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Flashcards in Pathophysiology 2 Deck (85):


-presence of new-onset grand mal seizures in a woman with preeclampsia
-more likely in cases in which new-onset seizures occur after 48-72hrs postpartum


Causes of seizures in addition to eclampsia?

-bleeding arteriovenous malformation
-ruptured aneurysm
-idiopathic seizure disorder


Pathophysiology of Hemotologic Changes?

-both thrombocytopenia and hemolysis may occur as part of unknown HELLP syndrome (unknown etiology)


Effect of Preeclampsia on baby?

-impaired uteroplacental blood flow or placental infarction
-intrauterine growth restriction
-placental abruption
-non-reassuring fetal status demonstrated on antepartum surveillance


Treatment of Preeclampsia?

-delivery: balance both maternal/fetal risks


How common is HTN in pregnancy?



What % of maternal deaths is HTN responsible for?



HTN disorders of Pregnancy?

-Gestational HTN (PIH)
-Superimposed Preeclampsia


Gestational HTN

-BP>140/90 after 20 wga
-no protein
-NL BP within 12 weeks postpartum
-25% of women with gestational hypertension will develop proteinuria (preeclampsia)



-like a C/S but need to get the baby out


Herpes Virology

-large, enveloped, double-stranded DNA virus
-glycoproteins 1 & 2 differentiates HSV 1 & 2
-replicated in host cell
-can form latent infection in dorsal root ganglion


HSV Epidemiology

-among most common STD
-HSV 1: 75-90% abs by age 10
-HSV 2: 25-60% reported prevalence of abs in young women, seroprevalence correlates with number of sexual partners
80% of new genital infections may be caused by HSV 1, may have surpassed HSV 2 as primary cause of genital herpes


HSV Epidemiology in Pregnancy

-incidence of new 1 or 2 in pregnancy is 2%
-about 10% of women who are seronegative have + partners
-with recurrent HSV
75% will have at least 1 recurrence during pregnancy
14% will have prodromal symptoms or lesions at delivery


Risk factors of HSV

-minority ethnicity
-previous genital infection
-lower family income
-# of sexual partners
-duration of sexual activity


HSV Treatment in Pregnancy

-at 37 weeks go on suppression therapy
-Acyclovir & Valacyclovir


Suppression therapy of HSV

->6 episodes a day that isn't pregnant
-1 or more episodes in pregnancy
-ACOG-pregnant women with history of recurrent HSV
-if mother is -, partner is + give suppression to partner


Invasive procedures in HSV

-if active: cesarean delivery
-if no lesions: "reasonable" to sue fetal scalp monitoring if indicated, invasive monitoring increases risk of neonatal infection


CMV Virology

-double stranded DNA enveloped
-Member of B-herpesvirus group
-primary & latent infections


CMV risk factors in pregnancy

-lower socioeconomic status
-birth outside US
-first pregnancy < 15 years old
-child care workers
-families with young children


Diagnosis of Maternal CMV

-incubation period: 28-60 days
-viremia can be detected 2-3 weeks following primary infection
-lab abnormalities: leukocytosis, lymphocytosis, elevated transaminases


Congenital CMV

-vertical transmission (transplacental infection, exposure to contaminated genital tract secretions during delivery, breastfeeding)
-hematogenous spread of virus across placenta (GREATEST RISK)


Diagnosis of CMV in pregnancy?



Ultrasound findings in CMV?

-cerebral calcifications
-echogenic bowel
-growth restrictions


KEY points of diagnosis of CMV?

-amniotic fluid for PCR is more sensitive than culture
-fetal blood sampling is less sensitive than fluid
-fetal infection may occur weeks to months after maternal infection (may need to repeat testing)
-timing of testing important (21 weeks, likely due to immaturity of fetal immune system & lag b/w maternal & fetal infection)
-detection of CMV in the amniotic fluid does not predict severity of disease


What predicts the severity of CMV?

-how early the baby was exposed in womb (early worse)


Intrauterine growth restriction is?

