All drugs Flashcards
(275 cards)
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
2
Q
Tylenol is metabolized
A
In the liver
3
Q
What do we give for a Tylenol overdose?
A
Charcoal & mucomyst (acetylcysteine)
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
5
Q
What drugs are acids?
A
propofol
NSAIDs
Barbiturates
6
Q
Why does acetaminophen cause liver failure?
A
Damage to the liver results from the metabolite (N-acetyl-p-benzoquinoneimine) which depletes glutathione
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
8
Q
What does NSAID stand for?
A
Non-steroidal anti-inflammatory drug
9
Q
What does Cox stand for?
A
Cyclooxygenase inhibitor
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
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
12
Q
How is ibuprofen metabolized?
A
By the liver, excreted by the kidneys
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
14
Q
The use of ibuprofen is limited in the OR setting because
A
It leads to GI dysfunction and platelet aggregation
15
Q
List the MAC, BP, VP, BG, & OG for desflurane.
A
MAC: 6%, BP: 24, VP: 669, BG 0.42, OG: 19
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
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
18
Q
List the MAC, BP, VP, BG, and OG for sevoflurane.
A
MAC: 2%, BP 59, VP: 157, BG 0.65, OG: 47
19
Q
What drug is used for inhalational inductions?
A
sevoflurane
20
Q
What does oil gas indicate?
A
potency
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
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
23
Q
The three A’s of anesthetics include
A
analgesia, areflexia, and amnesia
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
25
Describe the difference between PK and PD
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)
26
What is 'uncoupling'?
seen in anesthetic gases... it is where we have increased CBF and decreased CMRO2
27
What is the MOA of inhalational drugs?
unknown but possibly due to NMDA receptors, VGNa+ receptors, GABA receptors, glycine receptors, and potassium channels
28
Developmental neurotoxicity with gases
has not been demonstrated in human children... rule of thumb is to keep surgeries short and use short acting medications
29
What is a contraindication of using nitrous oxide?
pulmonary hypertension, pregnancy, surgeries involving the tympanic membrane or any surgery where gas can diffuse into an air filled space
30
Nitrous oxide has two good uses when used with other gases:
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
31
What agents are known to contribute to emergence delirium in kids?
desflurane and sevoflurane
32
Gases are beneficial to the pulmonary system in that they
reduce hypoxic pulmonary vasoconstriction
33
Sensitization means that
volatile agents reduce the quantity of catecholamines necessary to evoke arrhythmias
34
Preconditioning is
a phenomenon in which the heart is exposed to a cascade of intracellular events that protect it from ischemic and reperfusion insult
35
What inhalational agent undergoes the greatest metabolism?
sevoflurane at 5-8% in the liver
36
What is a MAC?
it is the minimal alveolar concentration where 50% of the population will not move on surgical incision
37
List the factors that increase MAC requirements
hyperthermia, drug induced increases in CNS activity, hypernatremia, chronic alcohol abuse
38
Factors that decrease MAC requirements:
hypothermia, increasing age, alpha-2 agonists, acute alcohol ingestion, pregnancy, and hyponatremia
39
Desflurane should not be given to
people with reactive airways because it is very pungent
40
Factoids about nitrous oxide
is supports combustion like oxygen so must be careful
| NMDA receptor antagonist so can lower risk of chronic pain after surgery
41
Malignant hyperthermia can be caused by:
volatile induction agents, succinylcholine, and stress
42
Malignant hyperthermia is due to
ryanodine receptor gene mutation on chromosome 19
43
Signs and symptoms of malignant hyperthermia include
increased CO2, muscle rigidity, metabolic acidosis, and high temperature
44
What is the metabolism of propofol?
metabolized in the liver, phase I
clearance exceeds hepatic blood flow
not influenced by hepatic/renal function
45
What is the MOA of propofol?
GABA allosteric agonist
46
What is the context sensitive half-time of propofol?
40 minutes
47
Propofol undergoes
first pass uptake in the lungs
48
What are the factors that make propofol an non-ideal drug?
