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Pharm Oral Boards > All drugs > Flashcards

All drugs Flashcards

1
Q

What does GABA stand for?

A

GABA is a gamma aminobutyric acid

We have many drugs that bind to GABA to elicit an action including propofol, benzodiazepines, and methohexital

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2
Q

Tylenol is metabolized

A

In the liver

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3
Q

What do we give for a Tylenol overdose?

A

Charcoal & mucomyst (acetylcysteine)

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4
Q

What is the dosage of Tylenol?

A

Q4-Q6 325-650 mg not to exceed 4 G/day
Can give IV Tylenol Ofirmev Q6 1000 mg
For alcoholics do not give more than 2000 mg/day

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5
Q

What drugs are acids?

A

propofol
NSAIDs
Barbiturates

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6
Q

Why does acetaminophen cause liver failure?

A

Damage to the liver results from the metabolite (N-acetyl-p-benzoquinoneimine) which depletes glutathione

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7
Q

Tylenol is a

A

Non selective cox inhibitor NSAID which provides antipyretic and analgesic properties (through activation of serotonergic pathways; antagonism of NMDA, substance P, nitric oxide)
It does NOT have anti inflammatory properties

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8
Q

What does NSAID stand for?

A

Non-steroidal anti-inflammatory drug

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9
Q

What does Cox stand for?

A

Cyclooxygenase inhibitor

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10
Q

Describe the difference between Cox 1 and Cox 2 pathways. What is the difference between selective and non-selective Cox inhibitors?

A

Cox 1: secretion of stomach protective enzymes, protects kidneys, and platelet aggregation through thromboxane A2
Tylenol, ibuprofen- non selective so get good and bad side effects (I.e. concern for stomach ulcers, kidney function)
Cox 2: fever, analgesia, inflammation
Example is Celebrex (selective Cox 2 drug) but can cause cause CV issues

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11
Q

What class of drug is ibuprofen and what does it do?

A

Non selective Cox inhibitor NSAID

Anti-inflammatory, anti-pyretic, and analgesia

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12
Q

How is ibuprofen metabolized?

A

By the liver, excreted by the kidneys

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13
Q

What is the volume of distribution of ibuprofen?

A

Very low Vd to the point where we really don’t care what the pKa is because it stays in the vasculature

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14
Q

The use of ibuprofen is limited in the OR setting because

A

It leads to GI dysfunction and platelet aggregation

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15
Q

List the MAC, BP, VP, BG, & OG for desflurane.

A

MAC: 6%, BP: 24, VP: 669, BG 0.42, OG: 19

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16
Q

List the MAC, BP, VP, BG, and OG for isoflurane.

A

MAC: 1.2%, BP 49, VP 238, BG 1.46, OG: 91

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17
Q

List the MAC, BP, VP, BG, and OG for nitrous oxide.

A

MAC: 104%, BP -88, VP 38,770, BG: 0.42, OG: 1.4

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18
Q

List the MAC, BP, VP, BG, and OG for sevoflurane.

A

MAC: 2%, BP 59, VP: 157, BG 0.65, OG: 47

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19
Q

What drug is used for inhalational inductions?

A

sevoflurane

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20
Q

What does oil gas indicate?

A

potency

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21
Q

What does blood gas indicate?

A

solubility; it indicates how much of the drug is bound to blood so for isoflurane there is 1.42 molecules of gas bound to blood for every 1 molecule that is not making it have a slower onset

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22
Q

Describe the stages of anesthesia.

