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AN80.1-7 | Fetal membranes — Practice Quiz

Practice 10 questions · Untimed · Unlimited attempts

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Q1 AN80.1 1 pt

Human chorionic gonadotropin (hCG) — the basis of the pregnancy test — is secreted by which structure?

A Decidua basalis
B Amnion
C Syncytiotrophoblast of the chorion
D Fetal liver

Correct! hCG is secreted by the SYNCYTIOTROPHOBLAST (the outer invasive layer of the trophoblast/chorion). It is detectable in urine and blood from Day 8–10 post-fertilisation and forms the basis of all pregnancy tests.

Syncytiotrophoblast produces: hCG (1st trimester, peaks at 10–12 wks), hPL, oestrogen (oestriol), progesterone. hCG maintains corpus luteum until placenta takes over progesterone production at ~10 weeks ("luteo-placental shift").

Incorrect. hCG is produced by the SYNCYTIOTROPHOBLAST. It maintains the corpus luteum → progesterone → maintains endometrium → prevents menstruation. Decidua, amnion, and fetal liver do not produce hCG.

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Q2 AN80.1 1 pt

A 30-week fetal anomaly scan shows excessive amniotic fluid (deepest pool >8 cm). The fetal stomach bubble is absent. The most likely cause of the polyhydramnios is:

A Bilateral renal agenesis — no urine production
B Oesophageal or duodenal atresia — fetus cannot swallow amniotic fluid
C Posterior urethral valves — bladder outlet obstruction
D Post-dates pregnancy — placental insufficiency

Correct! POLYHYDRAMNIOS + absent stomach bubble = GI ATRESIA (oesophageal or duodenal). The fetus cannot swallow normally → fluid accumulates. The "absent stomach bubble" sign on ultrasound indicates oesophageal atresia or duodenal atresia with associated anomalies.

Polyhydramnios causes (fluid accumulates = swallowing impaired OR over-production): GI atresias (oesophageal, duodenal), anencephaly (no swallowing), maternal diabetes, multiple pregnancy. Oligohydramnios causes: renal agenesis (no urine), posterior urethral valves, IUGR, post-dates.

Incorrect. Polyhydramnios + absent stomach bubble = GI obstruction (fetus cannot swallow). Renal agenesis → OLIGOHYDRAMNIOS (no urine). Posterior urethral valves → oligohydramnios. Post-dates → oligohydramnios.

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Q3 AN80.1 1 pt

Meckel's diverticulum, the most common congenital gut anomaly, is a remnant of which embryological structure?

A Allantois (urachus)
B Vitello-intestinal (omphalomesenteric) duct connecting the yolk sac to the gut
C Umbilical vein remnant
D Neural crest cell migration

Correct! Meckel's diverticulum = persistent VITELLO-INTESTINAL (omphalomesenteric) duct. Normally the duct connecting the yolk sac to the ileum obliterates by the 6th week. Persistence → Meckel's diverticulum: 2 cm long, 2 feet from ileocaecal valve, 2% of population, presents by age 2 (Rule of 2s).

Rule of 2s for Meckel's: 2 cm long, 2 feet from ileocaecal valve, 2% population, presents by age 2, 2 types of ectopic mucosa (gastric and pancreatic). Gastric mucosa → acid secretion → ulceration → bleeding per rectum — most common presentation in children.

Incorrect. Meckel's = OMPHALOMESENTERIC (vitello-intestinal) DUCT remnant (yolk sac stalk). Allantois → urachus → patent urachus or urachal cyst (different condition: urine drains from umbilicus). Neural crest → ganglia, not gut diverticula.

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Q4 AN80.2 1 pt

A normally formed umbilical cord contains which combination of vessels?

A 1 umbilical artery and 1 umbilical vein
B 2 umbilical arteries and 2 umbilical veins
C 2 umbilical arteries and 1 umbilical vein
D 1 umbilical artery and 2 umbilical veins

Correct! The NORMAL umbilical cord contains 2 ARTERIES and 1 VEIN (2:1 ratio). The arteries carry DEOXYGENATED blood from the fetus to the placenta. The vein carries OXYGENATED blood from the placenta to the fetus.

