Eduovisual
Pregnancy, Childbirth & Puerperium
Thyroid disease in pregnancy
— hCG cross-reacts with the TSH receptor → mild stimulation of thyroid, peaking late first trimester
— Estrogen ↑ thyroxine-binding globulin (TBG) → total T4/T3 rise ~1.5×; free hormone stays near normal
— Iodine requirements rise from 150 → 250 mcg/day (renal loss, fetal use, ↑ T4 production)
— Net effect: TSH is lower in pregnancy, especially T1; free T4 mildly higher early then normalizes
— T1: 0.1–4.0 mIU/L (ATA 2017; previously 2.5 upper limit, now relaxed)
— T2: 0.2–4.0; T3: 0.3–4.0
— Use assay/population-specific ranges if available; non-pregnant ranges misclassify many
— Hyperemesis gravidarum with weight loss, tachycardia, tremor → check TSH, free T4 (gestational transient thyrotoxicosis vs Graves)
— Fatigue, cold intolerance, constipation, goiter, dry skin → hypothyroidism
— Recurrent miscarriage, preterm delivery, fetal growth restriction, preeclampsia → screen TSH
— Personal/family hx autoimmune disease, T1DM, prior thyroid surgery, head/neck radiation, amiodarone/lithium use
— Goiter, neck nodule, or symptoms of pituitary dysfunction
— ATA/ACOG do not recommend universal screening
— Targeted screening (high-yield list): age >30, symptoms, goiter, TPO-Ab+, T1DM/autoimmune, prior thyroid disease, head/neck XRT, prior preterm/miscarriage, infertility, morbid obesity (BMI ≥40), amiodarone/lithium, iodine-deficient region, twin gestation
Board pearl: A low TSH with normal free T4 in T1 of a healthy-appearing woman is most often physiologic, not Graves — repeat in 4–6 weeks before treating. Differentiating physiology from disease anchors nearly every Step 3 stem on thyroid in pregnancy.
— TSH > upper trimester limit with low free T4, or TSH ≥10 regardless of free T4
— Symptoms: fatigue, weight gain beyond expected, cold intolerance, constipation, hair loss, depression, myalgia, carpal tunnel
— Pregnancy-specific clues: rising weight without edema explanation, persistent anemia despite iron, slow relaxation phase of reflexes
— TSH above trimester-specific upper limit, normal free T4
— Often asymptomatic — found on screening of high-risk patients
— Key distinction: TPO antibody status drives treatment thresholds (treat at lower TSH if TPO+)
— Suppressed TSH with elevated free T4/T3
— Heat intolerance, palpitations, tremor, anxiety, weight loss or failure to gain, hyperdefecation, lid lag, goiter, ophthalmopathy (Graves)
— Inappropriate tachycardia (>100) persisting after fluids in hyperemesis suggests true thyrotoxicosis
— Peaks 8–14 weeks, resolves by 14–18 weeks
— Hyperemesis gravidarum, molar pregnancy, multiple gestation
— No ophthalmopathy, no goiter, no TRAb, symptoms preceded by N/V — not Graves
— 1–6 months postpartum; classic triphasic: thyrotoxic → hypothyroid → euthyroid
— TPO+ before/during pregnancy is the strongest predictor
— Mistaken for postpartum depression or anxiety
— Prior thyroid disease, surgery, RAI; ATD use (methimazole exposure 6–10 wks = embryopathy window)
— Family hx of autoimmune thyroid disease
— Iodine intake, kelp/supplement use, amiodarone, lithium, biotin (assay interference)
— Prior pregnancy outcomes (loss, preterm, GDM, preeclampsia)
Step 3 management: When a woman on levothyroxine confirms pregnancy, empirically increase dose by ~25–30% (e.g., 2 extra tablets per week) and recheck TSH in 4 weeks — do not wait for symptoms or the next routine visit.
