Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Obstetrics > Pharmacology and Neuraxial Anesthesia in Pregnancy > Flashcards

Pharmacology and Neuraxial Anesthesia in Pregnancy Flashcards

1
Q

What law/ principle explains how drugs traverse a biologic membrane?

A

Fick prinicple

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the Fick principle? (formula)

A

Rate of diffusion = [diffusion coefficient x surface area x concentration gradient (between mom and fetus)] / membrane thickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the most important variables in determining rate of diffusion of a drug?

A

Diffusion coefficient

Concentration gradient between mother and fetus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does fetal acidosis affect drug transfer from mom to fetus?

A

It can increase the concentration gradient, leading to ion trapping

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What drug characteristics favor placental transfer of the drug?

A

Low molecular weight (< 500 Daltons)
High lipid solubility
Non- ionized
Non- polar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What drugs have significant placental transfer?

A

Local anesthetics (except choloroprocaine)

IV anesthetics (usually not a problem)

Volatile anesthetics

Opioids

Benzodiazepines

Atropine

Beta- blockers

Magnesium (not lipophilic, but small)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are special considerations for bupivicaine administration in pregnancy?

A

Low placental transfer d/t high protein binding and ionization

Greater sensory block relative to other locals

Risk of cardiac toxicity > cardiac sx before seizures in toxic doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does neuraxial ropivacaine compare to bupivacaine?

A

Less cardiac toxicity
Less potent
Less motor block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why is lidocaine unpopular for labor analgesia?

A

Strong motor block

Risk of neurotoxicity if given in the subarachnoid space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is 2-Chloroprocaine helpful for neuraxial labor analgesia?

A

Useful for emergency C-section when epidural is already in place d/t fast onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does 2-Chloroprocaine affect neuraxial opioids?

A

Antagonizes opioid (mu and kappa) receptors and reduces the efficacy of epidural morphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When administered in a neuraxial block, what is the relationship between opioids and local anesthetics?

A

Synergistic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How are neuraxial opioids beneficial when administered alone?

A

No loss of sensation or proprioception

No sympathectomy

Do not impair ability to push

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What opioid has local anesthetic properties?

A

Meperidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are side effects of neuraxial opioids?

A

Pruruitus (most common)
Nausea/ vomiting
Sedation
Respiratory depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are downsides of administering neuraxial opioids alone?

A

Lack of perineal relaxation

Less analgesia vs locals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why is lidocaine not used as a continuous epidural infusion?

A

Tachyphlylaxis is more likely to develop

Crosses the placenta to a greater degree than other locals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are three ways a patient can develop a total spinal?

A

An epidural dose injected into the subarachnoid space

An epidural dose injected into the subdural space

A single shot spinal after a failed epidural block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the patient management when an epidural dose is injected into the subarachnoid space?

A

Intubate the patient and stabilize her

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is subdural placement of an epidural catheter ruled out?

A

It is rare, but cannot be ruled out. Neither a test dose or catheter aspiration will rule out subdural placement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the symptoms of an epidural catheter placement in the subdural space?

A

Symptoms will occur 10- 25 minutes after epidural placement

The space is very low volume > higher block height than expected for the given dose in the epidural space

Sensory and autonomic block is usually more intense than a motor block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the presentation of a total spinal?

A

Usually rapid progression of sensory and motor block (prolonged onset in subdural injection)

Dyspnea, difficulty phonating, hypotension

Loss of consciousness occurs as a result of cerebral hypoperfusion sectondary to severe hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the anesthetic management for a total spinal?

A

Vasopressors, IVF, LUD, leg elevation to manage hemodynamics

Intubate trachea if pt loses consciousness or is unable to protect airway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are differential diagnoses for total spinal?

A

anaphylactic shock, eclampsia, amniotic fluid embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the objective of tocolytics?

A

Delay labor by suppressing uterine contractions (up to 24-48 hours). Provide a bridge for corticosteroids to take effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Why are corticosteroids given in the setting of preterm labor?

A

To hasten fetal maturity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How long does it take for corticosteroids to begin to take effect for lung maturity in the preterm fetus?

A

18 hours

28
Q

How long does it take for corticosteroids to reach peak effect for lung maturity in the preterm fetus?

A

48 hours

29
Q

How do beta-2 agonists work in the setting of premature labor?

A

Increase intracellular cAMP > turns on protein kinase, turns off myosin light-chain kinase, increases progesterone > relaxes the uterus

Also increases progesterone release > myometrial relaxation

30
Q

What are the side effects of beta-2 agonists to the fetus/ neonate?

A

Hyperglycemia (mother) > hypoglycemia (neonate)

Hypokalemia

Increase FHR

31
Q

What is the mechanism of action of magnesium sulfate as a tocolytic and anticonvulsant in the parturient?

