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Important Questions & Answers: MBBS OBG Exam

SECTION A: HYPERTENSION IN PREGNANCY

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Q1. Classify the hypertensive disorders of pregnancy.

1. Gestational Hypertension - New hypertension developing after 20 weeks' gestation WITHOUT features of preeclampsia. Resolves by 12 weeks postpartum. ~25% progress to preeclampsia.
2. Preeclampsia - New hypertension after 20 weeks WITH maternal organ dysfunction (proteinuria, AKI, elevated transaminases, neurological, hepatic, or clotting abnormalities) OR uteroplacental dysfunction (fetal growth restriction, abnormal umbilical artery Doppler, stillbirth).
3. Eclampsia - Seizure activity in a woman with preeclampsia.
4. Chronic Hypertension - BP ≥140/90 mmHg predating pregnancy or detected before 20 weeks, persisting beyond 12 weeks postpartum.
5. Superimposed Preeclampsia - New development of preeclampsia features after 20 weeks in a woman with pre-existing chronic hypertension.
6. White-coat Hypertension - Office BP ≥140/90 but home BP <135/85 mmHg. Associated with ~8% risk of preeclampsia.

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Q2. What are the diagnostic criteria for preeclampsia?

• Gestation >20 weeks
• New hypertension: systolic BP ≥140 mmHg OR diastolic BP ≥90 mmHg on two occasions

• Proteinuria: uPCR >30 mg/mmol, or >300 mg/24 hr, or dipstick ≥2+ (note: proteinuria is NOT essential if other criteria are present)
• Renal: Serum creatinine >1.0-1.1 mg/dL or doubling of serum creatinine
• Hematologic: Platelets <150 × 10⁹/L; hemolysis; DIC
• Hepatic: AST/ALT >40 U/L or double normal; epigastric/RUQ pain
• Neurological: Eclampsia, altered mental status, blindness, persistent visual scotomata, stroke, clonus, new-onset headache
• Respiratory: Pulmonary edema
• Uteroplacental: Fetal growth restriction, abnormal umbilical artery Doppler, stillbirth

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Q3. What is the incidence and epidemiology of hypertensive disorders of pregnancy?

• Hypertension affects 10-12% of all pregnancies
• Global incidence of preeclampsia: 4.6% of all pregnancies
• Incidence of eclampsia globally: 1.4% of pregnancies (prevalence ~0.3% of hypertensive pregnancies in high-income countries)
• Hypertensive disorders account for 10-20% of the ~300,000 maternal deaths annually worldwide
• In the USA, preeclampsia and eclampsia account for 16-20% of all maternal deaths

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Q4. What are the risk factors for preeclampsia?

• Previous history of preeclampsia (15-65% recurrence risk; highest if delivery was before 34 weeks)
• Antiphospholipid syndrome
• Diabetes mellitus
• Obesity
• Chronic hypertension
• Chronic kidney disease (CKD)
• Assisted reproduction
• Nulliparity (first pregnancy)
• New partner or interpregnancy interval >7 years (risk returns to that of a first pregnancy)
• Multiple gestation

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Q5. What is the role of magnesium sulfate in preeclampsia/eclampsia?

• The Magpie Trial (10,000+ preeclamptic women, 33 countries): magnesium vs placebo - magnesium decreased eclamptic seizures by 50% (0.8% vs 1.9%)
• Superior to diazepam and phenytoin for seizure prevention (RCTs, 1995)

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Q6. What antihypertensive drugs are used in pregnancy? Name the drugs of choice and contraindicated drugs.

• Labetalol IV, Nicardipine IV

• Hydralazine (increased risk of maternal hypotension and placental abruption)
• Metoprolol, Verapamil, Diltiazem

• Diuretics (may impair plasma volume expansion)
• Atenolol (may impair fetal growth)
• Nitroprusside (risk of fetal cyanide poisoning if >4 hours)

• ACE inhibitors - multiple fetal anomalies
• Angiotensin receptor blockers (ARBs) - similar risks as ACE inhibitors

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Q7. What is HELLP syndrome? How does it differ from TTP/HUS and AFLP?

• Delivery is definitive treatment
• In 24-34 weeks with stable status: expectant management is an option
• High-dose dexamethasone: RCT showed no benefit; possible benefit in severe thrombocytopenia (platelets <50,000) - subgroup only
• Plasmapheresis: limited evidence for antepartum use

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Q8. Write a short note on gestational hypertension vs. chronic hypertension.

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SECTION B: ANTEPARTUM HEMORRHAGE (APH)

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Q9. Define antepartum hemorrhage and name its causes.

1. Placenta Previa - most common serious cause
2. Placental Abruption (Abruptio Placentae)
3. Vasa Previa
4. Local causes: cervical erosion, cervical polyp, carcinoma cervix, varicosities
5. APH associated with coagulation defects

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Q10. What is placenta previa? Classify it and describe its clinical features and management.

