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60 Cards in this Set

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1.What tests done during the first trimester? 2.When? 3.What they indicate?
1. Free beta-hCG and PAPP-A to calculate risk for tri 18 and 21. Also US
2. between 10 4/7 and 13 6/7 wks
3. beta hCG - elevated and PAPP-A - decreased for tri 21.
What test done to confirm abnormal 1st trimester tests?
Chorionic villus sampling.
Tests for 2nd trimester screening? At what age?
Quad screen (if no 1st trim. tests) - alpha fetoprotein, total hCG, unconjugated estriol, inhibin A.
between 15 and 21 wks.
What indicate Quad abnormal results? How to confirm?
MSAFP and unconjugated estriol - low, hCG and inhibn A - elevated for Down s., also for tri 13 and 18. Amniocentesis to confirm.
If AFP level is elevated, what it is indicate?
In maternal serum - open neural tube defects, in amniotic fluids - abdominal wall defects, congenital nephrosis, intestinal atresia.
What is integrated screening?
US measurement of the fetal NT, done btw 10 4/7 and 13 6/7 wks. PAPP-A in 1st tri., Quad screen - in 2nd.
Sequential screening?
NT, PAPP-A, free beta-hCG are measured in 1st, and Quad test in 2nd. Has high false-positive rate.
Contingent sequential testing?
NT, PAPP-A, free beta-hCG in 1st, Quad in 2nd when an elevated risk is noted.
Calculation of gestational age.
Measure crown-rump length between 6 and 14 wks. After the 1st tri., a combination of biparietal diametr, head circumference, abdominal circ., femur length is used.
Definition of oligohydramnios? Maternal and fetal Causes?
When amniotic fluid index <5 cm, or < 10% on a gestational age-depending scale. Spontaneous rupture of membranes - most common, other maternal - placental insufficiency, chr. hypertension, postdates. Fetal - renal agenesis, bladder outlet obstruction, karyotypic abnorm., cardiac defects.
Polyhydramnios? Causes?
AFI > 25 cm. Associated with fetal anomalies - anencephaly, NTD, duodenal atresia, multiple gest. with twin-twin transf., nonimmune hydrops. Maternal - DM.
Biophysical profile?
Fetal movements, fetal breathing, tone, amniotic fluid volume. Done often after nonreactive NST. Useful after 26-28 wks. Score 10 - normal, 4-6 - chr. asphyxia, 0-2 - hi mortality.
Fetal well-being?
the baseline heart rate is normal, there are periodic accelerations in the FHR.
Reactive nonstress test (NST).
in a 20-min period, at least 2 accelerations of the FHR peaking 15 b/m above baseline, each acceleration lasting at least 15 sec. In a fetus < 32 wks - accel. 10 beats for 10 sec.
Nonreactive NST.
FHR does not meet the established criteria for 1 hrs.
Contraction stress test (CST).
Assess fetus at risk for uteroplacental insuf., Adequate - 3 contractions, each for 40-60 secs w/in period of 10 min. Normally, the FHR is increased with contractions. Normal (negative) - no late decel., the baseline FHR is normal. Positive - late decel. with 2 of 3 contractions over 10 min period. Delivery warranted.
The normal baseline FHR.
110 - 160 beats/min.
Fetal tachycardia. Causes.
> 160. Maternal or fetal infection, fetal hypoxia, thyrotoxicosis, maternal use of cardiac drugs.
Fetal bradycardia. Causes.
< 110. Hypoxia, complete heart block, maternal use of beta-blockers.
Variability. Indicate?
Causes of decreased or absent V.
Rapid fluctuations in the baseline fhr. Indicates a functioning sypathetic-parasympathetic NS, the most sensitive for fetal well being.
Decreased V. - sev. hypoxia, anencephaly, other NTD, complete heart block, maternal narcotics or magnesium, normal fetal sleep.
Late decelerations.
Result of uteroplacental insufficiency with fetal hypoxia. Causes - mat. hypotension, supine position, regional anesthesia, mat. hypertension, postdates, preeclampsia.
Variable decelerations. Causes.
Slowing of the FHR with abrupt onset and return to the baseline, with preceded and followed by small accelerations of the FHR.
Abrupt compression of the umbilical cord, or cord stretch, rapid fetal descend, cord prolapse.
Lecithin-sphingomyelin ratio.
Measure in amniotic fluid to check lung maturation. Lecithin - active component of surfactant, secreted by type 2 alveolar cells. Gradually incr. after 28 wks. Sphingomyelin secreted in body tissues other than the lungs. level constant. L-S = or > 2 - mature, less immature.
When lung maturation delayed?
Accelerated?
Delayed - in DM, Rh isoimmunization.
Accelerated - SCD, narcotic addiction, PROM, chr. hypertension, IUGR, smoking.
When is RhoGAM given?
Rh neg. mother with vaginal bleeding e.g. abortion, abruption, ectopic, trauma. Fetal-maternal hemorrhage ->isoimmunization. RhoGAM given as a prophylaxis at 28 wks gestation and at discharge in absence of sensitization. Dose - 50 mcg if < 12 wks, 300 mcg - > 12 wks.
Preeclampsia. Tx. Fetal effects.
Around or after 20 wks. Main features - incrsd BP, proteinuria, edema, if seizures - eclampsia. Tx - initially - magnesium, with severe - delivery.
Fetal effects - asymmetric IUGR due to uteroplacental insufficiency.
Preterm labor. Risk factors.
Labor occur before 37th wk gestation. Risk factors - multiple birth, cocaine, abruptio, alcohol, smoking,
Complicaitons of PROM.
premature labor, prolapsed cord, infection.
