High-yield algorithms, recognition patterns, and exam traps — built for rapid last-minute recall.
| Term | Definition |
|---|---|
| Gravidity | Total number of pregnancies (including current) |
| Parity | Number of pregnancies delivered beyond 20 weeks OR infant >500 g |
Example: G3P2012 → G3 = 3 total pregnancies; P2012 = 2 term, 0 preterm, 1 abortion, 2 living children.
Gestational Age (GA): weeks from first day of last menstrual period (LMP). Embryonic Age: weeks from fertilization (usually unknown; GA − 2 weeks).
| Method | Timing | Accuracy |
|---|---|---|
| Crown-rump length (CRL) | 6–12 weeks | Most accurate early dating |
| Biparietal diameter + Femur length | >13 weeks | Standard second trimester |
| Fundal height | >20 weeks | Reaches umbilicus at 20 weeks, then +1 cm/week |
| Quickening | 16–20 weeks | Primipara: 20 weeks; Multipara: 16 weeks |
| Fetal heart tones (Doppler) | 10–12 weeks | — |
Fundal height = GA in cm (approximately) only AFTER 20 weeks.
Gold standard for pregnancy diagnosis.
β-hCG doubles every 48 hours in the first 6–8 weeks. Failure to double → suspect ectopic or miscarriage.
| Ultrasound Route | β-hCG Level |
|---|---|
| Transvaginal US | 1500–3500 mIU/mL (use 1500 for board exams) |
| Transabdominal US | 6000–6500 mIU/mL |
Level at which an intrauterine pregnancy (IUP) should be visible on ultrasound.
| GA (weeks) | Finding |
|---|---|
| 5 | Gestational sac visible |
| 5.5 | Yolk sac visible |
| 6 | Fetal pole visible |
| 6–7 | Fetal cardiac activity |
“When should you see fetal cardiac activity?” → 6–7 weeks on transvaginal ultrasound.
| Parameter | Change | Peak / Timing | Mechanism |
|---|---|---|---|
| Cardiac output | ↑ 30–50% | 20–26 weeks | ↑ stroke volume + ↑ HR |
| Heart rate | ↑ 20% | Gradual | Progesterone effect |
| Stroke volume | ↑ 30% | Peaks at 19 weeks | Plasma volume expansion |
| Blood pressure | ↓ 10% | Lowest at 24–26 weeks, returns to baseline by term | ↓ peripheral vascular resistance |
| Peripheral resistance | ↓ 20% | Progressive | Progesterone → vasodilation |
| Parameter | Change | Result |
|---|---|---|
| Blood volume | ↑ 50% | — |
| Plasma volume | ↑↑ (more than RBC mass) | Dilutional (physiologic) anemia |
| Hemoglobin | ↓ slightly | Normal: 11–12 g/dL in pregnancy |
| Hematocrit | ↓ to 32–34% | Physiologic |
| WBC | ↑ to 15,000 | Can go up to 25,000 in labor |
| Platelets | Slight ↓ | Dilution + ↑ consumption |
| Fibrinogen | ↑ | — |
| Factors VII, VIII, X | ↑ | Hypercoagulable state |
| Protein S | ↓ | ↑ VTE risk |
Hb <11 g/dL in pregnancy = TRUE anemia (not physiologic) — investigate!
| Parameter | Change | Mechanism |
|---|---|---|
| Tidal volume | ↑ 40% | Progesterone → ↑ respiratory drive |
| Respiratory rate | Unchanged | — |
| Minute ventilation | ↑ 50% | ↑ tidal volume |
| Residual volume | ↓ 20% | Diaphragm elevation |
| Functional residual capacity | ↓ 20% | Diaphragm elevation |
Dyspnea of pregnancy (60–70% of patients) is benign; nasal congestion from mucosal edema is common.
| Parameter | Change | Result |
|---|---|---|
| Renal blood flow | ↑ 50% | — |
| GFR | ↑ 50% | — |
| Creatinine | ↓ to 0.4–0.6 mg/dL | Cr >0.8 mg/dL = abnormal in pregnancy |
| BUN | ↓ to 8–10 mg/dL | — |
| Serum sodium | ↓ 4–5 mEq/L | Dilution + ADH |
| Urinary frequency | ↑ | Bladder compression + ↑ GFR |
| Glucosuria | Common | ↓ renal glucose threshold |
“Cr 1.0 mg/dL in pregnancy?” → ABNORMAL (should be <0.8 mg/dL).
| Hormone | Change | Mechanism / Note |
|---|---|---|
| Estrogen | ↑↑↑ | Placental production |
| Progesterone | ↑↑↑ | Maintains pregnancy |
| Prolactin | ↑ | Lactation preparation |
| hCG | Peak at 10 weeks | Maintains corpus luteum |
| Total T3/T4 | ↑ | ↑ TBG (estrogen effect) |
| Free T3/T4 | Normal | — |
| TSH | ↓ in first trimester | hCG has TSH-like activity |
Total T4 ↑ in pregnancy is NORMAL; free T4 should remain normal.
| GA | Frequency |
|---|---|
| 0–28 weeks | Every 4 weeks |
| 29–36 weeks | Every 2 weeks |
| 37 weeks–delivery | Every week |
History:
Physical Examination:
Laboratory Tests:
| BMI Category | Total Weight Gain |
|---|---|
| Underweight (<18.5) | 12–18 kg (28–40 lb) |
| Normal (18.5–24.9) | 11–16 kg (25–35 lb) |
| Overweight (25–29.9) | 7–11 kg (15–25 lb) |
| Obese (≥30) | 5–9 kg (11–20 lb) |
| GA | Testing |
|---|---|
| 10–14 weeks | First-trimester screening (if desired): nuchal translucency + PAPP-A + free β-hCG; cell-free DNA (if desired) |
| 15–20 weeks | Quad screen (if first-trimester screening not done); MSAFP screening |
| 18–20 weeks | Anatomic ultrasound (fetal anomaly scan); Level II ultrasound if abnormalities detected |
| 24–28 weeks | Glucose challenge test (GCT): 50 g oral glucose, check at 1 hour; if ≥140 mg/dL → 3-hour 100 g GTT |
| 28 weeks | Rh(D) immune globulin if Rh-negative (after antibody screen); repeat CBC for anemia |
| 35–37 weeks | GBS culture: rectovaginal swab at 36–38 weeks; repeat CBC; consider repeat gonorrhea/chlamydia/HIV/syphilis in high-risk patients |
| 36–41 weeks | Weekly visits; cervical exam (if indicated); NST if high-risk pregnancy |
The most sensitive and specific screening test available.
| Detects | Sensitivity |
|---|---|
| Trisomy 21 (Down syndrome) | >99% |
| Trisomy 18 (Edwards syndrome) | >98% |
| Trisomy 13 (Patau syndrome) | >98% |
| Sex chromosome aneuploidies | — |
| Condition | AFP | hCG | Estriol | Inhibin A |
|---|---|---|---|---|
| Trisomy 21 (Down) | ↓ | ↑ | ↓ | ↑ |
| Trisomy 18 (Edwards) | ↓ | ↓↓ | ↓↓ | ↓ |
| Neural tube defect | ↑↑ | Normal | Normal | Normal |
| Abdominal wall defect | ↑↑ | Normal | Normal | Normal |
“2 up, 2 down”
“Still UNDER age at 18” — all markers DOWN.
Workup: 1) Repeat MSAFP → 2) detailed ultrasound (level II) → 3) amniocentesis for amniotic fluid AFP + acetylcholinesterase.
| Feature | CVS | Amniocentesis |
|---|---|---|
| Timing | 10–13 weeks | 15–20 weeks |
| Method | Transcervical or transabdominal aspiration of placental tissue | Transabdominal aspiration of amniotic fluid |
| Advantages | Earlier diagnosis | Lower miscarriage risk; can assess for NTD |
| Disadvantages | Higher miscarriage risk (~1%); cannot detect NTD | Later diagnosis |
| Miscarriage risk | 0.5–1% | 0.1–0.3% |
| Results | Karyotype, genetic testing | Karyotype, AFP, genetic testing, fetal lung maturity |
“When is amniocentesis done for lung maturity?” → Third trimester (NOT for aneuploidy).
| Screening | Detail |
|---|---|
| Timing | 36–38 weeks |
| Method | Rectovaginal swab |
| Situation | Regimen |
|---|---|
| First-line | Penicillin G 5 million units IV, then 2.5–3 million units IV q4h until delivery |
| Penicillin allergy (low risk) | Cefazolin 2 g IV, then 1 g IV q8h |
| Penicillin allergy (high risk of anaphylaxis) | Clindamycin or vancomycin (if susceptible) |
GBS bacteriuria ANY time in pregnancy = treat + give intrapartum prophylaxis (regardless of later culture).
