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Pharmacology > N926 Pharmacology Final Exam > Flashcards

N926 Pharmacology Final Exam Flashcards

1
Q

MAC of Desflurane

A

6%

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2
Q

VP of Desflurane

A

669

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3
Q

BGC of Desflurane

A

0.42

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4
Q

Oil Gas of Desflurane

A

19

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5
Q

MOA of Desflurane

A

Unknown

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6
Q

MAC of Isoflurane

A

1.2%

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7
Q

VP of Isoflurane

A

238

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8
Q

BGC of Isoflurane

A

1.4

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9
Q

Oil Gas of Isoflurane

A

91

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10
Q

MOA of Isoflurane

A

Uknown

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11
Q

MAC of Sevoflurane

A

2%

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12
Q

VP of Sevoflurane

A

157

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13
Q

BGC of Sevoflurane

A

0.65

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14
Q

OGC of Sevoflurane

A

47

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15
Q

MOA of Sevoflurane

A

Unknown

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16
Q

MAC of Nitrous Oxide

A

104%

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17
Q

VP of Nitrous Oxide

A

38770mmHg

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18
Q

BGC of Nitrous Oxide

A

0.46

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19
Q

OGC of Nitrous Oxide

A

1.4

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20
Q

MOA of Nitrous Oxide

A

Unknown

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21
Q

MOA of Propofol

A

Gamma Aminobutyric acid agonist

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22
Q

PK of Propofol

A

First pass effect in Lungs
Hepatic Metabolism CYP450
(4-hydroxypropofol) active metabolite
not influenced by hepatic or renal dysfunction
highly protein bound in blood
pain on inject
decrease dose in eldery, increase dose in children

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23
Q

PD of Propofol

A

rapid and pleasant loss and return to consciousness
may induce myoclonus
neuroprotective
decrease in sympathetic tone and vasodilation
mild resp. depression common in induction doses
mild bronchodilation

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24
Q

Induction dose of Propofol

A

1.5-2.5MG/kg

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25
Q

TIVA dose of Propofol

A

100-300mcg/kg/min

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26
Q

MAC dose of Propofol

A

25-100mcg/kg/min

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27
Q

Vd for propofol

A

3.5-4.5 L/kg

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28
Q

Half-Life of Propofol

A

0.5-1.5 hour

Context sensitive half-time <40 mins

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29
Q

MOA of etomidate

A

Gamma-aminobutyric agonist

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30
Q

PK of Etomidate

A

large Vd
75% protein bound
metabolism by hydrolysis and plasma esterases

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31
Q

Etomidate inhibits

A

conversion of cholestrol to cortisol
11B-hydroxylase
causes adrenal cortical suppression

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32
Q

Etomidate is contraindicated in

A

patients with porphyrias

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33
Q

PD of Etomidate

A

rapid onset, return to consciousness 5-15 minutes
CBF and CMRO2 decreased
involuntary myoclonic movements >50% of patients
maintains hemodynamic stability
decrease in MV, but increase in RR
consider for cardiac compromised patients
increased risk for PONV

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34
Q

Induction dose of Etomidate

A

0.2-0.4 mg/kg

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35
Q

Vd of Etomidate

A

2.2-4.5L/kg

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36
Q

Half time of Etomidate

A

2-5 hour

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37
Q

MOA of Ketamine

A

N-methyl D-aspartate (NMDA) antagonist

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38
Q

PK of Ketamine

A

racemic mixture
not significantly protein bound
highly lipid soluble, rapid transfer of BBB
demethylation of CYP450

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39
Q

PD of Ketamine

A

produces dissociative anesthesia
has both amnestic and analgesic properties
increase CBF, CMRO2, and ICP (can be attenuated w/ benzo or opioid)
produces nystagmus, increase IOP
increases HR BP and SVR
Increased oral secretions
maintain spontaneous resp; slightly bronchodilator
risk for emergence delirium (attenuate with benzo)
indicated for trauma patients; possibly asthmatics

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40
Q

Induction Dose of ketamine

A

1-2.5mg/kg IV

4-8mg/kg IM

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41
Q

Multi-modal pain management of Ketamine

A

0.5-1mg/kg

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42
Q

Vd of Ketamine

A

2.5-3.5L/kg

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43
Q

Half-time of Ketamine

A

2-3 hours

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44
Q

5 Principle Pharmacologic effects of Benzodiazepines

A 
anxiolysis
anticonvulsant activity
anterograde amnesia
sedation/hypnosis
skeletal muscle relaxation
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45
Q

Most common adverse effects of benzodiazepines

A

unexpected respiratory depression and oversedation

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46
Q

MOA of Midazolam

A

Gamma-Aminobutyric Acid (GABA) agonist

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47
Q

PK of Midazolam

A

water soluble with an imidazole ring (no discomfort on injection)
High lipid solubiltiy
highly pound to plasma proteins
metabolized by hydrolysis (1- hydroxymidazolam/4-hydroxymidazolam)
1-hydroxymidazolam half the activity
metabolism slowed by drugs that inhibit CYP450

