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OBGYN > High Risk OB > Flashcards

High Risk OB Flashcards

1
Q

What is the difference between GDMA1 and GDMA2?

A

A1 refers to GDM that is diet-controlled while A2 refers to GDM that requires medical therapy

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2
Q

What hormone causes insulin resistance during pregnancy, leading to GDM?

A

human placental lactogen

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3
Q

What are the two primary effects of human placental lactogen?

A
  • reduce insulin sensitivity/reduce glucose uptake

- promote lipolysis

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4
Q

Why is the use of urinary glucose levels of little help in the management of diabetes during pregnancy?

A

because there is an increase RBF and normal glucosuria of pregnancy in all patients

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5
Q

What causes glycosuria of pregnancy?

A

an increase in renal blood flow

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6
Q

What are the major fetal complications of gestational diabetes?

A
  • congenital anomalies, particularly affecting the heart, CNS, kidneys, and limbs; possibly sacral agenesis
  • spontaneous abortion or stillbirth
  • macroscomia or intrauterine growth restriction secondary to placental insufficiency
  • polyhydramnios
  • neonatal hypoglycemia, hyperbilirubinemia, hypocalcemia, or polycythemia
  • respiratory distress syndrome
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7
Q

Gestational diabetes is associated with what kinds of congenital anomalies?

A
  • cardiac, CNS, renal, and limb

- sacral agenesis is a rare but unique complications

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8
Q

Polyhydramnios is a risk factor for what three pregnancy complications?

A
  • placental abruption
  • preterm labor
  • postpartum uterine atony
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9
Q

What are the major maternal risks associated with pregestational diabetes during preganncy?

A
  • pre-eclapsia
  • progression from diabetic nephropathy to end-stage renal disease
  • worsening diabetic retinopathy
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10
Q

How do we screen for gestational diabetes?

A
  • a 50g, 1-hour oral glucose challenge between 24-28 weeks to start
  • patients whose glucose value exceeds the cut-off then undergo a 100g, 3-hour oral glucose tolerance test
  • two or more abnormal results of the 3-hour test establish the diagnosis
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11
Q

What are the blood sugar goals for patients with gestational diabetes?

A
  • fasting levels less than 95 mg/dL

- 1-hour post-prandial levels less than 140 mg/dL or 2-hour post-prandial levels less than 120 mg/dL

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12
Q

How is gestational diabetes managed during pregnancy?

A
  • patients should obtain morning fasting glucose levels as well as pre- and post-prandial levels throughout the day
  • the goal is fasting levels less than 95 and 1-hour postprandial levels less than 140 or 2-hour postprandial levels less than 120
  • the mainstay for therapy is insulin because oral hypoglycemics are thought to provide less optimal outcomes and more long-term effects on those exposed in utero
  • Glyburide and metformin are the preferred agents when oral hypoglycemics are used in pregnancy
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13
Q

How is gestational diabetes managed during labor, delivery, and the postpartum period?

A
  • most patients undergo induction at 39 weeks if well-controlled
  • once active labor begins or glucose levels decrease to 70 mg/dL, a constant glucose infusion of D5 is initiated at a rate of 100-150 mL/hr to maintain a glucose level of 100 mg/dL
  • we also monitor for material ketonuria
  • glucose tolerance screening is re-performed at 4-12 weeks postpartum and again every 1-3 years thereafter
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14
Q

Gestational Diabetes

A
  • divided into A1 and A2 depending on if it is diet- or medically controlled
  • caused by human placental lactogen which promotes lipolysis and inhibits glucose uptake
  • screen for using a 1-hour, 50g oral glucose challenge with a threshold between 130-140; diagnose with a 3-hour, 100g challenge if two time points are abnormal
  • risks to the fetus include cardiac, CNS, renal, and limb anomalies, including sacral agenesis; spontaneous abortion or stillbirth; macrosomia; polyhydramnios; and neonatal hypoglycemia, hyperbilirubinemia, hypocalcemia, polycythemia, and respiratory distress syndrome
  • maternal risks include pre-eclampsia, worsening renal status, and worsening diabetic retinopathy
  • manage primarily with insulin rather than oral hypoglycemic agents; goal is fasting less than 95 and 1 hour postprandial less than 140 or 2 hour postprandial less than 120
  • use D5 during active labor to maintain a glucose level of 100 mg/dL and monitor for ketonuria
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15
Q

What is postpartum thyroiditis?