| Drug/Agent | Defects | Notes |
|---|---|---|
| ACE inhibitors | Renal dysplasia, oligohydramnios, skull ossification defects | AVOID in pregnancy |
| Warfarin | Nasal hypoplasia, stippled epiphyses, CNS/eye abnormalities | “Wages war on fetus” |
| Isotretinoin (Accutane) | Craniofacial, cardiac, thymic, CNS defects | Category X |
| Valproic acid | Neural tube defects (spina bifida 1–2%) | ↑ folic acid to 4 mg |
| Carbamazepine | Neural tube defects, craniofacial | — |
| Phenytoin | Fetal hydantoin syndrome: microcephaly, dysmorphic facies, nail/digital hypoplasia, cardiac defects | — |
| Lithium | Ebstein anomaly (tricuspid valve) | — |
| Alcohol | Fetal alcohol syndrome: FGR, microcephaly, smooth philtrum, intellectual disability | Most common preventable cause of intellectual disability |
| Thalidomide | Limb reduction defects (phocomelia) | — |
| Methotrexate | Neural tube defects, skeletal abnormalities | Folic acid antagonist |
| Tetracyclines | Yellow-brown tooth discoloration, enamel hypoplasia | Generally avoid (doxycycline OK) |
| Aminoglycosides | CN VIII damage (ototoxicity) | — |
| Radiation | Microcephaly, intellectual disability | <50 mGy = safe |
| Androgens | Virilization of female fetus | — |
| Infection | Transmission | Key Features | Diagnosis | Treatment | Prevention |
|---|---|---|---|---|---|
| Toxoplasma | Transplacental (cat feces, raw meat) | Triad: hydrocephalus, intracranial calcifications, chorioretinitis | Serology, PCR | Pyrimethamine + sulfadiazine | Avoid cat litter, raw meat |
| Rubella | Transplacental (first trimester worst) | “Blueberry muffin” rash, cataracts, PDA, deafness | Serology | Supportive | MMR vaccine BEFORE pregnancy |
| CMV | Transplacental | Periventricular calcifications, microcephaly, sensorineural hearing loss | Urine culture, PCR of amniotic fluid | Ganciclovir (postpartum) | — |
| HSV | Intrapartum (active lesions) | Skin/eye/mouth vesicles, encephalitis, disseminated disease | Viral culture, PCR | Acyclovir from 36 weeks; C-section if active lesions at delivery | Avoid delivery through infected canal |
| HIV | In utero, delivery, breastfeeding | Failure to thrive, recurrent infections | ELISA + Western blot | HAART during pregnancy, AZT during labor, AZT for neonate | Viral load <1000; if >1000 → C-section |
| Syphilis | Transplacental | “Snuffles” (rhinitis), rash, hepatomegaly, saber shins, saddle nose, Hutchinson triad (deafness, keratitis, peg incisors) | Dark-field microscopy, RPR/VDRL, FTA-ABS | Penicillin (desensitize if allergic) | Screen and treat all pregnant women |
| Zika | Transplacental (mosquito-borne) | Microcephaly, craniofacial disproportion, eye abnormalities | Zika RNA | Supportive | Avoid endemic areas |
Loss of pregnancy before 20 weeks gestation OR fetus <500 g. Incidence: 10–20% of clinically recognized pregnancies (80% occur in first trimester).
Maternal Factors:
Environmental: smoking, alcohol, cocaine, excessive caffeine (>500 mg/day)
“The I’s are open” — Incomplete and Inevitable have an open os.
| Type | Bleeding | Cramping | Os | Fetal Cardiac Activity | POC Passed | Management |
|---|---|---|---|---|---|---|
| Threatened | Yes | ± | Closed | Yes | No | Expectant, follow-up US |
| Inevitable | Yes | Yes | Open | ± | No | Expectant, medical, or surgical |
| Incomplete | Yes | Yes | Open | No | Partial | Surgical (D&C or MVA) or medical |
| Complete | Stopped | Stopped | Closed | No | Yes | None (confirm with US) |
| Missed | No | ± | Closed | No | No | Expectant, medical, or surgical |
| Septic | Yes | Yes | Open | ± | ± | IV antibiotics + urgent D&C |
| Option | Detail |
|---|---|
| Expectant | Wait for spontaneous passage (success rate 50–80%) |
| Medical | Misoprostol 800 mcg vaginally (can repeat) |
| Surgical | Manual vacuum aspiration (MVA) if <12 weeks; dilation and curettage (D&C) if >12 weeks |
Fever, foul discharge, abdominal pain, cervical motion tenderness. Polymicrobial (E. coli, Streptococcus, anaerobes).
Management: broad-spectrum IV antibiotics (ampicillin + gentamicin + clindamycin) + urgent surgical evacuation.
≥2 consecutive losses OR ≥3 total losses.
Workup:
Treatment:
Always give Rh immune globulin to Rh-negative mothers after ANY pregnancy loss (including SAB, elective abortion, ectopic).
Implantation outside the uterine cavity. Location: 95% tubal (most commonly ampulla), 5% other (ovarian, cervical, abdominal, cornual/interstitial). Incidence: 1–2% of all pregnancies.
Classic triad (only 50% of patients): abdominal pain + vaginal bleeding + amenorrhea.
Best initial test: transvaginal ultrasound + quantitative β-hCG.
| Finding | Importance |
|---|---|
| β-hCG fails to double every 48 hours | Normal IUP doubles q48h → suspect ectopic or failed pregnancy |
| Discriminatory zone: β-hCG ≥1500 mIU/mL with no IUP on transvaginal US | Highly suspicious for ectopic |
| Absence of intrauterine gestational sac with β-hCG >1500 mIU/mL | Ectopic until proven otherwise |
| Adnexal mass (tubal ring, complex mass) | Supports ectopic |
| Free fluid in pelvis | Blood if ruptured |
| Pseudogestational sac (decidual cast) | Can mimic IUP — pitfall |
| Progesterone <5 ng/mL | Nonviable pregnancy (doesn’t distinguish ectopic from failed IUP) |
| Culdocentesis (rarely done) | Non-clotting blood from pouch of Douglas |
| Indications | Options |
|---|---|
| Hemodynamic instability, ruptured ectopic, failed medical management, contraindications to methotrexate, patient preference | Salpingostomy: linear incision in tube, remove ectopic, preserve tube (↑ recurrence risk) |
| Salpingectomy: remove affected tube (preferred if contralateral tube normal) | |
| Laparoscopy preferred over laparotomy (unless unstable) |
“When to use methotrexate?” → Stable, unruptured, <4 cm, β-hCG <5000, no cardiac activity.
Proliferative trophoblastic abnormalities (benign or malignant).
| Feature | Complete Mole | Partial Mole |
|---|---|---|
| Karyotype | 46,XX (or 46,XY) | 69,XXY (or 69,XXX) |
| Genetics | Diploid paternal (sperm fertilizes empty egg, duplicates) | Triploid (2 sperm + 1 egg) |
| Fetal tissue | None | Present (abnormal fetus) |
| Uterus size | Large for dates (50%) | Small or appropriate for dates |
| β-hCG | Very high (>100,000) | Moderately elevated |
| Theca-lutein cysts | Common (30–50%) | Rare |
| Medical complications | More common (hyperemesis, preeclampsia <24 weeks, hyperthyroidism) | Less common |
| Risk of malignancy | 15–20% | <5% |
| Chemotherapy (Malignant GTD) | Regimen |
|---|---|
| Indications: plateau or rise in β-hCG during follow-up; persistently elevated β-hCG >6 months after evacuation; metastatic disease; histologic choriocarcinoma | Low-risk: single-agent methotrexate or actinomycin D High-risk: multi-agent EMA-CO (etoposide, methotrexate, actinomycin D, cyclophosphamide, vincristine) |
Preeclampsia before 20 weeks is virtually diagnostic of molar pregnancy (or multiple gestation).
Persistent vomiting in pregnancy leading to: weight loss ≥5% of pre-pregnancy weight, ketonuria/ketonemia, electrolyte abnormalities.
Differentiate from normal nausea/vomiting of pregnancy (NVP): NVP is common (70–80%), mild, and self-limited. Hyperemesis is SEVERE.
Mild (outpatient): dietary modifications; Vitamin B6 (pyridoxine) 10–25 mg TID + Doxylamine 12.5 mg TID-QID (first-line, available as combination Diclegis).
Moderate (if no response): metoclopramide 10 mg PO/IV TID-QID OR promethazine 12.5–25 mg PO/PR/IM q4–6h OR prochlorperazine 5–10 mg PO/IM TID-QID.
Severe (hospitalization): IV hydration (NS/LR + dextrose), electrolyte correction (K¹, Mg¹), thiamine 100 mg IV daily (prevent Wernicke), antiemetics (ondansetron 4–8 mg IV q8h), enteral (NG) if oral fails, TPN if refractory.
Always rule out molar pregnancy with ultrasound in severe hyperemesis.
Incidence 1% of pregnancies. Key concept: poor glycemic control (especially periconceptional and first trimester) → ↑ congenital anomalies.
| Maternal Effects | Notes |
|---|---|
| Preeclampsia | 3–4× ↑ risk |
| Preterm labor | — |
| Polyhydramnios | Fetal polyuria from hyperglycemia |
| Diabetic ketoacidosis (DKA) | Type 1 DM; lower threshold in pregnancy |
| Hypoglycemia | ↑ insulin sensitivity early pregnancy |
| Worsening retinopathy/nephropathy | Screen at first visit, each trimester |
| Infection | UTI, candidiasis |
| Cesarean delivery | ↑ rate (macrosomia, shoulder dystocia risk) |
Structural anomalies (poor periconceptional control): cardiac (VSD, TGA, coarctation — most common structural defect), neural tube defects (spina bifida, anencephaly), caudal regression syndrome (sacral agenesis) — pathognomonic, renal anomalies.
