Pathology: Placenta

Question 1

Structure of normal placenta (and changes from first to third trimester)

Answer 1

First-trimester: chorionic villi composed of delicate mesh of central stroma surrounded by two discrete layers of epithelium—
• the outer layer consisting of syncytiotrophoblast and
• the inner layer consisting of cytotrophoblast.

Third-trimester: chorionic villi composed of stroma with dense network of dilated capillaries surrounded by markedly thinned-out syncytiotrophoblast and cytotrophoblast

Question 2

Causes of fetal growth restriction

Answer 2

May result from fetal, maternal, or placental abnormalities:

• Fetal: symmetric growth restriction may result from chromosomal disorders, congenital anomalies, and congenital infections (TORCH = Toxoplasmosis, Others such as syphilis, Rubella, CMV, Herpesvirus)
• Maternal: conditions that result in decreased placental blood flow, common causes include vascular dz (i.e., coagulopathies, pre-eclampsia) and chronic HTN
• Placental: asymmetric, spares the brain; uteroplacental insufficiency may result from umbilical-placental vascular anomalies, placental abruption, previa, thrombosis/infarction, infection, or mult. gestations

Question 3

Causes of spontaneous abortion/miscarriage

Answer 3

(defined as pregnancy loss before 20 weeks gestation)

• 50% have fetal chromosome anomalies
• maternal endocrine factors: luteal-phase defect uncontrolled DM, others
• physical defects of the uterus can prevent/disrupt implantation: submucosal leiomyoma, uterine polyps, uterine malformations
• systemic disorders affecting the maternal vasculature: antiphospholipid Ab syndrome, coagulopathies, HTN

Question 4

Major common causes of pregnancy loss in each trimester

Answer 4

1st - chromosomal anomalies
2nd - ascending infection; fetal/maternal anatomic defects
3rd - usually placental insufficiency

Question 5

Histologic findings of Listeria infection

Answer 5

necrotizing intervillositis

Question 6

Histologic findings of CMV infection

Answer 6

chronic villitis
Owl eye nuclear inclusions as well as cytoplasmic inclusions (herpes only has nuclear - that’s a distinction)
Also, the cell is HUGE (hence, -megalovirus)

Question 7

Histologic findings of Parvovirus B19 infection

Answer 7

• viral inclusions in erythroid precursors
• erythroblasts in the lumen of capillaries of placental villi show eosinophilic nuclear inclusions
  (the illness is called erythema infectiosum, or fifth disease; presents with body rash and a “slapped cheek” appearance)

Question 8

Twin-twin transfusion syndrome

Answer 8

a complication of monochorionic twin placentas where the blood is shunted to one twin at the expense of the other; one is underperfused and the other is fluid overloaded; may result in the death of one or both twins

Question 9

Ectopic pregnancy

Answer 9

a fertilized ovum implanted anywhere it’s not supposed to be; most common site is extrauterine fallopian tubes (~90% of cases)

Question 10

Placenta previa

Answer 10

a very low lying placenta or a placenta which cover the os; severe hemorrhage can result with cervical dilation and passage of the baby through the birth canal

Question 11

Placenta accreta

Answer 11

a lack of formation of a normal decidual plate (supposed to sit between the placenta and myometrium), therefore the chorionic villi interdigitate directly with the uterine myometrium. The placenta cannot separate normally following delivery; severe hemorrhage results

Question 12

Abruptio placenta

Answer 12

premature separation of the placenta prior to delivery, with formation of a retroplacental blood clot; a larger abruption more greatly compromises blood supply to the fetus

Question 13

Classification of placental invasion into myometrium

Answer 13

• accreta = superficial invasion into myometrium
• increta = deep invasion into myometrium
• percreta = invades through the myometrium

Question 14

Amnion nodosum

Answer 14

• Multiple yellow-tan superficial amniotic lesions, 0.2 to 0.4 cm and usually near insertion of umbilical cord
• micro: nodules of protuberant eosinophilic fibrinous material with entrapped squamous cells; associated with stratified squamous metaplasia
• 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

Question 15

Potter’s sequence - features and cause

Answer 15

• features: clubbed feet, pulmonary hypoplasia, and cranial anomalies, like flattened facies and low set ears
• due to oligohydramnios (not enough amniotic fluid)

Question 16

Preeclampsia

Answer 16

• disorder of pregnancy characterized by HTN and proteinuria
• causes villous ischemia of placenta, fibrinoid necrosis of maternal vessel walls in the decidua
• most placentas are smaller than expected, infarcts and retroplacental hematomas are common

Question 17

Hydatidiform Mole

Answer 17

• a non-viable fertilized egg that implants into the uterus
• associated with inc. risk of persistent trophoblastic disease (invasive mole) or choriocarcinoma
• check p57 IHC