A

Stage 1: amnesia and anesthesia… still following commands, reflexes maintained, spontaneous breathing, just sleepy
Stage 2: delirium and excitation stage… hemodynamically hyperactive, do not do anything to them in this stage as we could cause a laryngospasm or even death
Stage 3: surgical anesthesia… cessation of spontaneous breathing, reflexes no longer maintained,
Stage 4: anesthetic overdose; CV collapse, intervention required

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23
Q

The three A’s of anesthetics include

A

analgesia, areflexia, and amnesia

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24
Q

The 7 properties of an ideal drug include

A

bronchodilation, antiemetic, analgesia, quick on and offset, advantageous PK and PD, minimal CV and Resp. side effects, minimal toxicity and histamine release

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25
Q

Describe the difference between PK and PD

A

PK is what the body does to the drug (absorption, distribution, metabolism, and excretion)
PD is what the drug does to the body (receptor theory and dose/response curve)

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26
Q

What is ‘uncoupling’?

A

seen in anesthetic gases… it is where we have increased CBF and decreased CMRO2

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27
Q

What is the MOA of inhalational drugs?

A

unknown but possibly due to NMDA receptors, VGNa+ receptors, GABA receptors, glycine receptors, and potassium channels

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28
Q

Developmental neurotoxicity with gases

A

has not been demonstrated in human children… rule of thumb is to keep surgeries short and use short acting medications

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29
Q

What is a contraindication of using nitrous oxide?

A

pulmonary hypertension, pregnancy, surgeries involving the tympanic membrane or any surgery where gas can diffuse into an air filled space

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30
Q

Nitrous oxide has two good uses when used with other gases:

A

it can speed up the onset of action and make iso look more like des
-it can offset hemodynamics of other agents and keep blood pressure in a stable plane

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31
Q

What agents are known to contribute to emergence delirium in kids?

A

desflurane and sevoflurane

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32
Q

Gases are beneficial to the pulmonary system in that they

A

reduce hypoxic pulmonary vasoconstriction

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33
Q

Sensitization means that

A

volatile agents reduce the quantity of catecholamines necessary to evoke arrhythmias

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34
Q

Preconditioning is

A

a phenomenon in which the heart is exposed to a cascade of intracellular events that protect it from ischemic and reperfusion insult

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35
Q

What inhalational agent undergoes the greatest metabolism?

A

sevoflurane at 5-8% in the liver

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36
Q

What is a MAC?

A

it is the minimal alveolar concentration where 50% of the population will not move on surgical incision

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37
Q

List the factors that increase MAC requirements

A

hyperthermia, drug induced increases in CNS activity, hypernatremia, chronic alcohol abuse

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38
Q

Factors that decrease MAC requirements:

A

hypothermia, increasing age, alpha-2 agonists, acute alcohol ingestion, pregnancy, and hyponatremia

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39
Q

Desflurane should not be given to

A

people with reactive airways because it is very pungent

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40
Q

Factoids about nitrous oxide

A

is supports combustion like oxygen so must be careful

NMDA receptor antagonist so can lower risk of chronic pain after surgery

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41
Q

Malignant hyperthermia can be caused by:

A

volatile induction agents, succinylcholine, and stress

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42
Q

Malignant hyperthermia is due to

A

ryanodine receptor gene mutation on chromosome 19

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43
Q

Signs and symptoms of malignant hyperthermia include

A

increased CO2, muscle rigidity, metabolic acidosis, and high temperature

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44
Q

What is the metabolism of propofol?

A

metabolized in the liver, phase I
clearance exceeds hepatic blood flow
not influenced by hepatic/renal function

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45
Q

What is the MOA of propofol?

A

GABA allosteric agonist

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46
Q

What is the context sensitive half-time of propofol?

A

40 minutes

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47
Q

Propofol undergoes

A

first pass uptake in the lungs

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48
Q

What are the factors that make propofol an non-ideal drug?