Umbilical cord: 2 arteries (deoxygenated, fetus→placenta) + 1 vein (oxygenated, placenta→fetus). Single umbilical artery (SUA) → 30% associated anomalies. 50 cm long; Wharton's jelly. Left-sided helical coil. Cord prolapse = emergency → immediate CS.

Incorrect. Normal cord = 2 arteries + 1 vein. Single Umbilical Artery (SUA) = only 1 artery + 1 vein; associated with congenital anomalies in 30% (cardiac, renal). Remember: ARTERIES carry blood AWAY from the fetus; they are deoxygenated despite the name "artery".

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Q5 AN80.2 1 pt

A 34-year-old woman at 38 weeks presents in labour with sudden fetal bradycardia after spontaneous rupture of membranes. On vaginal examination, the examining finger feels a pulsating loop of cord ahead of the presenting part. Immediate management is:

A Administer tocolytics and transfer to hospital
B Emergency caesarean section while manually holding the cord up to relieve compression
C Allow normal vaginal delivery to proceed urgently
D Perform immediate forceps delivery in the labour ward

Correct! CORD PROLAPSE is an obstetric emergency. Management: (1) MANUALLY elevate the presenting part (per vaginum or by placing the woman in knee-chest position) to relieve cord compression; (2) EMERGENCY CAESAREAN SECTION immediately. Every minute of delay increases fetal hypoxia risk.

Cord prolapse: presenting part compresses cord against pelvis → cord vessels compressed → fetal anoxia → brain damage within 5–10 minutes. Risk factors: long cord, high presenting part, breech, PROM. Management: relieve compression manually → emergency CS.

Incorrect. Cord prolapse = immediate risk of fetal death from cord compression → EMERGENCY CS with manual relief of compression. Tocolytics alone are insufficient. Forceps delivery is only appropriate if the baby is fully descended (fully dilated, head on perineum).

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Q6 AN80.3 1 pt

The human placenta is classified as "haemochorial." This means:

A Maternal blood is separated from fetal blood by 3 layers of tissue
B The decidua forms a complete barrier between maternal and fetal circulations
C Maternal blood bathes the chorionic villi directly in the intervillous space
D Fetal blood mixes with maternal blood across a thin membrane

Correct! HAEMOCHORIAL = maternal blood (haemo-) directly bathes the chorionic (-chorial) villi in the intervillous space. The syncytiotrophoblast has eroded the maternal spiral arterioles; maternal blood jets into the intervillous space and directly surrounds the villi. There is NO separate maternal vessel wall.

Human placenta = haemochorial (most intimate type). Maternal blood in intervillous space → bathes chorionic villi → exchange across: syncytiotrophoblast → (cytotrophoblast, disappears after 4th month) → connective tissue → fetal capillary endothelium.

Incorrect. HAEMOCHORIAL = maternal BLOOD directly contacts the TROPHOBLAST of the chorionic villi (no maternal endothelium). Compare: endotheliochorial (cat, dog: maternal endothelium intact) and epitheliochorial (pig, horse: decidua + endometrium between). Human = most intimate contact.

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Q7 AN80.3 1 pt

A pregnant woman with deep vein thrombosis is started on anticoagulation. Which anticoagulant is preferred in pregnancy because it does NOT cross the placental barrier?

A Warfarin (vitamin K antagonist)
B Rivaroxaban (direct oral anticoagulant)
C Heparin (unfractionated or low-molecular-weight)
D Dabigatran (direct thrombin inhibitor)

Correct! HEPARIN (unfractionated and LMWH like enoxaparin) does NOT cross the placental barrier because it is a LARGE MOLECULE (not lipid-soluble). It is safe in pregnancy. WARFARIN does cross and is TERATOGENIC (warfarin embryopathy: nasal hypoplasia, stippled epiphyses in weeks 6–12; CNS defects in 2nd trimester).

Placental barrier crossing: DOES NOT cross = heparin (large), IgM (large), bacteria (mostly). DOES cross = IgG (Fc receptor), drugs (warfarin, aspirin, steroids, alcohol), oxygen/CO₂ (diffusion), glucose (facilitated), viruses (rubella, CMV, HIV).