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48
Q

PD of Midazolam

A

decreases CMRO2 and CBF
cerebral vasomotor responsiveness to CO2 is preserved
does not attenuate responses to intubation

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49
Q

Midazolam is synergisitc with

A

fentanyl

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50
Q

Midazolam at 0.2mg/kg produces

A

decrease in BP, increase in HR d/t changes in SVR

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51
Q

Midazolam should be avoided in patients with

A

acute porphyrias

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52
Q

Dosing of Midazolam

A

0.02-0.04mg/kg IV
0.4-0.8mg/kg oral
1-7mg/hr postoperative sedation

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53
Q

Vd of midazolam

A

1-1.7L/Kg

increased in elderly and obese

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54
Q

Half time of Midazolam

A

1.9 hours

2-4 Hours

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55
Q

MOA of diazepam

A

Gamma Aminobutyric Acid agonist

56
Q

PK of Diazepam

A

insoluble in water and painful on injection
highly lipid solubility
crosses the placenta
extensively protein bound
metabolized by oxidation (desmethyl diazepam/oxazepam)
Exhibits a near-linear relationship between elimination half-life and patient age

57
Q

Desmethyl Diazepam

A

may cause return of drowsiness at 6-8 hours and has a half life of 48-96 hours

58
Q

PD of diazepam

A

produces minmial depressive effects on ventilation

minimal decrease in BP, CO, SVR

59
Q

Diazepam has synergistic effects with

A

fentanyl that decreases BP and SVR

60
Q

Diazepam should be avoided

A

in patients with acute porphyrias

61
Q

Dosage of Diazepam for Seizures

A

0.1mg/kg IV effective in abolishing seizure activity

62
Q

Vd of Diazepam

A

0.8-1.3 L/kg

63
Q

Half time of Diazepam

A

20-50 hours

64
Q

MOA of Lorazepam

A

Gamma-aminobutyrc acid agonist

65
Q

PK of Lorazepam

A

most potent benzo, slowest onset of action
insoluble to water and pain on injection
conjugated with glucuronic acid in the liver (inactive metabolites)
less likely to be influenced by alteration in liver function

66
Q

PD of Lorazepam

A

Duration of sedative effects last longer (6-10 hours)

delayed emergence and weaning of ventilator

67
Q

Lorazepam should be avoided in patients with

A

porphyias

68
Q

Dosage of Lorazepam

A

50mcg/kg

max: 4mg

69
Q

Vd of Lorazepam

A

0.8-1.3L/kg

70
Q

Half time of Lorazepam

A

10-16 hours

71
Q

MOA of Flumazenil

A

Selective benzodiazepine antagonist (weak intrinsic agonist of GABA)

72
Q

PD of Flumazenil

A

not recommended for patients being treated with anti-epileptic meds for seizure control
will not cause acute HTN, tachycardia or anxiety
will not alter MAC requirements

73
Q

Dosing of Flumazenil

A

0.2mg IV followed by 0.1mg q1min
0.5-1mg completely abolish benzo effects
still unresponsive, have another problem

74
Q

MOA Thiopental

A

GABA agonist

75
Q

PK Thiopental

A

Rapid distribution

metabolized in liver by oxidation (pentobarbital active metabolite)

76
Q

PD Thiopental

A

Decrease in CRMO2, CBF, ICP
reverse steel effect
decrease MAP and CO (decrease in venomotor tone and neg inotropic effects)
respiratory depression

77
Q

Thiopental is contraindicated

A

intermittent porphyria

78
Q

When is thiopental an medical emergency

A

inadvertent arterial administration

79
Q

Induction dose of thiopental

A

2.5-5mg/kg

80
Q

Vd of Thiopental

A

Large

81
Q

Half life of Thiopental

A

relatively long (ten fold of propofol and prolonged in pregnacy d/t protein binding

82
Q

Methohexital is used for

A

ECT

83
Q

MOA of methohexital

A

GABA agonist

84
Q

PK of Methohexital

A

rapid distribution

metabolized in liver by oxidation (pentobarbital active metabolite)

85
Q

In Methohexital, what increases hypnotic potency but lowers seizure threshold and causes myoclonus

A

methyl on N

86
Q

PD of methohexital

A

Decrease in CRMO2, CBF, ICP
reverse steel effect
decrease MAP and CO (decrease in venomotor tone and neg inotropic effects)
respiratory depression

87
Q

INduction dose of methohexital

A

1-2 mg/kg

88
Q

Vd of Methohexital

A

large

89
Q

half life of methohexital

A

relatively long, (10 fold of propofol and prolonged in pregnancy due to protein binding)

