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Question 1

Describe how a blastocyst implants into the endometrium around days 8-9 post-fertilization?

Answer 1

It is likely that some adhesion molecules are essential for blastocyst attachment to the endometrium.Once the trophoblastic shell has attached, marked changes occur on its surface and invasion is accomplished by dissociation and ingestion of endometrial cells.

Question 2

What do placental ‘membranes’, that outline the uterine cavity where the fetus will develop,consist of?

Answer 2

Theseconsist of decidua on the outside, hyalinized villi and trophoblasts in the middle, and the chorion (and amnion) on the inside.

Question 3

What does the placenta develop from?

Answer 3

The placenta is a fetomaternal organ that has two components:A fetal part that develops from the chorionic sac, the outermost fetal membraneA maternal part that is derived from the endometriumThere is a placental membrane that acts as a location between the fetus and mother where blood and nutrients can be exchanges (villi)

Question 4

What genes regulate placental development?

Answer 4

Homeobox genes ( HLX and DLX3 ) expressed in the trophoblast and its blood vessels

Question 5

How does maternal blood enterthe intervillous space?

Answer 5

from the spiral endometrial arteries in the decidua basalis

Question 6

Describe the development of the urachus?

Answer 6

During the third week of development, the allantois protrudes into the area of the urogenital sinus.Between the 5th and 7th week of development, the allantois will become the urachus, a duct between the bladder and the yolk sac. A patent allantois can result in urachal cyst.

Question 7

What issymmetric growth restriction?

Answer 7

placental abnormalities/disruptions leading toall organ systems beingsimilarly affected

Question 8

What are some causes of symmetric growth restriction?

Answer 8

Chromosomal disorders, congenital anomalies, and congenital infections.

Question 9

What types of infections fall can cause symmetric growth restriction?

Answer 9

•TORCH group of infectionstoxoplasmosis,other viruses and bacteria, such as syphilis.rubella,cytomegalovirus,herpesvirus,

Question 10

T or F.asymmetric growth restriction spares the brain and is caused bya down-regulation of growth in the latter half of gestation due to placental disruptions

Answer 10

T.

Question 11

What are some common sources ofUteroplacental insufficiency that can cause asymmetric growth restriction?

Answer 11

-umbilical-placental vascular anomalies(such as single umbilical artery, abnormal cord insertion, placental hemangioma),-placental abruption,-placenta previa,-placental thrombosis and infarction,-placental infection, or-multiple gestations.

Question 12

Third trimester loss is usually due to what?

Answer 12

placental insufficiency, whereas earlier losses are more likely due to chromosomal abnormalities

Question 13

Asymmetric etal growth restriction may also be due to maternal abnormalities or illnesses, not just placenta disruptions. Name some.

Answer 13

maternal conditions that result in decreased placental blood flow, including:•Vascular diseases, such aspreeclampsia (toxemia of pregnancy)and chronic hypertension

Question 14

What is a spontaneous abortion defined as?

Answer 14

(aka miscarriage)- this is loss of a pregnancy before 20 weeks of gestation, whereas loss of pregnancy after 20 weeks is called a stillbirth

Question 15

Again, most early SABs are due to chromosomal abnormalities, while the majorty of third trimester stillbirths are due to placental insufficiency. What causes the majority of pregnancy loss in the second trimester?

Answer 15

maternal or fetal anatomical abnormalities and ascending infection

Question 16

What are some things included in ‘fetal or maternal structural abnormalities’ that commonly cause abortion in the second trimester?

Answer 16

• Maternal endocrine factors , including luteal-phase defect, poorly controlled diabetes, and other uncorrected endocrine disorders.• Physical defects of the uterus , such as submucosal leiomyomas, uterine polyps, or uterine malformations, may prevent or disrupt implantation• Systemic disorders affecting the maternal vasculature , such as antiphospholipid antibody syndrome, coagulopathies, and hypertension

Question 17

Infections are a common cause of fetal morbidity and mortality in the second trimester. What is one of the more common infections?

Answer 17

Infections can either be ascending (more common) or blood-bourne. A particularly common blood-bourne fetal infection arises from Listeriosis infection, in which Listeria spp. from food (delis, unpasteurized drinks, sushi) enters from the GI and passes through the placenta

Question 18

How does Listeria affect a fetus? What about the mother?