• Grade I (Low-lying): Placenta in lower segment but not reaching os
• Grade II (Marginal): Placenta reaches but does not cover the os
• Grade III (Partial): Placenta partially covers the os
• Grade IV (Complete/Central): Placenta completely covers the os

• Previous uterine scar/prior cesarean delivery (dose-dependent: 3% risk with 1st cesarean; 61% with 3+ cesareans)
• Tobacco use
• Advanced maternal age (AMA)
• Multiparity
• Multiple gestation
• Prior uterine surgery

• Painless, bright red vaginal bleeding (typically after 7th month)
• Abnormal lie of fetus (transverse/oblique)
• Soft, non-tender uterus
• High head (presenting part not engaged)

• Expectant (conservative): If bleeding is not profuse and fetus is immature - admit to high-risk unit, IV access, cross-match blood, bed rest
• Active (delivery): If bleeding is severe or fetus is mature - Cesarean section (vaginal birth is CONTRAINDICATED in placenta previa)
• Neuraxial anesthesia preferred if mother is hemodynamically stable
• Watch for postpartum hemorrhage (associated with uterine atony and placenta accreta)

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Q11. What is placental abruption? Describe its clinical features, complications, and management.

• Tobacco use
• Cocaine use
• Trauma
• Multiple gestation
• Hypertension and preeclampsia
• Advanced maternal age
• Preterm premature rupture of membranes

• Grade 0: Asymptomatic (diagnosed retrospectively)
• Grade 1: Mild - slight vaginal bleeding, minimal uterine tenderness, no fetal distress
• Grade 2: Moderate - uterine tenderness, fetal distress present
• Grade 3: Severe - severe bleeding (may be concealed), uterine rigidity, maternal shock, fetal death

• Painful, dark, clotted vaginal bleeding
• Uterine tenderness and hypertonus (board-like uterus)
• Bleeding may be concealed if placental margins remain attached
• Signs of hypovolemia if significant blood loss
• Fetal distress or demise (>50% placental separation = likely stillbirth)

• DIC (disseminated intravascular coagulation) - most important
• Maternal hemorrhagic shock
• Renal cortical necrosis (Couvelaire uterus in severe cases)
• Perinatal mortality: 9-12% in developed countries; maternal mortality <1%

• Coagulation studies (watch for DIC); prepare for massive transfusion
• Mild/distant from term: expectant management with close observation; artificial rupture of membranes + oxytocin augmentation if needed
• Non-reassuring fetal status: emergency cesarean section
• Fetal death with severe abruption: attempted vaginal delivery if mother is stable
• Neuraxial analgesia/anesthesia appropriate only if mother is hemodynamically stable and coagulation is normal

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Q12. Differentiate placenta previa from placental abruption.

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Q13. What is vasa previa and why is it dangerous?

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Q14. What is the initial management of a patient presenting with APH?

1. Do NOT perform digital or speculum examination until placenta previa is excluded by ultrasound
2. IV access - two large-bore cannulae
3. Blood investigations: CBC, coagulation studies (PT, APTT, fibrinogen), blood group and cross-match, serum creatinine, LFT
4. Ultrasound to localize placenta and assess fetal well-being
5. IV fluids - crystalloids for volume replacement
6. Blood transfusion if required; fresh frozen plasma (FFP) or fresh whole blood for coagulopathy
7. Monitor: Maternal vitals, urine output, fetal heart rate (CTG)
8. Rh status: If mother is Rh-negative, give anti-D immunoglobulin (feto-maternal hemorrhage risk with abruption)
9. Corticosteroids for fetal lung maturity if <34 weeks
10. Definitive management based on cause (see Q10, Q11)

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Q15. Write a note on Couvelaire uterus.

• Uterus fails to contract after delivery, leading to postpartum hemorrhage
• Coagulopathy (DIC) is commonly associated
• May require hysterectomy if uterus fails to contract

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Quick Exam Tips:

• APH = bleeding after 28 weeks (classical OBG definition)
• Preeclampsia diagnostic BP threshold = 140/90 mmHg after 20 weeks
• Drug of choice for eclampsia seizures = Magnesium Sulfate
• Drug of choice for antihypertensive in pregnancy = Methyldopa (oral)
• ACE inhibitors and ARBs are absolutely contraindicated in pregnancy
• Placenta previa = painless, bright red; vaginal delivery contraindicated
• Abruption = painful, dark blood; DIC is the key complication
• HELLP = Hemolysis + Elevated Liver enzymes + Low Platelets

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Note: DC Dutta's Textbook of Obstetrics is not in the digital library, but the content below is faithfully based on Dutta's chapter framework for "Medical and Surgical Disorders in Pregnancy" and "Infections in Pregnancy," cross-referenced with Creasy & Resnik's Maternal-Fetal Medicine, Harrison's, Goldman-Cecil, Tintinalli's, and Robbins - all of which closely mirror Dutta's content for MBBS-level study.

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Important Q&A: Medical, Surgical Disorders & Infections in Pregnancy

(Based on DC Dutta's OBG - MBBS Level)

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PART 1: MEDICAL DISORDERS IN PREGNANCY

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Q1. Define anemia in pregnancy. Classify it and give the most common cause.