-a fetus who fails to reach its growth potential
-less than 10th percentile of weight class (linked to morbidity & mortality)


Extrinsic Risk Factors of Intrauterine Growth Restriction

-Maternal Health: HTN, renal disease, constrictive lung disease, diabetes, cyanotic heart disease, collagen-vascular disease, hemoglobinopahties
-smoking/substance ebuse
-severe malnutrition


Intrinsic Risk Factors of Intrauterine Growth Restriction

-genetic syndromes
-congential anomalies
-primary placental disease
-multiple gestation


Maternal Vascular Disease: Intrauterine Growth Restriction

-25-30% of all IUGR
-most common cause of IUGR in nonanomalous infants
-decrease in uteroplacental perfusion
-most common etiology (early onset severe preeclampsia, CHTN/SIP)


Maternal Nutrition Abnormalities: Intrauterine Growth Restriction

-first dem. in WWII in Russia/Holland
-birth weight declined when under nutrition occurred in 3rd
-also gave evidence to importance of prepregnancy nutritional status
-10,000ft, cyanotic heart disease, hemoglobinopahties, chronic pulmonary disease


Infection: Intrauterine Growth Restriction

-Rubella (60%), capillary endothelial damage, hypoplasia, necrotizing angiopathy
-CMV - cytolysis, localized necrosis of organs
-Toxoplasma gondii, Plasmodium, Trypanosoma cruzi, syohilis
-Bacterial infections have not been linked


Placental Disease: Intrauterine Growth Restriction

-placental weight increases throughout gestation
-not to same degree as fetal weight
-IUGR placentas 24% smaller when compaired to AGA
(chorioangioma, placenta previa, abnormal cord insertions)


Toxins/Teratogens: Intrauterine Growth Restriction

-alcohol ingestion
-anticonvulsants (phenytoin)


Biophysical Profile of Fetal Wellbeing

1. Tone: extension with rapid return to flexion
2. Gross body movement: 4 discrete body movements in 30 min
3. Fetal Breathing movement: 30 sec of breathing, intermittent, hiccups cont.
4. Amniotic Fluid Evaluation: one pocket >2cm without cord


Genetic Factors: Intrauterine Growth Restriction

-overall chromosomal/multifactorial anomalies account for 20% of IUGR
-if early onset IUGR (<26 wks) up to 25% have abnormal karyotype (trisomy 13, 18, 21, Turners)
-cardiac malformations, anencephaly, pyloric stenosis


Multiple Gestation: Intrauterine Growth Restriction

Congential anomalies
maternal comlications
multifetal reduction
growth rate differences


Diagnosis of IUGR: Ultrasound

-fetal biometry (HC/BPD/AC/FL): best if growth followed at 2-4 week intervals
-Amniotic fluid volume: deepest pocket/AFI both acceptable
-Doppler studies
-Biophysical Profile
-Amniocentesis for genetic/infectious etiology


Diagnosis of IUGR: Fetal biometry

-confirms weight at less than 10th percentile
-should be followed by serial growth (if interval <2 weeks, risk or erroneous values)


Criteria for Diagnosis of Preeclampsia

-systolic bp >140, diastolic >90 at more than 20 weeks of gestation in a women with previously normal blood pressure
-proteinuria (0.3g protein or higher in 24hr urine)
-may be associated with myriad other signs and symptoms, such as visual disturbances, headache, & epigastric pain, & edema


Lab abnormalities in Preeclampsia

-elevated liver enzymes
-low platelet counts
(HELLP syndrome)


Disgnosis of Severe Preeclampsia

1 or more
-BP>160 (systolic), >110 (diastolic) (at least 2 times, 6hr apart on bed rest)
- >5g protein in 24hrs or 3+ greater on 2 random urine samples collected more than 4 hrs apart
-oliguria of less then 500mL in 24hrs
-serum creatinine>1.2mg/dL
-cerebral or visual distrubances
-pulmonary edema/cyanosis
-epigastric or right upper-quadrant pain
-impaired liver function (elevated AST/ALT)
-microangiopathic hemolysis, increased LDH
-thrombocytopenia, platelets less than 100,000


