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Repro II - PATH (Tobin) > Lecture 8.1: Gestational and Placental Disorders > Flashcards

Lecture 8.1: Gestational and Placental Disorders Flashcards

1
Q

Spontaneous abortion (aka miscarriage) is defined as pregnancy loss before ______ weeks of gestation

A

20 weeks of gestation (most often occurs before week 12)

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2
Q

What are 2 common fetal chromosomal anomalies associated with spontaneous abortion?

A

Turner Syndrome (45, XO) and trisomy 16

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3
Q

What are some maternal endocrine factors which may lead to spontaneous abortion?

A
  • Luteal-phase defect
  • Poorly controlled diabetes
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4
Q

Which systemic disorder of the vascular is associated with spontaneous abortions and a false positive syphilis test?

A

Antiphospholipid antibody syndrome

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5
Q

What is the most important predisposing condition (35-50%) for ectopic pregnancy?

A

Chronic salpingitis secondary to PID –> intralumenal fallopian tube scarring

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6
Q

What are some of the risk factors for ectopic pregnacy?

A
  • Chronic salpingitis secondary to PID
  • Scarring of fallopian tubes due to: appendicits, endometriosis, and/or prior surgery
  • IUD use = 2x ↑ risk
  • Smoking
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7
Q

Why is it important to recognize a potential ectopic pregnancy?

A
  • Rupture of tubal pregnancy = emergency!
  • May lead to intraperitoneal hemorrhage –> hemorrhagic shock –> DEATH!
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8
Q

Diagnosis of ectopic pregnancy is based on what?

A
  • ↑ serum levels of hCG
  • Pelvic sonography
  • Endometrial biopsy showing decidua w/o chorionic villi or implantation site
  • Laparoscopy
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9
Q

Typical clinical presentation of ectopic pregnancy?

A

Onset of moderate-severe abdominal pain + vaginal bleeding 6-8 weeks after last menstrual period

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10
Q

What are the 3 basic types of twin placentas?

A
  • Diamnionic dichorionic (may be fused)
  • Diamnionic monochorionic
  • Monoamnionic monochorionic
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11
Q

Twin-twin transfusion syndrome is a complication of what type of twin placenta; what occurs in this syndrome?

A
  • Complication of monochorionic twin pregnancy
  • Monochorionic placentas have vascular anastomoses that connect the circulation of each fetus; sometimes including one or more AV shunts
  • Shunt preferentially ↑ blood flow to one twin (polyhydramnios) at expense of other (oligohydramnios)
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12
Q

What is the placenta previa; leads to what complications?

A
  • Placenta implants in lower uterine segment or cervix, often leads to serious 3rd trimester bleeding
  • Complete placenta previa covers internal cervical os and requires delivery via C-section
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13
Q

What is placenta accreta; leads to what complication?

A
  • Partial or complete absence of the decidua, such that placental villous tissue adheres directly to myometrium
  • Leads to failure of placental separation at birth —> important cause of severe, life-threatening postpartum bleeding
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14
Q

Which pathway is the most common for placental infections and is caused by what?

A

Ascending infections caused by bacteria i.e., Gonorrhea and Chlamydia

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15
Q

Preeclampsia is what type of syndrome and due to dysfunction of what?

A

SYSTEMIC syndrome due to endothelial dysfunction

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16
Q

What is the triad of preeclampsia?

A
  1. HTN (endothelial dysf. –> vasoconstriction)
  2. Edema (↑ vascular permeability)
  3. Proteinuria (↑ vascular permeability)
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17
Q

Development of what makes preeclampsia become eclampsia?

A

Develop hyperreflexia and convulsions

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18
Q

Preeclampsia usually occurs in what trimester and which women are at greater risk?

A
  • Third trimester (after 34 weeks gestation)
  • Most common in primiparas (women pregnant for 1st time)
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19
Q

How is preeclampsia distinguished from gestational HTN?

A

Gestational HTN lacks proteinuria

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20
Q

Some women w/ severe preeclampsia can develop HELLP syndrome, which stands for what?

