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Principles III > Pregnancy and Coexisting Disease > Flashcards

Pregnancy and Coexisting Disease Flashcards

1
Q

What is the primary goal of gestational diabetes management?

A

Replicate low maternal glucose levels (70-120 mg/dl)

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2
Q

What is the primary goal of gestational diabetes management?

A

Replicate low maternal glucose levels (70-120 mg/dl)

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3
Q

What are normal maternal glucose levels during pregnancy?

A

Fetus continuously draws from maternal supplies creating blood glucose of 70-120 mg/dl

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4
Q

What is the key gestational diabetes management concept to remember regarding glucose and insulin?

A

glucose crosses the placenta but insulin does not

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5
Q

Why do mothers with gestational diabetes tend to have larger babies?

A
  • mother’s blood brings extra glucose to fetus
  • fetus makes more insulin to handle the extra glucose
  • extra glucose gets stored as fat and fetus becomes larger than normal
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6
Q

What are birth defects that can occur with gestational diabetes?

A 
neural tube defects
cardiac defects (most common)
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7
Q

When does a baby have macrosomnia from gestational diabetes?

A

> 4000 grams or 8.5 lbs

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8
Q

What are other complications that can occur during birth if the mother had gestational diabetes?

A

shoulder dystocia

brachial plexus injury

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9
Q

What are fetal complications of gestational diabetes?

A
  • respiratory distress syndrome (lung maturity delayed)
  • intrauterine fetal demise
  • hyperbilirubinemia
  • hypoglycemia post delivery (potential seizures, coma, brain damage)
  • childhood and adolescent obesity
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10
Q

What are maternal complications of GDM?

A
  • worsening of type I diabetes complications (retinopathy and nephropathy)
  • increased incidence of miscarriage, HTN, pre-eclampsia, C-section
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11
Q

When does maternal screening for GDM occur?

A
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12
Q

What is the treatment for GDM?

A
  • supplemental folic acid (decreases neural tube defects)
  • tight glucose control (capillary glucose monitoring 4-7 times/day–esp in 3rd trimester)
  • intensive fetal surveillance (serial ultrasounds for pregnancy dating, level 2 ultrasound for birth defects, fetal echocardiogram, amnio for fetal lung maturity for delivery
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13
Q

What do you do for glucose control in patient with GDM during labor and delivery?

A
  • diet-controlled diabetics (GDMA1) –> no glucose containing IV fluids
  • insulin-dependent diabetics (GDMA2) –> accu checks q1-2 hours with sliding scale coverage, combined glucose and insulin infusions during the intrapartum period (D5LR at 100 mL/hr and insulin gtt at 0.5-1 unit/hr)
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14
Q

What are the 4 types of HTN that can occur during pregnancy?

A
  • gestational HTN (HTN>20 weeks without proteinuria)
  • pre-eclampsia (HTN and proteinuria +/- edema >20 weeks)
  • chronic HTN
  • chronic HTN with superimposed pre-eclampsia
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15
Q

What are normal maternal glucose levels during pregnancy?

A

Fetus continuously draws from maternal supplies creating blood glucose of 70-120 mg/dl

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16
Q

What is the key gestational diabetes management concept to remember regarding glucose and insulin?

A

glucose crosses the placenta but insulin does not

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17
Q

Why do mothers with gestational diabetes tend to have larger babies?

A
  • mother’s blood brings extra glucose to fetus
  • fetus makes more insulin to handle the extra glucose
  • extra glucose gets stored as fat and fetus becomes larger than normal
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18
Q

What are birth defects that can occur with gestational diabetes?

A 
neural tube defects
cardiac defects (most common)
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19
Q

When does a baby have macrosomnia from gestational diabetes?

A

> 4000 grams or 8.5 lbs

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20
Q

What are other complications that can occur during birth if the mother had gestational diabetes?

A

shoulder dystocia

brachial plexus injury

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21
Q

What are fetal complications of gestational diabetes?

A
  • respiratory distress syndrome (lung maturity delayed)
  • intrauterine fetal demise
  • hyperbilirubinemia
  • hypoglycemia post delivery (potential seizures, coma, brain damage)
  • childhood and adolescent obesity
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22
Q

What is the one proposed theory explaining the cause of pre-eclampsia?

A

ulteroplacental ischemia causes production and release of biochemical mediators into the maternal circulation which then cause arteriolar constriction and vasospasm and vascular endothelial dysfunction

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23
Q

When does maternal screening for GDM occur?

