Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Lifecycle Unit 2 Test > Pathology of the Placenta & Gestational Trophoblastic Disease > Flashcards

Pathology of the Placenta & Gestational Trophoblastic Disease Flashcards

1
Q

How do hCG levels change in normal pregnancy, ectopic pregnancy, and trophoblastic disease states?

A

Normal pregnancy: Early rise to 10^5 or 10^6 range by fifth week, then fall to ~10^3 for remainder of pregnancy

Ectopic pregnancy: delayed rise to ~10^4 range before other evidence of ectopic pregnancy

Trophoblastic disease: slightly delayed rise compared to normal, but increase far above normal range and remain elevated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What hCG levels correlate with US detectable gestational sac?

A

1,500 IU/ml = 5-6 weeks and tranvaginal US

4,000 IU/ml = 7 weeks and abdominal US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where do the majority of ectopic pregnancies implant, and what are the diagnostic criteria?

A

90% implant in the fallopian tubes (other sites are ovary, abdominal cavity, and corneal tube)

35-50% associated with PID (also endometriosis, appendicitis)

Diagnostic:
Clinical symptoms (sudden onset pain), B-hCG levels, ultrasound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the definition of trophoblastic diseases?

A

Group of rare tumors that involve abnormal growth of cells. Starting in the cells that would normally develop into the placenta.

  • Can be either benign or malignant
  • Some result from an abnormal conception/pregnancy
  • Some are true neoplasms – uncontrolled tumor-forming proliferation of malignant trophoblast
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the two types of molar pregnancies and what causes each?

A

Complete mole is diandric diploid (46, XX or XY) No maternal tissue

Partial mole is diandric triploid (69, XXY) 1/3 maternal tissue

Need both maternal and paternal DNA for normal development
Mom = embryonic tissue
Dad = placental tissue (hence over development of placental tissue/function in molar pregnancies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the differences in US appearance and clinical consequences between partial and complete hydatidiform moles?

A

Partial: May have fetal parts
Large cystic spaces
Rarely recur or progress

Complete: Absence of fetal parts
“Snowstorm” appearance
Cystically dilated spaces without fetal parts
Potential to recur or become invasive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the signs and symptoms of a complete molar pregnancy?

A

Present with:

  • elevated β-hCG,
  • uterine size greater than dates,
  • hyperemesis gravidarum,
  • vaginal bleeding,
  • early pre-eclampsia,
  • hyperthyroidism

20% complete moles develop persistent Gestational Trophoblastic Disease
Recurrent or invasive Complete Hydatidiform Mole
Choriocarcinoma (1-2%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does a complete mole result in increased chances of gestational trophoblastic neoplasia?

A

Diandric cells have silenced p57kip2 genes.

p57kip2 is a cyclin dependent kinase inhibitor, loss of this gene may lead to neoplastic growth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the gestational trophoblastic neoplasms?

A

Choriocarcinoma (gestational)

Placental site trophoblastic tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the signs of a choriocarcinoma?

A

Vaginal bleeding,
High serum β-hCG
Single/multiple hemorrhagic well-circumscribed nodules in uterus
Biphasic pattern w hemorrhage and necrosis
Marked nuclear atypia and mitoses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the four anatomic components of the placenta?

A

Chorionic plate
Parenchyma
Villi
Basal (maternal) plate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the chorionic plate?

A

tough fibrous layer that carries fetal blood vessels, often with atrophied villous remains (chorion frondosum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is found in the parenchyma?

A

Villous Tree
Maternal Blood
Fetal Vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is found within the villi?

A

Stromal core with vessels
Cytotrophoblast - Inner, mononuclear
Syncytiotrophoblast - Outer, multinucleated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does G5 P2123 mean?

A 
P has four components (TPAL):
Term delivery
Preterm delivery
Abortion (Less than 20 week delivery – spontaneous or induced)
Living children
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the three categories of placental injury, and what results from each?

A

Inflammatory

  • Acute Chorioamnionitis
  • Chronic Villitis or Deciduitis

Fetal Vascular Supply

  • Maldevelopment – villous maturity, chorangioma
  • Obstruction or Rupture – myonecrosis, hemorrhage

Maternal Vascular Supply

  • Maldevelopment – abnormal implantation
  • Obstruction or Rupture – infarction, abruption
17
Q

What is chorioamnionitis?

A

Inflammation in the chorion
2° infection
Neutrophils (maternal) in fetal membranes
Poor correlation with clinical chorioamnionitis
Fever, leukocytosis, uterine tenderness, tachycardia
May be via ascending (cervico-vaginal flora) often GBS or trans-placental (hematogenous) routes often ToRCHeS (Toxoplasma, Rubella, CMV, HIV, HSV, Syphilis)

18
Q

What are the ToRCHeS infections?

A

ToRCHeS (Toxoplasma, Rubella, CMV, HIV, HSV, Syphilis)

19
Q

What is CMV Placentitis?

A

CMV = β-group herpesvirus, “owl’s eye” inclusion on histology
Common Infection
Primary or recurrent

Rarely problems (95% asymptomatic):

  • IUFD (Intra-uterine fetal demise)
  • IUGR (intra-uterine growth restriction)
  • Deafness

Detection:

  • Histology (placenta)
  • Antibody testing
  • Shell-virus urine culture
20
Q

What are the common causes of infectious villitis and what are the clinical implications?

