ERM2- Pregnancy Path

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jknell
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184368
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ERM2- Pregnancy Path
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2012-11-19 23:42:31
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Endocrine Reproductive Pathology
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Endocrine and Reproductive Pathology
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  1. Trophoblast Diffrentiation
  2. Villous Layer
    • -syncytiotrophoblast + cytotrophoblast
    • -separates off during parturition
  3. Extravillous Layer
    • -invasive layer (invade myometrium or spiral arteries)
    • -remodel decidual arterioles
    • -allow for interaction with maternal blood
  4. Endometrial Changes During Pregnancy
    -progesterone induced changes under the corpus luteum

    • Stromal Changes
    • -decidua (fried egg appearance)
    • -allows separation of placenta
    • -contains inflammatory cells

    • Gland Changes
    • -Arias Stella Effect: hypersecretory glands
  5. Ectopic Pregnancy: Epidemiology
    • -incidence = 1/80 spontaneous pregnancies
    • -mostly in Fallopian tubes
    • -cause 4-6% of maternal deaths in US
  6. Ectopic Pregnancy: Risk Factors
    • -IVF/assisted reproduction
    • -Hx of previous ectopic pregnancy
    • -pregnancy after tubal ligation/IUD
    • -Hx of PID
  7. Ectopic Pregnancy: Pathophysiology
    • -damage to tubal epithelium leads to delayed transport of the embryo
    • -abnormal implanatation of conceptus in a region with poor decidualization
    • -EVT invade and erode nearby vessels
  8. Ectopic Pregancy: Diagnosis
    • Classic Triad
    • 1. lower abdominal pain (100%)
    • 2. Missed menses (75-90%)
    • 3. Vaginal bleeding (>50%)

    • Tests
    • -positive pregnancy test
    • -transvaginal ultrasound (IUP absent)
    • -uterine curretage (absent chorionic villi)
    • *Arias Stella Changes will be present
  9. Ectopic Pregnancy: Management
    • Ruptured Ectopic
    • -hemodynamically stable/unstable --> laparotomy with salpingectomy

    • Probably Ectopic
    • -confirm diagnosis with U/S hCG and currettage --> laparoscopy with salpingectomy
  10. Placental Abruption: Epidemiology
    • -incidence: 1/120 deliveries
    • -most common in third trimester
  11. Placental Abruption: Pathophysiology
    • -small spiral arteries don't remodel well --> rupture and bleeding into the decidua
    • -less invasion by EVT
  12. Placental Abruption: Risk Factors
    • trauma
    • maternal HTN (pre-eclampsia)
    • smoking
    • advanced maternal age
    • cocaine
  13. Placental Abruption: Diagnosis
    • Classic Triad
    • 1. uterine contractions
    • 2. vaginal bleeding
    • 3. abdominal pain

    U/S
  14. Placental Abruption: Management
    • -hospitalize
    • -method and timing of deliver depends on gestational age of fetus
  15. Placenta Previa: Epidemiology
    -incidence: 0.3-0.5%
  16. Placenta Previa: Risk Factors
    • previous currettage
    • prior C-section
    • multiple vaginal deliveries
    • anatomic abnormalities (leiomyoma, malformation)
  17. Placenta Previa: Pathophysiology
    • -implantation of the placenta within the LUS/cervis
    • -placental tissue near or overylying cervical os
    • -reduced or absent decidua in this area of the uterus
  18. Placenta Previa: Diagnosis
    • -painless bleeding in second or third trimester
    • -usually prenatally diagnosed (if noticed before 26 wks it can move, so repeat at 28 wks)
  19. Placenta Previa: Management
    -delivery by C-section
  20. Placenta Previa: partial vs complete
    • Partial: retroplacental hematoma
    • Complete: may require postpartum hysterectomy
  21. Placenta Creta: Epidemiology
    • -incidence: 1/2500 deliveries
    • -10 fold increase over the past 10 years (increased c sections)
    • -10-25% associated with placenta previa
  22. Placenta Creta: Pathophysiology
    -implantation without intervening decidua, over uterine scar (complication of have too many C-sections)

