Membership of the Royal College of Obstetricians and Gynaecologists (MRCOG) Antenatal Care and Maternal Medicine Syllabus

What method of feticide is used before late termination for fetal anomaly (after ~22 weeks) and why?

Intracardiac or intrafunic potassium chloride (KCl) injection to ensure the fetus is not born alive, recommended for terminations performed at or beyond 21–22 weeks gestation.

Define gestational hypertension, chronic hypertension and pre-eclampsia.

Gestational hypertension: new hypertension ($\geq 140/90$) after 20 weeks without proteinuria/features. Chronic hypertension: hypertension before 20 weeks or pre-pregnancy. Pre-eclampsia: new hypertension after 20 weeks PLUS proteinuria or maternal organ/uteroplacental dysfunction.

State the blood pressure threshold defining severe hypertension in pregnancy and the BP treatment targets in pregnancy.

Severe hypertension: $\geq 160/110\ mmHg$. Target with treatment: aim for BP $\leq 135/85\ mmHg$.

Which women should take aspirin to reduce pre-eclampsia risk, at what dose and from when?

Women with $\geq 1$ high-risk or $\geq 2$ moderate-risk factors. Aspirin $75$–$150\ mg$ daily from 12 weeks until birth.

What is the definitive treatment of pre-eclampsia, and which drug is used for seizure prophylaxis/treatment in eclampsia plus its therapeutic monitoring?

Definitive treatment is delivery of the placenta (birth). Magnesium sulfate prevents and treats eclamptic seizures; monitor reflexes, respiratory rate and urine output, and reverse toxicity with calcium gluconate.

What are the first-line oral antihypertensives in pregnancy, and which classes are contraindicated?

First-line: labetalol; alternatives nifedipine and methyldopa. Contraindicated: ACE inhibitors, ARBs and thiazide diuretics (fetotoxic).

Define HELLP syndrome by its three laboratory components.

Haemolysis, Elevated Liver enzymes, Low Platelets — a severe variant of pre-eclampsia. (Low platelets typically $<100\times10^{9}/L$, raised LDH/bilirubin, raised transaminases.)

State the diagnostic OGTT thresholds for gestational diabetes used by NICE.

Fasting plasma glucose $\geq 5.6\ mmol/L$ OR 2-hour value $\geq 7.8\ mmol/L$ (after $75\ g$ glucose load).

What are the target capillary glucose values for women managing diabetes in pregnancy (fasting and 1-hour postprandial)?

Fasting $<5.3\ mmol/L$; 1 hour after meals $<7.8\ mmol/L$ (or 2 hours $<6.4\ mmol/L$); avoid levels $<4\ mmol/L$.

What is the first-line pharmacological treatment for GDM if diet/exercise fails, and when is insulin added?

Metformin is first-line. Insulin is added (or used first) if targets are not met, or initially if fasting glucose $\geq 7\ mmol/L$ at diagnosis, or $6$–$6.9$ with complications such as macrosomia/polyhydramnios.

When is delivery recommended in women with pre-existing versus gestational diabetes, assuming no complications?

Pre-existing (type 1/2) diabetes: offer elective birth between 37 and $38^{+6}$ weeks. Uncomplicated GDM: deliver no later than $40^{+6}$ weeks.

Which maternal cardiac conditions carry the highest risk in pregnancy and warrant advice against pregnancy (mWHO class IV)?

Pulmonary arterial hypertension, severe systemic ventricular dysfunction (EF $<30\%$/NYHA III–IV), severe mitral stenosis, severe symptomatic aortic stenosis, Marfan with aortic root $>45\ mm$, and severe coarctation.

How is warfarin managed in pregnant women with mechanical heart valves, and what is its main fetal risk?

Warfarin is teratogenic (warfarin embryopathy, especially weeks 6–12) and causes fetal haemorrhage. Options: switch to LMWH (esp. in first trimester) or continue warfarin if dose low; requires specialist counselling balancing valve thrombosis risk.

In chronic kidney disease, what pre-pregnancy creatinine/eGFR thresholds predict poorer pregnancy outcome?

Worse outcomes with serum creatinine $>125\ \mu mol/L$ (and markedly worse $>180$), eGFR $<60$, proteinuria and uncontrolled hypertension. Pregnancy may accelerate decline in moderate-severe CKD.

