Placental Abnormalities and Selected Pregnancy Complications Flashcards
What is the fetal portion of the placenta called and what is the layer which is closest to the fetus? What is its histology
Chorionic plate
First layer: amnion - formed by the amnionic cavity above the epiblast cells in the placenta.
-> single layer of cuboidal epithelial cells which lines the fetal surface of the placental disc as well as wraps around lining the amnionic sac
What is the structure of a chorionic villus?
- Central core of loose connective tissue made form extraembryonic mesoderm, containing fetal blood vessels
- Outer layer of trophoblasts (inner cyto, out syncytio)
- Intervillous space - Trophoblasts form lacunae which merge into a single space allowing close maternal blood flow
What are the fates of the cytotrophoblasts and syncytiotrophoblasts?
Cytotrophoblasts - eventually leave chorionic villi and migrate to form the “trophoblast layer”, between the placenta and the decidualized uterine endometrium.
Syncytiotrophoblasts - remain on outside of chorionic villi, secrete hCG
How are cotyledons formed in the placenta?
Collections of extravillous cytotrophoblasts + maternal decidua + fibrin deposits project into intervillous space
What is the maternal portion of the placenta called and what are its layers?
Basal plate:
Two fibrin layers surround the extravillous trophoblast layer from the fetus. Then closer to the mother is the decidua basalis (hormonally-stimulated stroma).
Then there are maternal spiral arteries (remodeled by extravillous trophoblasts) and normal endometrial glands.
When trying to determine if you have monozygotic or dizygotic twins, is it more helpful to have monochorionic placentas or dichorionic placentas?
Monochorionic - much more helpful, because they can only be formed when two babies share the same chorion.
Dichorionic placentas can be either a very early twinning (pre-morula completion, 0-4 days) or dizygotic
When does separation occur for a monochorionic diamnionic twin vs monochorionic monoamnionic twin? Which is more common?
Monochorionic diamnionic - separation occurs 4-8 days -> occurs after morula (compacted 8 cell embryo) has formed but before blastocyst has been made and implanted
-> most common twinning overall (even more than dichorionic)
Monochorionic monoamnionic -> very rare, occurs when cleavage happens in blastocyst stage, two embryos arise from same inner cell mass
(conjoined twins would be even later, but still monochorionic/amnionic)
What is a twin-twin transfusion syndrome?
When both twins share the same chorion, their parts of the placenta can share arteriovenous connections which lead to one twin drawing more oxygenated blood than the other
-> can lead to differential growth of the twins
What is a marginal vs velamentous cord insertion and what are the clinical consequences?
Marginal - cord inserts closer to disc margin (rather than centrally) -> minimal risk
Velamentous - cord inserts into fetal membranes (chorioamnion) rather than the placental disc -> vessels travel without Wharton jelly protection. Can result in vasa previa
What is vasa previa? What should be done?
When fetal vessels run over / close to cervical os
- > can lead to vessel rupture and fetal death if the membrane ruptures
- > Should do an Emergency C-section
What are the complications of a two-vessel umbilical cord?
This is a single umbilical artery
Usually asymptomatic,but may be associated with congenital anomalies or symmetric IUGR
What are the risks with having an excessively long umbilical cord?
Cord entanglements -> nuchal cord, which may strangle the baby
True knots and constrictures
-> fetal distress, neurologic impairment, and IGUR
What are the risks of having an abnormally short cord?
Increased risk of placental abruption (ripping off earlier than wanted), cord hemorrhage, and other congenital anomalies
What happens if you get a true knot in the cord?
If tight enough, can lead to intrauterine and intrapartum (during delivery) mortality, as well as neurologic damage
What is one common placental abnormality which increases the risk of retained placenta post-delivery as well as post-partum hemorrhage?
Multilobed placentas -> when lobes of the placenta are separated by intervening membranes
What does placenta previa mean?
Placenta comes before baby
-> placenta is implanted in maternal uterine segment, sometimes overlying internal cervical os
What are the complications of placenta previa and what should be done about it?
Can lead to significant maternal hemorrhage since the placenta is directly over the opening to the vagina, and the decidua is not well-formed in this area.
Baby should be delivered by C-section to prevent fatal maternal hemorrhage during delivery
What are the risk factors for placenta accreta/increta/percreta?