Incorrect. HEPARIN = safe in pregnancy (does not cross). Warfarin = TERATOGENIC in 1st trimester. Rivaroxaban and dabigatran = avoid in pregnancy (cross placenta, safety data insufficient).

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Q8 AN80.3 1 pt

A preterm neonate born at 28 weeks develops respiratory distress syndrome (RDS) due to surfactant deficiency. The obstetrician had administered antenatal corticosteroids to the mother 48 hours before delivery. The corticosteroids benefited the fetus because they:

A Cannot cross the placental barrier; they acted only on the mother
B Cross the placental barrier and stimulate fetal lung surfactant production
C Crossed via the umbilical arteries directly to fetal alveoli
D Are produced by the placenta itself in response to preterm labour

Correct! Corticosteroids (betamethasone, dexamethasone) ARE lipid-soluble and CROSS THE PLACENTAL BARRIER. They stimulate fetal type II pneumocytes to produce surfactant → reduces severity of RDS in preterm neonates. This is one of the most important evidence-based interventions in preterm care.

Lipid-soluble substances cross the placenta by simple diffusion: steroids, alcohol, most drugs, CO₂/O₂, fatty acids. Large/charged molecules do NOT cross easily: heparin, IgM, most bacteria. Antenatal corticosteroids (betamethasone 2 doses 24h apart, 24–34 wks) → gold standard for fetal lung maturity in preterm labour.

Incorrect. Corticosteroids DO CROSS the placental barrier (lipid-soluble). They act directly on fetal lung type II pneumocytes to upregulate surfactant synthesis. The beneficial effect requires 24–48 hours → urgency to administer before inevitable preterm birth.

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Q9 AN80.3 1 pt

A 30-year-old G3P2 with 2 previous caesarean sections presents at 34 weeks with sudden painless vaginal bleeding. Ultrasound confirms the placenta completely covers the internal cervical os. Regarding fetal circulation in this scenario, which vessel carries oxygenated blood FROM the placenta to the fetus?

A Two umbilical arteries
B One umbilical vein
C Ductus venosus
D Umbilical arteries (they carry blood to the placenta; return is via ductus arteriosus)

Correct! The UMBILICAL VEIN carries OXYGENATED blood FROM the placenta TO the fetus (into the fetal left branch of the portal vein → ductus venosus → IVC → fetal heart). The 2 umbilical ARTERIES carry DEOXYGENATED blood FROM the fetus TO the placenta.

Fetal circulation exception: Umbilical VEIN = oxygenated (placenta→fetus). Umbilical ARTERIES = deoxygenated (fetus→placenta). All other arteries carry oxygenated blood. Similarly: pulmonary artery carries deoxygenated blood (heart→lungs). These exceptions are standard exam questions.

Incorrect. Umbilical VEIN = oxygenated blood (placenta → fetus). Umbilical ARTERIES (×2) = deoxygenated (fetus → placenta). This is counterintuitive — "artery" normally = oxygenated — but in fetal circulation, the vessels are named by direction of flow, not oxygen content.

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Q10 AN80.3 1 pt

Placenta accreta occurs when chorionic villi implant directly into the myometrium. The absence of which layer normally separating placental villi from the myometrium explains this condition?

A Syncytiotrophoblast
B Cytotrophoblast (Langhans cells)
C Nitabuch's layer (fibrinoid layer of the decidua basalis)
D Wharton's jelly of the umbilical cord

Correct! NITABUCH'S LAYER (also called the fibrinoid layer or stria) is the zone of fibrinoid degeneration in the decidua basalis that acts as the natural cleavage plane for placental separation at delivery. Its absence (due to previous uterine scar from CS or surgery) → placenta accreta — villi attach directly to myometrium → cannot separate → massive PPH.

Placenta accreta spectrum: accreta (onto myometrium, 80%) → increta (into, 15%) → percreta (through, 5%). Risk: previous CS scar + placenta praevia = highest risk. Absent Nitabuch's layer in scar tissue. Treatment: planned CS + hysterectomy (if accreta confirmed on MRI/US pre-operatively).

Incorrect. NITABUCH'S LAYER = fibrinoid zone in decidua basalis = cleavage plane for placental separation. Its absence → placenta accreta (onto myometrium), increta (into myometrium), percreta (through myometrium).

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