A
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24
Q

What is the treatment for GDM?

A
  • supplemental folic acid (decreases neural tube defects)
  • tight glucose control (capillary glucose monitoring 4-7 times/day–esp in 3rd trimester)
  • intensive fetal surveillance (serial ultrasounds for pregnancy dating, level 2 ultrasound for birth defects, fetal echocardiogram, amnio for fetal lung maturity for delivery
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25
Q

What do you do for glucose control in patient with GDM during labor and delivery?

A
  • diet-controlled diabetics (GDMA1) –> no glucose containing IV fluids
  • insulin-dependent diabetics (GDMA2) –> accu checks q1-2 hours with sliding scale coverage, combined glucose and insulin infusions during the intrapartum period (D5LR at 100 mL/hr and insulin gtt at 0.5-1 unit/hr)
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26
Q

What are the 4 types of HTN that can occur during pregnancy?

A
  • gestational HTN (HTN>20 weeks without proteinuria)
  • pre-eclampsia (HTN and proteinuria +/- edema >20 weeks)
  • chronic HTN
  • chronic HTN with superimposed pre-eclampsia
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27
Q

What are the 3 triad of symptoms you see with pre-eclampsia?

A
  • labile HTN
  • proteinuria
  • non-dependent edema –> weight gain
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28
Q

When doe pre-eclampsia occur?

A

after the 20th week of pregnancy

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29
Q

What is eclampsia?

A

seizure activity in patient pre-eclampsia

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30
Q

What is the chance of a woman with pre-eclampsia progressing to eclampsia?

A

0.5-2%

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31
Q

What SBP and DBP define pre-eclampsia?

A

SBP >140 mmHg
DBP >90 mmHg
must be on 2 separate readings >6 hours apart

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32
Q

What amount of proteinuria defines pre-eclampsia?

A

> 300 mg protein/24 hours

>/= protein on dip stick (clean catch, no UTI)

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33
Q

What is the incidence of pre-eclampsia in different populations?

A
  • primipaternity (1st child)
  • extremes of age
  • african-americans
  • increased placental tissue (twins, moles)
  • co-existing disease (DM, chronic HTN, renal disease)
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34
Q

What is the etiology of pre-ecampsia?

A

unknown, but multiple theories around, possibly related to decreased placental perfusion and uteroplacental ischemia (but not sure which one came first to cause the other)

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35
Q

What is the one proposed theory explaining the cause of pre-eclampsia?

A

ulteroplacental ischemia causes production and release of biochemical mediators into the maternal circulation which then cause arteriolar constriction and vasospasm and vascular endothelial dysfunction

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36
Q

What is the treatment for pre-eclampsia?

A
  • delivery of fetus and placenta is definitive treatment
  • medical management - control of HTN, anticonvulsant prophylaxis, maintenance of renal function, determination of fetal lung maturity
  • strict bedrest
  • left uterine displacement
  • +/- low-dose aspirin treatment
  • intrapartum - fluid restriction, isotonic IV solutions, pharmacotherapy to treat HTN and prevent/treat seizures
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37
Q

What are the 3 primary manifestations of pre-eclampsia?

A

HTN
hypercoagulability
increased vascular permeability (decreased intravascular volume, end organ hypoperfusion, edema, proteinuria)

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38
Q

What are the CV effects of pre-eclampsia?

A
  • labile HTN
  • vascular leakage of fluid and proteins due to dec. colloid osmotic pressure, dec. intravascular volume, and edema
  • severe pre-eclampsia with SBP>/=160 or DBP>/=110
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39
Q

What are the pulmonary effects of pre-eclampsia?

A
  • upper airway edema

- severe pre-eclampsia –> pulmonary edema

40
Q

What are the hematologic effects of pre-eclampsia?

A
  • hypercoagulability
  • hemoconcentration
  • severe pre-eclampsia –> thrombocytopenia (most common), DIC
41
Q

What are the renal effects of pre-eclampsia?

A
  • proteinuria
  • low urine output
  • decreased uric acid clearance
  • severe pre-eclampsia –> oliguria and renal failure
42
Q

What are hepatic effects of pre-eclampsia?

A
  • impaired function
  • elevated LFTs
  • severe pre-eclampsia –> swelling of liver capsule causing epigastric pain, liver necrosis, subcapsular hematoma
43
Q

What are the CNS effects of pre-eclampsia?