- Prior C-section -> heals with scar tissue, and collagen cannot decidualize in response to hormones
- Uterine anomalies - leading to abnormal decidualization
- Placenta previa - lower uterus is not as hormone responsive as upper body -> improper decidualization
What is placenta accreta vs percreta vs increta?
Accreta - Placenta “attaches” to myometrium with no intervening decidua
Increta - placenta “invades” into myometrium
Percreta - placenta “penetrates” through myometrium into serosal surface, possibly attaching to nearby structures in peritoneal cavity
What are the potential complications of placenta accreta/increta/percreta?
- Retained placenta -> hard to get the placenta lose since it will be very adherent
- Retained placenta will cause post-parum hemorrhage and possible uterine rupture
- > significant bleeding, can lead to Sheehan syndrome
What should be done to prevent complications of placenta accreta/increta/percreta?
Usually a C-section with hysterectomy to prevent bleeding and to prevent this from happening again
What is placental abruption and what are the possible complications to the fetus?
Premature separation of placenta form uterine wall before delivery - may be partial or complete (whole placenta)
Fetal complications - Fetal distress, preterm delivery, IUGR, and death due to hypoxic/ischemic injury
What is the clinical presentation of placental abruption for the mother?
Abdominal pain / tenderness in the third trimester marked by:
- Painful vaginal bleeding
- Uterine contractions
- Disseminated intravascular coagulation and hypovolemic shock -> placenta releases procoagulant factors
What are the risk factors for placental abruption?
- Hypertension / preeclampsia - leads to poor placental disc perfusion
- Cocaine / nicotine use - poor perfusion due to vasocontriction
- Abdominal trauma
Are infarcts particularly common in the placenta? What are they and what do they look like grossly?
Small infarcts are very common
- > they are localized areas of pale necrosis, usually due to decreased maternal perfusion
- > they actually look like pale infarcts since there is poor collateral circulation in the villous space ->
What do placental infarcts look like microscopically, and what are the risk factors?
Coagulative necrosis with fibrin deposition, and often dystrophic calcification
Risk factors are maternal HTN and pre-eclampsia (similar to placental abruption)
-> may lead to fetal demise / IUGR if there are enough
What are the two major routes of placental infections and what usually causes them? What areas of the placenta get infected (I’m sorry mate you probs won’t remember this)?
- Acute chorioamnionitis - usually due to ASCENDING infections from vagina / cervix, associated with early membrane rupture. Almost always bacterial.
- Chronic villitis - (inflammation of chorionic villi) usually hematogenous dissemination in a TRANSPLACENTAL mechanism of TORCH pathogens. Almost always viruses and parasites
What are the etiologic agents of ascending infections of the placenta?
Again, these are chorioamnionitis
Commonly microbes from the vagina / cervix:
- Genital mycoplasmas (i.e. Mycoplasma hominis or Ureaplasma spp.)
- Gardnerella vaginalis
- Group B streptococcus
- E. coli
What is the immune response to ascending infections of the placenta?
- Maternal inflammation - purulent opacification of chorioamionic membranes due to neutrophilic infiltrate
- Fetal inflammation - begins in fetal vessels / umbilical cord -> involvement of Wharton’s jelly / umbilical arteries -> Funisitis (it sure is fun to infect the umbilical cord)
What are the clinical manifestations / complications of ascending placental infection?
Maternal fever / purulent discharge due to her immune response
Fetal complications include sepsis, ischemic brain injury, and death, especially if bacteria are in amnionic fluid and give the baby pneumonia
-> often causes preterm birth.
What type of inflammation is seen in transplacental infections, even syphilis?
TORCH microbes will usually be viral / parasitic -> cause chronic inflammation with lymphocytes, macrophages, and plasma cells (chronic villitis)
-> even syphilis will cause plasma cells since it is associated with obliterative endarteritis and chronic inflammation
What is the definition of pre-eclampsia?
Development of hypertensino, edema, and proteinuria during pregnancy, which may cause end-organ dysfunction
What are the severe symptoms of end-organ dysfunction in pre-eclampsia?
Headaches and visual disturbances secondary to hypertension, with hypercoagulability and acute kidney injury (due to fluid loss).
Pulmonary edema may result from proteinuria.
When does pre-eclampsia usually arise and what are the risk factors for it arising earlier?
