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MHD > Placenta > Flashcards

Placenta Flashcards

1
Q

The placenta is composed of two layers the amnion (inner layer) and the chorion the outer layer, what does the chorion attach to?

A

decidua=endometrium of pregnancy

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2
Q

What is the chorionic villi?

A

placenta composed of chorionic villi that sprout from the chorion to provide large contact area between fetal and maternal circulation
_BLOOD DOES NOT MIX

  1. central stroma
  2. epithelium
    - syncytiotrophoblast
    - cytotrophoblast

-3rd trimester villi are smaller and vasculature more pronounced and see fibrosis

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3
Q

Spontaneous abortion

A

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

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4
Q

Ectopic Pregnancy

A

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

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5
Q

Dizygotic

A

fertilization of 2 ova

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6
Q

Monozygotic

A

division of one fertilized ovum

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7
Q

Monochorionic placenta implies what? What is the number of amnions determined by?

A

monozygotic (identical twins)
-time of the splitting of the ovum
monochorionic diamniotic vs monochorionic mononamnionic

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8
Q

Placenta previa

A

attachment of placenta to lower uterine segment of cervix

-serious 3rd trimester bleeding-dilation of cervix disrupts placenta

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9
Q

Placenta accreta

A
  • 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
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10
Q

abruptio placentae

A

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
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11
Q

What happens if the placent tissue is retained postpartum?

A

postpartum hemorrhage

-potential infection

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12
Q

preeclampsia-eclampsia

A

systemic syndrome characterized by widespread maternal endothelial dysfunction presenting clinically during pregnancy with:
hypertension
edema
proteinuria

  • most common with 1st pregnancies
  • usually last trimester
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13
Q

What is the pathogenesis of preeclampsia-eclampsia?

A

placenta plays a key role
-symptoms rapidly disappear after delivery of placent

Principle theories

  1. 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)
  2. endothelial dysfunction and imbalance of angiogenic and anti-angiogenic factors
  3. coagulation abnormalities
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14
Q

What generalized processes also happen in preeclampsia-eclampsia? what happens to the placenta?

A

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
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15
Q

Preeclampsia

A

HTN, edema, proteinuria

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16
Q

severe preeclampsia

A

preeclampsia + headaches and vision changes

17
Q

eclampsia

A

preeclampsia + convulsions

18
Q

HEELP syndrome

A

severe preeclampsia + hemolysis, elevated liver enzymes, low platelets

19
Q

WHat is the managment? Are there maternal sequelae after the birth?

A

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

20
Q

Placental infections

2 pathways

A
  1. ascending
    - through birth canal
    - usually bacterial
    - result=premature rupture of membranes, pre-term delivery
  2. Hematogenous
    - transplacental
    - TORCH
21
Q

What do you see in acute chorioamnionitis?

A

green purulent membranes

PMNS

22
Q

TORCH infections

A 
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
23
Q

Hydatidiform Moles

A

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
24
Q

What chromosomes make up complete and partial moles?

A

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

25
Q 
Complete Mole
General
Gross
Microscopic
Clinical course
A 
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
26
Q

Partial Mole

General

A 
Some villi are edematous
Minimal Trophoblastic proliferation 
One egg, two/three sperm
Fetus, although abnormal, mostly present
Not increased risk for choriocarcinoma
27
Q 
Complete mole vs Partial mole
Karyotype 
Villous edema
Trophoblast proliferation
Atypia
Serum HCG
Fetal TIssue
Behavior
A 
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
28
Q

Invasive Mole

A

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

29
Q

Gestational Choriocarcinoma

A

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

30
Q

How does Gestational Choriocarcinoma present? What is the treatment?

A

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

MHD (81 decks)

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