Eduovisual
Endocrine
Thyroiditis: subacute, postpartum, and silent
— Subacute (de Quervain, granulomatous): post-viral, painful tender goiter, fever, elevated ESR/CRP, often follows URI by 2–8 weeks.
— Postpartum thyroiditis: occurs within 12 months of delivery or pregnancy loss, painless, autoimmune (TPO Ab+), affects ~5–10% of postpartum women.
— Silent (painless, sporadic) thyroiditis: autoimmune, non-pregnant patient, identical biochemistry to postpartum, often after immune perturbation (e.g., interferon, lithium, amiodarone, checkpoint inhibitors).
— Thyrotoxic symptoms (palpitations, heat intolerance, tremor, weight loss) without ophthalmopathy or pretibial myxedema.
— Low radioactive iodine uptake (RAIU) distinguishes thyroiditis from Graves'/toxic nodular disease.
— Recent pregnancy, recent viral illness, recent immunomodulator exposure, or new ICI initiation.
Board pearl: A thyrotoxic patient with a tender thyroid, high ESR, and low RAIU = subacute thyroiditis until proven otherwise — treat with NSAIDs, not methimazole.
Key distinction: Graves' = high uptake (gland overproducing); thyroiditis = low uptake (gland leaking stored hormone). This single data point reroutes therapy.
Step 3 management: In ambulatory practice, document the phase (thyrotoxic vs hypothyroid vs recovery), counsel on the expected timeline (weeks to ~12 months), and schedule TSH every 4–8 weeks to catch the hypothyroid transition before symptoms drive an ED visit.
— Preceded by viral URI (coxsackie, mumps, adenovirus, EBV, SARS-CoV-2).
— Anterior neck pain radiating to jaw/ear, low-grade fever, malaise, dysphagia.
— Symptoms peak over days, last 2–8 weeks in thyrotoxic phase.
— Peak incidence: women 30–50, HLA-B*35 association.
— Onset typically 1–6 months postpartum; thyrotoxic phase often missed because mistaken for "new-mom fatigue reversal" or anxiety.
— Hypothyroid phase 4–8 months postpartum — classic stem: fatigue, cold intolerance, depression, poor lactation, weight gain at 6 months postpartum.
— Risk factors: TPO Ab positivity in pregnancy (up to 50% develop PPT), type 1 diabetes (3× risk), prior PPT (~70% recurrence).
— Same biochemistry, no pain, no pregnancy link.
— Triggers: lithium, amiodarone, interferon-α, IL-2, checkpoint inhibitors (pembrolizumab, nivolumab), tyrosine kinase inhibitors.
— Often discovered on routine TSH monitoring.
— Recent delivery or miscarriage → PPT.
— Recent viral illness + neck pain → subacute.
— New oncology drug + abnormal TSH → ICI-induced silent thyroiditis.
— Family/personal autoimmune history (T1DM, vitiligo, celiac) → favors autoimmune (silent/PPT) over subacute.
Board pearl: A woman 4 months postpartum with palpitations and tremor, no neck pain, and low RAIU → postpartum thyroiditis in thyrotoxic phase — give propranolol, not methimazole.
Step 3 management: In any patient starting amiodarone, lithium, or a checkpoint inhibitor, document a baseline TSH and schedule recheck at 6–12 weeks; failing to do so is a classic Step 3 patient-safety gap that the question stem will punish.
— Exquisitely tender, firm, often asymmetric goiter; pain on swallowing or neck rotation.
— Low-grade fever (37.5–38.5°C), tachycardia, fine tremor, warm moist skin during thyrotoxic phase.
— No bruit, no ophthalmopathy (helps exclude Graves').
— Painless, small, firm, non-tender goiter (or normal-sized gland).
— Thyrotoxic phase: mild tachycardia, lid lag possible but no proptosis, brisk reflexes.
— Hypothyroid phase: dry skin, delayed relaxation of DTRs ("hung-up" reflex), bradycardia, periorbital puffiness, mood changes.
— Resting HR, BP, presence of AF (esp. >60 yo) — atrial fibrillation occurs in ~10–15% of thyrotoxic patients.
— Volume status: weight loss, orthostatics.
— Screen for high-output heart failure in elderly: JVD, S3, peripheral edema with warm extremities.
— Graves': diffusely enlarged gland with bruit, ophthalmopathy, pretibial myxedema, acropachy.