How does normal pregnancy alter thyroid function tests and TSH reference ranges in the first trimester?

hCG (TSH-like) stimulates the thyroid, suppressing TSH in the first trimester (lower reference range, e.g. ~$0.1$–$2.5\ mU/L$). Total T4/T3 rise due to increased thyroid-binding globulin; free T4 stays near-normal.

How should levothyroxine be adjusted in a hypothyroid woman who becomes pregnant?

Increase the dose promptly on confirming pregnancy (often by ~$25$–$50\%$, e.g. an extra 2 doses/week), aiming TSH in the lower half of the trimester-specific range; check TFTs every 4–6 weeks.

Which antithyroid drug is preferred in the first trimester versus later in pregnancy, and why?

Propylthiouracil (PTU) preferred in the first trimester (carbimazole is associated with aplasia cutis/embryopathy). Switch to carbimazole after the first trimester due to PTU hepatotoxicity risk.

What is the most common cause of hyperthyroidism in pregnancy and what fetal complication can its antibodies cause?

Graves disease. Maternal TSH-receptor antibodies (TRAbs) cross the placenta and can cause fetal/neonatal thyrotoxicosis; measure TRAbs in affected/treated women.

In pregnancy, what defines anaemia by trimester (haemoglobin thresholds)?

First trimester Hb $<110\ g/L$; second/third trimester $<105\ g/L$; postpartum $<100\ g/L$.

How does physiological haemodilution of pregnancy affect plasma volume and red cell mass?

Plasma volume increases ~$40$–$50\%$ and red cell mass increases ~$20$–$30\%$; the disproportionate plasma rise lowers haemoglobin concentration (physiological dilutional anaemia).

What thromboprophylaxis principle applies to pregnant women, and which agent is standard?

VTE risk is assessed at booking, on admission and postnatally; risk is ~4–5 fold increased. Low-molecular-weight heparin is the agent of choice (does not cross the placenta); warfarin and DOACs are avoided.

In sickle cell disease, list key pregnancy risks and a core management measure.

Increased risk of crises, acute chest syndrome, pre-eclampsia, FGR, preterm birth and VTE. Management: folic acid $5\ mg$, penicillin prophylaxis, aspirin, avoid iron unless deficient, prompt crisis management; partner screening for haemoglobinopathy.

Which connective tissue disease antibodies are associated with congenital heart block, and what management follows?

Anti-Ro (SSA) and anti-La (SSB) antibodies. Monitor fetal heart rate/rhythm (serial echocardiography ~16–26 weeks); congenital complete heart block may require neonatal pacing.

How does SLE typically behave in pregnancy and what is the cornerstone drug to continue?

SLE can flare in pregnancy and is associated with pre-eclampsia, FGR and loss (especially with antiphospholipid antibodies/active disease). Hydroxychloroquine should be continued throughout pregnancy.

In antiphospholipid syndrome with recurrent pregnancy loss, what is the standard treatment regimen?

Low-dose aspirin plus prophylactic LMWH (heparin) improves live birth rates; aspirin started preconception/early and LMWH once pregnancy confirmed.

Which maternal viral infection is the most common congenital infection, and what are its classic fetal effects?

Cytomegalovirus (CMV). Effects: sensorineural hearing loss, microcephaly, intracranial calcification, FGR, hepatosplenomegaly and chorioretinitis.

What is the risk of congenital rubella syndrome by gestation, and its classic triad?

Risk highest in first trimester (~$90\%$ if infected $<11$ weeks), low after 16–18 weeks. Classic triad: sensorineural deafness, cataracts/eye defects, and congenital heart disease (e.g. PDA).

In maternal primary varicella (chickenpox), what are the fetal/neonatal risks and the management of exposure in a non-immune woman?

Before 20 weeks: ~$1$–$2\%$ risk of fetal varicella syndrome. Around delivery ($<7$ days before to 7 days after): severe neonatal varicella. Non-immune exposed woman: check VZV IgG; give antivirals/VZIG (now oral aciclovir/valaciclovir per updated guidance) promptly.

What are the three classes of intervention to reduce vertical HIV transmission, and what is the achievable transmission rate?

Maternal combination antiretroviral therapy (aiming undetectable viral load), appropriate mode of delivery (vaginal if VL $<50$; PLCS if higher), and neonatal post-exposure prophylaxis plus avoiding breastfeeding. Transmission can be reduced to $<1\%$ (from ~$25\%$).

What is the classic tetrad/features of congenital toxoplasmosis and a key prevention message?

