Eduovisual
Endocrine
Hypopituitarism: workup and replacement
— Mass effect: pituitary adenoma, craniopharyngioma, Rathke cleft cyst, meningioma, metastasis (breast, lung)
— Iatrogenic: transsphenoidal surgery, sellar radiation (deficits emerge years later)
— Vascular: Sheehan syndrome (postpartum hemorrhage with failure to lactate), pituitary apoplexy (sudden headache + ophthalmoplegia + visual loss)
— Infiltrative/inflammatory: lymphocytic hypophysitis (peripartum, anti–CTLA-4/anti–PD-1 checkpoint inhibitors), sarcoidosis, hemochromatosis, IgG4 disease, Langerhans histiocytosis
— Traumatic: moderate–severe TBI, subarachnoid hemorrhage
— Congenital: PROP1, POU1F1 mutations; empty sella
— Chronic fatigue + hypotension + hyponatremia in a postpartum woman who never lactated
— Patient on ipilimumab/nivolumab with new headache, fatigue, low Na, low cortisol
— Post–pituitary surgery patient with polyuria + hypernatremia (central DI) or weight gain + cold intolerance
— Adult with bitemporal hemianopsia, decreased libido, amenorrhea, or short stature in a child
Board pearl: Always check and replace cortisol BEFORE thyroid hormone — giving levothyroxine first accelerates cortisol clearance and can precipitate adrenal crisis. This is among the most-tested Step 3 management traps in the endocrine section.
— Fatigue, weight loss, anorexia, nausea, postural lightheadedness
— Hyponatremia (euvolemic, SIADH-like from loss of cortisol's suppression of ADH)
— No hyperkalemia and no hyperpigmentation (aldosterone preserved; no ACTH/MSH excess) — this is the central vs primary distinction
— Crisis triggered by infection, surgery, steroid taper
— Cold intolerance, constipation, weight gain, bradycardia, dry skin
— TSH is low or inappropriately normal with low free T4 — never trust TSH alone here
— Women: oligo/amenorrhea, hot flashes, infertility, dyspareunia, low libido, osteoporosis
— Men: decreased libido, erectile dysfunction, loss of morning erections, decreased shaving frequency, gynecomastia, infertility, low energy
— Central adiposity, decreased lean mass, dyslipidemia, reduced QoL, low exercise tolerance, osteopenia
— Postpartum hemorrhage, transfusion requirements
— Prior sellar surgery or cranial radiation (dose, years out)
— Head trauma, especially with LOC
— Checkpoint inhibitor or opioid use (opioids suppress HPG and HPA axes)
— Family history of pituitary tumors (MEN1)
Key distinction: Primary adrenal insufficiency → hyperpigmentation + hyperkalemia + hyponatremia; secondary (pituitary) → hyponatremia only, skin pale. Same fatigue, very different lab signature on the exam.
— Pale, fine wrinkled "alabaster" skin (loss of MSH/androgen effect)
— Decreased axillary and pubic hair (loss of adrenal androgens and gonadotropins)
— Sarcopenia, central adiposity in chronic GH deficiency
— Children: proportionate short stature, delayed puberty, midline defects (cleft palate, single central incisor → suspect congenital hypopit)
— Orthostatic hypotension and resting tachycardia (cortisol deficiency)
— Bradycardia, hypothermia (central hypothyroidism)
— In apoplexy: hypotension out of proportion, may be shock-level
— Volume status: typically euvolemic; hypovolemic shock suggests apoplexy or concurrent illness
— Bitemporal hemianopsia from optic chiasm compression — confront fields; if abnormal → urgent MRI
— Cranial nerves III, IV, VI, V1, V2 traverse the cavernous sinus → ophthalmoplegia, ptosis, facial sensory loss in apoplexy or invasive macroadenoma
— Papilledema is uncommon (sella is below the suprasellar cistern)
— Testicular atrophy, small/soft testes in long-standing hypogonadism
— Vaginal atrophy, breast atrophy in women
— Galactorrhea suggests hyperprolactinemia from stalk compression
— SBP <90 despite fluids, AMS, hypoglycemia, hyponatremia <125, hypothermia → myxedema + adrenal crisis overlap is the classic Step 3 trap
— Glucose <60: hypoglycemia from cortisol and GH deficiency, especially in children
— Sudden severe headache + diplopia + visual loss = pituitary apoplexy — neurosurgical emergency
CCS pearl: On a hypotensive patient with suspected hypopit, simultaneously order IV hydrocortisone 100 mg, draw a cortisol and ACTH, normal saline bolus, dextrose if hypoglycemic, and an MRI of the pituitary. Do not wait for the cortisol result to treat empirically.