A

an autoimmune inflammation of the thyroid gland that presents as new-onset, painless hypothyroidism, transient thyrotoxicosis, or thyrotoxicosis followed by hypothyroidism within 1 year postpartum

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16
Q

Describe changes in TSH, total T4, free T4, and TBG during pregnancy.

A
  • TSH initially declines as B-hCG levels rise and stimulate thyroid receptors, but then return to normal as B-hCG levels drop around week 10
  • total T4 and TBG increase until about week 20 when they plateau; because they both increase, free T4 levels stay relatively constant through pregnancy
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17
Q

What happens to the thyroid gland during pregnancy?

A

it increases in size due to a decline in plasma iodide levels

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18
Q

How do we screen for thyroid problems during pregnancy?

A
  • routine screening is not recommended
  • but for those with evidence to warrant screening, TSH levels are measured since TSH does not cross the placenta and thus is an accurate measure of hormone function during pregnancy
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19
Q

Compare and contrast the use of methimazole and PTU for management of hyperthyroidism during pregnancy.

A
  • methimazole crosses the placental more and causes greater fetal thyroid suppression
  • methimazole has thus been associated with reports of aplasia cutis and choanal atresia
  • for this reason, methimazole is avoided during the first trimester
  • PTU has greater hepatotoxicity and thus isn’t recommended beyond the first trimester
  • both are compatible with breastfeeding
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20
Q

When does nausea and vomiting of pregnancy typically begin and resolve?

A

typically begins before 9 weeks gestation, peaks between 7-12 weeks, and resolves by 16 weeks

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21
Q

Nausea and Vomiting of Pregnancy

A
  • classified as mild (nausea alone), moderate (n/v), and severe (n/v leading to dehydration)
  • hyperemesis gravidarum is the most severe form, associated with ketonuria, dehydration, and significant weight loss
  • risk factors include multiple gestation, molar pregnancy, and personal or family history of hyperemesis gravidarum
  • typically begins before 9 weeks gestation, peaks between 7-12 weeks, and resolves by 16 weeks, in association with changing B-hCG levels
  • associated with lower miscarriage rates and the only negative effect is the impact on quality of life
  • can often be treated with lifestyle modification but first line medical therapy is vitamin B6 with or without the H1-antagonists doxylamine
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22
Q

What is hyperemesis gravidarum? What are the risks associated with it?

A
  • a severe form of nausea and vomiting of pregnancy, which is associated with ketonuria, dehydration, significant weightless, and biochemical hyperthyroidism
  • it is the most common indication for hospital admission in the first half of pregnancy
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23
Q

What are the risk factors for nausea and vomiting of pregnancy?

A

those associated with elevated hCG like multiple gestation or molar pregnancy as well as either a family or personal history of hyperemesis gravidarum

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24
Q

What is the preferred medical therapy for nausea and vomiting of pregnancy?

A

vitamin B6 with doxylamine

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25
Q

Intrahepatic Cholestasis of Pregnancy

A
  • a hepatic disorder unique to pregnancy
  • risk factors include multiple gestation and chronic hepatitis C
  • presents with generalized pruritus and elevated serum bile acid levels, typically in the second half of pregnancy
  • maternal risks are low but there is an increased risk of stillbirth and other fetal effects
  • diagnosed based on elevated fasting levels of bile acids, serum aminotransferases, and total and direct bilirubin concentrations
  • managed with ursodeoxycholic acid, which decreases plasma bile acid concentrations and improves itching
  • delivery is recommended at 37 weeks gestation
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26
Q

What labs are consistent with intrahepatic cholestasis of pregnancy?

A

elevated fasting bile acids, serum aminotransferases, and total and direct bilirubin

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27
Q

How is intrahepatic cholestasis of pregnancy managed?