    • -Accreta: to superficial myometrium
    • -Increta: into the myometrium
    • -Percreta: up to or through serosa
  23. Placenta Creta: Risk Factors
    • -maternal age > 35 years
    • -previous uterine instrumentation (C-section, currettage)
    • -uterine structural defects
  24. Placenta Creta: Diagnosis
    • 1. Prenatal: U/S MRI
    • -not very sensitive, often diagnosed at delivery

    • 2. Delivery
    • -retained placenta, PP hemorrhage
  25. Placenta Creta: Management
    • -manual delivery of placenta
    • -post partum uterine currettage
    • -c-section
    • -total abdominal hysterectomy
  26. Gestational Trophoblastic Disease/Neoplasias (GTD/GTN)
    -abnormal gestation or neoplasm arising from villous or extravillous trophoblasts
  27. GTD/GTN: Epidemiology
    • -Incidence in US: 1/2000
    • -Incidence in SE Asia: 1/100
  28. GTD/GTN: Risk Factors
    • -extremes of maternal age (<20, >40)
    • -race (highest in indonesia)
    • -prior hx
  29. Complete Mole
    • -defective egg (no maternal DNA)
    • -ferilized by one sperm --> duplicates
    • -only develop placental tissue, no fetal tissue

    • -bunches of grapes
    • *no fetal blood vessels or nRBCs
    • -increased choriocarcinoma risk
  30. Partial Mole
    • -egg is normal but fertilized by 2 sperm
    • -get excess DNA (69XXY)
    • -no increased risk for choriocarcinoma

    • -present fetal blood vessels and nRBCs
    • -associated with 3-4 syndactyly
  31. Molar Pregnancy: Management
    • -complete evacuation followed by uterine currettage
    • -F/U with b-hCG form 1 year
    • -postpone pregnancy for 1 year

    -methotrexate for metastases
  32. Invasive Mole
    • -persistent hCG levels after evacuation
    • -molar villi invade into myometrium

    • management
    • -chemo
    • -CT for mets (esp lungs)
    • -hysterectomy
  33. Choriocarcinoma: Incidence/Pathophysiology
    • -malignant tumor with propensity for hematogenous dissemination (lungs, brain, liver)
    • -usually follows a recent pregnancy (normal or molar)
    • -biphasic tumor with proliferation of CTB and STB
  34. Choriocarcinoma: Presentation
    • -vaginal bleeding
    • -most have signs and sx of metastatic disease (hemoptysis, HA)
  35. Choriocarcinoma: Management
    • -combination chemo
    • -radiation for CNS/Liver mets
    • -surgery in chemo resistant cases
    • -F/U serum hCG
  36. Placental Site Trophoblastic Tumor (PSTT)
    -rare tumor of extravillous trophoblast, mets through lymphatics
  37. PSTT: Presentation
    • -usually follows a normal pregnancy or pregnancy loss
    • -months to years later
    • -irregular vaginal bleeding
  38. PSTT: Diagnosis
    • -only mildly elevated hCG
    • -imaging --> complex mass in uterine wall
  39. PSTT: Management
    • -usually total hysterectomy
    • -adjuvant chemo for mets
  40. PSTT: Pathology
    • -poorly delineated mass in uterus
    • -usually NOT hemorrhagic
    • -"monophasic" tumor
    • -immunostain for diagnosis
  41. Teratogens
    -environmental agent that interferes with normal development of embryo or fetus

    • -10% of birth defects attributable to teratogens
    • -60% cause unknown
  42. Principles of Teratology
    • -unique pattern
    • -range of severity within the pattern
    • -species specificity
    • -genetic susceptibility
    • -timing of exposure varies results
    • -route of admin
    • -dose-response relationship
  43. Coumadin Derivatives
    • First Trimester:
    • -fetal warfarin syndrome (10% of exposed)
    • -nasal hypoplasia with stippled epiphyses
    • -critical exposure window: 6-9 weeks
    • -spontaneous abortion (16-18%)

