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Study Guide Questions Flashcards

1
Q

Organisms associated w/ UTI/pyelo and alkaline urine

A

Proteus, Klebsiella, Ureaplasma

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2
Q

Placental transport mechanism – Amino Acids

A

Active transport

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3
Q

Placental transport mechanism – Glucose

A

Facilitated diffusion

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4
Q

Placental transport mechanism – placental transfer of medications

A

Passive transport/simple diffusion

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5
Q

Umbilical venous PO2 is always lower than….

A

Uterine venous PO2

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6
Q

Prostaglandin that causes uterine relaxation

A

Prostacyclin

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7
Q

Trinucleotide repeat # associated with pre-mutation fragile X

A

55-200

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8
Q

Anti-inflammatory cytokine

A

IL-10

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9
Q

Disease associated with repeats of DNA

A

Fragile X
Huntingtons
Myotonic dystrophy

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10
Q

Maternal viral infections not compatible with breastfeeding

A

HIV
active/untreated TB
?Varicella

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11
Q

Paternal exposures associated with early pregnancy loss

A 
Mercury
Lead
Pesticides
Hydrocarbons
Anesthetic gases
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12
Q

Paternal exposures NOT associated with early pregnancy loss

A

Atomic radiation
Agent orange
Recreational drugs

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13
Q

Time in pregnancy that ciprofloxacin is recommended

A

anthrax exposure/treatment

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14
Q

Antibiotic to avoid in Myasthenia Gravis

A

Gentamycin

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15
Q

Gaucher disease is missing which enzyme

A

Glucocerebrosidase

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16
Q

Canavan disease is missing what enzyme

A

Aspartoacylase

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17
Q

Tay-Sachs is missing what enzyme

A

Hexosaminidase A

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18
Q

Niemann-Pick is missing what enzyme

A

Sphingomyelinase

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19
Q

Anesthesia med used for epidural hypotension that will decrease maternal HR

A

Phenylephrine

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20
Q 
Chemo toxicities:
Adriamycin
Bleomycin
Methotrexate
Cisplatin
Cyclophosphamide
A
  • Heart
  • Pulm fibrosis
  • Stomatitis
  • Ototoxicity, renal toxicity
  • Ovarian function
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21
Q

Acrocentric chromosomes

A

13,14,15,21,22,Y

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22
Q

Neonatal conjunctivitis caused by _____ in first 2 weeks postpartum

A

C. trichomoniasis

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23
Q

Neonatal conjunctivitis caused by ______ at 21 days postpartum

A

N. gonorrhea

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24
Q

Neonates get ppx for conjunctivitis against which bacteria?

A

N. gonorrhea

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25
Q

If you have to do GETA on asthmatic, which meds are preferred?

A

Ketamine– bronchodilation

Propofol – airway reflexes

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26
Q

Acute treatment for Guillan-Barre

A

IVIG and plasmapheresis (steroids not effective)

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27
Q

MCDA risk of co-twin death following twin demise

A

10%

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28
Q

MCDA risk of co-twin neurologic abnormality following death of 1 twin

A

10-30%

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29
Q

% uterine blood flow going to endometrium

A

80-90%

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30
Q

Another name for prostacyclin

A

PGI2

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31
Q

Cervical ripening –> increased tissue vascularization….what drives this?

A

VEGF

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32
Q

With advancing GA there is an increased water content to the cervix to allow ripening/dilation….this is due to accumulation of what substance in cervix?

A

Hyaluronan content

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33
Q

True/False there is a genetic component to timing of parturition?

A

True

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34
Q

What hormone steeply rises before onset of labor?

A

Estrogen

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35
Q

How does the fetus contribute to starting labor?

A

Fetus is thought to influence placental steroid hormone production through activation of the fetal HPA axis

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36
Q

Steroids produced by fetal adrenal gland

A

DHEAS

Cortisol

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37
Q

How can fetal DHEAS become an estrogen?

A

Directly aromatized to estrone in the placenta
OR
16-hydroxylated in the fetal liver, then converted to estriol in the placenta

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38
Q

In order for estrogen synthesis in the placenta to occur what must be present?

A

Fetal C19 androgens as a steroid precursor

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39
Q

What happens to maternal CRH in pregnancy?

A

Increase, mostly in 3rd trimester and then decrease sharply after delivery

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40
Q

What is the source of elevated CRH in pregnant women?

A

Placenta

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41
Q

Placenta CRH production is up-regulated by what?

A

Fetal corticosteroids

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42
Q

Placental enzyme that protects the fetus from high levels of maternal glucocorticoids?

A

11B-HSD2 (11 beta-hydroxysteroid dehydrogenase)

Converts cortisol to cortisone (inactive form)

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43
Q

Where is progesterone receptor located?

A

Nucleus

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44
Q

Perimortem TTTS occurs due to what anastomoses

A

AA and VV…the blood from living twin preferentially streams into the low pressure dead or dying twin

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45
Q

Peripartum TTTS is due to what anastomoses

A

AA and VV

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46
Q

Causes of acute peripartum TTTS

A

Delayed cord clamping
Pressure differences from contractions
Changes in fetal position

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47
Q

Hormone levels that are higher in recipient twin of TTTS

A

ANP
BNP
ENDOTHELIN 1

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48
Q

Protective anastomoses in TTTS

A

AA

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49
Q

Are VV anastomoses higher or lower in TTTS? AA?

A

Higher VV

Lower AA

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50
Q

If one twin of TTTS has a velementous cord and or smaller placental share, is it the donor or recipient twin?

A

Donor

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51
Q

TAPS is defined as severe twin discordance in….

A

Hemoglobin

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52
Q

TAPS occurs due to

A

Small inter-twin anastomoses leading to chronic blood transfusion

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53
Q

Why doesn’t poly-oli happen in TAPS?

