Pathology of Pregnancy Flashcards

1
Q

What structures are included in the placenta?

A

Placental disc, unbilical cord, extraplacental membranes

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2
Q

What are the two surfaces of the placenta?

A
  1. Fetal side: covered by amnion and chorion
  2. Maternal surface: The decidua
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3
Q

What is the decidua?

A

Border betwixt the fetal tissue and the uterus

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4
Q

What is the villus?

A

Placenta’s functional unit of exchange

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5
Q

What are the inner, middle, and outer layer of the villus?

A
  • Inner: Cytotrophoblast (Langhans cells)
  • Middle: Intermediate Trophoblast
  • Syncytiotrophoblast
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6
Q

What are Hofbauer cells?

A

Embryonal macrophages

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7
Q

What is the major secretion of the trophoblasts?

A

hCG

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8
Q

What is the fetal-placental weight ratio?

A

1 g placenta can oxygenate 7 grams of fetal tissue

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9
Q

What is the name of the condition when the placenta implants at the lower portion of the uterus and covers the internal os?

A

Placenta previa

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10
Q

What is ectopic pregnancy?

A

Placenta implants outside the uterine cavity

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11
Q

What is the term for an umbilical cord that inserts at the margin of the placental disk?

A

Marginal insertion

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12
Q

What is a velamentous insertion of the umbilical cord?

A

Umbilical insertion into the membranes

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13
Q

What is a life-threatening complication of velamentous insertion?

A

Vasa previa: Membranous blood vessels of the cord cover the cervical os. These vessels are easily ruptured and can cause life-threatening hemorrhage

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14
Q

Acute chorioamnionitis. What is this condition characterized by?

A

Neutrophils in the amnion and chorion

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15
Q

What is the order of inflammatory responses betwixt the mother and fetus?

A

Maternal inflammatory response occurs first, and if the infection persists the fetal inflammatory response will occur

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16
Q

Describe the inflammatory processes in the fetal inflammatory response to chorioamnionitis.

A
  • Acute funisitis - neutrophil migration into muscular walls of the umbilical vessels
  • Acute chorionic vasculitis - neutrophil migration into the large fetal vessels at the placental surface
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17
Q

What are the major risks of chorioamnionitis to the mother and infant?

A
  • Mother: Postpartum endometriosis and pelvic sepsis w/ venous thrombosis
  • Fetus: Neuro disease, stillbirth, neonatal sepsis and death
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18
Q

By what mechanism does villitis typically arise?

A

Results from transplacental passage of organisms usually from the maternal circulation (hematogenously)

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19
Q

Acute villitis. What is the most important consequence of acute villitis?

A

Establishment of an inflammatory focus that infects the fetus secondarily

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20
Q

What is villitis of unknown etiology?

A

Cause of chronic placental infsufficiency in which no infectious agent is found

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21
Q

What is the cause of fetal thrombotic vasculopathy?

A

Clotting in placental vessels

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22
Q

Avascular villi. What was the cause of this condition?

A

Villous capillaries have been replaced by fibrous tissue as a result of a chronic thrombus in a larger upstream stem villus

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23
Q

What is a “cushion defect”?

A

If a large chorionic vessel is thrombosed, thrombus can attach to and later be incorporated into the vessel wall

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24
Q

What is abruptio placentae?

A

Placental lining has separated from the uterus

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25
Q

What can abruptio placentae cause?

A

Retroplacental Hematoma

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26
Q

What is the outcome of retroplacental hematoma?

A

Depends on the size of hematoma

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27
Q

What does rupture of a chorionic villous blood vessel result in?

A

Causes blood to accumulate in the placenta and to form an intervillous thrombus/hematoma

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28
Q

What is placenta accreta? What is it caused by?

A

Abnormal adherence of the placenta to the uterus; Caused by failure to form decidua.

In this image, the chorionic villi are in contact with the underlying muscle

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29
Q

Placenta accreta is classified based on the depth of invasion of the villi into the myometrium. What are the 3 classifications?