    • Second/Third Trimester:
    • -CNS anomalies
    • -growth failure
    • -seizures
    • -mental deficiency
  44. Retinoids
    • First Trimester:
    • -20% of exposed
    • -heart defects
    • -ear anomalies (anotia, microtia)
    • -brain defects
    • -thymus defects
    • -after only a few doses
    • -spontaneous abortion (19%)
  45. Anticonvulsants (Valproic Acid)
    • First Trimester:
    • -12% of exposed --> minor structural defects
    • -facial features, fingernail hyperplasia
    • -neural tube defects
    • -increased risk of learning diabilities
  46. Alcohol
    • -short palpebral fissures
    • -smooth philtrum
    • -thin vermillion border of upper lip
    • -heart defects
    • -orofacial cleft
    • -pre/post natal growth deficiency
    • -signifcant learning and behaviour problems

    • -most common human teratogen
    • -most strongly associated with binge drinking
    • -no known safe threshold
  47. FDA Category A
    studies fail to demostrate risk
  48. FDA Category B
    • no adequte studies in pregnant women
    • OR
    • animal studies show risks but human studies don't
  49. FDA Category C
    • -animal studies show risk but no adequate studies in humans
    • -potential benefits may warrent use in pregnant women
  50. FDA Category D
    • -positive evidence for fetal risk based on human studies
    • -potential benefits may warrant use of drug in pregnancy
  51. FDA Category X
    • -studies in animals and humans show fetal abnormalities
    • -risk clearly outweighs benefits
  52. Lisinopril (ACEI)
    • C in first trimester
    • D in second/third trimester
  53. Examples of Category X Drugs
    • 1. Statins: Xol important for embryonic development
    • 2. Ribavirin: animal studies only
    • 3. Leflunomide: animal studies only (washout period before pregnancy)
  54. Fetal Risks of Advancing Maternal Age
    • -aneuploidy
    • -non-cytogenic congenital malformations
    • -mitochondrial DNA diseases
    • -spontaneous fetal losses and aneuploidy
  55. AFP Screen
    • -fetal albumin crosses into maternal circulation
    • -high and low values associate with problems
  56. Workup for elevated AFP
    • -U/S (gestational age, Number of fetuses)
    • -structural abnormalities (NTD, gastrochisis)
    • -Amniocentesis
  57. Neural Tube Defects: Epidemiology
    • -second most common serious malformation
    • -1/1000 births in US
  58. Neural Tube Defects: Pathophysiology
    • -failure of neural tube to close between weeks 3 and 4
    • -folate deficiency
    • -12-15% associated with chromosome defects
  59. Neural Tube Defects: Risk Factors
    • -diabetes
    • -anticonvulsants
    • -retinoic acid
    • -affected parent or sibling (biggest risk)
  60. Fetal Down Syndrome: Epidemiology
    • -most common pattern of human malformation
    • -1/800 live births
  61. Fetal Down Syndrome: Symptoms
    • developmental delay
    • characteristice faces
    • cardiac, renal, GI abnormalities
    • increased risk of childhood leukemia
  62. MSAFP Levels in congenital abnormalities
    • -slightly lower levels of AFP associated with Down's (huge overlap with normal)
    • -AFP highly increased in NTD
  63. Nuchal Translucency
    • -increased detection rates for Trisomy 21 and 18
    • -U/S to measure thickness at back of fetal neck
    • -measure between 11 wks 2 days and 14 weeks 2 days
  64. Screening Detection Rates for trisomies:
    • Full Integrated: T21 (90%), T18 (81%)
    • Serum Integrated: T21 (85%), T18 (79%)
    • Quad + NT: T21 (89%), T18 (72%)
    • Quad alone: T21 (80%), T18(67%)
  65. Invasive Fetal Testing
    • 1. CVS
    • 2. Amnio
    • 3. Fetal blood sampling
    • 4. Fetal skin/muscle bx
  66. Chorion Villus Sampling
    • -10-14 weeks
    • -1% loss risk
    • -bx of placenta
  67. Amniocentesis
    • -15-22 weeks
    • -1:400 loss risk
    • -AFAFP/AchE
  68. Non-Invasive Prenatal Testing
    -fetal cells get into blood (usually lymphocytes, can hang around for years, therefore testing --> previous pregnancies)