A

burns on injection
causes decreased BP through decrease in sympathetic tone and vasodilation
can cause hypersensitivity (still low incidence) d/t some of the additives

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49
Q

One of the biggest concerns with long-term propofol infusion is

A

PRIS syndrome; typically not seen in the surgical setting but it can cause death

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50
Q

The Vd of propofol is

A

large

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51
Q

Propofol has this effect on the respiratory system:

A

respiratory depression

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52
Q

Propofol has a

A

rapid and pleasant loss and return to consciousness

also has an active metabolite but we’re not very concerned with it

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53
Q

The pKa of propofol is

A

11

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54
Q

The pKa of etomidate is

A

4.2

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55
Q

The MOA of etomidate is

A

GABA allosteric agonist

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56
Q

The Vd of etomidate is

A

large

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57
Q

The effect of etomidate on the CV system is

A

to keep CV and BP steady

acts on alpha adrenergic receptors

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58
Q

Etomidate is metabolized by

A

hydrolysis in the liver (phase 1)

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59
Q

One frequent side effect of etomidate is

A

myoclonus

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60
Q

Etomidate is used as an induction agent

A

because it has a quick onset and offset (5-10 min.)

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61
Q

A concern with etomidate is

A

it can cause adrenocortical suppression via the enzyme 11 beta hydroxylase

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62
Q

These drugs are contraindicated in porphyrias

A

etomidate, barbiturates, and diazepam

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63
Q

Etomidate is

A

neuroprotectant… it decreases CBF and CMRO2

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64
Q

Ketamine’s MOA is

A

NMDA receptor antagonist

N-methyl-D apartate

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65
Q

The pKa of ketamine is

A

7.5

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66
Q

Vd of ketamine is

A

large

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67
Q

Ketamine produces

A

“dissociative anesthesia”, eyes open, corneal reflexes intact

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68
Q

Ketamine is given typically to

A

trauma patients because it causes an increase in BP, HR, and SVR

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69
Q

Ketamine should be avoided in patients with

A

head trauma or eye injury because it increases CBF, CMRO2, ICP, and IOP

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70
Q

Ketamine is metabolized by

A

liver in phase 1

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71
Q

____ should be given in conjunction with ketamine to avoid ______

A

benzodiazepines; emergence delirium

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72
Q

The elimination half time of ketamine is

A

2-3 hours

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73
Q

Ketamine can be good for pediatric

A

asthmatics…. “ketamine dart”

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74
Q

Ketamine can be used for

A

induction, analgesia, and TIVA

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75
Q

Mechanism of action of dexmedetomidine

A

works on alpha 2 agonist

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76
Q

Benefits of dexmedetomidine

A

easily arousable, lowers MAC and opioid requirements

causes sedation without decreased awareness

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77
Q

The half-life of dexmedetomidine

A

is 2-3 hours

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78
Q

Dexmedetomidine is metabolized by

A

the liver phase 1

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79
Q

The biggest concerns with dexmedetomidine is

A

bradycardia and hypotension

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80
Q

MOA of diazepam

A

GABA allosteric agonist

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81
Q

Vd of diazepam

A

large

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82
Q

Protein binding with diazepam

A

extensively protein bound so cirrhosis and renal insufficiency would increase unbound diazepam with increased side effects

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83
Q

Diazepam is metabolized by

A

phase I in the liver

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84
Q

The active metabolites of diazepam include

A

nordiazepam and oxazepam

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85
Q

The elimination half-time in diazepam is

A

long >40 hours, increases linearly with age

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86
Q

The five properties that benzodiazepines cause include

A

anxiolytic, sedative/hypnotic, spinal cord mediated relaxation, anterograde amnesia, anticonvulsant

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87
Q

The onset of action of lorazepam

A

slower than midazolam or diazepam so limits clinical anesthesia use
peak effect 20-30 minutes
antegrade amnesia may last up to 6 hours with minimal sedation

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88
Q

How is lorazepam metabolized?

A

stage 2 in the liver

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89
Q

What is the Vd of lorazepam?

A

large

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90
Q

The elimination half-time of lorazepam is

A

14 hours

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91
Q

Lorazepam may be used for

A

postoperative sedation of intubated patients

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92
Q

What is the mechanism of action for midazolam?

A

GABA allosteric agonist

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93
Q

What is the pKa of midazolam?

A

6.15

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94
Q

What is the volume of distribution of midazolam?

