B6: CM Repro Exam 4

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516 Terms

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respiratory distress syndrome

leading cause of death in preterm infants

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produce phospholipids that are packaged into lamellar bodies

alveoli are lined by type II pneumocytes that produce

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surfactant

-phospholipid compound released from lamellar bodies

-reduces surface tension with in alveolar spaces allowing for maximal gas exchange

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•Lecithin

•Sphingomyelin

•Phosphatidylglycerol: appears later in gestation

predominant components of surfactant

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-lecithin:sphingomyelin ratio (>2)

-tests for presence of phoshatidylglycerol

-lamellar body number density

amniocentesis tests for fetal lung maturity

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phosphatidyglycerol

•If present <1-5% of infants will develop respiratory distress syndrome (RDS)

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28 days

60% infants born 24-25 weeks survive at least

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-activation of maternal/fetal HPA axis

-inflammation/infection

-decidual hemorrhage

-pathologic uterine distention

potential pathophysiologies of pre-term labor

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•short cervical length

•multiple gestations

•vaginal bleeding

•UTIs

•genital track infections

•Periodontal disease

risks of pre-term labor during pregnancy

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•smoking

•substance abuse

•short interpregnancy interval

•low maternal pre-pregnancy weight

behavioral risks that result in preterm labor

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-birth 20-37 weeks

-regular contractions

-cervical change: effacement, dilation

the 3 criteria to preterm labor

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•No effective interventions for prevention regardless of risk factors.

-may try hydroxyprogesterone caproate, compounded product

meds to prevent preterm labor

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vaginal progesterone supplementation

drug to prevent pre term labor in women with shortened cervix

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•OB Exam including speculum exam

•Digital cervical exam if no ruptured membranes

•GBBS testing vaginal and rectal

•Chlamydia/GC testing based on H&PE

•Urinalysis and culture

workup associated with evaluation of pre term labor

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less than 30 mm

cervical length that increases risk of preterm labor

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fetal fibronectin

•Protein produced by throphoblasts and chorioamniotic membranes

•Acts like "glue" to maintain integrity of the membranes

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fetal fibronectin

•However, interventions based on fFN have not improved perinatal outcome

protein with a high negative predictive value for pre term labor

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-IV fluids: increased hydration decreases uterine muscle activity

-steroids to promote fetal lung maturity, decreasse necrotizing enterocolitiss

initial management of pre term labor

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steroids

med indicated from weeks 24-34 if t is at risk for delivery within 7 days

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antibiotics

recommended med for PTL pt with ruptured membranes and GBS

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Magnesium sulfate

med used in cases of pre term labor for neuroprotection (24-32 weeks)

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magnesium sulfate

•Given for neuroprotection if < 32 weeks @ risk for delivery

•Decreases risk of cerebral palsy and motor dysfunction in preterm infants

•Works by stabilizing fetal circulation and normalized cerebral blood flow

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when benefit of delaying delivery is greater than risk of therapy, not indicated prior to viability, no evidence has direct effect on neonatal outcomes or neonatal benefit

indication for tocolytics

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lethal anomaly, chorioamnionitis, fetal demise, severe pre-eclampsia, abruption, PPROM, maternal contraindications to medications

contraindications for tocolytics

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tocolytics

-used to prolong latency period for 48 hours to promote steroid activity on lung maturity

-muscle relaxers to prevent uterine contractions

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-beta agonist: terbutaline, ritodrine

-calcium channel blockers

-prostaglandin synthetase inhibitors

-magnesium sulfate

examples of tocolytics

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hyperglycemia (not for diabetics)

key side effect of beta agonist

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hypotension

key side effect of calcium channel blocker

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thrombocytopenia, anemia

key maternal side effects of prostaglandin inhibitors

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necrotizing enterocolitis

key fetal side effects of prostaglandin inhibitor tocolytic

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myasthenia gravis

magnesium sulfate is contraindicated in pts with

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-depressed reflexes, flushing, shortness of breath

rare: pulmonary edema

key side effects of magnesium sulfate

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at the best facilities, it is safe to deliver at ____ weeks

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cervical insufficiency: painless dilation of cervix with no contracitons

sign of PPROM in which tocolytics have no place in management

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cervical insufficiency --> PPROM

