188- Placental pathology Flashcards
most common site of ectopic pregnancy? How does it present? Often confused with? What will endometrial biopsy show? Risk factors?
fallopian tubes. Amenorrhea with lower-than-expected hCG and sudden lower abdominal pain. Appendicitis. Biopsy shows decidualization w/o chorionic villi. Risk factors: hx of infertlity, salpingitis (PID), ruptured appendix, prior tubal surgery
What happens in placenta previa? What increases your risk?
placenta implants very low in uterus, covering internal os. When cervix dilates for labor there will be severe hemorrhage. Risk increased by multiparity and prior c-section
Placenta accreta: what happens to cause it? what happens at birth? what increases your risk?
accreat=”encased”. Defective decidual layer allows placenta to invade myometrium so placenta doesn’t separate after birth so you get massive hemorrhage. Increased risk: prior c-section, inflammation, placenta previa.
What are the two possible routes of infection and their results and which is more common?
Hematogenous results in villitis. Ascending results in amniotic fluid infection (chorioamnionitis, funisitis) and is much more common
inflammatory response seen in membranes of placenta: where do the inflammatory cells come from? in umbilical cord inflammation?
maternal (decidua is only vascular layer)
fetal (come from mesenchymal mesoderm)
Placental abruption: what is it? What is it associated with? What increases risk?
premature detachment of placenta. May be associated with DIC. Increase risk with smoking, HTN, cocaine.
What are the features of preeclampsia? What can cause it?
HTN, proteinuria (edema no longer included). Caused by placental ischemia due to impaired spiral artery dilation leading to fibrinoid necrosis of vessels (acute atherosis)
Fetal thrombotic vasculopathy: what is it? what can cause it? what can it lead to?
term used to describe lesions of fetoplacental vasculature. Clotting results from Virchow’s triad. Can lead to retarded growth, fetal demise, cerebral palsy, amputation necrosis, low platelets
What would you call the spectrum of disease where villi are encased by perivillous fibrin
Massive pericillous fibrin deposition
Dizigotic vs mono? amnions? chorions? eggs? sperm?
Dizygotic: 2 eggs separately fertilized by 2 sperm. Always have separate amniotic sacs and separate placentas (chorions)
Monozygotic: 1 fertilized egg splits into 2 zygotes at variable times during pregnancy which determines number of chorions and amnions
Result of monozygotic twins splitting at 13 days?
(2-cell stage) separate placenta, separate amnion.
(Morula) common placenta, separate amnion
(blastocyst) common placenta, common amnion
(formed embryonic disc) common placenta, commo amnion, conjoined twins
what is a common complication of monochorionic twinning?
intertwin vascular connections resulting in twin-twin transfusion
Gestational trophoblastic disease: what is it? what is a good marker? What are some examples?
group of proliferative placental diseases (maternal tumor arising from fetal tissue).
High Beta-hCG
Hydatidiform mole (most common), choriocarcinoma, persistent GTD, placental site trophoblastic tumor
Hydatidiform mole: what is it? presentation? precursor to? Uterus appearance? Appearance of complete moles on sonogram?
cystic swelling of chorionic villi and proliferation of chorionic epithelium (trophoblast). Presents with vaginal bleeding. Most common choriocarcinoma precursor. Also can lead to uterine rupture. Honeycombed or cluster of grapes, abnormally enlarged. “snowstorm” appearance with no fetus.
what is the etiology of partial vs complete hydatidiform mole? what will their karyotype be? hCG levels? uterine size? conversion to choriocarcinoma? fetal parts?
complete: 1 or 2 sperm fertilize egg with no maternal DNA. 46 XX or XY. hCG very high. Enlarged uterus. 2% conversion to CA. No fetal parts.
Partial: two sperm fertilize egg with maternal DNA (triploid). 47 XXX, XXY, XYY. hCG mildly elevated. Normal uterine size. Rare conversion to CA. Contains fetal parts.