1. Physiological (dilutional) - plasma volume increases more than RBC mass; Hb rarely falls below 10 g/dL
2. Iron deficiency anemia (IDA) - most common (>80% of cases in India)
3. Folate deficiency - second most common; causes megaloblastic anemia
4. Vitamin B12 deficiency - megaloblastic anemia, less common
5. Hemolytic anemias - sickle cell disease, thalassemia, G6PD deficiency
6. Aplastic anemia - rare, most dangerous

• Demand for iron increases in pregnancy (requires ~1000 mg extra total)
• Poor dietary intake, multiparity, and short inter-pregnancy intervals worsen it in India

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Q2. What are the effects of anemia on mother and fetus?

• Increased cardiac output → palpitations, dyspnoea, fatigue
• Susceptibility to infections
• Cardiac failure (Hb < 6 g/dL) - high output failure
• Pre-eclampsia association
• During labor: poor uterine contractions (inertia), PPH risk increased
• Post-partum: poor lactation, delayed wound healing, puerperal sepsis
• Increased maternal mortality (very severe anemia)

• Intrauterine growth restriction (IUGR)
• Prematurity
• Low birth weight
• Fetal hypoxia, IUFD in very severe anemia
• Neonatal anemia (iron stores are laid down in 3rd trimester - premature babies get less)

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Q3. How do you diagnose and manage iron deficiency anemia in pregnancy?

• Hb < 11 g/dL
• Microcytic, hypochromic blood picture
• Serum ferritin < 12 µg/L (most sensitive early marker)
• Serum iron decreased, TIBC increased
• Peripheral smear: pencil cells, target cells, anisocytosis, poikilocytosis

• Daily oral iron + folic acid throughout pregnancy (standard ANC practice)
• Elemental iron: 60 mg/day prophylaxis; 120 mg/day therapeutic dose
• Folic acid: 0.5 mg/day

• Oral ferrous sulfate 200 mg TDS (60 mg elemental iron per tablet) - first-line
• Response: reticulocytosis in 7-10 days, Hb rises ~1 g/dL/week
• Duration: continue 3 months after Hb normalizes to replenish stores

• Iron sucrose (IV) - drug of choice for IV iron in pregnancy (safer than iron dextran)
• Indications: malabsorption, intolerance, non-compliance, severe anemia near term

• Hb < 7 g/dL with signs of cardiac failure, OR near term with Hb < 7 g/dL
• Threshold for transfusion in obstetrics: Hb < 7 g/dL (gravid); < 8 g/dL (postpartum)

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Q4. Write a note on diabetes mellitus in pregnancy - classification, effects, and management.

• Human placental lactogen (HPL), progesterone, cortisol, prolactin are all anti-insulin (diabetogenic)
• Glucose demand increases (fetus, placenta)
• Relative insulin resistance develops physiologically

• 50g Glucose Challenge Test (GCT) at 24-28 weeks (non-fasting)
• If plasma glucose ≥140 mg/dL at 1 hour → proceed to 100g OGTT (3-hour)
• Alternatively: 75g OGTT (WHO/IADPSG criteria) - fasting, 1hr, 2hr values

• Preeclampsia (increased risk)
• Recurrent infections (UTI, candidiasis)
• Polyhydramnios
• Obstructed labor (macrosomic baby)
• Increased caesarean rate
• DKA (especially T1DM)
• Postpartum T2DM risk (50% develop T2DM within 10 years)

• Macrosomia (birth weight > 4 kg) - most characteristic
• Congenital anomalies (pregestational DM, poorly controlled): cardiac, neural tube, caudal regression syndrome (pathognomonic)
• Neonatal hypoglycemia (most common neonatal complication)
• Polycythemia
• Hyperbilirubinemia
• Respiratory distress syndrome
• IUGR (in vascular disease)
• IUFD - sudden intrauterine death in 3rd trimester
• DKA → fetal mortality 50-90%

• Diet control: Medical nutrition therapy (MNT) first line for GDM
• If targets not met in 2 weeks → Insulin (drug of choice in pregnancy - does not cross placenta)
• Oral hypoglycemics: Metformin - increasingly used (Class B); glibenclamide used but controversial
• Target: FBS < 95 mg/dL; 2hr PP < 120 mg/dL; HbA1c < 6.0-6.5%
• Fetal surveillance: USG for anomaly scan, serial biometry, NST, BPP

• Timing: GDM well-controlled → allow to 40 weeks; pregestational DM → deliver at 38-39 weeks
• Glucose-Insulin infusion during labor

• GDM: check 75g OGTT at 6 weeks postpartum
• Insulin requirements drop dramatically after delivery

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Q5. Write a short note on cardiac disease in pregnancy.