A

Chronic nature of the pathophysiology

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54
Q

Renin levels in donor/recipient of TTTS

A

Donor - high renin

Recipient- low renin

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55
Q

Angioarchitecrture pattern of TAPS

A

Small, 3-4 AV

Few small AA and VV

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56
Q

In TRAP what type of anastomosis cause the problem

A

The acardiac twin is fed by an AA anastomosis

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57
Q

2 events that must happen to get TRAP

A
  1. One twin has circulator failure or nonfunctional heart in first trimester
  2. Placenta has a direct AA that can support acardiac twin
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58
Q

% acardiac twins with chromosomal problem

A

30-50%

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59
Q

Part of acardiac twin usually more developed

A

Lower limbs

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60
Q

PCIs for TRAP

A

Usually close together or share a common insertion site

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61
Q

Placental findings in sFGR

A

Unequal placental sharing, peripheral PCI of one or both twins

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62
Q

Embryo splits 8-12d post fertilization

A

Mono-mono

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63
Q

Twinning with embryo splitting at 13-16d post fertilization

A

Conjoined

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64
Q

PCIs of mono-mono

A

Close to each other and connected by large AA anastomoses

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65
Q

Conjoined twins with fused UC. How many vessels present in cord?

A

Variable, 3-8

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66
Q

T/F - peripheral PCI and SUA common in mono-mono

A

True

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67
Q

In fetal growth discordance of twins one twin must be…

A

FGR

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68
Q

Equation for growth discordance

A

Big-little/big

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69
Q

Zygosity of mole-fetus twin

A

Dizygosity

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70
Q

Zygote splits 0-3 days post fertilization

A

Di-di

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71
Q

Zygote splits 3-8 days post fertilization

A

Mono-di

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72
Q

CD4 count threshold for opportunistic infections in HIV

A

<200

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73
Q

CAART medication that can be associated with glucose intolerance

A

Protease inhibitor

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74
Q

PCP prophylaxis

A

TMP-SMX at CD4 <200

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75
Q

MAC prophylaxis

A

Azitrhomycin at CD4 < 50

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76
Q

Infections associated with increasing perinatal transmission in HIV

A

Hep C
CMV
BV
Genital ulcer

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77
Q

HIV transmission risk with +VL and no medications

A

25%

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78
Q

HIV transmission risk with +VL and ZDV

A

8%

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79
Q

HIV transmission risk with VL <1000 and meds

A

1-2% (some lower reports)

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80
Q

VL cutoff for cesarean in HIV+

A

> 1000 copies

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81
Q

Frequency of HIV RNA level checks

A

1st visit
2-4 weeks after initiating or changing meds
Monthly until undetectable, then at least q3 months
At 34-36 weeks to assess MOD

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82
Q

Timing of C-section for HIV+

A

38 weeks

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83
Q

ZDV regimen for c-section

A

3hours preop
1st hour - loading dose of 2mg/kg
2nd and 3rd hour - continuous infusion of 1mg/kg/hr
Continued as continuous until delivery

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84
Q

ZDV intrapartum for <1000 copies HIV

A

50-999 can give continuous infusion intrapartum , less than 50 the transmission seems less (expert opinion)

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85
Q

HIV+ scheduled for c-section for VL presents 1 week earlier with ROM…what is MOD?

A

Individualize – unclear if csection after onset of labor or ROM prevents transmission

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86
Q

HIV med that interferes w/ methergine

A

Protease inhibitors

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87
Q

Purpose of intrapartum ZDV

A

Pre-exposure ppx to the fetus

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88
Q

Neonatal HIV ppx should be initiated how quickly

A

6-12hrs after birth

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89
Q

Neonatal HIV ppx when VL <50

A

4 weeks of zidovudine

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90
Q

Neonatal HIV ppx when VL >50

A

cART (zidovudine, lamivudine, nevirapine OR raltegravir) for 6 week course

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91
Q

High risk neonatal HIV ppx for VL>50 and what other circumstances?

A

New diagnosis of HIV this pregnancy

Not taking any meds

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92
Q

cART general recommendations

A

Dual NRTI (nucleoside reverse transcriptase inhibitor) + Integrase inhibitor OR protease inhibitor

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93
Q

NRTI dual meds

A

Tenofovir + Lamivudine
Tenofovir + Emtricitabine
Abacavir + Lamivudine

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94
Q

Integrase inhibitor meds

A

Dolutegravir

Raltegravir

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95
Q

Protease Inhibitor

A

Atazanavir plus ritonavir

Darunivar plus ritonavir

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96
Q

Pre-conception or 1st visit lab tests in HIV+

A 
VL
CD4 count
Drug resistance genotype panel
Toxoplasmosis immunity
Hep B, Hep A, Hep C
TB screening
G6PD screening
HLA b7501 screening
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97
Q

If HLA-B5701 HIV genotype, which medication to avoid

A

Abacavir

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98
Q

Where is progesterone mostly produced?