A
  • Microangiopathic Hemolytic anemia
  • _E_levated _L_iver enzymes
  • _L_ow _p_latelets
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21
Q

Abnormal placental vasculature formation as part of the pathogenesis of preeclampsia is due to what 2 major events?

A
  • Abnormal trophoblastic implantation
  • Failure of physiologic remodeling of the maternal vessels
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22
Q

In response to hypoxia the ischemic placenta releases what 2 placenta-derived antiangiogenic factors into maternal circulation and what does each antagonize the effects of?

A
  • soluble FMS-like tyrosine kinase (sFltl) antagonizes VEGF
  • Endoglin antagonizes TGF-β
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23
Q

Preeclampsia is associated with a hypercoagulable state that may lead to formation of thrombi in the arterioles and capillaries of what main sites?

A

Liver + kidneys + brain + pituitary

24
Q

Hypercoagulablity in preeclampsia is related to what factors?

A
  • ↓ endothelial prod. of PGI2 (potent antithrombic factor)
  • Prod. of PGI2 is normally stimulated by VEGF, which is being antagonizd by sFlt1
25
Q

What 4 microscopic changes are seen in the placenta in women with preeclampsia?

A
  1. Infarcts, which are larger and more numerous
  2. Exaggerated ischemic change of chorionic villi and trophoblasts, consisting of ↑ syncytial knots***
  3. Frequent retroplacental hematomas
  4. Abnormal decidual vessels w/ thrombi, fibrinoid necrosis, or intraintimal lipid deposits (acute atherosis)**
26
Q

When liver lesions are present with preeclampsia what is seen?

A
  • Intraparenchymal hemorrhage
  • Fibrin thrombi in portal capillaries and foci of hemorrhagic necrosis
27
Q

What are the features of kidney lesions associated with preeclampsia, specifically the glomeruli?

A
  • Swelling of endothelial cells
  • Amorphous dense deposits on endothelial side of BM
  • Mesangial cell hyperplasia
28
Q

What will immunofluorescent studies of the kidney in preeclampsia show an abundance of?

A

Fibrin in glomeruli

29
Q

Preeclampsia will present earlier (before 34 weeks gestation) in women w/ what 4 underlying conditions?

A
  • Hydatidiform mole
  • Preexisting kidney disease
  • HTN
  • Coagulopathies
30
Q

Which sx’s assoc. w/ preeclampsia are serious events indicative of severe preeclampsia often requiring delivery?

A

Headaches and visual disturbances

31
Q

How is preeclampsia managed based on gestational age and severity?

A
  • Term pregnancies, delivery is tx of choice, regardless of severity
  • Pre-term requires close monitoring; if severe sx’s arise, delivery is indicated regardless of gestational age
  • Anti-HTN’s do NOT improve outcomes!!!
32
Q

What are some of the possible long-term complications of mother who had preeclampsia?

A
  • 20% develop HTN and microalbuminuria within 7 years of pregnancy
  • 2x ↑ risk of vascular disease of heart and brain
33
Q

The diagnosis of acute fatty liver of pregnancy rests on biopsy showing what?

A

Diffuse microvesicular steatosis of hepatocytes

34
Q

Pathogenesis of acute fatty liver of pregnancy is due to what type of dysfunction?

A
  • Mitochondrial; fetus produces metabolites that cannot be broken down by mother
  • Deficiency of mitochondrial long-chain 3-hydroxyacyl CoA dehydrogenase
35
Q

In preeclampsia/eclampsia, what catastrophic event may happen to blood under pressure inside the liver?

A

Coalesce and expand to form hepatic hematoma; dissection of blood under Glisson capsule —> catastrophic hepatic rupture

36
Q

Why are Hydatidiform moes important to recognize?

A

Assoc. w/ ↑ risk of persistent trophoblastic disease (invasive mole) or choriocarcinoma

37
Q

Hydatidiform moles are characterized histologically by what?

A

Cystic swelling of the chorionic villi accompanied by variable trophoblastic proliferation

38
Q

When and how are Hydatidiform moles usually diagnosed; there is an ↑ risk in which age groups?