A

Ca++ antagonist > relaxes smooth muscle by turning off myosin light- chain kinase in the vasculature, airway, and uterus

Hyperpolarizes membranes in excitable tissues = seizure prophylaxis

32
Q

How is Mg++ eliminated?

A

Renal elimination = careful with mothers with renal insufficiency

33
Q

How might Mg++ toxicity be tested at the bedside?

A

Reflex testing - if present > low risk of serious side effects, if absent > early sign of toxicity

34
Q

What is the range for normal magnesium level?

A

1.8-2.5 mg/dL

35
Q

What are symptoms of hypomagnesemia <1.2 mg/dL?

A

Tetany
Seizures
Dysrhythmias

36
Q

What are symptoms of hypomagnesemia 1.2-1.8 mg/dL?

A

Neuromuscular irritability
Hypokalemia
Hypocalcemia

37
Q

At what level does hypermagnesemia typically begin to become symptomatic?

A

~5 mg/dL

38
Q

What are symptoms consistent with a patient whose Mg++ level is 5-7 mg/dL?

A

Diminished deep tendon reflexes

Lethargy/ drowsiness

Flushing

N/V

39
Q

What are symptoms consistent with a patient whose Mg++ level is 7-12 mg/dL?

A

Loss of deep tendon reflexes

Hypotension

EKG changes

Somnolence

40
Q

What symptoms are consistent with a patient whose Mg++ level is >12 mg/dL

A

Respiratory depression -> Apnea

Complete heart block

Cardiac arrest

Coma

Paralysis

41
Q

How does hypermagnesemia affect a patient’s response to medications?

A

Skeletal muscle weakness -> potentiates neuromuscular blockers

Reduces responsiveness to ephedrine and phylephrine

42
Q

What are potential respiratory side effects of hypermagnesemia?

A

Pulmonary edema

Respiratory depression/ apnea

43
Q

How is hypermagnesemia treated?

A

Supportive measures based on symptoms

Diuretics > to facilitate excretion

IV calcium gluconate 1g over 10 minutes

44
Q

What is the mechanism of action of calcium channel blockers in the treatment of premature labor?

A

Block the influx of Ca++ into the uterine muscle > reduces Ca++ release from the sarcoplasmic reticulum > turns off myosin light- chain kinases and relaxes uterine muscle

45
Q

What is the first-line calcium channel blocker in the treatment of premature labor?

A

PO nifedipine

46
Q

How might co-administration of a calcium channel blocker with Mg++ affect the patient?

A

Increased skeletal muscle weakness

47
Q

What is the mechanism of action of nitric oxide donors in the treatment of premature labor?

A

Increases cGMP > turns off myosin light - chain kinases > relaxes uterine muscle

48
Q

Why are nitric oxide donors rarely used in the treatment of premature labor?

A

Risk of hypotension

49
Q

Where is endogenous oxytocin synthesized?

A

Paraventricular nuclei of the hypothalamus

50
Q

Where is endogenous oxytocin stored?

A

Posterior pituitary gland

51
Q

From where is endogenous oxytocin released?

A

Posterior pituitary gland

52
Q

What stimulates the release of endogenous oxytocin?

A

Cervical, vaginal, and breast stimulation

53
Q

What is the synthetic equivalent of oxytocin?

A

Pitocin

54
Q

What are indication for pitocin?

A

Augmentation of labor

Stimulate uterine contraction

Prevent hypotonia and hemorrhage post-delivery (administer after placental delivery in a c-section)

55
Q

What are side effects of pitocin?

A

Water retention (structurally similar to vasopressin)

Hyponatremia

Hypotension

Reflex tachycardia

Coronary vasoconstriction

56
Q

What are acceptable routes of administration for Pitocin?

A

IV

Injected directly into uterus

57
Q

How might rapid IV administration of Pitocin affect the patient?

A

May result in cardiovascular collapse

58
Q

How is Pitocin metabolized?

A

Hepatic metabolism

59
Q

What is the half-life of oxytocin?

A

4-17 minutes

60
Q

What is the first line uterontonic drug?

A

Pitocin

61
Q

What is the second-line uterotonic drug?

A

Methergine (Ergot alkaloid)

62
Q

What is the acceptable dose/ route of methergine?

A

0.2mg IM

63
Q

How might IV administration of methergine affect the patient?

A

significant vasoconstriction > hypertension > cerebral hemorrhage

64
Q

How is methergine metabolized?

A

Hepatic metabolism

65
Q

What is the half-life of methergine?

A

2 hours

66
Q

What is the third-line uterontonic?

A

Prostaglandin F2 (Hemabate or Carboprost)

67
Q

What is the acceptable dose/ route of prostaglandin F2?

A

250 mcg IM or injected into the uterus

Obstetrics (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions