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RDS Test 1 > B8.018 Prework 1: High Risk Pregnancies > Flashcards

B8.018 Prework 1: High Risk Pregnancies Flashcards

1
Q

specific pregnancy related concerns in obese gravidas

A

early screening for gestational diabetes or overt diabetes
sleep study to assess OSA
screen for pre-existing hypertension

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2
Q

how does pregnancy contribute to development of diabetes

A

human chorionic somatomammotropin (hCS) induces metabolic changes in the mother such as mobilization of fatty acids, insulin resistance, decreased glucose utilization, and increased availability of AAs
decreases maternal use of protein

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3
Q

who is at risk for diabetes in pregnancy?

A

obese
strong fam history of DM2
polycystic ovarian syndrome

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4
Q

diagnosis of overt diabetes

A

FPG = 126
A1C = 6.5%
random glucose = 200

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5
Q

adverse risks associated with diabetes in pregnancy

A 
preeclampsia
polyhydramnios
macrosomia
fetal organomegaly
maternal and infant birth trauma
perinatal mortality
neonatal respiratory problems and metabolic complications (hypoglycemia, hyperbilirubinemia, hypocalcemia, polycythemia)
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6
Q

direct effect of diabetes on offspring

A

risk of any congenital anomaly increases

long term risks: obesity, metabolic syndrome, autism

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7
Q

2 step approach for GDM testing

A

1 hr GTT (50g)
-if >135, do the 3 hr GTT (100g)
-fasting >95, 1 hr >180, 2 hr >155, 3 hr >140
need 2/4 values to be abnormal to meet criteria for GDM

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8
Q

1 step approach for GDM testing

A

2 hr GTT (75g load)
-fasting >92, 1 hr > 180, 2 hr > 153
if any value is abnormal, patient meets criteria

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9
Q

what to do once a diagnosis of GDM is made?

A

patient undergoes nutritional counseling and is then asked to check their blood sugars
initially > dietary changes, if this doesn’t work patient may receive pharmacologic treatment

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10
Q

medical interventions for GDM

A

insulin > gold standard

metformin and glyburide considered to be safe, oral alternatives

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11
Q

mechanism of metformin

A
  • decreases hepatic glucose production
  • decreases intestinal absorption of glucose
  • improves insulin sensitivity by increasing peripheral glucose uptake and utilization
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12
Q

metformin side effects

A

NO RISK of hypoglycemia

common adverse reactions: diarrhea, N/V, flatulence, indigestion, abdominal discomfort, anorexia, rash

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13
Q

mechanism of glyburide

A

stimulates the release of insulin from the pancreas

-dependent upon functioning beta cells in the pancreatic islets

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14
Q

side effects of glyburide

A

hypoglycemia, nausea, stomach pain, loss of appetite, rash

rarely: jaundice, confusion, weakness, easy bruising or bleeding

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15
Q

how to monitor fetal well being during GDM

A

non stress tests 2x weekly

biophysical profile weekly

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16
Q

non-stress test

A

fetal heart rate patterns measures for 20-30 min

pattern tells provider if the baby is getting adequate oxygenation from the placenta

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17
Q

biophysical profile

A

US assessment that includes documentation of how much the baby is moving, fetal muscle tone, diaphragmatic excursions observes, and the amt of amniotic fluid that is around the baby
if all are present in sufficient amounts: baby is getting adequate oxygenation

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18
Q

advanced maternal age

A

> 35 years

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19
Q

risks with AMA

A 
aneuploidy
early onset gestational diabetes
gestational HTN/ preeclampsia
preterm delivery
stillbirth
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20
Q

what should be offered to all pregnant mothers who are AMA

A
  1. genetic screening for trisomy 21, 18, 13
    - first trimester US at 11-14 weeks
    - offer additional serologic screening vs. chorionic villous sampling/amniocentesis
  2. first trimester/early second trimester screening for GDM
  3. detailed fetal anatomy scan around 20 wks
  4. fetal growth at 32 wks
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21
Q

AMA < 40

A

in absence of gestational diabetes, HTN disorders of pregnancy, fetal growth restriction, or evidence of impending placental insufficiency, routine prenatal care is sufficient until 39 wks

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22
Q

AMA > 40

A

initiate weekly surveillance 32-34 wks

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23
Q

why are pregnancies at risk of aneuploidy?

A

VERY RARELY does fam history have any role in risk for a cytogenetic error to occur
meiotic nondisjunction in 95% of cases
>90% the extra chromosome is from the mother

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24
Q

why offer aneuploidy screening?

