Pregnancy Complications Flashcards

1
Q

Who should be screened for GDM at first PNV?

A

Obese, prior GDM, physical inactivity, 1st degree relative w/ DM, high risk race (AA, asian, pacific islander), prior infant >9lb, HTN, high LPL, cholesterol, PCOS, a1c>5.7, other things associated w/ insulin resistance (BMI>40, acanthosis nigricans), hx cardiovascular disease.

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2
Q

What are values for 1hr and 3hr GTT?

A

Standard is Coustan (95, 180, 155, 140)
National diabetes group: 105, 190, 165, 145

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3
Q

What is White’s Classification?

A

Class A: diet alone, any duration or onset age
Class B: onset age 20yr +, duration <10yr
Class C: onset 10-19, duration 10-19 yr
Class D: onset < 10yrs age, duration 20+ yrs, retinopathy or HTN.
Class R: proliferative retinopathy
Class F: nephropathy w/ 500mg/d proteinuria
Class RF: R + F
Class H: arteriosclerotic heart disease
Class T: prior renal transplant

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4
Q

What is the risk of developing diabetes later in life if GDM?

A

Up to 70% of ppl w/ GDM will develop t2DM. Influenced by race, ethnicity, obesity. Hispanic have highest risk.

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5
Q

How do you counsel GDM pts on diet and exercise?

A

Carbs 40%, remaining divided between protein (20%) and fat (40%)
3 meals and 2-3 snacks to distribute carb intake and reduce postprandial glucose fluctuations.
Moderate exercise 30min at least 5x week.

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6
Q

What are pharmacologic treatments for GDM?

Who is a candidate for oral meds?

Mechanism of action of metformin?

Why don’t we recommend glyburide anymore?

A

Insulin recommended if fastings consistently >95, 1hr consistently above 140 adn 2hr >120
.0.7 units/kg in 1st tri, 0.8 in 2nd, 0.9 in 3rd

1st line=metformin. If decline insulin, can’t afford, can’t safely administer. Metformin crosses placenta and long-term metabolic effect on offspring is unknown but believed to be OK. absence of long-term neonatal follow up after metformin is why we recommend insulin

biguanide, inhibits hepatic gluconeogenesis and glucose absorption, stimulates glucose uptake in peripheral tissue.

Increases risk of neonatal hypoglycemia. Mechanism of action: sulfonylurea, increases insulin secretion and insulin sensitivity of peripheral tissues. Aovid if sulfa allergy.

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7
Q

What is dosing of metformin

What are side effects?

A

500mg nightly at initiation, increase to 500mg BID. max dose 300mg/day in 2-3 divided doses

GI (N, diarrhea), minimize by slowly increasing dose.

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8
Q

What is recommend APT for GDM?

What is delivery timing for GDMA1?
What is delivery timing for GDMA2?
When to delivery poorly controlled GDM?
When to deliver women who fail in-hospital admission for glycemic control?

A

Indicated if poorly controlled or medication requiring GDM at 32w No consensus for APT if GDMA1. j

GDMA1: 39-40w
GDMA2: 39-39w6d
GDM poorly controlled: 37w0d-38w6d
Requiring hospital admission and failed: 34-36w6d.

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9
Q

What is postpartum workup for GDM?

A

Risk of T2DM 15-70%. Recommend fasting and 2hr GTT.
Fasting >125 or 2hr >199→ definitely DM
Fasting <100 and 2hr < 140, normal. Anything in-between is impaired, refer for management and counseling.

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10
Q

What are glycemic goals for T2DM?

How do you prevent hyperglycemia in AM?

A

Avoid hypoglycemia <60. A1c <6% is best in 2nd and 3rd trimester.

Avoid carbs at bedtime, change dose of insulin, switch to different med.

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11
Q

How do you counsel someone w/ T2DM before pregnancy?

What is workup in 1st trimester?
2nd trimester?
3rd trimester?

A

Pre-conception: counsel on complications (anomalies, PTD, PEC, macrosomia, neonatal complications, worsening disease w/ retinopathy and nephrtopathy). Eval for hTN, nephropathy, cardiovascular disease. Optimize a1c <6.0. Increasing folic acid when getting pregnant bc incr risk neural tube defects/anomalies

1st tri: a1c, TSH, 24hr urine, EKG. Optho, dietician, endo, cardiologist or nephrologist if needed. Ongoing assessment of blood glucose, start LDA at 12w

2nd tri: anatomy US, a1c, fetal echo. Start LDA at 12wks.

3rd tri: a1c, growth US and weekly APT. delivery planning.

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12
Q

When do you deliver T2DM?

A

39-39w6d if no vascular complications and well controlled. If vascular complications: 36w0d-38w6d.

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13
Q

What are effects of elevated blood sugar on baby?

What are most common congenital defects?
What are neonatal consequences?

A

Major congenital anomalies
SAB
If a1c 5-6%, associated w/ fetal malformation rate close to normal pregnancies. IF a1c 10%, fetal anomaly rate of 20-25%.