A

large

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95
Q

The property that gives midazolam this characteristic is

A

the imidazole ring…. no discomfort on injection

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96
Q

Midazolam is metabolized by

A

CYP 450 via oxidation; phase 1 in the liver

liver disease can affect

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97
Q

The biggest concern side effect when giving midazolam is

A

strong synergism with opioids cause respiratory depression

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98
Q

The elimination half-time of midazolam is

A

1.9 hours

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99
Q

Midazolam cause these CNS effects

A

not neuroprotective, decreases CMRO2 and CBF, does not prevent increase in ICP with laryngoscopy

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100
Q

The MOA of flumazenil

A

selective benzodiazepine antagonist

weak intrinsic agonist activity attenuates abrupt reversal

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101
Q

Thiopental MOA

A

acts on GABA allosteric agonists

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102
Q

What is the volume of distribution of thiopental

A

large

effects terminated by redistribution

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103
Q

Where is thiopental metabolized?

A

in the liver; phase 1

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104
Q

Thiopental is contraindicated in

A

porphyrias

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105
Q

Inadvertent administration of thiopental necessitates

A

administration of papervine, heparinization, and vasodilation via regional block technique

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106
Q

Thiopental’s elimination half-time

A

long 3-8 hours

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107
Q

Thiopental is

A

an acid and a barbiturate

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108
Q

Thiopental’s effect on CV

A

decreased MAP and CO

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109
Q

Thiopental’s effect on CNS

A

reverse steal effect, burst suppresion, and isoelectric EEG

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110
Q

Thiopental’s effect on respiratory

A

respiratory depression, may cause apnea

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111
Q

Methohexital’s MOA

A

acts on GABA allosteric agonists

112
Q

Methohexitals Vd

A

large volume of distribution

113
Q

Methohexital is a

A

barbiturate, acid, and contraindicated in porphyrias

114
Q

The main use of methohexital is to

A

used in ECT to lower the seizure threshold

115
Q

Methohexital is metabolized in

A

the liver via phase 1

116
Q

Thiopental has an

A

active metabolite known as pentobarbital

117
Q

Methohexital’s half-life is

A

4 hours

118
Q

Methohexital and thiopental have an onset of action of

A

30 seconds

119
Q

Risk factors for PONV include:

A

young age, female gender, non-smoker, opioid usage (intraop and postop), previous hx., laparoscopic surgeries

120
Q

The mechanism of action of ondansetron is

A

acts as serotonin receptor antagonists (5-HT3)

mediates vomiting and is found in GI tract (abdominal vagal afferents) and brain (CTZ)

121
Q

Onset of ondansetron is

A

30 minutes

half-life is 4 hours so should be administered towards the end of the case

122
Q

Ondansetron is metabolized by

A

liver Phase 1 (hydrolysis) & Phase 2 (conjugation)

123
Q

Ondansetron produces mild side effects

A

HA & QT prolongation

124
Q

Promethazine MOA

A

Also known as phenergan

antihistamine, anticholinergic, and antimuscarinic

125
Q

The major side effect of promethazine is

A

can result in significant sedation when administered with opioids
also avoid in elderly because it can cause confusion and constipation

126
Q

Promethazine is metabolized in

A

the liver

127
Q

The mechanism of action of reglan is

A

centrally acting on dopamine receptor antagonist (D2) to CTZ

128
Q

Metoclopramide works by

A

increasing LES tone, speeding gastric emptying time, lowers gastric fluid volume

129
Q

metoclopramide is metabolized in

A

the liver

130
Q

The risk factors associated with metoclopramide include:

A

Extrapyramidal side effects; contraindicated in Parkinson’s disease, seizure, GI obstruction, and pheochromocytoma

131
Q

The mechanisms of action of dexamethasone

A

long-acting corticosteroid

synthetic glucocorticoid with anti-inflammatory and immunosuppressant properties

132
Q

Uses of dexamethasone

A

as a steroid to reduce inflammation or as an antiemetic (give early in the case)