Answer 18

Listeriosis is a rare disease that causes mild maternal illness, but can be devastating to the fetus. Listeria’s obligate intracellular naturemake it a difficult infection to diagnose and treatIt can also cause severe disease in the neonate, including death

Question 19

What is this?

Answer 19

Deciduitis- acute exuate inflammation with microabscess (3-5 neutrophils collected together) formation within the decidua

Question 20

What are the main ways placental infections can occur?

Answer 20

they can occur hematogenously or trans-placental. These are typically the TORCH infections and cause a chronic-villitis vs.ascending from the birthing canal and these cause acute chorioamnionitis

Question 21

What constitutes a fetal inflammatory response?

Answer 21

Inflammation of umbilical vessels (vasculitis) and cord substance (Wharton’s Jelly) (funisitis) occurs in response to infection, and constitutes the fetal inflammatory response (while choricoamnioitis is the maternal response)

Question 22

•Inflammation in the umbilical vein is called what?the umbilical arteries?

Answer 22

phlebitis and arteritis

Question 23

Established or long standing infections of the umbilical cordcan cause what?

Answer 23

tissue necrosis and accumulation of cellular debris (necrotizing funisitis)

Question 24

•Inflammation located at the periphery or surface of the umbilical cord may be the primary pattern seen. What is this called?

Answer 24

(peripheral funisitis)

Question 25

Describe umbilical infections caused by Candida albicans

Answer 25

Candida is a fungal organsm that is the most common cause of acute chorioamnionitis with peripheral funisitis.Most cases are diagnosed in preterm deliveries

Question 26

How would umbilica infections caused by Candida present grossly? histo?

Answer 26

●Gross description:well-circumscribed, pale yellow plaques scattered over the surface of the umbilical cord (top)●Micro description:microabscesses containing yeast in subamniotic layer of umbilical cord; chorioamnionitis or necrotizing funisitis may be present (bottom)

Question 27

What does this image show?

Answer 27

This is a chronic villitis with CMV

Question 28

How commonly does CMV cause chronic villitis?

Answer 28

It causes about 10% of chronic villitis cases, but often these infections present with no clinical symptoms

Question 29

When are fetal CMV infections most severe?

Answer 29

in placentas with plasmacytic villitis and inclusion bodies

Question 30

How would the placenta look during a chronic villitis due to CMV infection?

Answer 30

placenta may be large and edematous or small and fibroticMicro description:lymphocytic or plasmacytic villitis with hyalinized villi and mineralization; Hofbauer cell (fetal macrophage) hyperplasia, rare intranuclear and cytoplasmic inclusions

Question 31

T or F.Immunohistochemistry is often helpful in chronic villitis with CMV since histology often non-specific

Answer 31

T.

Question 32

How might a palcental Parvovirus B19 infection present?

Answer 32

B19 destroys early RBCs (normoblasts), causing anemia and resultant fetal hydrops with marked erythroid hypoplasia of bone marrow and occasional giant erythroblasts.Fetuses may also develop myocarditis

Question 33

Micro description:increased fetal erythroblasts with intranuclear inclusions and villous edema

Question 34

What are monochorionictwins?

Answer 34

monozygotic (identical) twins that share the same placenta

Question 35

What is twin-twin transfusion syndrome?

Answer 35

A complication of monochorionic twin pregnancy.Monochorionic twin placentas have vascular anastomoses that connect the circulations of the twins, and in some cases these connections include one or more arteriovenous shunts. If these shunts preferentially increase blood flow to one twin at the expense of the second, one twin will be underperfused, while the second will be fluid overloaded.It is this phenomenon that constitutes the twin-twin transfusion syndrome, which if severe may result in the death of one or both fetuses.

Question 36

During twin-twin transfusion syndrome, the twin that loses the blood when the blood supply is shunted to the other twin is called what?

Answer 36

donor twin (the other is the recipient twin)Both infants may have problems depending on how much blood is passed from one to the other. The donor twin may have too little blood, and the other may have too much blood.

Question 37

What are the symptoms of TTTS?

Answer 37

Most of the time, the donor twin is smaller than the other twin at birth. The donor infant often has anemia, is dehydrated, and looks pale.The recipient twin is born larger, with redness to the skin, too much blood, and a higher blood pressure. The twin that gets too much blood may develop cardiac failure because of the high blood volume.

Question 38

The unequal size of identical twins is referred to as _______

Answer 38

discordant twins.

Question 39

What isPlacenta previa?

