This document discusses several conditions related to pregnancy and childbirth: 1. Ectopic pregnancy occurs when a fertilized egg implants outside the uterus, most commonly in the fallopian tubes, and can cause severe abdominal pain and rupture. 2. Placental infections can occur through ascending or hematogenous routes of infection and cause inflammation of the chorionic villi that can lead to premature delivery. 3. Preeclampsia is a condition characterized by new onset hypertension and proteinuria during pregnancy, caused by endothelial dysfunction. It can progress to eclampsia and other complications if untreated. 4. Gestational trophoblastic disease includes conditions like hydatidiform moles and choriocarc

2. Ectopic pregnancy.
Placental infections.
Preeclampsia and eclampsia.
Gestational trophoblastic disease.

4. Ectopic Pregnancy.
Implantation of the fertilized ovum outside the uterine
cavity.
The most common site is within the fallopian tubes (90%).
Other sites: Ovary, abdominal cavity, and intrauterine
portion of the fallopian tube (cornual pregnancy).
Predisposing conditions:
Previous P.I.D. → fallopian tube scarring (chronic follicular
salpingitis) 35% to 50% of patients.
Appendicitis, endometriosis, and previous surgery →
peritubal scarring and adhesions.
I.U.D. Intrauterine contraceptive devices → ↑ risk of
ectopic pregnancy by about 2.5 fold.

5. Morphological features:
Tubes:
 Implantation of the embryonal sac & immature chorionic
villi in the lumen of the fallopian tube.
 Trophoblastic cells and chorionic villi → invade the
fallopian tube wall (thin wall & no decidualization).
 Erosion of tubal tissues & maternal blood vessels →
haemorrhage in gestational sac → rupture.
 Tubal lumen → tubal hematoma or hematosalpinx
(blood-filled fallopian tube).
 Peritoneal hemorrhage.
 Broad ligament → extraperitoneal haematoma.
Ectopic Pregnancy.

6. Morphological features:
Uterus:
Enlargement & formation of decidua.
Clinical features:
Severe abdominal pain, about 6 weeks after a previous
normal menstrual period.
Rupture of a tubal pregnancy → hemorrhagic shock with
signs of an acute abdomen.
Ectopic Pregnancy.

9. Two routes:
 Ascending infection through the birth canal.
 Hematogenous (transplacental) infection.
Ascending infections:
The most common, always bacterial.
Premature rupture of membranes and preterm delivery.
± Cloudy amniotic fluid & purulent exudate.
Edema, congestion & polymorphonuclear leukocytic
infiltrate of the chorion-amnion.
± Vasculitis of umbilical and fetal chorionic plate vessels.
Placental Infections.

10. Hematogenous (transplacental) infection:
Acute villitis:
Acute inflammatory cells infiltrating the chorionic villi.
Chronic villitis:
Chronic inflammatory cells infiltrating the chorionic villi ←
several hematogenous infections, classically TORCH
(toxoplasmosis and others [syphilis, tuberculosis,
listeriosis], rubella, cytomegalovirus, herpes simplex).
Placental Infections.

11. Systemic syndrome: Hypertension, edema, and proteinuria
during pregnancy.
Maternal endothelial dysfunction.
3% to 5% of pregnant women.
Last trimester.
More common in primiparas (women pregnant for the first
time).
Pathogenesis:
Diffuse endothelial dysfunction:
Vasoconstriction → hypertension.
Increased vascular permeability → proteinuria and edema.
The symptoms disappear rapidly after delivery of the
placenta.
PREECLAMPSIA.

12. Morphological features:
Malperfusion, ischemia, and vascular injury.
 Placental infarcts: Peripherally located, larger and more
numerous than that occurring in normal full-term
placentas.
 Exaggeration of ischemic changes in the chorionic villi
and trophoblasts.
 Increased frequency of retroplacental hematomas
(bleeding and instability of uteroplacental vessels).
 Abnormal implantation: Decidual vessels show
thrombosis, fibrinoid necrosis, or intraintimal lipid
deposition {acute atherosis}.
PREECLAMPSIA.

