyperthyroid
Weight loss, heat, anxiety, diarrhea, fast HR. Low TSH, high T4.
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🃏 Thyroid Hormones
Thyroid hormones — T3 vs T4, and calcitonin?
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🃏 Answer
T3 T4 — Triiodothyronine · Thyroxine · need Iodine
T4Thyroxine — main secreted form. Converted to T3 in tissues. Longer half-life.
T3Triiodothyronine — active form. 3-4× more potent than T4.
CalcitoninC cells — lowers calcium by inhibiting osteoclasts. Opposite of PTH.
HypothyroidWeight gain, cold, fatigue, constipation, slow HR. High TSH, low T4.
HyperthyroidWeight loss, heat, anxiety, diarrhea, fast HR. Low TSH, high T4.
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Adrenal Cortex Hormones
GFR — Glomerulosa · Fasciculata · Reticularis
Salt · Sugar · Sex — three zones three hormones
Three zones of the adrenal cortex — each makes a different hormone class
The adrenal cortex has three zones from outside to inside. Zona Glomerulosa (outer) → mineralocorticoids (aldosterone) — Salt. Zona Fasciculata (middle) → glucocorticoids (cortisol) — Sugar. Zona Reticularis (inner) → androgens (DHEA) — Sex. Memory trick: GFR from outside in, and "Salt Sugar Sex — the deeper you go." Addison's disease = adrenal insufficiency (low cortisol and aldosterone). Cushing's syndrome = excess cortisol (moon face, buffalo hump, striae).
Glomerulosa
Outermost — aldosterone. Na+ retention, K+ secretion, BP regulation.
Fasciculata
Middle (largest) — cortisol. Stress response, blood sugar, anti-inflammatory.
Reticularis
Inner — androgens (DHEA). Weak sex hormones, converted peripherally.
Addison's
Low cortisol + aldosterone → hypotension, hyponatremia, hyperkalemia, bronze skin.
Cushing's
Excess cortisol → moon face, buffalo hump, central obesity, purple striae.
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🃏 Adrenal Cortex Hormones
GFR
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🃏 Answer
GFR — Glomerulosa · Fasciculata · Reticularis
GlomerulosaOutermost — aldosterone. Na+ retention, K+ secretion, BP regulation.
FasciculataMiddle (largest) — cortisol. Stress response, blood sugar, anti-inflammatory.
ReticularisInner — androgens (DHEA). Weak sex hormones, converted peripherally.
Addison'sLow cortisol + aldosterone → hypotension, hyponatremia, hyperkalemia, bronze skin.
Cushing'sExcess cortisol → moon face, buffalo hump, central obesity, purple striae.
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Insulin vs Glucagon
Insulin IN (stores) · Glucagon OUT (releases)
Insulin = anabolic, lowers glucose · Glucagon = catabolic, raises glucose
The two pancreatic hormones — opposite effects on blood glucose
Insulin (beta cells) released when blood glucose rises after a meal → glucose enters cells, glycogen synthesis, fat storage. Lowers blood glucose. Glucagon (alpha cells) released when blood glucose falls → glycogenolysis (breaks down glycogen), gluconeogenesis (makes new glucose). Raises blood glucose. Type 1 diabetes: no insulin (autoimmune destruction of beta cells). Type 2 diabetes: insulin resistance — cells don't respond. Both result in hyperglycemia but through different mechanisms.
Insulin
Beta cells — post-meal. Glucose uptake, glycogen synthesis, fat storage. Lowers BG.
Glucagon
Alpha cells — fasting. Glycogenolysis + gluconeogenesis. Raises BG.
Type 1 DM
No insulin — autoimmune. Requires insulin injections. Ketoacidosis risk.
Type 2 DM
Insulin resistance — cells unresponsive. Lifestyle + oral medications + eventually insulin.
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🃏 Insulin vs Glucagon
Insulin vs glucagon — what does each do?
