DISEASES OF PREGNANCY

PLACENTAL INFLAMMATIONS AND INFECTIONS

ASCENDING
Cause – premature birth
PROM

Histology
Polymorphonuclear infiltrate in chorioamnion
Edema, congestion of vessels
Inflammation of umbilical cord and placental villi

Pathogens
Candida
Mycoplasma
Vaginal bacterial flora

DESCENDING
Hematogenous
TORCH infections, syphilis, TB, listeriosis

ECTOPIC PREGNANCY
Oviduct - tubal pregnancy
Ovaries - ovarian
Abdominal cavity - abdominal
Intrauterine portion of - interstitial
uterus

Morphology
Normal early development of embryo with placental tissue, amniotic sac and decidual
changes
Hematosalpinx, intraperitoneal hemorrhage
Distended upto 3-4 cmby a mall of blood with bits of placenta and fetal parts
Diagnosis by visualization of placental villi
Spontaneous proteolysis and absorption of the products of conception also occurs less
commonly

C/F
Until rupture occurs, indistinguishable from normal
Elevation of urine and placental hormones
Not elevated in poor attachment and necrosis of placenta

Treatment
Prompt surgical intervention
GESTATIONAL TROPHOBLASTIC DISEASE
Divided to
Hydatidiform mole
Invasive mole
Choreocarcinoma
All elaborate HCG in the increasing order from 1 to 3

HYDATIDIFORM MOLE
COMPLETE
CAUSE empty egg fertilized by 2
sperms
MORPHOLOGY Uterine cavity filled with a
delicae friable mass of thin
walled translucent cystic str
No fetal parts
All villi are edematous and
no vascularisation
Diffuse circumferential
trophoblastic proliferation
Atypia often present
HCG Serum – elevated
Tissue – very much elev
PROGNOSISt 2-3% progress to
choriocarcinoma
PARTIAL
normal egg fertilized by 2
sperms
Uterine cavity filled with a
delicate friable mass of thin
walled translucent cystic str
Fetal parts present
Only some of the villi
Haave a characteristic
scalloped irregular margin
Focal and slight
Not present
Less elevated
Elevated
Rarely gives rise to
choriocarcinoma

INVASIVE MOLE
Retains hydropic villi and invade the uterine wall deeply causing rupture and
hemorrhage.
Local spread to broad ligament and vagina

Morphology
Hyperplastic and atypical changes
Proliferation of both cuboidal and syncitial components

Prognosis
Removal technically difficult due to invasion
Cure possible through chemotherapy
Embolize to distant organs, but regress spontaneously

CHOREOCARCINOMA
Origin
Gestational chorionic epithelium or less frequently from totipotent cells withein the
gonads
Morphology
Hemorrhagic necrotic masses wihtn the uteus.
Early insinuation to myometrium and vessels
Primary lesion may self destruct
Chorionic villi are not formed, purely epithelial tumor with anaplastic cuboidal
cytotrophoblast and syncytiontrophoblast

C/F
Bloody brownish discharge accompanied by a rising titer of hCG
Absence of marked uterine enlargement
Dissemination mainly via blood, lymphatics uncommon

Treatment
Chemotherapy - nearly 100% cure even with neoplasms thea have spread beyond the
pelvis and vagina to lungs
Poor response to those arising from gonads

PLACENTAL SITE TROPHOBLASTIC TUMOR

Derived form placental site or intermediate trophoblast
Few months after pregnancy
hCG levels are only slightly elevated, more typically produce human placental lactogen
Not as sensitive to chemotherapy, so bad prognosis if extended beyond uterus

PREECLAMPSIA/ECLAMPSIA (TOXEMIA OF
PREGNANCY)
HT + proteinuria + edema in the 3rd trimester of pregnancy

Pathology
Musculoelastic walls of pregnancy
Blocked in eclampsia

Dilate to wide vascular sinusoids by fibrinous materials

This is caused by
Increase in Anti angiogenic factors sFlt1 and reduction in the level of
proangiogenic factor factor VEGF

The consequences are

Placental hypoperfusion
Development of ingarcts
Reduced elaboration by trophoblast the vasodilators prostacyclin, PGE2, NO
resulting in HT
Production by the ischemic placenta thromboplastic substances such as tissue
factor and thromboxane causing DIC
Morphology
Placental changes
More numerous infarcts
Retroplacental hemorrhages
Premature aging of placental villi with villous edema
Acute atherosis of spiral arteries with fibrinoid necrosis and lipid macrophages

Multiorgan changes
Due to DIC
Fibrin therombi within the glomerular capillaries
Endothelial swelling, mesangial hyperplasia
Finally cortical necrosis microvascular thrombi in brain, pituitary, heart

Treatment
Prompt early intervention in the eclampsia stage itself