90
Q

Morphine MOA

A

opioid receptor agonist

91
Q

PK of morphine

A

primary metabolism by conjugation and glucuronic acid

92
Q

metabolite of morphine

A

morphine 6 glucronide

93
Q

Morphine’s metabolite

A

longer DOA then morphine and higher analgesic potency 65x

94
Q

Renal Function and Morphine

A

impaired renal function can result in accumulation and unexpected respiratory depression

95
Q

PD of Morphine (CV)

A

bradycardia with sustained BP

orthostatic Hypotension

96
Q

Morphine is synergistic with

A

benzos and N20

97
Q

PD of Morphine (Resp)

A 
dose dependent ventilation depression accompanied by compensation in tidal volume
decrease responsiveness to CO2
decreased ciliary action
increased airway resistance
depression of medullary cough centers
98
Q

PD of Morphine (CNS)

A

decreased CBF and ICP
miosis d/t edinger-westphal nucleus of oculomotor nerve
“When pain is relieved, sedation can occur”

99
Q

PD of Morphine- General

A

muscle rigidity
spasms of biliary smooth muscle and sphincter of oddi
decreased gastric motility and constipation
increased N/V
urinary urgency
warmed flush skin and histamine release

100
Q

Dosing of Morphine

A

2-4 mg

101
Q

MOA Demerol (Meperidine)

A

Mu recpetor agonist

used for post-op shivering

102
Q

PK of Demerol

A

1/10 as potent as morphine
metabolized by demethylization and hydrolysis (normeperidine)
decreased renal function can result in accumulation of metabolites

103
Q

PD of Demerol

A

increase HR, mydriasis
delirium and seizures
Crosses the placenta

104
Q

Demerol and patients taking MAOi

A

serotonin syndrome

105
Q

Fentanyl MOA

A

opioid agonist

106
Q

Dosing of Demerol

A

12.5 mg is for post-op shivering

107
Q

PK of Fentanyl

A

rapid onset and highly lipid soluble
first pass uptake in lungs
metabolized by N-dealkylation and hydroxylation

108
Q

Cirrhosis with Fentanyl

A

does not prolong elimination half-time

109
Q

PD of Fentanyl

A

“secondary peaks” from pulmonary uptake
does not evoke histamine release
bradycardia is more prominent
increase ICP

110
Q

Fentanyl is synergistic with

A

propofol and versed

111
Q

Dosing of Fentanyl

A

1-3mcg/kg to blunt SNS to response and provide analgesia

112
Q

Vd of fentanyl

A

large

>80% leaves the plasma in less than 5 mins

113
Q

Fentanyl Context Sensitive 1/2 time

A

increases with infusion

>2hr

114
Q

Sufentanil MOA

A

opioid agonist

115
Q

PK of Sufentanil

A

5-10 more potent then fentanyl
extensive protein binding compared to fentanyl
significant first pass pulmonary uptake
Metabolized by N-deakylation and O-demethylation (desmethyl sufentanil)
clearance sensitive to hepatic flow and normal renal function important

116
Q

PD of Sufentanil

A

decreased CMRO2
decreased HR and CO
may cause chest wall rigidity

117
Q

Dosing of Sufentanil

A

0.1-0.4mcg/kg for analgesia (longer analgesia and respiratory depression than fentanyl)

118
Q

Vd of Sufentanil

A

large

119
Q

Context sensitive 1/2 time of Sufentanil

A

30 minutes

120
Q

MOA Alfentanil

A

opioid agonist

121
Q

PK of Alfentanil

A

less potent than fentanyl, shorter duration of action
metabolized by N-dealkylation
rapid onset

122
Q

PD of Remifentanil

A

seizure like activity
decrease in BP and ventilation
no post-op pain coverage

123
Q

Dosing of Reminfentanil

A

1-3 mcg/kg induction

0.1-0.3 mcg/kg/min infusion

124
Q

Vd of Reminfentanil

A

small

125
Q

Context sensitive 1/2 time of Reminfentanil

A

4 mins

126
Q

PD of Alfentanil

A

acute dystonia; avoid with untreated Parkinson’s

Significant decrease in BP

127
Q

Dosing of Alfentanil

A

15 mcg/kg

128
Q

Vd of Alfentanil

A

small

129
Q

Context sensitive 1/2 time fo Alfentanil

A

60 minutes

130
Q

MOA of Remifentanil

A

selective Mu agonist

131
Q

PK of Remifentanil

A

potency is the same as fentanyl
metabolized by non-specific plasma esterase
not affected by pseudocholinersterase deficiency

132
Q

Remifentanil is synergistic with

A

propofol

133
Q

1/2 Life of Fentanyl

A

2-4 hours

134
Q

Life Life of Remifentanil

A

0.1-0.3 hours

135
Q

1/2 Life of Sufentanil

A

2-5 hours

136
Q

1/2 Life of Alfentanil

A

1 hour

Pharmacology (14 decks)

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