    • -fetal DNA fragments (cleared withing 15 min), 10% from fetus
    • -look for increase total number of fragments of any chromsome
    • -99.2% detection rate
  69. Gestational Age estimations
    • 1. Menstrual Age
    • 2. Normal Gestation
    • 3. Trimesters
    • 4. Fetal/Embryologic Age
  70. Menstrual Age
    • -days past LMP
    • -follicular phase variable --> can be very off
  71. Normal Gestation
    • -280 days (40 wks)
    • - term = 37-40 wks
    • -perterm = 20-37 wks
    • -abortion/miscarriage = up to 20 wks
  72. Trimesters
    • -First: 14 wks
    • -Second: 28 wks
    • -Third: 42 wks
  73. Fetal/Embryologic Age
    • -embryo = 4-9 wks
    • -Fetus > 9 wks
  74. Birth
    delivery of the fetus > 20 weeks or >500g
  75. Abortion
    • -expulsion or extraction < 20 wks or < 500g
    • -elective or spontaneous
  76. Limit of Survival
    • -generally 23 weeks
    • -w/o handicap ~ 34 weeks
    • -w/ handicap ~ 28 wks
  77. Neonatal Period
    Birth - 28 days
  78. Perinatal Period
    20 wks - 28 wks
  79. Infant mortality
    -death of infant in first year of life
  80. Preterm Birth: Epidemiology
    • -delivery before 37 weeks
    • -leading cause of neonatal mortality (28%)
    • -US PTB rate one of the highest in the world (12.8%)
    • -highest in african americans
  81. Preterm Birth: Types
    • 1. Spontaneous (highest in developing world)
    • 2. Medically Indicated (fastest growing in US, IVF, multiples)
    • 3. Late PTB (rising rate in developing countries)
  82. Preterm Birth: Risk Factors
    • -multiple gestation
    • -prior history
    • -extremes of age (<17, >40)
    • -low socioeconomic status
    • -unmarried
    • -short pregnancy interval
    • -smoking/drugs
    • -BMI <19
    • -standing
    • -short cervix
    • -bleeding
    • -uterine infection
    • -STD
    • -pre-eclampsia
  83. Preterm Birth: Prediction
    • -risk scoring systems have low sensitivity
    • -Short cervix has good NPV but very poor PPV
  84. Normal Parturition
    • 1. Uterine Quiescence
    • 2. Release from Quiescence
    • 3. Preparation for labor
    • 4. Labor
  85. Uterine Quiescence
    -progesterone leads to myometrial unresponsiveness by down regulating contaction proteins

    -Cervical integrity (firm)
  86. Release from Quiescence
    • -cervical softening
    • -BUT: no predictable drop in progesterone in serum before this stage
  87. Preparation for Labor
    -estrogen/progesterone shift (estriol starts to rise, progesterone starts to plateau)

    -myometrial awakening (contraction associated proteins upregulated- oxytocin and PG receptors)

    -cervical ripening (hydrolysis of ground substance)
  88. Labor
    -forceful contactions (oxytocin release, decidual/membrane PGs)

    -myometrial cells communicate with each other (accelerate PG production)

    -membrane rupture (with contractions)