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
49
One of the biggest concerns with long-term propofol infusion is
PRIS syndrome; typically not seen in the surgical setting but it can cause death
50
The Vd of propofol is
large
51
Propofol has this effect on the respiratory system:
respiratory depression
52
Propofol has a
rapid and pleasant loss and return to consciousness
| also has an active metabolite but we're not very concerned with it
53
The pKa of propofol is
11
54
The pKa of etomidate is
4.2
55
The MOA of etomidate is
GABA allosteric agonist
56
The Vd of etomidate is
large
57
The effect of etomidate on the CV system is
to keep CV and BP steady
| acts on alpha adrenergic receptors
58
Etomidate is metabolized by
hydrolysis in the liver (phase 1)
59
One frequent side effect of etomidate is
myoclonus
60
Etomidate is used as an induction agent
because it has a quick onset and offset (5-10 min.)
61
A concern with etomidate is
it can cause adrenocortical suppression via the enzyme 11 beta hydroxylase
62
These drugs are contraindicated in porphyrias
etomidate, barbiturates, and diazepam
63
Etomidate is
neuroprotectant... it decreases CBF and CMRO2
64
Ketamine's MOA is
NMDA receptor antagonist
| N-methyl-D apartate
65
The pKa of ketamine is
7.5
66
Vd of ketamine is
large
67
Ketamine produces
"dissociative anesthesia", eyes open, corneal reflexes intact
68
Ketamine is given typically to
trauma patients because it causes an increase in BP, HR, and SVR
69
Ketamine should be avoided in patients with
head trauma or eye injury because it increases CBF, CMRO2, ICP, and IOP
70
Ketamine is metabolized by
liver in phase 1
71
____ should be given in conjunction with ketamine to avoid ______
benzodiazepines; emergence delirium
72
The elimination half time of ketamine is
2-3 hours
73
Ketamine can be good for pediatric
asthmatics.... "ketamine dart"
74
Ketamine can be used for
induction, analgesia, and TIVA
75
Mechanism of action of dexmedetomidine
works on alpha 2 agonist
76
Benefits of dexmedetomidine
easily arousable, lowers MAC and opioid requirements
| causes sedation without decreased awareness
77
The half-life of dexmedetomidine
is 2-3 hours
78
Dexmedetomidine is metabolized by
the liver phase 1
79
The biggest concerns with dexmedetomidine is
bradycardia and hypotension
80
MOA of diazepam
GABA allosteric agonist
81
Vd of diazepam
large
82
Protein binding with diazepam
extensively protein bound so cirrhosis and renal insufficiency would increase unbound diazepam with increased side effects
83
Diazepam is metabolized by
phase I in the liver
84
The active metabolites of diazepam include
nordiazepam and oxazepam
85
The elimination half-time in diazepam is
long >40 hours, increases linearly with age
86
The five properties that benzodiazepines cause include
anxiolytic, sedative/hypnotic, spinal cord mediated relaxation, anterograde amnesia, anticonvulsant
87
The onset of action of lorazepam
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
88
How is lorazepam metabolized?
stage 2 in the liver
89
What is the Vd of lorazepam?
large
90
The elimination half-time of lorazepam is
14 hours
91
Lorazepam may be used for
postoperative sedation of intubated patients
92
What is the mechanism of action for midazolam?
GABA allosteric agonist
93
What is the pKa of midazolam?
6.15
94
What is the volume of distribution of midazolam?
large
95
The property that gives midazolam this characteristic is
the imidazole ring.... no discomfort on injection
96
Midazolam is metabolized by
CYP 450 via oxidation; phase 1 in the liver
| liver disease can affect
97
The biggest concern side effect when giving midazolam is
strong synergism with opioids cause respiratory depression
98
The elimination half-time of midazolam is
1.9 hours
99
Midazolam cause these CNS effects
not neuroprotective, decreases CMRO2 and CBF, does not prevent increase in ICP with laryngoscopy
100
The MOA of flumazenil
selective benzodiazepine antagonist
| weak intrinsic agonist activity attenuates abrupt reversal
101
Thiopental MOA
acts on GABA allosteric agonists
102
What is the volume of distribution of thiopental
large
| effects terminated by redistribution
103
Where is thiopental metabolized?