— Toxic multinodular goiter: nodular gland, no pain, no eye disease.
— Suppurative thyroiditis: unilateral fluctuance, overlying erythema, high fever, systemic toxicity — surgical/ID consult.
Key distinction: Tender thyroid = subacute; painless thyroid + recent pregnancy = postpartum; painless thyroid + drug trigger = silent; bruit + eye disease = Graves'. This four-way exam triage answers most Step 3 thyroid stems.
Step 3 management: In any thyrotoxic patient age >60 or with palpitations, obtain an ECG at the visit to identify AF — anticoagulation decision (CHA₂DS₂-VASc) hinges on this, and the boards reward catching subclinical AF before discharge from the outpatient encounter.
— TSH (suppressed in thyrotoxic phase, elevated in hypothyroid phase).
— Free T4 and total T3 (T4 typically rises more than T3 in thyroiditis because the gland leaks stored hormone with a normal T4:T3 ratio, unlike Graves' where T3 synthesis predominates → T3:T4 ratio helps differentiate).
— TPO antibodies: positive in postpartum and silent (~80%), usually negative or low in subacute.
— TRAb / TSI: negative in thyroiditis, positive in Graves' — order when uptake scan cannot be done (e.g., pregnant, breastfeeding).
— ESR and CRP: markedly elevated (ESR often >50–100) in subacute; normal in silent/postpartum.
— CBC: mild leukocytosis possible in subacute; otherwise unremarkable.
— Beta-hCG in any reproductive-age woman before imaging or RAIU.
— LFTs and glucose if starting beta-blocker or considering steroids.
— Lipids and CK if hypothyroid phase confirmed (statin myopathy risk).
— Low TSH + high FT4 + low T3:T4 ratio + high ESR → subacute.
— Low TSH + high FT4 + TPO+ + postpartum window → PPT.
— Low TSH + high FT4 + TPO+ + drug trigger → silent.
— <20 suggests thyroiditis (preformed hormone leak).
— >20 suggests Graves' or toxic nodule (active synthesis favors T3).
Board pearl: ESR >50 + tender thyroid + suppressed TSH = subacute thyroiditis; you do not need a scan to start NSAIDs.
Step 3 management: Always document a pregnancy test before ordering radioactive iodine uptake — this is a recurring Step 3 patient-safety vignette where the wrong answer is "order RAIU" in a woman of reproductive age without ruling out pregnancy.
— Low/absent uptake (<5% at 24 h) = thyroiditis (any subtype), exogenous thyroid hormone ingestion, or recent iodine load.
— Diffusely elevated uptake = Graves'.
— Focal hot nodule(s) = toxic adenoma or toxic multinodular goiter.
— Contraindicated in pregnancy and breastfeeding (must stop nursing).
— Subacute: hypoechoic, ill-defined areas, decreased vascularity.
— Graves': diffusely enlarged with markedly increased vascularity ("thyroid inferno").
— Useful when RAIU unavailable or contraindicated (pregnancy, lactation, iodine-loaded patients).
— Elevated in thyroiditis (leak from damaged follicles).
— Low/undetectable in factitious thyrotoxicosis (exogenous levothyroxine ingestion) — both have low RAIU, so thyroglobulin separates them.
— Not routine; reserved for atypical persistent nodules or to exclude suppurative thyroiditis or malignancy mimicking subacute pain.
— Pregnant/lactating thyrotoxic patient: skip RAIU, use TRAb + ultrasound to distinguish Graves' from postpartum/silent thyroiditis.
— Amiodarone-induced thyrotoxicosis (AIT): ultrasound Doppler differentiates type 1 (increased vascularity, underlying nodular disease, treat with methimazole) vs type 2 (destructive thyroiditis, low vascularity, treat with prednisone).
Key distinction: Low RAIU + high thyroglobulin = thyroiditis; low RAIU + low thyroglobulin = exogenous hormone ingestion (think eating-disorder patient or surreptitious weight-loss use).
Step 3 management: In a lactating postpartum woman with thyrotoxicosis, order TRAb and ultrasound rather than RAIU; if she insists on a scan, Tc-99m pertechnetate with 24-hour interruption of breastfeeding is the safer alternative — a frequent CCS-style branching point.
— Thyrotoxic phase (weeks 0–8): symptomatic control only; no antithyroid drugs (the gland is not overproducing, methimazole won't help).
