Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
107 Cards in this Set
- Front
- Back
What is leading cause of neonatal mortality?
|
preterm labor
|
|
What causes preterm labor?
|
excessive uterine distension, decidual hemorrhage, activation of maternal and fetal hypothalamic pituitary system, intrauterine infection leading to inflammation
these cause production of uterine and cervical proteases and uterotonins which causes cervical ripening and dilation, weakening of the chorioamniotic membrane which leads to rupture, uterine contractions |
|
How does infection cause preterm labor?
|
trigger inflammatory response that releases cytokines, prostaglandins, and proteases which stimulate uterine activity, induce cervix softening dilation, and weaken chorioamniotic membranes
|
|
Is there genetic predisposition for preterm labor?
|
yes
|
|
Can thrombin cause preterm labor?
|
yes, associated with vaginal bleeding caused by placental abruption
|
|
Can increased corticotropin releasing hormone cause preterm birth?
|
yes, from maternal and fetal stress or infection
|
|
What are symptoms of preterm labor?
|
back ache and uterine contractions
|
|
Are contractions always detected in preterm labor?
|
not frequently, not painful, not a sensitive marker for preterm labor
|
|
What can exclude imminent preterm delivery if 24-34 weeks gestation with intact amniotic membranes, and cervical dilation less than 3 cm?
|
negative fibronectin
|
|
What does fibronectin predict?
|
delivery in next 1-2 weeks
|
|
What is the strongest predictor of preterm birth?
|
prior preterm birth, 4 fold increase if 1 previous, 6 fold if 2 previous
|
|
What risk factors for preterm birth?
|
less than 18 or greater than 35
black, low maternal wt before pregnancy, smoking, 2nd or 3rd trimester bleeding, multiple gestation, uterine anomalies shorter cervix maternal infections (UTIC, pneumonia) genital organisms: Gardnerella vaginalis, Chlamydia trachomatis, Neisseria gonorrhoeae, Ureaplasma urealyticum, Trichomonas vaginalis |
|
Do preterm deliveries only in occur in pts with risk factors?
|
no, only half do
|
|
What are tocolytics used for?
|
diminish contractions
|
|
When is glucocorticoid considered?
|
all women at risk for preterm birth within 7 days and between 24-34 weeks gestation
|
|
When is tocolytic less likely to be effective?
|
women with cervical dilation greater than 3cm and unsuccessful if pt is in advanced labor (greater than 5cm)
|
|
What should be ruled out before tocolytic is used?
|
other causes of preterm labor: UTI, choriamnionitis
|
|
What is most frequent parenteral tocolytic?
|
magnesium sulfate, also prevents and treats eclampsia
|
|
What level of mag sulfate is needed to relax uterine smooth muscle?
|
maternal serum level 5-8mg/dL
|
|
How does mag sulfate work as a tocolytic?
|
inhibits myosin ligh chain kinase activity by competition with intracellular calcium, reducing myometrial contractility
|
|
When is magnesium CI?
|
myasthenia gravis and renal failure
|
|
How does magnesium compare to beta agonist ?
|
equally effective and better tolerated
|
|
How is magnesium dose increased?
|
until she has fewer contractions per 10 minutes or max of 4g/hr
|
|
What should be monitored with mag sulfate?
|
DTR, respiratory rate, urine output, fluid balance (fluid overload), serum concentrations (every 6-12hrs)
|
|
Why DTR measured?
|
patellar reflex disappears with mag serum concentration between 9 and 10 mg/dL, as long as DTR present no need to measure concentration
|
|
What is used to prevent inadvertent overdoses from mag sulfate?
|
controlled infusion device to deliver as continuous infusion
|
|
What toxicities can occur with hypermagnesemia?
|
hypocalcemia and tetany
neuromuscular blockade and respiratory arrest (15-17mg/dL) cardiac arrest (greater than 17mg/dL) |
|
What is used to reverse toxic effects of magnesium sulfate?
|
1g parenteral calcium gluconate
|
|
What AE from mag sulfate?
|
common: transient hypotension, flushing, sense of warmth, HA, dizziness, lethargy, nystagmus, dry mouth
others: paralytic ileus and pulmonary edema |
|
Is pulmonary edema more common in mag sulfate or beta agonist?
|
beta agonist
|
|
How do fetal concentrations of mag compare to maternal?