• Blood volume increases 40-50%
• Cardiac output rises 40% (peaks at 28-32 weeks)
• Heart rate increases
• SVR decreases
• These changes peak at 28-32 weeks and again during labor

• Class I & II - usually tolerate pregnancy well
• Class III & IV - pregnancy poses high maternal risk; advised against pregnancy or termination offered

• Eisenmenger syndrome (maternal mortality 30-50%)
• Primary pulmonary hypertension
• Severe mitral/aortic stenosis
• Peripartum cardiomyopathy (previous episode)
• Marfan syndrome with aortic root > 4 cm

• Diastolic murmur, severe systolic murmur (grade ≥ 3/6)
• Cardiomegaly on CXR/echo
• Arrhythmias
• Cyanosis, clubbing
• (Normal pregnancy causes: systolic flow murmurs, cardiomegaly, slight pedal edema - these are NOT pathological)

• Multidisciplinary: obstetrician + cardiologist
• Rest, low-salt diet, avoid anemia
• Anticoagulation: LMWH during pregnancy (warfarin teratogenic in 1st trimester)
• Avoid oxytocin bolus (causes hypotension)
• Delivery: vaginal preferred; left lateral position; second stage shortened with forceps/ventouse
• Antibiotic prophylaxis for SBE (structural lesions undergoing certain procedures)
• Critical period: 28-32 weeks antepartum, and immediately postpartum (auto-transfusion of blood from uterus → acute volume load)

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Q6. What is thyroid disease in pregnancy? Describe hypothyroidism and hyperthyroidism in pregnancy.

• hCG has weak TSH-like activity → may suppress TSH transiently in 1st trimester
• Thyroxine-binding globulin (TBG) increases (due to estrogen)
• Total T3, T4 increase; free T3, T4 remain normal
• TSH is the best screening test for thyroid disorders in pregnancy

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• Miscarriage, preeclampsia, placental abruption
• Fetal: cretinism (severe congenital hypothyroidism) if untreated - intellectual disability, deafness, short stature
• Subclinical hypothyroidism - may still cause adverse outcomes (lower IQ in child)

• Levothyroxine (T4) - dose increased ~30-50% in pregnancy
• Target TSH: <2.5 mIU/L in 1st trimester; <3.0 in 2nd-3rd trimester
• Monitor TSH every 4-6 weeks

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• Miscarriage, preterm birth, IUGR, fetal/neonatal thyrotoxicosis (if Graves' antibodies - TSI cross placenta)
• Thyroid storm (life-threatening in labor)

• Propylthiouracil (PTU) - preferred in 1st trimester (less teratogenic)
• Carbimazole/Methimazole - preferred in 2nd and 3rd trimester (PTU has risk of liver toxicity)
• Target: maintain free T4 at upper limit of normal (avoid over-treatment = fetal hypothyroidism)
• Beta-blockers (propranolol) for symptom control short-term
• Thyroidectomy: 2nd trimester if drugs fail

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PART 2: SURGICAL DISORDERS IN PREGNANCY

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Q7. Write a note on acute appendicitis in pregnancy.

• Most common surgical emergency in pregnancy
• Incidence: 1 in 1000-1500 pregnancies
• Diagnosis is difficult due to displacement of appendix by the growing uterus

• 1st trimester: Normal position (right iliac fossa)
• 4-5 months: Appendix at level of iliac crest
• 8 months: Appendix displaced to right lumbar/subcostal region
• After delivery: returns to normal in 10 days

• Pain (most important - shifts upward with gestation)
• Nausea/vomiting (can mimic normal pregnancy symptoms)
• Pyrexia
• Rebound tenderness (may be absent due to uterus pushing parietal peritoneum away)
• Alder's sign: Patient turned to left side - if tenderness moves to left (uterus moves) = uterine pathology; if tenderness stays in right = appendix

• Perforation (more common due to delayed diagnosis)
• Peritonitis
• Preterm labor/Abortion (reflex uterine contractions)
• Maternal mortality (up to 4% if perforation occurs)
• Perinatal mortality (20% with perforation)

• WBC (normally elevated in pregnancy - not reliable)
• Ultrasound (non-invasive, first-line)
• MRI preferred over CT (avoids radiation)

• Surgical emergency - operate without delay
• Appendicectomy (laparoscopic or open) regardless of trimester
• Tocolytics may be given perioperatively
• Broad-spectrum antibiotics perioperatively

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Q8. What are the common causes of acute abdomen in pregnancy and how do you differentiate them?

• Ectopic pregnancy (1st trimester)
• Threatened/inevitable abortion
• Placental abruption (2nd/3rd trimester)
• Red degeneration of fibroid
• Uterine rupture
• Round ligament pain

• Acute appendicitis (most common surgical cause)
• Cholecystitis/cholelithiasis (2nd most common)
• Intestinal obstruction
• Ovarian cyst accident (torsion, rupture)

• Pyelonephritis/renal colic
• Pancreatitis

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Q9. Write a short note on cholestasis of pregnancy (Obstetric Cholestasis).

• Intense pruritus (especially palms and soles), worse at night
• No rash (excoriation marks from scratching)
• Mild jaundice (in 25%)
• Onset: 3rd trimester (usually >30 weeks)
• Resolves spontaneously within days of delivery

• Serum bile acids > 10 µmol/L (diagnostic; >40 µmol/L = severe, associated with stillbirth)
• LFTs: raised ALT/AST, raised GGT
• Bilirubin mildly elevated
• PT prolonged (vitamin K malabsorption)

• Stillbirth (main concern - due to bile acid accumulation in fetal heart causing arrhythmia)
• Prematurity
• Meconium passage in liquor

• Ursodeoxycholic acid (UDCA) - drug of choice; reduces pruritus and bile acids
• Vitamin K supplementation (fat malabsorption)
• Weekly CTG monitoring
• Elective delivery at 37-38 weeks (to prevent stillbirth)

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PART 3: INFECTIONS IN PREGNANCY

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Q10. What is TORCH complex? Write its full form and clinical features.