133
Q

Dexamethasone is metabolized by

A

the liver

134
Q

Do not give dexamethasone in cases of

A

hypersensitivity, uncontrolled infections, cerebral malaria, concurrent live vaccinations

135
Q

The mechanism of action of oxytocin is

A

lowers threshold for depolarization of uterine smooth muscle

increases prostaglandin production

136
Q

Oxytocin is used to

A

reduce blood loss after delivery; administered as soon as the cord is cut
at a low controlled rate it is also used to induce labor

137
Q

Oxytocin should never

A

be bolused IV… it causes vasodilation and decreased SVR which can cause hypotension and bradycardia

138
Q

Hemabate is a

A

prostaglandin and it works by increasing myometrial calcium levels and increasing MLCK activity and thus uterine contraction

139
Q

Hemabate is the

A

third line of defence for PPH

140
Q

The use of hemabate (resp)

A

can result in bronchospasm, V/Q mismatch and hypoxemia in women with reactive airways
monitor O2 and lung sounds

141
Q

Methergine MOA

A

methergine is an ergot alkaloid

MOA unclear- though to be an a-adrenergic agonist

142
Q

IV administration of methergine can result in

A

Profound hypertension, severe N/V, and cerebral hemorrhage

143
Q

Methergine is contraindicated in women with

A

hypertension, PVD or ischemic heart disease

N/V can occur; have vasodilating drugs available

144
Q

The mechanism of action of edrophonium

A

acetylcholinesterase inhibitor

allows for buildup of Ach at the NMJ and accelerates recovery from NMBD

145
Q

What are the side effects of edrophonium

A

bronchoconstriction, salivation, increased bowel motility, urination, severe bradycardia

146
Q

Edrophonium should be given to

A

reverse NMBD but only non-depolarizers

147
Q

Edrophonium should be given with

A

atropine

148
Q

The mechanism of action neostigmine is

A

acetylcholinesterase inhibitor

allows for buildup of Ach at the NMJ and accelerates recovery from NMBD

149
Q

Neostigmine should be given with

A

glycopyrolate to avoid effects such as bradycardia, increased bowel motility

150
Q

The mechanism of action of atropine is

A

anti-cholinergic drug

blocks mACHr

151
Q

The onset of edrophonium and neostigmine is

A

5-10 minutes

152
Q

The half-life of edrophonium is

A

110 minutes

153
Q

The half-life of neostigmine is

A

70-80 minutes

154
Q

The side effects of anticholinergic drugs (atropine & glycopyrolate) include

A

dry mouth, mydriasis, difficulty swallowing, tachycardia, dry skin, flushed, increased body temperature

155
Q

The mechanism of action of glycopyrrolate is

A

anti-cholinergic

156
Q

The mechanism of action of scopolamine is

A

anti-cholinergic

157
Q

Scopolamine can be used for

A

preoperative sedation, PONV

158
Q

Scopolamine can cause

A

amnesia and sedation, adverse effects include dry mouth, increased thirst, dry skin, constipation, drowsiness, dizziness, blurred vision, dilated pupils, light sensitivty

159
Q

Scopolamine is metabolized by

A

the liver

160
Q

The elimination half-life of scopolamine is

A

4.5 hours

161
Q

The MOA of succinylcholine is

A

depolarizing neuromuscular blocking drug

162
Q

The duration of action of succinylcholine is short

A

14 minutes due to rapid hydrolysis

163
Q

How is succinylcholine metabolized

A

via pseudocholinesterase or butrylcholinesterase in the blood

164
Q

How quickly does succinylcholine create intubating conditions?

A

60 seconds

165
Q

The Dibucaine number can be used to indicate

A

the level of butylcholinsterase in the blood which will indicate how prolonged the block of succinylcholine is

166
Q

What is the reversal for succinylcholine?