— Hypothyroid: periorbital puffiness, dry/coarse skin, brittle hair, macroglossia, hoarseness, slow speech
— Hyperthyroid: warm moist skin, fine tremor, hyperkinesis, weight inappropriate for gestational age
— Pregnancy can mimic both: palmar erythema, mild tachycardia, heat intolerance are physiologic
— Resting HR >100 persistently in T2–T3, especially after antiemetics and IVF, raises suspicion for thyrotoxicosis
— Wide pulse pressure, systolic flow murmur — physiologic in pregnancy but accentuated in hyperthyroidism
— Bradycardia and diastolic hypertension → hypothyroidism (uncommon presentation but classic)
— Diffuse non-tender goiter with bruit → Graves
— Tender goiter → subacute thyroiditis (rare in pregnancy)
— Painless firm goiter → Hashimoto
— Solitary nodule → ultrasound; FNA is safe in pregnancy for suspicious nodules
— Lid lag, proptosis, chemosis, restricted EOM → Graves orbitopathy (autoimmune, not from hyperthyroidism per se)
— Key distinction: Orbitopathy excludes GTT and points to Graves even when biochemistry overlaps
— Atrial fibrillation in pregnant patient → check TSH urgently; thyroid storm precipitant
— Listen for high-output flow murmur; if rales, consider thyrotoxic cardiomyopathy / peripartum cardiomyopathy overlap
— Hypothyroid: pericardial effusion (rare), pleural effusion, hypoventilation in myxedema
— Hung-up (delayed relaxation) ankle reflex → hypothyroidism
— Brisk reflexes with clonus → hyperthyroidism (also a preeclampsia red flag — check BP, urine protein)
— Fundal height vs dates: SGA in overt hypothyroidism or uncontrolled hyperthyroidism
— Fetal HR baseline >160 beats/min sustained → fetal thyrotoxicosis (TRAb crossing placenta in Graves)
Board pearl: Persistent fetal tachycardia + maternal Graves history (even post-thyroidectomy/RAI) mandates TRAb measurement — antibodies persist and cross the placenta even when mom is euthyroid.
— T1 upper limit ~4.0 mIU/L (ATA 2017); if institutional range exists, use it
— Lower limit drops because of hCG effect: TSH may be 0.1 in healthy T1
— Free T4 by direct dialysis or LC-MS/MS is most accurate; immunoassay free T4 underestimates in pregnancy
— Total T4 × 1.5 is an acceptable surrogate after week 16 if free T4 assay unreliable
— Free T3 helpful when TSH suppressed but free T4 normal (T3-toxicosis)
— TPO-Ab: drives treatment threshold in subclinical hypothyroidism; predicts postpartum thyroiditis
— TRAb (TSI): essential in any pregnant woman with current or prior Graves disease, even if euthyroid
— Check TRAb at initial visit; if elevated, recheck at 18–22 weeks and 30–34 weeks for fetal risk assessment
— ↑TSH, ↓free T4 → overt hypothyroidism → treat
— ↑TSH, normal free T4 → subclinical hypothyroidism → treatment depends on TPO and TSH level
— ↓TSH, ↑free T4 in T1 with hyperemesis, no goiter/TRAb → GTT → supportive care, recheck
— ↓TSH, ↑free T4, +TRAb, goiter/ophthalmopathy → Graves → PTU (T1) or methimazole (T2/T3)
— ↓TSH, normal free T4/T3 in T1 → physiologic; recheck in 4–6 weeks
— CBC (anemia in hypothyroidism, may worsen iron-deficiency picture)
— Hepatic panel before PTU (hepatotoxicity)
— Glucose/HbA1c (T1DM overlap); lipid panel if dyslipidemia suspected
— Avoid radioactive iodine uptake (RAIU) and thyroid scintigraphy — contraindicated in pregnancy
Step 3 management: Suppressed TSH in T1 with normal free T4 and no Graves features → do not treat; repeat TSH and free T4 in 4–6 weeks. Over-eager methimazole here causes iatrogenic fetal hypothyroidism and is a classic Step 3 wrong-answer trap.
— Safe in pregnancy — first-line imaging
— Indications: palpable nodule, asymmetric goiter, suspicious lymphadenopathy, evaluation of Graves vs nodular toxic goiter
— Findings: hypoechoic heterogeneous gland → Hashimoto; diffusely hypervascular gland → Graves; discrete nodule → assess size, composition, ACR TI-RADS features
— Safe at any gestational age for nodules meeting size/sonographic criteria (≥1 cm with suspicious features, or per TI-RADS)
— Do not delay FNA for benign-appearing nodules until postpartum if features are suspicious
— Bethesda III/IV nodules: consider deferring surgery to postpartum unless rapidly growing
— Contraindicated for diagnosis and treatment in pregnancy
— Inadvertent exposure before 10–12 weeks usually does not destroy fetal thyroid (fetal thyroid not yet trapping); after 12 weeks, risk of fetal hypothyroidism/cretinism rises sharply
— Pregnancy must be excluded (hCG) within 72 hours before any RAI in a reproductive-age woman
— Measure if: active Graves, prior Graves treated with surgery/RAI, prior infant with neonatal Graves
— TRAb >3× upper limit at 18–22 weeks → high risk of fetal/neonatal thyrotoxicosis → serial fetal ultrasound for goiter, growth, HR; involve MFM
— Serial growth ultrasounds in poorly controlled disease
— Fetal goiter on US in mother on excessive ATD → consider dose reduction; rarely intra-amniotic levothyroxine
— Central hypothyroidism (low TSH + low free T4) → MRI pituitary, prolactin, cortisol — Sheehan if peripartum hemorrhage history
Key distinction: Graves vs gestational transient thyrotoxicosis — Graves has goiter, ophthalmopathy, +TRAb, persistent symptoms beyond T1, and free T3 disproportionately high; GTT resolves with falling hCG and lacks autoimmune markers. This is the single most tested differential on Step 3 thyroid-pregnancy stems.
