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Board Exam COPY > OB > Flashcards

OB Flashcards

1
Q

What causes swelling of the maternal airway?

A

Increased progesterone, estrogen, and relaxin combined with an increase in ECF.
These tissues also become very friable

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2
Q

Risk of difficult and failed intubation

A

8x higher than normal

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3
Q

What things make airway edema even worse in parturients?

A

Pre-eclampsia, tocolytics, and prolonged trendelenburg position

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4
Q

This hormone is a respiratory stimulant

A

Progesterone
Causes MV to increase by 50%
(40% increase in TV + 10% increase in RR)

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5
Q

Lung volume changes in pregnancy

A

Increased:

  • TV and MV
  • RR

Decreased:
- FRC (d/t decreases in ERV and RV)

No changes in other lung volumes! It’s actually pretty easy to think this through.

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6
Q

CV changes in pregnancy

A
  • O2 consumption increased 20%
  • CO increased 40% (up to 80% in 3rd stage of labor)
  • HR increased 15%
  • SV increased 30% (similar to respiratory, with volume increasing more than rate)
  • SBP and MAP unchanged (increase in blood volume and decrease in SVR even out)
  • DBP decreased 15%
  • SVR and PVR both increased d/t NO
  • No change in filling pressures (CVP or PAOP)
  • Left axis deviation (d/t pushing of diaphragm)
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7
Q

3 Major effects of progesterone

A

1) Increases RAAS activity
- Increased blood volume and CO

2) Vascular muscle relaxation
- Decreased SVR and increased flow

3) Increased MV
- Rightward shift of dissociation curve

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8
Q

With LUD, the right torso should be elevated ___ degrees

A

15 degrees

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9
Q

Heme changes in pregnancy

A

Overall, increasing circulating blood volume and preparing for hemorrhage in labor

  • Increase circulating volume and erythrocyte volume (dilution anemia)
  • Increased clotting factors
  • Decreased natural anticoagulants (C&S)
  • Decreased fibrin polymerization and increased fibrin breakdown

Mom makes more clot, but breaks it down faster too

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10
Q

What happens to serum albumin?

A

Decreases

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11
Q

What happens to pseudocholinesterase?

A

Decreases (not enough to be clinically relevant though)

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12
Q

Drug characteristics that favor placental transfer

A
  • Low MW
  • Non-ionized and non polar
  • Lipid soluble
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13
Q

Stages of labor

A

Stage 1

  • Beginning of regular contraction to full dilation
  • Divided into latent, and then active phases
  • Most cervical dilation occurs during active phase
  • Thoracic pain (T10-L1)

Stage 2

  • Full dilation to delivery
  • Perineal pain begins here (Sacral S2-4)

Stage 3
- Delivery of placenta

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14
Q

2 Major effects of uncontrolled pain in labor

A

1) Catecholamine release
- Maternal HTN and reduced UBF

2) Hyperventilation (leftward shift and decreased O2 transfer to fetus)

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15
Q

Only LA that decreases efficacy of morphine

A

2-Chlorprocaine

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16
Q

How is chlorprocaine metabolized?

A

Pseudocholinesterase (minimal placental transfer)

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17
Q

Presentation of high spinal

A

Rapid sensory and motor block
Dyspnea
Difficulty phonating
Hypotension (hypotension leads to apnea)

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18
Q

Management of high spinal

A

Get her BP back up so she will start breathing on her own! (Overall pressers and increase venous return)

  • Pressors
  • IVF
  • LUD
  • Leg elevation

If unable to manage her own airway, then INTUBATE

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19
Q

Normal fetal heart rate (FHR)

A

110-160

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20
Q

Fetal and maternal causes of low FHR (

A

Fetal:

  • Asphyxia
  • Acidosis

Maternal:

  • Hypoxia
  • Drugs that decrease placental perfusion
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21
Q

Fetal and maternal causes of high FHR (>160)

A

Fetal:

  • Hypoxia
  • Arrhythmias

Maternal:

  • Fever
  • Placental infection (chorioamnionitis)
  • Meds given to mother (atropine, ephedrine, or terbutaline)
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22
Q

These things decrease FHR variability

A
  • CNS depressants (opioids, sedatives, propofol, barbs, and magnesium)
  • Hypoxia
  • Fetal sleep
  • Acidosis
  • Anencephaly
  • Cardiac anomalies
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23
Q

Type of decels and what they mean

A

1) Early
- Occur with uterine contraction
- Compression of fetal head increased vagal tone
- Loss of variability with each deceleration
- NO RISK OF FETAL HYPOXIA (benign)

2) Late
- Deceleration occurs AFTER contraction
- Due to decreased placental perfusion leading to fetal compromise**
- GRADUAL decal that happens with each contraction
- Caused by maternal hypotension, hypovolemia, acidosis, and preeclampsia

3) Variable
- No pattern between contraction and FHR
- RAPID drop in FHR
- Variability is maintained during decel
- Often due to compression of cord (causing baroreceptor mediated reduction in FHR)

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24
Q

Three-tier system for evaluation of FHR

A

Category I

  • FHR is normal
  • Fetus is good

Category II

  • There’s some weird shit going on with the FHR
  • Could be ok, but maybe not

Category III

  • There’s some serious shit going on
  • Oh fuck
  • Oh God, why?
25
Q

What is sinusoidal pattern?

A

Regular up and down waves of FHR

26
Q

Corticosteroids for fetal lung maturity begin to work at ___ hours and peak at ___ hours

A

Begins at 18 hours

Peaks at 48 hours

27
Q

Tocolytic agents stop labor for how long?