A
  • Diagnosed early in preg. (average 9 weeks) by sonogram (US)
  • ↑ incidence in teens and btw 40-50 y/o
39
Q

Hydatidiform moles are more common in what part of the world?

A

2x more common in Southeast Asia

40
Q

What does a complete mole result from and what are the karyotypes seen?

A
  • Fertilization of an egg that has lost its female chromosomes; as result genetic material is completely paternally derived
  • 90% = 46,XX from duplication of genetic material from one sperm
  • NO fetal tissue
41
Q

What occurs in a Partial mole and what is the resultant karyotype?

A
  • Fertilization of an egg with 2 sperm
  • Karyotype = triploid (i.e., 69,XXY) or tetraploid (i.e., 92,XXXY)
42
Q

How do complete moles differ from partial moles in terms of presence of fetal tissue and risk of future complications?

A
  • Complete moles ↑ risk for choriocarcinoma and persistent or invasive mole; no fetal tissue
  • Partial moles will usually have fetal tissue present; are not associated with choriocarcinoma
43
Q

What is the classic morphological appearance of hydatidiform moles?

A

Delicate, friable mass of thin-walled, translucent, cystic, grapelike structure w/ swollen edematous (hydropic) villi

44
Q

Most women with partial and early complete moles present how?

A
  • Spontaneous miscarriage

or

  • Undergo curettage because of US findings of abnormal villous enlargment
45
Q

Levels of what will be greatly increased with complete moles and this level can be used to monitor for successful removal?

A

β-hCG levels

46
Q

Continous elevation of β-hCG after removal of a hydatiform mole likely indicates what?

A

Persistent or Invasive mole

47
Q

Invasive hydatidiform moles are characterized by invasion where and what events follow?

A
  • Penetration or perforation of uterine wall; invasion of myometrium by hydropic chorionic villi
  • Proliferation of both cyto- and syncytiotrophoblasts
  • Tumor is locally destructive and may invade parametrial tissue and blood vessels –> hydropic villi may embolize to sites, such as lung and brain
48
Q

What are signs/sx’s and tx for invasive mole?

A
  • Vaginal bleeding + irregular uterine enlargement
  • Responds to chemo but may result in uterine rupture and necessitate hysterectomy
49
Q

What is a choriocarcinoma, which cells are involved and is it benign or malignant?

A
  • Malignant neoplasm of trophoblastic cells derived from previously normal or abnormal pregnancy
  • Rapidly invasive and metastasize widely, but responds well to chemo
50
Q

List 4 conditions which most often precede development of choriocarcinoma?

A
  • 50% arise in complete mole
  • 25% arise in previous abortion
  • 22% after normal pregnancy
  • Remainder in ectopic pregnancy
51
Q

How does choriocarcinoma appear grossly?

A

Soft, fleshy, yellow-white tumor w/ large pale areas of necrosis and extensive hemorrhage

52
Q

What is the typical presentation of a choriocarcinoma?

A
  • Irregular vaginal spotting of bloody, brown fluid
  • Sometimes sx’s don’t arise until months after preceding event
  • hCG is typically ↑↑↑, unless tumor is necrotic they may be low
53
Q

Choriocarcinoma has a high propensity for what route of spread and what are the most common site of metastasis?

A
  • Hematogenous
  • Lungs (50%) and vagina (30-40%)l followed by brain > liver > bone and kidney
54
Q

What is the tx for choriocarcinoma and the prognosis?

A
  • Depends on stage and usually consists of evacuation of the uterus contents + chemotherapy
  • Nearly 100% remission and high cure rate w/ chemotherapy
55
Q

Placental site trophoblastic tumor is composed of what cells?

A

Neoplastic proliferation of extravilous trophoblasts (aka intermediate trophoblasts)

56
Q

Which hormone is produced by normal extravillous trophoblasts and may be ↑ in placental site trophoblastic tumor?

A

Human placental lactogen (hPL)

57
Q

Histologically what is seen with placental site trophoblastic tumors?

A

Malignant trophoblastic cells diffusely infiltrating the endomyometrium

Repro II - PATH (Tobin) (7 decks)

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