— Euthyroid phase: monitor.
— Hypothyroid phase (weeks 8–24): treat with levothyroxine if symptomatic or TSH >10, otherwise observe and recheck.
— Recovery phase: confirm with TSH at 6–12 months.
— Subacute: ~5–15% permanent.
— Postpartum: ~20–40% permanent at 5–10 years, especially with high TPO titers or severe hypothyroid phase.
— Silent: ~20% permanent; recurrence common with re-exposure to trigger.
— Severe pain in subacute → escalate from NSAIDs to prednisone 40 mg daily, tapered over 4–6 weeks.
— Atrial fibrillation in thyrotoxic phase → rate control with beta-blocker, anticoagulation per CHA₂DS₂-VASc (do not assume reversibility excuses anticoagulation if score qualifies).
— Pregnant patient → endocrine consult, avoid radioactive isotopes, careful drug selection.
— Checkpoint-inhibitor thyroiditis → continue ICI (thyroid irAEs rarely require holding), treat symptomatically; replace thyroid hormone in hypothyroid phase.
Board pearl: Do not prescribe methimazole or PTU for thyroiditis — the gland is leaking, not synthesizing. Picking an antithyroid drug is a high-yield Step 3 trap.
Step 3 management: Build the longitudinal plan at the index visit: TSH at 4–6 weeks, then every 6–8 weeks through the phases, with explicit instructions on when to call (worsening palpitations, weight gain, depression, lactation problems) — closing the loop is the CCS-style win.
— Beta-blockers: propranolol 10–40 mg PO q6–8h (also inhibits peripheral T4→T3 conversion) or atenolol 25–50 mg daily.
— Indication: HR >90, palpitations, tremor, anxiety.
— Avoid in asthma/severe COPD (use cardioselective or CCB alternative).
— No antithyroid drugs (methimazole/PTU are ineffective — these block synthesis, not release).
— First line: NSAIDs (ibuprofen 600–800 mg q8h or naproxen 500 mg BID) for 2–4 weeks.
— Refractory or severe pain/fever: prednisone 40 mg PO daily × 1–2 weeks, taper over 4–6 weeks.
— Response to steroids is rapid (within 24–48 h) — failure to improve should prompt reassessment.
— Treat with levothyroxine if: TSH >10, symptomatic, planning pregnancy, or lactating.
— Dose: 1.6 μg/kg/day in young healthy; start 25–50 μg in elderly or CAD.
— Recheck TSH in 6 weeks, titrate to TSH 0.5–2.5.
— Plan a withdrawal trial at 6–12 months in PPT and silent thyroiditis to identify those with permanent disease vs recovery.
— Aspirin in thyrotoxic phase — displaces T4 from TBG, can worsen thyrotoxicosis. NSAIDs other than ASA are fine for pain.
— Iodinated contrast — can prolong or worsen thyrotoxicosis.
— Amiodarone — perpetuates the cycle if it was the trigger.
Board pearl: In subacute thyroiditis, NSAIDs first, steroids if severe; in all thyroiditis-induced thyrotoxicosis, propranolol for symptoms, never methimazole.
Step 3 management: When starting levothyroxine in a postpartum woman who is breastfeeding, reassure that levothyroxine is safe in lactation and titrate to TSH 0.5–2.5 — undertreatment risks postpartum depression and impaired milk supply.
— Prednisone 40 mg daily × 1–2 weeks → taper by 5–10 mg/week over 4–6 weeks.
— Indications: severe subacute pain, type 2 amiodarone-induced thyroiditis, ICI-related thyroiditis with severe symptoms (rare; usually self-limited).
— Counsel on glycemic effects, bone protection if course extended, adrenal suppression with abrupt cessation.
— Type 1 (Jod-Basedow on nodular gland): methimazole 20–40 mg daily ± potassium perchlorate.
— Type 2 (destructive thyroiditis): prednisone 40 mg daily.
— Mixed cases: both. Decision to discontinue amiodarone is individualized (cardiology co-management).
— Most common endocrine irAE (~10% on anti–PD-1; up to 20% combination therapy).
— Brief thyrotoxic phase → permanent hypothyroidism in majority.
— Continue ICI; treat hypothyroidism with levothyroxine.