Usually arises in third trimester
Earlier in molar pregnancies, pre-existing HTN, kidney disease, or coagulopathy.
What is the proposed pathogenesis of pre-eclampsia?
Inadequate extravillous trophoblast remodelling of maternal spiral arteries leads to placental factors are released into circulation and cause diffusion endothelial dysfunction:
- > Vasoconstriction (damaged endothelium releases less NO)
- > Increased vascular permeability leading to edema / proteinuria
- > hypercoagulability due to endothelial damage
What are eclampsia and HELLP syndrome?
Eclampsia - Preeclampsia + seizures
HELLP - Severe pre-eclampsia leading to
- > Hemolysis, Elevated Liver Enzymes, Low Platelets
- > microangiopathic hemolytic anemia involving liver damage
What are the placental factors released into circulation causing maternal endothelial dysfunction and hypercoagulability?
Placental ischemia -> induces release of angiogenesis modulating factors like endoglin
-> systemic endothelial dysfunction
Hypercoagulability -> caused by endothelial damage causing decreased prostacyclin production and increased prothrombotic factors -> systemic thrombi formation
What are the findings in the placenta pathologically in pre-eclampsia?
Thrombi, fibrinoid necrosis, and abnormal lipid deposition -> acute atherosis. This is due to leakage of plasma proteins from maternal vessels. Hematomas and ischemic infarcts are often seen
What are the treatments for pre-eclampsia and severe pre-eclampsia, eclampsia, and HELLP syndrome?
Pre-eclampsia - antihypertensives, IV magnesium sulfate (seizure prevention and later control). May deliver is baby is full term
Severe pre-eclampsia, eclampsia, and HELLP syndrome - delivery of baby immediately
What is the cause of a complete mole vs a partial mole? How many chromosomes will they have?
Complete mole - completely paternal DNA -> either two sperm in one empty ovum, or one sperm which replicates in empty ovum -> 46 chromosomes
Partial mole - 2 sperm + 1 eggs -> 69 chromosomes
What are the possible karyotypes of complete mole?
46,XX or 46,XY, I don’t think 46,YY would lead to a viable mole
What is seen on the pathology of a complete vs partial mole?
Complete mole - proliferation of trophoblasts and “grape-like” edematous villi
Partial mole - some normal villi, but others are edematous from excess trophoblastic proliferation.
-> fetal tissue may be present in this case because maternal chromosomes are there to work past imprinting
How does molar pregnancy usually present / what is the usual way you know it’s happening?
Usually presents as spontaneous miscarriage or with increased uterine size and hCG levels which are TOO HIGH for gestational age (trophoblastic proliferation)
-> increased hCG may lead to theca cell cysts, hyperthyroidism, and early pre-eclampsia
How is molar pregnancy dealt with and what are the risks associated with it? Who are these more common in?
Endometrial curettage
-> monitor hCG for recurrence, as it may develop into:
- Invasive mole (more common in complete mole than partial)
- Gestational choriocarcinoma (complete mole only)
How does complete mole classically appear on ultrasound?
“Snowstorm” appearance -> areas where trophoblast masses appear and do not appear, looks like a blizzard of white and black.
What is the clinical presentation of invasive mole and what is happening pathologically?
Pathologically - myometrium has been invaded by proliferating trophoblasts AND chorionic villi which can lead to uterine rupture
Presents as uterine bleeding / elevated hCG after mole removal
What is the treatment for invasive mole?
Methotrexate chemotherapy -> tumor is highly responsive.
What gives rise to a gestational choriocarcinoma?
Complete hydatidiform mole most commonly, but can arise from any pregnancy, including abortion, normal pregnancy, and ectopic pregnancy
How does a choriocarcinoma differ from a invasive mole?
Choriocarcinoma - there will be NO chorionic villi. It an invasive mole, the chorionic villi are present.
What is the clinical presentation of a choriocarcinoma?
uterine bleeding and elevated hCG levels.
Shortness of breath with hemoptysis is common due to early widespread dissemination hematogenously, including lungs, brain, liver, etc (trophoblasts are invasive).
How does gestational choriocarcinoma differ from germ cell choriocarcinoma?
They both look the same (malignancies of trophoblasts), but gestational-related choriocarcinomas have a far better prognosis, and respond well to chemotherapy.
Germ cell choriocarcinoma will probs kill you.