-finding amninotic fluid bulging into cervical canal is predictive

-1st trimester ultrasound shortening of cervix <2.5 cm

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-previous preterm delivery

-earlier delivery in subsequent pregnancies

-cervical procedures

-uterine anomalies

risk factors for cervical insufficiency

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cervical dilation or PPROM in 2nd trimester

clinical presentation of cervical insufficiency

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cervical cerclage

-a surgical suture placed in purse string fashion placed near internal cervical os

-placed by 14 weeks for cervical insufficiency

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prelabor rupture of membranes (PROM)

•rupture of membranes before onset of labor

•Historically referred to as premature rupture of membranes

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PPROM (preterm premature rupture of membranes)

•Preterm rupture

•PROM before 37 weeks

•rupture preterm AND prior to labor

•associated with 30% preterm deliveries

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-infections

-history of PPROM

-uterine distention: twins, polyhydamninoss, fibroids

-short cervix

-2nd or 3rd trimester bleeding

-lower BMI, lower SES, smokers and drug users

risk factors for pre-labor rupture of membranes

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tests pooling fluid in vagina on fern test and nitrazine test

-arborization and pH >7.1 indicates rupture of membranes

how do you diagnose pre-labor rupture of membranes?

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blood, mucus, or semen present in vaginal fluid raising the pH

what could cause a false positive nitrazine test

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-intrauterine infection: increases with duration of latency

-cord prolapse

-placental abruption

main risks of term PROM

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latency period

• time from PROM to labor

inversely related to gestational age

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24 hours

if there is PROM at term, spontaneous labor typically occurs within

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•Placental abruption

•Postpartum endometritis

•sepsis

maternal complications of PPROm

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•Mortality 34% <26 weeks 15% >26 weeks

•Pulmonary hypoplasia

•Musculoskeletal deformities

•Cord prolapse

neonatal complications of PPROM

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NO digital exam if membranes are ruptured and not in active labor

should you do a digital exam if pt present PPROM?

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expectant management (in hospital) until maternal or fetal signs require delivery

-GBS prophylaxis, NSTs, ultrasound

typical management of PPROM

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fever, non-reassuring NST, poor BPP, spontaneous labor, reach 37 weeks gestation

indications to deliver a PPROM pt

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-all pregnancies at risk for delivery prior to 37 weeks

-no signs of chorioamnionitis

-reduce risk of RDS and intraventricular hemorrhage

indications for PPROM steroids

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celestone

most commonly used PPROM steroid

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give antivirals

•if recurrent disease- expectant management

•if active lesion when labors - cesarean delivery

management of PPROM ppt with HSV

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antiretroviral therapy

•zidovudine during labor

• evaluate viral load to determine risk of vertical transmission

management of PPROM pt with HIV

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ascending infection from vagina/cervix

maternal blood

penetrating trauma

sources of vertical transmission

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•Toxoplasmosis

•Other (varicella, parvovirus B19, listeria)

•Rubella

•Cytomegalovirus

•HIV

•Herpes, Hepatitis B & C

•Syphilis

list the TORCHHeS infections

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rubella and syphilis at first prenatal visit

-some countries also screen for toxoplasmosis

pregnant women should be screened during 1st trimester for these TORCH infections at their first prenatal visit

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HIV

syphilis

hep B and C

chlamydia

ALL women are screened for these during first trimester

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HHSV and gonorrhea

diseases screened during first prenatal visit only if high risk

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group B strep

screened in ALL women during 36-37 weeks gestation

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HIV, syphilis, chlamydia, gonorrhea

screened during third trimester if high risk

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-rubella

-toxo and CMV

TORCH infections associated with blueberry muffin rash

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blueberry muffin rash

extramedullary hematopoiesis in the dermis

<p>extramedullary hematopoiesis in the dermis</p>
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T. gondii

-intracellular parasite found in undercooked meat, unwashed fruit, and litter box

-cats the only definitive hosts

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oocyts--> tachyzoites in acute form---> bradyzoites (chronic)

-oocytes infectious found in feces, contaminated foods

acute and chronic forms of T. gondii

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-typically asymptomatic and self limited; symptoms are typically mono like

-prior infection results in immunity

presentation of maternal toxoplasmosis

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•Tachyzoite replication destroys infected cells

•Necrosis can become tissue calcification---> intracranial calcifications

pathogenesis of congenital toxoplasmosis

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chorioretinitis, hydrocephalus, intracranial calcifications