A

ursodeoxycholic acid decreases plasma bile acid concentrations to improve itching and delivery is recommended at 37 weeks gestation

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28
Q

Acute Fatty Liver of Pregnancy

A
  • the most common cause of acute liver failure in pregnancy
  • may, in some cases, be caused by a recessive mitochondria abnormality of fatty acid oxidation similar to that seen in Reye-like syndromes
  • typically presents in the third trimester as persistent nausea and vomiting; other symptoms include hypertension, proteinuria, malaise, anorexia, abdominal pain, edema, and progressive jaundice
  • diagnosis is supported by elevated serum aminotransferases, elevated bilirubin, decreased fibrinogen levels, thrombocytopenia, leukocytosis, and liver dysfunction
  • liver biopsy, though rare, would show microvesicular steatosis and canalicular cholestasis
  • managed with delivery to stop further decline in liver function; recovery may be prolonged
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29
Q

What is the most common cause of acute liver failure in pregnancy?

A

acute fatty liver of pregnancy

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30
Q

What similarities do pre-eclampsia and acute fatty liver of pregnancy share? How are they best differentiated?

A
  • acute fatty liver may present with some combination of hypertension, proteinuria, and edema
  • acute fatty liver can be differentiated, however, because decreased fibrinogen levels, increased bilirubin, and liver dysfunction are rare in pre-eclampsia
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31
Q

How is acute fatty liver of pregnancy managed?

A

with delivery to halt the progression

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32
Q

What is the most common presentation of acute fatty liver of pregnancy?

A

persistent nausea and vomiting into the third trimester with declines in liver function

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33
Q

How does asymptomatic bacteriuria differ in pregnancy? Why?

A
  • in pregnancy, it is more likely to lead to cystitis and pyelonephritis
  • thought to be because of pregnancy-associated urinary stasis, glucosuria, and increased urine pH secondary to bicarbonate excretion
  • urinary stasis is secondary to progesterone-induced decreased ureteral tone and motility, mechanical compression of the ureters at the pelvic brim, and compression of the bladder and ureteral orifices
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34
Q

What three factors contribute to urinary stasis of pregnancy?

A
  • progesterone-induced decreased ureteral tone and motility
  • mechanical compression of the ureters at the pelvic brim
  • compression of the bladder and ureteral orifices
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35
Q

Urinary Tract Infections of Pregnancy

A
  • asymptomatic bacterium is more likely to lead to cystitis and pyelonephritis during pregnancy
  • due to progesterone-induce smooth muscle relaxation, mechanical compression of the ureters at the pelvic brim, compression of the bladder and ureteral orifices, increased bicarbonate excretion, and glucosuria
  • screen for asymptomatic bacteria at the onset of prenatal care and treat with ampicillin, cephalexin, or nitrofurantoin
  • suppressive antimicrobial therapy is indicated only if there are repetitive UTIs during pregnancy or if there is pyelonephritis during pregnancy
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36
Q

How are urinary tract infections treated during pregnancy?

A
  • we screen for and treat asymptomatic bacteriuria at the onset of prenatal care and treat with ampicillin, cephalexin, or nitrofurantoin
  • suppressive antimicrobial therapy is then used for those with repetitive UTIs
  • pyelonephritis is treated with cephalosporins or ampicillin and gentamicin followed by suppressive therapy
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37
Q

What symptoms are consistent with cystitis? With pyelonephritis?

A
  • cystitis presents with dysuria, urinary frequency, and urgency
  • pyelonephritis patients are more acutely ill with fever, costovertebral tenderness, general malaise, and often dehydration
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38
Q

What are the major complications of pyelonephritis in pregnancy?

A
  • increased uterine activity leading to preterm labor

- septic shock and maternal mortality

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39
Q

Pyelonephritis During Pregnancy

A
  • presents with fever, costovertebral tenderness, general malaise, and often dehydration
  • complicated by increased uterine activity and preterm labor or septic shock and maternal mortality
  • treated with a cephalosporin or ampicillin and gentamicin; consider tocolytics to prevent preterm labor and follow treatment with suppressive therapy
40
Q

Why does pyelonephritis lead to preterm labor?

A
  • because E. coli produce PLA, which promotes prostaglandin synthesis, driving uterine activity
  • furthermore, fever is known to induce contractions
41
Q

Describe the presentation and management of nephrolithiasis in pregnancy.

A
  • presents with symptoms similar to pyelonephritis, including costovertebral tenderness, general malaise, and urinary symptoms, but without fever
  • less likely to see renal colic in pregnant women because of the progesterone-induced relaxation of ureteral tone
  • likely to find microhematuria on UA
  • treat with expectant management and hydration
42
Q

How does pre-existing renal disease affect pregnancy outcome?