Diagnostic Criteria for Superimposed Preeclampsia

-new onset proteinuria >300mg/24hrs in a women with HTN before 20 weeks of gestation, but no proteinuira prior to 20wga
-a sudden increase in proteinuria if already present in early gestation
-a sudden increase in HTN or dev. of HELLP syndrome
-onset of headache, scotomata, or epigastric pain


Risk factors for Preeclampsia

-multifetal gestations
-H/o preeclampsia
-chronic hypertension
-pregestational diabetes
-vascular/connective tissue disease
-antiphospholipid antibody syndrome
-BMI >34 or <19.8
-35 or older
-African-American race
-may have genetic basis


Pathophysiology of Preeclampsia

-invasion by the trophoblast appears to be incomplete
-severity of HTN may be related to degree of trophoblastic invasion
1.abnormal trophoblastic invasion of uterine vessels
2.immunological intolerance b/w maternal & fetalplacntal tissue
3.maternal maladaptation to cardiovascular or inflammatory changes in pregnancy
4.dietary deficiencies
5.genetic influences


Hemotologic changes in preeclampsia

-both thrombocytopenia & hemolysis may occur as part of HELLP syndrome, etiology is unknown
-hematocrit may be very low because or very high secondary to hemoconcentration in absence of hemolysis
-lactate dehydrogenase is present in erythrocytes in high conc. (or a sign of hemolysis)


HELLP Syndrome

1. hemolysis
2. elevated liver enzymes
3. low platelets


Hepatic Changes in Preeclampsia

-hepatic function may be altered
-alanine aminotransferase & aspartate aminotransferase may be elevated
-hepatic hemorrhage (subcapsular hematoma)
-rare: hepatic rupture (high mortality)


Incidence of HELLP with preeclampsia?



HELLP increases risk of?

-placental abruption
-renal failure
-subcapsular hepatic hematoma
-recurrent preeclampsia
-preterm delivery
-fetal or maternal death


Neurologic issues with preeclampsia?

-intracranial hemorrhage
-temporary blindness (hours to week)
-blurred vision


Treatment of Preeclampsia

-continued observation with preterm fetus (if mild)
-weekly nonstress tests, biophysical profiles
-testing twice weekly for suspected fetal gorwth restriction or oligohydramnios
-ultrasound every 3 weeks
-platelet count, renal function, urine protein - repeat as needed


Treatment with HELLP syndrome

-delivered regardless of gestational age


Management of preeclampsia during labor

1. prevent seizures
2. control of HTN
(Mg sulfate)


Peripartum Cardiomypathy

1. development of cardiac failure in the last month of pregnancy or within 5 months after delivery
2. absence of an identifiable cause for the cardiac failure
3. absence of recognizable heart disease prior to the last month or pregnancy
4. left ventricular systolic dysfunction demonstrated by classic echocardiographic criteria such as depressed shortening fraction or ejection fraction


Diagnosis of Peripartum Cardiomyopathy

-diagnosis of exclusion
-similar to those in nonpregnant adults
-acute disease


Risk Factors for Peripartum Cardiomyopathy

-Superimposed Pre-E
-obestiy + CHTN
-H/o Peripartum Cardiomyopathy
-Extremes of Age
-Multiple Gestation


Most common cause of heart failure during pregnancy?

-chronic HTN with superimposed preeclampsia


Obesity and Peripartum Cardiomyopathy

-common cofactor with chronic HTN (cause/contribute to underlying ventricular HTN)
-Framingham increased by 2x risk in nonpregnant


Dilated Cardiomyopathy is also found in???