Metabolic/Other: macrosomia (>4000 g or >90th percentile), FGR (if maternal vasculopathy), polyhydramnios, IUFD, RDS (delayed lung maturity), neonatal hypoglycemia (hyperinsulinemia), hypocalcemia, hypomagnesemia, polycythemia → hyperbilirubinemia, birth trauma (shoulder dystocia, brachial plexus injury).
“HbA1c >8% in diabetic pregnancy?” → High risk for cardiac defects; get fetal echo.
Incidence 6–9% of pregnancies. Pathophysiology: placental hormones (hPL, progesterone, cortisol) → insulin resistance → relative insulin deficiency.
| Step | Test | Positive |
|---|---|---|
| Step 1 | 50-gram 1-hour glucose challenge test (GCT) — non-fasting | ≥140 mg/dL (some use ≥130 mg/dL); ~15–25% screen positive |
| Step 2 | 100-gram 3-hour OGTT — fasting required; glucose at 0, 1, 2, 3 hours | Diagnosis: ≥2 values abnormal |
| Time | Threshold |
|---|---|
| Fasting | ≥95 mg/dL |
| 1 hour | ≥180 mg/dL |
| 2 hours | ≥155 mg/dL |
| 3 hours | ≥140 mg/dL |
Alternative: one-step approach (75-gram 2-hour OGTT) — diagnose if ≥1 value abnormal.
GDM diagnosed in first trimester suggests preexisting diabetes (not true GDM).
Target BP: 120–160/80–110 mm Hg (avoid over-treatment → placental hypoperfusion).
First-line antihypertensives (safe): methyldopa 250–500 mg PO BID-TID (max 3 g/day); labetalol 100–400 mg PO BID-TID (max 2400 mg/day); nifedipine (extended-release) 30–90 mg PO daily.
Avoid: ACE inhibitors/ARBs (fetal renal dysgenesis, oligohydramnios, IUGR, neonatal renal failure); atenolol (IUGR).
New-onset HTN (≥140/90) at ≥20 weeks WITHOUT proteinuria or end-organ dysfunction. Up to 25% progress to preeclampsia.
New-onset HTN (≥140/90) at ≥20 weeks PLUS proteinuria (≥300 mg/24 h OR urine protein/Cr ratio ≥0.3) OR end-organ dysfunction (even without proteinuria): thrombocytopenia (<100,000/µL), renal insufficiency (Cr >1.1 mg/dL or doubling), elevated LFTs (>2× ULN), pulmonary edema, new-onset headache unresponsive to meds, visual disturbances. Incidence: 3–5%.
Abnormal placentation → endothelial dysfunction → vasospasm → end-organ ischemia.
“Signs of magnesium toxicity?” → Loss of DTRs first, then respiratory depression, then cardiac arrest.
| Severity | GA | Management |
|---|---|---|
| Without severe features | <37 weeks | Expectant (outpatient if compliant; frequent monitoring: twice-weekly BP, labs, fetal testing; no antihypertensives unless severe-range BP) |
| Without severe features | ≥37 weeks | Deliver |
| With severe features | <34 weeks | Expectant (inpatient; give betamethasone); deliver if maternal/fetal deterioration |
| With severe features | ≥34 weeks | Deliver |
| Magnesium Level | Clinical Findings | Management |
|---|---|---|
| 4–7 mEq/L | Therapeutic | Continue |
| 8–10 mEq/L | Loss of DTRs | Stop infusion; monitor closely |
| 10–12 mEq/L | Respiratory depression | Stop infusion; calcium gluconate 1 g IV over 3 min |
| >12 mEq/L | Cardiac arrest | Calcium gluconate; prepare for resuscitation |
Antidote: calcium gluconate 1 g (10 mL of 10% solution) IV over 3 minutes.
Preeclampsia PLUS any of:
Complications: hepatic rupture (rare, life-threatening), DIC, placental abruption, acute renal failure, pulmonary edema, maternal death (1–2%).
Management: same as severe preeclampsia → DELIVER.
HELLP can occur without hypertension or proteinuria.
New-onset grand mal seizures in a patient with preeclampsia (NOT attributable to other causes).
During seizure: protect airway — left lateral position, O₂, suction; do NOT restrain; monitor fetal heart rate.
After seizure:
“Can eclampsia occur postpartum?” → YES, up to 25% occur postpartum (usually within 48 hours).
UTIs are more common in pregnancy due to: urinary stasis (progesterone → ↓ ureteral peristalsis), vesicoureteral reflux, glycosuria. Organisms: E. coli (80–90%), Klebsiella, Proteus, Enterococcus, GBS.
≥10&sup5; CFU/mL on urine culture WITHOUT symptoms. Incidence 2–10%. 30–40% progress to pyelonephritis if untreated → preterm labor, low birth weight.
Avoid: fluoroquinolones (cartilage damage), trimethoprim (folate antagonist — especially first trimester), sulfonamides (kernicterus risk near term).
Most common serious medical complication of pregnancy. Risk factors: untreated asymptomatic bacteriuria, previous pyelonephritis, urinary tract abnormalities.
Presentation:
Diagnosis: UA (pyuria, WBC casts, bacteriuria); urine culture ≥10&sup5; CFU/mL; blood cultures often positive; leukocytosis.
Pyelonephritis in pregnancy ALWAYS requires hospitalization (unlike non-pregnant).
Reversible cholestasis in late pregnancy causing pruritus and elevated bile acids. Incidence 0.5–2% (higher in Chile, Scandinavia). Pathophysiology: ↑ estrogen → impaired hepatic bile secretion → bile acid accumulation.
Presentation:
Diagnosis:
Management:
Complications: stillbirth (↑ risk especially if bile acids >40 µmol/L), preterm delivery, meconium-stained fluid, postpartum hemorrhage (vitamin K malabsorption).
“Intense itching on palms/soles in third trimester with elevated bile acids” → Intrahepatic cholestasis of pregnancy.
Rare, life-threatening microvesicular fatty infiltration of liver in third trimester. Incidence 1 in 10,000. Pathophysiology: mitochondrial dysfunction in fetal fatty acid oxidation (often associated with fetal LCHAD deficiency).
Presentation: third trimester (30–38 weeks) or early postpartum; persistent nausea/vomiting, RUQ/epigastric pain, malaise, jaundice (late); fulminant hepatic failure: encephalopathy, coagulopathy, hypoglycemia.
Diagnosis — Labs:
Complications: maternal mortality 10–20% (higher if delayed diagnosis); DIC; hepatic encephalopathy; acute renal failure; pancreatitis; GI bleeding; fetal/neonatal mortality 20–30%.
Any vaginal bleeding after 20 weeks gestation. Incidence 3–5%. Most common causes: placental abruption, placenta previa, vasa previa. Other causes: cervical lesions, vaginal trauma, bleeding disorders, uterine rupture.
Premature separation of normally implanted placenta from the uterine wall (BEFORE delivery). Incidence 1 in 100. Most common cause of antepartum hemorrhage.
Other features: uterine hypertonicity (tetanic contractions), fetal distress (bradycardia, late decelerations), maternal hypovolemia/shock, concealed hemorrhage (20%).
Primarily a clinical diagnosis.
Maternal complications: hemorrhagic shock, DIC (thromboplastin release), acute kidney injury (ATN), Couvelaire uterus (may require hysterectomy), maternal death.
Fetal complications: hypoxia/acidosis, fetal anemia, intrauterine fetal demise, preterm delivery. Recurrence: 5–15%.
Abnormal placental implantation in the lower uterine segment, near or covering the internal cervical os. Incidence 1 in 200.
Classic: painless, bright red vaginal bleeding — usually third trimester (peak 32–34 weeks); often stops spontaneously within 1–2 hours; recurrent episodes common.
Transvaginal ultrasound — gold standard (>95% sensitivity); safe (does NOT cause bleeding). Transabdominal US less accurate.
Can precipitate massive hemorrhage. Speculum exam may be done carefully if needed.
| Situation | Action |
|---|---|
| Asymptomatic/incidental (second trimester) | Pelvic rest (no intercourse, no vaginal exams); repeat US at 28–32 weeks; many low-lying placentas “migrate” upward (differential growth, not true movement) |
| Bleeding episode <34 weeks, stable | Hospitalize until bleeding stops ×24–48 h; large-bore IV, type and cross; fetal monitoring; betamethasone; tocolytics if contractions (only if stable); consider admission at 30–32 weeks for complete previa |
| Bleeding episode ≥34 weeks OR unstable | Deliver by C-section |
| Delivery planning | All previas: C-section at 36–37 weeks (after steroids at 34–36 weeks); low-lying >2 cm from os may attempt trial of labor |
Maternal complications: hemorrhage (massive transfusion), placenta accreta spectrum (especially with prior C-section), emergency C-section, postpartum hemorrhage, hysterectomy, maternal death.
Fetal complications: vasa previa (associated), preterm delivery, PROM, FGR, congenital anomalies (slightly ↑). Recurrence: 4–8%.
Fetal blood vessels crossing the internal cervical os, running through the membranes unsupported by placenta or umbilical cord. Incidence 1 in 2500–5000.
“Painless bleeding + fetal bradycardia at ROM” → Vasa previa (EMERGENCY C-section).