— Cortisol + ACTH (cortisol <3 µg/dL with low/normal ACTH = central AI; 3–15 indeterminate → stimulation test; >15–18 essentially excludes AI)
— Free T4 + TSH (low free T4 with low/normal TSH = central hypothyroidism — never diagnose central hypothyroidism on TSH alone)
— LH, FSH, total testosterone (men, 8 AM) or estradiol (women) — low gonadal steroid with low/normal gonadotropins is central
— Prolactin — low in Sheehan; mildly elevated (<150 ng/mL) suggests stalk effect from compression; >200 suggests prolactinoma
— IGF-1 as screen for GH deficiency (age- and sex-adjusted)
— Basic chemistry: Na (hyponatremia common), glucose, BUN/Cr
— CBC: normocytic anemia is common
— In suspected DI: serum Na, serum and urine osmolality, urine specific gravity
— MRI pituitary with and without gadolinium, dedicated sellar protocol — the test of choice for any biochemical hypopituitarism
— CT only if MRI contraindicated or for acute apoplexy hemorrhage detail
— Look for: macroadenoma (>10 mm), microadenoma, empty sella, stalk thickening (hypophysitis, sarcoid), Rathke cleft cyst, suprasellar mass (craniopharyngioma — calcifications in a child)
Board pearl: A morning cortisol >15 µg/dL essentially rules out adrenal insufficiency; <3 rules it in; the 3–15 zone needs cosyntropin stimulation. In acute central AI (<2 weeks post-pituitary insult), the adrenals haven't atrophied yet, so cosyntropin can give a falsely normal response — use insulin tolerance or metyrapone instead.
— Standard-dose (250 µg) cosyntropin stimulation: Cortisol <18 µg/dL at 30 or 60 min = AI. Reliable for chronic central AI (atrophied adrenals fail to respond).
— Insulin tolerance test (ITT): Gold standard for both ACTH and GH axes. Induce glucose <40; cortisol should rise >18, GH should rise >5 ng/mL. Contraindicated in CAD, seizure disorder, elderly.
— Metyrapone test: Blocks 11β-hydroxylase; intact axis raises 11-deoxycortisol >7 µg/dL. Useful when ITT contraindicated.
— Random GH is useless (pulsatile). Use IGF-1 as screen.
— Confirm with provocative testing: ITT, glucagon stimulation, or macimorelin (oral ghrelin agonist, FDA-approved). Diagnose adult GHD only with ≥3 other pituitary deficiencies + low IGF-1 without provocative test (high pretest probability).
— Men: low 8 AM total testosterone confirmed on a second morning sample, with inappropriately low/normal LH/FSH. Check SHBG and free T if borderline.
— Women premenopausal: low estradiol with low/normal FSH and amenorrhea. Postmenopausal women should have FSH >30; a postmenopausal woman with a "normal" FSH has central hypogonadism until proven otherwise.
— Water deprivation test: urine osm fails to concentrate (<300); after desmopressin, urine osm rises >50% (central) vs <50% (nephrogenic).
— Copeptin (surrogate for ADH) after hypertonic saline is replacing classical testing where available.
— Stalk thickening → ACE, calcium, chest CT (sarcoid), β-hCG/AFP (germinoma in young patients), IgG4
— Apoplexy → coags, platelets, type and screen for OR
Step 3 management: When ordering a cosyntropin test, do not give hydrocortisone in the 24 hours before (it cross-reacts on cortisol assays); dexamethasone is acceptable as cover because it does not.