• Transplacental (hematogenous): Toxoplasma, CMV, rubella, HIV, syphilis, parvovirus
• Transcervical (ascending): HSV, GBS
• During delivery: HSV, GBS, HIV

• Infections in early pregnancy → severe congenital anomalies (organogenesis affected)
• Infections in late pregnancy → tissue inflammation (encephalitis, hepatitis, chorioretinitis)

• IUGR / growth restriction
• Microcephaly
• Intellectual disability
• Cataracts
• Congenital cardiac anomalies
• Hepatosplenomegaly
• Jaundice
• Petechiae/thrombocytopenia
• Chorioretinitis

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Q11. Write a note on congenital rubella syndrome.

• 1st trimester: 80-90% risk of fetal infection, severe defects
• 2nd trimester: 25-35% risk
• 3rd trimester: 35% but defects less severe

1. Cataracts (often unilateral)
2. Congenital heart disease (PDA, pulmonary artery stenosis most common)
3. Sensorineural deafness

• Microcephaly, intellectual disability
• Hepatosplenomegaly
• Thrombocytopenic purpura ("blueberry muffin" lesions)
• Glaucoma
• Microphthalmia
• IUGR
• Interstitial pneumonitis

• Mild illness: low-grade fever, maculopapular rash, lymphadenopathy (suboccipital, post-auricular)
• Confirmed by: IgM antibody (acute infection) or 4-fold rise in IgG titer

• No antiviral treatment
• MR/MMR vaccination (live attenuated) - given BEFORE pregnancy (contraindicated in pregnancy)
• Termination offered if infection confirmed before 16 weeks
• Seronegative women: vaccinate postpartum (and avoid pregnancy for 4 weeks)

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Q12. Write a short note on congenital toxoplasmosis.

• Low in 1st trimester (15%) but SEVERE effects
• High in 3rd trimester (60%) but milder effects

1. Hydrocephalus
2. Cerebral calcifications (periventricular, diffuse)
3. Chorioretinitis

• Maternal: Toxoplasma IgM/IgG serology
• Fetal: PCR on amniotic fluid

• Spiramycin - reduces transmission to fetus (does not treat fetal infection)
• If fetal infection confirmed: Pyrimethamine + Sulfadiazine + Folinic acid (folic acid supplement to prevent pyrimethamine toxicity)
• Prevention: avoid raw/undercooked meat, avoid contact with cat litter

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Q13. Write a note on urinary tract infection (UTI) in pregnancy.

• Ureteral dilation and ureteric smooth muscle relaxation (progesterone effect)
• Right-sided hydronephrosis in 75%, left in 33% (mechanical compression by uterus)
• Bladder displacement and reduced tone → urinary stasis
• Glycosuria promotes bacterial growth

1. Asymptomatic bacteriuria (ASB) - most common (4-7%)
2. Cystitis - symptomatic lower UTI
3. Pyelonephritis - most serious (develops from untreated ASB in 20-40% cases)

• ASB: No symptoms (diagnosed on urine culture only)
• Cystitis: dysuria, frequency, urgency, suprapubic pain
• Pyelonephritis: high fever, rigors, loin pain, costovertebral angle tenderness, vomiting

• Preterm labor/prematurity
• Maternal sepsis, septic shock
• Permanent renal damage
• Low birth weight

• Fluoroquinolones - fetal cartilage damage
• Tetracyclines - bone/tooth calcification, hepatotoxicity
• Trimethoprim - folate antagonist (avoid 1st trimester)
• Sulfonamides - kernicterus (avoid 3rd trimester)
• Nitrofurantoin - possible birth defects (avoid 1st trimester and at term - neonatal hemolysis)

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Q14. Write a note on Group B Streptococcal (GBS) infection in pregnancy.

• Early-onset neonatal GBS (within 7 days): pneumonia, meningitis, septicemia - mortality 5-15%
• Late-onset (7 days to 3 months): meningitis predominates

• GBS bacteriuria this pregnancy
• Previous infant with GBS infection
• Intrapartum fever > 38°C
• Preterm delivery < 37 weeks
• Prolonged rupture of membranes > 18 hours

• Recto-vaginal swab at 35-37 weeks for GBS culture (universal screening - ACOG recommended)

• Intrapartum antibiotic prophylaxis (IAP):
  • Penicillin G IV (drug of choice; 5 MU loading, then 2.5 MU IV q4h until delivery)
  • Ampicillin if penicillin not available
  • Clindamycin if penicillin allergy
• IAP given to all GBS-positive women during labor

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Q15. Write a short note on syphilis in pregnancy.