    -cervical dilation and fetal descent

    ***last two are clinical markers for labor
  89. Maternal Contribution to Initiation of Labor
    • 1. Progesterone withdrawal
    • - early in pregnancy PR-B is expressed (classic R)
    • -during labor expression switches to PR-A and PR-C (dominant negative receptors)

    • 2. Oxytocin Secretion
    • -produced by paternal pituitary
    • -minor role

    3. Stress Related Cortisol Release
  90. Fetal Contribution to Initiation of Labor
    • 1. Fetal/Placental cortisol releasing hormone
    • 2. Increased uterine stretch
    • 3. Fetal pulmonary surfactant protein A (immune and inflammatory function)
    • 4. Chorioamnionic membrane PGs
  91. Inititiation of Labor
  92. Initiation of Labor 2
    • -in late pregnancy CRH is produced by the placenta
    • -CRH stimulates pituitary to produce ACTH
    • -ACTH stimulates cortisol production from the adrenal gland
    • -CRH acts directly on muscle to induce contraction
    • -a little bit of CRH enters the fetal circulation activating the fetal adrenal gland
    • -fetal adrenals produce DHEA-S, cross into the myometrium and placenta --> converted to estriol
  93. Preterm Labor: Diagnosis
    1. Regular painful contractions and cervical dilation (false + rate of 40-60%)

