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after 20 weeks
to be defined as gestational hypertension, onset of HTN must be
Abnormal placentation → placental ischemia → systemic endothelial dysfunction
what is the core mechanism of the pathophys of preeclampsia-eclampsia
Kidneys: glomerular endotheliosis → proteinuria
Liver: ischemia → elevated LFTs, RUQ pain
Brain: cerebral edema/vasospasm → headaches, seizures
Placenta: hypoperfusion → IUGR, abruption
describe the multisystem effects of HTN in pregnancy
first pregnancy has greatest risk
is there a greater risk of preeclampsia depending on how many pregnancies you've had?
Multiple gestation
Molar pregnancy
IVF / assisted reproduction
pregnancy related risk factors for preeclampsia
≥300 mg/24 hr urine
Protein/creatinine ratio ≥0.3
define proteinuria indicative of preeclampsia
Platelets <100,000
Creatinine >1.1 or doubling
Elevated AST/ALT
Pulmonary edema
New-onset headache or visual changes
signs of end organ dysfunction defining preeclampsia
delivery
definitive treatment of preeclampsia
placental
preeclampsia is a ________ disease
not if there are severe features present/end organ dysfunction
is proteinuria required to define preeclampsia
Hospitalization
Magnesium sulfate (seizure prophylaxis)
Control severe BP (≥160/110):
IV labetalol
IV hydralazine
PO nifedipine
immediate management of preeclampsia with severe features
Deep tendon reflexes
Respiratory rate
Urine output
how to look for magnesium sulfate toxicity
A severe variant of preeclampsia characterized by:
Hemolysis Elevated Liver enzymes Low Platelets
define HELLP syndrome
↑ LDH
Schistocytes
Indirect hyperbilirubinemia
signs of hemolysis in HELLP syndrome
no
is proteinuria and severe HTN required to diagnose HELLP
≥160/110
define severe HTN
RUQ or epigastric pain
Nausea/vomiting
Malaise
Headache
Hypertension (often)
Can progress rapidly
typical clinical presentaiton of HELLP
Immediate delivery (regardless of gestational age)
Magnesium sulfate
Control BP
management of HELLP
Liver hematoma or rupture
DIC
Renal failure
Placental abruption
Maternal death
complications of HELLP
no, prevents seizures
does magnesum sulfate lower BP?
HELLP until proven otherwise
RUQ pain + ↓ platelets in pregnancy=
Affects ~6–10% of pregnancies in the U.S.
incidence of gestational diabetes
Typically develops in 2nd or 3rd trimester
when does gestational diabetes usually develop?
fetal osmotic diuresis
why is polyhydramnios bigger risk in gestational diabetes
fetal hyperinsulinemia
what causes macrosomia in GDM
↑ placental hormones (hPL, cortisol, progesterone)
→ progressive insulin resistance
pathophys of gestational diabetes
24–28 weeks gestation (earlier if high risk)
when to screen for gestational diabetes
Step 1: Screening Test
50-g oral glucose load (non-fasting)
Measure glucose at 1 hour
Abnormal if ≥130–140 mg/dL (institution dependent)
Step 2: Diagnostic Test
100-g oral glucose tolerance test (fasting)
Abnormal if ≥2 values elevated
most common test for GD
75-g OGTT (fasting)
Diagnosis if any value elevated
one step method to test for GD
Obesity
Prior GDM
Known impaired glucose tolerance
indications for early testing of GDM
Dietary modification
Exercise
Glucose monitoring
first line management of GDM
Fasting: <95 mg/dL
1-hr PP: <140 mg/dL
2-hr PP: <120 mg/dL
glucose targets in tolerance test
insulin
if diet control fails for GDM, this treatment is gold standard
Well-controlled on diet → deliver by 40 weeks
Insulin-treated or poorly controlled → 39 weeks
delivery timing for GDM
75-g OGTT at 6–12 weeks postpartum
Counsel on future type 2 DM risk
postpartum management of GDM patients
neonatal hypoglycemia
most common neonatal complication
insulin
safest GDM med
IgG anti-D antibodies
Abs associated alloimmunization
Fetal anemia
Hydrops fetalis
Heart failure
Stillbirth (severe cases)
complications of alloimmunization
indirect coombs test (maternal serum); positive=maternal antibodies present
-antibody titer
tests for diagnose alloimmunization
maternal antibodies
indirect coombs identifies
fetal/neonatal RBCs with antibodies
direct coombs tests for
Binds fetal Rh-positive RBCs in maternal circulation
Prevents maternal immune system from recognizing antigen
Passive immunity — not effective once sensitized
MOA of rhogam
28 weeks gestation
Within 72 hours postpartum if infant is Rh-positive
After sensitizing events
timing to give Rhogam
Vaginal bleeding
Abortion or miscarriage
Ectopic pregnancy
Trauma
Amniocentesis/CVS
External cephalic version
sensitiing events indicating need for RhoGAM therapy
Standard: 300 mcg
Covers ~30 mL fetal whole blood
standard dose of RhoGAM
cell free DNA
how can you test fetal Rh
Middle cerebral artery (MCA) Doppler
↑ velocity = fetal anemia
fetal surveillance method for alloimmunization
Hydrops fetalis
Ascites
Pleural/pericardial effusion
in alloimmunization you ultrasound to check for
Intrauterine transfusions
Early delivery if viable
Neonatal intensive care at birth
mgmt of moderate-severe alloimmunization
hydrops fetalis
end-stage hemolytic disease