A

there is none because it is metabolized so quickly in the blood

167
Q

Side effects of succinylcholine include:

A

hyperkalemia, myoglobinuria, bradycardia, dysrthymias, increased intraocular pressure, increased intracranial pressure, myalgias, & masseter spasm

168
Q

Succinylcholine should not be given to

A

patients < 5 years old b/c it is contraindicated in patients with duchene muscular dystrophy, and cardiac arrest from hyperkalemia can occur

169
Q

succinylcholine lasts for

A

9 to 13 minutes

170
Q

Atricurium’s MOA is

A

non-depolarizing muscular blocking drug

specifically a benzylisoquinolium

171
Q

What limits the usage of atricurium?

A

Histamine release

172
Q

How is atricurium eliminated?

A

through ester hydrolysis and spontaneous degradation

Hoffman elimination

173
Q

What is the MOA of ciastricurium?

A

non-depolarizing muscular blocking drug

specifically a benzylisoquinolium

174
Q

Atricurium has an active metabolite

A

known as Laudanosine and it is implicated in convulsions although not seen in a typical anesthesia dose

175
Q

Atricurium and cisatricurium have (onset)

A

an intermediate onset

176
Q

Cisatricurium is metabolized by

A

Hoffman elimination

177
Q

Cisatricurium is different from atricurium in that

A

it does not cause histamine release

178
Q

What is the volume of distribution of NMBDs?

A

small

179
Q

The steroidal compounds of NMBDs include:

A

pancuronium, vecuronium, and rocuronium

180
Q

Pancuronium is a

A

long acting NMBD

181
Q

The onset time to maximum block of pancuronium is

A

2.9 minutes

182
Q

Pancuronium is cleared by

A

the kidney

183
Q

Pancuronium is used during

A

cardiac surgeries because it has vagolytic inhibiting properties to help maintain HR & BP

184
Q

Vecuronium is a

A

intermediate-acting neuromuscular blocking drug

185
Q

The onset time to maximum block of vecuronium is

A

2.4 minutes

186
Q

Vecuronium is different from pancuronium in that

A

there is a slight decrease in potency and loss of vagolytic properties

187
Q

Vecuronium is metabolized in

A

the liver

188
Q

The relationship between potency and onset with NMBDs

A

increased potency= slower onset

189
Q

List the factors that increase the potency of NMBDs

A

antibiotics- clindamycin, hypothermia, magnesium sulfate, local anesthetics, quinidine, inhalational agents

190
Q

Rocuronium is an

A

intermediate-acting neuromuscular blocker

191
Q

The time to maximum block for rocuronium is

A

1.7 miutes

192
Q

Rocuronium is primarily metabolized

A

in the liver

193
Q

Adverse effects of NMBDs include:

A

can have bradycardia and hypotension, histamine release can cause lots of issues

194
Q

Which of the NMBDs has the highest potential for allergic reactions?

A

rocuronium (because it is given so frequently)

195
Q

Neostigmine has

A

a ceiling effect, once threshold is reached, additional doses have no effect
cannot antagonize profound or deep levels of blockade
maximum block depth that can be antagonized corresponds to return of the fourth twitch in TOF

196
Q

To ensure adequate reversal we want to see

A

TOF >0.9 with qualitative monitoring
only true objective monitoring
(it will not give you a number until you’ve had 4 twitches)

197
Q

Sugammedex can be used

A

to reverse steroidal agents

198
Q

Sugammedex side effects

A

possible allergic reactions and bleeding, can make pulmonary hypertension in peds worse, and can cause oral contraceptives to be ineffective

199
Q

Sugammedex works by

A

encapsulating and deactivating NMBDs

it is a modified gamma cylcodextrin

200
Q

Toradol should not

A

be given to patients with impaired renal function

201
Q

Non-selective NSAIDs usage is limited in preop because

A

causes GI toxicity, platelet dysfunction, and delayed bone healing (safe in the setting of primary bone healing)