— Untreated overt disease → miscarriage, preeclampsia, abruption, preterm birth, low birth weight, impaired neurocognitive development
— Goal: TSH within trimester-specific range, ideally <2.5 mIU/L
— TSH > 10: treat regardless of antibodies
— TSH above trimester upper limit but <10 and TPO+: treat
— TSH above upper limit, TPO−: treatment controversial; ATA suggests considering treatment given low risk of harm
— TSH 2.5–4.0, TPO+: not routinely treated unless infertility/recurrent loss — individualize
— Normal TSH, low free T4 — do not treat; no benefit shown in trials (CATS, controlled antenatal thyroid screening)
— Untreated → preeclampsia, heart failure, thyroid storm, preterm labor, IUGR, stillbirth
— Graves: ATD therapy (PTU in T1, switch to methimazole T2/T3)
— Toxic nodule/multinodular: ATD, plan definitive therapy postpartum
— Not associated with adverse outcomes; do not treat in pregnancy
— Supportive: IV fluids, antiemetics, electrolyte repletion; β-blocker (propranolol) short-term for symptoms if needed
— No ATD — resolves with hCG decline
— Thyrotoxic phase: β-blocker for symptoms; no ATD (destructive, not synthetic)
— Hypothyroid phase: levothyroxine if symptomatic, planning pregnancy, or breastfeeding; trial off after 6–12 months
Step 3 management: Algorithmic order in subclinical hypothyroidism — (1) get trimester-specific TSH, (2) measure TPO, (3) decide treatment using TSH cutoff + antibody status, (4) recheck TSH 4 weeks after starting/adjusting levothyroxine, (5) repeat every 4 weeks until 20 weeks, then once T3.
— Start dose in newly diagnosed overt: 1.6 mcg/kg/day (use ideal body weight)
— Already on LT4 + new pregnancy: increase 25–30% immediately (2 extra tablets/week is the common rule)
— Take on empty stomach, 30–60 min before food; separate from iron, calcium, PPIs by ≥4 hours
— Use brand-name or consistent generic; avoid switching
— Do not use T3, desiccated thyroid, or combination T4/T3 in pregnancy
— TSH every 4 weeks until 20 weeks, then once between 26–32 weeks
— Target: TSH within trimester-specific range, ideally lower half (<2.5 in T1)
— Postpartum: return to pre-pregnancy dose, check TSH in 6 weeks
— Propylthiouracil (PTU): preferred first trimester (lower teratogenicity than methimazole)
— Dose: PTU 50–150 mg PO TID; titrate to lowest effective
— Methimazole (MMI): switch in T2/T3 (PTU hepatotoxicity risk)
— Dose: MMI 5–20 mg/day; conversion ratio ~PTU 20 mg = MMI 1 mg
— Goal: maternal free T4 at or just above upper normal — the lowest dose that controls symptoms to minimize fetal exposure
— MMI 6–10 weeks: aplasia cutis, choanal/esophageal atresia, omphalocele (methimazole embryopathy)
— PTU: less severe, milder face/neck/urinary defects; hepatotoxicity in mother (rare fulminant)
— Propranolol or labetalol short-term for symptom relief (palpitations, tremor)
— Avoid prolonged use → IUGR, fetal bradycardia, neonatal hypoglycemia
— 150 mcg iodine in prenatal vitamin; total intake 250 mcg/day
— Avoid kelp, high-dose iodine supplements (can induce dysfunction)
Board pearl: The classic Step 3 trap is starting methimazole at 8 weeks for new Graves — switch to PTU through end of T1, then back to MMI. Document the switch and rationale.
