Click any card to flip · 34 cards organized by LO 1–6In-House + In-House Anki + BnB 5.01 / Bootcamp 2.01 / FA 3.01 / Physeo 6.02
LO 1 · Anatomy In House · FA 2.01
Where is the pituitary located? What connects it to the hypothalamus? Which lobe is glandular vs neural?
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Answer
Pituitary sits in the sella turcica of the sphenoid bone. Hypothalamus is in the diencephalon, superior to the pituitary. Connected by the infundibulum (pituitary stalk).
Adenohypophysis (anterior) = Rathke's pouch, oral ectoderm (glandular epithelium). Neurohypophysis (posterior) = neuroectoderm of diencephalon (true neural tissue). Pars intermedia (also Rathke's pouch) — MSH; mostly nonfunctional in adults.
LO 1 · Hypophyseal Portal System In House · BnB 5.01
Trace a hypothalamic releasing hormone from its nucleus to the anterior pituitary target cell.
Why it matters: allows very high local concentrations of tiny amounts of releasing hormone at the AP without systemic exposure. The median eminence is a circumventricular organ (lacks BBB) — essential for this hypothalamus→AP communication.
LO 1 · Three Output Pathways In House
By what THREE routes does the hypothalamus control endocrine organs?
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Answer
1. Hypophyseal portal system → anterior pituitary (vascular; releasing/inhibiting hormones). 2. Direct axonal projections → posterior pituitary (neural; ADH + oxytocin stored in Herring bodies). 3. Sympathetic nervous system → direct preganglionic innervation of adrenal medulla chromaffin cells (fight-or-flight, fastest endocrine reflex, seconds).
LO 2 · Portal-System Hormones In House · FA 3.01
List the seven hypothalamic hormones that travel via portal system to the anterior pituitary.
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Answer
Releasing hormones: TRH (→TSH + PRL), CRH (→ACTH), GnRH (→FSH + LH), GHRH (→GH). Inhibiting hormones: Somatostatin (GHIH) (→↓GH + ↓TSH), Dopamine (PIH) (→↓PRL — tonic), GnIH (→↓FSH + ↓LH; 8-AA peptide from dorsomedial nucleus). Most are peptides; dopamine is the exception (amine).
LO 2 · PVN and SON In House
Which two hypothalamic nuclei make the nonapeptides ADH and oxytocin? How are they transported?
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Answer
Supraoptic nucleus (SON) — primarily ADH (+ some oxytocin). Paraventricular nucleus (PVN) — primarily oxytocin (+ some ADH, also CRH & TRH).
Both are nonapeptides (9 amino acids). Synthesized as preprohormones → packaged on neurophysin carriers → axonal transport to nerve terminals in posterior pituitary → stored in Herring bodies → released into fenestrated capillaries on stimulus.
LO 2 · Circumventricular Organs In House
What are CVOs and which four are endocrine-relevant?
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Answer
CVOs are brain regions near the ventricles with minimal or absent BBB → allow direct blood–brain hormonal exchange.
1. Median eminence — hypophyseal portal system first plexus. 2. Neurohypophysis — ADH/oxytocin release into fenestrated capillaries. 3. OVLT — osmosensors on anterior wall of 3rd ventricle; drives ADH release + thirst. 4. Pineal gland — melatonin release.
LO 2 · OVLT In House · Bootcamp 2.01
How does the OVLT sense plasma osmolarity and regulate ADH?
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Answer
The organum vasculosum of the lamina terminalis (OVLT) sits on the anterior 3rd-ventricle wall — a CVO without BBB. Specialized osmoreceptor neurons shrink in hypertonic plasma and project to SON/PVN → trigger ADH release from posterior pituitary. Also stimulates thirst via cortex projections. OVLT is how the brain "tastes" the plasma.
LO 3 · Acidophils vs Basophils In House · FA 2.01
How are anterior pituitary cells classified on H&E and which hormones does each type secrete?
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Answer
Acidophils (eosin-pink granules) — 2 of 6 AP hormones: GH (somatotropes), PRL (lactotropes). Basophils (hematoxylin-blue) — other 4 AP hormones: TSH (thyrotropes), ACTH (corticotropes), FSH + LH (gonadotropes). Mnemonic: "B-FLAT" = Basophils secrete FSH, LH, ACTH, TSH. Chromophobes — pale, non-secretory supporting / stem / degranulated cells.
LO 3 · Herring Bodies & Pituicytes In House · FA 2.01
What are Herring bodies and pituicytes? What do they tell you about posterior pituitary embryology?
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Answer
Herring bodies — eosinophilic swellings at axon terminals of SON/PVN neurons in the posterior pituitary. Store ADH + oxytocin in secretory vesicles, ready for release into fenestrated capillaries. Pituicytes — glial support cells (similar to astrocytes) of the posterior lobe. Both confirm the posterior pituitary is NEURAL tissue (diencephalic neuroectoderm), NOT glandular. Contrasts with the adenohypophysis (glandular cells + fenestrated capillaries, but no neural parenchyma).
LO 3 · Pars Intermedia In House · FA 2.01
What is produced there? How do you recognize it histologically?
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Answer
The pars intermedia is derived from Rathke's pouch (oral ectoderm) and sits between the anterior and posterior lobes. It secretes MSH (melanocyte-stimulating hormone) and is mostly nonfunctional in adult humans — active in fetuses and young children. Histology: densely packed basophilic cells + cysts filled with eosinophilic colloid — the characteristic finding. Remnant cysts are the origin of craniopharyngiomas.
LO 3 · Pituitary Embryology Bootcamp 3.01 · FA
Different embryologic origins of the two pituitary lobes — and their clinical significance?
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Answer
Adenohypophysis (anterior + pars intermedia) = Rathke's pouch from oral ectoderm — glandular epithelial cells. Remnants can form craniopharyngioma (children, calcified suprasellar mass with "motor-oil" cyst fluid). Neurohypophysis (posterior) = neuroectoderm of diencephalon — true neural tissue (Herring bodies, pituicytes). Different blood supply from the AP (hypophyseal arteries vs portal veins) — which is why the posterior is SPARED in Sheehan syndrome.
LO 4 · Six Anterior Pituitary Hormones In House · FA 3.01
Classify each anterior pituitary hormone by its hypothalamic releaser/inhibitor and target.
LO 5 · Long, Short, Ultra-Short Loops In House · FA 3.01
Define each feedback loop with one concrete example.