Abnormal adherence of placenta to the uterine wall due to defective decidua basalis.
| Type | Definition | Incidence |
|---|---|---|
| Accreta | Villi attach to myometrium (no decidua) | 75% |
| Increta | Villi invade INTO myometrium | 15% |
| Percreta | Villi penetrate THROUGH myometrium to serosa (may invade bladder) | 5% |
“Placenta previa + prior C-section” → High risk for placenta accreta; plan delivery at tertiary center.
| Feature | Placental Abruption | Placenta Previa | Vasa Previa |
|---|---|---|---|
| Bleeding | Painful, dark | Painless, bright red | Painless |
| Onset | Sudden | Gradual, recurrent | At ROM |
| Uterine tone | Hypertonic, tender, rigid | Soft, non-tender | Soft |
| Fetal status | Distress common | Usually reassuring | Severe bradycardia |
| Ultrasound | Low sensitivity (50%) | High sensitivity (>95%) | Color Doppler shows vessels over os |
| Risk factors | HTN, trauma, cocaine | Prior C-section, multiparity | Velamentous insertion, low-lying placenta |
| Management | Deliver (often emergent) | C-section at 36–37 weeks | Emergency C-section |
“What’s the difference between abruption and previa?” → Use the table above.
Pregnancy with ≥2 fetuses. Incidence 3% of live births (increasing due to ART and advanced maternal age).
One egg splits after fertilization; chorionicity/amnionicity depends on timing:
| Split Timing | Chorionicity/Amnionicity | Frequency | Risk |
|---|---|---|---|
| 0–3 days | Dichorionic, diamniotic | 30% | Lowest |
| 4–8 days | Monochorionic, diamniotic | 65% | Moderate (TTTS risk) |
| 9–12 days | Monochorionic, monoamniotic | 4% | High (cord entanglement) |
| >13 days | Conjoined twins | 1% | Highest |
Imbalanced blood flow through placental vascular anastomoses in monochorionic twins. Donor twin transfuses blood to recipient → donor becomes anemic/oligo, recipient polycythemic/poly.
| Type | Timing |
|---|---|
| Dichorionic-diamniotic | 38 weeks |
| Monochorionic-diamniotic | 34–37 weeks |
| Monoamniotic | 32–34 weeks (C-section) |
“Monozygotic twins always monochorionic?” → NO, 30% are dichorionic (if split 0–3 days).
Estimated fetal weight (EFW) <10th percentile for gestational age. Also called IUGR. Incidence 5–10%.
Fetal: chromosomal abnormalities (trisomy 13, 18, 21, Turner), congenital infections (CMV, rubella, toxoplasmosis), congenital anomalies, multiple gestation
Placental: placental insufficiency, previa/abruption, abnormal cord insertion
Maternal:
“What’s the most sensitive ultrasound parameter for FGR?” → Abdominal circumference.
Birth weight >4000 g (8 lb 13 oz) OR >4500 g (some definitions) OR >90th percentile for GA. Incidence 10% of births.
Increases C-section rate without improving outcomes.
Excessive amniotic fluid: AFI ≥24 cm OR single deepest pocket ≥8 cm. Incidence 1–2%.
| Severity | Management |
|---|---|
| Mild (AFI 24–30, asymptomatic) | Expectant; serial ultrasounds; antenatal testing |
| Moderate-severe (AFI >30 OR symptomatic) | Therapeutic amniocentesis (amnioreduction) — remove 1–2 L slowly, may repeat; indomethacin (↓ fetal urine production) with caution — risk premature ductus arteriosus closure, usually avoid after 32 weeks |
| Delivery | Consider at 39 weeks if persistent |
“Polyhydramnios + absent stomach bubble on ultrasound?” → Esophageal atresia.
Decreased amniotic fluid: AFI <5 cm OR single deepest pocket <2 cm. Incidence 1–5%.
| Cause | Management |
|---|---|
| PROM | See rupture of membranes management |
| Uteroplacental insufficiency | Treat underlying cause; antenatal testing 1–2×/week; consider delivery if worsening |
| Fetal renal anomalies | Prognosis depends on severity; bilateral renal agenesis (Potter) = lethal; multidisciplinary counseling |
| Post-term pregnancy | Deliver (typically induce at 41 weeks) |
| Delivery | Induce if ≥36–37 weeks, non-reassuring testing, or worsening oligohydramnios; continuous fetal monitoring (↑ cord compression → variable decelerations); amnioinfusion during labor if variable decelerations |
Maternal production of anti-D (Rh) antibodies against fetal Rh+ RBCs → maternal IgG crosses placenta → fetal hemolysis. Only occurs in Rh-negative mother carrying Rh-positive fetus.
Hemolytic disease of fetus/newborn (HDFN) → fetal anemia → high-output cardiac failure → hydrops fetalis; neonatal jaundice → kernicterus risk; fetal demise.
Correct: A) 3 pregnancies: 2 term deliveries, 0 preterm, 1 abortion, 2 living children
Concept: TPAL system & obstetric terminology Recall
Why A: G3P2012 = G3 (3 total pregnancies); P2012 = 2 term, 0 preterm, 1 abortion, 2 living children.
Discriminator: Parity counts deliveries beyond 20 weeks; the four TPAL digits each map to a specific category.
| B) 0 term, 2 preterm | Reverses the first two digits of P2012 |
| C) 2 pregnancies | Gravidity is 3, not 2 |
| D) 2 preterm | Second digit is 0, not 2 |
| E) 1 living child | Fourth digit is 2, not 1 |
Trap: Digit misreading — each position of TPAL is a different category.
Future alert: Read TPAL left to right: term-preterm-abortions-living.
Correct: A) Consider the pregnancy ectopic until proven otherwise and evaluate further
Concept: Ectopic pregnancy — discriminatory zone Interpretation
Why A: At β-hCG ≥1500 mIU/mL (transvaginal), an intrauterine pregnancy should be visible. No IUP at 2000 mIU/mL is highly suspicious for ectopic, so the patient stays in workup (serial β-hCG, careful evaluation).
Discriminator: The discriminatory zone number (1500 on board exams) plus the absence of an IUP.
| B) Reassure and repeat US later | Delays a potentially life-threatening diagnosis |
| C) OCPs | Irrelevant and harmful in a possible ectopic |
| D) Transabdominal US only | TVUS is the required test at this β-hCG range |
| E) RhoGAM and discharge | RhoGAM may be needed later, but evaluation comes first |
Trap: Anchoring on “early pregnancy loss” when the real issue is location.
Future alert: No IUP at β-hCG ≥1500 = ectopic until proven otherwise.
Correct: B) This is true anemia in pregnancy and warrants investigation
Concept: Physiologic vs true anemia in pregnancy Interpretation
Why B: Hemoglobin normally falls only to 11–12 g/dL in pregnancy; values <11 g/dL are true anemia and need investigation regardless of symptoms.
Discriminator: The threshold: 11 g/dL, not 9 or 10.
| A) Physiologic, no workup | Dangerous dismissal of a true anemia |
| C) Transfuse immediately | Transfusion is not first-line for asymptomatic mild anemia |
| D) Normal at 9 g/dL | Wrong threshold — <11 is abnormal |
| E) Iron only if symptomatic | Investigation, not symptom-based treatment, is the point |
Trap: Physiologic dilutional anemia is real but has limits — 10.2 is past them.
Future alert: Hb <11 g/dL in pregnancy = investigate.
Correct: B) Rh(D) immune globulin if Rh-negative and repeat CBC
Concept: Prenatal visit schedule (28 weeks) Recall
Why B: At 28 weeks: Rh immune globulin for Rh-negative mothers (after antibody screen) plus repeat CBC to check for anemia.
Discriminator: Time-stamp each screening test: GBS swab 36–38 weeks, GCT 24–28 weeks, quad screen 15–20 weeks.
| A) GBS culture | 36–38 weeks, not 28 |
| C) Quad screen | 15–20 weeks |
| D) 50-g GCT | 24–28 weeks — already due, but “28 weeks” specifically flags Rh + CBC |
| E) Anatomic ultrasound | 18–20 weeks |
Trap: Overlapping windows (GCT is 24–28) — the 28-week visit pair is Rh + CBC.
Future alert: 28 weeks = RhoGAM + repeat CBC.
Correct: A) Fundal height equals gestational age in cm only after 20 weeks, so this is appropriate
Concept: GA determination — fundal height Interpretation
Why A: After 20 weeks, fundal height in cm approximates GA in weeks (reaches umbilicus at 20 weeks, +1 cm/week). 26 cm at 26 weeks is appropriate.
Discriminator: The “after 20 weeks” qualifier makes the rule valid here.
| B) Unreliable before 30 weeks | Rule applies from 20 weeks onward |
| C) FGR | FGR is suspected when lag >3 cm |
| D) Polyhydramnios | Growth matches dates exactly |
| E) Always 20 cm | Ignores weekly growth |
Trap: Applying the fundal-height rule before 20 weeks.
Future alert: Fundal height = GA in cm only after 20 weeks.
Correct: A) Trisomy 21
Concept: Quadruple screen interpretation Recall
Why A: Trisomy 21 gives “2 up, 2 down”: hCG ↑ and inhibin A ↑; AFP ↓ and estriol ↓.