Answer 39

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

Question 40

What isPlacenta accreta?

Answer 40

results from a lack of formation of a normal decidual plate. Thus, the chorionic villi extend into myometrium, and the placenta cannot separate normally following delivery. Severe hemorrhage results.

Question 41

What is abruptio placenta?

Answer 41

Thisresults from premature separation of the placenta prior to delivery, with formation of a retroplacental blood clot. The blood supply of oxygen and nutrients to the fetus is compromised to a greater degree with increasing size of the abruption.

Question 42

What isAmnion Nodosum?

Answer 42

This is seen in placentas affected by oligohydramnios, which may be associated with fetal renal agenesis and pulmonary hypoplasiaMay be due to desquamated skin or membrane injury

Question 43

Grossly describe amnion nodosum

Answer 43

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

Question 44

Provide a micro description of amnion nodosum

Answer 44

•Nodules of protuberant eosinophilic fibrinous material with entrapped squamous cells•Associated with stratified squamous metaplasia

Question 45

What is Potter sequence?

Answer 45

the atypical physical appearance of afetusorneonatedue to oligohydramniosexperienced in the uterus.Oligohydramnios is the decrease inamniotic fluidvolume sufficient to cause deformations inmorphogenesisof the fetusclubbed feet,pulmonary hypoplasia, and cranial anomalies = potters sequence

Question 46

What are some causes of oligohydramnios?

Answer 46

It can be caused by renal diseases such as bilateralrenal agenesis(BRA),atresiaof the ureter or urethra causing obstruction of the urinary tract, polycystic or multicystic kidney diseases, renal hypoplasia,amniotic rupture, toxemia, oruteroplacental insufficiencyfrom maternal hypertension.

Question 47

What is preeclampsia?

Answer 47

The presentation of edema, HTN, and proteinuria typically beyond 20 weeks.

Question 48

How is the placenta involved in pereclampsia?

Answer 48

An ischemic placenta releases factors that affect the maternal endothelium

Question 49

How can the placenta appear in cases of preeclampsia?

Answer 49

Most placentas are smaller than expected (left: normal; right: preeclampsia)andInfarcts and retroplacental hematomas are more common

Question 50

How do placental infarcts from preeclampsia affect a neonate?

Answer 50

small infarcts may be of no consequence to the fetus, but if more than a third or half of the placental parenchyma is infarcted or lost in some fashion, then the blood supply to the fetus can become severely compromised and fetal demise may occur.

Question 51

What areSyncytiotrophoblastic knots or syncytial knots?

Answer 51

These areaggregates of syncytial nuclei at the surface of terminal villi, commonly seen in preeclampsia.In the term placenta, most syncytial knots are thought to be artifacts from tangential sectioning while the minority are syncytial sprouts, bridges, or apoptotic knots. Syncytial knots are consistently present, increasing with increasing gestational age, and can be used to evaluate villous maturity. Increased syncytial knots are associated with conditions of uteroplacental malperfusion and are important in placental examination.

Question 52

There is fibrinoid necrosis of the vessel wall (strong eosinophilic staining areas). These are maternal vessels in the decidua.

Question 53

What is a molar pregnancy?

Answer 53

also known as hydatidiform mole —this is a noncancerous (benign) tumor that develops in the uterus. A molar pregnancy starts when an egg is fertilized, but instead of a normal, viable pregnancy resulting, the placenta develops into an abnormal mass of cysts, often described as a grapelike cluster

Question 54

What is a complete molar pregnancy?

Answer 54

Acomplete moleis caused by a single (incidence is about 90%) or two (incidence is about 10%) sperm combining with an egg which has lost itsDNA(the sperm then reduplicates forming a “complete” 46chromosomeset),Thegenotypeis typically 46,XX (diploid) due to subsequentmitosisof the fertilizing sperm, but can also be 46,XY (diploid).46,YY (diploid) is not observed

Question 55

What risks are associated with complete molar pregnancies?

Answer 55

an increased risk of persistent trophoblastic disease (invasive mole) or 3% chance of turning into a choriocarcinoma

Question 56

T or F.In a complete molar pregnancy, there’s no embryo or normal placental tissue

Answer 56

T.

Question 57

What is a partial molar pregnancy?

Answer 57

Apartial moleoccurs when a haploid egg is fertilized by two sperm or by one sperm which reduplicates itself yielding the genotypes of 69,XXY (triploid) or 92,XXXY (tetraploid).In a partial molar pregnancy, there’s an abnormal embryo and possibly some normal placental tissue. The embryo begins to develop but is malformed and can’t survive.