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Answer
Long loop — target-organ hormone → hypothalamus + pituitary. Cortisol → ↓CRH + ↓ACTH. Short loop — pituitary hormone → hypothalamus. ACTH → ↓CRH. Ultra-short loop — hypothalamic hormone inhibits its own release via axon collaterals. CRH → ↓CRH. Creates pulsatility (prevents receptor desensitization).
LO 5 · Positive Feedback In House · FA
Two classic positive-feedback loops in the H-P system?
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Answer
1. LH surge (mid-cycle ovulation): Rising estradiol late in follicular phase SWITCHES from negative to positive feedback on GnRH + LH → massive LH surge → ovulation ~24 h later. 2. Oxytocin & labor (Ferguson reflex): Uterine stretch → oxytocin release → contractions → more cervical stretch → more oxytocin. Terminates with delivery. Both are self-terminating — positive loops need an end-point to avoid runaway.
LO 5 · Pulsatility & Desensitization In House
Why does pulsatile hormone secretion prevent receptor desensitization?
Rule: the problem is where the hormone LEVEL DROPS first — everything UPSTREAM rises (compensating); everything DOWNSTREAM falls. "Primary" = farthest downstream. Same logic for cortisol/ACTH and sex-steroid axes.
LO 6 · Exogenous Prednisone In House · FA
Predict CRH, ACTH, and endogenous cortisol levels on chronic oral prednisone. Why does sudden withdrawal cause crisis?
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Answer
Pattern: ↓ CRH, ↓ ACTH, ↓ endogenous cortisol — long-loop feedback suppresses the entire axis. Adrenal atrophy develops from chronic ACTH deficiency. Abrupt withdrawal: no endogenous cortisol + atrophied adrenal can't respond → adrenal crisis (hypotension, hypoglycemia, shock). Always TAPER steroids after prolonged use (>3 weeks of supraphysiologic dosing).
LO 6 · Exogenous Testosterone In House
In a young man on anabolic steroids — predict GnRH, LH/FSH, testes size, sperm count.
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Answer
Exogenous T → long-loop suppression: ↓ GnRH → ↓ LH + ↓ FSH → ↓ endogenous testosterone (Leydig cells silenced) → testicular atrophy. ↓ FSH → ↓ Sertoli cell/germ-cell support → ↓ spermatogenesis → oligospermia / azoospermia (infertility). Serum total T may look normal (exogenous replaces endogenous) but LH/FSH and intratesticular T are suppressed. hCG (LH-like) is used to preserve fertility during testosterone therapy.
LO 6 · Stalk Section Pattern In House · BnB 5.02
What happens to each AP hormone after complete pituitary stalk transection?
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Answer
Stalk section cuts ALL hypothalamic input to the AP. PRL RISES — only hormone under tonic DOPAMINE inhibition; losing inhibition = disinhibition. (Unique exception.) All other AP hormones fall — TSH, ACTH, FSH, LH, GH — losing their releasing hormones. Posterior pituitary also affected: loss of SON/PVN axonal input → central DI (hours–days). Over weeks, pituitary atrophy develops from absent trophic input.
LO 4 · Prolactinoma Bootcamp 3.06 · FA 3.04
Typical presentation, biochemical findings, and first-line treatment?
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Answer
Female: amenorrhea, galactorrhea, infertility, ↓ libido. Male: hypogonadism, decreased libido/erectile dysfunction, gynecomastia; mass effect (bitemporal hemianopia) more common. Lab: PRL often >200 ng/mL (vs mild ↑ in stalk effect). Tx:cabergoline (D2 agonist, first-line) or bromocriptine — shrink tumor and normalize PRL in >80%. Medical-first approach is unique to PRL because of tonic dopamine inhibition (LO 4 biology applied). Watch out for "hook effect" — extremely high PRL may read falsely low; dilute sample.
Who gets it, why is the anterior pituitary uniquely vulnerable, and first clinical sign?
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Answer
Who: postpartum women with obstetric hemorrhage / hypotension. Why: pregnancy doubles lactotrope mass, outstripping portal blood supply → hypertrophied AP is uniquely vulnerable to ischemic necrosis. First sign: failure to lactate (PRL loss). Later: fatigue (↓GH); amenorrhea (↓FSH/LH); hypothyroidism (↓TSH); adrenal insufficiency (↓ACTH). Posterior pituitary is SPARED — different blood supply (hypophyseal arteries, not portal system).
LO 3 · Pituitary Apoplexy BnB 5.02
Classic presentation, imaging, and the EMERGENT treatment step?
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Answer
Sudden hemorrhage or infarction within a pre-existing pituitary adenoma → acute thunderclap headache, bitemporal hemianopia, cavernous sinus syndrome (CN III, IV, V1-2, VI), altered mental status. Labs: acute secondary adrenal insufficiency — hypotension, hypoglycemia. MRI: hemorrhagic sellar mass with suprasellar extension. EMERGENT step:IV hydrocortisone FIRST (empirically, life-saving), THEN surgical decompression for vision threat. Never give T4 before cortisol — accelerated cortisol clearance precipitates crisis.
LO 3 · Craniopharyngioma Bootcamp · FA
Typical patient, imaging buzzwords, and embryologic origin?
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Answer
Typical: child / young adult with growth failure, bitemporal hemianopia (chiasmal compression from below), polyuria (stalk/posterior pituitary involvement → DI), delayed puberty. Imaging buzzwords:calcified suprasellar mass with "motor-oil" cyst fluid. Origin: remnants of Rathke's pouch (oral ectoderm). Same embryologic origin as adenohypophysis → arises from adamantinomatous cells. Bimodal age distribution (children + older adults).
LO 4 · Central vs Nephrogenic DI Bootcamp 2.04
Distinguish lab-wise. What test discriminates?
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Answer
Both: polyuria with dilute urine + hypernatremia. Central DI: ADH deficient. Causes — pituitary surgery, tumor, trauma, autoimmune. Nephrogenic DI: ADH ineffective at kidney — V2-R mutation (X-linked), AQP2 mutation (AR), lithium, hypercalcemia. Desmopressin (DDAVP) challenge: central → urine osm rises >50%; nephrogenic → no response. Tx: Central — desmopressin. Nephrogenic — stop offending drug, HCTZ + low-salt, amiloride (for lithium-induced).
LO 4 · SIADH Bootcamp 2.03
Classic electrolyte picture, common triggers, and treatment?
Classic triad and underlying developmental defect?
