Pregnancy pathology Flashcards
Umbilical cord
Normally have 3 vessels- 2 Arteries and One vein
About 1% have only 2 vessesl one of each
80% is an isolated finding, 20 % have other fetal anomalies (most often GU or cardiac)
the 2 arteries and 1 vein is surrounded by whartons jelly (help maintain patency of vessels)
Membranes
Amnion- cuboidal layer of surface epithelium
Chorion laeve- pauci cellular connective tissue layer
Decidua capsularis (trophoblast, vessels and ghosted villi)
Villous parenchyma histology
Chorionic villi (gets smaller and more vascular with age or ischemia, syncytial knotting and calcifications increase with age)
Fetal stem vessels and villous capillaries--> fetal blood Intervillous space (star)--> maternal blood
the functional lung
Maternal decidua
Decidua basalis- can be quite cellular, often scattered lymphocytes, remodeled maternal spiral arteries
Why are spiral arteries remodeled?
Normal arteries- smooth muscle in walls allows for contraction/constriction–> increase cardiac out put in times of blood loss
if maternal spiral arteries constrict–> no flow to fetus/placenta–> fetal demise
Maternal spiral arteries remodel–> fibrin replaces smooth muscle during first/second trimesters
Lack of remodeling is pathologic
Abnormal cord insertion
Marginal cord insertion- inserts at disk edge
Velamentous cord insertion- inserts into membrane (tears easily)
Acute infections involving the placenta
Ascending infections: E coli, Group B strep, mycoplasma, candida, derived from Genitourinary/gastrointestinal tracts, can lead to umbilical cord inflammation (funisitis), acute chorioamnionitis, fetal/neonatal spesis, maternal fever
Hematogenous infection- listeria, (camplyobacter and gram negatives), maternal blood stream, acute villitis/ intervillositis (acute inflammation of villi and intervillous space), fetal loss, maternal illness, premature labor
Ascending infections in placenta
Acute inflammatory cells (PMNs) react to inflammatory stimulus in amniotic fluid- sometimes referred to as amniotic fluid infection sequence
Fetal inflammatory response- PMNs come from fetal circulation–> funisitis (umbilical cord inflammation)
Maternal inflammation response- PMNs com from maternal circulation–> chorioamnionitis (inflammation in membrane)
Acute intervillositis
abcess with PMN invasion involving numerous villi and the space between them, Intervillositis
when you see it think LISTERIA INFECTION, pregnancy patients present with fever, flu- like symptoms, risk of fetal dmise and neonatal sepsis usually acute
chrnic inflammation in placenta
Usually chorionic inflammatory cells in villi ( chronic villitis)
inflammatory cells- lymphocytes, histiocytes, plasma cell (b cells)- when an infection think TORCH
When there are plasma cells, rule out CMV and syphilis **
Preeclampsia
Sometimes called Toxemia of pregnancy
Clinically- usually the 1st pregnancy, advanced maternal age, symptoms- HTN, proteinuria, edema, if there are seizures– eclampsia
HELLP syndrome- plus elevated liver enzymes, microangiopathic hemolytci anemia, thrombocytopenia, dissemintate intravascular coagulation- deliver it
preeclampsia pathophysiology
abnormalities of maternal spiral arteries decrease blood flow to the placenta, incomplete remodeling/ retained smooth muscle in artery walls, result–> insufficient blood flow to placenta
Placenta releases substances (sFIt1, sEng) that lead to endothelial cell dysfunction, vascular hyperreactivity
will have a thick smooth muscle and could have fibrosis can lead to retroplacenta hemorrhage,
Ectopic pregnancy
inmplantation of a fertilized ovum anywhere other than the uterine cavity (1% of all pregnancies)- fallopian tube (90% of ectopic pregnancies), ovaries, peritoneal surfaces of the abdomen
risk factors- anything that obstructs the fallopian tubes (chronic inflammation (salpingitis PID), tubal ligation
Early stages of pregnancy are unremarkable (b-hCG usually increases normallay and mensttuation stops)
Eventuallu- embryo dies du to inadequate attachement), Placental invasion causes rupture with massive hemorrhage and shock–> medical emergency
Gross/ histopathology of ectopic pregnancy
hemorrhage within tube lumen (hematosalpinx) with ddistension, embryo or placental parts visible
Hist- placental villi and embryo components
gestational trophoblastic disease
Abnormal proliferation of fetal trophoblast cells
2 categoris per WHO
Molar lesions- Partial Mole, complete Mole, invasive mole
Non molar lesion–> choriocarcinoma
Common factor- all secrete hCG in blood and urine
hydatiform moles
result from abnormal fertilization due to excess paternal genetic maternal material
Complete mole- 46XX, 46XY- single sperm undergoes duplication of chromosomes in an empty ovum/ without active maternal chromosomes (90% of cases) or 2 sperm fertilize an empty ovum (10% of cases)
Partial mole (69 XXy)–> normal egg fertilized by 2 sperm
Clinical presentation- elevated maternal hCG, absent fetal hr, Dan de monitoring of serum hCG
Swolledn edematoud villi