13. Clinical features:
Condition starts after 34 weeks of gestation.
Earlier presentation in cases of hydatidiform mole,
preexisting kidney disease, hypertension, or
coagulopathies.
PREECLAMPSIA.

14. Complications:
Eclampsia: Preeclampsia progressing to convulsions.
Hypercoaguability.
Acute renal failure.
Pulmonary edema.
HELLP syndrome : Hemolysis, elevated liver enzymes, and
low platelets (10% of severe preeclampsia cases).
PREECLAMPSIA.

16. Proliferation of placental tissue, either villous or
trophoblastic.
Vesicular (hydatidiform) mole.
Choriocarcinoma.
↑ H.C.G. → theca lutein ovarian cysts & high titers of
ß H.C.G.

17. Vesicular Mole.
Proliferation of trophoblastic tissue & cystic swelling of
chorionic villi.
Risk Factors:
 Maternal age :
Teens and between the ages of 40 and 50 years.
 Previous molar gestation.

18. Vesicular Mole.

19. Complete Mole.
Diploid 46, paternal in origin , 46,XX (46, XY), (empty
ovum fertilized by one or two sperms).
Morphological features:
Enlarged uterus.
Uterine cavity:
Delicate, friable mass of cystic grape-like
translucent structures.
Enlarged & edematous villi (core of loose edematous
stroma → cistern formation & absent blood vessels).
Marked circumferential trophoblastic proliferation.
Fetal vessels and fetal parts (extremely rare).
2.5% risk of subsequent choriocarcinoma.

20. Partial Mole.
Triploid, 69 XXY, (ovum fertilized by two sperms),
Morphological features:
Enlarged uterus.
Uterine cavity: delicate, friable mass of cystic grape-like
translucent structures.
Focal villous edema.
Focal and moderate trophoblastic proliferation.
Fetal vessels and fetal parts (commonly present).
Not considered to have an increased risk for
choriocarcinoma.

21. Mole that penetrates or even perforates the uterine wall →
chorionic villi invading the myometrium + proliferation
of both cytotrophoblast and syncytiotrophoblast.
Locally destructive tumor.
Invasive Mole.

22. Clinical Features:
Abnormal uterine bleeding.
Thin watery fluid discharge.
Irregular uterine enlargement
Preeclampsia.
Spontaneous pregnancy loss (especially with partial and
early complete moles).
Abnormalities in ultrasound showing diffuse villous
enlargement.
↑ ß H.C.G.
Vesicular Mole.

23. Complications:
Severe haemorrhage.
Invasive mole:
Parametrial tissue invasion → rupture uterus.
Vascular invasion → distant spread → lungs and brain.
Regression after hysterectomy.
Malignant change.
Vesicular Mole.

26. CHORIOCARCINOMA.
Malignant neoplasm of trophoblastic tissue.
More with vesicular mole (50%) than with normal, ectopic
pregnancy or abortion.
Rapidly invasive and widely metastasizing.
Morphological features:
Soft fleshy yellow white tumor.
Large areas of necrosis & haemorrhage.
Malignant trophoblastic proliferation (pleomorphic cyto &
synctiotrophoblasts, anaplasia & mitosis).
No chorionic villi.
Infiltration (uterine wall, blood vessels & lymphatics).

27. CHORIOCARCINOMA.
Spread:
Direct: Invasion of the myometrium ± extension to the
serosa and adjacent structures.
Early invasion of blood vessels and lymphatics.
Early lung metastases:
Single, large → cannon-ball,
or multiple, small → snow storm.

28. CHORIOCARCINOMA.
Clinical Features:
 Irregular vaginal spotting (bloody, brown fluid).
 Spread (chest, bones).
Usually, by the time the tumor is discovered, chest and
bone X ray show metastatic deposits.
Frequent sites of metastasis:
Lungs (50%).
Vagina (30% - 40%).
Brain.
Liver.
Kidney.
 Elevated titers of H.C.G. to levels above those
encountered in hydatidiform moles.