Drugs contraindicated in pregnancy.
Thalidomide Androgens Progestins
Aspirin & indomethacin Phenytoin
Metronidazole Chloramphenicol Aminoglycoside Tetracycline
Live vaccines Warfarin Valproic ACE inhibitors
Effect of maternal smoking on fetus.
Reduced birth wt and lenght (asymmetric IUGR).Dose related.
Nicotine -> vasoconstriction ->reduced placental blood flow ->chr. hypoxia and icrsd carbon monoxide level.
S/s of maternal Magnesium toxicity.
Decreased deep tendon reflexes, respiratory depression.
Fetal side effects of Indomethacin.
Olygo-, ductul constriction, increased risk for NEC and IVH.
Effect of maternal PIH on fetus.
Asmmetric IUGR, perinatal asphyxia, polycythemia, prematurity, increassed risk of placental abruption.
Complications of maternal cardiac d. on fetus.
genetic factors,alterations in placental perfusion and exchange, the impact of maternal drugs.
Fetal malformations due to maternal warfarin therapy.
1st trimester - nasal hypoplasia, epiphyseal stippling, ASD, PDA, mental and growth retardation.
2nd - eyes and CNS abnormalities.
Fetal response to acute blood loss?
Hypoxemia and acidosis lead to bradycardia, vasospasm, initial shunt of blood to vital organs ->brain damage, demise.
Effect of increased maternal glucose level on fetus.
Early in pregnancy - congenital malformations, later - fetal hyperglycemia, increased fetal insulin production.
Can insulin and glucose cross the placenta?
When the fetal pancreas produce insulin?
What trigger fetal growth?
Glucose cross the placenta, insulin - does not.
20 wks.
The combination of elevated blood glucose and insulin level. Rapid organs growth combined with increased fat and glycogen stores.
How fetus can acquire TB?
Directly from mother's blood or swallowing amniotic fluids although most transmission occurs post-partum thru maternal contact.
Can mother with TB breastfeed?
Yes, if mother with inactive disease and taking meds.
Maternal complications with low Hgb?
At risk for infection, pre-eclampsia, postpartal hemorrhage. With severe low Hgb - mother at risk for cardiac failure. Fetus at risk for stillbirths, low BW, neonatal death.
Is maternal iron-deficiency anemia affect fetus?
Neonates are not deficient of iron at birth, but have low store and may develop iron deficiency.
Maternal folic acid deficiency is associated with what fetal problems?
Open neural tube defects.
True or false.
Folic acid deficiency is associated with iron deficiency.
True.
How maternal hyperthyroidism affect the fetus?
Thyroid-stimulating antibodies and drugs used for tx, cross the placenta and can increase fetal thyroid hormone production.
S/s of Grave's d. in fetus and neonates.
Tachycardia, growth retardation, goiter, CHF.
Causes of fetal cretinism.
Maternal iodine deficiency.
How maternal PKU affect the offsprings?
Microcephaly, mental retardation, growth retardation,cardiac disease.
Tolerance of distress as relation to gestational age?
The preterms tolerate longer periods of distress, than full terms, whereas the postterms may be in significant distress without displaying late decelerations.
Rh sensitivity.
Rh negative mother's blood contact blood of an Rh-positive fetus ->anti-D antibodies cross the placenta and attack the fetal Rh-positive RBCs, resulting in hemolysis. Problem during the 2nd and subsequent pregnancies.
Why the fetus can develop erythroblastosis fetalis with hemolysis?
Hemolysis triggers increased RBC production (erythroblastosis fetalis) which if left untreated results in severe /fatal edema (hydrops fetalis) that cause CHF.
when ABO incompatibility will happen? Why?
When mom is O and fetus is A or B.Anti-A or anti-B antibodies cross the placenta and hemolysis occur in fetus.
The bigest problem when mom takes PCP(phenilcyclidine)?
Mother may have overdose or psychotic response that can result in hypertension, hyperthermia and coma which will compromise the fetus.
Effect of amphetamines on mother during the pregnancy?
They are CNS stimulants. Use of these substances causes hypertension and tachycardia which can cause miscarriage, abruptio placentae, premature delivery.
Effect of amphetamines on fetus?
Symptoms of neonatal withdrawal?
Cross the placenta. Cause fetal hypertension, prenatal stroke. Symmetric SGA.
Abnormal sleep pattern (lethargy), poor feeding, tremor, diaphoresis, miosis, frantic fist sucking, hi-pitch cry, fever, yawning, hyperreflexia.
Effect of heroin on mother?
Heroin users are at increased risk of poor nutrition, iron deficiency anemia, pre-eclampsia-eclampsia.
Neonatal withdrawal from heroin?
Symptoms begin 48 to 72 hrs after delivery and include CNS and GI dysfunction, frequent yawning, sneezing, sweating, fever, tachycardia.
Methadone.
Used to treat heroin addiction. Exposure to methadone causes miscarriage, stillbirth, IUGR, fetal distress, low birth rate. Withdrawal symptoms the same as heroin.
Effect of maternal smoking on fetus?
Symmetric IUGR, increased rate of congenital birth defects (cleft lip/palate, limb reduction, urinary tract defects), placenta previa, placental abruption, preterm birth.
Cocaine.
Cross the placenta, act as vasoconstrictor. Causes fetal cardiac dysfunction. Increase risk of prematurity. Causes cerebral infarctions, nonduodenal intestinal atresia, anal atresia, NEC, GU defects, limb defects. Direct effect on neonatal CNS