A
  • pregnancy outcome is related to the degree of serum creatinine elevation and presence of hypertension
  • creatinine less than 1.5 carries little risk, 1.5-3.0 has moderate risk, and above 3.0 has severe risk
  • added hypertension is associated with an increased incidence of intrauterine growth restriction in patients with chronic renal disease
43
Q

An acute abdomen in pregnancy has what gynecologic differential?

A
  • early in gestation, consider ectopic pregnancy and torsion

- later in pregnancy, consider placental abruption and uterine rupture

44
Q

Why are surgical cases more complicated during pregnancy?

A
  • requires monitoring of fetal status
  • the supine position needs to be avoided to prevent supine hypotensive syndrome
  • patients have lower residual lung volume and diminished reserve for respiratory function
  • delayed gastric emptying makes aspiration of stomach contents more likely
45
Q

Why is cholelithasis more common in pregnancy and how is it managed?

A
  • pregnancy is a risk factor for new-onset and exacerbation of cholelithiasis due to slowed gallbladder emptying and increased residual gallbladder volume
  • managed expectantly; use hydration, pain control, dietary restriction, and NG tube for biliary colic; progress to immediate surgical management for cholecystitis
46
Q

Why can appendicitis be more difficult to diagnose during pregnancy?

A

leukocytosis of pregnancy may mask the leukocytosis associated with appendicitis and the appendix may be displaced upward during pregnancy, shifting the expected location of abdominal pain

47
Q

Trauma during pregnancy may lead to what complications?

A

maternal injury and death, direct fetal injury, placental abruption, uterine rupture, fetal-maternal hemorrhage, PROM, or preterm labor

48
Q

How is trauma during pregnancy managed?

A
  • place the patient in the decubitus lateral tilt position if beyond 20 weeks gestation
  • monitor for at least four hours after minor trauma
  • if during those four hours there are signs of uterine tenderness, irritability or contractions, vaginal bleeding, rupture of membranes, or a non-reassuring fetal status continue monitoring for 24 hours
  • monitor for at least 24 hours after major trauma
49
Q

If a gravid woman undergoes cardiopulmonary arrest, how long after should cesarean delivery be considered? Why?

A
  • consider after 4 minutes of failed resuscitation because long-term outcomes for children are more likely to be favorable if the infant is delivered within five minutes of loss of maternal circulation and maternal resuscitation is also made easier by delivery
  • fetal survival is unlikely after 15-20 minutes without maternal circulation
50
Q

What aspect of CT and MRIs is generally contraindicated in pregnant patients?

A

CT and MRI without contrast are suitable for pregnant patients, but contrast is avoided

51
Q

Describe a tension headache and the preferred treatment during pregnancy.

A
  • they present as a painful pressure or tightness all around the head, originating over the forehead and radiating over the crown to the posterior neck
  • the preferred treatment is acetaminophen as NSAIDs are avoided during pregnancy
52
Q

What effect does pregnancy have on migraines?

A

most patients experience an improvement in the frequency and severity of migraines during pregnancy

53
Q

What is the preferred treatment for migraines during pregnancy?

A
  • acetaminophen is preferred, avoiding NSAIDs
  • acetaminophen may be combined with codeine, metoclopramide, or butalbital-caffeine
  • triptans are avoided because they cause vasoconstriction and increase uterotonic activity
  • beta-blockers and oral magnesium can be used as prophylaxis
54
Q

Describe the course and aggravating factors associated with postdural puncture headaches.

A
  • they generally develop within 48 hours of the procedure and resolve with another 48 hours
  • they are positional, worse with standing or sitting and relieved by lying supine
55
Q

What prenatal supplement is known for altering serum levels of many anti-epileptics?

A

high dose folate supplements

56
Q

What are the two major risks associated with epilepsy during pregnancy?

A
  • fetal injury, including abruption

- oxygen deprivation from a prolonged maternal seizure

57
Q

Which anti-epileptic carries the highest risk for congenital malformations? What is that particular malformation?

A

valproate greatly increases the risk neural tube defects

58
Q

What is carpal tunnel syndrome? Why is it more common during pregnancy and how is it managed?