— Distinguish from hypophysitis (more common with ipilimumab): low TSH with low FT4 and other pituitary axis deficits → MRI pituitary, replace cortisol before levothyroxine.
— Monitor TSH at baseline, then every 3–6 months.
— Lithium can cause hypothyroidism, goiter, or silent thyroiditis; usually does not require lithium discontinuation if psychiatrically indicated — add levothyroxine.
— In a thyrotoxic patient with thyroiditis, avoid elective iodinated contrast for 4–6 weeks if possible.
CCS pearl: For suspected ICI hypophysitis vs primary thyroiditis: order AM cortisol, ACTH, LH/FSH, prolactin, IGF-1, and pituitary MRI before reflexively prescribing levothyroxine — giving thyroid hormone to a cortisol-deficient patient can precipitate adrenal crisis.
Step 3 management: Always replace glucocorticoids before levothyroxine in any patient with suspected combined adrenal and thyroid insufficiency — a perennially tested sequencing question.
— Thyrotoxicosis may present apathetically: weight loss, depression, atrial fibrillation, heart failure — without classic adrenergic symptoms.
— Higher baseline cardiovascular risk → lower threshold for beta-blockade and AF anticoagulation.
— Start levothyroxine at 12.5–25 μg/day, titrate every 6–8 weeks; goal TSH 0.5–4.0 (higher TSH acceptable in age >70 to avoid AF and osteoporosis from over-replacement).
— Watch for subclinical hyperthyroidism during overshoot — increases fracture and AF risk.
— Beta-blocker choice: atenolol requires dose reduction in CKD (renally cleared); metoprolol or propranolol preferred when GFR <30.
— NSAIDs for subacute: avoid or limit in CKD stage ≥3, HF, or volume depletion — use acetaminophen + short steroid course instead.
— Levothyroxine dosing unchanged in CKD, but ESRD patients absorb erratically — separate from phosphate binders and sevelamer by 4 h.
— Propranolol undergoes hepatic metabolism — reduce dose in cirrhosis.
— Avoid prolonged NSAIDs in cirrhosis (variceal bleed, hepatorenal risk).
— Steroids relatively safe but worsen ascites and glycemic control.
— Reconcile levothyroxine absorption interferences: calcium, iron, PPIs, sucralfate, bile acid sequestrants — take levothyroxine 30–60 min before breakfast, separate from other meds by 4 h.
Board pearl: New-onset AF in an elderly patient with weight loss and depression — check TSH; apathetic thyrotoxicosis from thyroiditis or Graves' is a classic miss.
Step 3 management: When starting levothyroxine in an elderly patient with CAD, start 12.5–25 μg/day and uptitrate slowly to avoid precipitating angina or MI — rapid replacement is a tested patient-safety error.
— Thyrotoxicosis in first trimester is more often gestational transient thyrotoxicosis (hCG-mediated) than Graves' or thyroiditis; hyperemesis gravidarum is a clue.
— RAIU is contraindicated; use TRAb and ultrasound to differentiate.
— Postpartum thyroiditis can occur after miscarriage or termination, not just live birth — ask about all pregnancy outcomes within 12 months.
— Thyrotoxic phase: propranolol if symptomatic; safe in lactation (low milk transfer); avoid atenolol (higher milk levels).
— Hypothyroid phase: levothyroxine if symptomatic, TSH >10, breastfeeding, or planning another pregnancy.
— Trial off levothyroxine at 6–12 months unless planning pregnancy — about 20–40% will be permanently hypothyroid.
— Screen for PPT in any woman with postpartum depression, fatigue, or lactation failure — overlap is enormous and missed PPT prolongs symptoms.
— 70% recurrence risk with subsequent pregnancies — counsel preconception.
— TPO Ab+ women should have TSH checked in early pregnancy and at 6 weeks, 3 months, 6 months postpartum.
— Annual TSH lifelong even if recovered — high lifetime risk of permanent hypothyroidism.
— Subacute thyroiditis is uncommon in children; consider after viral illness with neck pain.
— Hashimoto's is the dominant pediatric thyroid pathology — distinguish by chronic course and persistent TPO+.
Board pearl: A woman 4 months postpartum presenting with "depression" — check TSH before starting an SSRI; missed hypothyroid-phase PPT is a recurring vignette.
Step 3 management: In any woman planning pregnancy with prior PPT or TPO+, target preconception TSH <2.5; this improves obstetric outcomes and is a high-yield ambulatory checkpoint.