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Answer
Triad: (1) anosmia / hyposmia; (2) delayed puberty with hypogonadotropic hypogonadism; (3) absent olfactory bulbs on MRI. Mechanism: failed migration of GnRH neurons from olfactory placode → hypothalamus during embryogenesis. GnRH is deficient → low LH/FSH → low sex steroids. Tx: pulsatile GnRH (restores fertility) OR exogenous LH/FSH (hCG + FSH); testosterone for virilization without fertility need. Contrast with Klinefelter (primary testicular failure, HIGH LH/FSH).
LO 6 · GH Deficiency in Child Bootcamp 3.05
Clinical picture, stimulation test, treatment?
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Answer
Child: short stature, normal body proportions, delayed bone age. Midline defects (cleft palate, central incisor) can indicate congenital pituitary malformation. Adult GH deficiency: central obesity, low muscle mass, fatigue, ↓ bone density — less obvious than pediatric. Stimulation tests: insulin tolerance test (hypoglycemia should stimulate GH), arginine, clonidine. Random GH unhelpful (pulsatile). Tx: recombinant human GH (somatropin) SC; contraindicated in open-angle pituitary adenoma, active cancer.
LO 4 · Hypothalamic Drug Targets FA · Pharm
Summarize the key drugs that act on the H-P axis and their mechanisms.
Step 1-Style MCQs: single best answer. Each question cross-references the in-house LO and the mapped 3rd-party resource that teaches it.
Question 1 of 10 · LO 1 — Anatomy of the Stalk In House · FA 2.01
A 42-year-old woman with a non-functioning sellar mass has progressive visual field loss on confrontation. Which of the following best describes the anatomic connection between the mass's origin (pituitary gland) and the hypothalamus?
AA peripheral nerve extending from the medulla
BThe infundibulum (pituitary stalk), containing both the hypophyseal portal system and axonal projections
CDirect contact through the sella turcica bone
DCerebrospinal-fluid diffusion via the fourth ventricle
ELymphatic channels in the cavernous sinus
B. The infundibulum (pituitary stalk) carries (1) hypophyseal portal veins from median eminence to anterior pituitary and (2) axons from SON/PVN to posterior pituitary. Compression of the stalk disconnects both pathways — hence patients present with panhypopituitarism AND prolactin elevation (loss of tonic dopamine). Pituitary sits in the sella turcica of the sphenoid; hypothalamus in the diencephalon — they are connected ONLY through the infundibulum.
Question 2 of 10 · LO 2 — Nonapeptide Source In House · FA 3.03
A 55-year-old man develops polyuria (6 L/day) and hypernatremia 2 days after transsphenoidal pituitary adenoma resection. Which hypothalamic structure most directly produces the hormone that is now deficient?
AArcuate nucleus
BPeriventricular nucleus
CSupraoptic nucleus (SON)
DMedial preoptic nucleus
EVentromedial nucleus
C — SON. The patient has central diabetes insipidus from disruption of SON (and PVN) axons traversing the stalk. SON is the primary source of ADH; PVN is primary for oxytocin (plus CRH, TRH). Arcuate (A) = dopamine (PIH); periventricular (B) = somatostatin; medial preoptic (D) = GnRH; ventromedial (E) = GHRH. Desmopressin (V2 agonist) is the treatment.
Question 3 of 10 · LO 3 — Acidophil vs Basophil FA 2.01
On H&E staining of a pituitary biopsy, cells with prominent eosinophilic (pink) granules are seen. Which two anterior pituitary hormones are most likely produced by these cells?
AACTH and TSH
BFSH and LH
CGH and prolactin
DADH and oxytocin
EMSH and ACTH
C. Acidophils are somatotropes (GH) and lactotropes (PRL). Basophils (blue) are thyrotropes (TSH), corticotropes (ACTH), and gonadotropes (FSH + LH) — mnemonic "B-FLAT". ADH/oxytocin (D) are posterior-pituitary hormones stored in Herring bodies, not made by adenohypophyseal cells. MSH (E) is from pars intermedia.
Question 4 of 10 · LO 4 — Prolactin Tonic Inhibition In House · Bootcamp 3.06
A 30-year-old woman reports 12 months of amenorrhea and galactorrhea. She is not pregnant. PRL is 340 ng/mL; TSH 2.0; free T4 normal. MRI shows a 9-mm sellar mass. What is the best first-line therapy?
ATranssphenoidal surgery
BCabergoline (dopamine D2 agonist)
COctreotide (somatostatin analog)
DLevothyroxine
EPituitary radiation
B — Cabergoline. Dopamine tonically inhibits PRL release via D2; D2 agonists (cabergoline, bromocriptine) shrink prolactinomas AND normalize PRL in >80%. Surgery (A) is reserved for drug-intolerant, vision-threatening, or drug-resistant tumors. This "medical-first" approach is unique among pituitary tumors and directly reflects the LO 4 biology of PRL control.
Question 5 of 10 · LO 4 — TRH / PRL Cross-Stimulation FA 3.04
A 28-year-old woman has amenorrhea and galactorrhea. PRL 85 ng/mL, TSH 8.2 mIU/L, free T4 0.6 ng/dL (low). What is the PRIMARY mechanism of her hyperprolactinemia?
AProlactin-secreting pituitary adenoma
BPrimary hypothyroidism → ↑TRH → stimulates both TSH and PRL
CHypothalamic dopamine deficiency
DExcess GnRH suppressing dopamine
EPrimary gonadal dysfunction
B. TRH has TWO pituitary targets: TSH (main) and PRL (lactotropes have TRH receptors). In primary hypothyroidism, low T4 → loss of feedback → ↑ TRH → ↑ TSH AND ↑ PRL. Treat the hypothyroidism (levothyroxine) → both labs normalize. Prolactinoma (A) would typically have PRL >200 and NORMAL TSH. Always check thyroid function in hyperprolactinemia.
Question 6 of 10 · LO 4 — Acromegaly Screening FA 3.02 · Bootcamp 3.04
A 52-year-old man with progressive jaw enlargement, carpal tunnel syndrome, and sleep apnea has suspected acromegaly. Which test is best for initial screening?
ARandom serum GH
BSerum IGF-1
CMRI pituitary
DSerum prolactin
E24-hour urine cortisol
B — IGF-1. GH is secreted in pulses (GHRH pulses + ultra-short autoregulation), so random GH can miss active disease. IGF-1 is produced by liver in response to GH and integrates GH exposure over 24 hours → stable index. If IGF-1 elevated → confirm with OGTT (normal GH suppresses with glucose; acromegaly does NOT). MRI (C) follows positive biochemistry, not the screen.