Discriminator: Inhibin A direction splits Down from Edwards (Edwards = all markers down).
| B) Trisomy 18 | All four markers are down (“still under age at 18”) |
| C) NTD | Isolated high AFP with normal others |
| D) Gastroschisis | Isolated high AFP |
| E) Normal pregnancy | Matched marker pattern points to aneuploidy |
Trap: Using hCG alone (up in both Down and, to a lesser degree, some normals).
Future alert: Down = ↑hCG + ↑inhibin A + ↓AFP + ↓estriol.
Correct: A) Incorrect dating
Concept: Elevated MSAFP workup Recall
Why A: The most common cause of elevated MSAFP is incorrect dating; others include NTDs, abdominal wall defects, multiple gestation, fetal demise, and placental abnormalities.
Discriminator: “Most common” is the keyword — always the benign dating error.
| B) Fetal demise | A cause, but far less common |
| C) Abruption | A cause, not the most common |
| D) Anencephaly | Classic association, not the most common cause |
| E) Omphalocele | Raises AFP but is uncommon |
Trap: Picking the flashiest diagnosis instead of the most frequent one.
Future alert: ↑MSAFP — first think incorrect dating; workup = repeat + level II US + amniocentesis.
Correct: A) It cannot detect neural tube defects
Concept: cfDNA screening limitations Recall
Why A: cfDNA screens trisomies and sex chromosome aneuploidies but cannot detect NTDs (MSAFP/ultrasound remain the NTD tools).
Discriminator: “Cannot detect NTDs” is the classic cited limitation plus non-diagnostic status.
| B) Lower sensitivity than quad | False — cfDNA is the most sensitive |
| C) Must combine with NT | Optional, not required |
| D) Requires amniocentesis | It is a blood test |
| E) Diagnostic | It is screening; positive results need amniocentesis |
Trap: Confusing “most sensitive” with “diagnostic and complete.”
Future alert: cfDNA = aneuploidy only; NTDs still need MSAFP and anatomy scan.
Correct: A) Give intrapartum penicillin prophylaxis regardless of the negative culture
Concept: GBS prophylaxis indications Interpretation
Why A: GBS bacteriuria at ANY time in pregnancy is a prophylaxis indication at delivery, independent of the later rectovaginal culture.
Discriminator: The “any time” rule overrides a subsequent negative culture.
| B) No prophylaxis with negative culture | Ignores the bacteriuria rule |
| C) Amoxicillin only with fever | Prophylaxis is routine, not fever-triggered |
| D) Reculture in labor | No time for results; treat |
| E) Only if ROM >18 h | That is one risk factor path, not the rule here |
Trap: Letting a fresh negative culture override a historical indication.
Future alert: GBS bacteriuria anytime = intrapartum prophylaxis, always.
Correct: A) Ebstein anomaly
Concept: Teratogen-specific malformations Recall
Why A: Lithium exposure is classically associated with Ebstein anomaly (tricuspid valve abnormality).
Discriminator: Pairing teratogen to its signature defect is the entire question.
| B) Caudal regression | Diabetes |
| C) Fetal hydantoin syndrome | Phenytoin |
| D) Phocomelia | Thalidomide |
| E) Tooth discoloration | Tetracyclines |
Trap: Cross-matching the wrong drug-defect pair.
Future alert: Lithium → Ebstein anomaly.
Correct: A) Increase folic acid to 4 mg daily
Concept: Valproate teratogenicity prevention Recall
Why A: Valproic acid causes neural tube defects (spina bifida 1–2%); preconception folic acid is raised to 4 mg daily.
Discriminator: 4 mg folic acid is the specific dose for prior NTD or valproate/carbamazepine use.
| B) Switch to lithium | Lithium has its own teratogenicity (Ebstein) |
| C) Oral iron | Does not address NTD risk |
| D) Penicillin | No role here |
| E) Levothyroxine | Only if hypothyroid |
Trap: Standard 400 mcg dose confusion — high-risk women need 4 mg.
Future alert: Valproate/carbamazepine or prior NTD → folic acid 4 mg.
Correct: A) CMV
Concept: ToRCHHeS specific features Recall
Why A: Periventricular calcifications + microcephaly + sensorineural hearing loss is the CMV signature.
Discriminator: Calcification pattern is the split: periventricular = CMV; diffuse intracranial + chorioretinitis = toxoplasma.
| B) Toxoplasmosis | Diffuse intracranial calcifications + chorioretinitis + hydrocephalus |
| C) Rubella | Blueberry muffin rash, cataracts, PDA, deafness |
| D) Zika | Microcephaly with craniofacial disproportion |
| E) HSV | Skin/eye/mouth vesicles, encephalitis |
Trap: Any calcification reads as toxoplasma; location decides.
Future alert: Periventricular calcifications = CMV.
Correct: A) Hutchinson triad
Concept: Congenital syphilis stigmata Recall
Why A: Hutchinson triad — sensorineural deafness + interstitial keratitis + peg incisors — is classic late congenital syphilis.
Discriminator: All three components must be recognized as one named triad.
| B) Potter sequence | Renal agenesis + oligohydramnios + pulmonary hypoplasia |
| C) Turner stigmata | Lymphedema, webbed neck, streak gonads |
| D) Quintero stage III | TTTS staging |
| E) Liley zone III | Rh disease amniotic-fluid bilirubin |
Trap: Syndrome-name recall — know the eponym and its parts.
Future alert: Deafness + keratitis + peg incisors = Hutchinson triad (syphilis).
Correct: A) Incomplete abortion; surgical evacuation (D&C or MVA) or medical management
Concept: Types of spontaneous abortion Interpretation
Why A: Open os + partial passage of products = incomplete abortion; options are surgical (D&C or MVA) or medical.
Discriminator: “Open os” + “partial POC” is the incomplete signature (“the I’s are open”).
| B) Threatened | Closed os, bleeding, viable fetus |
| C) Complete | Everything passed, closed os, no treatment |
| D) Missed | Closed os, no bleeding, no cardiac activity |
| E) Septic | Fever, foul discharge — needs IV antibiotics + D&C |
Trap: Missing the “partially passed” detail that makes it incomplete.
Future alert: Open os + partial POC = incomplete abortion.
Correct: A) Crown-rump length of 8 mm with no cardiac activity
Concept: Ultrasound criteria for nonviable pregnancy Recall
Why A: CRL ≥7 mm without cardiac activity is a criteria for nonviability; 8 mm meets it.
Discriminator: The 7 mm CRL threshold (or sac ≥25 mm with no embryo).
| B) CRL 5 mm, no activity | Below threshold — repeat in 7–10 days |
| C) Sac 15 mm, no embryo | Below the 25 mm threshold |
| D) Yolk sac, no pole at 5 wk | Still early and normal |
| E) Visible heartbeat | Clearly viable |
Trap: Applying thresholds loosely on either side.
Future alert: CRL ≥7 mm no heartbeat or sac ≥25 mm no embryo = nonviable.
Correct: A) Single-dose methotrexate 50 mg/m² IM with day 4 and 7 β-hCG
Concept: Ectopic pregnancy — methotrexate candidacy Interpretation
Why A: Stable, unruptured, mass <3.5–4 cm, no cardiac activity, β-hCG <5000, normal organ function — all methotrexate criteria are met.
Discriminator: Verify every criterion, especially β-hCG <5000 and hemodynamic stability.
| B) Emergency salpingectomy | For ruptured/unstable |
| C) Expectant only | Reserved for very low β-hCG with falling titers |
| D) Mifepristone | Not the ectopic regimen |
| E) Immediate laparotomy | Surgery is for failed medical management or contraindications |
Trap: Jumping to surgery when medical management is clearly indicated.
Future alert: MTX when: stable + unruptured + <4 cm + no cardiac activity + β-hCG <5000.
Correct: A) Resuscitate and proceed to emergency surgery for ruptured ectopic
Concept: Ruptured ectopic — surgical emergency Analysis
Why A: Hemodynamic instability + shoulder pain (diaphragmatic irritation from hemoperitoneum) = ruptured ectopic: resuscitate, cross-match, and operate.
Discriminator: Shoulder pain + hypotension in early pregnancy = ruptured ectopic until proven otherwise.
| B) Methotrexate | Contraindicated in ruptured/unstable disease |
| C) Discharge | Life-threatening |
| D) Antibiotics | No infection picture |
| E) Routine US + clinic follow-up | Delays definitive care |
Trap: Treating a surgical abdomen as an outpatient workup.
Future alert: Shoulder pain + shock in early pregnancy = ruptured ectopic, operate.
Correct: A) Breastfeeding
Concept: Methotrexate contraindications Recall
Why A: Breastfeeding, hemodynamic instability, ruptured ectopic, immunodeficiency, liver/kidney disease, and blood dyscrasias contraindicate methotrexate.
Discriminator: The question asks for an absolute contraindication, not a relative caution or borderline value.
| B) β-hCG 4500 | Below 5000 — acceptable |
| C) Mass 3 cm | Below 3.5–4 cm — acceptable |
| D) Mild pain | Pain alone is not the instability that contraindicates |
| E) Primigravida | Not a contraindication |
Trap: Confusing eligibility criteria with contraindications.
Future alert: No MTX: breastfeeding, unstable, ruptured, immunodeficiency, organ disease.
Correct: A) Complete hydatidiform mole
Concept: Gestational trophoblastic disease Analysis
Why A: Preeclampsia before 20 weeks + “snowstorm” ultrasound + no fetal parts + very high β-hCG + theca-lutein cysts = complete mole.
