Placenta Flashcards

1
Q

What cells of the blastocyst attach to the endometrial lining?

A

Trophblasts bind to the endometrial lining and invade the tissue to implant the blastocyst

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2
Q

What are the layers of the placenta?

A
  • *Amnion**
  • *Chorion**
  • *Decidua** - bascially the endometrium of the uterus. Provides a barrier between chorion and myometrium.
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3
Q

Deoxygenated is carried in the ___________ while oxygenated blood is carried in the ___________.

A

Deoxygenated is carried in the umbilical artery while oxygenated blood is carried in the umbilical vein.

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4
Q

What structures make up the chorionic villus?
• compare the appearance of the chorionic villus at 10 weeks to the villus near term.

A

Villus Structure:
Outer Layer - Synciotrophoblasts
Inner Layer - Cytotrophoblasts

Within the Villus:

  • *Fetal Blood Vessels**
  • *Hofbauer** bodies (macrophages)

• In the course of pregnancy the Synciotrophoblasts on the outside of the villi become increasingly nodular and the overall thickness of the villus is reduced .

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5
Q

________ and _________ are two genes found in _________ and ____________ that regulate placental development.

A

HLX and DLX3 are two genes found in Trophoblasts and Blood Vessels that regulate placental development.

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6
Q

What is the intervillus space?
• How does this show up histologically?

A
Intervillus space 
• **Maternal Blood is Dumped here** so that nutrients can diffuse across the chorionic villi (remember synciotrophoblasts don't have MHC class I) 

Histologically the intervillus space shows up as white empty space surrounding the Cellular (fetal) blood filled Villus

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7
Q

Blood from _________ enters the Intervillus space to exchange nutrients.

A

Endometrial Spiral Arteries

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8
Q

What happens to the allantois at weeks 5-7 of development?

A

The Allantois becomes the Urachus

Allantois - connects umbilicus directly to urogenital sinus

Urachus - connects umbilicus to the bladder

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9
Q

What should you see in a cross-section of the umbilical cord?

A

Allantois (possibly)
Placental Vein
Whartons Jelly
2 Placental Arteries

****NL has 3 BVs total***

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10
Q

Symmetric Growth Restrictions
• What is it?
• What causes it?

A

What is it?
- All organ systems are equally affected

Causes:

  • *- Chromosomal Disorders
  • Congenital Abnormalities
  • Congenital TORCH infections
  • Conditions that decrease fetal blood flow**(pre-eclampsia, chronic HTN)
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11
Q

What is the most common cause of a 1st trimester spontaneous abortion?

A

Chromosomal Abnormalities

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12
Q

What are 3 common factors that lead to 2nd trimester fetal loss?

A
  • *1. Maternal Endocrine Factors
    2. Fetal Physical Defects
    3. Infection**
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13
Q

What infection might you contract from eating deli meat that can be extremely harmful to the fetus?

A

Listeria can penetrate the Placental Barrier much like it can cross the BBB

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14
Q

What paremeters define a spontaneous abortion?

A

Fetal Loss Before 20 weeks

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15
Q

Listeria can cause both necrotizing intervillositis and chorioamnioitis.
• Which of these is a maternal and which is a fetal inflammatory response.

A

These are probably both maternal inflammatory responses

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16
Q

What are two inflammatory processes that may occur in the umbilical cord?
• are these maternal or fetal responses?

A

FETAL immune system is responsible for Vasculitis (Phlebitis and Arteritis) and Funisitis in the umbilical cord

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17
Q

What two types of funisitis are seen in the umbilical cord?
• What do these look like?

A

Necrotizing Funisitis - long standing inflammation and cellular debris

Peripheral Funisitis - found at the periphery of the umbilical cord (in wharto

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18
Q

What is the most common cause of acute chorioamnionitis with peripheral funisitis?
• What is the implication of this infection?

A

CANDIDA ALBICANS
• Often this occurs leading to Pre-Term Deliveries

19
Q

What Gross and Microscopical findings would you expect to see on an umbilical cord affected by acute chorioamnionitis and peripheral funisitis?

A

Gross:
• Well Circumscribed yellow plaques on the umbilical cord

Micro:
• Microabscesses with yeast in wharton’s jelly

20
Q

CMV
• What inflammatory Process does it cause?
• What do you expect to see histologically?
• Gross?

A

CMV causes Chronic Villitis

Histo:
Lymphocytic/PLASMOCYTIC villi with inclusion bodies
Hofbauer body (macrophage) Hyperplasia

Gross:
Placenta may be large and edematous or small and fibrotic

21
Q

Parvovirus B19
• Name of Disease Caused
• Pathophysiology
• Histology

A

Disease Caused
Erythemia Infectiosum

Pathophysiology
Destroys early RBCs (normoblasts) causing anemia and hydrops fetalis
• MYOCARDITIS in the fetus is also a potential outcome

Histology:
Eosinophilic Nuclear inclusion in Erythroid Precursors in villi
Viral inclusions in erythroblast precursors

22
Q

Twin-Twin Transfusion Syndrome
• Pathophysiology

A

In Monochorionic twins vascular anastomoses exist between the circulations of the 2 fetuses some of these form AV shunts that favor shunting to one twin over the other

This leads to one big erythematous recipient twin and one small anemic donor twin at birth (if they both make it to term)

23
Q

What structure is lacking in placenta accreta?
• what complications are associated with this pathology?