Hydrocephalus, intracranial calcifications, chorioretinitis (plus convulsions). Prevention: avoid undercooked meat, wash produce, avoid cat litter/soil contact; treat with spiramycin to reduce transmission.

Why is asymptomatic bacteriuria screened and treated in pregnancy, and which organism predominates?

Untreated asymptomatic bacteriuria (~$2$–$5\%$, commonly E. coli) progresses to pyelonephritis and is linked to preterm birth and low birth weight, so it is screened by MSU at booking and treated with antibiotics.

What is the approach to Group B Streptococcus (GBS) in the UK and the intrapartum prophylaxis used?

UK uses a risk-based (not universal screening) strategy. Offer intrapartum IV antibiotic prophylaxis (benzylpenicillin) for: previous GBS-affected baby, GBS detected in current pregnancy, intrapartum pyrexia, prematurity or prolonged rupture of membranes.

Define maternal sepsis and name a commonly used early-warning/scoring approach in obstetrics.

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection. Recognition uses MEOWS (Modified Early Obstetric Warning Score) charts; the Sepsis Six bundle (cultures, lactate, urine output, oxygen, IV fluids, IV antibiotics) is delivered within 1 hour.

What is the most common causative organism of severe genital tract sepsis in pregnancy/puerperium?

Group A Streptococcus (Streptococcus pyogenes), which can cause rapidly progressive, fulminant maternal sepsis; E. coli is also common.

Define fetal growth restriction (FGR) and distinguish it from small-for-gestational-age (SGA).

SGA: estimated fetal weight or abdominal circumference $<10^{th}$ centile, which may be constitutionally small. FGR: a fetus failing to reach its genetic growth potential, usually due to placental insufficiency, with Doppler/growth-velocity abnormalities; severe SGA is $<3^{rd}$ centile.

In surveillance of the growth-restricted fetus, describe the typical sequence of Doppler deterioration.

Increasing umbilical artery resistance $\to$ absent then reversed end-diastolic flow; middle cerebral artery shows reduced PI (brain-sparing, cerebroplacental ratio falls); finally ductus venosus a-wave abnormality/absent or reversed, and abnormal CTG/STV — indicating decompensation and need for delivery.

Which uterine artery Doppler finding at the second trimester is associated with increased risk of FGR and pre-eclampsia?

Persistent high-resistance pattern with an early diastolic 'notch' and raised pulsatility index, reflecting failed trophoblastic invasion of spiral arteries.

How does routine antenatal anti-D prophylaxis (RAADP) reduce Rhesus sensitisation, and what is the single-dose regimen timing?

Prophylactic anti-D immunoglobulin given to non-sensitised RhD-negative women neutralises fetal RhD cells. Single-dose RAADP: $1500\ IU$ at ~28 weeks (or two-dose at 28 and 34 weeks).

What test quantifies large fetomaternal haemorrhage to calculate additional anti-D dose, and the rule of thumb for dosing?

Kleihauer test (acid-elution) detects/quantifies fetal cells in maternal blood. Approximately $500\ IU$ of anti-D covers ~$4\ mL$ of fetal red cells; additional anti-D and repeat Kleihauer guide large bleeds.

In a sensitised RhD-negative pregnancy, what non-invasive Doppler measurement detects fetal anaemia and what value triggers action?

Middle cerebral artery peak systolic velocity (MCA-PSV). A value $>1.5$ multiples of the median (MoM) for gestation suggests moderate/severe fetal anaemia and warrants referral for possible intrauterine transfusion.

How is chorionicity in twins best determined and at what gestation, including the ultrasound signs?

Best determined by ultrasound before 14 weeks. Dichorionic = 'lambda' (twin-peak) sign; monochorionic = 'T-sign' at the membrane-placenta junction. Chorionicity (not zygosity) drives risk and surveillance.

Describe twin-to-twin transfusion syndrome (TTTS), the pregnancies at risk, and its definitive treatment.

TTTS occurs in monochorionic diamniotic twins due to unbalanced placental vascular anastomoses: donor (oligohydramnios, 'stuck twin') and recipient (polyhydramnios, possible hydrops). Staged by Quintero. Treatment of choice for severe (Stage II+) cases is fetoscopic laser ablation of anastomoses.

Compare the recommended timing of delivery for uncomplicated dichorionic, monochorionic diamniotic, and monochorionic monoamniotic twins.