— Emergent (admit, ICU consideration): pituitary apoplexy, adrenal crisis, myxedema coma, severe hyponatremia <125 with symptoms, DI with hypernatremia and altered access to water
— Urgent (admit or rapid clinic): new biochemical panhypopituitarism, macroadenoma with visual field defect, postoperative DI
— Outpatient: stable chronic deficiencies, isolated GH or gonadotropin deficiency without red flags
— 1. Glucocorticoid first (always, if any doubt about cortisol)
— 2. Levothyroxine only after glucocorticoid is on board
— 3. Sex steroids once cortisol/thyroid stable
— 4. GH last, after other axes optimized
— 5. Desmopressin as needed for confirmed DI (and watch for unmasking after steroid replacement — cortisol is required for free water excretion, so DI may emerge only after starting hydrocortisone)
— Prolactinoma (even macro): medical first — cabergoline (preferred) or bromocriptine. Surgery only if dopamine agonist intolerant, resistant, or apoplexy with visual loss.
— Other pituitary tumors with mass effect, visual compromise, or hormonal hypersecretion (GH, ACTH): transsphenoidal surgery is first-line.
— Incidentaloma <10 mm, no hormonal excess, no mass effect: observe with MRI at 6–12 mo, then yearly × 3, then less frequently.
— Medical alert bracelet
— Sick-day stress-dose steroid rules (covered in chunk 15)
— Injectable hydrocortisone kit at home
Board pearl: A patient with a macroprolactinoma and visual field cut typically does NOT go to surgery first — start cabergoline; tumors usually shrink within weeks and vision improves. This counterintuitive pattern is a frequent Step 3 distractor.
— Hydrocortisone 15–20 mg/day PO, divided (10 mg AM, 5 mg early afternoon) to mimic diurnal rhythm; or prednisone 3–5 mg daily
— Avoid dexamethasone for chronic replacement (long half-life, no diurnal flexibility, harder to dose-adjust)
— No mineralocorticoid needed in central AI (aldosterone is RAAS-regulated and intact) — key distinction from Addison disease, which requires fludrocortisone
— Monitor clinically: weight, BP, energy, signs of over-replacement (weight gain, hyperglycemia, osteoporosis). No reliable lab — do not chase ACTH (it's already suppressed) and 24-hr urinary cortisol does not validate hydrocortisone replacement well.
— Levothyroxine 1.6 µg/kg/day in healthy adults; start lower (25–50 µg) in elderly or CAD
— Target: free T4 in the upper half of the reference range. Do NOT titrate to TSH — TSH is unreliable in central hypothyroidism.
— Re-check 6 weeks after dose change
— Testosterone (gel, IM enanthate/cypionate, undecanoate, or transdermal patch) — target mid-normal total T, monitor hematocrit (<54%), PSA, lipids
— Contraindicated in active prostate or breast cancer, untreated severe OSA, polycythemia, recent MI, desire for fertility (use gonadotropins/hCG + FSH instead)
— Premenopausal: combined estrogen + progestin (oral, patch, or vaginal ring) until age of natural menopause (~50–51); progestin required if uterus is present
— Fertility desired: pulsatile GnRH or gonadotropin therapy
Step 3 management: When initiating levothyroxine in an older patient with possible undiagnosed adrenal insufficiency, give hydrocortisone first or empirically cover — failure to do so causing adrenal crisis is a very common exam vignette and a real medicolegal event.