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🃏 Answer
Insulin IN (stores) · Glucagon OUT (releases)
InsulinBeta cells — post-meal. Glucose uptake, glycogen synthesis, fat storage. Lowers BG.
GlucagonAlpha cells — fasting. Glycogenolysis + gluconeogenesis. Raises BG.
Type 1 DMNo insulin — autoimmune. Requires insulin injections. Ketoacidosis risk.
Type 2 DMInsulin resistance — cells unresponsive. Lifestyle + oral medications + eventually insulin.
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Calcium Regulation
PTH UP · Calcitonin DOWN · Vitamin D UP
Three hormones that regulate blood calcium levels
Calcium homeostasis — three hormones, opposite effects
PTH (parathyroid hormone): released when calcium is LOW. Raises calcium by activating osteoclasts (bone resorption), increasing renal reabsorption of calcium, and activating vitamin D. Calcitonin (thyroid C cells): released when calcium is HIGH. Lowers calcium by inhibiting osteoclasts. Vitamin D (activated in kidneys from sunlight precursor): increases intestinal absorption of calcium. Hypoparathyroidism → hypocalcemia → tetany (muscle spasms). Hyperparathyroidism → hypercalcemia → stones, bones, groans, psychic moans.
PTH
Low Ca2+ → PTH released → osteoclasts, renal reabsorption, activate Vit D.
Calcitonin
High Ca2+ → calcitonin released → inhibits osteoclasts → lowers Ca2+.
Vitamin D
Increases GI absorption of calcium. Activated in kidneys (1,25-dihydroxycholecalciferol).
Hypocalcemia
Tetany, Chvostek's sign, Trousseau's sign. Cause: hypoparathyroidism, Vit D deficiency.
Hypercalcemia
Stones, bones, groans, psychic moans. Cause: hyperparathyroidism, malignancy.
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🃏 Calcium Regulation
Calcium regulation — what do PTH, calcitonin and vitamin D do?
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🃏 Answer
PTH UP · Calcitonin DOWN · Vitamin D UP
PTHLow Ca2+ → PTH released → osteoclasts, renal reabsorption, activate Vit D.
CalcitoninHigh Ca2+ → calcitonin released → inhibits osteoclasts → lowers Ca2+.
Vitamin DIncreases GI absorption of calcium. Activated in kidneys (1,25-dihydroxycholecalciferol).
HypocalcemiaTetany, Chvostek's sign, Trousseau's sign. Cause: hypoparathyroidism, Vit D deficiency.
HypercalcemiaStones, bones, groans, psychic moans. Cause: hyperparathyroidism, malignancy.
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Negative Feedback
More hormone = Less signal · Less hormone = More signal
Negative feedback maintains hormonal homeostasis
How negative feedback controls hormone levels — the most important endocrine concept
Most endocrine systems use negative feedback — the product inhibits its own production. Example: Low thyroid hormone → hypothalamus releases TRH → pituitary releases TSH → thyroid produces T3/T4 → high T3/T4 feeds back to inhibit TRH and TSH release. The thermostat analogy: when the room is warm enough, the heater turns off. Understanding negative feedback explains virtually every endocrine lab interpretation — high TSH + low T4 = hypothyroidism. Low TSH + high T4 = hyperthyroidism.
Thyroid axis
TRH → TSH → T3/T4. High T4 inhibits TRH and TSH (negative feedback).
Adrenal axis
CRH → ACTH → cortisol. High cortisol inhibits CRH and ACTH.
Lab interpretation
High TSH + low T4 = hypothyroid. Low TSH + high T4 = hyperthyroid.
Positive feedback
Rare exception — LH surge (ovulation) and oxytocin (labor) are positive feedback loops.
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🃏 Negative Feedback
Negative feedback — how does it work?
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🃏 Answer
More hormone = Less signal · Less hormone = More signal
Thyroid axisTRH → TSH → T3/T4. High T4 inhibits TRH and TSH (negative feedback).