— ICU admission, fetal monitoring, treat precipitant (infection, labor, preeclampsia, surgery)
— PTU 600–1000 mg loading then 200–250 mg q4h (preferred over MMI for blocking T4→T3 conversion)
— Iodine (SSKI or Lugol) 1 hour after PTU to block hormone release
— Propranolol 60–80 mg PO q4h (or IV); use cautiously if heart failure
— Hydrocortisone 100 mg IV q8h (blocks T4→T3, treats relative adrenal insufficiency)
— Cooling, acetaminophen (avoid aspirin — displaces T4 from TBG)
— Treat heart failure: diuretics, oxygen; consider digoxin
— Reserved for: allergy/intolerance to both ATDs, agranulocytosis, requirement for very high ATD doses, large compressive goiter, suspected thyroid cancer
— Optimal timing: second trimester (lowest risk of miscarriage and preterm labor)
— Pre-op: β-blocker + iodine to render euthyroid; avoid in T1 (organogenesis) and T3 (preterm labor)
— Pre-conception: women must avoid pregnancy for 6 months after RAI
— Breastfeeding contraindicated for I-131 ablation indefinitely (or until cessation per protocol)
— Differentiated thyroid cancer in pregnancy: if found early T1/T2, surgery in T2; if late T2/T3 with stable disease, defer surgery to postpartum
— TSH suppression with LT4 for known DTC: continue, target TSH per risk category
— RAI ablation deferred until ≥6 weeks postpartum and after cessation of breastfeeding
— Iron, calcium, magnesium, aluminum hydroxide, PPIs, sucralfate, cholestyramine, soy
— Estrogen ↑ TBG → may need higher LT4 dose; not relevant in pregnancy where increase already done
CCS pearl: Pregnant patient in thyroid storm — order in this sequence: IV access, labs (TSH, free T4/T3, CBC, CMP, blood cultures), continuous fetal monitoring, PTU first, then iodine 1 hour later, β-blocker, hydrocortisone, treat precipitant, MFM/endocrine/ICU consults.
— Pregnancy normally lowers creatinine; "normal" Cr (≥1.0) may signal CKD
— LT4 dose generally unaffected by CKD; monitor TSH q4 weeks
— PTU and MMI: no dose adjustment in mild–moderate CKD; both renally and hepatically cleared
— Preeclampsia and severe hypothyroidism share features (edema, fatigue, hypertension) — check TSH if atypical course
— PTU: rare fulminant hepatic necrosis (boxed warning) — check LFTs at baseline and if symptoms; do not use beyond T1 unless MMI contraindicated
— MMI: cholestatic injury, usually mild
— Pre-existing liver disease (AIH, HBV/HCV cirrhosis): prefer MMI if hyperthyroid in T2/T3; if T1, weigh PTU teratogenicity vs hepatic risk
— Pre-existing AFib, valvular disease, cardiomyopathy + hyperthyroidism → high risk for storm and heart failure
— Tight TSH control; rate control with β-blocker; anticoagulation considerations (LMWH preferred in pregnancy)
— Hypothyroidism worsens diastolic dysfunction; treat aggressively
— T1DM strongly associated with autoimmune thyroid disease — screen TSH preconception and in T1
— Hypothyroidism worsens insulin resistance; correcting it may reduce insulin needs
— GDM is more frequent in untreated hypothyroidism
— BMI ≥40 is a high-risk indication for thyroid screening
— LT4 dose based on ideal body weight to avoid overtreatment
— Higher hCG → more pronounced TSH suppression in T1; interpret cautiously
— IVF patients on LT4: increase dose by 25% at positive pregnancy test
Key distinction: PTU's risk is maternal hepatic while MMI's risk is fetal embryopathy — this asymmetry drives the T1-PTU / T2-T3-MMI sequencing rule that Step 3 tests repeatedly.
— Affects 5–10% of postpartum women; up to 25% in T1DM, 50% in TPO+
— Triphasic: thyrotoxic (1–4 mo) → hypothyroid (4–8 mo) → euthyroid by 12 mo
— 20–40% develop permanent hypothyroidism — annual TSH screening for life if TPO+ or persistent disease
— Differentiate from Graves: PPT has low RAI uptake (can check after weaning), no TRAb, smaller/non-tender gland
— LT4: fully compatible with breastfeeding
— MMI ≤20 mg/day and PTU ≤450 mg/day: compatible; minimal transfer to breast milk; monitor infant TFTs if higher doses
— Take ATD after breastfeeding sessions to minimize infant exposure
— RAI: contraindicated during lactation; cessation of breastfeeding required before ablation
— Neonatal Graves: TRAb-mediated; transient (clears 3–12 weeks as antibodies decline)
— Signs: tachycardia, irritability, poor feeding, goiter, exophthalmos, advanced bone age, craniosynostosis
— Fetal/neonatal hypothyroidism: from maternal ATD overdose; suspect if maternal dose high in T3
— Universal newborn screening catches congenital hypothyroidism; treat within 2 weeks of life
— Return to pre-pregnancy dose immediately after delivery
— Recheck TSH 6 weeks postpartum
— New-onset hypothyroidism diagnosed in pregnancy: trial dose reduction by 25–50% postpartum; reassess in 6 weeks
— Optimize TSH <2.5 before conception
— Women with Graves wanting pregnancy: consider definitive therapy (surgery > RAI) before conception; if RAI, wait 6 months
— Folic acid 400–800 mcg, iodine 150 mcg in prenatal vitamin
Board pearl: Postpartum depression that doesn't fit the timeline, plus tachycardia or unexplained weight changes 2–6 months after delivery → check TSH before escalating psychiatric workup.
