Placenta Flashcards
The placenta is composed of two layers the amnion (inner layer) and the chorion the outer layer, what does the chorion attach to?
decidua=endometrium of pregnancy
What is the chorionic villi?
placenta composed of chorionic villi that sprout from the chorion to provide large contact area between fetal and maternal circulation
_BLOOD DOES NOT MIX
- central stroma
- epithelium
- syncytiotrophoblast
- cytotrophoblast
-3rd trimester villi are smaller and vasculature more pronounced and see fibrosis
Spontaneous abortion
lost before 20 weeks
1/3 of all pregnancies lost
-more than half due to chromosomal abnormalities
-defective implantation
-fetal abnormalities
-maternal causes (inflammation, uterine deformity, DM, luteal-phase defects)
-unkown
Ectopic Pregnancy
Implantation occurs outside uterus
1:150 pregnancies
90% fallopian tubes
10% ovary and abdominal cavity
Predisposing factors
- inflammation and scarring
- intrauterine device
Presentation-abdominal pain, acute abdomen
Clinical complications: rupture and hemorrhage; high mortality unless removed surgically
Dizygotic
fertilization of 2 ova
Monozygotic
division of one fertilized ovum
Monochorionic placenta implies what? What is the number of amnions determined by?
monozygotic (identical twins)
-time of the splitting of the ovum
monochorionic diamniotic vs monochorionic mononamnionic
Placenta previa
attachment of placenta to lower uterine segment of cervix
-serious 3rd trimester bleeding-dilation of cervix disrupts placenta
Placenta accreta
- partial or complete absence of decidua with adherence of decidua with adherence of placental villous tissue directly to myometrium -failure of placental separation
- cause of postpartum bleeding
Predisposing factors:
- placenta previa (60%)
- previous cesarean section
abruptio placentae
premature separation of placenta prior to delivery
formation of retroplacental blood clot
- blood supply of oxygen and nutrients to fetus compromised to greater degree with increasing size of abruption
- painful maternal bleeding
- potential fetal death
What happens if the placent tissue is retained postpartum?
postpartum hemorrhage
-potential infection
preeclampsia-eclampsia
systemic syndrome characterized by widespread maternal endothelial dysfunction presenting clinically during pregnancy with:
hypertension
edema
proteinuria
- most common with 1st pregnancies
- usually last trimester
What is the pathogenesis of preeclampsia-eclampsia?
placenta plays a key role
-symptoms rapidly disappear after delivery of placent
Principle theories
- abnormal placenta vasculature
- failure of uterine spinal artery to remodel-maternal vascular hypoperfusion-placental ischemia-generalized endothelial cell injury (cytotrophoblasts allow for arteries to remodel) - endothelial dysfunction and imbalance of angiogenic and anti-angiogenic factors
- coagulation abnormalities
What generalized processes also happen in preeclampsia-eclampsia? what happens to the placenta?
Generalized
liver: fibrin thrombi, hemorrhage, necrosis
kidney: fibrin in glomeruli and capillaries, renal cortical necrosis
brain: hemorrhage and thrombosis
heart and anterior pituitary
Placenta Malperfusion, ischemia, vascular injury -infarcts -retroplacental hematoma -villous ischemia -acute atherosis of uterine vessels ***-fibrinoid necrosis, macrophages, inflammation
Preeclampsia
HTN, edema, proteinuria
severe preeclampsia
preeclampsia + headaches and vision changes
eclampsia
preeclampsia + convulsions
HEELP syndrome
severe preeclampsia + hemolysis, elevated liver enzymes, low platelets
WHat is the managment? Are there maternal sequelae after the birth?
Term=delivery
Preterm
-Mild-expectant management
-Severe-deliver regardless of fetal age
20% develop HTN and microalbuminuria within 7 years
-2X increased heart and brain vascular disease
Placental infections
2 pathways
- ascending
- through birth canal
- usually bacterial
- result=premature rupture of membranes, pre-term delivery - Hematogenous
- transplacental
- TORCH
What do you see in acute chorioamnionitis?
green purulent membranes
PMNS
TORCH infections
T-toxoplasma gondii O-others: parvovirus B 19, Syphilis, TB, listeria R-rubella C-CMV H-Herpes simplex virus, HIV
- all may evoke:
1. fever
2. encephalitis
3. chorioretinitis
4. hepatosplenomegaly
5. pneumonitis
6. myocarditis
7. hemolytic anemia
8. vesicular or hemorrhagic skin lesions
Hydatidiform Moles
cystic swelling of chorionic villi with trophoblastic proliferation
- infrequent
- women present with miscarriage and undergo D&C based on US/HCG findings
- BENIGN-we want to know and distinguish them with regard to invasive mole or choriocarcinoma
What chromosomes make up complete and partial moles?
Complete Mole 90%
- both chromosomes are of male origin
- homozygous complete mole
- 46XX
Complete Mole 10%
- both chromosomes are of male origin
- heterozygous complete mole
- 46XX and 46XY
Partial Mole MOST COMMON
Sperm and ovum
-69XXX, 69XXY, 69XYY
Complete Mole General Gross Microscopic Clinical course
Most villi enlarged, edematous Diffuse trophoblast hyperplasia Androgenic (empty ovum) Embryo dies very early (fetal parts rarely seen) 2.5% risk of choriocarcinoma
Gross:
Delicate friable mass of thin walled, translucent, cystic friable, grape like structures
Microscopic
- swollen villi with almost no fetal blood vessels
- diffuse cytotrophoblast and syncytial trophoblast proliferation
- marked atypia at implantation site
Clinical course Abnormal uterine bleeding passage of fluid and tissue ultrasound diagnostic (snow storm) -serum HCG increase -roved via curettage; serum HCG levels monitored -10% develop into invasive moles -2.5 risk choriocarcinoma
Partial Mole
General
Some villi are edematous Minimal Trophoblastic proliferation One egg, two/three sperm Fetus, although abnormal, mostly present Not increased risk for choriocarcinoma
Complete mole vs Partial mole Karyotype Villous edema Trophoblast proliferation Atypia Serum HCG Fetal TIssue Behavior
Complete Karyotype: 46 XX or 46XY Villous edema: all villi Trophoblast proliferation: diffuse, circumfrential Atypia: often present Serum HCG: elevated Fetal TIssue: absent Behavior: 2.5% choriocarcinoma
Partial Karyotype: triploid Villous edema: some villi Trophoblast proliferation: focal; slight Atypia: absent Serum HCG: less elevated Fetal TIssue: present Behavior: rare
Invasive Mole
Mole that penetrates uterine wall
Hydropic chorionic villi invade myometrium
-may embolize to distant sites
Clinical
vaginal bleeding
persistently elevated HCG
risk of uterine rupture
Treatment
chemotherapy
Gestational Choriocarcinoma
Malignant
- rapidly invasive, widely metastatic
- rapidly growing
- necrotic
- hemorrhagic
Neoplasm of trophoblast derived cells
- proliferation neoplastic cytotrophoblasts and syncytiotrophoblast
- NO CHORIONIC VILLI
Uncommon 1:20,000-30,000 Us preg
50% from complete moles
25% from previous abortions
22% normal pregnancy (intraplacental choriocarcinoma)
Ectopic pregnancy
How does Gestational Choriocarcinoma present? What is the treatment?
Presents as vaginal blood, brown fluid spotting
- during pregnancy, after miscarriage, after curettage
- can be months delay
Metastases usually at time of any signs
HCG elevations
-unless very necrotic
Chemo EXTREMELY effective
-paternal antigens evoke immune response in mother