Adrenal axisCRH → ACTH → cortisol. High cortisol inhibits CRH and ACTH.
Lab interpretationHigh TSH + low T4 = hypothyroid. Low TSH + high T4 = hyperthyroid.
Positive feedbackRare exception — LH surge (ovulation) and oxytocin (labor) are positive feedback loops.
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Cortisol Effects
BIDE — Blood sugar · Immunity suppressed · Decreased inflammation · Everything broken down
Four major effects of cortisol — the stress hormone
What cortisol actually does — four effects to know for every exam
Cortisol is released by the adrenal cortex in response to ACTH and stress. Blood sugar: raises glucose via gluconeogenesis — breaks down protein and fat for fuel. Immunity: suppresses immune response — why corticosteroids are used for inflammation but increase infection risk. Decreased inflammation: stabilizes cell membranes, reduces prostaglandins. Everything broken down: catabolic — muscle wasting, bone loss, thin skin with prolonged excess. Diurnal rhythm: peaks at 8 AM, lowest at midnight. Stress response essential for survival.
Blood sugar ↑
Gluconeogenesis — breaks down muscle and fat to make glucose.
Immunity ↓
Suppresses lymphocytes — used therapeutically but increases infection risk.
Anti-inflammatory
Inhibits prostaglandins and histamine — why steroids reduce swelling.
Catabolic
Muscle wasting, bone loss, skin thinning with chronic excess (Cushing's).
Diurnal rhythm
Peaks 8 AM, lowest midnight. Disrupted in shift workers and Cushing's.
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🃏 Cortisol Effects
BIDE
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🃏 Answer
BIDE — Blood sugar · Immunity suppressed · Decreased inflammation · Everything broken down
Blood sugar ↑Gluconeogenesis — breaks down muscle and fat to make glucose.
Immunity ↓Suppresses lymphocytes — used therapeutically but increases infection risk.
Anti-inflammatoryInhibits prostaglandins and histamine — why steroids reduce swelling.
CatabolicMuscle wasting, bone loss, skin thinning with chronic excess (Cushing's).
Diurnal rhythmPeaks 8 AM, lowest midnight. Disrupted in shift workers and Cushing's.
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Adrenal Medulla
ENA — Epinephrine · Norepinephrine · Adrenaline rush
Catecholamines released during fight or flight response
Adrenal medulla hormones — modified sympathetic neurons that act like a gland
The adrenal medulla is essentially modified postganglionic sympathetic neurons — it releases epinephrine (80%) and norepinephrine (20%) directly into the bloodstream. Epinephrine: increases HR, bronchodilation, blood glucose (glycogenolysis), dilates skeletal muscle vessels. Norepinephrine: primarily vasoconstriction, increases BP. Both prepare the body for fight or flight. Pheochromocytoma = adrenal medulla tumor → excess catecholamines → hypertensive crises, headache, palpitations, sweating (the classic triad).
Epinephrine (80%)
↑HR, bronchodilation, ↑glucose, vasodilation in muscle. Classic EpiPen response.
Norepinephrine (20%)
Vasoconstriction, ↑BP. Also a CNS neurotransmitter.
Pheochromocytoma
Tumor → episodic hypertension, headache, palpitations, sweating. Rule of 10s.
Adrenal cortex vs medulla
Cortex = steroids (slow, sustained). Medulla = catecholamines (fast, brief).
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🃏 Adrenal Medulla
ENA
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🃏 Answer
ENA — Epinephrine · Norepinephrine · Adrenaline rush
Epinephrine (80%)↑HR, bronchodilation, ↑glucose, vasodilation in muscle. Classic EpiPen response.
Norepinephrine (20%)Vasoconstriction, ↑BP. Also a CNS neurotransmitter.
PheochromocytomaTumor → episodic hypertension, headache, palpitations, sweating. Rule of 10s.
Adrenal cortex vs medullaCortex = steroids (slow, sustained). Medulla = catecholamines (fast, brief).
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