Most common: Cardiac anomalies, CNS (anencephaly, spina bifida), sacral agenesis

NICU admission, hypoglycemia, higher rate RDS, hyperbilirubenamia, electrolyte disturbances, incr risk metabolic syndrome and cardiac disease in adult life.

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14
Q

How do you manage insulin on L&D?

A

Give usual dose of insulin at bedtime. Hold morning dose depending on timing of admission.
IV NS
In active labor or glucose <70, switch to 5% dextrose and give at 100-150cc/hr to achieve glucose level of 100mg/dL.
Check glucose hourly w/ bedside meter.
Regular insulin via IV if glucose >100. Give at rate of 1.25units/hr.

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15
Q

What are risk factors for DKA?

How do you manage DKA?

A

New onset DM, Infection, non-compliance with insulin, insulin pump failure, tx w/ beta mimetic tocolytic meds (terbutaline).

Present w/ abdominal pain, N/V, AMS. Lab findings: Low arterial pH<7.3, low bicarb <15, Elevated AG, elevated ketones

IV Hydration w/ NS at 1-2L/hr (total replacement 4-6L in first 12hr)
Potassium: if K<3.3, hold insulin and give 20meQ. If >3.3, give K??
Insulin: give IV, loading dose 0.1-0.2u/kg as bolus. Then 0.1units/hr. When glucose reaches 200, reduce dose.
Bicarb: if pH >7, no bicarb.
Hourly labs in iCU
and IV insulin
Monitor glucose and potassium

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16
Q

What is delivery timing for various complications?

A

Placenta previa: 36w-37w6d
Vasa Previa: 34 0/7 - 37 0/7
PAS: 34 0 /7 - 35 6/7
Prior classical 36 0/7 - 37 0/7
Prior myomectomy: 37 0/7 - 38 6/7
Prior uterine rupture 36 0/7 - 37 0/7
FGR 3-10%: 38-39 0/7, <3 %: 37w0d
Absent UAD: 33 0/7 - 34 0/7
Reversed UAD: 30 0 /7 - 32 0/7
Di-di twins: 38-38 6/7
Mono-di: 34 0 /7 - 37 6/7
Mono-mono: 32 0 /7 - 34 0/7
Di-di twins w/ FGR: 36 0 /7 - 37 6/7
Mono di with selective FGR: 32 0 /7 - 34 6/7
Alloimmunization: 37 0/7 - 38 6/7
Alloimmunization requiring IUT: individualized.
cHTN no meds: 38 0 /7 - 39 6/7
chTN on meds: 37 0 /9 - 39 6/7
cHTN difficult to control: 36 0 /7 - 37 6/7
T2DM well controlled: 39 0 /7 - 39 6/7
T2DM w/ vascular complications or prior stillbirth: 36 0 /7 - 38 6/7
GDM well controlled: 39 0/7 - 40 6/7
GDM on meds: 39 - 39 6/7
HIV if VL <1000: 38wks
HIV if VL < 1000: 39 weeks
Cholestasis bile acids <100: 36 0 /7 - 39 0/7
Cholestasis bile acids > 100: 36 0 /7 or at diagnosis.

17
Q

What is amniotic fluid embolism?

A

rare cause maternal cardiac arrest
- mortality 20% to 60%
- Diagnostic triad: Sudden hypoxia | Hypotension | Coagulopathy

  • Treatment: CPR, TTE once stabilized to diagnosed R heart strain. Meds for RHF. Manage DIC, may need MTP.
18
Q

Who is LDA recommended for?

A

High risk PEC w/ 1+ following RF: hx PEC, multiple gestation, HTN, pregestational DM, kidney disease, autoimmune (SLE, APLS)
1 or more RF: Nullips, obesity, fam hx, black race, low income, age 35+, IVF

19
Q

What are effects of obesity on fetus development?

Effects of obesity on pregnancy?

Intrapartum effects of obesity?

What is antepartum care for obese patient?

A

SAB, Fetal anomalies (NTD, hydrocephaly, cardiovascular, orofacial, limbs)

cardiac dysfunction, OSA, NAFLD, GDM, PEC, stillbirth. In postpartum: postpartum weight retention, metabolic dysfunction, early termination of breastfeeding, depression

PTB, CS, failed TOL, endometritis, wound issues, venous thrombosis.

Genetic screening, early US, anatomy US. detection of incr NF, echogenic bowel and EIF NOT altered by BMI.
LDA, nutrition, a1c, baseline PEC labs, early GCT. serial growth scans

20
Q

What are causes of FGR?

A

aneuploidy, HDP, tobacco/substance use, T2DM, intra-uterine infections, velamentous cord, maternal cardiovascular disease, SLE, poor maternal weight gain

21
Q

What are recommendations for epilepsy in pregnancy?

A
  • continue AED
  • Keppra (Levetiracetam) and Lamotrigine are best
  • need normal amount folic acid 0.4mg/day
  • single agent is best, monitor drug levels and adjust pro, assess for nTD, confirm fetal growth
  • 1MG FOLIC ACID PRE-CONCEPTION.