|
similar
|
|
What are most common neonatal AE from mag sulfate?
|
hypotonia and sleepiness
|
|
What potential role does mag sulfate have?
|
prevention of cerebral palsy
|
|
Why are B adrenergic agonist not first line for preterm labor?
|
high costs and maternal AE
|
|
What is the only medication FDA approved for tx of preterm labor?
|
ritodrine, b agonist
|
|
What are the B2 agonists?
|
ritodrine and terbutaline, bind to B2 receptors in uterine smooth muscle and inhibit smooth muscle cell contractility
|
|
What can continued use of B agonists lead to?
|
tachyphylaxis
|
|
What route for terbutaline?
|
IV, SQ, and PO
|
|
When is SC terbutaline used?
|
mild contraction and cervical dilation less than 2cm
|
|
When is IV terbutaline used?
|
more severe and frequent contractions anc cervical dilation greater than 2cm
|
|
Why do B agonists have high incidence of AE?
|
not selective for myometrial B2 adrenergic receptors at pharmacologic doses
|
|
What maternal AE from B agonists?
|
pulmonary edema, palpitations, tachycardia, myocardial ischemia, hyperglycemia, hypokalemia, and hepatotoxicity
|
|
How often d/c from B agonists?
|
10%
|
|
What can pulmonary edema lead to from B agonists?
|
ARDS and death
|
|
When should B agonist not be used?
|
underlying cardiac disease or arrhythmias, HTN, DM, severe anemia, thyrotoxicosis
|
|
What AE for fetus?
|
tachycardia, hypotension, hypoglycemia, hypocalcemia
increased risk of neonatal intraventricular hemorrhage |
|
What prostaglandins are important regulators of myometrial contractility and cervical ripening?
|
F2alpha and E2
|
|
What is action of indomethacin?
|
COX1 inhibitor, prostaglandin synthetase inhibitor, decrease prostaglandin production and thereby decrease contractions and inhibit cervical change
|
|
Indocin
|
indomethacin, prostaglandin synthetase inhbitor
|
|
What is used for GI upset from Indocin?
|
antacids
|
|
Does indocin cross placenta?
|
yes, rapidly and approaches maternal levels
|
|
What AE for indomethacin?
|
decrease fetal urine output leading to oligohydramnios
constriction of ductus arteriosus increased risk for maternal postpartum hemorrhage |
|
When should indomethacin be d/c based the amniotic fluid index?
|
if below 5cm, oligohydramnios
|
|
When does oligohydramnios resolve?
|
48-72hrs after d/c indomethacin
|
|
What increases risk of neonatal AE from indomethacin?
|
drug exposure more than 48hrs and used after 32 weeks when premature closure of ductus occurs more frequently
|
|
When should indomethacin not be used?
|
presence of oligohydramnios or suspected fetal renal or cardiac anomaly
|
|
When is indomethacin used as tocolytic?
|
second line for preterm between 24-32 weeks with CI to other tocolytics
|
|
What route is loading dose of indomethacin?
|
rectal or PO
|
|
What route is maintenance dose of indomethacin?
|
PO
|
|
How long is indomethacin given?
|
24-48hrs
|
|
Why might COX 2 inhibitors be more effective than COX 1 inhbitors or nonselective?
|
only amniotic COX2 is increased during labor
|
|
How do CCB work as tocolytics?
|
decrease calcium influx into uterine smooth muscle and inhibit myometrial contractions
|
|
What CCB are used as tocolytics?
|
nifedipine (most common) and micardipine
|
|
What maternal AE for CCB?
|
tachycardia, HA, flushing, dizziness, nausea, hypotension
|
|
Does nifedipine adversely affect uteroplacental blood flow or fetal circulation?
|
no
|
|
What DI with CCB?
|
magnesium, may potentiate neuromuscular blockade
|
|
What is max dose of nifedipine in first hr?
|
40mg in first hr
|
|
How long is nefedipine used?
|
through week 34
|
|
How long is magnesium sulfate tx?
|
12-24hrs after successful tocolysis, or the time to complete corticosteroids
|
|
What is used for chronic tocolytic?
|
continuous SC low dose terbutaline infusion through portable pump
|
|
Why is glucocorticoid given?