Discriminator: Preeclampsia <24 weeks is virtually diagnostic of molar pregnancy (or multiples); no fetal parts + snowstorm favors complete mole.
| B) Partial mole | Has abnormal fetal tissue, lower hCG, fewer cysts |
| C) Choriocarcinoma | Follows moles; diagnosed on histology/surveillance |
| D) PSTT | Rare, different presentation |
| E) Multiple gestation | Fetal parts would be present |
Trap: Labeling early preeclampsia as idiopathic instead of molar.
Future alert: Preeclampsia <20–24 weeks = think mole.
Correct: A) To distinguish a new pregnancy from malignant transformation by β-hCG trends
Concept: Post-molar surveillance Recall
Why A: A new pregnancy would raise β-hCG and confuse surveillance for choriocarcinoma; contraception keeps the β-hCG signal unambiguous.
Discriminator: The purpose is interpretive clarity of the tumor marker.
| B) Ovarian hyperstimulation | Unrelated |
| C) Uterus cannot support pregnancy | Not the reason |
| D) DVT risk | Unrelated |
| E) Theca-lutein cyst resolution | Cysts resolve on their own |
Trap: Picking a plausible-sounding gynecologic reason instead of the monitoring rationale.
Future alert: Contraception 6–12 months post-mole = clean β-hCG surveillance.
Correct: A) Vitamin B6 (pyridoxine) 10–25 mg TID plus doxylamine 12.5 mg TID-QID
Concept: Hyperemesis gravidarum first-line therapy Recall
Why A: Pyridoxine + doxylamine is the first-line pharmacologic combination for nausea/vomiting in pregnancy.
Discriminator: Stepwise ladder — dietary changes and B6/doxylamine first, then metoclopramide/promethazine, then hospitalization.
| B) Ondansetron IV | Hospital-level, not first-line outpatient |
| C) Metoclopramide IV | Second step |
| D) Thiamine only | Adjunct for hospitalized patients (Wernicke prevention) |
| E) Promethazine PR | Second step |
Trap: Choosing the hospital drug when the patient is still outpatient.
Future alert: First-line hyperemesis: B6 + doxylamine.
Correct: A) Thiamine 100 mg IV daily
Concept: Hyperemesis complications — Wernicke prevention Recall
Why A: Thiamine replacement prevents Wernicke encephalopathy (ataxia, confusion, ophthalmoplegia) in prolonged vomiting.
Discriminator: Match the specific complication to its specific prevention.
| B) Potassium | Corrects hypokalemia, not Wernicke |
| C) Ondansetron | Controls vomiting |
| D) NS boluses | Corrects dehydration |
| E) NG feeding | Nutritional support, not targeted prevention |
Trap: Treating the vomiting but missing the vitamin deficiency.
Future alert: Severe hyperemesis → thiamine before dextrose to avoid Wernicke.
Correct: A) Cardiac defects — fetal echocardiography is indicated
Concept: Pregestational diabetes — fetal surveillance Recall
Why A: HbA1c >8% in diabetic pregnancy marks high risk for cardiac defects; fetal echocardiography is indicated alongside the anatomic scan.
Discriminator: The >8% threshold triggers the fetal echo.
| B) Cystic hygroma | Aneuploidy marker, not diabetic |
| C) Diaphragmatic hernia | Not diabetes-associated |
| D) Duodenal atresia only | Associated with aneuploidy, not the priority here |
| E) Skeletal dysplasia | Not the classic diabetes lesion |
Trap: Knowing diabetes causes anomalies but forgetting the echo trigger.
Future alert: HbA1c >8% + pregnancy → fetal echo.
Correct: B) Gestational diabetes — 2 of 4 values exceed thresholds
Concept: GDM diagnosis — Carpenter-Coustan Interpretation
Why B: Fasting 92 (normal, <95), 1-hour 195 (abnormal, ≥180), 2-hour 160 (abnormal, ≥155), 3-hour 135 (normal, <140). Two abnormal values diagnose GDM.
Discriminator: Apply each threshold individually before counting; ≥2 abnormal = diagnosis.
| A) 3 of 4 exceed | Only 1-hour and 2-hour are abnormal |
| C) Only 1 value exceeds | Two values exceed |
| D) All normal | Two values clearly exceed |
| E) Pregestational diabetes | Label depends on timing of onset, not thresholds |
Trap: Counting the 92 and 135 as abnormal; they are normal.
Future alert: CC thresholds: 95/180/155/140; ≥2 abnormal = GDM.
Correct: A) Screen with a 75-gram 2-hour OGTT at 6–12 weeks postpartum
Concept: GDM postpartum screening Recall
Why A: All GDM women need a 75-g 2-hour OGTT at 6–12 weeks postpartum to detect persistent dysglycemia, then rescreening every 1–3 years (50% develop type 2 DM within 10 years).
Discriminator: OGTT timing postpartum (6–12 weeks), not immediate discharge testing.
| B) Continue glyburide | Discontinue agents immediately postpartum |
| C) HbA1c at discharge | Not the standard immediate postpartum test |
| D) No follow-up | High future type 2 DM risk demands screening |
| E) Metformin prophylaxis | Not routine |
Trap: Stopping surveillance after a normal pregnancy course.
Future alert: GDM → postpartum OGTT at 6–12 weeks, then 1–3 yearly.
Correct: A) Preeclampsia without severe features
Concept: Hypertensive disorders classification Interpretation
Why A: New HTN ≥20 weeks + proteinuria with BP below the severe range (160/110) and no end-organ dysfunction = preeclampsia without severe features.
Discriminator: Proteinuria moves it from gestational HTN to preeclampsia; the BP (150/95) keeps it non-severe.
| B) Severe features | Requires SBP ≥160, DBP ≥110, or organ dysfunction |
| C) Gestational HTN | No proteinuria by definition |
| D) Chronic HTN | Diagnosed before 20 weeks |
| E) Eclampsia | Requires seizures |
Trap: Calling any preeclampsia “severe” based on anxiety, not criteria.
Future alert: Preeclampsia severity = BP ≥160/110 or any severe end-organ feature.
Correct: A) Expectant management with twice-weekly monitoring; deliver at 37 weeks
Concept: Preeclampsia without severe features — delivery timing Interpretation
Why A: At 33 weeks without severe features, manage expectantly with twice-weekly BP, labs, and fetal testing; deliver at 37 weeks.
Discriminator: No severe features → no magnesium, no immediate delivery, no aggressive BP goal.
| B) Immediate C-section | Only for severe features/deterioration |
| C) Magnesium + deliver at 34 | Magnesium is for severe features |
| D) Labetalol to <120/80 | Goal is <160/110, not normotension (placental hypoperfusion) |
| E) Induce today | Premature at 33 weeks with a stable picture |
Trap: Over-treating non-severe preeclampsia to the severe protocol.
Future alert: Non-severe preeclampsia <37 wk → expectant, deliver at 37.
Correct: A) Stop the infusion and monitor closely
Concept: Magnesium toxicity management Recall
Why A: At 8–10 mEq/L (loss of DTRs), stop the infusion and monitor closely; calcium gluconate is for respiratory depression or higher levels.
Discriminator: Loss of DTRs (8–10) vs respiratory depression (10–12): the antidote is given at 10–12+.
| B) Calcium gluconate now | Reserved for respiratory depression/cardiac arrest levels |
| C) Intubate | Not yet indicated |
| D) Double the infusion | Opposite of correct care |
| E) Diazepam | No role in magnesium toxicity |
Trap: Giving the antidote at the wrong level.
Future alert: Mg levels: >8 DTRs lost (stop), >10 respiratory depression (calcium gluconate), >12 arrest.
Correct: A) HELLP syndrome
Concept: HELLP syndrome recognition Analysis
Why A: Hemolysis (LDH 800, low haptoglobin) + elevated liver enzymes (AST 180) + low platelets (60,000) = HELLP, which can occur WITHOUT hypertension or proteinuria.
Discriminator: The normal BP/urine does not exclude HELLP — that is the classic trap.
| B) AFLP | Hypoglycemia, coagulopathy, jaundice dominate; no hemolysis triad |
| C) Gestational thrombocytopenia | Mild, isolated, no hemolysis/LFT elevation |
| D) TTP | Neurologic changes, fever, more profound anemia |
| E) Chronic HTN | No hemolysis or liver injury |
Trap: Demanding hypertension/proteinuria before diagnosing HELLP.
Future alert: HELLP can be normotensive and non-proteinuric.
Correct: A) Postpartum eclampsia is recognized and most occurs within 48 hours
Concept: Eclampsia timing Recall
Why A: Eclampsia is antepartum 50%, intrapartum 25%, postpartum 25% (up to 4 weeks, most within 48 hours); magnesium continues 24 hours postpartum.
Discriminator: Postpartum occurrence is expected, not impossible.
| B) Cannot occur after delivery | 25% occur postpartum |
| C) Almost always fatal | Serious but maternal death ~1–2% |
| D) Stop magnesium at delivery | Continue 24 hours postpartum |
| E) Always epilepsy after 24 h | Eclampsia can occur up to 4 weeks |
Trap: Stopping seizure prophylaxis at the moment of delivery.
Future alert: Postpartum eclampsia: up to 25%, mostly within 48 h — continue magnesium 24 h.