— Most common long-term complication; rates: subacute ~5–15%, silent ~20%, PPT ~20–40% at 5–10 years.
— Risk factors: high TPO antibody titers, severe hypothyroid phase, multiparity (PPT), prior episodes.
— Atrial fibrillation (10–15%, higher in age >60) — anticoagulate by CHA₂DS₂-VASc.
— High-output heart failure, exacerbation of CAD, angina, MI.
— Sinus tachycardia without intervention rarely causes harm but is a marker of poor symptom control.
— Depression (especially postpartum), cognitive slowing, weight gain, hyperlipidemia, lactation failure.
— Myxedema coma is rare in thyroiditis-induced hypothyroidism (usually mild and transient).
— Severe pain (occasionally requiring steroids), dysphagia, rare airway compromise.
— Transient vocal cord issues from inflammation.
— PPT during the next pregnancy may unmask underlying autoimmune hypothyroidism — increased risk of miscarriage, preterm delivery, and impaired fetal neurodevelopment if untreated.
— Over-replacement with levothyroxine during a recovering hypothyroid phase → iatrogenic thyrotoxicosis, AF, osteoporosis. Always plan a withdrawal trial.
— Inappropriate methimazole prescribed for thyroiditis → drug-induced agranulocytosis or hepatotoxicity for no benefit.
— Missed Graves' disease mislabeled as thyroiditis → untreated thyrotoxicosis, thyroid storm risk.
Board pearl: Annual TSH lifelong after any thyroiditis — even "recovered" patients carry 2–4× lifetime risk of permanent hypothyroidism.
Step 3 management: Schedule a levothyroxine withdrawal trial at 6–12 months in PPT and silent thyroiditis; failure to do so leads to indefinite unnecessary therapy and is flagged as low-value care in value-based vignettes.
— Suspected thyroid storm (rare in thyroiditis but possible if severe leak): high fever, AMS, HR >140, HF, GI dysfunction — ICU admission, beta-blocker, steroids, supportive care; antithyroid drugs unhelpful since the gland is not synthesizing.
— Suppurative thyroiditis: high fever, fluctuant tender mass, leukocytosis — ENT/surgery and ID consult, IV antibiotics, drainage, look for pyriform sinus fistula in children (recurrent left-sided abscess).
— Severe pain unresponsive to NSAIDs → outpatient prednisone, rare admission.
— New AF with RVR, decompensated HF, ACS → inpatient rate/rhythm control, anticoagulation, cardiology consult.
— Myxedema coma (very rare in thyroiditis) → ICU, IV levothyroxine + hydrocortisone.
— Endocrinology: pregnancy with thyrotoxicosis, ICI-induced disease, amiodarone-induced thyrotoxicosis, diagnostic uncertainty, recurrence.
— Cardiology: AF, HF, ACS in thyrotoxic phase.
— OB: pregnant patient with thyrotoxicosis or PPT planning next pregnancy.
— Psychiatry: postpartum depression overlap, severe mood symptoms in hypothyroid phase.
— Stable vitals, oral intake intact, symptoms controlled with beta-blocker → outpatient.
— Hemodynamic instability, suspected storm, suppurative infection, severe cardiac decompensation → admit.
CCS pearl: In a CCS case with thyrotoxic patient + new AF + HR 140 + fever, do not order methimazole reflexively — verify uptake/labs first; if thyroiditis is the cause, the correct orders are propranolol IV, IV fluids, acetaminophen, cooling, and steroids.
Step 3 management: In suspected suppurative thyroiditis, order CT neck with contrast to evaluate for abscess and pyriform sinus fistula — missing the fistula leads to recurrence and is a tested ENT pitfall.
— Diffuse goiter with bruit, ophthalmopathy, pretibial myxedema.
— High RAIU, TRAb positive, T3:T4 ratio >20.
— Treat with methimazole, RAI, or surgery — not symptomatic only.
— Older patients, nodular gland.
— RAIU with focal hot spots; no eye disease.
— Definitive therapy: RAI or surgery.
— Chronic autoimmune hypothyroidism with TPO Ab+, firm bumpy goiter.
— Can have transient "Hashitoxicosis" — overlaps clinically with silent thyroiditis; differentiated by chronicity.
— Rare; rock-hard, fixed, fibrotic gland with compressive symptoms.