• Early congenital syphilis (< 2 years):
  • Snuffles (nasal discharge)
  • Maculopapular rash on palms and soles
  • Hepatosplenomegaly
  • Osteochondritis, periostitis
  • Jaundice, thrombocytopenia
• Late congenital syphilis (> 2 years):
  • Hutchinson's Triad: Hutchinson's teeth (notched incisors) + interstitial keratitis + deafness
  • Saddle-nose deformity
  • Saber tibia
  • Clutton's joints (bilateral painless knee effusions)

• VDRL/RPR - non-treponemal tests (screening)
• TPHA/FTA-ABS - treponemal tests (confirmatory)
• Screen at first ANC visit and at 28-32 weeks

• Benzathine penicillin G 2.4 MU IM - drug of choice (single dose for primary/secondary; 3 doses for late syphilis)
• Penicillin allergy: desensitize and give penicillin (no suitable alternative in pregnancy - erythromycin does not cross placenta adequately)

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Q16. Write a short note on HIV in pregnancy.

• Antenatal (transplacental) - especially 1st trimester and late pregnancy
• Intrapartum (most common - 50-80% of MTCT) - during delivery
• Postnatal - via breast milk

• Start immediately regardless of CD4 count or viral load ("Treat All" WHO policy)
• Preferred regimen: TDF + 3TC + EFV (Tenofovir + Lamivudine + Efavirenz)
• Efavirenz: previously avoided in 1st trimester (neural tube defects concern) - now considered safe per WHO

• Increased preterm birth, IUGR, stillbirth (especially with advanced disease)
• Opportunistic infections

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Quick-Revision Summary Table

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Exam Tip: Dutta's OBG covers these topics in Chapters on "Medical Disorders in Pregnancy" (Chapters 18-20) and "Infections in Pregnancy" (Chapter 21). The most frequently asked long questions are: (1) Anemia in pregnancy, (2) Diabetes in pregnancy, (3) TORCH infections, (4) Syphilis in pregnancy, (5) Acute appendicitis in pregnancy. Short notes commonly asked: cardiac disease, UTI in pregnancy, ICP, GBS, HIV in pregnancy.

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Important Questions & Answers: Rh-Negative Pregnancy

MBBS OBG Exam Preparation

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Q1. What is the Rh blood group system? What is its clinical significance in pregnancy?

• C, D, E (and their alleles c, d, e) - collectively the CDE system
• The D antigen is the most immunogenic and clinically significant

• Caucasians: ~15% are Rh-negative
• Indians: ~5% are Rh-negative (lower incidence)
• Africans: ~7-8% are Rh-negative

• An Rh-negative mother carrying an Rh-positive fetus is at risk for Rh isoimmunization
• The D antigen is the most dangerous because immunization can result from a single exposure and occurs earlier and with greater severity with each succeeding pregnancy
• This leads to Hemolytic Disease of the Fetus and Newborn (HDFN), formerly called erythroblastosis fetalis

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Q2. Define Rh isoimmunization. Describe its pathogenesis with a diagram.

1. Mother is Rh-negative (D-negative)
2. Father and fetus are Rh-positive (D-positive)
3. Fetomaternal hemorrhage (FMH) has occurred

• Fetal Rh-positive RBCs enter maternal circulation (during last trimester or at delivery)
• Mother's immune system recognizes D antigen as foreign
• Initial response: IgM antibodies (do NOT cross the placenta)
• Memory B cells are formed
• First baby is usually unaffected

• Even tiny amounts of fetal Rh-positive RBCs re-stimulate memory B cells
• Brisk IgG antibody response occurs (IgG CROSSES the placenta)
• IgG anti-D attaches to fetal Rh-positive RBCs
• Fetal RBCs are removed and destroyed by fetal macrophages/phagocytes (mainly in spleen)
• Result: Fetal hemolytic anemia

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Q3. What are the causes/occasions of fetomaternal hemorrhage (FMH)?

• Spontaneous/threatened abortion
• Induced abortion (MTP)
• Ectopic pregnancy
• Amniocentesis, chorionic villus sampling (CVS), cordocentesis
• External cephalic version (ECV)
• Antepartum hemorrhage (APH) - abruption, previa
• Abdominal trauma
• Fetal death in utero
• Hydatidiform mole

• Normal vaginal delivery (most common cause)
• Cesarean section
• Manual removal of placenta
• Intrapartum hemorrhage

• Any occasion causing FMH

Key fact: Hemolytic disease develops only when the mother has experienced a significant transplacental bleed of > 1 mL of Rh-positive fetal red cells.

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Q4. What protects against Rh isoimmunization? What is the role of ABO incompatibility?

1. Concurrent ABO incompatibility - Most important natural protective factor:
   • If the fetus is ABO-incompatible with mother (e.g., mother O, fetus A/B), fetal RBCs entering maternal circulation are rapidly coated and destroyed by naturally occurring anti-A or anti-B IgM antibodies
   • These antibodies clear fetal cells before the immune system is sensitized to the D antigen
   • ABO IgM antibodies do NOT cross the placenta - so fetus is unaffected
2. Small volume of FMH - Sensitization requires >1 mL Rh-positive fetal blood
3. Anti-D immunoglobulin (prophylaxis) - Administered before sensitization occurs
4. Low D antigen expression on fetal RBCs
5. Weak immune responders - ~30% of Rh-negative women never become sensitized even after repeated exposures (due to inherent immune hypo-responsiveness)

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Q5. Describe the effects of Rh isoimmunization on the fetus and newborn. What is erythroblastosis fetalis?

