Flashcards in Pregnancy related pathology Deck (12):
-primary- no menarche- hypoplastic uterus, imperforate hymen, endocrine problems
-secondary- after initiation of menarche- pregnancy, lactation, endocrine, stress
fertilized ovum implanted outside the uterine cavity, tubes cervix, ovary, abdomen
-tubal pregnancy- 1% of all pregnancies
-increase because of PID with tubal adhesions
-endometriousis with fibrosis is also higher risk, fibrosis blocks the passage of fertilized ovum
-lack of space poor vasculature, limited placental size
-ruptures 2-6 weeks after fertilization, embryo dies, rarely it is implanted in abdomen.
- ruptured- acute abdominal pain after amenorrhea- severe hemorrhage shock- mimics acute appendiciitis if right side, ultrasound shows abscenc of appropriate uterine nelargmenet, expansion of adnexz
-peritoneal aspiration yields blood
- beta hCG elevated due to preganancy, once the embryo dies, bhCG drops, decrease in bhCG leads to degenerationof corpus luteum which leads to drop in estrogen and progesterone
-endometrium breaks down leading to bleeding.
-endometrial curettings show no chorionic villi but have hypersecretory glands, R/O spontaneous abortion(chorionic villi)
Delivery of embryo(8 weeks) or fetus(20 weeks) , premature delivery (20-40 weeks)
- usually defective chromosomes, vaginal bleeding is rapid and can be severe(shock)
- lower abdominal pain due to uterine contraction,
-demonstrate chorionic villi or embryo for diagnosis.
-retroplacental hemorrhage at the interface of placenta and myometrium-
-disruption of the fetal vessels in terminal villi may produce a significant loss of fetal blood with injury or death
- can be caused by abnormal placental implantation or development, or material vascular disease, the effects may range from mild intrauterine growth retardation to sever uteroplacental ishcemia and maternal preeclampsia.
preamuter separtion of placent, ante partum hemorrhage, shock, DIC featal daeath, premature labor
placenta implants in the lower uterine segment or cervix, often the serious third trimester bleeding. a complete placenta previa covers the internal cervical os and thus requires delivery via cesarean section in avert placental rupture and fatal maternal hemorrhage during vaginal delivery.
leads to ante partum hemorrhage
caused by partial or complete absence of the decidua with adherance of the placental villous tissue directly to the myometrium and failure of placental separation.
-important cause of post partum bleeding which often may be life threatenint to the mother, common predisposing factors are placenta prevai and history of previous cesarean section.
last trimester- gestational edema with proteniuria and hypertension (GEPH)
synrome: EPH usually in third trimester
-distinct from a hypertensive person becoming pregnant
-5% of pregnancies
-1-% of PE develop seizures (Eclampsia)
-induce labor or do caesarian section
-disappears after labor.
-predisposing factor- primigravida, over 35 years age
-multiple pregnancies, hydramnios, prexisting hypertension, hydatidiform mole.
etiology- undetermined- placental ishcemia
-autoimmune reaction to placenta
-decrease production of PGE2 and NO by placenta- increased sensitivity to renin angiotensin
-DIC in eclampsia- due to thromboplastic tissue factor thromboxane released by ischemic placenta
-diffuse endothelial dysfunction, vasocontriction
- increased vascular permeability (proteinuria, edema)
Pathology- degenerated placenta ischemia-hyaline calcification, congestion, infarcts, thrombosed spiral arteries, hemorrhage (spnal arteies fail to dilate and thin out like in normal pregnancy due to lack of smooth muscle coat
-acute atherosis- foamy macrophages in necrotic vessel wall characterisitc later
-macrophages and lymphocytes.
-- glomerular and endothelial swelling, mesangial proliferation, fibrin thrombi, cortical necrosis
-- liver, periportal hemorrhage, other organs edema, hemorrhages.
Gestational trophoblastic disease
hydatidiform mole(molar pregnancy)- complete, incomplete
-invasive mole (chorioadenoma destruens
-placental site trophoblastic tumor
-bhCG levels more important than anatomic classification
Uterus filled with translucent, grape-like clusters of edematous, distoreted villous structures, deficiency of fetal blood vessels.
- More common in Far East, large edematous avascular villi, degeneration of stroma, proliferation of trophoblasts, partial or complete.
Complete mole- ovum has lost all its chromosomes- empty ovum, fertilized by two sperms or a single diploid sperm- 46XX, 46 XY, genotype of complete mole is purely paternal, embryo dies early, no fetal parts seen, uterus is enlarged fileld with grape like vesicles, beta hCG markedly elevated , may produce bilateral theca lutein cysts, 2% develop choriocarcinoma
Partial mole- ovum fertilized by two sperms 23 x and 23 y, so moles are triploid- 69XXY
- embryo develops for a short period, fetal parts may be seen,
-molar changes partial, uterus minimally enlarged, no risk of malignancy
clinical features- amenorrhea, vomiting, positive pregnancy test, uterus larger compared to amenorrhea , 3-4 months of vaginal bleeding, grape like structures,
-enlarged cystic placenta, absent fetus
-beta hCG greatly elevated in serum, urine, curettage to remove the lesion
-monitor beta hCG for 2% that develop choriocarcinoma
10% of complete moles develop invasive feature, deep invasion of villi and trophoblasts into the myometirum
-associated with necrosis, hemorrhage of myometrium
-Uterus may rupture, villi may embolize to lungs, treat with chemotherapy.
50% follow a mole, 25% follow abortion, 23% follow normal pregnancy, 2% follow ectopic pregnancy
-friable hemorrhagic mass, extenxive infiltration and metastasis- lung, brain, liver
- malignant cyto, syncitiotrophoblasts,
-hemorrhage and necorsis (bloody discharge per vagina)
-NO chorionic villi
- beat HCG elevated confirm diagnosis by biopsy, chemotherpay yeilds good results,- cure
follow up beta hCG levels monitored.