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EOR Exam - Women's Health > Obstetrics Part 2 > Flashcards

Obstetrics Part 2 Flashcards

1
Q

Differentiate between augmentation and induction as it relates to labor and state how they are achieved.

A

Aug: inc already present contractions
Induc: initiating labor before spontaneous onset.
Both performed via PGs, oxytocic agents, mechanical dilation, artificial ROM

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2
Q

What is used to predict the success of labor induction and how is it evaluated?

A

Bishop Score –> rates five categories - position of cervix, consistency of uterus, effacement, dilation, and station - scored on a scale from 0 to 2 or 3 with zero being least favorable. Bishop score < 5 predicts failed induction as much as 50% of the time.

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3
Q

Define station of labor.

A

Rates the position of the baby’s head (or other presenting part) in relation to the ischial spines of the pelvis.

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4
Q

If a patient scores 5 or less on Bishop Scale, what can be done to improve likelihood of induction success?

A

PGE2 gel, pessary, or miso used to ripen the cervix.

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5
Q

What are the contraindications to induction of labor?

A

asthma, glaucoma, prior section, non reassuring fetal testing

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6
Q

What signs seen in fetal monitoring indicate potential need for augmentation/induction?

A

HR > 160 indicating distress secondary to hypoxia, infection, or anemia.
Decels > 2 minutes with HR < 90 requires immediate action.

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7
Q

Define and describe decelerations during labor.

A

Decreases in fetal HR furing labor that are characterized as either early, variable, or late relative to uterine contractions.

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8
Q

Define early deceleration.

A

Symmetrical decrease and return of FHR associated with uterine contraction. Nadir of HR will correspond to peak of contraction strength

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9
Q

Define variable deceleration.

A

Occur at any time and drop more precipitously than early or late decels.

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10
Q

Define late deceleration.

A

Start at the peak of contraction and return to baseline after contraction has concluded.

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11
Q

Which deceleration pattern is most worrisome?

A

Late

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12
Q

How should repetitive decels be managed and what is the contraindication to this management?

A

Monitoring with fetal scalp electrode.

CI: Maternal hepatitis or HIV or fetal thrombocytopenia

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13
Q

Define the three categories of fetal HR tracing.

A

1: Normal - normal baseline, moderate variability, and no variable or late decelerations
2: Indeterminate - many different tracings. Could be variable/late decels, brady, tachy, etc.
3: Abnormal - absent variability plus recurrent late/variable decels or bradycardia. Sinusoidal pattern also abnormal (cat 3)

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14
Q

What does a sinusoidal fetal HR tracing indicate?

A

Fetal anemia

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15
Q

Define Montevideo Units.

A

Method of measuring uterine contractions. Intrauterine Pressure Catheter (IUPC) monitors changes that are summed over a 10 minute period. 200 or above is adequate.

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16
Q

If fetal HR tracing is concerning, what additional monitoring may be done and what values are normal or concerning?

A

Fetal scalp pH to assess for fetal hypoxia and acidemia. Reassuring when pH > 7.25 is reassuring. Bad when pH < 7.20. Normal fetal SpO2 > 30%.

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17
Q

Describe the VEAL CHOP acronym used to categorize decelerations.

A 
Variables = Cord compression
Early = Head compression
Accelerations = Ok
Late = Placental insufficiency (worst)
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18
Q

What is the most common cause of infant morbidity and mortality in the developed world?

A

Pre-term labor

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19
Q

Define pre-term labor.

A

Sustained, progressive uterine contractions which lead to cervical dilatation and effacement between 20 and 37 weeks gestation

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20
Q

What is the term for sustained uterine contractions before 20 weeks gestation?

A

Inevitable spontaneous abortion.

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21
Q

What are the fours broadly classified causes of preterm uterine contractions?

A
  1. pathologic uterine distension
  2. decidual hemorrhage and abruption
  3. exaggerated response to infection/inflammation
  4. premature HPA axis activation s/p maternal or fetal stress.
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22
Q

What are the 2 primary causes of pathological uterine distension?

A

Multiple gestation and polyhydraminos

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23
Q

What is the decidua and what is the primary cause of damage to the decidual blood vessels?

A

Decidua: modified endometrium ion pregnancy

Damage most commonly s/p maternal HTN

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24
Q

Describe the pathophysiology of inflammation or infection leading to premature uterine contractions.

A

Activation of tissue necrosis factor (TNF) causes increased apoptosis of amniotic epithelial cells and PROM.

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25
Q

Describe the pathophysiology of HPA axis activation causing premature uterine contractions.

