Obstetric and Gynaecological Pathology

ACEM Primary

Table of Contents

Miscarriage

Pregnancy loss before 20 weeks gestation
Causes:
- Foetal = chromosomal abnormalities ~ 50%
- Maternal = luteal phase defect, diabetes, physical defects of uterus, APLS, coagulopathy, HTN and infection (Toxoplasma, Mycoplasma, Listeria)

Implantation of foetus at any site other than normal intrauterine location
~90% fallopian tubes
1 in 150 pregnancies
Predisposing factors = PID resulting in fallopian tube scarring, endometriosis or previous surgery causing adhesions, IUD
Morphology = haematosalpinx, thinning/ rupture of fallopian tube as trophoblastic cells try to invade wall -> intraperitoneal haemorrhage
Clinical features = severe abdominal pain, 6 weeks post LNMP, haemorrhagic shock

Pre-eclampsia = systemic syndrome, characterised by widespread maternal endothelial dysfunction

Clinical presentation:

Occurs in 3-5% pregnant women, usually in third trimester and in primiparas.

Eclampsia = pre-eclampsia progresses to seizures and coma

Complications:

Pathogenesis:
Placenta plays a central role

Abnormalities =

Abnormal placental vasculature
- Abnormal trophoblastic implantation and lack of physiological alterations in maternal vessels needed for adequate perfusion of placenta
- Placenta is ill equipped to meet circulatory demands of late gestation
Diffuse endothelial dysfunction
- Ischaemic placenta releases factors into maternal circulation which cause imbalance of angiogenic and anti-angiogenic factors
Vasoconstriction -> hypertension
Increased vascular permeability -> proteinuria and oedema
Hypercoagulability
- Due to reduced endothelial production of PGI2 (anti-thrombotic factor)
- Thrombosis of arterioles and capillaries in liver, kidney, brain and pituitary

Morphology:

Placental infarcts, ischaemic changes in chorionic villi and trophoblast
Increased syncytial knots
Retroplacental haematoma due to bleeding and instability of uteroplacental vessels

= Infection of the placenta

Develop by either ascending through birth canal (most common) or haematogenous spread (TORCH infections)
Can cause premature rupture of membranes and preterm delivery
Amniotic fluid is cloudy with purulent exudate

= Abnormal proliferation of placental tissue, either villous or trophoblastic

Hydatidiform Mole	Invasive Mole	Choriocarcinoma
= Cystic swelling of chorionic villi with variable trophoblastic proliferation Increased risk of invasive mole or choriocarcinoma Present with PV bleeding in 4-5^th month of pregnancy Complete Fertilization of egg that has lost chromosomes (genetic material is completely paternal) – 90% have 46, XX diploid pattern – 10% have 46, XX and 46, XY from fertilisation of empty egg by two sperm Enlarged, oedematous villi and diffuse trophoblastic hyperplasia Foetal parts and vessels are rare. 2.5% risk of subsequent choriocarcinoma Partial Fertilisation of an egg with two sperm – Triploid (69, XXY) – Tetraploid (92, XXXY) Oedematous villi Foetal parts more common than in complete moles. Nil increased risk of choriocarcinoma	= Mole that penetrates the uterine wall Locally destructive tumour Hydropic villi may embolise to distant sites such as lungs and brain, but do not grow as true metastases Manifests as PV bleeding, uterine enlargement and persistently elevated HCG Responds well to chemotherapy	= Malignant neoplasm of trophoblastic cells Rapidly invasive, metastases widely Responds well to chemotherapy 50% arise from hydatidiform mole

Last Updated on August 25, 2021 by Andrew Crofton