— Spontaneous abortion (especially TPO+)
— Gestational hypertension and preeclampsia
— Placental abruption
— Postpartum hemorrhage (impaired uterine contractility)
— Anemia, myopathy, cardiac dysfunction
— Low birth weight, preterm birth
— Neurocognitive impairment — most established for overt disease; benefit of treatment for SCH on IQ outcomes is uncertain (CATS trial: no IQ benefit at age 3 or 9)
— Stillbirth (rare, with severe disease)
— Preeclampsia, heart failure, atrial fibrillation
— Thyroid storm — precipitated by labor, infection, preeclampsia, C-section, abruption
— Placental abruption
— IUGR, preterm birth, stillbirth
— Fetal goiter (from ATD excess or from TRAb stimulation)
— Fetal/neonatal thyrotoxicosis (TRAb crossing placenta)
— Neonatal central hypothyroidism (from prolonged maternal hyperthyroidism suppressing fetal pituitary)
— Craniosynostosis, advanced bone age
— LT4 over-replacement → maternal AFib, bone loss, low birth weight
— MMI in T1 → embryopathy (aplasia cutis, choanal atresia, omphalocele, esophageal atresia)
— PTU → maternal hepatic failure, ANCA vasculitis (rare)
— Prolonged β-blocker → IUGR, neonatal hypoglycemia, bradycardia
— Postpartum thyroiditis (often missed)
— Permanent hypothyroidism (20–40% after PPT)
— Relapse of Graves disease 3–12 months postpartum
Key distinction: Maternal free T4 should be at or just above the upper limit of normal in Graves — pushing into the normal range causes fetal hypothyroidism because the fetus is more sensitive to ATD than the mother. Over-treatment is as harmful as under-treatment.
— New diagnosis of overt hyperthyroidism in pregnancy
— Graves requiring ATD dose escalation or with poorly controlled symptoms
— TSH not normalizing despite LT4 titration
— Thyroid nodule with suspicious features or large goiter
— History of thyroid cancer requiring TSH suppression
— Active Graves with elevated TRAb (>3× ULN at 18–22 weeks)
— Fetal goiter, fetal tachycardia, IUGR
— Thyroid storm management
— Need for thyroidectomy in pregnancy
— Thyroid storm (Burch-Wartofsky score ≥45 highly suggestive)
— Severe hyperemesis with electrolyte derangement and thyrotoxicosis
— Myxedema coma (rare in pregnancy): hypothermia, hypoventilation, altered mental status
— Atrial fibrillation with rapid ventricular response
— Hyperthyroid heart failure
— Pre-op admission for thyroidectomy in T2
— Thyroid storm with hyperthermia >40°C, tachyarrhythmia, CHF, altered mental status
— Myxedema coma
— Need for invasive monitoring during delivery in cardiac decompensation
— Active Graves: anesthesia, neonatology, endocrine, MFM team meeting before delivery
— Plan for cord blood TSH/free T4/TRAb at delivery if maternal Graves
— Neonatology to evaluate infant for thyrotoxicosis within 24–48 hours
— TSH out of range on two consecutive checks despite adherence → reassess for malabsorption, drug interactions, non-adherence, alternative diagnosis (central hypothyroidism)
— New goiter or rapid growth → ultrasound and endocrine referral
CCS pearl: For a pregnant patient with new AFib and palpitations, the first three orders are TSH, free T4, free T3 alongside the cardiac workup — uncovering hyperthyroidism changes management entirely (β-blocker + ATD, not just rate control + anticoagulation decision).
— Diffuse goiter, ophthalmopathy, pretibial myxedema, +TRAb/TSI
— Most common cause of overt hyperthyroidism in pregnancy
— Free T3 disproportionately elevated; symptoms persist through pregnancy
— Treatment: PTU (T1) → MMI (T2/T3); avoid RAI
— hCG-mediated; peaks 8–14 weeks, resolves by 14–18
— Associated with hyperemesis gravidarum, multiple gestation, molar pregnancy
— No goiter, no ophthalmopathy, no TRAb
— Treatment: supportive only; short-course β-blocker if needed
— Older gravidas, longstanding goiter; nodule(s) on ultrasound
— No autoimmune stigmata; TRAb negative
— Treatment: ATD during pregnancy; definitive therapy (surgery or RAI) postpartum
— Painful tender goiter, post-viral, elevated ESR
— Rare in pregnancy
— Treatment: β-blocker, acetaminophen, prednisone if severe; no ATD (destructive process)
— Postpartum thyroiditis is the pregnancy-related variant
— Low RAIU (post-weaning), low/normal thyroglobulin pattern variable
— Self-limited; treat symptoms
— Most common cause of hypothyroidism in pregnancy in iodine-sufficient regions
— TPO+, ± TgAb; firm goiter; ultrasound shows heterogeneity
— Treatment: LT4
— Still a global cause; iodine-sufficient US population usually adequate
— Goiter, hypothyroidism, increased risk of cretinism if severe
— Prevention: 150 mcg iodine in prenatal vitamin
— From amiodarone, iodinated contrast, kelp supplements
— Can cause hypo- or hyperthyroidism
Key distinction: GTT is hCG-driven and self-resolves with falling hCG; Graves is autoimmune and progresses without treatment. Time course (T1 only vs persistent), autoimmune markers, and presence of orbitopathy/goiter separate them — Step 3's favorite hyperthyroid-in-pregnancy fork.