A
  1. Placenta accreta: attachment of villi to the surface of the uterine wall w/o further invasion
  2. Placenta increta: Villi invading the underlying myometrium
  3. Placenta percreta: Villi penetrating the full thickness of the uterine wall
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30
Q

What is the most common presenting sign of a patient with placenta accreta?

A

Third trimester bleeding

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31
Q

What is a possible major consequence of placenta accreta?

A

Post-partum hemorrhage

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32
Q

What is chronic uteroplacental malperfusion an important cause of?

A

Perinatal morbidity and mortality

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33
Q

What causes villous hypoplasia?

A

Decreased maternal bloodflow to the placenta especially due to disease of the spiral arterioles

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34
Q

Villous Hypoplasia. What are the characteristic uscopic features?

A

Chronic ischemia with small shrunken villi with stromal fibrosis and clumped trophoblasts

35
Q

What can increased perivillous fibrin result in?

A

Placental insufficiency

36
Q

What is massive perivillous fibrin deposition?

A

Placental fibrion deposition and transmural villous necrosis from the maternal (decidual) to fetal (chorionic) surface

37
Q

What is maternal floor infarction?

A

Fibrin deposit throughout the lower half of the placenta including the decidua

38
Q

What are the two most frequent causes of placental infarction?

A

Hemorrhage b/w the base of placenta and uterine wall and occlusion/thrombosis of the uterine spiral artery

39
Q

Chorioangiosis. What is chorioangiosis?

A

Abnormally increased chorionic vessels due to chronic fetal hypoxia

40
Q

What do increased syncytial knots indicate?

A

Chronic uteroplacental malperfusion

41
Q

What are the two subtypes of Intrauterine growth restriction?

A

Symmetric and asymmetric

42
Q

From what is asymmetric intrauterine growth restriction usually caused?

A

Chronic uteroplacental insufficiency

43
Q

What is another name for Asymmetric IUGR?

A

“Head sparing IUGR”

44
Q

What is the most important prevetable cause of asymmetric IUGR?

A

Maternal cigarette smoking

45
Q

What is Dx of Asymmetric IUGR?

A

Ponderal Index of

46
Q

What is another name for spontaneous abortion?

A

Miscarriage

47
Q

What is the definition of spontaneous abortion?

A

Expulsion of a conceptus before the 20th week of gestation

48
Q

What are dizygotic twins?

A

Fertilization of two separate ova resulting in genetically different twins

49
Q

What are monozygotic twins?

A

Early division of a signle fertilized ovum resulting in genetically identical twins of the same sex

50
Q

What is the name of the condition in which monozygous twins do not separate?

A

Conjoint fetuses w/i a monoamniotic, monochorionic placenta

51
Q

What are two complications of pregnancy that result in maternal death?

A
  1. ARDS
  2. DIC
52
Q

What is preeclampsia? Eclampsi?

A

HTN, Proteinuria, Edema; Preeclampsia + seizures

53
Q

What is believed to be the basis of preeclampsia?

A

Faulty remodeling of uterine spiral arteries that supply the placenta with oxygenated maternal blood

54
Q

Describe the pathogenesis of acute atherosis.

A

Spiral arteries escape invasion by trophoblastic tissue and never dilate. these arteries commonly show fibrionoid ncerosis, clusters of lipid-rich macrophages and perivascular infiltrate of monoculcear cells

55
Q

What is the central pathogenetic abnormality in preeclampsia?

A

Placental ischemia

56
Q

What vascular changes that normally occur in pregnancy do not occur in preeclampsia?

A

Vessels still reactive to vasoconstrictors

57
Q

Describe the general pathogenesis leading to preeclampsia

A
  1. Inadequate cytotrophoblastic invasion of maternal spiral arteries
  2. Placental ischemia
  3. Generalized endothelial cell injury
  4. Reduced renal BF, Increased VR, Increased arterial pressure, Enhanced pressor response (HTN, Proteinuria, Edema)
  5. Preeclampsia
58
Q

What is a pathologic change in the mother that is always seen in (pre)eclampsia?

A

Maternal kidneys always shown glomerular change

59
Q

What abnormalities are seen in the majority of women dying from preeclampsia?

A

Liver abnormalities

60
Q

What is HELLP syndrome?