    2. Cervical length (good NPV, bad PPV)

    3. Fetal fibronectin (comes out of cervix during active labor (good NPV, poor PPV)
  94. Preterm Labor: Pathways
    • 1. Infection and inflammation (25%)
    • 2. Stress (25%)
    • 3. Abruption Bleeding (35%)
    • 4. Mechanical Stretch (15%)
  95. Infection and inflammation
    • -can be infection of amniotic fluid, chorioamnion, decidua
    • -from ascending or resident bacteria (ureaplasma, mycoplasma, strep, E coli, fusobacter)
    • -cytokine/chemokine response (PGF and protease activation of labor)
    • -exascerbated by immunosuppression in pregnancy
  96. Stress
    • -maternal or fetal cortisol
    • -enhances placental CRH
    • -enhances amniochrion PG synthesis
    • -estriol shift via DHEA-S
    • -myometrial awakening
  97. Abruption Bleeding
    • -increase tissue factor in decidual cells
    • -increases MMP and IL8 expression
    • -risks: smoking, trauma, HTN, implantation defects
  98. Mechanical Stretch
    • -activates CAP genes in the myometrium
    • -induces cervical ripening
    • -risks: mutliple gestation, polyhudramnios
  99. Preterm Labor: Management
    • 1. Tocolysis
    • 2. Antenatal Glucocorticoids
    • 3. Cerclage
    • 4. Progesterone
  100. Tocolytics (23-34 wks)
    • -Magnesium Sulfate
    • -Indocin (NSAID)
    • -Nifedipine (CCB)
    • -Terbut (B-mimetic)
    • -Atosiban (oxytocin antagonist)
  101. Magnesium Sulfate
    • -inhibits sarcoplasmic Ca influx
    • -doesn't delay delivery
    • -doesn't improve health
  102. Indocin (NSAID)
    • -decrease choriodecidual COX1 and PGs
    • -delays delivery
    • -? improve health
  103. Nifedipine
    • -Calcium channel blocker
    • -delays delivery
    • -doesn't improve health
  104. Terbut
    • -B mimetic
    • -activate beta adrenergic Rs and cAMP
    • -delays delivery
    • -doesn't improve help
  105. Atosiban
    • -oxytocin antagonist
    • -delays delivery
    • -doesn't improve health
  106. Tocolysis: Risk Factors
    • -Pulmonary edema
    • -Sepsis
    • -Toxicity
    • -Premature closure of fetal ductal arteriosis
  107. Tocolysis: Contraindications
    • -severe pre-eclampsia
    • -non-reassuring fetal status
    • -significant bleeding
    • -chorioamnionitis
    • -lethal fetal anmalies
    • -maternal cardiac disease
  108. Antenatal Glucocorticoids
    • -23-34 weeks
    • -high dose maternal betamethasone/desamethasone
    • -accelerates fetal lung, brain and gut maturation
    • -works much better than tocolysis
  109. Fetal Pulmonary Development
    • -fetal lungs are quite delayed in development
    • -only see significant alveolar development around 36 weeks
  110. Cerclage
    • -indicated for cervial insufficiency
    • -mechanical
    • -marginally effective if short cervix and hx of PTB
  111. Progesterone
    • -maintain quiescent labor
    • -works in the right patient population
  112. Preterm Premature Ruptured Membranes (PPROM)
    • -rupture of membranes prior to 37 wks
    • -20-30% of all preterm labor
    • -75% deliver within a week of rupture
  113. PPROM: Risk Factors
    • -smoking
    • -bleeding
    • -polyhydramnios/distention (strongest factor)
    • -infections (STDs)
    • -low SES
  114. PPROM: Mechanism
    • -inapropriate activation of collagenase/protease
    • -apoptosis of amniochorion
    • -initiated by infection or inflammation
  115. PPROM: Diagnosis
    • -sterile speculum examination
    • -pooling, ferning, increased pH
    • -alpha microglobulin 1
    • -dye test amniocentesis
  116. PPROM: Management
    • -expectant hospitalization
    • -antenatal glucocorticoids (if < 32 wks)
    • -"latency" abx (prolong ~ 14 days)
  117. Pre-eclampsia: Background
    • -hypertensive disorder of pregnancy
    • -syndrome of vascular dysfunction (HTN, proteinuria, end organ disease)
    • -reversible (only cure is delivery)
    • -cause unknown
  118. Preeclampsia-Eclampsia
    • -new onset HTN and proteinuria
    • -eclampsia (seizure)
  119. Superimposed Preeclampsia
    -worsening of pre-existing HTN and/or proteinuria
  120. Gestational HTN
    -new onset HTN w/o proteinuria or organ injury
  121. Chronic HTN
    -stable HTN without evidence of maternal injury
  122. Chronic HTN: Diagnosis
    • -present before pregnancy or detect before week 20 or detected after wk 20
    • -doesn't resolve 12 wks postpartum
    • -Systolic > 140
    • -Diastolic > 90
    • -no proteinuria (or no change)
  123. Preeclampsia-Eclampsia: Diagnosis
    • -de novo HTN and proteinuria
    • -HTN usually onset after 20 wks
    • -Proteinuria (>30 mg/dL)
  124. Severe Preeclampsia: Diagnosis
    • Severe end organ dysfxn
    • -increased proteinuria
    • -liver damage
    • -thrombocytopenia
    • -fetal growth restriction
  125. HELLP Syndrome
    • -Preeclampsia Variants
    • H: hemolysis
    • EL: elevated liver enzymes
    • LP: low platelets

    • -acute fatty liver of pregnancy
    • -TTP/HUS
    • -severe getational HTN (>160, but stable)
  126. Superimposed Preeclampsia: Diagnosis
    • -difficult
    • -new onset proteinuria or sudden worsening of chronic proteinuria
    • -sudden worsening of well controlled BP
    • -lab evidence of end organ dysfunction
  127. Gestational HTN: Diagnosis
    • -de novo HTN (after 20 weeks)
    • -no other manifesations of preeclampsia
  128. Gestational HTN: Morbidity and Mortality
    • 10/100,000 die with huge demographic variation
    • one of the top three causes of maternal mortality
  129. Gestational HTN: Epidemiology
    • -3-5% of pregnancies
    • -5-8% of first pregnancies
    • -rates increasing
  130. Preeclampsia: Maternal Clinical Consequences
    • -eclampsia
    • -stroke/CVA
    • -pulmonary edema
    • -hepatic rupture
    • -renal failure
    • -DIC
  131. Preeclampsia: Fetal Clinical Consequences
    • -mostly due to PTB
    • -placental abruption
    • -growth restriction
    • -cerbral palsy
    • -fetal death
  132. Preeclampsia: Risk Factors
    1. Maternal Vascular Factors (renal disease, diabetes, chronic HTN, obesity, PCOS, >40 yrs, pregnancy interval)