A

Inc ACTH –> inc cortisol –> inc corticotropin releasing hormone –> activation of PGs –> PGs cause cervical ripening and rupture of membranes.

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26
Q

What is Ehlers-Danlos Syndrome and how does it impact pregnancy?

A

EDS is a genetic disorder causing weakened connective tissue s/p impaired collagen formation. EDS causes cervical incompetence increasing risk for premature or precipitous labor. Also increased risk for fetal injuries and maternal bleeding during labor.

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27
Q

Define cervical insufficiency.

A

Inability of the cervix to retain a pregnancy without uterine contractions –> aka cervical ripening that occurs far from term. Rarely occurs in isolation. More commonly part of a complex preterm syndrome.

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28
Q

List common congenital and acquired causes of cervical insufficiency.

A

Con: EDS and other collagen disorders, uterine anomalies, in utero diethylstilbestrol (synthetic estrogen) exposure
Acq: Cervical trauma, rapid mechanical dilation, treatment of cervical intraepithelial neoplasm

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29
Q

What is the common presentation of cervical insufficiency and how is diagnosis commonly made?

A

S/S: asymptomatic or pelvic pressure, vaginal discharge, and mild uterine contractions. Pelvis in late pres is soft, effaced, and dilated with prolapsed or ruptured membranes.
Dx: Usually dependent on recurrent mid-trimester loss, risk factors, and transvaginal US measurement showing shortened cervical length.

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30
Q

How is cervical insufficiency managed?

A

Patients with Hx of cervical insufficiency should have cerclage (single stitch to keep cervix closed) at 12-14 weeks gestation. Patients should also be educated to avoid coitus during pregnancy.

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31
Q

What measurement of the cervix is diagnostic for cervical insufficiency and what measurement is normal?

A

Lentgth < 25mm on transvaginal US is diagnostic

Normal length is 40mm

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32
Q

What is the definition of low birth weight?

A

< 2500g

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33
Q

List risk factors for low birth weight.

A

PROM, chorioamnionitis, multiple gestations, uterine anomalies, pre-pregnancy weight < 50kg, Hx of pre-term delivery, abruption, infections, intra-abdominal disease/surgery, low socioeconomic status, smoking, cocaine.

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34
Q

Describe general management strategies for treatment of pre-term labor.

A

Bed rest, hydration, Abx if infection, Steroids for fetal lung maturity, tocolytics, cerclage.

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35
Q

How does maternal hydration status affect labor?

A

ADH is similar to oxytocin and will cause contractions. Dehydration = inc ADH = inc contractions.

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36
Q

Which steroid is used to decrease fetal respiratory distress syndrome in pre-term labor?

A

Betamethasone (celestone)

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37
Q

Which medications are used as tocolytics (decrease uterine contractions) during pre-term labor? HINT: Acronym “It’s Not My Time”

A

I: Indomethacin (inhibits PGs)
N: Nifedipine (CCB inhibits Ca entry into cells)
M: Magnesium Sulfate (acts as Ca antagonist)
T: Terbutaline

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38
Q

What are the AEs associated with magnesium sulfate?

A

flushing, HA, fatigue, diplopia, N/V, muscle weakness, decrease DTRs

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39
Q

What is a toxic level of magnesium sulfate and what results at toxic levels? What is the therapeutic serum level?

A

> 10 mg/dl can cause respiratory depression, hypoxia, and cardiac arrest
Therapeutic range = 4.2 - 8.4 mg/dl

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40
Q

What is the antidote for magnesium sulfate toxicity?

A

Calcium gluconate

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41
Q

What is the dosing for magnesium sulfate in the management of pre-term labor?

A

6g bolus over 15-30 min followed by 2-3 g/hr infusion

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42
Q

What is the black box warning for terbutaline?

A

may cause maternal cardiac events and death s/p tachycardia, hyperGLC, hypoK, pulmonary edema.

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43
Q

What is administered to patients with risk factors to reduce rate of pre-term labor/death?

A

Weekly injections of 17-alpha hydroxyprogesterone caporate from 16 - 36 weeks.

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44
Q

Define PROM.

A

Premature Rupture Of Membranes –> rupture prior to onset of labor or regular uterine contractions.

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45
Q

What are the major complication risks of PROM?

A

infection and cord prolapse

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46
Q

What combination of S/S is considered diagnostic for PROM?

A

Sudden gush of clear or pale yellow fluuid after 38 weeks and pooling of amniotic fluid in vaginal formix.