Pathway 1 - Anemia:

• Hemolysis → progressive fetal anemia
• Fetus compensates by extramedullary hematopoiesis (liver, spleen enlarge and produce RBCs)
• Immature nucleated RBC precursors (erythroblasts) appear in peripheral blood → Erythroblastosis fetalis
• Severe anemia → cardiac hypoxia → cardiac failure
• Cardiac failure + reduced plasma oncotic pressure → generalized edema, ascites, pleural effusions, pericardial effusion = Hydrops fetalis
• Hydrops fetalis is a life-threatening condition that can lead to intrauterine fetal death (IUFD)

Pathway 2 - Hyperbilirubinemia/Jaundice:

• Hemoglobin from destroyed RBCs → converted to unconjugated (indirect) bilirubin
• In utero: bilirubin crosses placenta and is cleared by mother's liver - so fetus is not jaundiced
• After birth: Neonatal liver is immature and cannot conjugate bilirubin fast enough
• Unconjugated bilirubin accumulates → Neonatal jaundice (within first 24 hours - pathological)
• Unconjugated bilirubin is lipid-soluble, crosses the immature blood-brain barrier
• Deposits in basal ganglia, hippocampus, cerebellum → Kernicterus

Clinical spectrum of HDFN:

• High-pitched cry, seizures, opisthotonos, hypotonia/hypertonia
• Permanent sequelae: intellectual disability, choreoathetosis, sensorineural deafness, cerebral palsy

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Q6. Describe the incidence and progression of erythroblastosis fetalis across pregnancies.

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Q7. How do you investigate a woman with Rh-negative pregnancy?

At First ANC Visit (Booking):

1. Blood group and Rh typing (ABO + Rh)
2. Indirect Coombs Test (ICT) / Indirect Antiglobulin Test (IAT) - screens for circulating anti-D antibodies in mother's serum
   • Negative ICT = mother NOT sensitized (unsensitized)
   • Positive ICT = mother IS sensitized (sensitized - antibodies present)

If ICT is Negative (Unsensitized mother):

• Repeat ICT at 28 weeks, then monthly thereafter
• Check husband's blood group
• Give anti-D prophylaxis

If ICT is Positive (Sensitized mother):

• Quantitate antibody titre
  • Titre < 1:8 (or < 1:16 in some centers) = mild risk, monitor with serial titres
  • Titre ≥ 1:16 (Dutta's critical titre) = significant risk, proceed to fetal assessment

Fetal Assessment (when titre ≥ critical level):

1. Middle Cerebral Artery Doppler (MCA-PSV)
   • Gold standard for non-invasive assessment of fetal anemia
   • MCA-PSV > 1.5 MoM (multiples of median) = significant fetal anemia
2. Serial USG - for hydrops (ascites, pleural/pericardial effusion, skin edema, polyhydramnios)
3. Amniocentesis - measure bilirubin in amniotic fluid (OD450 - optical density at 450 nm)
   • Plotted on Liley's chart (or Queenan chart for earlier gestations)
   • Zone I = mild, Zone II = moderate, Zone III = severe (immediate delivery/IUT)
4. Cordocentesis (PUBS - Percutaneous Umbilical Blood Sampling)
   • Direct fetal blood sampling for Hb, Hct, blood group
   • Can proceed to intrauterine transfusion (IUT) at the same sitting

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Q8. What is the Indirect Coombs Test and Direct Coombs Test? How do they differ?

• ICT: Mother's serum + Rh-positive test cells → add Coombs serum → agglutination = positive (antibodies present in serum)
• DCT: Neonate's washed RBCs + Coombs serum → agglutination = positive (antibodies coating the RBCs)

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Q9. What is Liley's chart? How is it used?

• Valid only from 27 weeks onwards (Liley's original chart)
• For earlier gestation (18-26 weeks): Queenan's chart is used

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Q10. What is anti-D immunoglobulin? Describe its dose, timing, and mechanism of action.

• 300 µg (1500 IU) IM at 28 weeks gestation (antenatal prophylaxis)
• 300 µg (1500 IU) IM within 72 hours of delivery if baby is confirmed Rh-positive
• 50 µg (250 IU) after abortion/ectopic if < 12 weeks gestation (smaller FMH expected)
• 300 µg after abortion/ectopic if > 12 weeks gestation
• Additional doses required if Kleihauer-Betke test shows large FMH (>30 mL fetal blood)

• After delivery, abortion, ectopic pregnancy, APH, amniocentesis, CVS, ECV, trauma
• Antenatally at 28 weeks (routine prophylaxis - before any intrapartum FMH)
• Some centers also give at 34 weeks (double-dose schedule)

1. Clearance of fetal RBCs: Anti-D antibody coats Rh-positive fetal RBCs entering maternal circulation → they are rapidly removed by macrophages before the immune system can be sensitized
2. Central inhibition: Anti-D may directly inhibit B lymphocyte activation/antibody production in the mother against the D antigen

• Mother is already sensitized (ICT positive) - too late, prophylaxis has no benefit
• Baby confirmed Rh-negative
• Mother is Rh-positive

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Q11. What is the management of a sensitized Rh-negative mother?