A

Syphilis- Perivascular fibrous proliferation
Toxoplasmosis - Granulomatous with cysts
Herpes- Multinucleated cells with inclusions
Listeria - Acute inflammation destroying villi

Clinical implications:
Treatment for mother and child
Unsuspected maternal immunosuppression
Generally does not recur
Public health/epidemiologic tracking
Closure for family in poor outcomes
21
Q

What are the two classes of villitis?

A

Infectious villitis

Villitis of unknown etiology

22
Q

What is the histological findings in Villitis of Unknown Etiology and the clinical consequences?

A

Results in:
Agglutination/clumping of villi
Maternal lymphocytes attacking & destroying villi

Recurrence risk = 10-15% recur; ~2/3 IUFD or IUGR
Evaluation for infectious villitis
With stem villous/chorionic plate vasculitis = obliterative fetal vasculopathy
Independent risk factor for poor long-term fetal outcome

23
Q

What conditions may lead to fetal vascular injury?

A

Meconium myonecrosis - meconium is toxic to vascular smooth muscle

Intervillous Thrombi - 1/5 of term placentas, leads to fetopmaternal hemorrhage (Kleinhauer-Betke test), laminated appearance (lines of Zahn)

Placental infarct - Acute cessation of maternal flow with live fetus Central more significant than peripheral Associated with IUGR, fetal hypoxia, IUFD

24
Q

What are some conditions caused by abnormal placental location?

A

Placental accreta - Failure of decidual formation
Trophoblast invade abnormally deeply
Chorionic villi adhere to myometrium

Placenta Increta - Villi INVADE into myometrium

Placenta Percreta - Villi PENETRATE through serosa

Placenta Previa - Placenta covers the internal os
Increased risk for abruption, postpartum hemorrhage, C-section

Abruptio placentae - detachment of placenta from decidual seat, vaginal bleeding, abdominal/back pain, rapid uterine contractions

25
Q

What is pre-eclampsia and what are some risk factors?

A

Hypertension + proteinuria after 20 weeks gestational age (clinical)
Endothelial cell activation, exaggerated inflammatory response (physiology)

Risk factors:

  • Family history
  • Pre-existing disease (HTN, DM, APA, autoimmune, renal)
  • Pre-e in prior pregnancy
26
Q

What is eclampsia and what is a treatment option?

A

With seizures = Eclampsia

Attempt to prevent/treat seizures with magnesium sulfate administration- unknown mechanism of action; give for 24 hours following birth

27
Q

What are the structural differences that may lead to pre-eclampsia?

A

Normal development leads to ↓ uteroplacental resistance by widening arterial lumens and impairing contractility
Trophoblast invade & replace endothelium, forming trophoblastic plugs; dual phenotype
Loss of elastic fibers and smooth muscle cells
Intramural fibrin and fibrinoid replace vessel wall with increase in luminal diameter

Pathologic development:
When trophoblast invasion is too superficial, smooth muscle coat of vessels persists
Proliferative activity of intimal and muscle cells with damage to endothelium  decidual vascular thrombosis
Fibrinoid necrosis of media
Infiltration of fatty macrophages (athetosis)
Overall increase in resistance

28
Q

What are the fetal and maternal consequences of pre-eclampsia and what is the treatment?

A

Fetal:

  • 35% higher risk stillbirth
  • IUGR & preterm delivery
  • Hypoxia, neurologic injury
  • ↑ risk stroke & (maybe) CAD as adults

Maternal:

  • Abruption, DIC, stroke
  • Organ failure: liver, kidney, pulmonary edema
  • Risk for chronic HTN

Treatment = DELIVERY

29
Q

What are the two types of abruptio placentae and what are the sequelae for the fetus and the mother?

A

Acute abruption - Intravillous hemorrhage due to sudden placental ischemia with disruption of capillaries

Chronic abruption - Pathologic lesion due to the clinical condition of abruption Fibrin clot with rim of villous infarction May see evidence of bleeding during pregnancy

Fetal

  • Deprivation of oxygen & nutrients
  • Premature birth
  • Stillbirth

Maternal

  • Shock (2º blood loss)
  • Clotting problems (DIC)  blood transfusions
  • Organ failure
30
Q

What are some complications of post partum hemorrhage?

A

Disseminated intravascular coagulation (DIC)

HELLP = Hemolysis, Elevated Liver Enzymes, Low Platelets

31
Q

What are the common categories of defects that lead to spontaneous abortions in each trimester?

A

First trimester - chromosomal
Second trimester - structural defects, placental, infectious
Third trimester - placental, structural defects

32
Q

What are the common structural defects that lead to SAB?

A 
Intrauterine growth restriction
Fetal Hydrops
Neural tube defects
Acardiac twin
Teratomas
33
Q

What are the common chromosomal defects that lead to SAB?

A 
Monosomy X (Turner's syndrome)
Trisomy 21 (Down)
Trisomy 13 (Patau)
Trisomy 18 (Edwards)
Triploidy 69 XXX or 69 XXY
- if digynic = non-molar triploidy
- if diandric = partial hyditidiform mole

Lifecycle Unit 2 Test (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions