Free UKMLA obstetrics and gynaecology questions with explanations

A. Intramuscular betamethasone

A course of antenatal corticosteroid given when preterm birth is expected accelerates maturation of fetal type II pneumocytes and surfactant production, cutting the risk of respiratory distress syndrome, intraventricular haemorrhage, necrotising enterocolitis and neonatal death. Benefit is greatest when birth occurs 24 hours to 7 days after the first dose. Steroids are offered when preterm birth is anticipated between 24 and 34 weeks and considered up to about 36 weeks. Magnesium sulfate is given to the same women for a different reason, neuroprotection against cerebral palsy, and has no effect on lung maturity.

B. Oral erythromycin

In preterm prelabour rupture of membranes, prophylactic oral erythromycin is given for up to 10 days or until established labour, because it reduces chorioamnionitis and prolongs the latency to delivery. Co-amoxiclav is specifically avoided because it was associated with an increased rate of neonatal necrotising enterocolitis in the ORACLE trial. Intravenous benzylpenicillin is intrapartum prophylaxis against group B streptococcus once labour starts, not a latency antibiotic. Metronidazole and nitrofurantoin have no role in preventing intrauterine infection here. If signs of chorioamnionitis develop, prophylaxis is abandoned in favour of broad-spectrum intravenous antibiotics and delivery.

D. Serum bile acids

Pruritus without a rash in the third trimester, typically of the palms and soles and worse at night, is the classic presentation of intrahepatic cholestasis of pregnancy. The diagnosis is confirmed by a raised non-fasting serum bile acid concentration (19 micromol/L or above) in the absence of another cause; transaminases may be mildly raised and jaundice is uncommon. Bile acids matter beyond diagnosis because the peak level stratifies stillbirth risk and dictates the timing of birth. Ultrasound and hepatitis serology help exclude other causes when the picture is atypical but neither confirms cholestasis of pregnancy.

D. Low molecular weight heparin

Pregnancy is prothrombotic and hyperemesis adds dehydration, immobility and hospital admission, so every woman admitted with hyperemesis gravidarum should receive thromboprophylaxis with low molecular weight heparin unless contraindicated, stopped on discharge once she is mobile and rehydrated. The other core measures are isotonic crystalloid with potassium replacement, a regular antiemetic and thiamine to prevent Wernicke's encephalopathy. Corticosteroids are third-line, for women still vomiting despite combinations of standard antiemetics. Enteral or parenteral nutrition is reserved for the rare woman who continues to lose weight despite all of this, and glucose-containing fluids are avoided as the initial fluid because they can precipitate Wernicke's encephalopathy in a thiamine-depleted woman and do not correct sodium.

E. Real-time ultrasound scan to assess fetal cardiac activity

Intrauterine death must be confirmed by real-time ultrasound demonstrating absence of fetal cardiac activity, performed by someone trained to do so, because auscultation and CTG can record the maternal pulse or placental flow and be falsely reassuring or falsely alarming. The scan is done promptly, the finding is explained to the woman clearly and honestly using plain words such as 'died', ideally with her partner present or contacted, and a second scan or opinion is offered if she wishes. Repeated attempts with Doppler or a Pinard prolong the uncertainty without excluding death, and a CTG cannot make the diagnosis. Once death is confirmed, the bereavement midwife is involved and the discussion moves to the timing and method of birth and the investigations that will be offered.

A. Velamentous cord insertion

Vasa praevia occurs when unprotected fetal vessels traverse the membranes over or near the internal cervical os, and velamentous cord insertion, where the umbilical cord inserts into the chorioamniotic membranes rather than the placental disc, is the strongest associated risk factor. Other recognised associations include bilobed or succenturiate-lobed placentas, low-lying second-trimester placenta, multiple pregnancy, and IVF conception.

E. Ovarian torsion

Abrupt, severe, unilateral lower abdominal pain with repeated vomiting and a tender adnexal mass in an adolescent is ovarian torsion until proven otherwise. The ovary twists on its vascular pedicle, usually because a cyst or enlarged ovary acts as a lead point, and venous congestion followed by arterial compromise produces intense pain and reflex vomiting. Torsion is a surgical emergency because ovarian salvage falls with every hour of ischaemia. A ruptured cyst causes sudden pain too, but the pain tends to ease rather than persist and there is no enlarging tender mass; appendicitis builds over hours with anorexia and fever; and the recent normal period makes ectopic pregnancy unlikely.

D. Repeat the sample in 3 months

When the high-risk HPV test is positive but the reflex cytology is inadequate, the cytology cannot triage the result, so the whole sample is repeated no sooner than 3 months to allow cellular regeneration. If cytology is again inadequate on the repeat sample, referral for colposcopy follows. The short interval applies specifically to inadequate samples, distinguishing them from the 12-month surveillance pathway used when cytology is adequate and normal.

D. Insulin resistance with compensatory hyperinsulinaemia

Insulin suppresses hepatic synthesis of sex hormone-binding globulin. In an obese woman with polycystic ovary syndrome, insulin resistance drives high circulating insulin, the globulin falls, and a normal total testosterone leaves a large free, biologically active fraction; this is why the free androgen index is a better marker of androgen excess than total testosterone. Insulin also stimulates theca cell androgen production directly. Raised LH increases ovarian androgen output but does not regulate the binding globulin, and oestrogen, which raises it, is not deficient in this condition.

E. Punch biopsy of the lesion edge

Vulval cancer is diagnosed on histology that shows the depth of invasion, so a representative punch or incisional biopsy is taken under local anaesthetic from the edge of the lesion, including a rim of adjacent skin and avoiding the necrotic centre. The lesion is not excised at this stage: a diagnostic excision compromises later planning of margins and sentinel lymph node mapping and removes the landmark the oncology team needs. Cytology and aspiration give cells without architecture and cannot distinguish intraepithelial neoplasia from invasive carcinoma or measure depth, which decides whether the groin nodes must be assessed. HPV status is prognostic but does not make the diagnosis.