Question 7 of 10 · LO 5 — Feedback Hierarchy In House · FA
"Rising CRH inhibits its own subsequent release via axon collaterals within the hypothalamus." Which type of feedback loop does this describe?
ALong loop
BShort loop
CUltra-short loop
DPositive feedback
EFeed-forward
C. Ultra-short loop = hypothalamic hormone inhibits ITSELF via axon collaterals within the hypothalamus. This autoregulation creates pulsatile release and prevents receptor desensitization at the pituitary (LO 2 integration). Long loop (A) = target hormone → hypothalamus + pituitary. Short loop (B) = pituitary → hypothalamus.
Question 8 of 10 · LO 5 — Positive Feedback In House · FA
Mid-cycle, estradiol rises to peak levels and triggers a surge of LH. Which statement best captures the physiology?
AEstradiol exerts continuous negative feedback throughout the cycle
BSustained high estradiol SWITCHES feedback from negative to positive on GnRH, generating the LH surge (self-terminating)
CFSH stimulates estradiol release which directly causes ovulation
DProgesterone drives the LH surge
ELH suppresses GnRH via short-loop feedback
B. Estradiol normally suppresses GnRH/LH (negative feedback). At mid-cycle, sustained high estradiol (from the dominant follicle) SWITCHES to positive feedback on GnRH pulse frequency + pituitary sensitivity → massive LH surge → ovulation ~24h later. The loop is self-terminating: ovulation removes the follicle, progesterone from corpus luteum restores negative feedback.
Question 9 of 10 · LO 6 — Cushing Localization FA · Bootcamp
A 45-year-old woman has central obesity, striae, hyperglycemia. Morning cortisol elevated, ACTH elevated. Low-dose dexamethasone fails to suppress cortisol, but HIGH-dose dexamethasone DOES suppress. Which best describes the source?
B — Cushing disease. Classic pattern: low-dose dex fails to suppress (any cortisol excess), high-dose dex SUPPRESSES → pituitary adenoma retains SOME feedback sensitivity at high dex doses. ACTH mildly elevated. Ectopic ACTH (C) doesn't suppress at any dose + usually higher ACTH + hypokalemic alkalosis. Adrenal (D) and exogenous (A) have LOW ACTH (feedback-suppressed pituitary). Tests the LO 5/6 logic of feedback applied clinically.
Question 10 of 10 · LO 6 — Continuous Leuprolide FA · Physeo 6.02
A 66-year-old man with metastatic prostate cancer starts continuous leuprolide. Week 1: worsening bone pain, urinary retention, testosterone RISES. Week 4: symptoms improve, testosterone at castrate level. Which mechanism explains this biphasic response?
ALeuprolide directly stimulates Leydig cells
BInitial LH/FSH surge (flare) followed by GnRH-receptor down-regulation from continuous (non-pulsatile) agonism
CAnti-leuprolide antibodies develop after week 3
DAromatase converts androgens to estrogens
ELeuprolide stimulates adrenal androgens
B. Pulsatile GnRH is the physiologic signal. Continuous leuprolide initially AGONIZES GnRH receptors → LH/FSH surge → testosterone spike ("tumor flare"). After 1–2 weeks, constant stimulation → receptor down-regulation → LH/FSH fall → castrate testosterone. Bicalutamide (anti-androgen) is co-administered to blunt the flare. Directly applies LO 5 pulsatility principle.
Vignette 1 of 6 · LO 3 — Pituitary Apoplexy BnB 5.02 · FA
A 54-year-old man with a known non-functioning pituitary macroadenoma presents with acute thunderclap headache, bitemporal visual loss, and right-sided ptosis with a fixed mid-dilated pupil. He becomes progressively somnolent. BP 80/50, glucose 58. MRI: hemorrhagic sellar mass with suprasellar extension and right cavernous sinus involvement. What is the most appropriate IMMEDIATE next step?
AEmergent transsphenoidal decompression
BIV hydrocortisone 100 mg
CIV levothyroxine 500 µg
DContinuous IV desmopressin
EHigh-dose dexamethasone suppression test
B — IV hydrocortisone. Pituitary apoplexy causes acute secondary adrenal insufficiency within hours. Hypotension + hypoglycemia + altered mental status = adrenal crisis until proven otherwise. Give steroids FIRST (empiric, life-saving); surgery follows for vision-threatening compression. Never start T4 before cortisol — accelerated cortisol clearance precipitates crisis.
Vignette 2 of 6 · LO 3 — Craniopharyngioma Bootcamp · FA
A 9-year-old boy presents with growth failure (<3rd percentile), polyuria, and worsening peripheral vision. Exam: bitemporal hemianopia, delayed puberty (Tanner 1). Labs: IGF-1 LOW, urine osm 110, Na⁺ 148. MRI: suprasellar mass with calcifications and cystic components containing "motor-oil" fluid.
AMedulloblastoma
BGerminoma
CCraniopharyngioma
DPituitary adenoma
EMeningioma of the tuberculum sellae
C — Craniopharyngioma. Buzzwords: child + suprasellar + calcified + motor-oil cyst + bitemporal hemianopia + growth failure + DI. Origin: Rathke's pouch remnants (oral ectoderm). Constellation of AP failure (↓GH → short stature; ↓FSH/LH → delayed puberty) + central DI (stalk involvement) + chiasmal compression is classic. Pituitary adenoma (D) is rare in children and usually doesn't calcify.
Vignette 3 of 6 · LO 4/6 — Post-Op Central DI Bootcamp 2.04
A 55-year-old woman undergoes transsphenoidal resection of a non-functioning pituitary macroadenoma. On post-op day 1: polyuria (550 mL/hr dilute urine), thirst, Na⁺ rises 141 → 149. Urine osm 95, serum osm 305. Desmopressin 2 µg IV → urine osm rises to 420 within 2 hours. What best explains her condition?
ANephrogenic DI from post-op contrast exposure
BCentral DI from surgical disruption of ADH-producing neurons or their axons
CPrimary polydipsia from pain-related anxiety
DSIADH with inappropriate urine dilution
EOsmotic diuresis from hyperglycemia
B — Central DI. SON/PVN neurons or their axons through the stalk can be disrupted during transsphenoidal surgery → ADH deficiency → polyuria + dilute urine + hypernatremia. Desmopressin response (urine osm >50% rise) distinguishes central from nephrogenic. Often evolves through a classic triphasic response: DI days 0–5 → transient SIADH days 5–10 (stored ADH released as cells die) → permanent DI. Reinforces LO 4 posterior-pituitary physiology.