A

Corpus luteum until 7-9 weeks, then placenta

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99
Q

Progesterone function in mid-late pregnancy

A

Uterine quiescence – limits PG production, inhibits expression of CAP genes (contraction associated protein)

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100
Q

T/F - estrogen exert effect by binding to nuclear receptors

A

True

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101
Q

Type of PG secreted by:

  • Fetal membranes
  • Decidua
  • Myometrium
A
  • Fetal membranes: PGE2
  • Decidua: PGF2a
  • Myometrium: PGI2
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102
Q

PGs that promote uterine contractions

A

PGF2a, PGE1, PGE3, Thromboxane

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103
Q

PGs that inhibit uterine contractions

A

Prostacyclin, PGE2, PGD2

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104
Q

PG regulation occurs within what cascade

A

Arachidonic acid cascade

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105
Q

In general how are PGs formed

A

from free arachidonic acid that is released from membrane phospholipids through phospholipase enzymes

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106
Q

How do PGs induce myometrial contractions

A

Increasing calcium influx into myometrial cells

Enhancing gap junction formation

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107
Q

Oxytocin is released from what organ

A

posterior pituitary

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108
Q

T/F: during pregnancy oxytocin is degraded primarily by placenta

A

True - oxytocinase

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109
Q

What happens when myometrial Oxytocin receptor is activated (on cellular level)

A

Interaction w/ G-binding protein, simulates phospholipase C activity, increase production of ITP and influx of calcium

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110
Q

Myometrial contractions lead to increased intracellular concentrations of

A

Calcium

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111
Q

Substances that cross placenta via pinocytosis (4)

A

IgG
Insulin
LDL
Transferrin

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112
Q

Molecules that corss placenta via active transport

A 
Amino acids 
Ca
Iron
Phosphorus 
Iodine
Vit C
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113
Q

Molecules that follow simple diffusion across placenta

A

CO2, O2, free fatty acids

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114
Q

Drugs that work on afferent arterioles of kidney

A

NSAIDs

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115
Q

Drugs that work on efferent arterioles of kidney

A

ACEi ARBs

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116
Q

Factors that promote surfactant associated protein A production

A

cAMP analogues
Epidermal growth factor
T3

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117
Q

C-19 steroids are the precursor to….

A

estrogens

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118
Q

Enzyme that is present in fetal adrenal gland but NOT in placenta

A

17-hydroxylase (needed to convert C-21 steroids to C-19 steroids)

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119
Q

enzymes needed for estrogen formation in placenta, located in what cells?

A

synctiotrophoblasts

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120
Q

low maternal estrogen levels

A

anencephaly
fetal demise
umbilical cord ligation

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121
Q

What day does blastocyst implant on endometrium?

A

Day 8-10 after ovulation

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122
Q

Majority of implantation sites are located where in uterus

A

upper 2/3 of uterus, more commonly on side of corpus luteum

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123
Q

_____ are thought to be essential for allowing the blastocyst (trophoblast specifically) and endometrium to “attach”

A

Integrins (alphav-beta3)

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124
Q

Controlled invasion of maternal vascular system by the ______ during implantation

A

Cytotrophoblast

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125
Q

3 factors that regulate trophoblastic invasion of maternal vascular system

A

Stimulate invasion:

  1. Epidermal growth factor
  2. Interleukin-1B

Inhibit invasion:
3. Trnasforming growth factor-B

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126
Q

Peak trophoblastic invasion of maternal vessels occurs at what GA

A

12 weeks

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127
Q

Functional unit of placenta

A

Chorionic villi

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128
Q

Structure of a chorionic villi

A

Core: connective tissue and abundant capillaries that connect with fetal circulation
Inner layer: cytotrophoblasts
Outer layer: synctiotrophoblasts

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129
Q

Type of hormones made by (1) cytotrophoblasts (2) syncytiotrophoblasts

A

(1) peptide

(2) peptide, steroid

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130
Q

Elevated NK cells in endometrium associated with….

A

recurrent implantation failure

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131
Q

hCG is structurally similar to what hormones

A

alpha subunit: TSH, LH, FSH

beta subunit: LH

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132
Q

Predominant producer of hCG

A

syncytiotrophoblasts

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133
Q

when can hCG be detected in urine/serum

A

7-8 days before expected menses

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134
Q

when is peak hCG production (100,000)

A

9-10 weeks gestation

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135
Q

What is the role of hCG in early pregnancy?

A

Rescue corpus luteum from premature demise

Can also stim CL to make estradiol, 17-hydroxyprogesterone, relaxin, inhibin through the LH receptor

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136
Q

Placenta takes over progesterone production at what GA

A

9-10 weeks GA

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137
Q

T/F: fetal ovary is active

A

False - it does not secrete estrogens until puberty

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138
Q

T/F - the fetal teste is active in utero

A

True - Leydig cells produce testosterone levels equivalent to adult male

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139
Q

Hormone that provides initial stimulus for teste development

A

hCG

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140
Q

What hormones/hormone conversions are needed to allow final maturation of male genital structures in the fetus?

A

Local conversion of testosterone to dihydrotestosterone by 5a-reductase

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141
Q

What placental hormone protects maternal system from being affected by fetal testosterone?

A

Placental aromatase

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142
Q

During first 6weeks of gestation, CL makes progesterone. What type of progesterone is elevated?

A

17alpha-OHP

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143
Q

Precursor to placental progesterone synthesis

A

Maternal LDL cholesterol

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144
Q

Placental enzyme converting Cholesterol –> Pregnenolone

A

CYP450

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145
Q

Placental enzyme converting Pregnenolone –> Progesterone

A

3beta-hydroxysteroid dehydrogenase

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146
Q

Location of placental conversion of cholesterol –> progesterone

A

Mitochondria

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147
Q

Major estrogen formed in pregnancy

A

Estriol

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148
Q

How is estriol different from estradiol and estrone?

A

Estriol is cleared more rapidly and has low affinity for sex hormone-binding globulin

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149
Q

Precursor substrate for estrogen synthesis in pregnancy

A

Androgen precursors (DHEAS)

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150
Q

Placental cells responsible for estrogen synthesis

A

Syncytiogrophoblasts

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151
Q

Placental enzymes needed to make estrogen

A
  1. sulfatase to take 16alpha-OH-DHEAS to DHEAS

2. aromatase to take DHEAS to 17beta estradiol (–>estriol) + estrone

152
Q

X-linked condition cause by placental sulfatase deficiency

A

Congenital X-linked ichthyosis

153
Q

Effects of placental aromatase deficiency

A

Virilization of fetus and mother

154
Q

Low levels of maternal serum estrogen caused by….