    2. Immunologic Factors (primiparity, new partner, cohabitation, IVF/egg donor)

    3. Genetic Factors (FHx, father hx of prior preeclampsia, trisomy 13)

    4. Placental Factors (multiples, uterine artery/prenatal screening abnormalities)

    5. Other (SMOKING DECREASES!!!)
  133. Preeclampsia: Pathogenesis
    • Two Stage Disease Hypothesis
    • 1. Placental Stage (shallow invasion, failed remodeling, hypoxia, oxidative stress)
    • -releases circulating factors -->

    2. Maternal Stage (endothelial dysfunction --> end organ injury, inflammation)
  134. Normal Implantation
    • -EVT from placenta line maternal spiral arterioles
    • -two waves of invasion (decidual, myometrial)
    • -mimic endothelial cells (pseudovascularization)
  135. Shallow Implantation
    • -limited trophoblast invasion (first wave only)
    • -defective integrin switching
    • -immune tolerance (NK/T cell killing)
    • --> chronic hypoxia
  136. Poor Placental Perfusion
    • -abnormal doppler velocity waveform of uterine artery
    • -low velocity diastole
    • -severe notching
  137. Placental Injury
    • atherosclerosis of spiral arteries
    • placental abruption with large clots
    • infarction
    • small dystrophic placenta
  138. Maternal Vascular Function in Normal Pregnancy
    • -decreased tone (decreased SVR)
    • -Increased capacitance (increase blood volume)
    • -Uteroplacental angiogenesis (increase uterine artery flow)
  139. Preeclampsia: Maternal Vascular Function
    • -Endothelial Dysfunction (los of refractoriness to vasopressors)
    • -Vasospasm/focal ischemia/HTN
    • -decreased cardiac output
    • -Proteinuria (damage to glomerular endothelium)
  140. Preeclampsia: Vascular Pathology
    • -oxidative stress (increase ROS)
    • -inflammation
    • -Trophoblast debris
    • -Low grade DIC
    • -increased sympathetic tone (increased work, decreased output)
  141. Preeclampsia: Angiogenic Factors
    • -VEGF (increase refractoriness to vasopressors)
    • -produced by trophoblast
    • -paradoxically elevated in preeclampsia

    -PlGF
  142. Preeclampsia: Anti-angiogenic Factors
    • -sFLT1 (blocks VEGF, produced by placenta)
    • -soluble endoglin (inhibits TGF and NO)
  143. Preeclampsia: sFLT1
  144. Preeclampsia: PlGF
  145. Preeclampsia: Soluble Endoglin
    • -markedly elevated in women with preterm PE
    • -doesn't increase significantly in normal pregnancy
  146. Preeclampsia: New Theory Pathogenesis
    • -sick placenta produces more anti-angiogenic factors preventing normal action of angiogenic factors
    • --> dysfxn endothelium
  147. Preeclampsia: Management
    • -prevent or tx eclamptic seizures (Mag sulfate)
    • -tx severe HTN to prevent CVA
    • -prevent pulm edema (restrict fluids)
    • -accelerate fetal maturity if preterm (steroids)
    • -cure (delivery)
  148. Unsafe anti-HTN medicines in Pregnancy
    • ACEI
    • AngII R Blockers
    • Diuretics
  149. Preeclampsia: effects on future maternal health
    • 1. underlying vasculopathies
    • -precede pregnancy
    • -not accelerated by preeclampsia

    • 2. remote outcomes
    • -HTN
    • -MI-Stroke
    • -Renal disease
    • -decreased risk of Breast CA

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