A
  • HA

- hyperreflexia

44
Q

What are the CNS effects in a patient with SEVERE pre-eclampsia?

A 
visual disturbances
cerebral edema
eclamptic seizures
cerebral hemorrhage
maternal death
45
Q

What are placental effects of pre-eclampsia?

A
  • hypoperfusion

- severe pre-eclampsia –> infarct, abruption

46
Q

What are the fetal effects of pre-eclampsia?

A
  • IUGR
  • prematurity
  • severe pre-eclampsia –> hypoxemia, fetal distress, IUFD
47
Q

What lab values would you want to check for someone with pre-eclampsia?

A
  • Hgb/Hct
  • platelet count
  • 24 hour urine >/= 300 mg/dl protein
48
Q

What lab values would you want to check for someone with SEVERE pre-eclampsia?

A
  • BUN and Cr
  • LDH, ALT, and AST
  • uric acid
  • PT (DIC)
49
Q

What is the treatment for pre-eclampsia?

A
  • delivery of fetus and placenta is definitive treatment
  • medical management - control of HTN, anticonvulsant prophylaxis, maintenance of renal function, determination of fetal lung maturity
  • strict bedrest
  • left uterine displacement
  • intrapartum - fluid restriction, isotonic IV solutions, pharmacotherapy to treat HTN and prevent/treat seizures
50
Q

What are the drugs of choice to manage pre-eclampsia?

A 
magnesium sulfate
hydralazine
labetalol
May also include:
phenytoin
midazolam, diazepam
nifedipine
nitroprusside
51
Q

What is the anticonvulsant of choice with pre-eclampsia?

A

magnesium sulfate, controls seizures in 95% of cases

52
Q

What is the dose of magnesium sulfate?

A

4-6 grams loading dose over 20 minutes then maintenance infusion of 1-2 grams/hr

53
Q

What other drugs can be given as anticonvulsant prophylaxis?

A
  • phenytoin can be added in eclampsia

- diazepam/midazolam may be used to control seizures resistant to magnesium sulfate

54
Q

What is the dose of phenytoin?

A

20 mg/kg IV at a rate of 12.5 mg/min, max dose of 1500 mg/day

55
Q

What are the doses of midazolam/diazepam?

A

titrate to effect

56
Q

How does magnesium sulfate work?

A

antagonizes calcium channels in the smooth muscle cells, vasodilates and increases uterine blood flow, decreases Ach release at the neuromuscular junction

57
Q

What are therapeutic levels of MgSO4?

A

4-8 mEq/L, actual levels monitored only in renal impairment of symptomatic toxicity

58
Q

What are adverse side effects of MgSO4?

A
  • respiratory depression
  • CNS depression
  • cardiac conduction block at toxic levels
59
Q

What are signs and symptoms of MgSO4 toxicity?

A
  • respirations
60
Q

What is the treatment for MgSO4 toxicity?

A

10-20 mL of 10% calcium gluconate IV (remember that it reverses beneficial effects of MgSO4)

61
Q

What are some anesthetic implications with MgSO4?

A
  • Can increase neuromuscular blockade with both depolarizers and nondepolarizers (decreases endplate senstivity to Ach motor end-plate release)
  • Increases NMB with aminoglycoside abx
  • May cause significant hypotension when used concurrently with antihypertensives
  • decreased uterine tone
62
Q

What is the goal DBP in treatment of HTN in pre-eclampsia?

A

DBP 90-100 mmHg

63
Q

What is the antihypertensive of choice?

A

hydralazine - vasodilates arterioles and increases HR, increasing CO, and improves placental blood flow

64
Q

What is the 2nd line of therapy for HTN with pre-eclampsia?

A

labetalol - vasodilates without increased HR, also improves placental blood flow

65
Q

What is the dose of hydralazine?

A

5-10 mg IV q20 mins to maximum of 60 mg (remember delayed onset time of ~20 mins)

66
Q

What is the dosing of labetalol?

A

step-wise IV dosing (20-40-80 mg) q10 mins to maximum of 300 mg

67
Q

What is the dose of nifedipine?

A

10-40 mg PO TID

68
Q

What is the dosing of nitroprusside?

A

0.2-10 mcg/kg/min IV, increased prn

69
Q

What differentiates eclampsia from pre-eclampsia?

A

seizure activity

70
Q

When can eclampsia occur?