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47
Q

If clinical diagnosis of PROM is unclear, what lab testing may be performed? Describe a positiv efinding of the test.

A

pH testing of vaginal fluid using nitrazine paper.
Normal: amniotic pH = 7.0-7.3, vag. fluid pH = 3.8-4.2
Strips turn blue if vag fluid > 6.0 indicating presence of amniotic fluid.

48
Q

What evaluation of vaginal fluid is considered a secondary method of diagnosing PROM?

A

Presence of arborization (aka ferning) on microscopic evaluation.

49
Q

What is a final method of evaluation for PROM if diagnosis remains uncertain after all other testing?

A

US for oligohydraminos (reduced amniotic fluid. Normal amniotic fluid level on US essentially r/o PROM.

50
Q

What evaluation should be avoided if PROM is suspected?

A

Digital exam

51
Q

What is the treatment for PROM at gestation of 37 or greater?

A

Hospitalize and monitor, induce labor with oxytocin or PG cervical gel.

52
Q

What is the treatment for PROM before 37 weeks gestation?

A

Abx: ampicillin +/- erythromycin
May add tocolytics and/or steroids
Daily non-stress test/biophysical profile of fetus
Most common to deliver at 34 weeks

53
Q

What is the management for a fetus that is small for gestational age (SGA)?

A

Treat underlying etiology
No mgmt if SGA consistent throughout pregnancy
Biophysical profile if SGA acute

54
Q

Define macrosomia and state how it is managed.

A

Def: birth weight > 4500g. Fetal weight greater than 90th percentile at any gestation is concerning. Management is avoid excessive maternal weight gain and induce labor before macrosomia.

55
Q

What are risk factors for macrosomia?

A

Maternal obesity, Pre-pregnancy DM.

56
Q

Define oligohydraminos and state the risk of perinatal fetal mortality?

A

Def: too little amniotic fluid. In absence of PROM, it is associated with 40 fold increase in perinatal mortality.

57
Q

How is diagnosis of oligohydraminos made?

A

Amniotic fluid index (AFI) < 5cm measured by US

58
Q

Where is amniotic fluid produced?

A

Fetal lungs and kidneys

59
Q

What is the treatment of oligohydraminos?

A

Dependent on etiology –> induce labor and/or dilute meconium to decrease aspiration risk

60
Q

How is diagnosis of polyhydraminos made?

A

AFI > 20-25cm by US

61
Q

What complications are associated with polyhydraminos?

A

Cord prolapse, fetal structural and chromosomal abnormalities, hydrops fetalis, neural tube defects, obstruction of fetal alimentary canal. R/F - maternal DM (pre-preg or gest), and multiple gestations.

62
Q

How is polyhydraminos diagnosed and treated?

A

Dx: US, Tx: rupture of membrane

63
Q

Describe the pathophysiology of Rh incompatibility.

A

Mother = Rh (-) and fetus is Rh (+). Maternal abs cross the placenta and cause hemolysis of fetal RBCs. Result is erythroblastosis and hydrops causing a hyperdynamic state, HF, edema, ascites, pericardial effusion.

64
Q

Define hydrops fetalis.

A

Accumulation of excess fluid in at least 2 body compartments.

65
Q

What is used to prevent Rh incompatibility?

A

RhoGAM if any risk –> 300mg

66
Q

What risks indicate need to administer RhoGAM?

A

Any time maternal and fetal blood could have mixed in Rh (-) woman –> miscarriage, amniocentesis, maternal trauma in delivery

67
Q

What is the timing of RhoGAM administration when indicated?

A

at 28 weeks gestation and within 72 hours of delivery.

68
Q

What is anti-D immunoglobulin and when is it administered?

A

Anti-D IG neutralizes any abs against Rh antigen. Given to Rh (-) mothers within 72 hours of delivery of an Rh (+) baby to prevent sensitization of the mother.

69
Q

What test can be used to determine presence if fetal blood is present in maternal circulation when risk of mixing is high?

A

Kleihauer-Betke test

70
Q

How is pregnancy managed when death of the fetus is confirmed prior to delivery?

A

< 20 weeks: dilation and evacuation with mifepristone (progesterone antagonist) and misoprostil (induce contractions)
> 20 weeks: induce labor
Test for etiology

71
Q

What is the normal effect of pregnancy on maternal BP?

A

BP decreases early in pregnancy with nadir at mid-second trimester followed by progressive return to baseline at delivery.

72
Q

What is the triad of S/S associated with pre-eclamspia?