Vignette 4 of 6 · LO 4/5 — Ectopic ACTH vs Cushing Disease BnB 5.02 · FA
A 68-year-old male smoker has 3 months of weight loss, muscle weakness, BP 200/110, hyperpigmentation, K⁺ 2.7, pH 7.52 (metabolic alkalosis). Morning cortisol markedly elevated; ACTH 420 pg/mL. Neither low-dose nor high-dose dexamethasone suppresses cortisol. CT chest: 4-cm central lung mass.
B — Ectopic ACTH (SCLC). Key distinguishers: failure of BOTH low- and high-dose dex to suppress (tumor feedback-independent), very high ACTH, hyperpigmentation (POMC-cleavage products include α-MSH), severe hypokalemic metabolic alkalosis (extreme cortisol excess overwhelms 11β-HSD2 → cortisol acts on MR at kidney). Pituitary Cushing (A) suppresses at high dose. Adrenal (C) and exogenous (D) = LOW ACTH. Integrates LO 4 + LO 5/6 feedback logic.
Vignette 5 of 6 · LO 3/4 — Sheehan Syndrome BnB 5.02 · FA
A 32-year-old woman had a major post-partum hemorrhage 4 weeks ago requiring multiple transfusions. She now reports inability to lactate, fatigue, cold intolerance, and amenorrhea. Labs: low cortisol, low free T4, low FSH/LH, low IGF-1. Serum Na⁺ and urine-concentrating ability are normal.
AAutoimmune lymphocytic hypophysitis
BSheehan syndrome — ischemic necrosis of the hypertrophied anterior pituitary
CPanhypopituitarism from craniopharyngioma
DPrimary adrenal insufficiency (Addison's)
EEmpty sella syndrome
B — Sheehan. Pregnancy doubles lactotrope mass → hypertrophied anterior pituitary outstrips its low-pressure portal blood supply. Obstetric hemorrhage precipitates AP infarction. Failure to lactate is the EARLIEST sign (PRL loss). Followed by GH ↓ (fatigue), FSH/LH ↓ (amenorrhea), TSH ↓ (hypothyroidism), ACTH ↓ (adrenal insufficiency). Posterior pituitary SPARED — different blood supply (hypophyseal arteries, not portal) — explaining normal Na⁺ / urine-concentrating ability.
Vignette 6 of 6 · LO 4 — Kallmann Syndrome FA · BnB
A 17-year-old boy presents with delayed puberty. He has not reached Tanner 2. Testicular volume is 3 mL. He also reports being unable to smell — tested formally with olfactory discrimination cards: severely impaired. Labs: FSH 1.2, LH 0.8, testosterone 80 ng/dL. MRI: absent olfactory bulbs.
AKlinefelter syndrome (47,XXY)
BKallmann syndrome — failed migration of GnRH neurons
CConstitutional delay of growth and puberty
DProlactinoma
EPrimary testicular failure
B — Kallmann. Classic triad: anosmia + delayed puberty + absent olfactory bulbs. GnRH neurons normally migrate from olfactory placode → hypothalamus during embryogenesis; KAL1 (X-linked) or FGFR1 mutations disrupt this → GnRH deficient → low LH/FSH → low T (hypogonadotropic hypogonadism). Contrast Klinefelter (A): primary testicular failure → LH/FSH HIGH. Tx: pulsatile GnRH pump (restores fertility), or hCG + FSH; testosterone for virilization alone.
Step 1 Traps: each statement is TRUE or FALSE. Many reverse facts or mix up similar concepts.
Trap 01 · LO 1 — Sheehan Blood Supply In House · BnB 5.02
"In Sheehan syndrome, the posterior pituitary infarcts before the anterior pituitary because it has higher metabolic demand."
FALSE — reversed. The ANTERIOR pituitary is vulnerable in Sheehan. Pregnancy-induced lactotrope hypertrophy outstrips the low-pressure hypophyseal portal blood supply → ischemic necrosis of AP. The POSTERIOR pituitary has a different blood supply (hypophyseal arteries) and is spared.
Trap 02 · LO 4 — Prolactinoma Treatment In House · FA 3.04
"D2 agonists like cabergoline INCREASE prolactin secretion, making them ideal for lactation induction."
Trap 03 · LO 6 — Ectopic ACTH & High-Dose Dex FA · BnB
"Ectopic ACTH-secreting tumors suppress cortisol with HIGH-dose dexamethasone because the pituitary-adrenal axis retains feedback sensitivity."
FALSE. Ectopic ACTH sources (SCLC, carcinoid) are FEEDBACK-INDEPENDENT — they don't suppress even at high dex doses. HIGH-dose dex suppression is the SIGNATURE of pituitary Cushing disease (retained partial sensitivity). Neither low nor high dex suppresses ectopic ACTH.
Trap 04 · LO 3 — Hormone Replacement Order In House · FA
"In a patient with pituitary apoplexy and panhypopituitarism, levothyroxine should be started immediately, before steroid replacement."
FALSE. Always cortisol BEFORE T4. Thyroid hormone accelerates cortisol clearance — giving T4 first in an ACTH-deficient patient can precipitate adrenal crisis. Start IV hydrocortisone empirically when acute adrenal insufficiency is possible (apoplexy, Sheehan, acute hypopituitarism).
Trap 05 · LO 4 — Stalk Section & Prolactin In House
"Complete pituitary stalk transection causes all six anterior pituitary hormones — including prolactin — to fall precipitously."
FALSE — PRL is the exception. Prolactin is under TONIC DOPAMINE INHIBITION. Cutting the stalk removes dopamine → PRL RISES. All five other AP hormones (TSH, ACTH, FSH, LH, GH) fall because they lose their positive hypothalamic releasing hormones. Mnemonic: stalk section = everything down EXCEPT PRL.
Trap 06 · LO 4 — DDAVP Test Bootcamp 2.04
"Desmopressin significantly raises urine osmolality in both central and nephrogenic DI, so the test cannot distinguish them."
FALSE — it does distinguish. Central DI = ADH deficient → kidney V2 receptors are normal → DDAVP works → urine osm rises >50%. Nephrogenic DI = ADH adequate but V2/AQP2 broken → DDAVP does NOT raise urine osm. This is THE bedside test for telling them apart.