A

risk assessment
balance consequences of having a child with the particular disorder against the risk of an invasive diagnostic test
prenatal mental preparation
pregnancy monitoring
recommendations for delivery at tertiary center

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25
Q

first trimester aneuploidy screening option

A

nuchal translucency

thicker = abnormal

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26
Q

what is cffDNA

A

cell free fetal DNA
can be isolated from maternal plasma
result of apoptosis of the placental syncytiotrophoblasts (technology relies on the premise that the fetus and placenta originate from a single, fertilized egg)

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27
Q

predictive value of cffDNA

A

NOT good in lower risk populations

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28
Q

carrier screening performed

A

CF and SMA offered to all
some ethnic specific
fragile X in those with personal or family history of premature ovarian failure, autism, intellectual dysfunction, movement disorders

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29
Q

delivery in AMA pregnancies

A

most deliver in 39th week

  • increased risk of stillbirth after this
  • low risk of neonatal morbidity/mortality at this GA
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30
Q

drugs given to premature infants to reduce risks of morbidity and mortality

A

corticosteroids

magnesium sulfate

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31
Q

which pregnant mothers are given corticosteroids?

A

patients expected to deliver prematurely (<37 wks GA)

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32
Q

function of steroids in premature birth

A

stimulate fetal lungs to develop type 1 and 2 pneumocytesand surfactant
decreased rates of newborn mortality
decrease intraventricullar hemorrhage, necrotizing enterocolitis, and infections

33
Q

when can steroids have a positive impact on premature infants

A

after 22-23 wks GA

34
Q

which steroids can be given in pregnancy

A

bethamethasone
dexamethasone
need to be fluorinated to cross the placenta

35
Q

conditions where you should defer delivery for steroid benefit x 48 hrs

A 
labor
platelets <100K
elevated LFTs
HELLP
fetal growth restriction
oligohydramnios
critically abnormal umbilical artery doppler indices
new onset renal dysfunction or deteriorating renal function
36
Q

when should you NOT delay delivery to give sterois

A 
uncontrolled severe BPs
eclampsia
pulmonary edema
GA < 23 wks
placental abruption
DIC
non-reassuring fetal status
intrapartum demise
37
Q

use of magnesium sulfate in delivery

A

if administered within 24 hours of delivery, newborns have less incidence of cerebral palsy and lower rate of death

38
Q

magnesium sulfate administration recommendation

A

any pregnancy that is threatened to delivery < 32 weeks GA

neuro morbidity decreases after 32 weeks

39
Q

mechanism of magnesium sulfate

A

stabilization of cerebral circulation by stabilizing blood pressure and normalizing cerebral blood flow
prevention of excitation injury by stabilization of neuronal membranes and blockade of excitatory neurotransmitters
protection against oxidative injury
protection against inflammatory injury via anti-inflammatory effects

40
Q

hypertensive disorders in pregnancy

A

preeclampsia/ eclampsia
chronic HTN
chronic HTN with superimposed preeclampsia
gestational HTN

41
Q

chronic HTN (pre-existing)

A

documentation of systolic BP >140 or diastolic BP >90 on 2 separate occasions at least 4 hrs apart
PRIOR to 20 wks GA
or diagnosis prior to pregnancy altogether

42
Q

preeclampsia

A

new onset HTN: systolic BP >140 or diastolic BP >90 on 2 separate occasions at least 4 hrs apart
AFTER 20 wks GA
+ proteinuria >300 in 24 hr urine collection

43
Q

gestational HTN

A

same as preeclampsia but without proteinuria

44
Q

eclampsia

A

new onset tonic-clonic seizures associated with new onset HTN

45
Q

other findings in preeclampsia

A 
proteinuria
-not required, don't want to delay diagnosis
new onset systemic findings:
-thrombocytopenia (<100K)
-doubling of LFTs
-doubling of Cr > 1.1 mg/dL
-cerebral/visual disturbances
-pulmonary edema
46
Q

preeclampsia with severe features

A

new onset HTN criteria plus any of the following:

  • persistent severe BP >160/105
  • thrombocytopenia
  • doubling of LFTs
  • doubling of Cr > 1.1 mg/dL
  • cerebral/visual disturbances
  • pulmonary edema
  • HELLP
  • GI symptoms
47
Q

GI symptoms w preeclampsia w severe features

A

persistent mid-epigastric/RUQ pain
new onset n/v
severe indigestion

48
Q

preeclampsia prevention

A

aspirin (81 mg)

to women w history of delivery prior to 34 wks due to preeclampsia or >1 pregnancy affected by preeclampsia