Question 18

Complete mole

Answer 18

an egg that has no DNA that gets fertilized; has no embryo, no normal placenta, marked villous enlargement , edema, and circumferential trophoblastic proliferation
all paternal No fetal parts
Snowstorm appearance on ultrasound
Labs: HIGH hCG

Question 19

Partial mole

Answer 19

an egg with DNA that gets fertilized by 2 sperm (so often ends up as triploid); some villi will appear normal, others swollen, avascular, and grape-like; minimal trophoblastic proliferation
- can have fetal parts
Labs: elevated hCG, not as high as complete mole

Question 20

Choriocarcinoma

Answer 20

• malignant neoplasm of trophoblastic cells derived from a previously normal or abnormal pregnancy
• histo will see proliferating syncytiotrophoblasts and cytotrophoblasts; mitoses are abundant and sometimes abnormal
• soft, fleshy, yellow-white tumor; usually with large pale areas of necrosis and extensive hemorrhage
• rapidly invasive and metastasizes widely, gets into the underlying myometrium, frequently penetrates blood vessels
• very high hCG levels; responds well to chemo

Question 21

Placental site nodule or plaque

Answer 21

a rare proliferation of intermediate trophoblast that is microscopic; of no major clinical consequence

Question 22

Placental Site Trophoblastic Tumor

Answer 22

a rare localized proliferation of intermediate trophoblast that can produce a grossly visible nodule; most are benign but there are rare malignant cases

Question 23

Necrotizing enterocolitis (NEC)

Answer 23

a complication of premature birth consisting of infarction and transmural necrosis of the bowel, wall becomes perilously thin with impending perforation
-Grossly, submucosal gas bubbles may be seen (pneumonitis intestinalis)

Question 24

Neonatal respiratory distress syndrome, also known as hyaline membrane disease

Answer 24

• results from reduced surfactant synthesis/storage/release and increased alveolar surface tension
• alternating atelectasis and dilation of the alveoli with eosinophilic thick hyaline
• leads to hypoxemia and CO2 retention and acidosis, pulm. VC and hypoperfusion means endothelial damage and plasma leak into alveoli; fibrin/debris form hyaline membrane

Question 25

Fetal hydrops

Answer 25

• accumulation of edema fluid in the fetus during intrauterine growth
• causes include CV, chromosomal, fetal anemia, Parvo B19, homozygous alpha-thalassemia, twin-twin, etc.
• Immune hydrops (MCC) = reactions of the Rh antigens and ABO blood groups that occurs in second and subsequent pregnancies; Abs to Rh+ RBCs cause their removal, get anemia, cardiac decompensation, and hydrops, as well as Hgb degradation, bilirubin, jaundice
• Strong association with Turner’s Syndrome (45X)

Question 26

Cystic hygroma

Answer 26

• a condition in which fluid accumulates in the soft tissues of the neck; looks like a fan around the neck
• characteristically seen, but not limited to, in chromosomal anomalies like 45X

Question 27

SIDS

Answer 27

• the sudden death of an infant from an unexplained cause (remains unexplained after investigation and autopsy)

Question 28

Klinefelter syndrome

Answer 28

• XXY
• lost Sertoli cells, lost inhibin, and inc. FSH
• FSH –> aromatase, inc. estrogen
• female SSCs at puberty

Question 29

Androgen Insensitivity Syndrome (AIS)

Answer 29

• XY phenotypic female
• no testosterone receptor activity, no conversion to DHT, no male structural development
• AMH is present so there’s no female structures, but the distal 2/3 (vagina) and breasts form due to estrogen

Question 30

Premature ovarian failure

Answer 30

• loss of ovarian function, so dec. estrogen and inhibin feedback results in inc. FSH/LH
• presents as female, >40yo, with amenorrhea; progesterone withdrawal test is negative for bleeding

Question 31

Polycystic ovarian syndrome (PCOS)

Answer 31

• increased LH increases testosterone and conversion to estrogen
• high LH inhibits FSH; no follicle development and follicle becomes a cyst
• female presents with hirsutism, amenorrhea; progesterone test is positive for bleeding

Question 32

Turner syndrome

Answer 32

• 45X– monosomy
• presents as lymphedema at birth, primary amenorrhea
• patient is short, shield chest, wide nipples, webbed neck, low hair line, coarctation of aorta, streak ovaries, little estrogen, elevated FSH/LH

Question 33

Kallman syndrome

Answer 33

• defective production of GnRH

- associated with anosmia (inability to smell)

Question 34

Inflammation of umbilical vessels (vasculitis) and cord substance (funisitis) occurs in response to infection, and constitutes the fetal or maternal inflammatory response?

Answer 34

Fetal