Antenatal Management:

• Serial anti-D antibody titres (4-weekly)
• If titre < critical level (< 1:16): close monitoring only
• If titre ≥ 1:16: proceed to fetal assessment

• MCA Doppler (MCA-PSV) every 1-2 weeks from 18 weeks
  • MCA-PSV > 1.5 MoM → significant anemia → perform cordocentesis
• Serial USG for signs of hydrops
• Amniocentesis + Liley's chart (if MCA not available)

• Indication: Fetal hemoglobin below threshold (Hct <30%) confirmed on cordocentesis, OR hydrops, OR MCA-PSV >1.5 MoM
• Route: Intravascular transfusion via umbilical vein (cordocentesis) - preferred
  • Old method: Intraperitoneal transfusion (absorbed via lymphatics - now rarely used)
• Blood used: O-negative, CMV-negative, irradiated, leukodepleted, cross-matched with mother's serum
• Can be repeated every 2-3 weeks

Timing of Delivery:

Mode of delivery:

• Vaginal delivery preferred if stable
• Cesarean section for obstetric indications or severe fetal compromise

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Q12. Describe the management of a newborn with HDFN (erythroblastosis fetalis).

Immediate Assessment at Birth:

• Cord blood: Hb, Hct, bilirubin, blood group, Direct Coombs Test (DCT)
• DCT positive = confirms HDFN

Treatment:

• Indication: Mild-moderate hyperbilirubinemia
• Blue-green light (wavelength 430-490 nm) converts unconjugated bilirubin in skin into water-soluble photoisomers excreted in bile/urine
• Does NOT treat anemia

• Indication: Severe hyperbilirubinemia (bilirubin approaching kernicterus threshold), severe anemia (Hb < 10 g/dL at birth), hydrops
• Procedure: Replace neonate's Rh-positive blood with Rh-negative blood (removes antibody-coated RBCs, anti-D antibodies, and bilirubin)
• Done over 1.5 hours (double-volume exchange = ~160 mL/kg)
• Performed via umbilical vein catheter
• Bilirubin level drops by ~50% immediately
• May need to be repeated

• Reduces need for exchange transfusion in moderate cases
• Blocks Fc receptors on macrophages → reduces hemolysis

• Correct hypoglycemia, hypocalcemia (common in hydrops)
• Respiratory support
• Monitor closely for 6-8 weeks (maternal anti-D persists in infant for ~6 weeks)

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Q13. Write a short note on ABO incompatibility. How does it differ from Rh incompatibility?

• Occurs almost exclusively in Group A or B babies of Group O mothers
• Group O mothers may have IgG anti-A/anti-B antibodies naturally (without sensitization), hence first baby can be affected
• Severity is mild because: (1) fetal RBCs express A/B antigens weakly, (2) many other fetal tissues absorb the antibody
• Effective protection using prophylaxis does not exist

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Q14. What is hydrops fetalis? Classify it.

• Caused by Rh isoimmunization (most common) or ABO incompatibility
• Pathogenesis: Hemolytic anemia → cardiac failure + reduced plasma oncotic pressure → generalized edema
• Since widespread use of anti-D prophylaxis, immune hydrops has drastically decreased

• Skin/scalp edema (> 5 mm)
• Ascites
• Pleural effusion
• Pericardial effusion
• Polyhydramnios
• Placental thickening (> 6 cm)
• "Buddha position" - fetus with distended abdomen

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Q15. Write the Kleihauer-Betke test and its significance.

• Adult RBCs (containing HbA) - eluted (appear as "ghost cells")
• Fetal RBCs (containing HbF) - retain Hb (appear as darkly staining cells)

• Quantifies the volume of fetomaternal hemorrhage (FMH)
• Determines whether a single standard dose of anti-D (300 µg) is sufficient or extra doses are needed

• 300 µg anti-D covers up to 30 mL of Rh-positive fetal whole blood (or 15 mL fetal RBCs)
• If KB test shows FMH > 30 mL → give additional 300 µg for every extra 30 mL fetal blood

• After delivery in Rh-negative mothers
• After significant abdominal trauma
• After abruption

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Quick Revision Summary

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Exam Tips for MBBS:

• Long questions: "Rh isoimmunization - pathogenesis, investigations, management" and "Erythroblastosis fetalis"
• Short notes: Liley's chart, Anti-D immunoglobulin, Kleihauer-Betke test, Hydrops fetalis, ABO incompatibility, Kernicterus
• Remember: Anti-D prevents sensitization but cannot reverse existing sensitization
• The MCA Doppler has replaced invasive amniocentesis as the primary tool for fetal monitoring in sensitized pregnancies