A
  1. placental sulfatase deficiency
  2. placental aromatase deficiency
  3. fetal demise
  4. anencephaly
  5. complete mole
  6. pseudocyesis
155
Q

Which progesterone receptor is upregulated at the time of labor?

156
Q

How is progesterone thought to regulate uterine contractions

A

The ratio of PR receptors (PR-A to PR-B) in myometrial tissue predicts overall uterine contractile state.

When PR-B > PR-A progesterone promotes relaxation and anti-inflammatory genes
When PR-A > PR-B progesterone promotes uterine contractions and proinflammatory genes

157
Q

Functions of elevated estrogen

A
  1. increase gap junctions for myometrial contraction
  2. increase uteroplacental blood flow
  3. prepare breast for lactation
  4. fetal development, organ maturation, surfactant production
158
Q

Low 1st trimester PAPP-A levels associated with…

159
Q

2nd trimester low PAPP-A

160
Q

Function of PAPP-A

A

Cleaves IGF-binding proteins to make IGF available for trophoblast invasion and early fetal development

161
Q

where is PAPP-A made?

A

Embryo

Syncytiotrophoblast

162
Q

What is PGF? Where is it produced?

A

VEGF analogous

Made in extravillous cytotrophoblasts

163
Q

How is PGF a biomarker for preeclampsia?

A

increased sFLt:PGF levels associated with preeclampsia

164
Q

Human chorionic somatomammotropin (AKA hPL) is produced by? function?

A

Syncytiotrophoblasts

Nutritional needs of fetus met

165
Q

Function of pregnancy specific glycoproteins

A

modulate the maternal immune response

low levels = SAB, FGR

166
Q

Metabolic changes of pregnancy

A 
Hyperinsulinemia
Insulin resistance
Fasting hypoglycemia
Increased circulating lipids
Hypoaminoacidemia
167
Q

Etiology of insulin resistance in pregnancy

A

Human chorionic somatomammotropin and placental GH thought to be responsible

168
Q

T/F – maternal beta cell islet hyperplasia in pregnancy

169
Q

When do HDL and LDL cholesterol increase in pregnancy?

A

HDL in early pregnancy

LDL in late pregnancy

170
Q

T/F - if prolonged maternal fast, gluconeogenesis will occur

A

False – ketonemia, hypoinsulinemia and hyopglycemia

171
Q

Where is Relaxin produced?

A 
Corpus luteum
Decidua
Placenta
Prostate
Atria
172
Q

Causes of elevated Relaxin levels

A

Multiples

OHSS

173
Q

T/F - Prolactin can be found in amniotic fluid

A

True - made by decidua, thought to function in regulation of solute and water transport

174
Q

Period when breast most permeable to drugs?

A

During colostrum phase, 1st week PP

175
Q

Factors that increase transfer of drugs into breastmilk

A
  1. Non-ionized molecules
  2. Non-protein bound molecules
  3. Smaller molecules (<200)
  4. Water soluble molecules (lipid barrier)
  5. Long half-life
  6. High pKa (breastmilk is more acidic 7.0)
176
Q

Breastfeeding contraindications

A
  1. HIV
  2. Active/untreated TB
  3. Active drug use
  4. Infant with galactosemia
  5. Ebola, Lassa, Marburg, Dengue viruses
  6. Breast CA
  7. Certain medications
177
Q

Hormone causing myoepithelial contraction for milk expression

178
Q

Hormone that produces breastmilk

179
Q

Soft markers, highest to lowest LR for aneuploidy

A
  1. Nuchal thickening
  2. Echogenic bowel
  3. Short humerus
  4. Short femur
  5. EIF
  6. UTD
180
Q

Top 5 causes of pregnancy-related death

A
  1. CV conditions
  2. Infection or sepsis
  3. Cardiomyopathy
  4. Hemorrhage
  5. Embolism
181
Q

Physiology changes in:

  1. Blood/plasma volume
  2. HR
  3. CO
  4. SVR
A
  1. Increase 40%/50%
  2. Increase ~15bpm
  3. Increase 40%
  4. Decrease 20%
182
Q

Aldosterone levels _____ in pregnancy

A

Increase (leading to Na and H20 retention)

183
Q

T/F: the local anesthetic requirement is decreased in pregnancy

184
Q

Treatment regimen to improve AFE outcomes

A

AOK - atropine, ondansetron, Ketorolac

185
Q

NYHA Classes

A

1 - no symptoms
2 - symptoms with greater than normal activity
3 - symptoms with normal activity
4 - symptoms with rest

186
Q

MOA of Terbutaline

A

Beta-agonist

187
Q

Medications that can increase pulmonary resistance

A 
Hemabate
Methergine
Misoprostol 
Stadol
Systemic narcotics if hypoventilation and increased CO2 occurs
188
Q

Oxytocin as a large bolus can lead to….

