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Pharm Flashcards

1
Q

Drugs that decrease lower esophageal sphincter tone (increased aspiration risk):

A

sodium nitroprusside
anticholinergics
dopamine
thiopental
opioids
propofol
tricyclic antidepressants

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2
Q

Drugs that increase lower esophageal sphincter tone (decreased aspiration risk):

A

metoclopramide
prochlorperazine
edrophonium
neostigmine
pancuronium
alpha-adrenergic agents
antacids

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3
Q

Medication doses based on ideal body weight:

A

rocuronium
vecuronium
cisatracurium
remifentanil infusion

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4
Q

Medication doses based on lean body weight:

A

propofol induction
sufentanil maintenance

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5
Q

Medication doses based on total body weight:

A

succinylcholine
fentanyl loading
propofol maintenance

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6
Q

List the Class 1 antiarryhthmics and their MOA:

A

Na+ channel blockers

1A: quinidine, procainamide, disopyramide
Moderate depression of Phase 0
Prolong Phase 3 repolarization (increase QT)

1B: lidocaine, phenytoin
Weak depression of Phase 0
Shortened Phase 3 repolarization

1C: flecaininde, propafenone
Strong depression of Phase 0
Little effect Phase 3 repolarization

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7
Q

List the Class 2 antiarryhthmics and their MOA:

A

Beta Blockers: esmolol, metoprolol, etc.
Slow Phase 4 depolarization in SA node

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8
Q

List the Class 3 antiarryhthmics and their MOA:

A

Potassium Channel Blockers: Amiodarone, Bretyium
Prolong Phase 3 repolarization (increase QT)
Increase effective refractory period

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9
Q

List the Class 4 antiarryhthmics and their MOA:

A

Calcium Channel Blockers: verapamil, diltiazem
Decrease conduction velocity through AV node

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10
Q

How does succinylcholine stimulate bradycardia and tachycardia?

A

It is two acetylcholine molecules.
Brady is caused by stimulating the M2 receptor in the SA node.
Tachy is caused by mimicking Ach action at the sympathetic ganglia.

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11
Q

List 7 side effects of succinylcholine:

A
  1. bradycardia
  2. tachycardia
  3. increased potassium
  4. increased intraocular pressure
  5. increased intracranial pressure
  6. increased intragastric pressure
  7. MH
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12
Q

What enzymes metabolize acetylcholine and what is their primary location?

A

NMJ

acetylcholinesterase
genuine cholinesterase
type 1 cholinesterase
true cholinesterase
specific cholinesterase

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13
Q

What enzymes metabolize succinylcholine, mivacurium, and ester LAs and what is their primary location?

A

Plasma

butyrylcholinesterase
pseudocholinesterase
type 2 cholinesterase
false cholinesterase
plasma cholinesterase

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14
Q

Where is pseudocholinesterase produced?

A

Liver. Is an indicator of hepatic synthetic function.

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15
Q

Where is pseudocholinesterase located?

A

Liver, smooth muscle, intestines, white matter of brain, heart, and pancreas.

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16
Q

Where is pseudocholinesterase located?

A

Liver, smooth muscle, intestines, white matter of brain, heart, and pancreas.

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17
Q

What medications reduce pseudocholinesterase activity (and therefore increase succinylcholine duration)?

A

echothiopate
neostigmine
metoclopramide
esmolol
cyclophosphamide
oral contraceptives/estrogen
MAOIs
nitrogen mustard

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18
Q

What diseases reduce pseudocholinesterase activity?

A

atypical PChE
pregnancy (late stage)
chronic renal disease
severe liver disease
burns
organophosphate poisoning
neoplasm
malnutrition
advanced age

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19
Q

What conditions are sensitive to non-depolarizers and risk hyperK with succinylcholine administration?

A

Duchenne’s muscular dystrophy
Guillain-Barre
Multiple sclerosis
Amyotrophic lateral sclerosis

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20
Q

What conditions risk hyperK with sux and have a normal response to non-depolarizers?

A

Upregulation of AChRs
Charcot-Marie-Tooth
Hyperkalemic periodic paralysis

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21
Q

What conditions risk MH with sux but have a normal response to non-depolarizers?