A

Abscence of a Decidua is what allows for the placental tissue to attach to the myometrium

Placenta accreta may lead to massive hemorrhage in delivery

24
Q

Note: In Abruptio Placenta there is often a RETROPLACENTAL blood clot that forms

A
25
Q

Amnion Nodosum
Associated with what conditions?
Cause?
Gross?
Micro?

A

Seen in placentas affected by oligohydramnios, which may be associated with fetal renal agenesis and pulmonary hypoplasia​

May be due to desquamated skin or membrane injury​

Gross description​
​Multiple yellow-tan superficial amniotic lesions, 0.2 to 0.4 cm and usually near insertion of umbilical cord​

Micro description​

Nodules of protuberant eosinophilic fibrinous material with entrapped squamous cells​

Associated with stratified squamous metaplasia​

26
Q

What is Potter’s Sequence?

A

Clubbed Feet
Pulmonary Hypoplasia
Cranial Anomalies

27
Q

Potter’s Sequence
• What are some reasons we might see this?

A

Bilateral Renal Agenesis
Atresia of Ureter or Obstruction
Polycistic Kidney Disease
Amniontic Rupture
UTEROPLACENTAL INSUFFIENCY FROM MATERNAL HYPOTENSION

28
Q

T or F: Choriocarcinomas can arise both in gestation and not in gestation.

Explain.

A

True,
NON-GESTATION
*Germ Cell Neoplasma

GESTATION
*Normal or abnormal Pregnancy
* COMPLETE MOLE

29
Q

How does the prognosis for a choriocarcinoma change if it occurs inside or outside of pregnancy?

A

Pregnancy associated choriocarcinomas respond much better to chemotherapy than germ cell neoplasms that cause choriocarcinoma

30
Q

Are choriocarcinomas invasive?
• If so how?

A

Yes, they metastasize my invading through the myometrium and getting into the blood vessels (remember these trophoblasts are trained to find blood)

31
Q

Choriocarcinoma
• Histology
• Gross

A

Histology:
• Abundant mitosis and entirely composed of synciotiotrophoblasts and cytotrophoblasts

Gross:
• Soft fleshy, yellow tumor with extensive necrosis

32
Q

What are some causes of Fetal Hydrops?

A

CV, Chromosomal, and Twin-Twin Transfusion

Anemias:
Alpha Thalessemia
Parvovirus B19
Rh Mismatch

33
Q

What chromosomal abnormality is associated with Cystic Hygroma?

A

TURNER SYNDROME 45 XO

34
Q

What triad of factors are needed to see SIDS?

A
  1. Vunerable Infant
  2. Critical Development Period in Homeostatic Control
  3. Exogenous Stress (smoke, insects, laying on back)
35
Q

Compare the Gross appearance of a pre-eclamptic placenta to a NL placenta.

A

Pre-eclamptic placentas are typically smaller

36
Q

Pre-eclampsia
• What microscopic changes are associated with this condition?

A
  • *1. SYNCYTIAL KNOTS** - caused by villous ischemia
  • *2. FIBRINOID NECROSIS** in maternal decidual vessels
37
Q

What is a Hydatidiform mole?

A

Non-cancerous (benign) tumor from a proliferation of trophblasts only

38
Q

Hydratidiform Mole
• Presentation
• What mediator of pregnancy is present in large amounts and what are the effects of its presence?

A

Presentation:
Vaginal bleeding with more uterine enlargement than expected and **increased pelvic pressure

hCG mediated Effects:
• EARLY PRE-ECLAMPSIA
• HYPERTHYROIDISM
• HYPEREMESIS GRAVIDARUM
• THECA LUTEAL CYSTS**

39
Q

What conditions can a Hydratitiform mole progress to if not treated?

A

Invasive Mole
Choriocarcinoma

40
Q

Hydatidiform Moles
• Compare Gross appearance of complete and partial.

A

COMPLETE
• Entire Specimen consists of Grape-like clusters

PARTIAL
• Some NL tissue is present among the grape-like clusters

41
Q

Hydatidiform Moles
• Compare Microscopic appearance of complete and partial moles.

A

Complete:
Villous enlargement and Edema with Peripheral Proliferation of Trophoblasts

Partial:
Minimal Trophoblastic proliferation with some NL villi and some swollen avascular villi

42
Q

Which type of hydatidiform mole shows up as a honeycomb/snowstorm appearance on ultrasound?

A

Complete Hydratidiform Moles

43
Q

Compare the following for a complete vs. partial hydatidiform moles
• Karyotype Possibilities
• Components Responsible for Its formation
• Presence of Fetal Parts

A

Complete
Karyotype - 46 XX (90%) or 46 XY
Components - 1 sperm (maybe 2) + 1 empty egg
Fetal Parts - NEVER PRESENT

Partial
Karyotype - 69 XXX, 69 XXY, 69 XYY
Components - 2 sperm + 1 egg
Fetal parts - OFTEN PRESENT

44
Q

Compare the following for a complete vs. partial hydatidiform moles
• hCG levels
• Risk of Trophoblastic Neoplasia
• Risk of Choriocarcinoma

A

hCG levels:
• WAY more elevated in COMPLETE moles

Trophoblastic Neoplasia
• WAY more likely with COMPLETE moles

Choriocarcinoma
• MUCH more likely with COMPLETE moles