A

Decreased SVR and subsequent hypotension

189
Q

Contraindications to Methergine

A

Severe HTN or preeclampsia
Ischemic heart disease
Vasoconstrictive disease
Pulmonary HTN

190
Q

Hemabate contraindications

A

Severe asthma

Pulmonary HTN

191
Q

MOA of Magnesium as dilating vascular beds

A
  • Increasing prostacyclin release
  • Decreasing plasma renin activity
  • Decreasing angiotensive-converting enzyme activity
192
Q

Anti-HTN that increases arteriolar vasodilation

A

Hydralazine

193
Q

Hydralazine increased blood flow notably to what organs

A

Uterus and kidneys

194
Q

Side effects of Hydralazine

A

Reflex tachycardia

Possible ventricular arrhythmia without b-blockade

195
Q

T/F - Nitroprusside preserves uterine blood flow

196
Q

Negative side effects of Nitroprusside

A

Reflex tachycardia
Cyanide toxicity with long term use
Cerebral vasodilation

197
Q

Negative effect of Nitroglycerin

A

Uterine relaxant

198
Q

Anti-HTN that increases renal perfusion and urine output

199
Q

Medications that can be used if eclamptic seizure is prolonged

A

Propofol

Midazolam

200
Q

IV fluid restriction in preeclampsia

A

80-100mL/hr

201
Q

T/F - IV fluid preloading decreases hypotension following regional anesthesia

202
Q

Muscle relaxants that should be avoided with Mg use

A

Vecuronium and Rocuronium – nondepolarizing muscle relaxants

203
Q

ABG values in pregnancy

A 
pH - 7.44
pO2 - 104
pCO2 - 27-32
HCO3 - 18-22
Base excess - -3
204
Q

How would ABG in pregnancy be different in morbidly obese pregnant woman

A

Decrease pO2 to 85, decrease pCO2 to 30 and increase in base excess to -4

205
Q

If bronchoconstriction in asthmatic needing GETA, what induction agents can be used?

A

Ketamine and/or Propofol

206
Q

What causes shortened interval from apnea to desaturation and hypoxia in GETA

A

Decreased FRC and increased oxygen consumption

207
Q

GETA induction agents if hemodynamic instability is a concern

A

Ketamine and/or Etomidate

208
Q

Muscle relaxant good for GETA

A

Succinylcholine

209
Q

Historic definitions of sepsis

A
  • Temp >38 or <36
  • HR >90
  • RR >20
  • WBC >12k or <4k
210
Q

Most common causes of sepsis

A
  1. UTI/pyelo
  2. Chorio/Endometritis
  3. Septic AB
  4. NEC fasciitis
  5. Septic thrombophlebitis
211
Q

In those using amphetamines or cocaine - hypotension tends to respond better to what pressor?

A

Phenylephrine

212
Q

Induction agent to be avoided in active amphetamines or cocaine use?

213
Q

Agents to prevent hypertension when needing GETA for amphetamines or cocaine use?

A

Nicardipine or short-acting opioids like remifentanyl

214
Q

Why might hypotension after regional anesthesia occur in those with active amphetamines or cocaine use?

A

Endogenous catecholamine depletion

215
Q

What is test dose for epidural?

A

3mL of Lidocaine + 5mcg Epinephrine – to assess if accidental intravascular or subacrachanoid placement

Motor block = subarachnoid placement
HR increase 20bpm = intravascular placement

216
Q

Drugs of choice for epidural

A

Bupivacaine or Ropivacaine (long acting)

Fentanyl

217
Q

Why not lidocaine or chloroprocaine in epidural?

A

Lidocaine - shorter duration, higher motor block (good for instrumental delivery or second-stage block)
Chloroprocaine - rapid onset but short duration

218
Q

Common side effect of spinal opioids?

219
Q

Vasopressors/Inotropes to use in AFE

A

Vasopressor - norepinephrine

Inotropes - Dobutamine, Milrinone

220
Q

Suspected trigger for AFE

A

entrance of material from the fetal compartment into the maternal circulation resulting in abnormal activation of proinflammatory mediator systems

221
Q

What happens to uterus in AFE?

A

oxygenated blood is shunted away from uterus

catecholamine induced uterine hypertonus

222
Q

Risk factors for AFE

A 
Operative delivery (cesarean or vaginal)
Placenta previa
Placenta accreta
Placenta abruption
Smaller: uterine rupture, cervical lacerations, eclampsia, poly, multiples
223
Q

1st signs of AFE

A

Hypotension and hypoxia

224
Q

Goal of serum glucose following AFE (critical illness)

225
Q

Temperature recommendations following cardiac arrest

A

32-36 degrees

226
Q

Risk of therapeutic hypothermia

A

Hemorrhage

227
Q

Common echo finding following AFE

A

Dilated and hypokinetic right ventricle

228
Q

How to improve RV function following AFE?

A

Inotropes - dobutamine and milrinone

Decreasing pulmonary vascular restriction - the inotropes as well as sildenafil, prostacyclin, inhaled NO

229
Q

What is the trend in heart function/failure following AFE?

A

RV failure followed by LV failure

230
Q

Platelet goal in massive DIC

231
Q

Factor VII only as last resort for DIC, why?

A

excessive diffuse thrombosis and multiorgan failure

232
Q

Diff dx of AFE?

A 
MI
PE
Air embolism 
Anesthetic complications
Anaphylaxis
Eclampsia
Sepsis
233
Q

Risk of congenital varicella if maternal infection occurs < ——- weeks

234
Q

Findings in congenital varicella

A 
Dermal scarring - 73%
CNS delay, microcephalic - 62%
Chorio retinitis/eye defects - 52%
Limb hypoplasia 
Rudimentary digits 
FGR 
CNS abnormalities
235
Q

% of fetuses with congenital varicella after primary maternal infection

236
Q

Neonatal varicella risk highest if maternal infection occurs

A

5 days before delivery through 2 days postpartum highest risk but 1-4 weeks before delivery is still possible

237
Q

Neonatal varicella rx

A

Varicella IgG

238
Q

Time between maternal varicella and US detection of fetal effects

A

Five weeks

239
Q

If seronegative mother exposed to VZV what is tx

A

VZV IgG within 4 days of exposure (continue until 10 days post exposure)

240
Q

Maternal chicken pox infection treatment

A

Oral acyclovir

241
Q

If neonatal VZV occurs what is treatment

A

IV Acyclovir

242
Q

Pulmonary VZV treatment

A

IV Acyclovir

243
Q

VZV vaccine schedule

A

2 doses, one month apart

244
Q

Part of TSH molecule that confers specificity

A

Beta subunit

245
Q

Difference between Iodine and Iodide

A 
Iodine = taken in by diet
Iodide = reduced form that is taken up by thyroid gland
246
Q

Organs that can uptake/clear Iodide

A

Thyroid

Kidney

247
Q

Function of thyroglobulin versus TBG?