202
Q

Celebrex is

A

the only available cox-2 inhibitor
has less GI toxicity
increased CV risk

203
Q

Risk factors for the development of GI complications due to NSAIDs include

A

elderly, H. pylori infection, hx. of previous ulcer, concomitant use of aspirin, anticoagulants, or corticosteroids

204
Q

Celebrex is associated with

A

increased risks of MI, HF, and HTN

205
Q

In patients with CV risks,

A

naproxen is NSAID of choice

206
Q

Hypersensitivity with NSAIDs can be seen with a combination of

A

allergic rhinitis, nasal polyps, and asthma

207
Q

Lidocaine is used for

A

multimodal pain management plan to supplement general anesthesia

208
Q

The mechanism of action for lidocaine is

A

uncertain; may involve sodium channels or block priming of polymorphonuclear granulocytes

209
Q

What drugs undergo first pass extraction in the lungs?

A

lidocaine & propofol

210
Q

Lidocaine is metabolize in

A

the liver

211
Q

Morphine is a

A

naturally occurring opiate

212
Q

In appropriate doses, opioid agonists

A

produce analgesia; do not cause loss of touch, loss of proprioception, and loss of consciousness

213
Q

The mechanism of action of opioids

A

Opioids are agonist that work on the GPCRs of opioid receptors, decreases neurotransmission and mimics the actions of endogenous ligands
Specifically, exogenous substances act on postsynaptic neurons to increase K+ conductance and decrease function

214
Q

Opioids do not

A

block nerve impulses or alter responsiveness of afferent nerve endings to noxious stimulation

215
Q

Opioid receptors are primarily found

A

in the brain and spinal cord

216
Q

All opioids are metabolized in

A

the liver except for remifentanil

217
Q

A common CV side effect of opioid administration is

A

bradycardia with sustained BP, orthostatic hypotension, cardiac protectant effect

218
Q

Common respiratory side effects of opioids include

A

slow and deep
decreased responsiveness to CO2
dose-dependent depression of ventilation
increase airway resistance

219
Q

Common CNS side effects of opioids include

A

awareness is possible they are not anesthetics
sedative and euphoric effects, decreased CBF, used cautiously in head trauma patients b/c it alters wakefulness, miosis is d/t to action of Edinger-Westphal nucleus of oculomotor nerve

220
Q

Morphine causes sedation

A

that precedes analgesia

221
Q

In the biliary tract

A

opioids cause spasm of biliary smooth muscle and the sphincter of Oddi
morphine can contract pancreatic ducts and mimic acute pancreatitis

222
Q

Opioids exert effects on the GI tract including

A

constipation, decreased GI motility, and N/V

223
Q

GU effects of opioids include

A

urinary retention

224
Q

Morphine is the biggest culprit in

A

cutaneous changes- causes histamine release and lots of itching

225
Q

The overdose triad includes

A

miosis, hypoventilation, and coma

226
Q

Morphine side effects include

A

nausea, body warmth, pruritis (nose), dry mouth, and extremity heaviness

227
Q

The onset of action of morphine is

A

15-30 minutes

228
Q

Morphine has significant

A

renal metabolism and metabolism in the liver phase 2

229
Q

Morphine has a long half-life due to

A

active metabolite

230
Q

Meperidine MOA

A

MU-receptor agonist

anti-shivering is d/t stimulation of kappa receptors

231
Q

Meperdine is (potency)

A

1/10th as potent as morphine

232
Q

the duration of action of meperdine is

A

2-4 hours

233
Q

Meperdine is metabolized in

A

the liver

234
Q

Meperdine should not

A

be given to patients with decreased kidney function because it will result in accumulation