Signs/Symptoms of Congestive Heart Failure

-chest pain


Clinical Findings of Peripartum Cardiomyopathy

-impressive cardiomegaly
-echo show EF less than 45%


Management for Peripartum Cardiomyopathy

-treatment for heart failure
1. Diuretics: reduce preload
2. Hydralazine: reduce afterload (vasodilator)
3. Digoxin: intropic effects (unless complex arrhythmias)
-prophylactic heparin: thromboembolism


Short Term Prognosis for Peripartum Cardiomyopathy

-immediate mortality rate is approximately 2%


Long Term Prognosis for Peripartum Cardiomyopathy

-long term mortality is significant (5-10 yr survival is lower in nonpregnant patients with idiopathic cardiomyopathy)
100% vs 25%
-peripartum that regain ven. function within 6 months have god prognosis (if not, bad)
-if ejection fraction is <50%, be reserved to have another baby


Diagnosis of IUGR

-Clinical Evaluation (fundal height, searching for etiologies)
-Ultrasound (growth, anatomy, genetic testing, amniotic fluid, doppler studies, antenatal testing)


Clinical Evaluation of IUGR

-fundal height for screening only (PE alone misses/inaccurate about 50% of time)
-important in evaluating risk factors
-often with gives an index of suspicion for IUGR
-prompt examination if concern for lagging growth


Diagnosis of IUGR: Amniotic Fluid

-single deepest pocket <5cm


Diagnosis of IUGR: Oligohydramnios

-result of chronic hypoxia with blood diverted from kidneys to vital organs
-increased risk of perinatal mortality
-normal fluid less likely to end in demise


Management of IUGR: Doppler Ultrasonography

-important tool: reduction in number of antenatal admission
induction of labor is decreased
cesarean section for distress is reduced
reduction in perinatal death


Doppler: Umbilical Artery

-placental vascular resistance
(reversed flow when >70% of arteries are obliterated)


Doppler: Middle Cerebral Artery

-detect "brain sparing effect"
(increased blood flow directed away from abdominal organs to the brain)


Doppler: Venous Circulation

-reflect cardiac dysfunction


Doppler: Uterine Arteries

-used in high risk pregnancies to predict IUGR, preeclampsia


Components of Doppler Assessment

-arterial circulation: umbilical artery, middle cerebral artery
-venous circulation: umbilical vein, ductus venosus


Delivery Management with HSV

-important facts to remember when managing HSV in pregnancy
-risk of transmission to neonate during primary infection at the time of delivery (30-60%)
-risk of transmission to neonate during recurrent infection at time of delivery 1-3%
-cesarean delivery doesn't completely prevent vertical transmission


HSV Cesarean Delivery

1. active lesions
2. prodromal symptoms-culcar pain & burning w/history of HSV


Women w/history of genital HSV but no active genital lesions at time of delivery?

-risk of vaginal transmission is very low
-sterile speculum exam for lesions
-non-genital lesions should be covered w/occlusive dressing



-premature pre-rupture of membranes
-seen with HSV


Risk factors for CMV infection

-11% childcare workers seroconvert in 10 months of hire
-families with young children


Risk for Congenital CMV

-primary CMV in pregnancy - 1/2 will infect fetus
-risk of transmission is greatest when infection occurs in 3rd trimester
-severe fetal injury is greatest when infection occurs in 1st trimester
-recurrent CMV in pregnancy: 5-10% will infect fetus (rarely symptomatic fetus)


Clinical Manifestations of CMV

-not highly contagious: saliva, urine, sexual, transplantation of organ
-mono-like syndrome: fever, malaise, myalgia, chills, cervical lymphadenopathy
-sever: pneumonia, hepatitis, guillian-barre, aseptic meningitis


Diagnosis of Maternal CMV

-serologic studies
CMV specific IgM (first) & IgG (long term)
CMV IgG avidity (how long has it been around, if <25% previous 3 months)
-PCR of blood, urine, salvia, amniotic fluid, cervical secretions


Diagnosis of CMV in pregnancy

-serum samples collected 3-4 weeks apart & tested in parallel CMV spec. IgG
-sero conversion from - to +


Is CMV IgM reliable?

-not completely
1. may not be + during acute infection
2. may persist for several months after primary inf
3. may be + with recurrent infection
4. should not be used alone to diagnose


Treatment of CMV in Pregnancy

-no therapies available
-antiviral treatment with ganciclovir is approved for treatment of CMV retinitis in women with AIDS
-live attenuated vaccine-concern about the ability of the vaccine to reactivate & infect the host