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Repro - Pathology > Ob shit > Flashcards

Ob shit Flashcards

1
Q

What is the definition of placenta?

A
  1. temporary organ that connects mother and fetus and provides respiratory and renal functions.
  2. Composed of chorionic villi sprouting from chorion, villi increases SA for blood exchange
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2
Q

What are the 5 components of a placenta?

A
  1. Amnion - membranous sac, surrounds fetus, contains serous fluid
  2. Chorion - plate shaped, has villous projections w/ fetal blood vessels into villous space w/ maternal spiral arteries
  3. Decidua - outer layer of placenta attached to myometrium, layered is peeled during placental delivery
  4. Trophoblast - outermost layer of blastocyst that implants into uterus, forms placenta
  5. Syncytiotrophoblast - outer covering of chorionic villi, clumped nuclei to decrease diffusion barrier
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3
Q

What happens w/ the blood flow in the placenta?

A
  1. maternal O2-blood enters mature placenta via spiral arteries and ciruclates through villi
  2. fetal deO2 blood enters placenta via 2 umbilical arteries, branch into chorionic arteries
  3. Fetal umbilical vein carries O2 maternal blood to baby
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4
Q

Is there any mixing of blood that takes place in the placenta?

A

no

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5
Q

What is the most common site of an ectopic pregnancy?

A

fallopian tube –> MCC is Fallopian tube scarring.

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6
Q

What are other causes of an ectopic pregnancy?

A
  1. adhesion from appendicitis
  2. surgery
  3. endometriosis
    * all of these prevent the ovum from reaching the fallopian tube
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7
Q

What are the consequences of an ectopic pregnancy?

A
  1. trophoblasts invade fallopian tube walls but it’s not designed for implantation so no growth/development of the yolk sac can take place –> leads to rupture –> Hemorrhage
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8
Q

What happens in pathology of an ectopic pregnancy?

A

hemtaosalpinx (blood filled fallopian tube); belly full of blood (can lead to ileus)

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9
Q

How does an ectopic pregnancy present?

A

severe onset of ab pain and pelvic hemorrhage – symptoms usually 6 wks post-normal menstrual cycle

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10
Q

What is spontaneous abortion?

A
  1. Miscarriage - pregnancy loss before 20 wks gestation
  2. most occur before 12 wks gestation
  3. increase w/ increasing age
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11
Q

What are causes of an miscarriage in the different trimesters?

A

1st trimester - Genetics (chromsomal abnormalities)
2nd trimester - Infectious - Acute chorioamnionitis
3rd trimester - Vascular - uteroplacental insufficiency; Pre-eclampsia
Recurrent SAB (>3) - AntiPhospholipid Syndrome
Recurrent Stillbirth (>20 wks gestation) - Hypercoagulable state

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12
Q

What are the 2 different times of Twin Placentas?

A
  1. Dichorionic Diamnionic
  2. Monochorionic Diamnionic
  3. Monochorionic Monoamnionic
    * Di-di twins are dizygotic
    * mono placentas are monozygotic
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13
Q

What is twin-transfusion syndrome in Mono-mono twin placentas?

A

Unbalanced vasculature due to vascular anastomoses leads to abnormal sharing of blood leads to abnormal circulatory volumes –> donor twin dies from decreased blood flow –> releases nectoric material into anastomoses leading to death of twin and even mother

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14
Q

What is placenta previa?

A

placenta implants in lower uterus or cervix –> leads to severe bleeding and placental rupture –> hemorrhage/death

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15
Q

What is placenta accreta

A

defective decidua –> Severe postpartum bleeding (80%), adherence of villous tissue to myometrium.

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16
Q

What is placental increta

A

defective decidua –> Severe postpartum bleeding (15%). penetration of villous tissue to myometrium

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17
Q

What is placental percreta

A

defective decidua –> Severe postpartum bleeding (5%). Penetration of villous tissue to entire uterine wall.

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18
Q

What is the treatment for a defective decidua

A

hysterectomy > resection

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19
Q

What are the causes of a hematogenous placental infection?

A
  1. Toxoplasma Gondii - protozoan, cat feces
  2. Others - syphilis, HIV, TB ( rare w/ PNC)
  3. Rubella
  4. CMV: most common transplacental infxn in US
  5. HSV: acquired intrapartum from maternal lesions of active infxn
    TORCH!!!
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20
Q

What are the clinical presentations for TORCH?

A
  1. Toxo: microcephaly, seizures, rash/fever in neonates
  2. Rubella - deafness, neurologic defects, cardiac malformation
  3. CMV - deafness + neurologic defects
  4. HSV - skin lesions/infxns in neonates –> prevent w/ C-section
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21
Q

What are the consequences of a hematogenous placental infxn?

A

premature rupture and preterm delivery

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22
Q

What is the cause of an ascending placental infxn?

A

Acute Chorioamnionitis

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23
Q

What is the etiology of acute chorioamnionitis?

A

polymicrobial infxn w/ vaginal flora bacteria ascending up the genital tract.