Correct: A) Hospitalize and start IV antibiotics
Concept: Pyelonephritis in pregnancy Recall
Why A: Pyelonephritis in pregnancy ALWAYS requires hospitalization with IV antibiotics (ceftriaxone/cefazolin/ampicillin+gentamicin) until afebrile 24–48 hours.
Discriminator: The pregnancy modifies management to inpatient care.
| B) Outpatient cephalexin | Inpatient care required |
| C) Nitrofurantoin 7 days | Wrong agent/scenario — this is pyelo, not ASB |
| D) Single-dose fosfomycin | For uncomplicated cystitis/ASB |
| E) Reassure and repeat | Dangerous delay |
Trap: Treating pregnancy pyelonephritis like a non-pregnant UTI.
Future alert: Pyelo in pregnancy = always admit + IV antibiotics.
Correct: A) Trimethoprim
Concept: Antibiotic safety in pregnancy Recall
Why A: Trimethoprim is a folate antagonist and is particularly avoided in the first trimester; sulfonamides are avoided near term (kernicterus); fluoroquinolones are avoided altogether (cartilage).
Discriminator: The stem pins first trimester — the strongest avoid-at-this-gestation answer with a mechanism.
| B) Amoxicillin-clavulanate | Safe in pregnancy |
| C) Cephalexin | Safe in pregnancy |
| D) Fosfomycin | Safe single dose |
| E) Nitrofurantoin preferred/safe | False as stated — nitrofurantoin is also avoided in the first trimester (theoretical G6PD hemolysis); it is used from the second trimester onward |
Trap: Nitrofurantoin is avoid-in-first-trimester too; the option鈥檚 claim of being “preferred and safe at this gestation” is what makes it wrong.
Future alert: First trimester: avoid trimethoprim and nitrofurantoin; near term: avoid sulfonamides.
Correct: A) Ursodeoxycholic acid
Concept: Intrahepatic cholestasis of pregnancy Recall
Why A: UDCA 10–15 mg/kg/day divided BID improves pruritus and bile acids; bile acids 38 µmol/L is below the >40 threshold prompting even earlier delivery.
Discriminator: “Pruritus on palms/soles + elevated bile acids” = cholestasis → UDCA.
| B) Antihistamines alone | Only adjunctive |
| C) Cholestyramine alone | Less effective than UDCA |
| D) Prednisolone | No role |
| E) Immediate delivery | Delivery considered at 36–37 weeks, not immediately at 31 |
Trap: Delivering prematurely when medical therapy exists.
Future alert: Cholestasis → UDCA; deliver 36–37 weeks; stillbirth risk ↑ if bile acids >40.
Correct: A) Acute fatty liver of pregnancy; deliver immediately
Concept: AFLP recognition & management Analysis
Why A: Nausea/vomiting, RUQ pain, jaundice, profound hypoglycemia (42), coagulopathy, thrombocytopenia in the third trimester = AFLP — a medical emergency requiring immediate delivery regardless of GA.
Discriminator: Profound hypoglycemia is the pathognomonic pointer to AFLP over HELLP.
| B) HELLP, deliver at 37 | No hemolysis triad; delayed delivery is wrong |
| C) Viral hepatitis | Does not deliver; hypoglycemia/coagulopathy point to AFLP |
| D) Cholestasis | Pruritus + bile acids, not hypoglycemia/coagulopathy |
| E) Cholecystitis | No jaundice/hypoglycemia picture |
Trap: Waiting for confirmatory tests instead of delivering.
Future alert: Late-pregnancy RUQ pain + hypoglycemia + coagulopathy = AFLP, deliver now.
Correct: A) Continue labetalol; avoid ACE inhibitors/ARBs and atenolol
Concept: Chronic hypertension — medication safety Interpretation
Why A: Labetalol (with methyldopa and nifedipine) is first-line safe; ACE inhibitors/ARBs cause fetal renal dysgenesis/oligohydramnios and atenolol is associated with IUGR.
Discriminator: Which agents are safe vs avoidable in pregnancy.
| B) Switch to enalapril | ACE inhibitor — teratogenic |
| C) Switch to atenolol | Associated with IUGR |
| D) Stop all antihypertensives | Leaves chronic HTN untreated |
| E) Add spironolactone | Not the safe first-line picture |
Trap: Choosing a familiar BP drug that is unsafe in pregnancy.
Future alert: Pregnancy-safe antihypertensives: methyldopa, labetalol, nifedipine.
Correct: A) Digital vaginal examination
Concept: APH — contraindicated exam Recall
Why A: A digital vaginal exam can precipitate massive hemorrhage if placenta previa is present; it is contraindicated until previa is ruled out. Speculum and ultrasound are acceptable.
Discriminator: Digital vs speculum — one is forbidden, the other permitted.
| B) Speculum exam | Acceptable in APH |
| C) Transabdominal US | Safe imaging |
| D) Transvaginal US | Safe and the gold standard for previa |
| E) Fetal monitoring | Always indicated |
Trap: Treating all pelvic exams as equally risky.
Future alert: Painless APH: no digital exam until previa excluded.
Correct: A) Abruption is a clinical diagnosis; negative ultrasound does not exclude it
Concept: Placental abruption — diagnosis Interpretation
Why A: Ultrasound is only ~50% sensitive for abruption; the diagnosis is clinical (painful bleeding + board-like uterus + fetal distress).
Discriminator: The low sensitivity number is the whole trap.
| B) 95% sensitive, excluded | Inverts the true sensitivity |
| C) Vasa previa | Painless bleeding at ROM, not constant pain/rigidity |
| D) Placenta previa | Painless bright red, soft uterus |
| E) Uterine rupture | Different risk set; board-like uterus + fetal distress here is abruption |
Trap: Trusting a negative ultrasound over a classic clinical picture.
Future alert: Abruption = clinical diagnosis; US 50% sensitive.
Correct: A) Scheduled C-section at 36–37 weeks after corticosteroids
Concept: Placenta previa — delivery planning Recall
Why A: All placenta previas deliver by C-section at 36–37 weeks (after steroids at 34–36 weeks), balancing prematurity against bleeding risk.
Discriminator: 36–37 weeks is the fixed previa window — not immediate, not term.
| B) Vaginal at 38 | Contraindicated in complete previa |
| C) Immediate C-section | Only for unstable bleeding ≥34 wks |
| D) Reassess at 40 | Too late — bleeding risk climbs |
| E) ECV and trial of labor | Dangerous and wrong |
Trap: Waiting to term in a previa.
Future alert: Previa → C-section at 36–37 weeks after steroids.
Correct: A) Vasa previa; emergency C-section
Concept: Vasa previa — acute presentation Interpretation
Why A: Painless bleeding at ROM + acute severe fetal bradycardia = ruptured fetal vessels (vasa previa) → EMERGENCY C-section with neonatal resuscitation.
Discriminator: The pairing of ROM-timed bleeding with bradycardia is unique to vasa previa.
| B) Abruption, expectant | Painful bleeding + rigidity; and never expectant with distress |
| C) Previa, later C-section | Previa bleeds before labor, usually no acute bradycardia |
| D) Uterine rupture, hysterectomy | Different maternal picture |
| E) Cord prolapse, continue labor | Bleeding + bradycardia at ROM is vasa previa; emergent delivery |
Trap: Anagramming toward abruption because it “also causes bleeding.”
Future alert: Bleeding + bradycardia at ROM = vasa previa, emergency C-section.
Correct: A) Plan delivery at a tertiary center with scheduled C-section hysterectomy at 34–36 weeks
Concept: Placenta accreta spectrum — management Analysis
Why A: Previa + ≥2 prior C-sections (40–60% accreta risk) with US findings of lacunae and lost hypoechoic zone = accreta. Deliver at 34–36 weeks at a tertiary center via planned C-section hysterectomy with placenta left in situ.
Discriminator: Risk-stratify (previa + prior CS) then match the protocol (tertiary, scheduled, hysterectomy).
| B) Vaginal with induction | Catastrophic in accreta |
| C) Manual placental removal | Explicitly forbidden — causes massive hemorrhage |
| D) Methotrexate now | Only in selected conservative cases, not the plan |
| E) C-section at 40 without steroids | Wrong timing and no preparation |
Trap: Treating accreta like a routine previa delivery.
Future alert: Previa + prior C-section = suspect accreta; tertiary planned C-section hysterectomy.
Correct: A) Twin-twin transfusion syndrome; fetoscopic laser ablation of communicating vessels
Concept: Twin-twin transfusion syndrome — diagnosis and treatment Interpretation
Why A: Monochorionic-diamniotic twins at 18 weeks with a deepest vertical pocket ≤2 cm around the donor and ≥8 cm around the recipient meet Quintero criteria for TTTS. Definitive treatment is fetoscopic laser photocoagulation of the communicating placental vessels; expectant management is reserved for selected stage I cases.
Discriminator: The donor-oligo/recipient-poly pairing with the 2 cm/8 cm DVP cut-offs.
| B) TTTS, expectant management alone | Only selected stage I is expectant; laser is the definitive treatment |
| C) Cord entanglement, immediate C-section | Entanglement is the monoamniotic problem, not the picture here |
| D) Selective IUGR, delivery at 38 weeks | No poly/oligo discrepancy in sIUGR |
| E) TAPS, transfusion of the recipient | TAPS is chronic anemia/polycythemia without oligo-poly sequence |
Trap: Choosing the “less invasive” option because laser sounds aggressive — in TTTS it is the definitive therapy.