A

non-dependent edema, HTN, proteinuria

73
Q

What are risk factors for pre-eclampsia?

A

Chronic HTN, renal disease, DM, advanced maternal age, African-American, any auto-immune disease (SLE, etc.), pre-eclampsia Hx, nulliparity, multiple gestation, abnormal placenta.

74
Q

What S/S are associated with mild pre-eclampsia?

A

2 BP measurements > 140/90 taken 4-6 hours apart
Proteinuria > 300mg per 24 hours
Non-dependent edema (usually face or hands)
Proteinuria of 1+ on 2 occasions or 2+ at any time.

75
Q

What does it mean when proteinuria is designated as 1+, 2+, etc?

A

Such a scale is used to estimate amount of protein in urine when a quantitative test wasn’t performed.

76
Q

What S/S are associated with severe pre-eclampsia?

A 
Severe HA not relieved by APAP
Visual changes, scotoma (blind spot)
SBP > 160 or DBP > 110
Pulmonary edema
Acute renal failure with inc creatinine
Oliguria < 500 ml/day
RUQ abdominal pain with elevated AST and ALT
Platelets < 100,000
Hemolytic anemia
DIC
Intrauterine growth restriction
Abnormal umbilical doppler (US showing flow through umbilical artery)
77
Q

What is the goal in pre-eclampsia and how is this accomplished?

A

Prevent eclampsia with maternal BP control (hydralazine, nifedipine, or labetalol) and delivery of baby. May use magnesium sulfate for seizure prophylaxis. Try to hold off delivery until 32 weeks gestation.

78
Q

How is a pre-eclampsia patient managed after delivery?

A

Effects can linger for weeks - continue magnesium and BP control until marked improvement.

79
Q

When are corticosteroids indicated for pre-eclampsia?

A

Presence of HELLP syndrome –> hyemolysis, elevated liver enzymes, and low platelets.

80
Q

What is done to reduce pre-eclampsia risk in a patient with pre-eclampsia Hx?

A

Low dose ASA or calcium supplementation.

81
Q

What is the sign of eclampsia and what is the treatment?

A

Seizures –> treat with magnesium

82
Q

What findings are required to diagnose HELLP Syndrome?

A

At least 2 of:

  • Abnormal blood smear (achistocytes, burr cells)
  • bilirubin > 1.2
  • low haptoglobin
  • Significant dec in Hgb unrelated to blood loss
  • AST/ALT more than 2x upper limit of normal
  • Platelets < 100,000
83
Q

What is the treatment for HELLP syndrome?

A

Delivery

84
Q

What blood lab abnormalities are found in acute fatty liver disease during pregnancy?

A

Increased ammonia, BGL < 50 mg/dl, decreased fibrinogen, decreased antithrombin III.

85
Q

How often do eclamptic seizures occur before, during, and after labor?

A

25% before, 50% during, 25% after

86
Q

How is chronic HTN treated in pregnancy?

A

Labetalol, nifedipine, baseline CrCl and ECG

87
Q

Define pregnancy induced HTN.

A

HTN that manifests after 20 weeks with no other S/S.

88
Q

How is asthma treated differently in pregnancy?

A

No difference in treatment - all asthma meds safe.

89
Q

Describe the pathophysiology of gestational DM.

A

Impairment in carbohydrate metabolism s/p pancreatic B-cell dysfunction and tissue insulin resistance. Postprandial BGL elevated. Fasting BGL may be elevated.

90
Q

What complications are associated with gestational DM?

A

Fetal: macrosomia and birth injuries, hypoGLC, hypoCa, hyperbilirubinemia, and polycythemia at birth, delayed lung maturity.
Maternal: pre-eclampsia, traumatic birth/shoulder dystocia, 4-10 fold increased risk of future T2D

91
Q

What are the risk factors of developing gestational DM?`

A

Previous large for gestational age infant, obesity, age > 25, family Hx of DM, race - African American, Asian, Hispanic, American Indian

92
Q

Describe how gestational DM is diagnosed.

A

Patients usually asymptomatic. All screened at 24-28 weeks with glucose tolerance test. Start with 50g GLC test: BGL of >130-140 at 1 hour is positive. When positive, 100g GLC test. Pos. if: >90 before test (fasting), >165-180 at 1hr, >145-155 at 2hr, or >125-140 at 3hr.

93
Q

What fetal monitoring is performed, and when, in a mother diagnosed with gestational DM?`

A

biophysical profile and non-stress test at 34 weeks.

94
Q

What post-partum testing is done in a mother diagnosed with gestational DM?