Trap 07 · LO 5 — LH Surge Driver In House · FA
"The LH surge that triggers ovulation is caused by rising progesterone levels exerting positive feedback on GnRH/LH."
FALSE. The mid-cycle LH surge is driven by rising ESTRADIOL (from the dominant follicle) switching from negative to POSITIVE feedback on GnRH/LH. Progesterone rises AFTER ovulation (from the corpus luteum) and restores negative feedback. Don't confuse cause (estradiol) with consequence (progesterone post-ovulation).
Trap 08 · LO 2 — Osmoreceptor Location In House
"Because the hypothalamus lies above the blood-brain barrier, all its neurons can directly sense plasma sodium levels."
FALSE. Most of the hypothalamus IS behind the BBB. Osmoreceptors are localized to circumventricular organs — especially the OVLT — which lack BBB and CAN directly sense plasma osmolarity. OVLT projects back to SON/PVN → ADH release + thirst. Damage to this specific region causes adipsic DI (loss of thirst drive + ADH).
Trap 09 · LO 6 — Adrenal Medulla & ACTH In House
"A patient with panhypopituitarism from Sheehan syndrome will be unable to produce epinephrine in response to stress because their ACTH-driven adrenal output has failed."
FALSE. ACTH controls the adrenal CORTEX (cortisol, aldosterone, androgens) — NOT the MEDULLA. The adrenal medulla is a modified sympathetic ganglion, innervated directly by preganglionic sympathetic fibers. Sheehan abolishes cortisol but catecholamine release from chromaffin cells is PRESERVED. This separation explains why Addisonian/hypopit patients get hypoglycemia + hypotension but maintain tachycardic stress response.
Trap 10 · LO 5 — Continuous GnRH Direction In House · FA
"Continuous GnRH agonist therapy INCREASES LH and FSH throughout treatment because it is the opposite of a GnRH antagonist."
FALSE. Continuous GnRH agonism causes an INITIAL LH/FSH surge ("flare"), but within ~2 weeks it DOWN-REGULATES GnRH receptors on gonadotropes → LH/FSH fall to castrate levels. Pulsatility is required for stimulation — continuous agonism is effectively suppressive (medical castration). Antagonists (degarelix) block receptors directly, no flare.
Trap 11 · LO 3 — Stain Reversal FA 2.01
"Anterior pituitary basophils secrete GH and prolactin; acidophils secrete FSH, LH, ACTH, and TSH."
FALSE — reversed.Acidophils = GH + PRL. Basophils = B-FLAT = FSH, LH, ACTH, TSH. Easy memory: acidophils are the "2" (GH, PRL); basophils cover the "4" (FLAT).
Trap 12 · LO 1 — Rathke's Pouch FA · Bootcamp 3.01
"Rathke's pouch gives rise to the posterior pituitary (neurohypophysis), while the anterior pituitary arises from neuroectoderm."
FALSE — reversed.Rathke's pouch (oral ectoderm) → ANTERIOR pituitary (adenohypophysis) + pars intermedia. Neuroectoderm of diencephalon → POSTERIOR pituitary (neurohypophysis). Remnants of Rathke's pouch cysts give rise to craniopharyngioma.
Trap 13 · LO 4 — Oxytocin Neuropeptide In House
"Oxytocin functions only in the uterus (labor) and breast (milk let-down); it has no CNS effects."
FALSE. Beyond classical uterine contraction and milk let-down, oxytocin acts as a CNS neuropeptide influencing pair bonding, social recognition, memory, anxiety, and appetite. Active research as therapy for autism spectrum, social anxiety, and postpartum depression (efficacy uncertain).
Trap 14 · LO 6 — Kallmann Pattern FA · BnB
"A 17-year-old with anosmia and delayed puberty has LH/FSH HIGH and testosterone LOW (primary testicular failure)."
FALSE — inverted. Kallmann = HYPOGONADOTROPIC hypogonadism. GnRH-neuron migration failure → low GnRH → LOW LH/FSH → LOW T. Contrast with Klinefelter (primary testicular failure) → HIGH LH/FSH. Anosmia is the telltale — olfactory bulbs share embryologic origin with GnRH-producing neurons.
Matching drills: click an item on the left then its match on the right. Four drills: hypothalamic nucleus → hormone, cell type → AP hormone, hypothalamic hormone → target, pituitary disease → mechanism.
Drill 1 · LO 2 — Hypothalamic Nucleus → Principal Hormone
From the in-house lecture's hypothalamic-nucleus map.
Postpartum hemorrhage → ischemic necrosis of hypertrophied anterior pituitary
Loss of ADH-producing SON/PVN neurons or axons via stalk
Autonomous PRL secretion escaping tonic dopamine D2 inhibition
Score: 0/6 correct
Clinical correlates + HY testing notes: signature H-P diseases and testing patterns that connect each LO to mapped 3rd-party Step 1 content. Click Expand for mechanism.
LO 4 · Lactotrope Bootcamp 3.06 · FA 3.04 · BnB 5.02
Prolactinoma — Medical Therapy First
Functional pituitary adenoma from lactotropes. Classic female: amenorrhea + galactorrhea + infertility. Classic male: hypogonadism + mass effect. PRL typically >200 ng/mL. First-line treatment is medical (cabergoline / bromocriptine) — unique among pituitary adenomas.
Why medical first: PRL is the only AP hormone under tonic dopamine inhibition (LO 4). D2 agonists mimic dopamine → shrink tumor AND normalize PRL in >80%. Surgery reserved for drug-intolerant, drug-resistant, or vision-threatening cases. Hook effect: extremely high PRL may saturate immunoassay → falsely low reading; dilute sample. Differentials for ↑PRL: prolactinoma (PRL >200), stalk effect (mild ↑ from non-functioning mass compressing stalk), primary hypothyroidism (↑TRH → ↑PRL), D2-antagonist drugs (antipsychotics, metoclopramide).
LO 4 · Somatotrope Bootcamp 3.04 · FA 3.02 · BnB 5.02
Acromegaly & Gigantism — GH Excess
Somatotrope adenoma → autonomous GH → IGF-1 excess. In adults (closed epiphyses) → acromegaly: jaw/brow enlargement, hands/feet growth, carpal tunnel, sleep apnea, diabetes, cardiomyopathy. In children (open epiphyses) → gigantism.