A

up to 48 hours post partum

71
Q

What is the maternal and fetal mortality rate from eclampsia?

A

maternal - 1%

fetal - 12%

72
Q

When do majority of seizures with eclampsia occur?

A

prior to delivery (75%, 25% prior to onset of labor and 50% occur during labor)

73
Q

What type of seizures are associated with eclampsia?

A

tonic-clonic, lasting 60-70 secs, followed by post-ictal phase

74
Q

What is the treatment for eclampsia?

A
  • clear/secure airway as indicated (don’t intubate unless become hypoxic)
  • administer oxygen
  • left uterine displacement
  • initiate MgSO4 therapy
  • C-section usually elected shortly after eclamptic seizure, though labor may be induced if cervix is favorable
75
Q

What are some anesthetic implications for a c-section with an eclamptic patient?

A
  • stabilize patient prior to c-section to prevent further renal impairment due to surgical stress
  • may need swan-ganz catheter and a-line
  • GETA usually done because thrombocytopenia/coagulopathy contraindicate regional anesthesia and airway is secured
76
Q

What is HELLP syndrome?

A

defined as Hemolysis, Elevated Liver enzymes, and Low Platelet count

77
Q

When can HELLP syndrome occur?

A

occurs in 10% of pre-eclamptics and 30-50% of eclamptics

78
Q

How is the liver affected by HELLP?

A

hepatocellular necrosis and liver dysfunction occur which can cause DIC and hemorrhage

79
Q

What is “vertical transmission” of HIV?

A

transmission from mother to infant

  • 25% in untreated women
  • 2% in treated women
80
Q

What is the mean survival time of HIV infected infants?

A

10 years

81
Q

When can vertical transmission occur?

A
  • prenatally
  • intrapartum (most common)
  • breastfeeding
82
Q

What are the 2 routes of transmission of HIV from mother to fetus?

A
  • hematologically across the placenta

- across the amniotic membranes (especially if inflamed/infected)

83
Q

How does intrapartum transmission occur?

A

neonatal contact with maternal blood and cervicovaginal secretions, transmission rate increases with time and amount of neonatal exposure

84
Q

How can postnatal transmission of HIV be prevented?

A

no breastfeeding

85
Q

What is the treatment of HIV during pregnancy?

A

prenatal, perinatal, and fetal postnatal antiviral therapy along with elective c-section, lowers vertical transmission rate as low as 2%

86
Q

What are the CDC guidelines for prenatal antiviral treatment?

A

Zidovudine (AZT, ZDV, Retrovir) 300 mg PO bid

87
Q

What are the CDC guidelines for perinatal antivital treatment?

A

continuous IV zidovudine infusion at 1 mg/kg/hr, discontinue with cord clamping

88
Q

What are the CDC guidelines for postnatal antivital treatment?

A

Zidovudine within the first 6-12 hours of life until 6 weeks old, may be discontinued at 6 weeks if HIV tests are negative

89
Q

When should rupture of the membranes (ROM) occur with HIV mom?

A

after elective c-section

90
Q

What is the most common coexisting medical condition affecting reproductive-aged women?

A

asthma

91
Q

What is the course of asthma during pregnancy?

A

1/3 improve
1/3 remain normal
1/3 become worse
- pregnancy can have any effect on asthma

92
Q

Which gestational weeks tend to be most difficult for asthmatics?

A

24-36 because of displacement of the diaphragm and reduced FRC

93
Q

When does asthma severity return to baseline?

A

3 months post-partum

94
Q

What is the treatment of asthma during pregnancy?

A
  • control and avoidance of triggers (allergens, irritants, GERD, UTIs, exercise)
  • pharmacotherapy (uncontrolled asthma poses greater risk to fetus than medications during pregnancy)
95
Q

What is the outpatient asthma pharmacotherapy regimen?

A
  • inhaled corticosteroids
  • beta 2 agonists as rescue med.
  • theophylline (3rd line treatment)
  • leukotriene receptor antagonists/synthesis inhibitors (singulair, accolate, zyflo), role in pregnancy unclear
96
Q

What is the treatment of acute asthma exacerbation?

A
  • oxygen (should be used liberally, maintain O2 sats >95%)
  • systemic corticosteroid course
  • beta 2 agonists (administered via nebulizer or MDI with spacer, ipatropium may be added)
  • theophylline (limited use in acute exacerbations)

Principles III (12 decks)

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