A
  • it is a compression of the median nerve as it passes through the carpal tunnel, causing pain, tingling, and numbness
  • it is more common as pregnancy advances because fluid retention is thought to be a causative factor
  • managed with wrist splints
59
Q

How do we define perinatal depression?

A

as a major or minor depressive episode that occurs during pregnancy or during the first 12 months after delivery

60
Q

What risks are associated with perinatal depression?

A
  • poor compliance with prenatal care
  • inadequate nutrition
  • increased alcohol, tobacco, or other substance use
  • poor maternal-infant bonding
  • disruptive family environemnts
61
Q

Depression is a greater cause of maternal mortality than what other pregnancy complications?

A

hemorrhage and hypertensive disorders

62
Q

What medications are typically used to treat perinatal depression?

A

all SSRIs except paroxetine during the first trimester as it increases the risk for cardiac defects

63
Q

Postpartum Blues

A
  • an extremely common mood disorder arising in the postpartum period
  • characterized by depressed affect, tearfulness, and fatigue starting 2-3 days after delivery
  • treatment is supportive as it usually resolves in 10 days
  • follow-up for possible postpartum depression
64
Q

Postpartum Depression

A
  • irritability, labile mood, difficulty falling asleep, phobias, and anxiety, which are worse in the evening
  • typically arises 2 weeks to 12 months postpartum and lasts 3-14 months
  • preferred treatment is SSRIs
65
Q

Postpartum Psychosis

A
  • mood-congruent delusions, hallucinations, and thoughts of harming the baby or self
  • risk factors include history of bipolar or psychotic disorder, first pregnancy, family history, and recent discontinuation of a psychotropic medication
  • treat with hospitalization and initiation of atypical antipsychotics; ECT if necessary
66
Q

How is chronic hypertension defined with regards to pregnancy?

A

as hypertension present before pregnancy, before the 20th week of pregnancy, or beyond the postpartum period

67
Q

How is gestational hypertension defined?

A

hypertension that develops for the first time after 20 weeks gestation in the absence of proteinuria

68
Q

How is pre-eclampsia defined and what are the specific criteria for this definition?

A

the development of hypertension with proteinuria after 20 weeks of gestation

  • blood pressure with systolic greater than 140 or diastolic greater than 90
  • proteinuria defined as urinary excretion of 0.3g protein or higher in a 24-hour urine specimen
69
Q

What are severe features of pre-eclampsia?

A
  • blood pressure with systolic greater than 160 or diastolic greater than 110
  • renal insufficiency defined as serum creatinine greater than 1.1 or a doubling
  • cerebral or visual disturbances such as headache or scotomata, pulmonary edema, epigastric or RUQ pain
  • evidence of hepatic dysfunction
  • thrombocytopenia less than 100
70
Q

Why can RUQ pain be a symptom of pre-eclampsia?

A

it is likely pain caused by sub capsular hepatic hemorrhage or stretching of the capsule secondary to hepatocellular edema

71
Q

How do we define eclampsia?

A

as pre-eclampsia with the additional presence of convulsions, which can’t be explained by a neurologic disorder

72
Q

What are the features of HELLP syndrome?

A
  • microangiopathic hemolysis
  • elevated liver enzymes
  • low platelet count
73
Q

What is the predominant pathophysiologic finding in those with pre-e and gestational hypertension?

A

maternal vasospasm

74
Q

Describe the pathophysiology of pre-eclampsia.

A
  • a genetic predisposition contributes to inadequate trophoblastic invasion of maternal spiral arteries
  • this, combined with parity and maternal vascular disease, contribute to placental ischemia
  • placental ischemia leads to generalized endothelial cell injury, which then promotes vasospasm and vascular permeability manifesting as hypertension, proteinuria, and edema
75
Q

What vascular changes have been linked to the cause of maternal vasospasm and pre-eclampsia?

A
  • the normally trophoblast-mediated vascular changes in the uterine vessels such as decreased musculature in the spiral arterioles which is necessary for a low-resistance, low-pressure, high-flow system are inadequate
  • endothelial damage has also been noted within the vessels
76
Q

What prostanoid differences or changes have been linked as potential causes of pre-eclampsia?

A

a shift towards more TXA2 and less PGI2, which promotes vasoconstriction and platelet aggregation

77
Q

What changes have been postulated as potential causes of pre-eclampsia?