Future alert: MCDA + donor DVP ≤2 cm + recipient DVP ≥8 cm = TTTS → fetoscopic laser.
Correct: A) The twins are dichorionic and at lowest TTTS risk
Concept: Chorionicity by first-trimester ultrasound Interpretation
Why A: A thick dividing membrane plus the lambda (twin peak) sign at the inter-twin membrane insertion is diagnostic of dichorionic diamniotic twins. Separate placentas mean placental anastomoses are absent, so TTTS risk is lowest and routine TTTS screening is not needed.
Discriminator: Lambda sign = dichorionic; T sign = monochorionic.
| B) Monochorionic, TTTS screening from 16 weeks | That is the T-sign picture, not lambda |
| C) The twins are monoamniotic | Monoamniotic twins have no dividing membrane at all |
| D) The twins are conjoined | Not a chorionicity question |
| E) Chorionicity cannot be determined | First trimester is the best time to determine it |
Trap: Reversing the lambda and T signs — the classic twin-anatomy error.
Future alert: Lambda (twin peak) = dichorionic; T sign = monochorionic.
Correct: A) Abdominal circumference <10th percentile; deliver at 38–39 weeks
Concept: Fetal growth restriction — screening parameter and delivery timing Analysis
Why A: Abdominal circumference is the single most sensitive ultrasound parameter for FGR because liver glycogen stores deplete first and the AC lags earliest. With a normal umbilical artery Doppler (late-onset FGR), delivery is planned at 38–39 weeks — there is no indication for preterm rescue delivery.
Discriminator: AC for detection + normal Doppler = no urgency, deliver at 38–39 weeks.
| B) BPD, deliver 32–34 weeks | BPD is insensitive; 32–34 weeks is for severe early FGR with abnormal Dopplers |
| C) Femur length, deliver immediately | FL is insensitive and immediate delivery is unjustified with normal Doppler |
| D) Head circumference, deliver at 37 weeks | HC is a late finding and 37 weeks is not the standard timing |
| E) AFI <5, deliver at 40 weeks | AFI is an associated finding, not the sensitive parameter; 40 weeks is too late |
Trap: Rushing to deliver on a single lagging measurement without Doppler evidence of compromise.
Future alert: FGR detection = AC <10th percentile; normal UA Doppler → deliver at 38–39 weeks.
Correct: A) Assessing lung maturity in the third trimester (L/S ratio)
Concept: Indications for amniocentesis Recall
Why A: Fetal lung maturity testing (lecithin/sphingomyelin ratio ≥2 or lamellar body count) is a third-trimester amniocentesis performed when early delivery is contemplated. That is the only listed indication that matches the technique.
Discriminator: L/S ratio = lung maturity sample; karyotype = aneuploidy sample. Timing differs (3rd vs 2nd trimester).
| B) Aneuploidy screening at 16 weeks | Karyotyping is a second-trimester amnio, not a lung-maturity test |
| C) Ruling out NTDs at 12 weeks | NTD screening is maternal serum AFP plus ultrasound |
| D) Diagnosing GBS colonization | GBS is a vaginal/rectal swab |
| E) Evaluating placenta previa | Previa is diagnosed by ultrasound |
Trap: Conflating the karyotype amnio (2nd trimester) with the maturity amnio (3rd trimester).
Future alert: Lung-maturity amniocentesis = third trimester, L/S ratio.
Correct: A) Inpatient monitoring and C-section at 32–34 weeks
Concept: Monoamniotic twins — management Analysis
Why A: Monoamniotic twins share a single sac, so cord entanglement threatens both fetuses at any time. Management is inpatient (or intensive in-hospital) monitoring from viability onward with planned C-section at 32–34 weeks to prevent late fetal death.
Discriminator: Monoamniotic = C-section at 32–34 weeks with monitoring, not a wait-and-deliver approach.
| B) Outpatient, delivery at 38 weeks | Too late; entanglement risk climbs steeply after 32 weeks |
| C) Vaginal delivery at 37 weeks | Monoamniotic twins are delivered by planned C-section |
| D) Trial of labor at 36 weeks | No trial of labor for monoamniotic twins |
| E) C-section at 40 weeks without monitoring | Unscreened delay is the worst option |
Trap: Managing monoamniotic twins like uncomplicated MCDA twins and deferring delivery.
Future alert: Monoamniotic twins → inpatient monitoring + C-section at 32–34 weeks.
Correct: A) Elective C-section
Concept: Macrosomia — delivery planning in a non-diabetic woman Analysis
Why A: An estimated fetal weight of 5100 g in a non-diabetic woman exceeds the 5000 g threshold, so elective C-section is indicated to prevent shoulder dystocia and brachial plexus injury. (In diabetic women the threshold is 4500 g.)
Discriminator: The 5000 g non-diabetic / 4500 g diabetic cut-offs.
| B) Induction for suspected macrosomia | Induction does not reduce shoulder dystocia and raises C-section risk |
| C) Trial of labor, expectant | Vaginal delivery of a 5100 g fetus carries high injury risk |
| D) Forceps at full dilation | Instrumental delivery increases dystocia risk |
| E) Deliver at 41 weeks if no labor | Awaiting only worsens the macrosomia |
Trap: Inducing for suspected macrosomia — a proven non-beneficial intervention in this situation.
Future alert: EFW ≥5000 g (non-diabetic) or ≥4500 g (diabetic) → elective C-section.
Correct: A) Esophageal atresia
Concept: Polyhydramnios — fetal causes Interpretation
Why A: Polyhydramnios (AFI 26 cm) with an absent fetal stomach bubble in an otherwise normal fetus points to failure of amniotic-fluid swallowing — classically esophageal atresia, usually with a distal tracheoesophageal fistula.
Discriminator: Polyhydramnios + absent stomach bubble = obstruction to swallowing.
| B) Bilateral renal agenesis | Causes oligohydramnios, not polyhydramnios |
| C) Posterior urethral valves | Urinary obstruction → oligohydramnios |
| D) Diaphragmatic hernia | Stomach herniates into the chest; classically not the absent-bubble-with-poly pattern |
| E) Omphalocele | No effect on amniotic fluid volume |
Trap: Reaching for renal causes of abnormal fluid — they cause oligo, not poly.
Future alert: Polyhydramnios + absent stomach bubble = esophageal atresia.
Correct: A) Pulmonary hypoplasia
Concept: Early severe oligohydramnios — fetal complications Interpretation
Why A: Severe oligohydramnios starting at 16 weeks (deepest pocket 1.5 cm) removes the amniotic-fluid cushion and mechanical distension needed for lung development, so pulmonary hypoplasia is the most serious associated fetal complication; limb compression and Potter sequence features follow.
Discriminator: The early gestational timing — the lung grows during this window.
| B) Shoulder dystocia | Associated with macrosomia, not oligohydramnios |
| C) Postpartum hemorrhage | A maternal, not fetal, complication |
| D) Neonatal jaundice | Unrelated to fluid volume |
| E) Polycythemia | Not the classic serious consequence of oligohydramnios |
Trap: Offering generic neonatal complications instead of the mechanism-specific one.
Future alert: Pre-viable severe oligohydramnios → think pulmonary hypoplasia first.
Correct: B) 300 mcg
Concept: Rh immune globulin in threatened abortion Recall
Why B: Any bleeding in an Rh-negative, unsensitized woman is an indication for anti-D prophylaxis regardless of whether the pregnancy is ultimately viable. The standard full dose is 300 mcg, which covers up to 30 mL of fetal whole blood (about 15 mL of fetal RBCs).
Discriminator: Bleeding in Rh-negative pregnancy → RhIG now; viability is assessed, not assumed.
| A) 50 mcg | A microdose option, not the standard indicated dose for this event |
| C) 1000 mcg | Not a standard single anti-D dose |
| D) None, pregnancy not viable | Cannot assume non-viability from a threatened abortion |
| E) None, sensitization has not occurred | Prophylaxis exists precisely to prevent sensitization |
Trap: Withholding anti-D because “the pregnancy may abort anyway.”
Future alert: First-trimester bleeding in Rh-negative → 300 mcg Rh immune globulin.
Correct: A) Intrauterine transfusion via cordocentesis
Concept: Fetal anemia in Rh alloimmunization Analysis
Why A: A critical anti-D titer (≥1:16–1:32) with a rising MCA peak systolic velocity >1.5 MoM indicates significant fetal anemia from hemolysis. At 26 weeks the management is intrauterine transfusion via cordocentesis to buy gestational time before delivery.
Discriminator: MCA PSV is the noninvasive marker of fetal anemia; IUT is the definitive in-utero treatment.
| B) RhoGAM 300 mcg now | Anti-D is prophylaxis for the unsensitized; useless once sensitized |
| C) Exchange transfusion of the mother | Maternal exchange does not treat fetal anemia |
| D) Deliver immediately at 26 weeks | Too premature; IUT aims to delay delivery safely |
| E) Oral iron supplementation | This is hemolytic anemia, not iron deficiency |
Trap: Giving anti-D to an already-sensitized woman — the classic auto-pilot error.
Future alert: Critical titer + MCA PSV >1.5 MoM = fetal anemia → intrauterine transfusion.