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MHD II Test 3 > Placental and Gestational Disorders > Flashcards

Placental and Gestational Disorders Flashcards

1
Q

Placenta: Functions (3)

A
  1. establish effective communication between mother and the developing fetus while maintaining the immune and genetic integrity of both individuals;
  2. allows intimate apposition of maternal and fetal circulations for exchange of nutrients, oxygen, and waste products;
  3. secretes a variety of hormones including human chorionic gonadotropin (hCG)
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2
Q

Define

  1. Amnion
  2. Chorion
  3. What does the chorion attach to?
  4. Define Chorionic Villi
A
  1. inner layer of the membrane surrounding the developing fetus, forms the amniotic cavity
  2. outer layer of the surrounding the developing fetus, forms the amniotic cavity
  3. decidua (endometrium of pregnancy)
  4. Placenta composed of chorionic villi that sprout from the chorion to provide a large contact are between the fetal and maternal circulations
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3
Q

Chorionic Villi

  1. Histo look
  2. What are the two layers of epithelium?
A
  1. central stroma, w/ vascularity

2. syncytiotrophoblast, cytotrophoblast

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4
Q

Fetal Circulation

  1. Under normal circumstances, when do the maternal and fetal blood mix?
  2. What are the umbilical vessels?
  3. How does maternal blood move?
A
  1. never
  2. 1 vein (carries oxygenated blood to baby), 2 arteries (carries deoxygenated blood back to receive oxygen and nutrients
  3. enters placenta via endometrial arteries and leaves via endometrial veins
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5
Q

Spontaneous Abortion (Miscarriage)

  1. When does it usually occur?
  2. How often does it occur?
  3. What are more than half due to?
  4. What are some other causes?
A
  1. pregnancy loss before 20 weeks
  2. 1/3 of all pregnancies are lost (10-15% of recognized pregnancies)
  3. chromosomal abnormalities (tri/monosomy)
  4. Defective implantation, fetal abnormalities, maternal causes (inflammation, uterine deformity, DM, luteal-phase defects) unknown
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6
Q

Ectopic Pregnancy

  1. Define
  2. How often does it occur?
  3. Where?
  4. Predisposing Factors
  5. Presentation
  6. Complications
A
  1. implantation occurs outside uterus
  2. 1:150 pregnancies
  3. 90% fallopian tubes, 10% ovary/abdom. cavity; may also implant in corn (horn) of uterus
  4. inflammation and scarring (pelvic inflamm disease –> constrictions and fibrosis of fallopian tube); intrauterine devices can increase risk
  5. abdominal pain, acute abdomen
  6. rupture and hemorrhage (esp of fallopian tube)
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7
Q

Twin Placentas

  1. 3 types of twin placentas
  2. What implies monozygotes?
  3. What determines the number of amnions?
A
  1. diamnionic, dichorionic; diamnionic, monochorionic; monoamnionic, monochorionic;
  2. monochorionic placenta; however, dichorionic can also be identical twins
  3. time of splitting of ovum
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8
Q

When does to ovum split to create:

  1. dichorionic, diamnionic placenta?
  2. monochorionic, diamnionic placenta?
  3. Monochorionic monoamnionic placenta?
A
  1. day 0-4
  2. day 4-8
  3. day 8-12
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9
Q

Twin-Twin Transfusion

  1. What happens?
  2. What happens to each twin?
A
  1. 1 fetus gets more blood than the other

2. the less perfused twin often does not survive; well perfused twin may not make it as well

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10
Q

Placenta Previa

  1. Define
  2. Symptom
  3. how is baby delivered?
  4. Risk factor?
A
  1. attachment of placenta to lower uterine segment or cervix
  2. painless, serious 3rd trimester bleeding due to dilatation of cervix;
  3. C-section
  4. previous C-sections
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11
Q

Placenta Accreta

  1. Define
  2. Causes what?
  3. What can it do?
  4. Predisposing factors
A
  1. partial or complete absence of decidua with adherence of placental villous tissue directly to myometrium (failure of placental separation)
  2. post-partum bleeding
  3. Can invade into other structures, like the bladder
  4. Placenta Previa, previous C-section (scarring of endometrium)
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12
Q