A

Potentially fatal condition of pregnant women and infants in the third trimester

Hemolytic anemia, elevated liver enzymes and low platelet count

61
Q

What is believed to be the cause of amniotic fluid embolism?

A

Amniotic fluid, fetal squamous cells, hair and other amniotic material enter te maternal circulation through the uterine veins in the devidual bed at the base of the placenta

62
Q

What is considered the distinctive feature of amniotic fluid embolism?

A

Fetal squamous epithelial cells in both alveolar capillaries or in larger blood vessels

63
Q

What is gestational diabetes?

A

Pregnanat woman without previous diabetes develops abnormally high blood glucose levels

64
Q

What is the hallmark of gestational diabetes?

A

Resistance to maternal insulin

65
Q

Describe the pathogenesis and consequences of gestational diabetes

A
  • Pregnancy hormones/factors interfere w/ insulin binding resulting in hyperglycemia
  • Glucose crosses the placenta and fetus increases output of insulin
  • Insulin stimulates growth leading to large fetal size (Macrosomia)
66
Q

What is acute fatty liver pregnancy?

A

Rare life-threatening condition of pregnancy caused by disordered metabolism of fatty acids by maternal mitochondria

67
Q

What enzyme is deficient in acute fatty liver of pregnancy?

A

Mitochondrial enzyme long chain 3-hydroxyacyl-coenzyme A dehydrogenase (LCHAD)

68
Q

What is Dx of Acute fatty liver of pregnancy?

A

Liver biopsy showing characteristic uvesicular fat droplets in the cytoplasm of enlarged hepatocytes w/ central nuclei

69
Q

What is the leading avoidable cause of morbidity and mortalty in pregnant women and their infants?

A

SMOKING

70
Q

What are the two main factors that contribute to morbidity and mortality of the fetus in smokers?

A
  1. Carbon Monoxide: Decreases fetal O2
  2. Nicotine: Potent vasoconstrictor of uterus and placenta
71
Q

What is gestational trophoblastic disease?

A

Spectrum of disorders with abnormal trophoblast proliferation and maturation

72
Q

What is a hydatidiform mole?

A

A placenta with grossly swollen chorionic villi, resembling bunches of graphes, and showing varying degrees of trophoblastic proliferation

73
Q

How does a hydatidiform mole form?

A

Complete moles result from fertilization of an empty ovum that lacks functional maternal DNA

74
Q

Complete hydatidiform mole. What is the most common type?

A

Haploid (23,X)

75
Q

How are complete hydatidiform moles typically monitored? What is the most serious complication?

A

Serum hCG levels are monitored; Development of choriocarcinoma

76
Q

What is a partial hydatidiform mole? How is it formed?

A

A mole with three sets of chromosomes, 1 from the mother and 2 sets from the father (normal ovum fertilized by either 2 sperm or 1 sperm that did not successfully undergo meiosis)

77
Q

How is a partial hydatidiform mole histo different than a complete?

A
  • Contain two types of chorionic villi
  • Normal villi
  • Hydropically swollen villi

Trophoblastic proliferation is focal and less pronounced than in complete mole

78
Q

What is an invasive hydatidiform mole?

A

A mole that penetrates the underlying myometrium

79
Q

What is the typical histo of invasive hydatidiform moles?

A

Trophoblastic proliferation

80
Q

From what is gestational choriocarcinoma derived?

A

Fetal trophoblasts

81
Q

Choriocarcinoma. What are the typical histo findings?

A

Malignant cytotrophoblasts, and syncytiotrophoblasts

82
Q

A tumor contains villous structures but seem cancerous. Dx?

A

HYDATIDIFORM MOLE. Tumors containing any villous structures, EVEN IF METASTATIC, are considered hydatidiform moles and NOT choriocarcinoma

83
Q

What is the typical presentation of a patient with choriocarcinoma? How is it monitored?

A

Abnormal uterine bleeding; Monitor hCG levels

84
Q

What distinguishes placental site trophoblastic tumor from choriocarcinoma?

A

Monomorphic trophoblastic proliferation unlike the dimorphic patter of trophoblast in choriocarcinoma