A

Hypokalemic periodic paralysis
MH

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22
Q

Discuss sux and non-depolarizers in the patient with myasthenia gravis:

A

Resistant to sux
Sensitive to non-depolarizers

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23
Q

Intubating dose, time to max block (onset), time to return to 25% control (duration): Mivacurium

A

0.15 mg/kg
3.3 min
16.8 min

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24
Q

Intubating dose, time to max block (onset), time to return to 25% control (duration): Cisatracurium

A

0.1 mg/kg
5.2 min
45 min

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25
Q

Intubating dose, time to max block (onset), time to return to 25% control (duration): Vecuronium

A

0.1 mg/kg
2.4 min
45 min

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26
Q

Intubating dose, time to max block (onset), time to return to 25% control (duration): Atracurium

A

0.5 mg/kg
3.2 min
45 min

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27
Q

Intubating dose, time to max block (onset), time to return to 25% control (duration): Rocuronium

A

0.6 mg/kg
1.7 min
35 min

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28
Q

Intubating dose, time to max block (onset), time to return to 25% control (duration): Pancuronium

A

0.08 mg/kg
2.9 min
85 min

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29
Q

Metabolism, liver elimination, renal elimination, metabolites: Atracurium

A

Hofmann (33%) and non-specific plasma esterases (66%)
None
10-40%
Laudanosine (seizures)

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30
Q

Metabolism, liver elimination, renal elimination, metabolites: Cisatracurium

A

Hofmann (77%)
None
16% of total clearance
Laudanosine (seizures)

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31
Q

Metabolism, metabolites: Mivacurium

A

Pseudocholinesterases
No active metabolism

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32
Q

Metabolism, liver elimination, renal elimination, metabolites: Rocuronium

A

None
>70%
10-25%
None

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33
Q

Metabolism, liver elimination, renal elimination, metabolites: Vecuronium

A

Liver (30-40%)
40-50%
50-60
3-OH vecuronium

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34
Q

Metabolism, liver elimination, renal elimination, metabolites: Pancuronium

A

Liver (10-20%)
15%
85%
3-OH pancuronium

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35
Q

Rank volatile anesthetics in order of greatest to least potentiation of NMBs:

A

Des > Sevo > Iso > N2O > propofol

36
Q

Which antibiotics prolong NMB?

A

aminoglycosides
polymixins
clindamycin
lincomycin
tetracycline

37
Q

Which antidysrhythmics potentiate NMB?

A

verapamil
amlodipine
lidocaine
quinidine

38
Q

What diuretic can potentiate NMBs?

A

Furosemide

39
Q

Which electrolyte disturbances can potentiate NMB?

A

HyperMagnesium (decreased Ach release from presynaptic nerve
HyperLithium (activates potassium channels)
HypoKalemia (decreased resting membrane potential)
HypoCalcemia (decreased Ach release from presynaptic terminal)

40
Q

What patient factors contribute to NMB potentiation?

A

Hypothermia (decreased metabolism and clearance)
Gender (women > sensitive than men)

41
Q

What 3 NMBs release histamine?

A

Succinylcholine
Atracurium
Mivacurium

42
Q

What NMBs affect M2 receptors on the heart?

A

Succinylcholine - stim (brady)
Pancuronium - moderate blockade
Rocuronium - 0/slight blockade

43
Q

Which NMB can stimulate the autonomic ganglia and produce tachycardia?

A

succinylcholine

44
Q

What NMB should be avoided in HOCM and why?

A

Pancuronium has a vagolytic effect that leads to increased HR and CO with no change in SVR. This leads to increased LV outflow obstruction.

45
Q

Which 2 NMBs are most likely to cause anaphylaxis?

A

Succinylcholine (more likely)
Rocuronium

46
Q

What blood level can be used to diagnose anaphylaxis related to a NMB?

A

Elevated tryptase - peaks 15-120 minutes after exposure

47
Q

How is Ach inhibited by edrophonium?

A

Competitive inhibition by an electrostatic bond at the anionic site and a hydrogen bond at the esteratic site.
These are weak bonds, so duration of action is short.

48
Q

Describe the mechanism of action of acetylcholinesterase( AchE) and where it is located:

A

AchE terminates the effects of Ach by hydrolyzing it to choline + acetate. It is concentrated around the nicotinic receptors at the neuromuscular junction.

49
Q

What is the mechanism of action of AchE inhibitors?

A

AchE inhibitors prevent the breakdown of Ach. This leaves more Ach available at the NMJ to compete with the alpha binding sites on the nicotinic receptor and antagonize the block.

50
Q

Discuss pseudocholinesterase:

A

Resides in plasma.
Metabolizes succinylcholine.
Is inhibited by neostigmine and pyridostigmine, but NOT edrophonium.
The duration of sux is prolonged if given after neostigmine or pyridostigmine.

51
Q

In what two ways do AchE inhibitors increase Ach concentration at the nicotinic receptor?

A

Enzyme inhibition
Presynaptic effects

52
Q

Which AchE inhibitors form a carbamyl ester at the esteratic site?

A

neostigmine
pyridostigmine
physostigmine

53
Q

Why do neostigmine, pyridostigmine, and physostigmine have a longer duration of action?

A

Carbamyl ester bonds are strong, leading to longer duration of action.