Abruptio Placentae

  1. Define
  2. What forms?
  3. What happens to the fetus?
  4. What happens to the mother?
A
  1. premature separation of the placenta prior to delivery
  2. retroplacental blood clot
  3. blood supply of O2 and nutrients to the fetus is compromised to a greater degree with increasing size of the abruption; potential fetal death
  4. painful bleeding, hemorrhage
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13
Q

Retained Placental Tissue

  1. Define
  2. May cause what?
A
  1. retention of tissue after spontaneous miscarriage or elective abortion
  2. post-partum hemorrhage, infection,
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14
Q

Preeclampsia- Eclampsia

  1. Define
  2. Can also cause…
  3. Who gets it? When?
  4. Which pregnancy is it most common in?
A
  1. systemic syndrome characterized by widespread maternal endothelial dysfunction presenting clinically with hypertension, edema, and proteinuria during pregnancy
  2. fetus problems due to insufficient blood supply to developing fetus
  3. 3-5% of pregnancies; 3rd trimester;
  4. 1st pregnancy, those w/ underlying HTN or diabetes
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15
Q

Preeclampsia- Eclampsia: Pathogenesis

  1. How do we know that the placenta plays a role in symptoms?
  2. Theories of pathogenesis (3)
A
  1. symptoms disappear after delivery of placenta
  2. abnormal placental vasculature;
    endothelial dysfunction and imbalance of angiogenic and anti-angiogenic factors (more anti-angiogenic factors);
    Coagulation abnormalities (imbalance btwn thromboxane and prostacyclin- abnormally high thromboxane)
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16
Q

Preeclampsia- Eclampsia

1. What happens to spiral arteries?

A
  1. They fail to remodel; usually, the musculature around them regresses allowing them to be high capacitance vessels;
    when this fails to occur, blood vessels can’t carry as much blood to the fetus
17
Q

Preeclampsia- Eclampsia: How are the following organs involved?

  1. Liver
  2. Kidney
  3. Brain
  4. Other organs involved
A
  1. fibrin thrombi, hemorrhage, necrosis
  2. fibrin in glomeruli and capillaries, renal cortical necrosis
  3. hemorrhage and thrombosis
  4. heart and anterior pituitary
18
Q

Placenta Morphology in Preeclampsia- Eclampsia

  1. What happens to placenta?
  2. What does that cause?
A
  1. Malperfusion, ischemia, vascular injury
  2. –> infarcts, retroplacental hematoma, villous ischemia, acute therosis of uterine vessels (fibrinoid necrosis, macrophages, inflammation)
19
Q

Distinctions between Preeclampsia and Eclampsia

  1. What defines Preeclampsia?
  2. Severe Preeclampsia?
  3. Eclampsia?
  4. HELLP Syndrome
  5. Other complciations (3)
A
  1. HTN, edema, proteinuria
  2. preeclampsia + headache and vision changes
  3. Preeclampsia + convulsions
  4. severe preeclampsia + hemolysis, elevated liver enzynes, low platelets
  5. hypercoaguability, acute renal failure, pulmonary edema
20
Q

Management of Preeclampsia- Eclampsia

  1. If baby is at term
  2. If baby is preterm
  3. Long term consequences
A
  1. deliver
  2. mild- expectant management; severe- delivery regardless of fetal age
  3. none for mother;
    20% of children develop HTN and microalbuminemia w/in 7 years;
    2x increased heart and brain vascular disease
21
Q

Placental Infections: Ascending

  1. How common
  2. How does it get there?
  3. What causes it?
  4. Result
A
  1. more common
  2. through birth canal
  3. usually bacterial,
  4. premature rupture of membranes, pre-term delivery
22
Q

Placental Infections: Hematogenous

  1. How common
  2. How does it get there?
  3. What causes it?
  4. What does it result in?
A
  1. less common than ascending
  2. hematogenous, blood spread
  3. TORCH infections
  4. neonate fever, encephalitis, chorioretinitis, hepatosplenomegaly, penumonitis, myocarditis, hemolytic anemia, and vesicular or hemorrhage skin lesions
23
Q

What are the TORCH infections?