235
Q

Meperedine should not be given to patients taking

A

MAOI or fluoxetine because it may cause serotonin syndrome

236
Q

Side effects of meperedine include

A

increase in heart rate, mydriasis, delirium and seizures

237
Q

Fentanyl structure

A

phenylpiperdine ring

238
Q

With fentanyl, the lungs have

A

a large first pass uptake

239
Q

Fentanyl’s pKa is

A

8.4 but it is highly lipid soluble

240
Q

Morphine’s pKa is

A

7.9

241
Q

Fentanyl has a large

A

volume of distribution

242
Q

The elimination half-time of fentanyl

A

is longer than that of morphine

243
Q

The context sensitive half-time of fentanyl

A

increases with infusion >2 hours

244
Q

What enzyme is inhibited by etomidate

A

11 beta hydroxylase

245
Q

Side effects of fentanyl include

A

“secondary peaks” d/t release from pulmonary uptake, bradycardia, myoclonus, associated with modest increases in ICP, synergism with propofol and versed

246
Q

The side effect commonly dissociated with agonist-antagonist opioids include

A

dysphoria d/t kappa agonism

247
Q

The potency of phenylpiperdines is

A

sufentanil, fentanyl, remifentanil, and alfentanil

248
Q

Sufentanil is known to produce

A

longer analgesia and less respiratory depression than fentanyl

249
Q

Doses required for intubation with sufentanil

A

can cause chest wall rigidity

250
Q

Lidocaine can cause

A

sedation

251
Q

Phenylpiperdines that have high protein binding

A

sufentanil and alfentanil have extensive alpha 1 glycoprotein

252
Q

Sufentanil has a significant

A

first pass pulmonary uptake

253
Q

Sufentanil is metabolized by

A

phase 1 in the liver

254
Q

For sufentanil clearance is dependent on

A

hepatic blood flow; clearance should be greater than 0.7

255
Q

Alfentanil has a

A

rapid onset of action

pKa is 6.5

256
Q

Most to least ionized phenylpiperdines

A

fentanyl, sufentanil, alfentanil, and remifentanil

257
Q

Volume of distribution of the phenylpiperdines:

A

fentanyl, sufentanil, remifentanil, and alfentanil

258
Q

Alfentanil is metabolized in

A

the liver

259
Q

Side effects of alfentanil include

A

more significant decrease in BP, acute dystonia- don’t give to Parkinson’s patients

260
Q

Remifentanil MOA

A

selective mu agonist

261
Q

Remifentanil is structurally significant in that

A

it has an ester linkage which allows for it to be metabolized by plasma esterases in the blood so allows for quick metabolism

262
Q

Remifentanil Vd

A

small Vd

263
Q

The context sensitive half-time of remifentanil is

A

4 minutes

264
Q

Side effects of remifentanil:

A

important to administer a longer acting opioid for postop analgesia; can induce “seizure like” activity, N/V, depress ventilation/ decrease systemic BP

265
Q

Butorphanol MOA

A

agonist-antagonist on opioid receptors
low affinity for mu receptors (antagonism)
moderate affinity for kappa receptors (analgesia and anti-shivering)

266
Q

Butorphanol pearls:

A

limited intraop use

metabolized in the liver

267
Q

Side effects of butorphanol:

A

dysphoria, sedation, nausea, diaphoresis, depression of ventilation

268
Q

Nalbuphine MOA:

A

agonist antagonist- chemically related to oxymorphone and naloxone

269
Q

Nalbuphine is metabolized in

A

the liver

270
Q

Antagonist effects of nalbuphine

A

occur at mu receptors; if given before an opioid may diminish effects of morphine-like drugs preoperatively
if after administration of opioid it can reverse depression of ventilation effects but maintain analgesia

271
Q

Nalbuphine has less

A

dysphoria than butorphanol

sedation most common

272
Q

Naloxone half-life

A

30-45 minutes (shorter than most opioids so needs to be redosed)

273
Q

Naloxone is metabolized

A

by the liver (phase II)

274
Q

The dose of naloxone is

A

1-4 mcg/kg IV

275
Q

Side effects of naloxone administration:

A

increased sympathetic nervous system activity, sudden onset of pain, tachycardia, hypertension, pulmonary edema, N/V, reversal of analesia

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