49
Q

management of preeclampsia without severe features

A 
2x weekly visits
-BP, physical
2x weekly fetal surveillance
1x weekly assessment of LFTs and platelets
serial fetal growth assessment
umbilical artery velocimetry
50
Q

anti-hypertensives safe for pregnancy

A

labetalol
procardia
hydralazine
started if persistent BP > 160/110

51
Q

BP goals in preeclamptic pts

A

decrease by 10-20 mmHg

systolic 120-150

52
Q

when should preeclampic pts be delivered

A

37-39 wks

if severe, no later than 34 weeks

53
Q

role of magnesium sulfate in preeclampsia

A

prevents eclampsia

triggers cerebral vasodilation, thus reducing ischemia generated by cerebral vasospasm during an eclamptic event

54
Q

when should magnesium sulfate be administered in preeclampsia

A

severe signs/symptoms OR is eclampsia has already occurred

55
Q

cure for preeclampsia

A

DELIVERY

56
Q

preterm labor

A

regular uterine contractions accompanied by a change in cervical dilation, effacement, or both
initial presentation with regular contractions and cervical dilation of at elast 2 cm

57
Q

problem w preterm labor

A

mild irregular contractions are normal, so its hard to distinguish true labor (results in cervical change) from false labor (contractions that do not result in cervical change)

58
Q

preterm premature rupture of membranes

A

premature rupture of the amniotic membrane anytime prior to 37 weeks gestational age

59
Q

pathophys of preterm labor

A

activation of the maternal or fetal HPA axis associated with either maternal anxiety and depression or fetal stress

  • inflammation or infection
  • decidual hemorrhage
  • pathological uterine distention
60
Q

pathophys of PPROM

A

shearing forces created by uterine contractions

intraamniotic infection

61
Q

risk factors for PTL and PPROM

A 
history of PTL or PPROM
UTI
STI
short cervical length
2nd and 3rd trimester bleeding
low BMI
low SES
cig smoking
illicit drug use
62
Q

evaluation for suspected PTL/PPROM

A

maternal physical and vital assessment
external monitors that assess for contractions and fetal heart rate
sterile speculum exam
digital cervical exam (if no concern for ruptured membranes)
send urine culture
send swab of vagina/perirectal area to assess presence of GBS

63
Q

sterile speculum exam in suspected PTL

A

assess dilation
assess for rupture of amniotic membranes
collect samples of vaginal secretions for STI testing

64
Q

signs of PPROM on speculum exam

A

fluid pooling in vaginal vault
ferning: appearance of dried amniotic fluid on light microscopy
nitrazine test: detects pH, amniotic fluid is basic

65
Q

management of PTL

A

antibiotics for GBS prophylaxis
steroids for fetal lung maturation (over 48 hrs)
IV fluids

66
Q

meds to stop contractions

A

tocolytics

given for 48 hrs to allow the full effect of the steroids to take place for fetal benefit

67
Q

tocolytic options

A 
COX inhibitors (indomethacin)
Ca2+ channel blockers (Nifedipin)
B-agonists
oxytocin receptor antagonists
magnesium sulfate
NO
68
Q

COX inhibitors mechanism

A

reduce prostaglandin production by inhibition of both COX 1 and 2

69
Q

concerns about use of COX inhibitors

A

after 32 wks, risk of premature closure of the fetal ductus arteriosus which can result in right heart failure in utero

70
Q

when not to use COX inhibitors

A

dont use after 32 weeks or for >48 hours

71
Q

Ca2+ channel blockers mechanism

A

block influx of Ca2+ through cell membrane and inhibit release of intracellular Ca2+ from sarcoplasmic reticulum
increase Ca2+ efflux from the cell
leads to myometrial relaxation

72
Q

risks with Ca2+ channel blockers

A

no known fetal side effects but can lead to maternal side effects due to vasodilatory actions

  • headache, nausea, hypotension
  • should be avoided if mothers have a pre-load dependent cardiac lesion or are already hypotensive
73
Q

antibiotic management of PPROM vs PTL

A

for PPROM give for 7 days

for PTL, stop when threat has ceased

74
Q

why use prophylactic antibiotics in PTL and PPROM?

A

prolong latency and reduce risk of neonatal and maternal infection

75
Q

antibiotics used in pregnancy

A

Macrolides: ureaplasmas and chlamydia

ampicillin and amoxicillin: GBS and many gram neg bacilli, some anaerobes

76
Q

delivery timing in PPROM

A

> 34 wks GA

77
Q

chorioamnionitis

A

intrauterine or intraamniotic infection

associated with maternal and newborn morbidity

78
Q

diagnosis of chorioamnionitis

A

fever >39 deg C
OR
fever > 38 on 2 occasions 30 min apart PLUS
-fetal HR >160 for >10 min
-maternal WBC >15,000 w left shift
-purulent appearing fluid coming from the cervical os visualized by speculum exam

79
Q

treatment of chorioamnionitis

A

DELIVER

RDS Test 1 (22 decks)

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