A

TBG binds T3/T4 in maternal serum

Thyroglobulin binds T3/T4 in thyroid follicle colloid

248
Q

Thyroid peroxidase is needed for what?

A

Converts Iodide –> Iodine in thyroid follicle

249
Q

T3/T4 bind to what type of receptors

A

Nuclear receptors, T3>T4

250
Q

Testing of which thyroid level is most accurate in critical illness and why?

A

Free T4

Critical illness leads to elevated rT3 as physiologic response

251
Q

Effects of pregnancy on:

  1. TBG
  2. TSH (thyrotropin)
  3. Total T4
  4. Free T4
A
  1. TBG increased due to estrogen stimulation
  2. TSH decreases due to elevated hCG levels (mostly 1st trimester)
  3. Total T4 increases
  4. Free T4 slight increase due to hCG stimulation
252
Q

How does T4 convert to T3 in peripheral tissues

A

Via deiodinase enzyme

253
Q

Deiodinases found in placenta

A

Converts T4 –> T3
Type II: in placenta to make T3
Type III: in placenta to make rT3

254
Q

T/F: Dietary Iodine is taken up by placenta

255
Q

When does fetal thyroid start to function

A

~12-14wks GA (12 wks starts concentrating iodine)

256
Q

Most of the fetal T4 is converted to what and how in the fetus?

A

T4 converted to rT3 by placenta type III deiodinase

257
Q

What type of thyroid hormone does fetal brain depend on

A

T3, made by T4 conversion to T3 by type II placental deiodinase

258
Q

Does maternal T4 cross placenta? Maternal TSH?

A

T4 - yes

TSH - no

259
Q

Amniotic fluid levels of thyroid hormone are reflective of maternal or fetal serum levels?

260
Q

What happens to thyroid hormone levels in neonate?

A

Surge in TRH/TSH following birth leads to high levels of T3 (mostly) and T4 for 4-6 weeks after birth (thought to happen for thermoregulation function)

261
Q

Effect of neonatal cooling on neonatal thyroid hormones

A

Exacerbate the normal increase in neonatal thyroid hormone production

262
Q

T/F: Iodine renal clearance increases in pregnancy

263
Q

How to assess if maternal iodine intake is sufficient?

A

If iodine excrection >100ug in 24hrs

264
Q

Dietary Iodine recommendation for pregnancy/lactation

A

WHO: 250ug of Iodine daily

ACOG/IOM: 220ug pregnant, 290ug lactation

265
Q

Fetal brain development relies on thyroid hormone for development…is it maternal or fetal thyroid hormone that supplies this need?

A

1st and 2nd trimester - maternal T4 converted to T3

3rd trimester - fetal T4 converted to T3

266
Q

T/F: GTN and hyperemesis can present with serum/clinical evidence of hyperthyroidism

A

True - GTN can present as thyroid storm and need treatment. Don’t treat with HG as it doesn’t improve symptoms and is transient

267
Q

Why does goiter happen when Iodine deficiency?

A

Elevated TSH stimulates thyroid glandular hypertrophy

268
Q

Nutritional deficiency that can exacerbate Iodine deficiency?

269
Q

Symptoms of cretinism

A

Mental retardation
Deaf-mutism
Pyramidal syndromes

270
Q

Most common etiology of hypothyroidism?

A

autoimmune thyroiditis AKA Hashimoto’s thyroiditis

271
Q

What are the anti-thyroid antibodies that can cause hypothyroidism?

A

Anti-TPO

Anti-Thyroglobulin

272
Q

T/F: Anti-TPO can cross placenta?

A

True – but doesn’t have any fetal effects

273
Q

Positive anti-TPO but no evidence of clinical hypothyroidism — what are they at risk for?

A

Becoming hypothyroid in pregnancy, developing postpartum thyroiditis

274
Q

Most common antibody in Hashimoto’s thyroidits

275
Q

Medications associated with causing hypothyroidism

A

Lithium

Amiodarone

276
Q

If no pregnancy/trimester specific free T4 or TSH lab ranges, what can you use as estimate?

A

T4 - 1.5x higher than nonpregnant state (AKA about 50% increase after 16wks)
TSH - <3-4 (lower limit decrease by 0.4, and upper limit decrease by 0.5)

277
Q

Levothyroxine dose change in pregnancy

A

Increase 30% in first trimester

278
Q

Preconception TSH goal for hypothyroid patients

279
Q

Levothyroxine dosing

A

1.6mcg/kg/day

280
Q

Can you use dessicated thyroid or T3 replacement for hypothyroidism in pregnancy?

A

No – doesn’t cross placenta for fetal brain development

281
Q

What are the types of TSH receptor antibodies?

A

TSI - thyroid stimulatory antibodies (TRAb)

TBII - thyroid inhibitory antibodies

282
Q

Can thyroid stimulating (TSI) and thyroid inhibitory binding (TBII) antibodies cross placenta?

A

Yes — can cause fetal thyroid dysfunction

283
Q

T/F: anti-TPO or anti-thyroglobulin may be seen in hyperthyroidism

284
Q

Most common cause of hyperthyroidism?

A

Graves disease (hyperthyroidism, goiter, thyroid eye disease, myxedema)

285
Q

When should you test for TSI (TRAb) in hyperthyroidism?

A

After 20 weeks, as they may be falsely negative with high hCG levels

286
Q

MOA of thioamide therapy

A

Prevent iodination of thyroglobulin and prevent thyroglobulin production
PTU also prevents peripheral conversion of T4–>T3

287
Q

Which thioamides should be used in each trimester?