|
increase production of fetal lung surfactan and reduce incidence and severity of RDS
|
|
What glucocorticoids are used?
|
betamethasone and dexamethasone
|
|
What other benefits from steroids?
|
decreased intraventricular hemorrhage, necrotizine enterocolitis, neonatal death
|
|
Why are repeat weekly courses of CS discouraged?
|
decreased birthweight and head circumference, hypothalamic pituitary adrenal axis suppression, deleterious effects on cerebral myelination and lung growth, neonatal death
|
|
When is CS recommended?
|
preterm labor between 24 and 34 weeks gestation
|
|
Which CS is preferred?
|
betamethasone, fewer IM injections, greater reduction in RDS
|
|
When can CS be given in preterm premature rupture of membrane?
|
up to 32 weeks in absence of chorioamnionitis
|
|
What is used as indicator for fetal lung maturation?
|
phosphatidylglycerol or lecithin to sphingomyelin ratio (L:S) greater than 2
|
|
When is CS not recommended?
|
greater than 34 weeks unless indication of fetal lung immaturity
|
|
Why are AB given in preterm labor?
|
treat bacterial vaginosis, occult or documented intra-amniotic infections in preterm premature rupture of membrane, prophylactic against neonatal GBS
|
|
What is risk from bacterial vaginosis?
|
preterm delivery
|
|
Are vaginal AB effective for bacterial vaginosis?
|
no
|
|
What AB must be included in regimen for bacterial vaginosis?
|
metronidazole (Flagyl)
|
|
Does tx of bacterial vaginosis reduce risk of preterm delivery if no history of preterm birth?
|
no
|
|
What week should tx for bacterial vaginosis begin?
|
37
|
|
Where is most bacteria in amniotic fluid and placenta from?
|
vagina
|
|
When does spontaneous delivery occur when preterm premature rupture of membrane occurs?
|
within 7 days, AB increase this
|
|
What is sign of choriamnionitis?
|
temp 100.4 (38C) or more
|
|
How many women are colonized with GBS?
|
10-30% women in vagina or rectum
|
|
What neonates get GBS?
|
1-2% born to GBS mother
|
|
What organism causes GBS?
|
Streptococcus agalactiae
|
|
How is GBS transmitted to fetus?
|
vertical: mother to infant during labor and delivery
|
|
What is mortality rate of GBS?
|
5-20%
|
|
What does GBS cause to mother?
|
UTI, amnionitis, endometriosis, wound infection
|
|
What has reduced incidence of GBS?
|
AB prophylaxis
|
|
When is mother treated with intrapartum AB for GBS?
|
positive vaginal GBS
or one or more of the following: previous infant with GBS, GBS bacteriuria during current pregnancy, preterm labor less than 37 weeks, preterm premature rupture of membrane 18hrs or more, intrapartum temp 38 (100.4) or more |
|
What is tx if GBS positive and onset of labor less than 37 weeks?
|
Pen V for 48 hrs and intrapartum AB prophylaxis
if no GBS culture, start Pen until result of culture |
|
What is optimal prophylaxis for GBS?
|
AB at least 4 or more hrs before delivery
|
|
What is preferred tx for GBS?
|
Pen G over amp because of narrower spectrum of antimicrobial activity
|
|
What is required for intrapartum prophylaxis for GBS?
|
AB given immediately before and during delivery
|
|
When is intrapartum prophylaxis for GBS indicated?
|
previous infant with invasive GBS, GBS bacteriuria during current pregnancy, positive GBS culture during current pregnancy (unless planned cesarean delivery in absence of labor or amniotic membrane rupture is performed), unknown GBS status and any of the following (delivery less than 37 weeks gestation, amniotic membrane rupture 18hrs or more, intrapartum temp 100.4)
|
|
Is previous pregnancy with positive GBS indicated for tx?
|
no
|
|
Is planned cesarean delivery in absence of labor or membrane rupture indicated for GBS prophylaxis?
|
no
|
|
What is recommended tx for GBS?
|
Pen G
|
|
What is alternative tx for GBS?
|
ampicillin
|
|
What is tx if pt has pen allergy but not at high risk for anaphylaxis?
|
cefazolin
|
|
What is tx if pt at high risk for anaphylaxis?
|
clindamycin or erythromycin if susceptible
vanc is resistant to clindamycin or erythromycin or unknown |