— Indications: macroadenoma with visual compromise, hormone-hypersecreting tumor (acromegaly, Cushing, TSHoma), most non-prolactin tumors >10 mm, apoplexy with neurologic deficits, dopamine agonist–resistant or intolerant prolactinomas
— Endoscopic endonasal approach is now standard
— Pre-op: stress-dose hydrocortisone (50–100 mg IV at induction, then 50 mg q8h tapering); baseline visual fields and hormones; MRI; cardiac clearance as indicated
— Q2h urine output, q6h serum Na, daily I/O for DI (often transient, occasionally triphasic: DI → SIADH at days 5–10 → permanent DI)
— Cortisol POD 1–3 to assess axis; if <5–10 µg/dL, continue hydrocortisone and reassess in 4–6 weeks
— Post-op precautions: no nose blowing, no straws, no positive-pressure ventilation if avoidable; head of bed elevated
— Watch for CSF rhinorrhea (test for β-2 transferrin), meningitis, epistaxis, and visual deterioration
— Immediate IV hydrocortisone 100 mg, fluids, correct electrolytes
— Urgent neurosurgical and ophthalmology consult
— Surgical decompression if visual loss, decreased mental status, or worsening ophthalmoplegia; otherwise selected cases managed conservatively with close monitoring
— Reserved for residual or recurrent tumors after surgery, especially aggressive secretory tumors
— Conventional fractionated or stereotactic radiosurgery (Gamma Knife) — latter for small, well-defined residuals
— Long-term consequence: progressive hypopituitarism (50%+ at 10 years) — these patients need lifelong annual axis screening
— Dopamine agonist for prolactinomas (non-surgical, see chunk 6)
— Somatostatin analogs (octreotide, lanreotide) and GH-receptor antagonists (pegvisomant) for acromegaly
— Pasireotide, ketoconazole, osilodrostat, metyrapone for Cushing disease
CCS pearl: After TSS, the very first electrolyte derangement you'll see is hypernatremia + dilute polyuria (DI) within 24–48 hours. Reflexively order strict I/Os, q6h Na, and have desmopressin available — and don't be surprised by SIADH about a week later.
— Symptoms (fatigue, weight loss, cognitive slowing, low libido) overlap with normal aging — under-recognized
— Start levothyroxine low (12.5–25 µg/day) and titrate slowly every 6 weeks; rapid replacement can precipitate atrial fibrillation, angina, or MI
— Lower hydrocortisone dose (15 mg total daily) — older adults are more sensitive to glucocorticoid side effects (osteoporosis, hyperglycemia, skin atrophy)
— Testosterone replacement requires especially careful CV risk assessment, hematocrit, prostate exam, PSA
— GH replacement: more side effects (edema, arthralgia, insulin resistance); use only with clear indication and lower starting dose (0.1–0.2 mg/day)
— Elderly hypopituitary patients have markedly increased fracture risk from hypogonadism, GH deficiency, and over-replacement of glucocorticoid/thyroid
— DXA at baseline and every 1–2 years; vitamin D, calcium, weight-bearing exercise; bisphosphonate when indicated
— Levothyroxine: no dose adjustment, but reassess as nephrotic syndrome can cause increased thyroid hormone loss → may need higher doses
— Hydrocortisone: no significant adjustment
— Desmopressin: risk of hyponatremia — start lower, monitor Na closely; avoid in CKD with fluid restriction issues
— Testosterone: monitor more closely for erythrocytosis (CKD already alters EPO physiology)
— Reduced cortisol-binding globulin synthesis → falsely low total cortisol; use free cortisol or salivary cortisol if available
— Levothyroxine metabolism slowed — same dose, longer steady state
— Oral estrogens contraindicated in significant liver disease (use transdermal estradiol)
— IGF-1 reduced from hepatic dysfunction independently — interpret GHD testing cautiously
Board pearl: In an elderly patient with new AF and recent dose increase of levothyroxine, back off the dose rather than just rate-controlling — iatrogenic thyrotoxicosis is reversible and avoidable. This is the classic "what would you do next" Step 3 stem.
— Hydrocortisone: Increase dose by ~50% in 2nd–3rd trimester due to rising CBG and cortisol clearance; stress dose in labor (hydrocortisone 100 mg IV at active labor onset, then q8h, taper postpartum)
— Levothyroxine: Demand rises ~30% early — increase by 25–30% as soon as pregnancy confirmed (some endocrinologists add 2 extra weekly doses immediately); target free T4 in upper half of trimester-specific range
— Desmopressin: Safe in pregnancy; placental vasopressinase increases ADH degradation, so dose may need to rise
— Gonadotropin therapy may be needed for ovulation induction in central hypogonadism
— Sheehan syndrome: Postpartum hemorrhage with hypotension → pituitary infarction. Hallmark: failure to lactate, then amenorrhea, fatigue, hyponatremia. Diagnose with MRI (empty sella later) + axis testing. Lifelong replacement.