Screening: IGF-1 (GH is pulsatile; random GH unreliable). Confirmation: OGTT — normal GH suppresses with glucose; acromegaly does NOT. Treatment: transsphenoidal surgery first line. Adjuncts: • Octreotide / lanreotide — somatostatin analogs → ↓GH • Cabergoline — D2 agonist adjunct • Pegvisomant — GH-receptor antagonist (refractory disease) GH signals via JAK2-STAT5; diabetogenic effects result from direct GH action (anti-insulin) + IGF-1 independent pathways.
LO 3 · AP Blood Supply BnB 5.02 · FA 4.03 · Bootcamp 3.07
Sheehan Syndrome — Postpartum Panhypopituitarism
Postpartum hemorrhage → hypotension → ischemic necrosis of the lactotrope-hypertrophied anterior pituitary. First sign: failure to lactate. Progressive AP failure over weeks-years.
Why AP is vulnerable: pregnancy doubles lactotrope mass, outstripping the low-pressure hypophyseal portal blood supply. Hemorrhage precipitates infarction. Order of symptom emergence: PRL (lactation failure) → FSH/LH (amenorrhea) → GH (fatigue) → TSH (hypothyroidism) → ACTH (adrenal insufficiency — can be life-threatening). Posterior pituitary SPARED — different blood supply (hypophyseal arteries, not portal). Treatment: replace deficient hormones; cortisol BEFORE T4.
LO 3 · Acute Sellar Emergency BnB 5.02 · FA · Bootcamp 3.07
Pituitary Apoplexy — Steroids First
Sudden hemorrhage or infarction within a pre-existing pituitary adenoma. Thunderclap headache + visual loss + ocular paresis + altered mental status. Life-threatening if adrenal crisis ensues.
Pathophysiology: pituitary adenoma outgrows its blood supply OR hemorrhages into itself → sudden expansion in the rigid sella → compression of optic chiasm (bitemporal hemianopia) + cavernous sinus (CN III, IV, V1-2, VI) + stalk. Labs: acute secondary adrenal insufficiency (hypotension, hypoglycemia, hyponatremia). MRI: hemorrhagic sellar mass with suprasellar extension. IMMEDIATE:IV hydrocortisone 100 mg empirically (life-saving), THEN imaging/surgery for vision threat. Transsphenoidal decompression indicated for vision-threatening compression. Never give T4 before cortisol.
LO 3 · Suprasellar Mass Bootcamp 3.01 · FA · BnB 5.02
Craniopharyngioma — Rathke's Pouch Remnant
Benign but locally aggressive tumor from Rathke's pouch remnants. Bimodal age: children and older adults. Classic child presentation: growth failure + visual loss + polyuria.
Origin: same oral ectoderm that gives rise to the adenohypophysis → adamantinomatous craniopharyngioma (children) or papillary (adults). Imaging: calcified suprasellar mass with cystic components containing "motor-oil" cholesterol-rich fluid — pathognomonic. Clinical cascade: (1) AP failure → GH deficiency (growth failure) + FSH/LH deficiency (delayed puberty); (2) chiasmal compression → bitemporal hemianopia; (3) stalk/posterior pituitary involvement → central DI; (4) hypothalamic compression → temperature regulation, obesity. Treatment: surgical resection ± radiation. High recurrence.
LO 4 · Posterior Pituitary Bootcamp 2.04 · FA 4.02 · In-House Anki
Diabetes Insipidus — Central vs Nephrogenic
Insufficient water reabsorption at collecting duct → polyuria (>3 L/day), dilute urine, polydipsia, hypernatremia. Central DI = ADH deficient. Nephrogenic DI = ADH effective signal failure at kidney.
Central DI causes: pituitary surgery, trauma, tumor (craniopharyngioma, germinoma), autoimmune hypophysitis, idiopathic. Nephrogenic DI causes: V2-R mutation (X-linked), AQP2 mutation (AR), lithium, demeclocycline, hypercalcemia, hypokalemia. Diagnosis: water deprivation test — failure to concentrate urine → DI confirmed. Desmopressin challenge — central responds (urine osm ↑>50%); nephrogenic does NOT. Treatment: • Central: desmopressin (V2 agonist; also nasal, PO). • Nephrogenic: stop offending drug; paradoxical HCTZ + low-salt diet; amiloride (for lithium). Triphasic post-surgical DI: early DI → SIADH (days 5-10) → permanent DI.
LO 4 · Posterior Pituitary Bootcamp 2.03 · FA 4.01 · In-House Anki
SIADH — Euvolemic Hyponatremia
Inappropriate (excess) ADH → water retention → dilutional hyponatremia with inappropriately concentrated urine. Patient appears clinically euvolemic.
Labs: hyponatremia (<135), serum osm LOW, urine osm HIGH (inappropriately concentrated), urine Na⁺ >40. BUN and uric acid LOW (dilution). Common causes: SCLC (ectopic ADH), CNS disease (stroke, trauma, meningitis), pulmonary disease (pneumonia), drugs (SSRIs, carbamazepine, cyclophosphamide, NSAIDs), postop, HIV, pain/nausea. Treatment: • First line — fluid restriction. • Chronic — salt tablets ± loop diuretic. • Vaptans (tolvaptan, conivaptan — V2 antagonists) for resistant cases. • Severe/symptomatic (seizures) — hypertonic saline, but correct slowly (<0.5 mEq/L/hr) to avoid central pontine myelinolysis.
LO 4 · GnRH FA 3.01 · BnB 5.01 · In-House Anki
Kallmann Syndrome — Migration Defect
Hypogonadotropic hypogonadism + anosmia + absent olfactory bulbs. GnRH-producing neurons fail to migrate from the olfactory placode into the hypothalamus during embryogenesis.
Genetics: KAL1 (X-linked, Anosmin-1), FGFR1 (AD), PROKR2, CHD7, others. Clinical: delayed/absent puberty, microphallus, cryptorchidism, infertility, anosmia (usually noticed only when asked). Labs: LOW LH, LOW FSH, LOW T/E2 — hypogonadotropic hypogonadism. Distinguishes from Klinefelter (HIGH LH/FSH, primary testicular failure). Imaging: MRI shows absent olfactory bulbs. Treatment: pulsatile GnRH pump (restores fertility) OR hCG + FSH; testosterone/estrogen for virilization only (no fertility needed).
LO 5 · Ovarian Cycle In House · FA 3.01 · Physeo 6.02
The LH Surge — Positive Feedback Physiology
Mid-cycle ovulation is driven by the mid-cycle LH surge. The surge is generated when sustained high estradiol SWITCHES from negative to POSITIVE feedback on GnRH/LH — a rare example of positive feedback in the endocrine system.