A

1st: PTU

2nd/3rd: MMI

288
Q

Concerns with PTU use?

A

Liver toxxicity

289
Q

Concerns with MMI use?

A 
Cutis aplasia
Choanal atresia
TE fistula
Abdominal wall defects
VSD
Facial anomalies
290
Q

PTU:MMI dosing equivalents

A

20:1 (100mg PTU:5mg MMI)

291
Q

Thioamide side effects

A

rash, itching, lupus-like syndrome, bronchoconstriction, agranulocytosis, transient leukopenia

292
Q

When to take thioamide when breastfeeding

A

3-4hours before feeding

293
Q

Goal T4 of thioamide treatment

A

Upper limit of normal

294
Q

Fetal signs of over-treatment of maternal hyperthyroidism?

A

Signs of fetal hypothyroidism – bradycardia, FGR, goiter

295
Q

Rate of fetal hyperthyroidism

296
Q

What predicts higher chance of fetal hyperthyroidism?

A

Maternal TSI level >300% measured at 18-22 weeks

297
Q

T/F: women s/p radiodide ablation can have fetal hyperthyroidism

A

Yes – check for presence of ab in serum

298
Q

Fetal symptoms of hyperthyroidism

A

Tachycardia, goiter, FGR, craniosynostosis, advanced bone age, hydrops

299
Q

Treatment of fetal hyperthyroidism?

A

Maternal thioamide treatment

300
Q

After radioactive iodine therapy, how long to avoid pregnancy?

301
Q

What to do if accidental radioactive iodine treatment in early pregnancy?

A

Potassium Iodide and thionamide treatment within 7-10 days of exposure

302
Q

If thyroid surgery needed in pregnancy, what can you give preop to decrease thyroid vascularity?

A

potassium iodide

303
Q

Effect of potassium iodide on thyroid function

A

decreases t3/t4 levels by inhibiting release from thyroid

304
Q

Risks of thyroid surgery

A

hypoparathyroidism, recurrent laryngeal nerve paralysis

305
Q

Protocol for thyroid storm treatment

A
  1. PTU loading dose then continuous dosing
  2. Potassium Iodide 1hr after PTU (can also use sodium iodide, lugol solution, lithium carbonate)
  3. Dexamethasone to block peripheral conversion
  4. B-blockers
306
Q

Reason to do thyroidectomy in pregnancy for CA

A

lymph node metastasis or substantial growth before 24 weeks

307
Q

Serum level checked to determine if biochemical evidence of thyroid CA following thyroidectomy

A

Thyroglobulin

308
Q

Typical course of postpartum thyroid disease

A

Hyperthyroidism followed by hypothyroidism (treat the hypothyroidism)

309
Q

T/F: thyroid gland enlargement in pregnancy

A

True - 30%

310
Q

If thyroid storm patient has iodide anaphylaxis history, what can you give instead?

A

lithium carbonate

311
Q

US characteristics of malignant thyroid nodule

A

hypoechoic pattern
irregular margins
microcalcifications

312
Q

Deficiency of what enzyme predisposes to fetal hydantoin syndrome

A

Epoxide hydrolase

313
Q

Fetal hydantoin syndrome associated with use of what medication

314
Q

Features of fetal hydantoin syndrome

A 
Hypoplasia of nails/distal phalanges
Developmental delays
Flat, broad nose
Webbing of neck
Microcephaly
Growth restriction
315
Q

CVR >1.6 is predictive of what

A

hydrops
need for early surgery
RDS at birth

316
Q

Signs of fetal hyperthyroidism

A
  • High FH
  • Goiter
  • Advanced bone age
  • Poor growth
  • Craniosynostosis
  • Hydrops
317
Q

Anti-inflammatory cytokine

Pro-inflammatory cytokine associated w/ PTL

A

anti: IL10
pro: IL6

318
Q

For smooth muscle relaxation – what things must happen (2 major things)

A
  • decreased intracellular Ca levels

- increased myosin light chain phosphatase

319
Q

Effect of NO2 on smooth muscle

A

relaxation

320
Q

Difference between ephedrine and phenylephrine for post-anesthesia hypotentions

A

Ephedrine - alpha and beta agonists. Associated with fetal tachycardia
Phenylephrine - drug of choice

321
Q

Weight gain recommendations for twins

A

18.5-224.9: 37-54lbs
25-29.9: 31-50lbs
>30: 25-42lbs

322
Q

Weight gain recommendations singletons

A

<18.5: 28-40lbs
19-24.9: 25-35lbs
25-29.9: 15-25lbs
>30: 11-20lbs

323
Q

Clinical manifestations of hyperparathyroidism

A 
Nephrolithiasis
Fractions
Hypercalcemia
Hyperemesis
Pancreatitis
324
Q

Fetal/neonatal effects of maternal hyperparathyroidism

A 
Hypocalcemia
Tetany
PTB
FGR
IUFD
325
Q

Cause of acromegaly

A

GH secreting adenoma in pituitary

326
Q

Increased risk of what outcomes for acromegaly in pregnancy

327
Q

Medical therapies for acromegaly

A

Somatostatin analogues (avoid in pregnancy)

Ocretotide

328
Q

Elevated hormone levels in acromegaly

A

IGF-1

Prolactin (compression or mixed type adenoma)

329
Q

What drives increased fetal calcium needs in pregnancy?

330
Q

Placental transport mechanism of Calcium

A

Active transport

331
Q

Immediate treatment for K of 6.9

A

Ca gluconate (or calcium chloride) followed by insulin and glucose

332
Q

Most common chorioangioma location

A

In the placenta on the fetal side near the cord insertion (appears to bulge into amniotic cavity)

333
Q

Vascular flow through chorioangioma is maternal or fetal in origin?