A

24-48 hours

28
Q

Examples of tocolytic agents

A

1) Beta- 2 Agonists
- Work by increasing intracellular cAMP
- Ex- Terbutaline and Ritodrine
- SE include hyperglycemia (places fetus at risk for hypoglycemia), hypokalemia, and may cross placenta to increase FHR

2) Mag Sulfate
- Ca++ antagonist

3) CCBs
- Block influx of Ca+2 into uterine muscle
- Ex- oral Nifedipine
- Given with mag sulfate can exacerbate weakness

4) NO Donors
- Rarely given d/t hypotension

29
Q

How does mag sulfate work?

A

Calcium Antagonist

Turn off myosin light chain kinase and hyper polarizes excitable membranes

30
Q

Order of magnesium’s effects with increasing serum concentrations

A 
Normal Level
Tocolysis
Anticonvulsant
Patellar Reflex Abolished
Skeletal muscle weakness
Resp Depression
Apnea
Cardiac Arrest
31
Q

SE of mag sulfate

A

Hypotension and decreased response to ephedrine and phenylephrine
Pulmonary edema
Muscle weakness
CNS depression (b/c it depresses excitable tissue)

32
Q

Treatment for hpermagnesemia

A
  • IV Calcium! (Mag antagonist)
  • Diuretics (to excrete Mag)
  • Supportive measures
33
Q

Details of Oxytocin (Pitocin)

A
  • Endogenous oxytocin is release after stimulation of cervix, vagina, and/or breasts
  • Can be given IV or injected into uterus
  • Metabolism: hepatic
  • 1/2 life = 4-7 minutes (very short acting!)
  • SE = water retention and hyponatremia, hypotension, reflex tachycardia, and coronary vasoconstriction
34
Q

Details of Methergine

A
  • Ergot alkaloid
  • Second line uterotonic (after pitocin)
  • Dose = 0.2mg IM
  • Giving IV can cause massive HTN (may result in cerebral hemorrhage)
  • 1/2 life is 2 hours
35
Q

Details of Hemabate/Carboprost

A
  • Prostaglandin F2
  • Third line uterotonic
  • Dose = 250mcg IM or injected into uterus
  • SE = bronchoconstrition, N/V/D, and hypoTN or HTN
36
Q

In the case of coagulopathy, which is preferred for C/S? Regional or GA?

A

GA

37
Q

In the case of fetal distress, which is preferred for C/S? Regional or GA?

A

GA (d/t greater hemodynamic stability –> no sympathectomy)

38
Q

Triple prophylaxis against respiration

A

1) Bicitra
2) H2 antagonist (Ranitidine)
3) Gastrokinetic agent (Reglan)

39
Q

VA usage in GA for emergent C/S

A

0.8 MAC with 50% Nitrous

VAs relax the uterus and can contribute to bleeding post-delivery

40
Q

When is oxtocin given during C/S

A

After delivery of the placenta

41
Q

When can opioids and benzos be used during C/S?

A

After delivery of newborn

42
Q

Why is C/S tried to be performed as quickly as possible?

A

Risk of neonatal acidosis increases if time from incision to delivery exceeds 3 minutes

This is also why patient is prepped and draped prior to induction

43
Q

Why are NSAIDs avoid for women after their first trimester?

A

They can close the ductus arteriosus

When it comes to GA in parturients, KISS! Keep it simple, stupid! Stick to things with a proven track record. Nothing risky.

44
Q

Aspiration prophylaxis if mother is > ___ weeks

A

14 weeks

Triple prophylaxis and RSI

45
Q

Patho of pre-eclampsia

A

Abnormal placental implantation results in elevated uterine VR and reduction in BF. Placenta and fetus thus don’t get enough O2 and nutrients to develop normally.

The shitty placenta ends up making 7x more thromboxane than prostacyclin (normally 1:1).

  • Results in vasoconstriction, plt aggregation, and further decreased placental BF.
  • Diseased placenta also releases cytokines that damage vascular endothelium
46
Q

Why do we treat BP in preeclampsia?

A

Only need it once severe (>160/110) to prevent MI, cerebral hemorrhage, and placental abruption.

47
Q

Dose of mag sulfate for sz prophylaxis

A

4g loading dose > 10 minutes

Then infusion of 1-2g/hr

48
Q

Dose of calcium for mag toxicity

A

1g

10mL of 10% calcium GLUCONATE

49
Q

Major risk of placenta accreta

A

Uterine contractility is impaired –> potential for massive blood loss!

50
Q

This med can provide uterine relaxation for placental extraction

A

NTG

51
Q

These situations in pregnancy may lead to DIC

A

Intrauterine demise
Amniotic fluid embolism
Placental abruption

52
Q

Meaning of APGAR score at 1 and 5 minutes

A

1 minute = acid-base balance
5 minutes = neurologic outcome

8-10 = Normal
4-7 = Moderate  distress
0-3 = Impending demise
53
Q

SpO2 immediately after delivery

A

60%

Should rise to 90% by 10 minutes

54
Q

This is the best indicatory of adequate ventilation in the newborn

A

Resolution of bradycardia

55
Q

3 routes that emergency drugs can be given to newborn

A

1) Umbilical vein
2) ETT
3) Intraosseous

56
Q

Dose of epic for newborn

A

10-30mcg/kg IV

OR

0.05 - 0.1mg/kg via ETT

57
Q

Volume expander dose for newborn

A

10mL/kg over 5-10 minutes for
PRBCs
NS
LR

58
Q

Chest compressions are initiated in newborn if HR

A

60

Board Exam COPY (21 decks)

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