-chorioretinitis is later sequelae

classic diagnostic triad of congenital toxoplasmosis

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congenital toxoplasmosis

-more severe manifestations usually indicate infection earlier in gestation

-no symptoms at birth= still at risk

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-PREVENTION

-treatment of acutely infected women reduce risk of fetal transmission, reduce severity

best option of toxoplasmosis treatment

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-RNA virus, familly matonaviridae, genus rubivirus

-aka german measles

virus family of rubella

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children: generalized maculopapular rash on face, spreads to trunk

adults: prodrome fever, generaliized rashes, polyarthralgias

presentation of rubella

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rubella

-associated with forchheimer spots (rose spots) on the soft palate

<p>-associated with forchheimer spots (rose spots) on the soft palate</p>
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rubeola

associated with koplik spots, white spots on buccal mucosa

-pathognomonic for measles

<p>associated with koplik spots, white spots on buccal mucosa</p><p>-pathognomonic for measles</p>
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highest risk in first 12 weeks

when is the highest risk of congenital rubella transmission?

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sensorineural deafness, cataracts, congenital heat disease (eye <3 ruby earrings)

clinical triad of congenital rubella syndrome

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-prevent with vaccine prior to pregnancy and avoidance

-supportive care only, close monitoring of infant over first year; no effective antiviral for baby

-isolate infected mom, shed virus in urine, stools secretions for one year

treatment of congenital rubella

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rubella

virus that can be isolated from blood, urine, CSF, and throat swab specimens

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human herpesvirus-5

-family herpesviridae; enveloped, dsDNA

virus family of CMV

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cytomegalovirus

leading cause of nonhereditary sensorineural hearing loss; most common congenital viral infection

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cytomegalovirus

•Lytic replication inside endothelial cells results in owl’s eye inclusion bodies

•Viral protein UL16 prevents expression of NK cell activating receptor ligands

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cytomegalovirus

symptoms/presentation is inversely proportional to gestational age at time of transmission

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-usually asymptomatic or subclinical

-symptomatic = mononucleosis (not EBV)

-primary infections have higher risk of transmission to baby

presentation of CMV in mom

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congenital CMV

Chorioretinitis, Microcephaly, periVentricular calcifications

-petichiae, microcephaly

-intracranial calcifications, chorioretinitis

-hearing loss

-blueberry muffin rash

-hepatomegaly

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-IV ganciclovir for infants with symptomatic congenital CMV

-maternal antiviral therapy not routinely recommended

treatment for congenital CMV

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ssRNA, enveloped human retrovirus

virus type of HIV

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-very LOW with combination of low viral load and ART therapy

-may occur antepartum, intrapartum, or posttpartum through breastfeeding

rate of vertical transmissio nof HIV

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5 months

In untreated infants, the mean incubation period for developing an AIDS-defining condition after vertical transmission is

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•Treat with ART within 12 hours of birth

•Bathe infant prior to administering vaccines

tx of HIV in neonates

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38 weeks

•Planned cesarean delivery at ____ weeks of gestation is recommended for women who have a HIV viral load greater than 1,000 copies/mL

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•Failure to thrive, neurodevelopmental delay, lymphadenopathy, Opportunistic infections (thrush, diaper rash), interstitial pneumonitis, frequent diarrhea, hepatosplenomegaly

-molluscum contagiosum

presentation of congenital HIV

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HIV

congenital infection defined by recurrent bacterial infections, lymphoid hyperplasia, chronic parotid swelling, progressive neurologic deterioration, pneumocystis jirovecii

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dsDNA virus

•HSV-1 primarily cold sores; HSV-2 primarily genital herpes

•Either strain can cause genital herpes

viral family of herpes simplex

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gingivostomatitis

inflammation of the mouth and gums associated with HSV 1

<p>inflammation of the mouth and gums associated with HSV 1</p>
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primary HSV

infection type of HSV that causes the greatest risk to fetus

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•C-section recommended if herpes lesions are identified on the cervix, in the vagina, or on the vulva at the time of labor or spontaneous rupture of membranes

•Acyclovir is safe and can be used during pregnancy if symptoms are severe and to reduce risk of viral shedding or C-section delivery

prevention of congenital HSV

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-rash of skin, eyes, and mouth

-localized CNS disease

-disseminated disease involvign multiple organs

3 patterns of presentation of neonatal HSV

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IV acyclovir unntil PCR of CSF is negative ---> then long erm antiviral therapy

treatment of neonatal HSV

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motile spirochete treponema pallidum

cause of syphilis

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