334
Q

Fetal complications of chorioangioma

A

Hydrops
Poly
FGR
Anemia

335
Q

Chorioangioma size more likely to have complications

336
Q

T/F: chorioangioma is not a true neoplasm

A

True – is the result of reactive proliferation

337
Q

T/F: vascularity of chorioangioma may change over gestation

338
Q

Location of placental teratoma

A

Between amnion and chorion

339
Q

Associated abnormalities in cases of chorioangioma

A

Fetal hemangiomas
SUA
Beckwith-Wiedmann

340
Q

How do anti-epileptic medications decrease birth control efficicay?

A

Induce hepatic enzymes that accelerate metabolism of OCPs

341
Q

Antiepileptics associated with NTD’s

A

Valproate (highest at 1-2%)

Carbamazepine (0.9%)

342
Q

Coagulation factors that decrease in pregnancy

A

Protein S
Factor XI (likely unchanged or slight decrease)
Factor XIII

343
Q

For vWD you want vWF Ag and Factor VIII levels to be > ____ for delivery

344
Q

Difference between the types of vWD

A

Type 1: AD, quantitative problem, responds to DDAVP

Type 2: AD, qualitative problem, 1st line is vWF concentrates/Factor VIII

Type 3: AR, severe quantitative problem, doesn’t respond to DDAVP

345
Q

MOA of DDAVP

A

Stimulates relase of vWF and Factor VIII from endothelial cells

346
Q

% chance of PPH with vWD

A

30% chance for immediate and/or delayed

347
Q

Platelet count thresholds for non-bleeding women nearing delivery

A

Vaginal >30,000

Cesarean >50,000

348
Q

Therapy to raise platelet counts in ITP

A

Steroids
IVIG
^^require 1 week to work

Platelet transfusion - if needed immediately

349
Q

General platelet count goals in pregnancy

A

> 30k with >50k at term

350
Q

For ITP if you give steroids when will effect take place

A

3-7 days after initiation

351
Q

When is IVIG used for ITP?

A
  • refractory to steroids

- perioperative setting when platelet count <10k

352
Q

If using IVIG for ITP when do you see response?

A

7-10 days and it lasts for about 30 days

353
Q

Incidence of stillbirth per 1,000 within 1 week of (a) BPP (b) modified BPP (c) CST (d) NST

A

a - 0.8
b - 0.8
c - 0.3
d - 1.9

354
Q

Change EDD if discrepancy is more than ____ days at

(a) less than 8w6d
(b) between 9w and 13w6d
(c) between 14w and 15w6d
(d) between 16w and 21w6d
(e) between 22w and 27w6d
(f) between 28w and beyond

A 
a - 5 days
b  - 7 days
c - 7 days
d - 10 days
e - 14 days
f - 21 days
355
Q

Teratogenicity associated with efavirenz

356
Q

T/F: Warfarin crosses placenta

357
Q

GA that warfarin has highest risk of teratogenicity

A

6-12 weeks

358
Q

T/F: Warfarin can cause fetal bleeding at any GA

359
Q

Clinical manifestations of warfarin embryopathy

A

Defects in cartilage/bone formation – nasal hypoplasia, short limbs, short digits, stippled epiphyses

360
Q

Hep B treatment

361
Q

Interpretation:
HbsAg - negative
Anti-HBc - negative
Anti-HBs - negative

A

Not immune or acutely infected. Susceptible to infection.

362
Q

Interpretation:
HbsAg - Negative
Anti-HBc - Positive
Anti-HBs - Positive

A

Immune through natural infection

363
Q

Interpretation:
HbsAg - Negative
Anti-HBc - Negative
Anti-HBs - Positive

A

Immune through vaccination

364
Q

Interpretation:
HbsAg - Positive
Anti-HBc IgM - negative
Anti-HBs - negative

A

Acute infection

365
Q

Hep B - what antigen stays positive once chronically infected

366
Q

What factors (2) in chronic Hep B increases chance of perinatal transmission

A
  1. Positive HBeAg (increase from 10-30% to 90-95%)

2. Maternal viral load >5 log copies/mL (>1 million)

367
Q

Neonatal tx for maternal Hep B positive

A

HBIg and HBV within 12hrs of life

368
Q

If diagnosed with chronic Hep B what other virus should be tested for

369
Q

T/F: lamivudine for hep B treatment

A

False – higher rates of viral resistance

370
Q

Chronic Hep B — treat or don’t treat in pregnancy?

A

Consider treatment after 28-32 weeks if viral load >6-8 log (1-100 million) copies/mL

371
Q

T/F: Hep D has no effect on pregnancy or fetus

372
Q

RF for PVL

A
  1. pretermers with IVH

3. chorio

373
Q

most likely outcome of neonatal PVL

A

spastic diplegia, seizures

374
Q

Phenylalanine is converted to ____ by _____

A

Tyrosine by phenylalanine hydroxylase

375
Q

HIV/HepB coinfection – which meds to avoid

A

Telbivudine
Emtricitabine
Adefovir
Lamivudine

376
Q

Idiopathic intracranial HTN treatment

A 
Carbonic anhydrase inhibitors - acetazolamide (try to use after 20 weeks)
Topamax
Furosemide
Serial LP's
Short course of steroids (vision loss)
377
Q

CHD lesions that will lead to neonatal cyanosis (Ductal dependent)

A 
HLHS
Severe/critical AS
Critical coarctation (differential cyanosis)
Interrupted aortic arch (differential cyanosis)
TOF w/ pulm stenosis
Pulmonary atresia, intact septum
TOF - varies
Tricuspid atresia/ebstein
TGA

cyanosis but not ductal depd
TAPVC
Truncus

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