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24
Q

What happens in acute chorioamnionitis?

A
  1. Maternal polys acess intervillous space –> polys progress to infect fetus via chorionic blood vessels.
  2. The fetus has an immune response that leads to an inflammatory state ==> pro-coagulable
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25
Q

What is the gross pathology of acute chorioamnionitis?

A

tan exudate w/ congestion and green discoloration of amniotic surface. Funisitis of umbilical cord can occur.

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26
Q

What is the microscopic pathology of acute chorioamnionitis?

A
  1. wavefront of polys from chorion to amnion to amniotic fluid
  2. Granulation tissue occurs where infxn damaged the BM
  3. sloughing of amniotic epithelium and fetal thrombosis
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27
Q

What is the clinical presentation of acute chorioamnionitis?

A

TUFF Luck

  1. Tachycardia
  2. uterine tenderness
  3. foul smelling amniotic fluid
  4. fever
  5. Leukocytosis
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28
Q

What are the complications of acute chorioamnionitis?

A

fetal sepsis, cerebral plasy, and endometritis

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29
Q

What is a cause of acute chorionamnionitis?

A

premature rupture of membranes and premature labor/delivery (caused by inflammatory cytokines)

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30
Q

Who is more commonly to get hydatidiform mole?

A

southeast asians, women less than 20 or women greater than 40

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31
Q

What is a hydatidiform mole?

A

abnormal fertilization leading to abnormal gestation. Complete vs Partial

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32
Q

How does a complete mole form?

A
  1. empty egg + duplication of single sperm
  2. empty egg + two sperm
    * diploids!
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33
Q

how does a partial mole form?

A

normal egg w/ 2 sperm – Triploid

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34
Q

What is the pathology of hydatidiform moles?

A
  1. Gross: cystic swelling – grapelike

2. Micro: edematous villi; complete mole has trophoblast hyperplasia

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35
Q

how do you dx a hydatidiform mole?

A

ultrasound will show diffuse villous enlargement and increased beta-hCG

36
Q

What is a related disease for a hydatidiform mole?

A

can become an invasive mole leading to a choriocarcioma. Complete moles more than partial. Invasive moles appear like choriocarcinomas but DON’T metastasize

37
Q

what is a choriocarcinoma? how does it mets?

A

trophoblastic neoplasms; via blood to lung, liver, brain, spleen, kidney

38
Q

What does a choriocarcinoma look like>

A
  1. fleshy soft yello white tumor –> rapid growth can lead to ischemic necrosis and hemorrhage
  2. micro: mixed trophoblasts
39
Q

What is the most common first symptom of a choriocarcinoma?

A

uterine bleeding

40
Q

What is the prognosis of a choriocarcinoma?>

A

70% survival w/ hysterectomy/chemo even w/ metastasis

41
Q

What are causes of acute abdomen of pregnancy?

A
  1. ovarian torsion
  2. appendicitis
  3. volvulus
  4. ruptured ectopic pregnancy
  5. diverticulitis
42
Q

What is ovarian torsion?

A

twisting of ovary on ligamentous support leading to obstruction of venous drainage and blood supply = ischemia and eventually infarction

43
Q

When is ovarian torsion most common?

A

in women of childbearing age w/ ovarian mass or pregnancy (increased mass from corpus luteum in 1st trimester)

44
Q

What does an ovarian torsion present as?

A

acute onset of pelvic pain, N/V

45
Q

What causes appendicitis?

A

overgrowth of appendix from normal flora overgrowth trapped by occluding fecalith, associated with a decreased fiber diet

46
Q

When does appendicitis usually present in pregnanacy

A

2nd trimester. Initial periumbilical pain that becomes RLQ pain. rebound tenderness at McBurney’s point

47
Q

Where is the McBurney’s point found

A

1/2 btw umbilicus and ASIS

48
Q

What is volvulus

A

twisting of colonic segment on its mesentery –> obstruction, dilation, and ischemia –> infarction. Untwisting can release colonic bacteria into blood and cause sepsis.

49
Q

What is the classic presentation of volvulus

A

intermittent camping lower abdominal pain, gradual abdominal distention/tympani (no stools, flatus)

50
Q

how can you differentiate causes of acute abdomen from pregnancy

A

Pregnancy will have leukocytosis up to 14,000
Labor will have leukocytosis up to 30,000
But neither have bandemia which is present in acute abdomen

51
Q

what are the causes of acute abdomen in order

A
  1. ruptured ectopic pregnancy
  2. corpus luteum rupture/hemorrhage
  3. PID
  4. appendicitis
  5. ovarian torsion
52
Q

what is diverticulitis

A

inflammation of a transmural outpouching of colonic mucosa due to perforation +/- abscess

53
Q

What is the presentation of diverticulitis

A

abdominal pain for more than one day.
LLQ pain = whites; RLQ pain = Asians
Leukocytosis, constipation, diarrhea, N/V
Common in old men