— Severe N/V, weight loss >5%, ketonuria, electrolyte derangement
— TSH may be suppressed from hCG cross-reactivity; free T4 mildly elevated
— Do not treat as Graves if no autoimmune features; supportive care
— Palpitations, tremor, diaphoresis overlap with thyrotoxicosis
— Distinguish: weight loss with normal/increased appetite, persistent tachycardia, lid lag, goiter favor thyroid
— Check TSH before initiating psychiatric treatment
— Hypertension, proteinuria, edema, hyperreflexia — can mimic hyperthyroidism
— Severe features (HELLP, AKI) require delivery; check TSH if features are atypical
— Severe hypothyroidism can predispose to preeclampsia
— Both 1–6 months postpartum
— PPT: ± palpitations, weight loss, tremor (thyrotoxic phase) or fatigue, cold intolerance (hypo phase)
— Always check TSH in postpartum mood/anxiety presentations
— Episodic hypertension, headache, palpitations, diaphoresis
— Rare but life-threatening in pregnancy; plasma/urine metanephrines
— Distinguish from thyrotoxicosis by paroxysmal nature, headaches, hypertension predominance
— Postpartum hemorrhage → pituitary necrosis → central hypothyroidism, adrenal insufficiency, agalactia
— Low TSH with low free T4 (vs primary hypothyroidism with high TSH)
— Workup: full pituitary panel, MRI
— Fatigue, dyspnea, weakness overlap with hypothyroidism
— Always check CBC alongside TSH
— Fatigue, weight changes — overlap with thyroid disease
— Screen both; bidirectional risk associations
Board pearl: In a postpartum woman with fatigue, low blood pressure, failure to lactate, and history of severe peripartum hemorrhage → think Sheehan, not Hashimoto. The TSH will be inappropriately low or normal despite hypothyroid symptoms — the giveaway for central etiology.
— Return to pre-pregnancy dose immediately after delivery
— New-diagnosis pregnancy hypothyroidism: reduce dose by 25–50% postpartum; some can stop entirely (gestational-only requirement)
— Recheck TSH at 6 weeks postpartum
— ATD typically continued postpartum; relapse common 3–12 months
— Compatible with breastfeeding (MMI ≤20 mg/day, PTU ≤450 mg/day) — take after feeds
— Plan definitive therapy (surgery or RAI) after weaning, especially if next pregnancy planned
— RAI: 6-month contraception requirement before next conception
— Defer FNA-confirmed DTC surgery to postpartum if low-risk and stable
— Continue LT4 with appropriate TSH suppression for known DTC
— Goal TSH <2.5 mIU/L before conception in known hypothyroid
— Graves: ideally definitive therapy + euthyroid x6 months before conception
— Iodine 150 mcg in prenatal vitamin; folate 400–800 mcg
— Annual TSH — 20–40% develop permanent hypothyroidism
— TPO+ women: lifetime risk of autoimmune thyroid disease elevated; screen at any future pregnancy
— Hyperthyroid patients on ATDs can use any contraception; avoid pregnancy until disease controlled and on stable T2/T3-appropriate regimen
— Levonorgestrel IUD, etonogestrel implant excellent options
— Ensure smooth handoff from OB to PCP for ongoing thyroid care at 6-week postpartum visit
— Medication reconciliation: confirm LT4 dose, brand, and timing
Step 3 management: At the postpartum visit, three thyroid action items: (1) confirm LT4 dose returned to pre-pregnancy or adjusted, (2) check TSH at 6 weeks, (3) document need for annual TSH screening in TPO+ or PPT history. Missing any of these is a transition-of-care failure.