Phase-by-phase: • Early follicular — low E2, modest FSH, negative feedback dominant. • Mid/late follicular — dominant follicle produces rising E2; above a threshold (~200 pg/mL for 48 hours), feedback switches sign. • Pre-ovulatory — sustained high E2 drives GnRH pulse frequency up AND increases pituitary gonadotrope sensitivity → massive LH surge (+ smaller FSH surge). • LH surge triggers ovulation within ~24–36 hours. • After ovulation — corpus luteum secretes progesterone → restores negative feedback; estrogen also drops. Self-terminating: ovulation removes the high-E2 source, preventing runaway. Clinical: continuous exogenous estrogen (OCPs) prevents the LH surge (maintains negative feedback) → contraception.
LO 5 · Pulsatility FA · Physeo 6.02 · BnB 5.01
Leuprolide Flare — The Pulsatility Principle in Clinical Practice
Leuprolide is a GnRH agonist used for prostate cancer, endometriosis, and central precocious puberty. Continuous administration initially STIMULATES (flare) then SUPPRESSES LH/FSH via receptor down-regulation.
Flare phenomenon (first 1–2 weeks): continuous GnRH agonism → initial LH/FSH surge → testosterone/estradiol spike. In prostate cancer this causes pain crisis / urinary retention / spinal cord compression risk. Co-administer bicalutamide (AR antagonist) during the flare window. Suppression (week 3+): sustained agonism → GnRH-receptor down-regulation + desensitization on gonadotropes → LH/FSH fall → castrate T in ~2 weeks. Alternative:GnRH ANTAGONISTS (degarelix, cetrorelix) block receptors directly with no flare — more expensive but no need for anti-androgen cover. Directly illustrates the LO 5 principle that pulsatility matters: continuous agonism is effectively suppressive.
High-Yield Testing Notes
Pattern-matching, buzzwords, and axis rules that recur on Step 1 for LOs 1–6.
Buzzword → Diagnosis Pattern Bank
"Bitemporal hemianopia + headache + ↑PRL": Prolactinoma (or stalk effect from non-functioning macroadenoma) (LO 4). "Calcified suprasellar mass + motor-oil cyst in a child": Craniopharyngioma (LO 3). "Postpartum hemorrhage + failure to lactate": Sheehan syndrome (LO 3). "Thunderclap headache + visual loss + pituitary mass": Pituitary apoplexy (LO 3/4). "Jaw enlargement + carpal tunnel + sleep apnea": Acromegaly (LO 4). "Moon facies + striae + low-dose dex fails": Cushing → check ACTH + high-dose dex (LO 5/6). "Smoker + hyperpigmentation + dex non-suppressible": Ectopic ACTH (SCLC) (LO 6). "Polyuria + hypernatremia post-pituitary-surgery": Central DI (LO 4). "Delayed puberty + anosmia": Kallmann syndrome (LO 4). "Flat / empty pituitary on MRI": Empty sella syndrome (LO 3). "Euvolemic hyponatremia + concentrated urine": SIADH (LO 4).
Rules of the H-P Axis High-Yield
Steroids before thyroid: in panhypopituitarism, always give cortisol BEFORE T4 (T4 accelerates cortisol clearance). PRL is the exception: only AP hormone under tonic INHIBITION → stalk section RAISES it; all other AP hormones fall. Pulsatile GnRH matters: continuous GnRH agonism = receptor downregulation (medical castration). Pulsatile = stimulation (fertility). Posterior pituitary is spared in Sheehan: different blood supply (hypophyseal arteries, not portal system). Hook effect: extremely high PRL may read FALSELY LOW — dilute sample. High-dose dex SUPPRESSES Cushing disease, NOT ectopic ACTH or adrenal sources. Taper steroids: >3 weeks of supraphysiologic dosing suppresses HPA — abrupt stop = crisis. Triphasic post-op DI: DI (days 0-5) → transient SIADH (days 5-10) → permanent DI.
Mnemonics Memory Hooks
B-FLAT (basophils): FSH, LH, ACTH, TSH. Acidophils do 2: GH, Prolactin. SON / PVN → posterior: nonapeptides (ADH + oxytocin). "PRL loves TRH, hates dopamine": TRH stimulates, dopamine inhibits PRL. Three output pathways: Portal → AP · Axons → PP · Sympathetic → adrenal medulla. "Ultra-short = ME ME ME": hypothalamic hormone inhibits ITSELF → pulsatility. Rathke's pouch (oral ectoderm) = ANTERIOR; neuroectoderm = POSTERIOR.
Trap Corner Common Errors
Do NOT reverse: PRL goes UP (not down) with stalk section. Do NOT reverse: acidophils = GH + PRL; basophils = other 4 (FLAT). Do NOT reverse: Rathke's pouch = anterior (oral ectoderm); neuroectoderm = posterior. Do NOT confuse: Kallmann (low LH/FSH, GnRH migration defect) with hypergonadotropic hypogonadism (Klinefelter, Turner — gonadal failure with HIGH LH/FSH). Do NOT confuse: SIADH (euvolemic, dilute plasma, concentrated urine) with cerebral salt wasting (volume-depleted). Do NOT confuse: low-dose dex fails = "Cushing present"; high-dose dex fails = "ectopic or adrenal source." Do NOT confuse: adrenal medulla is innervated directly by SNS — Sheehan does NOT abolish epinephrine response.
Hypothalamic Nuclei & Hormones (quick map)
Nucleus
Hormone(s)
Pituitary Effect
Memory Hook
Supraoptic (SON)
ADH (primary); some oxytocin
Posterior → water retention
"SON keeps you dry"
Paraventricular (PVN)
Oxytocin (primary); CRH, TRH, some ADH
Posterior + AP releasing hormones
"PVN = many jobs"
Arcuate
Dopamine (PIH)
↓ Prolactin (tonic)
"Arc → dope → no milk"
Periventricular
Somatostatin (GHIH)
↓ GH and ↓ TSH
"Peri = stop GH"
Ventromedial
GHRH
↑ GH
"Ventro = grow"
Medial preoptic
GnRH (pulsatile)
↑ FSH + LH
"Pre-optic = puberty"
Dorsomedial
GnIH (8-AA peptide)
↓ FSH + LH
"Dorsal = damper"
In-house slide note: "Don't memorize" the exact nucleus names for exams, but know the SON/PVN → posterior (nonapeptides) and arcuate → dopamine rules, plus the functional categories.