54
Q

What is pre-eclampsia

A

systemic syndrome w/ widespread maternal endothelial dysfunction w/ HTN, EDEMA, and PROTEINURIA

55
Q

What are the risk factors for pre-eclampsia

A 
1st pregnancy, multiple pregnancies, increased intervals btw pregnancies
Age <20; .40
Obesity, DM, HTN
New Paternity
previous pre-eclampsia
56
Q

What is the pathogenesis of pre-eclampsia

A

Abnormal placental vasculature. The pre-eclamptic trophoblasts fail to convert spiral arteries (increase their capacitance to accommodate increased blood flow) –> leads to an ISCHEMIC PLACENTA

57
Q

What happens due to an ischemic placenta

A
  1. release of anti-angiogenic factors: sFlt1 and endoglobin –> decreased NO and PGI2 leads to maternal HTN, Edema, and proteinuria
  2. Ischemic placenta releases pro-inflammatory cytokines :TNF alpha
58
Q

What does sFlt1 do?

A

truncated form of VEGA-R that binds up circulating maternal VEGF

59
Q

What does endoglobin do?

A

TGF-b receptor that binds up circulating maternal TGF-b

60
Q

What kind of state does the inflammation lead to?

A

PRO-COAGULABLE State leads to endothelial dysfunction and increases TPR and MAP

61
Q

What is the placental pathology for pre-eclampsia?

A

Atheroscleorsis of placental vessels, Villous Hypoplasia, Fibrin clots in intervillous space (can lead to necrosis),

62
Q

What happens to the fetus in pre-eclampsia

A

intrauterine growth restriction, hypoxia, and death may occur

63
Q

What happens to the maternal pathology in pre-eclampsia

A

fibrinoid necrosis of uterine blood vessels and subendothelial macrophages

64
Q

When does one make the dx of pre-eclampsia

A

new onset of HTN and proteinuria post 20 wks of gestation

65
Q

What are complications of pre-eclampsia

A

eclampsia

10% pts get HELLP

66
Q

What is HELLP

A

hemolysis, elevated liver enzymes, low platelets

67
Q

What is the pathogenesis of HELLP

A

platelets and clotting factors are activated –> fibrin clots in capillaries/hepatic sinusoids, destruction of RBCs, platelet aggregation

68
Q

What are complications of HELLP

A

DIC, hepatorenal syndrome, pulmonary edema/ARDS

69
Q

what is the pathology of HELLP

A

peripotal zone of hepatic lobule showing fibrin deposition

70
Q

what are the causes of maternal death in order?

A
  1. thromboembolism
  2. hemorrhage
  3. pre-eclampsia
  4. others
71
Q

What are 2 reasons for resulting in placenta ischemia

A
  1. decreased blood supply

2. increased flow resistance to placenta

72
Q

How much infarction of the placenta can the fetus tolerate

A

50%

73
Q

What are consequences of extensive placental infarction

A

IUGR, neurologic injury, and fetal demise

74
Q

what does and older and a new infarct of the placenta look like

A

Old- tan

Subacute- red granulation tissue

75
Q

What are some etiologies of a placental ischemia/infarction

A
  1. pre-eclampsia
  2. hypercoagulable state (lupus)
  3. AI vasculitis
  4. Smoking
76
Q

What is oliohydraminos

A

deficiency in amniotic fluid – leads to Potter sequences

77
Q

What is the pathogenesis of oligohydramnios

A
  1. decreased amniotic fluid by renal agenesis leads to decreased urine production which is the main component of amniotic fluid
78
Q

What are the consequences of oligohydraminos

A

fetal compression and pulmonary hypoplasia, nose and ears are especially flattened, contracture of hands/feet

79
Q

What is an amniotic band

A

mechanical fibrotic lesions causing limb structures, may result in amputations

80
Q

what are umbilical knots

A
  • can cause fetal demise especially in 2nd trimester w/ increased fetal pulling/movement
  • true knots - cord tied up
    False knots - hyper/hypocoiling (associated w/ poor obstretical outcomes)
81
Q

What is placental abruption

A

bleeding at decidual-placenta interface causing partial of total placental detachment before delivery – forms a retroplacental hemorrhage (1/3 can occur w/out abruption)

82
Q

What is the pathogenesis of an amniotic fluid embolism

A

fetal/amniotic elements enter maternal veins as decidue detaches and can embolize to lungs causing vasospasms, HTN, and RH failure

83
Q

What is seen on pathology for an amniotic fluid embolism

A

small calcifications from placenta, elongated flattened light/purplish strucutres - squamoid/squamous cells from amnion

84
Q

What are consequences of an amniotic fluid emboli

A

DAD, DIC, hemorrhage

85
Q

What is peripartum cardiomyopathy

A

myocarditis resolving spontaneously(1/3) or leads to dilated cardiomyopathy (2/3) – usually 3 months before or after delivery

86
Q

Who is more likely to get a peripartum cardiomyopathy

A

multiparous AA

Repro - Pathology (5 decks)

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