— TSH every 4 weeks until 20 weeks gestation
— TSH once between 26 and 32 weeks
— Within 4 weeks of any dose change
— Postpartum: dose return + TSH at 6 weeks; then per stability
— Free T4 (and TSH, free T3) every 2–4 weeks until stable, then monthly
— Goal: maternal free T4 at or just above upper limit of normal on lowest effective ATD dose
— CBC + LFTs at baseline; recheck if symptoms (sore throat, fever, jaundice)
— TRAb at initial visit, 18–22 weeks, and 30–34 weeks if Graves
— Serial ultrasound q4–6 weeks from 20 weeks: growth, fetal HR, goiter, hydrops
— Fetal goiter → reassess maternal ATD dose (often too high)
— Fetal tachycardia >160 sustained → consider fetal thyrotoxicosis
— LT4 timing: empty stomach, 30–60 min before food, away from iron/calcium/PPI
— Take LT4 daily even when nauseated; rectal LT4 has been used in severe hyperemesis
— Report symptoms of hepatotoxicity on PTU (RUQ pain, jaundice, dark urine)
— Report agranulocytosis symptoms on either ATD (fever, sore throat) — stop drug, get CBC
— Adherence: missing doses risks miscarriage, preterm birth
— Continue prenatal vitamin with 150 mcg iodine (not all brands include — verify)
— Avoid kelp/seaweed supplements and excessive iodine
— Smoking cessation (worsens Graves ophthalmopathy)
— Adequate sleep, hydration, mood monitoring
— Hypothyroidism mimics depression; check TSH before/during treatment of perinatal depression
— Postpartum mood + thyroid screening linked at 6-week visit
Board pearl: In Graves on ATD, the single most useful number to follow is the maternal free T4, not TSH (which stays suppressed for months). Aim for high-normal/just-above-normal — this protects the fetus while controlling mom.
— Disclose teratogenicity of methimazole (aplasia cutis, choanal atresia, omphalocele) and PTU (less severe defects, maternal hepatotoxicity)
— Document discussion of risks of untreated disease vs treatment risks
— Decisional capacity intact and patient autonomy respected — even if patient refuses treatment, document risks of refusal (storm, preterm birth, stillbirth)
— Mandatory hCG within 72 hours before RAI in any reproductive-age woman
— Document negative test in chart before administration
— Counsel 6-month contraception post-RAI before attempting pregnancy
— Inadvertent RAI exposure in pregnancy: urgent endocrine + MFM + radiation safety consultation; fetal thyroid most vulnerable after 12 weeks
— Discuss safety of LT4 (fully compatible), ATDs (dose limits), and absolute contraindication of RAI during lactation
— Respect patient's choice; document shared decision
— Highest-risk handoff: OB to PCP at 6 weeks postpartum
— Failure to adjust LT4 back to pre-pregnancy dose causes iatrogenic hyperthyroidism
— Failure to follow TPO+ women for postpartum thyroiditis misses permanent hypothyroidism
— Use structured discharge summary including dose, target TSH, follow-up date
— All maternal Graves cases: communicate to neonatology before delivery
— Cord blood TSH, free T4, TRAb at delivery if indicated
— Neonatal screening within first 24–48 hours; TRAb-mediated neonatal thyrotoxicosis may emerge 1–2 weeks later
— Congenital hypothyroidism detected on newborn screening is reportable in many states
— Birth defects from MMI exposure may be reported to teratogen registries
— Iodine deficiency more common in vegan diets, restrictive eating; ensure prenatal vitamin contains iodine — many OTC brands omit it
— Cost of brand-name LT4 may impede adherence; confirm formulary, avoid frequent generic switching
Step 3 management: A reproductive-age woman scheduled for RAI ablation — order urine or serum hCG within 72 hours and document negative result. Forgetting this single step is a high-frequency Step 3 safety/ethics vignette.
— hCG ↑ → TSH ↓; total T4 ↑ 1.5× due to TBG; free T4 stays near normal
— Iodine needs: 250 mcg/day in pregnancy and lactation
— Trimester-specific TSH ranges: ~0.1–4.0 mIU/L
— LT4 starting dose: 1.6 mcg/kg ideal body weight
— Already on LT4 + pregnancy → ↑ 25–30% immediately
— Target TSH <2.5 in T1, then trimester-specific
— Treat SCH if TSH >10 or TSH > ULN with TPO+
— Untreated overt → miscarriage, preeclampsia, neurodevelopmental impairment
— Most common cause = Graves
— PTU in T1, methimazole in T2/T3
— MMI embryopathy: aplasia cutis, choanal atresia, omphalocele, esophageal atresia
— PTU hepatotoxicity (rare, severe), agranulocytosis (both drugs)
— Goal: free T4 at/just above upper normal — lowest effective dose
— Check in any Graves patient (active or history)
— Recheck 18–22 and 30–34 weeks if positive
— TRAb >3× ULN → fetal/neonatal Graves risk
— GTT: T1, hyperemesis, no TRAb, no goiter, no orbitopathy → supportive
— Graves: persistent, +TRAb, goiter, orbitopathy → ATD
— TPO+ predicts; triphasic course; β-blocker for thyrotoxic phase, LT4 for hypo phase if symptomatic
— 20–40% permanent hypothyroidism — annual TSH
— 150 mcg in prenatal vitamin; avoid kelp/excess
— Severe deficiency → cretinism
— RAI (diagnostic or therapeutic)
— Combination T4/T3 or desiccated thyroid
— Long-term β-blocker (use shortest possible)
Board pearl: Free T4 just above upper limit + lowest ATD dose + serial TRAb + MFM involvement + fetal ultrasound = the five-element framework for managing Graves in pregnancy. If a stem omits any, that's likely the answer.