— Lymphocytic hypophysitis: Peripartum (late pregnancy or early postpartum); stalk thickening on MRI; ACTH most commonly affected first; consider biopsy if diagnosis unclear
— Short stature is the cardinal presentation of childhood GHD; check IGF-1, IGFBP-3, bone age, and provocative GH testing (arginine, clonidine, glucagon)
— Congenital midline defects (septo-optic dysplasia, holoprosencephaly, cleft lip/palate, single central incisor) → suspect congenital hypopit
— Hypoglycemia + microphallus + prolonged jaundice in a newborn is congenital hypopituitarism until proven otherwise
— Delayed/absent puberty → check LH, FSH, sex steroids; differentiate constitutional delay from permanent hypogonadotropic hypogonadism (Kallmann — anosmia + low LH/FSH)
— Dose hydrocortisone 8–10 mg/m²/day in children — lower per kg than adults — to preserve growth
— Sex steroid replacement timed to match physiologic puberty with gradually escalating doses to allow normal growth spurt and bone accrual
Step 3 management: A pregnant patient on chronic levothyroxine who calls reporting a positive home test → increase levothyroxine immediately by 25–30% and check TSH/free T4; don't wait for the first OB visit.
— Triggered by infection, surgery, trauma, missed doses, GI illness, untreated hyperthyroidism
— Presents with hypotension refractory to fluids, AMS, hyponatremia, hypoglycemia, abdominal pain mimicking acute abdomen
— Treatment: immediate IV hydrocortisone 100 mg, normal saline, dextrose, treat underlying trigger
— Mortality 6% per crisis; lifetime risk in chronic AI patients is 50%+
— Severe untreated central hypothyroidism, often with concurrent adrenal insufficiency
— Hypothermia, bradycardia, hyponatremia, hypoventilation, AMS
— Treatment: IV hydrocortisone first, then IV levothyroxine 200–400 µg load + T3, warming, ventilatory support
— Central obesity, dyslipidemia, hypertension, insulin resistance, accelerated atherosclerosis — particularly in untreated GHD
— Standardized mortality ratio ~1.5–2× general population, driven by CV deaths
— Fatigue, low mood, decreased exercise tolerance, cognitive complaints — significantly improved with adequate replacement
— Over-replacement of cortisol → iatrogenic Cushing, osteoporosis, weight gain, hyperglycemia
— Over-replacement of levothyroxine → AF, bone loss, anxiety
— Testosterone → erythrocytosis, OSA worsening, infertility, prostate issues
— Desmopressin → hyponatremia (especially with concurrent water intake)
— GH → carpal tunnel, edema, glucose intolerance, intracranial hypertension
Key distinction: Adrenal crisis in primary AI features prominent hyperkalemia, acidosis, and hyperpigmentation; central AI crisis lacks these — but is equally lethal and still demands stress-dose hydrocortisone. Do not be reassured by a normal K+.
— Suspected pituitary apoplexy (sudden severe headache + ophthalmoplegia or visual loss)
— Adrenal crisis (hypotension, AMS, hypoglycemia, severe hyponatremia)
— Myxedema coma (hypothermia, AMS, hypoventilation)
— New visual field defect from sellar mass
— Severe hyponatremia (<125) or hypernatremia (>150) with symptoms
— Postoperative DI/SIADH with fluctuating Na
— Hemodynamic instability requiring vasopressors after stress-dose steroids
— Airway compromise (myxedema)
— Status epilepticus from severe hyponatremia or hypoglycemia
— Postop pituitary patient with deteriorating mental status, CSF leak with meningitis, or refractory Na derangements
— Endocrinology: every newly diagnosed hypopituitarism, replacement initiation, complex axis testing, pregnancy planning
— Neurosurgery: any sellar mass with mass effect, secretory tumor, apoplexy, suspected craniopharyngioma
— Neuro-ophthalmology / ophthalmology: baseline and follow-up visual fields and OCT
— Radiation oncology: residual/recurrent tumors after surgery
— Obstetrics + MFM: pregnant patients on multi-axis replacement
— Cardiology: elderly initiating levothyroxine with known CAD; testosterone candidates with CV risk
— Patient is hemodynamically stable
— Na, glucose, and vitals are normal
— Patient understands sick-day rules and has emergency hydrocortisone access
— Reliable follow-up within 2–4 weeks established
CCS pearl: A patient calling from home with vomiting and dizziness on chronic hydrocortisone replacement should be told to double the oral dose and come to the ED if unable to keep it down within 1 hour — escalation to IM/SC hydrocortisone 100 mg at home before EMS arrival can be lifesaving and should be in every action plan.