54
Q

Dose, onset, duration, metabolism and elimination, and best anticholinergic pairing: Edrophonium

A

0.5 - 1.0 mg/kg
1-2 min
30-60 min
renal 75% , liver 25%
atropine

55
Q

Dose, onset, duration, metabolism and elimination, and best anticholinergic pairing: Neostigmine

A

0.02 - 0.07 mg/kg
5-15 min
45-90 min
renal 50%, liver 50%
glycopyrrolate

56
Q

Dose, onset, duration, metabolism and elimination, and best anticholinergic pairing: Pyridostigmine

A

0.1 - 0.3 mg/kg
10-20 min
60-120 min
renal 75% , liver 25%
glycopyrrolate

57
Q

Is a dose adjustment needed for AchE inhibitors in renal failure? Why or why not?

A

No, both drugs remain in the body longer, so no need to re-dose or adjust dose of AchE inhibitor.

58
Q

How is onset of action of an AchE inhibitor affected with a deeper degree of NMB?

A

Onset of action is longer
Ex: neostigmine will take longer to reach peak effect with 90% twitch suppression vs 50% twitch suppression

59
Q

What could happen if an AchE inhibitor is administered at full recovery?

A

Paradoxical muscle weakness

60
Q

What could happen if an AchE inhibitor is administered at full recovery?

A

Paradoxical muscle weakness

61
Q

List 4 drugs that reduce the incidence of shivering in the PACU

A

Physostigmine
Meperidine
Clonidine
Dexmedetomidine

62
Q

Why do AchE inhibitors cause parasympathetic side effects?

A

Increased Ach at the muscarinic receptor leads to parasympathetic stimulation

63
Q

Discuss cholinergic side effects:

A

DUMBBELLS
Diarrhea
Urination
Miosis
Bronchoconstriction
Bradycardia
Emesis
Lacrimation (increased tear production)
Laxation (elimination of fecal waste)
Salivation

64
Q

What are the MAC values of the inhalation agents?

A

Iso - 1.2%
Sevo - 2%
Des - 6.6%
Nitrous - 104%

65
Q

What is MAC-awake? When does it occur during induction? During emergence?

A

alveolar concentration where a patient opens their eyes
induction ~0.4 - 0.5 MAC
emergence ~ 0.15 MAC

66
Q

What is MAC-bar?

A

alveolar concentration required to Block the Autonomic Response to a supramaximal painful stimulus. it is ~ 1.5 MAC

67
Q

At what MAC is movement prevented in 95% of the population?

A

~1.3 MAC

68
Q

At what MAC are awareness and recall assumed to be prevented?

A

~0.4 - 0.5 MAC

69
Q

What is the most important site of volatile anesthetic action in the brain?

A

GABA-A receptor stimulation. This increases chloride influx through the ligand-gated chloride channel to hyper polarize the neurons. This impairs firing of the neurons. They most likely increase the time the channels remain open.

70
Q

Where do volatile anesthetics produce immobility?

A

In the ventral horn of the spinal cord
NOT due to GABA-A receptors in the spinal cord

71
Q

What are the most important sites of volatile anesthetic action in the spinal cord?

A

glycine receptor stimulation
NMDA receptor inhibition
Na channel inhibition

72
Q

How do gaseous anesthetics (Nitrous oxide and xenon) work?

A

NMDA antagonism
potassium 2P-channel stimulation

73
Q

What are the primary targets where volatile anesthetics produce unconsciousness?

A

cerebral cortex
thalamus
reticular activating system

74
Q

What are the primary targets where volatile anesthetics produce amnesia?

A

amygdala
hippocampus

75
Q

What are the primary targets where volatile anesthetics modulate autonomic tone?

A

pons
medulla

76
Q

What are the primary targets where volatile anesthetics produce immobility?

A

ventral horn in spinal cord

77
Q

What are the primary targets where volatile anesthetics produce analgesia?

A

spinothalamic tract

78
Q

Which inhalation agents increase heart rate?

A

Des
Iso
Nitrous

79
Q

Which inhalation agent decreases BP the most?

A

Iso

80
Q

What is the potency of coronary artery vasodilating abilities of volatile anesthetics from greatest to least?

A

Iso
Des
Sevo

81
Q

What conditions might the duration of succinylcholine be prolonged in due to decreased concentration of plasma cholinesterase?

A

muscular dystrophy
pregnancy
newborns
patients with acute infections
myocardial infarction

82
Q

Which NMB is associated with both vagal blockade and catecholamine release?

A

pancuronium

83
Q

Length of time to recovery at adductor pollicis with intubating dose of sux 1 mg/kg:

A

7 - 13 minutes

84
Q

How is etomidate metabolized?

A

This drug is metabolized by hepatic microsomal enzymes and undergoes extra hepatic clearance via plasma esterases.

85
Q

How is midazolam metabolized?

A

CYP3A4 enzymes in the liver and small intestine

86
Q

How is dexmedetomidine metabolized?

A

Extensively in the liver

87
Q

Renal clearance of NMBs from LEAST to MOST:

A

Cisatracurium
Rocuronium
Vecuronium
Pancuronium

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