A
  • inadequate trophoblast-mediated vascular changes in the spiral arterioles
  • endothelial damage
  • increased platelet activation secondary to increased endothelial fibronectin and decreased antithrombin III and a2-antiplasmin
  • a shift toward TXA2 rather than PGI2, promoting vasoconstriction
  • a decrease in nitric oxide
78
Q

What happens to the kidneys in a patient with pre-eclampsia?

A

there is a decline in GFR secondary to atherosclerotic-like changes and vasospasm of renal vessels, leading to increased serum creatinine and uric acid, and the onset of proteinuria

79
Q

What are the neurologic consequences of pre-eclampsia?

A
  • hyperreflexia/hypersensitivity
  • headache
  • blurred vision or scotomata
80
Q

What causes pulmonary edema in those with pre-eclampsia?

A

decreased colloid oncotic pressure, pulmonary capillary leak, left heart failure, or iatrogenic fluid overload

81
Q

What are the fetal effects of pre-eclampsia?

A
  • decreased intermittent placental perfusion responsible for IUGR and oligohydramnios
  • increased risk of placental abruption
  • intrapartum uteroplacental insufficiency when the placenta is unable to adequately oxygenate the fetus during conrtactions
82
Q

What sort of peripheral edema is abnormal during pregnancy and may signal the onset of pre-eclampsia?

A

that which is unresponsive to resting in the supine position or involves the upper extremities, sacral region, or face

83
Q

How is chronic hypertension managed during pregnancy?

A
  • the major task is closely monitoring maternal blood pressure and watching for the superimposition of pre-eclampsia
  • antihypertensives are typically recommended for pressures greater than 160/105 in order to reduce the likelihood of stroke or major cardiac events
  • labetalol is considered first-line
  • other medications include calcium channel blockers like nifedipine or amlodipine or methyldopa
84
Q

Which medications are safe for the treatment of hypertension during pregnancy?

A

labetalol is the preferred treatment but hydralazine, calcium channel blockers, and methyldopa are other options

85
Q

How is pre-eclampsia without severe features managed?

A
  • with delivery if at term

- with rest and expectant management otherwise, including monitoring fetal growth and amniotic fluid features

86
Q

How is pre-eclampsia with severe features managed?

A
  • treatment with magnesium sulfate, antihypertensive therapy, and corticosteroids if fetal lung maturity is in question
  • delivery if patient is more than 34 weeks gestation or unstable; expectant management with frequent monitoring if less than 34 weeks and stable
87
Q

What is the therapeutic level of magnesium sulfate?

A

4-6 mg/dL

88
Q

How is magnesium toxicity reversed?

A

slow IV administration of 10% calcium gluconate

89
Q

What is the blood pressure goal when managing those with pre-eclampsia with severe features?

A

140-150/90-100 because less than this may impair uterine blood flow

90
Q

How is eclampsia managed?

A
  • begin IV administration of magnesium sulfate
  • stabilize the mother
  • deliver once stabilized or if seizures and uterine hyperactivity persist for more than 20 minutes
91
Q

What is the threshold for platelet transfusion in patients with HELLP?

A
  • 20K if it is a vaginal delivery

- 50K if it is a c-section

92
Q

What fetal risks are associated with maternal cardiac disease?

A

low birth weight and prematurity

93
Q

How should patients with cardiac disease be managed during the labor process?

A
  • they should labor in the lateral position
  • they should aim for a vaginal delivery to avoid the stresses associated with cesarean section
  • the second stage of labor should be shortened if possible, using forceps or vacuum, because cardiac output increases significantly during this stage
  • monitor them in the hours after since there is an additional 500 mL of blood volume added to the maternal circulation as the uterus contracts
94
Q

What is permpartum cardiomyopathy?

A

that which is identified in the last month of pregnancy or first 6 months following delivery

95
Q

Asthma carries what fetal risks?

A

low birth weight and prematurity

96
Q

What is the first line controller and rescue medication for asthma in pregnant patients?

A
  • budesonide inhaled corticosteroid is the controller

- inhaled albuterol is the preferred rescue

97
Q

Maternal flu carries what fetal risks?

A
  • exposure to hyperthermia
  • preterm labor secondary to the systemic inflammatory response
  • consequences of maternal hypoxia

OBGYN (21 decks)

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