— Distinguishing features: hyperpigmentation, hyperkalemia, metabolic acidosis, high ACTH, requires fludrocortisone
— Etiology: autoimmune adrenalitis (most common in US), TB (worldwide), bilateral hemorrhage (Waterhouse-Friderichsen, antiphospholipid), metastases
— Cosyntropin stim: cortisol fails to rise in BOTH primary and chronic secondary, but ACTH levels diverge
— High TSH + low free T4 vs central pattern of low/normal TSH + low free T4
— Hashimoto thyroiditis with positive anti-TPO antibodies; usually no other axis involvement
— Men: low T + high LH/FSH (Klinefelter, mumps orchitis, chemo, radiation, testicular trauma)
— Women: premature ovarian insufficiency with high FSH and low estradiol before age 40
— Pituitary axis fully intact — gonadotropins are appropriately elevated
— Mild elevation (<100 ng/mL) — stalk effect from any sellar mass, medications (antipsychotics, antiemetics, SSRIs, opioids, verapamil), hypothyroidism, renal failure, pregnancy
— Marked elevation (>200) — almost always prolactinoma
— Always check TSH, β-hCG, BUN/Cr, and medication list before imaging
— APS-1 (AIRE mutation): chronic mucocutaneous candidiasis + hypoparathyroidism + adrenal insufficiency
— APS-2: Addison + autoimmune thyroid + type 1 DM — far more common in adults
— Iatrogenic Cushing from supraphysiologic hydrocortisone is identifiable by exam findings + history; tapering replacement resolves it
Key distinction: Always pair the target-organ hormone with the pituitary hormone in the same blood draw. The single most diagnostic move in any "low cortisol/T4/T/E2" stem is what is the ACTH/TSH/LH-FSH doing simultaneously? Low or inappropriately normal = pituitary problem until proven otherwise.
— Overlap with hypogonadism, GHD, mild central hypothyroidism in presentation (fatigue, low libido, anhedonia, weight changes)
— Differentiate with biochemistry; treat the endocrine deficit, but co-manage mood disorder
— Critically ill patients have low T3, sometimes low T4, low/normal TSH — looks like central hypothyroidism
— Do not start levothyroxine in ICU patients with non-thyroidal illness — recheck after recovery
— Same caution with cortisol (acutely elevated in illness, returns to baseline)
— Amenorrhea with low LH/FSH/estradiol; normal MRI
— Reversible with weight restoration; treat underlying disorder rather than chronic estrogen replacement when possible (though estrogen for bone protection is considered)
— Low T3, mildly low cortisol can mimic hypopit
— Chronic opioids suppress HPA and HPG axes (opioid-induced androgen and cortisol deficiency)
— Chronic glucocorticoid use (oral, inhaled, topical, intra-articular) → tertiary adrenal suppression — treat as central AI with taper and stress dosing
— Megestrol — glucocorticoid-like activity, can cause adrenal suppression
— Checkpoint inhibitors — ipilimumab >> nivolumab for hypophysitis; pembrolizumab more often causes thyroid issues
— Antipsychotics, metoclopramide — hyperprolactinemia mimicking pituitary disease
— Iron deposition in pituitary causes hypogonadotropic hypogonadism (often the first clinical manifestation); also affects liver, pancreas, heart, joints
— Screen with ferritin and transferrin saturation in any "unexplained" hypogonadism, especially in men with arthropathy or LFT abnormalities
— Tuberculosis, syphilis, fungal infections can infiltrate pituitary
— Sarcoidosis and Langerhans histiocytosis — stalk thickening, DI often the first finding
Board pearl: In any patient on chronic opioids with fatigue, low libido, ED, and amenorrhea, check morning cortisol, total testosterone, LH/FSH — opioid-induced endocrinopathy is widely under-diagnosed and frequently appears on Step 3.