Dichorionic diamniotic: ~37 weeks. Monochorionic diamniotic: ~36 weeks (with steroids). Monochorionic monoamniotic: 32–34 weeks by caesarean (high cord-entanglement risk).

What defines reduced fetal movements and what is the initial assessment if RFM is reported after 28 weeks?

There is no fixed threshold count; maternal perception of reduced movements is significant. Assessment: confirm fetal heart with handheld Doppler/CTG, then CTG; if further concern, ultrasound for growth, liquor and Doppler. RFM is associated with stillbirth and FGR.

Define stillbirth in the UK and name two leading associated/causative factors.

Stillbirth: a baby born with no signs of life at or after 24 completed weeks of gestation. Common associations: placental insufficiency/FGR, placental abruption, congenital anomaly, infection, and pre-existing maternal disease (e.g. diabetes).

What investigations are recommended after a stillbirth to determine cause?

Maternal: Kleihauer, infection screen, thrombophilia/antiphospholipid, glucose/HbA1c, TFTs, bile acids, autoimmune screen. Fetal/placental: postmortem examination (with consent), placental histology, fetal karyotype/microarray, and surface/skin swabs.

Define polyhydramnios using amniotic fluid index and deepest vertical pocket, and list common causes.

Polyhydramnios: AFI $>25\ cm$ or deepest vertical pocket $>8\ cm$. Causes: maternal diabetes, fetal anomalies impairing swallowing (e.g. oesophageal/duodenal atresia, anencephaly), fetal anaemia/hydrops, TTTS (recipient), and infection; many are idiopathic.

Define oligohydramnios by deepest vertical pocket/AFI and list its principal causes.

Oligohydramnios: AFI $<5\ cm$ or deepest vertical pocket $<2\ cm$. Causes: ruptured membranes, placental insufficiency/FGR (reduced fetal renal perfusion), fetal renal anomalies (e.g. renal agenesis, posterior urethral valves) and post-term pregnancy.

What is the Potter sequence and how does it relate to amniotic fluid?

Potter sequence results from severe, prolonged oligohydramnios/anhydramnios (often bilateral renal agenesis or obstruction): pulmonary hypoplasia, limb contractures and characteristic flattened (Potter) facies — frequently lethal due to lung hypoplasia.

At booking, which factors place a woman in the higher-risk category requiring consultant-led (rather than midwifery-led) care?

Examples: pre-existing medical disease (cardiac, renal, diabetes, epilepsy, hypertension), previous obstetric complications (pre-eclampsia, stillbirth, preterm birth, abruption), high or very low BMI, age extremes, multiple pregnancy, and previous caesarean/significant surgery.

What is the recommended weight-gain guidance and the management priority for a pregnant woman with BMI $\geq 30$?

No formal UK weight-gain targets, but excess gain discouraged. Priorities: folic acid $5\ mg$, vitamin D, aspirin for pre-eclampsia prophylaxis, GDM screening (OGTT), VTE risk assessment, and consultant-led care with anaesthetic review.

In epilepsy, how does pregnancy affect seizure control and what monitoring is advised for lamotrigine?

Seizure frequency may increase due to altered drug pharmacokinetics, nausea, sleep deprivation and reduced adherence. Lamotrigine levels fall in pregnancy (increased clearance) so levels are monitored and the dose often increased, then reduced postpartum.

What is obstetric cholestasis (intrahepatic cholestasis of pregnancy), its hallmark symptom/biochemistry, and main fetal concern?

Pruritus (typically palms/soles) without rash, with raised serum bile acids (and often transaminases). Associated with increased risk of stillbirth, especially with bile acids $\geq 100\ \mu mol/L$; managed with monitoring and timed delivery.

What is the most common cause of jaundice/severe liver dysfunction unique to late pregnancy that presents with hypoglycaemia and coagulopathy?

Acute fatty liver of pregnancy (AFLP) — a rare third-trimester emergency with nausea, vomiting, hypoglycaemia, deranged LFTs, coagulopathy and renal impairment; treatment is prompt delivery and supportive care.

How does maternal parvovirus B19 infection affect the fetus and what surveillance is required?

Parvovirus B19 suppresses fetal erythropoiesis causing aplastic anaemia, which can lead to hydrops fetalis and loss. Surveillance: serial MCA-PSV Doppler for 8–12 weeks; intrauterine transfusion if severe anaemia/hydrops develops.