Question 58

T or F. AComplete mole occurs when anegg that has lost its female chromosomes, and as a result the genetic material is completely paternally derived

Answer 58

T.A partial mole occurs due tofertilization of an egg with two sperm

Question 59

Are hCG levels elevated with a mole?

Answer 59

hCG very elevated in complete mole, slightly elevated in partial compared to normal levels for gestation

Question 60

What is the buzzword for a complete hydatidiform mole?

Answer 60

‘Snowstorm”

Question 61

What is this?

Answer 61

A partial hydatidiform mole- some villi appear normal, whereas others are swollen, avascular, and grape-like (though not as large as a complete mole).There is minimal trophoblastic proliferation

Question 62

What are gestational choriocarcinomas?

Answer 62

a malignant neoplasm of trophoblastic cells derived 50% fromin moles, 25% in SAB,and 22% in normal pregnancies.

Question 63

How do gestational choriocarcinomas progress?

Answer 63

Choriocarcinoma is rapidly invasive and metastasizes widely to the lungs, but once identified responds well to chemotherapy.Mitoses are abundant and sometimes abnormal. The tumor invades the underlying myometrium, frequently penetrates blood vessels, and in some cases extends out onto the uterine serosa and into adjacent structures.

Question 64

How do gestational choricocarcinomas appear histologically?

Answer 64

The tumor is composed ofsyncytiotrophoblastic giant cellsin association withcytotrophoblasts ona highlyhemorrhagic background.

Question 65

How do gestational choricocarcinomas appear grossly?

Answer 65

Choriocarcinoma is a soft, fleshy, yellow-white tumor that usually has large pale areas of necrosis and extensive hemorrhage

Question 66

What serum marker is usally high in gestational choriocarcinomas?

Answer 66

hCG

Question 67

What are some main sequelae associated with premature delivery?

Answer 67

-Neonatal respiratory distress syndrome, also known as hyaline membrane disease-Necrotizing enterocolitis-Sepsis-Intraventricular and germinal matrix hemorrhage

Question 68

What is this?

Answer 68

Necrotizing enterocolitis (NEC).A,entire small bowel is markedly distended with a perilously thin wall (impending perforation).B,The congested portion of the ileum corresponds to areas of hemorrhagic infarction and transmural necrosis microscopically. Submucosal gas bubbles(pneumatosis intestinalis)can be seen in several areas(arrows).

Question 69

What is fetal hydrops?

Answer 69

accumulation of edema fluid in the fetus during intrauterine growth.

Question 70

What causes hydrops fetalis?

Answer 70

cardiovascular, chromosomal, fetal anemia (immune, Parvo B19, homozygous alpha-thalassemia), twin-twin, etc

Question 71

What are the main immune causes of hydrops fetalis?

Answer 71

Immune hydrops - The major antigens known to induce clinically significant immunologic reactions are certain of the Rh antigens and the ABO blood groups.The reaction occurs in second and subsequent pregnancies in an Rh-negative mother with an Rh-positive father.

Question 72

Why does hydrops fetalis develop via RH factor differences (ie RH negative mom and RH positive fetus)?

Answer 72

Rh+ eryhtrocytes get into maternal circulation where they are recognized as foreign bodies and an immune response is made against them where IgG ABs are made that can cross the placenta and enter the fetal circulation causing:lysis of RBCs, leading to anemia, and then extramedullary hematopoiesis and cardiac decompensation (causes the edema), as well asbilirubin release from degraded hemoglobin which produced jaundice and kernicterus

Question 73

What is this? When does it classically occur?

Answer 73

Fluid accumulation is particularly prominent in the soft tissues of the neck, and this condition has been termedcystic hygroma.Cystic hygromas are characteristically seen, but not limited to, constitutional chromosomal anomalies such as 45,X karyotypes (aka Turner syndrome)

Question 74

What is SIDS?

Answer 74

defined as “the sudden death of an infant under 1 year of age which remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of the clinical history.”sudden unexpected infant death (SUID)

Question 75

What causes SIDS?

Answer 75

A “triple-risk” model of SIDS has been proposed, which postulates the intersection of three overlapping factors:(1) a vulnerable infant,(2) a critical developmental period in homeostatic control, and(3) an exogenous stressor.