Inc risks:
- FGR
- IUFD
- PEC
- congenital anomalies
- pTD
- maternal mortality

22
Q

Who needs early GCT?

A

BMI >40
1st degree relative w/ DM
prior macrosomia/SD/stillbirth
prior GDM
PCOS
physical inactivity

–postpartum: 75 gm GTT, screen ALL at 6-12weeks.

23
Q

What is White classification?

A

a1 - GDM diet controlled
a2 - GDM requiring meds

B: onset age >20, duration <10
C: onset age 10-20, duration 10-20
D: onset < 10, duration >20

F: ne-F-phropathy
H - HEART involvement (CAD)
R - Retinopathy

24
Q

What are recs for cardiovascular disease in pregnancy?

A

RF: risk of heart attack: Race, obesity, HTN, age
- most common: HF, MI, arrhythmia, aortic dissection.

Do: fetal echo

NYHA classification
- Class 1: asymptomatic
Class 2: mild fatigue w/ ordinary activity
Class 3: marked fatigue w/ less than ordinary activity
Class 4: fatigue at rest.

L&D:
- avoid fluid overload, get epidural, vaginal delivery preferred (Avoid valsalva, shorten 2nd stage w/ operative delivery)
- supplemental o2
- PP is highest risk: inc.

Highest risk (pregnancy contra-indicated):
- pulm HTN, severe cardiomyopathy, severe AS, Marfan w/ dilated aortic root, class 4 disease.

– corrected valvular disease is lower risk!

25
Q

What is management of sickle cell disease in pregnancy?

A

autosomal recessive disorders involving abnormal hemoglobin (hemoglobin S)
- Asymptomatic individuals with heterozygous Hb S genotypes (carriers) are said to have sickle cell trait

  1. hgb status of partner -> genetic counseling, diagnostic testing
  2. Maternal complications: PEC, sickle cell crisis, VTE
  3. Fetal complications: FGR, PTD
  4. Risk-reducing: folic acid 4mg qd and LDA
  5. Labs: PEC labs to assess renal function, CBC

TTE if symptoms

26
Q

What is APLS?

A

1 clinical + 1 lab criteria
CLINICAL:
- vascular thrombosis
- fetal death > 10 wks w/ structurally normal fetus
- severe PEC before 34wks
- 3+ SAB < 10 wks

LAB (2 occasions 12wks apart)
- LAC (predicts poor pregnancy outcome)
- B2 glycoprotein
- anti-cardiolipin

Risks:
- thrombosis, fetal loss, PEC, PTL FGR

Tx:
- prophylactic anticoagulation + LDA
- avoid estrogen COC postpartum.

27
Q

What are causes of symmetric vs asymmetric FGR?

A

Symmetric: early, 2/2 genetic causes, symmetrically small
- TORCH, syphilis, genetics, congenital anomalies, malaria

Asymmetric: occurs later in pregnancy. head and organ sparing
- 2/2 placental insufficiency.

28
Q

What are risk factors for IUFD?
What is evaluation?

A
  • black race
  • obesity
  • smoking
  • T2DM
  • HTN
  • AMA
  • nulips
  • IVF
  • alcohol use
  • male fetal sex
  • late/post term pregnancy
  • maternal history/exam
  • placental exam
  • fetal autopsy
  • fetal karyotype/microarray
  • test for KB
  • test for syphilis
  • test for APLS

– can delivery at 39w

29
Q

What is oligo?
Causes?
Delivery timing?

A

DVP <2cm
Causes: FGR, smoking, PPROM, velamentous cord, issue w/ fetal bladder. Know more.
When do you deliver? 36-37wks.

30
Q

What is poly?
Causes?
Delivery timing?

A

AFI >25cm. causes=T2DM, GDM, idiopathic, hydrops, infections, multiple gestation, fetal TEF or duodenal atresia

  • not before 39wks
31
Q

What is nausea/vomiting in pregnancy?
What is regimen?
What is differential?

A
  • small frequent meals
  • Non-pharmacologic: convert PNV to those with folic acid, ginger capsules
  • Pharmacologic: B6 10-25mg, Diclegis (B6 + doxylamine 10mg of both, can increase dose) QID, Reglan, Phenergan, Zofran. Read practice bulletin. Avoid zofran in organogenesis period 2/2 small risk birth defects.

DD n/V: hyperemesis (>5% body weight loss, inability to tolerate oral intake), molar pregnancy, twin gestation. GI (PUD, gastroparesus), GU (pyelo, kidney stones, torsion), metabolic (DKA), neurologic (migraines, CNS tumors), pregnancy (PEC, AFLP), miscellaneous (drug toxicity)

32
Q

What is the NPV of reactive NST? BPP?

PPV of NST?

What affect BPP parameters adversely?

A

NST is 99.8% and 99.9% for BPP

PPV is 10%

Fetal sleep status, maternal meds/intoxication, maternal smoking, fetal CNS abnormalities.