— Hydrocortisone 10 mg AM + 5 mg early afternoon (or 15+5; or prednisone 4–5 mg daily)
— Levothyroxine at body-weight–appropriate dose, target free T4 mid-upper reference
— Testosterone in men or estrogen + progestin in women — to age of natural menopause
— Desmopressin for confirmed DI, lowest effective dose
— GH in adults with documented severe deficiency + symptoms — shared decision-making (cost, injection burden)
— Minor illness, fever, vomiting once: double or triple the hydrocortisone dose for 2–3 days
— Persistent vomiting, severe illness, surgery: IM/SC hydrocortisone 100 mg at home, then go to ED
— Major surgery: IV hydrocortisone 100 mg at induction, then 50 mg q8h × 24 h, taper over 2–3 days
— Dental procedure / colonoscopy: double dose morning of procedure
— DXA at baseline and every 1–2 years
— Calcium 1000–1200 mg/d (diet preferred), vitamin D to maintain 25-OH-D >30 ng/mL
— Weight-bearing exercise
— Bisphosphonate if T-score ≤ –2.5 or fracture
— Lipid panel annually; statin per ASCVD risk
— BP control to <130/80
— Smoking cessation, diet, exercise counseling
— Diabetes screening yearly (HbA1c) given metabolic effects
Step 3 management: At every visit, explicitly re-teach sick-day rules and verify the patient has an unexpired hydrocortisone injection kit at home. This single counseling action is the highest-yield secondary prevention intervention in chronic adrenal insufficiency.
— Initial titration phase: visits every 4–8 weeks until each axis is optimized
— Stable maintenance: every 6 months, then annually
— Post-TSS or post-radiation: at 6 weeks, 3 months, then every 6–12 months indefinitely (radiation-induced hypopit may emerge decades later)
— Pregnancy: monthly endocrinology + MFM co-management
— Cortisol replacement: No reliable biochemical target; assess clinically — symptoms, weight, BP, glucose, signs of Cushingoid changes
— Levothyroxine: Free T4 every 6–8 weeks during titration; annually when stable. TSH is meaningless in central hypothyroidism — do not chase it.
— Testosterone: Total T 2–4 weeks after starting, target mid-normal. Check hematocrit at 3 and 6 months then annually (stop if Hct >54%), PSA in men >40, lipids
— Estrogen: Clinical symptom relief, breast exam, mammography per screening guidelines
— GH: IGF-1 every 6 weeks during titration; annually maintenance; glucose/HbA1c, lipids
— Desmopressin: Na every 1–2 weeks during titration; periodic Na and symptom check thereafter
— Macroadenoma after TSS: MRI at 3 months, 1 year, then yearly × 5, then less frequently
— Microincidentaloma observed: MRI at 6–12 months; if stable and non-secretory, extend interval
— Visual fields whenever tumor abuts chiasm
— Sick-day rules (verify understanding each visit)
— Fertility planning and reproductive options
— Bone health and falls prevention
— Cardiovascular risk modification
— Medication adherence — missed doses of hydrocortisone are the #1 cause of crisis
— Mental health screening (depression and anxiety are common)
— Driving and occupational considerations during initial titration
Board pearl: In central hypothyroidism, a suppressed TSH on levothyroxine does NOT indicate over-replacement — titrate to free T4 in the upper half of normal. Cutting the dose because of a low TSH is a common but incorrect step that exam writers love to test.
— Patients need explicit discussion of lifelong dependence, sick-day rules, and crisis risk
— Testosterone counseling must include infertility risk (suppression of spermatogenesis) — critical for younger men; consider sperm banking or alternative gonadotropin therapy if fertility desired
— GH replacement: discuss cost (often >$10,000/year), injection burden, theoretical malignancy/recurrence concerns — shared decision-making is essential
— ED triage error is the most common patient safety event in chronic AI — missed crisis, delayed steroid administration. Solution: medical alert bracelet, wallet card, and standardized hospital order sets.