A 
Toxoplasma gondii
Others- (parvovirus B19, Syphilis, TB, listeria)
Rubella
CMV
HSV
24
Q

Gestastional Trophoblastic Disease

  1. What is it?
  2. Types (4)
A
  1. tumors, proliferation of placental tissue (villous or trophoblastic)
  2. Hydatiform mole (complete and partial)
    Invasive mole
    Choriocarcinoma
    Placental-site trophoblastic tumor (very rare)
25
Q

Hydatiform Moles

  1. What are they?
  2. How common?
  3. Who is evaulated?
  4. Why are they evaluated?
A
  1. cystic swelling of chorionic villi with trophoblastic proliferation
  2. infrequent in US, more common in China or Japan
  3. most women who rpesent with miscarriage undergo D&C based on Uterus Size (US)/hCG findings
  4. benign, but want to know and distinguish them with regard to increased risk of invasive mole or choriocarcinoma
26
Q

Complete Mole

  1. What happens?
  2. What happens to villi?
  3. What can it make?
  4. what happens to the embryo?
  5. risk of what?
A
  1. 2/3 sperm fertilize an empty ovum
  2. most villi are enlarged & edematous; diffuse trophoblastic hyperplasia
  3. androgens
  4. dies very early, fetal parts rarely seen
  5. 2.5% risk of choriocarcinoma
27
Q

Complete Mole

  1. Gross look
  2. Close-up Gross look
  3. Microscopic
A
  1. entire placenta, all villi edematous, delicate friable mass of thin-walled, translucent, cystic, grape like structures
  2. villi look like balloons
  3. Swollen villi with almost no fetal blood vessels; diffuse cytotrophoblast and syncytial trophoblastic proliferation; marked atypica at implantation
28
Q

Complete Mole

  1. Clinical Course
  2. Diagnostic Test
  3. What is increased?
  4. How is it removed?
  5. What can develop?
A
  1. abnormal uterine bleeding, passage of fluid and tissue
  2. ultrasound (snow storm- larger than expected uterus)
  3. serum hCG
  4. curretage,serum hCG levels are followed
  5. invasive moles (10%), choriocarcinoma (2.5%)
29
Q

Partial Mole

  1. What happens?
  2. What happens to villi?
  3. Genomes
  4. Is the fetus present?
  5. What is risk for choriocarcinoma?
A
  1. 2/3 sperm fertilize a normal ovum;
  2. edematous
  3. Triploid (69, XXY or 69,XXX) or tetraploid (92, XXXY)
  4. fetus mostly present, although abnormal
  5. NOT increased risk
30
Q

Partial Mole

  1. Gross look
  2. Microscopic look
A
  1. some villous swelling, lots of solid parts

2. swollen villus, trophoblast proliferation

31
Q

Invasive Mole

  1. define
  2. what can it do to distant sites?
  3. Presentation
  4. Risk of what?
  5. Treatment
A
  1. mole that penetrates uterine wall, hydropic chorionic villi invade myometrium
  2. may embolize, does not disseminate
  3. vaginal bleeding, persistantly elevated hCG
  4. uterine rupture
  5. chemotherapy
32
Q

Gestational Choriocarcinoma

  1. Malignant or Benign?
  2. course
  3. What cells
  4. How common?
  5. What lesions/situations contribute to it?
A
  1. Malignant;
  2. rapidly invasive, widely metastatic; rapidly growing,
  3. neoplasm of trophoblast derived cells
  4. uncommon
  5. 50% from complete moles
    25% previous abortion
    22% normal pregnancy (intraplacental choriocarcinoma)
    Ectopic pregnancy
33
Q

Choriocarcinoma

  1. Gross look
  2. Histo look
  3. Presentation
  4. When does it present?
  5. How advanced is it at the time of presentation?
A
  1. necrotic, hemorrhagic, rapidly growing
  2. proliferation of neoplastic cystotrophoblasts and syncytiotrophoblasts (NO chorionic villi)
  3. vaginal blood, brown fluid spotting
  4. during pregnancy, after miscarriage, after curretage, can occur months after
  5. usually already metastasized
34
Q

Choriocarcinoma

  1. What is elevated? When is it not?
  2. Treatment
A
  1. hCG; unless necrotic

2. surgery, chemo (extremely effective); paternal antigens evoke immune response in mothers

35
Q

Difference between ovarian and gestational choriocarcinoma

  1. ovarian is result of…
  2. response to chemo
  3. what choriocarcinoma is rare?
A
  1. extra-embryonic differentiation of malignant germ cells
  2. ovarian- poorly responsive to chemo, poor prognosis
  3. testis

MHD II Test 3 (14 decks)

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