— T1 woman with hyperemesis, weight loss, tachycardia; TSH suppressed, free T4 mildly elevated, no goiter or orbitopathy
— Answer: gestational transient thyrotoxicosis — supportive care, recheck in 4–6 weeks
— Wrong answers: start methimazole, start PTU, order RAI uptake
— Woman on LT4 100 mcg for Hashimoto presents at 8 weeks pregnant
— Answer: increase LT4 dose by 25–30% now and recheck TSH in 4 weeks
— Wrong answers: continue same dose and recheck, decrease dose, stop LT4
— 10-week pregnant patient with Graves; what's the best ATD?
— Answer: PTU through T1, then switch to MMI in T2
— Wrong answers: continue MMI, RAI ablation, immediate thyroidectomy
— Patient with prior Graves treated by thyroidectomy 5 years ago, now euthyroid on LT4, 20 weeks pregnant
— Answer: measure TRAb — antibodies can persist and cross placenta, threatening fetal thyrotoxicosis
— Wrong answer: no further workup needed since maternal disease cured
— Woman 3 months postpartum with fatigue, weight gain, depression; previously had palpitations at 6 weeks postpartum
— Answer: check TSH — postpartum thyroiditis (hypothyroid phase)
— Postpartum hemorrhage, failure to lactate, fatigue, hypotension; TSH low, free T4 low
— Answer: central hypothyroidism / Sheehan — pituitary MRI, full pituitary panel, replace cortisol before LT4
— Reproductive-age woman scheduled for RAI ablation of Graves
— Answer: hCG within 72 hours before procedure
— Graves patient with TRAb 5× ULN, fetal HR 180 sustained on US
— Answer: assess for fetal goiter, adjust maternal ATD, MFM co-management
Step 3 management: When the stem describes pregnancy + new thyroid findings, your first two clicks are nearly always trimester-specific TSH and free T4 — not free T3, not RAI uptake, not antibodies first.
Thyroid disease in pregnancy hinges on three rules: use trimester-specific TSH ranges, treat overt disease aggressively while keeping antithyroid drug doses at the lowest effective level (PTU in T1, methimazole in T2/T3), and increase levothyroxine by 25–30% the moment pregnancy is confirmed.
— Increase LT4 by 25–30% at conception; target TSH <2.5 in T1, trimester-specific thereafter
— Monitor TSH q4 weeks until 20 weeks, then once between 26–32 weeks
— Treat overt disease always; treat SCH if TSH >10 or > ULN with TPO+
— Untreated disease → miscarriage, preeclampsia, neurodevelopmental impairment
— Graves = most common cause; differentiate from gestational transient thyrotoxicosis (no TRAb, no goiter, resolves with hCG)
— PTU in T1 (avoids methimazole embryopathy), switch to MMI in T2/T3 (avoids PTU hepatotoxicity)
— Target maternal free T4 at or just above upper normal on lowest effective dose
— Check TRAb at intake and at 18–22 and 30–34 weeks in any current/prior Graves patient
— Return LT4 to pre-pregnancy dose at delivery; check TSH at 6 weeks postpartum
— Postpartum thyroiditis: TPO+ predisposes; triphasic course; 20–40% permanent hypothyroidism — annual TSH
— RAI absolutely contraindicated in pregnancy and lactation; confirm negative hCG within 72 hours before any RAI; 6-month contraception after RAI
— LT4 and low-dose ATDs (MMI ≤20 mg, PTU ≤450 mg) are compatible with breastfeeding
— GTT vs Graves (TRAb, orbitopathy, goiter, time course)
— Postpartum thyroiditis vs postpartum depression (always check TSH)
— Sheehan vs Hashimoto (central → low TSH + low free T4 + pituitary failure stigmata)
Board pearl: If you remember nothing else, remember: trimester-specific ranges, PTU→MMI by trimester, +25–30% LT4 at conception, TRAb in Graves, hCG before RAI, and TSH at the 6-week postpartum visit — these six anchors solve nearly every Step 3 thyroid-pregnancy stem.