— Associated with IgG4-related disease and retroperitoneal fibrosis.
— Treat with tamoxifen, steroids, or rituximab; surgery for compression.
— Bacterial (S. aureus, strep) infection; unilateral fluctuant tender mass, fever.
— Antibiotics, drainage, evaluate for pyriform sinus fistula.
— Low RAIU + low thyroglobulin + history of OTC supplements or surreptitious use.
— Rare ovarian teratoma producing thyroid hormone — low neck uptake, high pelvic uptake on whole-body scan.
Key distinction: Tender + high ESR = subacute; painless + TPO+ + recent pregnancy = PPT; painless + drug trigger = silent; eye disease + bruit + high uptake = Graves'; nodular + focal uptake = toxic nodule; rock-hard fixed gland = Riedel.
Step 3 management: When RAIU is unavailable or contraindicated, use the TRAb + ultrasound Doppler algorithm: TRAb+ with hypervascular gland = Graves'; TRAb− with hypovascular gland = thyroiditis.
— Episodic palpitations, headache, sweating, hypertension.
— Normal TSH; elevated plasma/urine metanephrines.
— Palpitations, tremor, sweating but normal TSH — always check TSH before psychiatric label.
— Tachycardia, tremor, anxiety; normal TSH.
— Drug screen helpful.
— Tremor, tachycardia, agitation; history and timeline reveal etiology.
— Overlaps with PPT — check TSH before initiating SSRI in any postpartum woman with mood symptoms.
— Mimic the neck pain of subacute thyroiditis; exam localization and ultrasound distinguish.
— First-trimester thyrotoxicosis from high hCG; resolves by 14–18 weeks; supportive care.
— Fatigue, weight loss, hypotension; coexisting hypophysitis can produce central hypothyroidism (low TSH and low FT4).
— TSH-secreting adenoma (rare): high FT4 with inappropriately normal/high TSH.
Board pearl: Low TSH with low FT4 = central hypothyroidism (think pituitary, especially ipilimumab-induced hypophysitis), not primary thyroid disease — get an AM cortisol before replacing thyroid hormone.
Step 3 management: In any postpartum woman presenting with fatigue, depression, or "anxiety," include TSH, FT4, and TPO Ab in the workup — anchoring on psychiatric diagnosis without thyroid testing is a tested safety lapse.
— Annual TSH after any thyroiditis episode — recovered patients still have elevated risk of future permanent hypothyroidism.
— TPO Ab+ women: TSH every 6–12 months, more often in pregnancy.
— 70% recurrence with future pregnancies — preconception counseling.
— Check TSH at 6 weeks, 3 months, 6 months, 12 months postpartum in TPO+ women or those with prior PPT.
— Withdraw trial at 6–12 months post-hypothyroid phase except in women planning pregnancy or breastfeeding.
— Persistent TSH elevation 6–8 weeks after withdrawal = permanent hypothyroidism → resume therapy indefinitely.
— Target TSH 0.5–2.5 in young/pregnant; 0.5–4.0 in elderly.
— Amiodarone: TSH every 3–6 months.
— Lithium, interferon, IL-2, ICIs, TKIs: baseline TSH then every 4–12 weeks during therapy.
— Document recurrence risk; do not necessarily stop the offending drug if medically necessary.
— No specific dietary restrictions; iodine excess can re-trigger silent thyroiditis — caution with kelp/seaweed supplements.
— Smoking worsens Graves' ophthalmopathy but not thyroiditis per se — still counsel cessation.
— Bone health: assess in postmenopausal women with thyrotoxic phase or over-replacement.
Board pearl: A patient on chronic amiodarone with new TSH abnormality — do not stop amiodarone reflexively; characterize as type 1 vs type 2 and co-manage with cardiology and endocrinology.
Step 3 management: Build a problem list entry "history of thyroiditis — annual TSH" so it surfaces in every annual visit; this longitudinal continuity is the kind of ambulatory follow-up the Step 3 exam rewards.
— Initial diagnosis → recheck TSH, FT4 in 4–6 weeks to track phase transition.
— Through thyrotoxic and hypothyroid phases → TSH every 6–8 weeks.
— After recovery → TSH at 6 and 12 months, then annually.
— Thyrotoxic: HR, weight, sleep, tremor, mood, AF symptoms.