— Inpatient-to-outpatient transition: Ensure discharge medications include a clear hydrocortisone taper schedule and stress-dose plan written for the patient
— Surgical scheduling: Pre-op communication with anesthesia and surgical team about stress dosing — missed perioperative steroids cause preventable crises
— Pharmacy errors: Hydrocortisone (replacement) confused with hydrochlorothiazide (HCTZ) or hydrocodone in handwritten or verbal orders — use full names and confirm
— No specific reporting requirement for hypopituitarism, but TB-associated pituitary disease triggers TB reporting
— Driving: Patients with active visual field defects from sellar tumors may not meet state vision standards — counsel and document
— Hypoglycemia from cortisol/GH deficiency may impair driving — assess
— GH therapy in idiopathic short stature without true GHD raises ethical questions about treating non-disease; insurance often denies; engage families in informed shared decision-making
— Assent of older children/adolescents for chronic injectable therapy
— Acute adrenal crisis or myxedema coma → patient lacks capacity; treat under implied/emergency consent, document, involve surrogate ASAP
— Chronic glucocorticoid dependence can affect mood and cognition; periodically reassess capacity for complex medical decisions
Step 3 management: When a hypopituitary patient is admitted under another service (surgery, OB, ortho), personally communicate the stress-dose steroid plan to the primary team and document it in the chart and on the med rec — this transition-of-care intervention prevents the most common preventable death in this population.
Key distinction: Pituitary apoplexy presents with thunderclap headache that mimics subarachnoid hemorrhage — but MRI/CT shows hemorrhage in the sella, not subarachnoid space. Add it to your headache differential.
"A 32-year-old woman presents 6 months postpartum with fatigue, cold intolerance, amenorrhea, and inability to breastfeed her infant. She had a postpartum hemorrhage requiring 4 units PRBC..."
→ Answer: check morning cortisol, free T4, TSH, prolactin, LH/FSH; MRI pituitary; start hydrocortisone first, then levothyroxine
"A patient with newly diagnosed panhypopituitarism is started on levothyroxine. Two days later, he presents with hypotension and altered mental status..."
→ Answer: adrenal crisis precipitated by starting thyroid hormone without cortisol coverage; treat with IV hydrocortisone
"A 55-year-old man with a known pituitary macroadenoma presents with sudden severe headache, diplopia, and decreased visual acuity. BP 85/50..."
→ Answer: IV hydrocortisone 100 mg STAT, IV fluids, urgent MRI, neurosurgery consult
"A patient with hypopituitarism on levothyroxine has TSH <0.01 and free T4 in upper-normal range. Next step?"
→ Answer: continue current dose — TSH is unreliable in central disease
"Patient with bitemporal hemianopsia and prolactin 850 ng/mL. Best next step?"
→ Answer: start cabergoline, monitor visual fields and prolactin; surgery only if intolerant/resistant
"POD 1 from transsphenoidal surgery, urine output 400 mL/hr, urine SG 1.002, serum Na 148..."
→ Answer: central DI; give desmopressin, strict I/O, q4–6h Na
"Patient on ipilimumab for melanoma develops fatigue, headache, low Na, low cortisol, low ACTH..."
→ Answer: immune-related hypophysitis; start hydrocortisone (with high-dose steroids if mass effect), continue checkpoint inhibitor cautiously per oncology
"Patient with chronic AI develops gastroenteritis, takes usual hydrocortisone, presents with hypotension..."
→ Answer: failure to stress-dose; IV hydrocortisone now, educate
"45-year-old man with arthropathy, fatigue, low T, low LH/FSH, elevated LFTs..."
→ Answer: check ferritin and transferrin saturation; HFE mutation analysis
"Patient with central hypothyroidism on stable levothyroxine reports positive pregnancy test..."
→ Answer: increase dose by 25–30% immediately, recheck free T4 in 4 weeks
Board pearl: The exam loves the "two-step" management question — first stabilize hemodynamics with hydrocortisone + fluids, then pursue diagnostic confirmation. If a question offers "obtain MRI" vs "start IV hydrocortisone" in an unstable patient — choose hydrocortisone first.
Hypopituitarism is the loss of one or more pituitary hormones — diagnose by pairing each target-organ hormone with its pituitary counterpart in a morning blood draw, image the sella with MRI, and replace deficient axes in the correct order: glucocorticoid ALWAYS before thyroid, then sex steroids, then GH, with desmopressin for DI — and counsel every patient on sick-day stress dosing and emergency injectable hydrocortisone for life.
Step 3 management: Treat first, test second when unstable — empiric IV hydrocortisone saves lives, never confirmatory MRI.