A

Screen for DM 6 weeks post-partum and at yearly intervals after that.

95
Q

What is the management of gestational DM?

A

Mild exercise, 2200 cal/day with 200-220 from carbs, regular GLC checks in morning and after meals, induce labor at 40 weeks (well controlled) or 38 weeks (not well controlled).

96
Q

When is insulin therapy indicated in gestational DM?

A

Short-acting plus intermediate insulin if fasting GLC > 105 or 2hr GLC > 120.

97
Q

What is the risk of developing T2D after being diagnosed with gestational DM?

A

25-35% develop T2D. Lifetime risk is 50%. Risk of recurrence is 60-90%.

98
Q

What is the primary risk when a DM patient becomes pregnant?

A

4x more likely to develop pre-eclampsia/eclampsia.

99
Q

Describe the management of a DM patient during pregnancy.

A

T1D: Aggressive GLC control. Maintain A1C 6-6.5. Monitor thyroid function. Slight inc in insulin req 1st half of pregnancy. Significant inc in insulin 2nd half.
T2D: Typically req insulin (PO hypoglycemics may be teratogenic). Weekly NST and BPP 32-36 weeks.

100
Q

Define interhepatic cholestasis of pregnancy and state how common it is.

A

Impaired release of bile from liver during pregnancy. Most common in third trimester. Recurs in over half of pregnancies.

101
Q

What are the S/S of interhepatic cholestasis of pregnancy?

A

Pruritis concentrated on palms of hand and soles of feet, elevated serum bile acids and LFTs.

102
Q

What is the treatment of interhepatic cholestasis of pregnancy?

A

Ursodeoxycholic acid –> inc hepatic bile flow. Induction of labor at 36-37 weeks.

103
Q

What is the primary risk of interhepatic cholestasis of pregnancy?

A

Intrauterine fetal demise –> most common after 37 weeks.

104
Q

Describe the risk and treatment of urinary infections in pregnancy.

A

5% have increased risk of cystitis and pyelonephritis s/p asymptomatic bateriuria. Lower UTIs treated with PO abx. Pyelonephritis require IV abx. Symptomatic bacterial vaginosis associated with pre-term delivery –> treat with metronidazole x 7 days.

105
Q

What is the leading cause of noenatal sepsis and when is screening performed?

A

Group B Strep –> Screen at 35 and 37 weeks.

106
Q

How is chorioamnionitis diagnosed and treated?

A

Maternal fever, uterine tenderness, elevated maternal WBCs, fetal tachycardia.
Treated with IV abx and delivery.

107
Q

How is hyperemesis gravidarum diagnosed and when is it most common?

A

Persistent vomiting, weight loss > 5% of pre-pregnancy weight, ketonuria. Most common in molar pregnancy.

108
Q

What is the treatment for hyperemesis gravidarum?

A

1st: phenergan –> then Reglan, compazine, or etigan –> droperidol and zofran.
Rehydrate and give electrolyte solution. Corticosteroids if condition persists.

109
Q

How are patients with seizure disorder managed during pregnancy?

A

Taper to lowest possible dose monotherapy. May stop meds if seizure free for > 2 years. Many seizure meds are teratogenic.

110
Q

How is hyperthyroidism and hypothyroidism managed during pregnancy?

A

Hyper: Serial NSTs, PTU and methimazole at minimum dose.
Hypo: increase levothyroxine dose

111
Q

How is SLE treated in pregnancy?

A

Stop: cyclophosphamide and methotrexate
Continue: ASA, heparin, steroids

112
Q

What are the fetal risks of alcohol use in pregnancy?

A

growth retardation, CNS effects, abnormal facies

113
Q

How is alcohol withdrawal managed in pregnancy?

A

Barbiturates –> benzos are teratogens

114
Q

What are the fetal risks of smoking during pregnancy?

A

spontaneous abortion, pre-term birth, placental abruption, low birth weight, SIDS, respiratory distress.

115
Q

What are the fetal risks of cocaine use in pregnancy?

A

placental abruption, pre-term labor/delivery, intrauterine growth retardation (IUGR).

116
Q

What are the fetal risks of opiate use in pregnancy?

A

Non-teratogenic. Major risks in withdrawal –> miscarriage, pre-term delivery, fetal death. Treat with suboxone or methadone.

117
Q

What seizure medication is specifically contraindicated in pregnancy and which is used in its place?

A

Depakote (valproic acid). Keppra is DOC or may also use lamictil.

EOR Exam - Women's Health (7 decks)

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