— Hypothyroid: fatigue, cold intolerance, constipation, weight, depression, cognition.
— Counsel when to call: palpitations, syncope, chest pain, significant weight change, severe depression, suicidal ideation, lactation failure.
— Beta-blocker users: HR, BP, exercise tolerance; taper off as symptoms resolve and TSH normalizes (usually 4–8 weeks).
— Levothyroxine users: TSH 6 weeks after each dose change; adjust by 12.5–25 μg increments.
— Postpartum: integrate thyroid follow-up with postpartum visit and well-child visits.
— Explain triphasic course with a written timeline to set expectations and prevent unnecessary ED visits.
— Levothyroxine administration: empty stomach, 30–60 min before food, separate from calcium, iron, PPIs, sevelamer by 4 hours.
— Reassure most patients recover fully; emphasize annual surveillance.
— Postpartum: PHQ-9 at each thyroid follow-up; thyroid abnormality may explain or coexist with PPD.
— Hypothyroid-phase depression often improves with levothyroxine alone — recheck mood 6–8 weeks after replacement.
Board pearl: Recheck TSH 6 weeks after any levothyroxine change — checking sooner gives misleading values because of T4's 7-day half-life.
Step 3 management: Document a shared decision-making conversation about levothyroxine withdrawal trial at 6–12 months — this is the kind of patient-engagement entry that anchors value-based Step 3 vignettes.
— RAI and RAIU are absolutely contraindicated in pregnancy; failure to obtain a documented pre-procedure pregnancy test in any reproductive-age woman is a sentinel safety event and a recurring Step 3 negligence vignette.
— Counsel post-RAI patients to avoid pregnancy for 6 months and breastfeeding entirely until isotope decay confirmed.
— Propranolol, atenolol (less ideal), methimazole ≤20 mg/day, PTU 300 mg/day, and levothyroxine are compatible with breastfeeding.
— Diagnostic radioisotopes require timed cessation — Tc-99m: ~24 h; I-131: stop nursing permanently for the current child.
— Steroid use in subacute thyroiditis — discuss glycemic, infection, and bone risks.
— Levothyroxine indefinite vs trial withdrawal — patient preference matters.
— Patients discharged after AF cardioversion in thyrotoxic phase must have explicit endocrinology follow-up and TSH check within 4–6 weeks — missed handoffs are a tested error.
— Medication reconciliation across OB, primary care, and endocrinology in PPT — duplicate or omitted levothyroxine prescriptions are a common error.
— When amiodarone, lithium, or ICI triggers thyroiditis, document the adverse drug reaction in the chart and notify the prescribing service; consider MedWatch reporting for newer agents.
— Not applicable directly to thyroiditis, but postpartum depression identified during evaluation may trigger maternal-mental-health referral and, in some states, structured screening reporting.
— Postpartum follow-up gaps disproportionately affect underinsured women — proactive scheduling improves outcomes.
Step 3 management: Before ordering RAIU in any reproductive-age woman, chart-document a same-day urine or serum hCG; this single safety step is repeatedly tested.
Board pearl: Tender thyroid + viral prodrome + high ESR = subacute thyroiditis; painless thyroid + recent baby = postpartum; painless thyroid + new oncology drug = silent thyroiditis. Three stems, three answers, one underlying mechanism.
Board pearl: When the stem hands you a low RAIU and a tender thyroid, the answer is never methimazole. When it hands you low RAIU and a postpartum patient, the answer is never methimazole either. The only thyrotoxic stems that get antithyroid drugs are high-uptake ones.
Step 3 management: Lead with the distinguishing data point (RAIU, T3:T4 ratio, TRAb, ESR, timing relative to pregnancy) before choosing therapy — Step 3 punishes premature treatment selection.
Thyroiditis — subacute, postpartum, and silent — is a self-limited triphasic destructive process (thyrotoxic → euthyroid → hypothyroid → recovery) characterized by low radioactive iodine uptake, treated with symptomatic beta-blockade in the thyrotoxic phase and levothyroxine in the hypothyroid phase when symptomatic, planning pregnancy, lactating, or TSH >10 — never with methimazole.
Board pearl: Three painless thyrotoxic patients walk into the clinic — one just delivered, one started pembrolizumab, one is on amiodarone — all three get propranolol, none get methimazole, and all three need a hypothyroid-phase plan and lifelong TSH surveillance.