in the liver; phase 1
104
Thiopental is contraindicated in
porphyrias
105
Inadvertent administration of thiopental necessitates
administration of papervine, heparinization, and vasodilation via regional block technique
106
Thiopental's elimination half-time
long 3-8 hours
107
Thiopental is
an acid and a barbiturate
108
Thiopental's effect on CV
decreased MAP and CO
109
Thiopental's effect on CNS
reverse steal effect, burst suppresion, and isoelectric EEG
110
Thiopental's effect on respiratory
respiratory depression, may cause apnea
111
Methohexital's MOA
acts on GABA allosteric agonists
112
Methohexitals Vd
large volume of distribution
113
Methohexital is a
barbiturate, acid, and contraindicated in porphyrias
114
The main use of methohexital is to
used in ECT to lower the seizure threshold
115
Methohexital is metabolized in
the liver via phase 1
116
Thiopental has an
active metabolite known as pentobarbital
117
Methohexital's half-life is
4 hours
118
Methohexital and thiopental have an onset of action of
30 seconds
119
Risk factors for PONV include:
young age, female gender, non-smoker, opioid usage (intraop and postop), previous hx., laparoscopic surgeries
120
The mechanism of action of ondansetron is
acts as serotonin receptor antagonists (5-HT3)
| mediates vomiting and is found in GI tract (abdominal vagal afferents) and brain (CTZ)
121
Onset of ondansetron is
30 minutes
| half-life is 4 hours so should be administered towards the end of the case
122
Ondansetron is metabolized by
liver Phase 1 (hydrolysis) & Phase 2 (conjugation)
123
Ondansetron produces mild side effects
HA & QT prolongation
124
Promethazine MOA
Also known as phenergan
| antihistamine, anticholinergic, and antimuscarinic
125
The major side effect of promethazine is
can result in significant sedation when administered with opioids
also avoid in elderly because it can cause confusion and constipation
126
Promethazine is metabolized in
the liver
127
The mechanism of action of reglan is
centrally acting on dopamine receptor antagonist (D2) to CTZ
128
Metoclopramide works by
increasing LES tone, speeding gastric emptying time, lowers gastric fluid volume
129
metoclopramide is metabolized in
the liver
130
The risk factors associated with metoclopramide include:
Extrapyramidal side effects; contraindicated in Parkinson's disease, seizure, GI obstruction, and pheochromocytoma
131
The mechanisms of action of dexamethasone
long-acting corticosteroid
| synthetic glucocorticoid with anti-inflammatory and immunosuppressant properties
132
Uses of dexamethasone
as a steroid to reduce inflammation or as an antiemetic (give early in the case)
133
Dexamethasone is metabolized by
the liver
134
Do not give dexamethasone in cases of
hypersensitivity, uncontrolled infections, cerebral malaria, concurrent live vaccinations
135
The mechanism of action of oxytocin is
lowers threshold for depolarization of uterine smooth muscle
| increases prostaglandin production
136
Oxytocin is used to
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
Oxytocin should never
be bolused IV... it causes vasodilation and decreased SVR which can cause hypotension and bradycardia
138
Hemabate is a
prostaglandin and it works by increasing myometrial calcium levels and increasing MLCK activity and thus uterine contraction
139
Hemabate is the
third line of defence for PPH
140
The use of hemabate (resp)
can result in bronchospasm, V/Q mismatch and hypoxemia in women with reactive airways
monitor O2 and lung sounds
141
Methergine MOA
methergine is an ergot alkaloid
| MOA unclear- though to be an a-adrenergic agonist
142
IV administration of methergine can result in
Profound hypertension, severe N/V, and cerebral hemorrhage
143
Methergine is contraindicated in women with
hypertension, PVD or ischemic heart disease
| N/V can occur; have vasodilating drugs available
144
The mechanism of action of edrophonium
acetylcholinesterase inhibitor
| allows for buildup of Ach at the NMJ and accelerates recovery from NMBD
145
What are the side effects of edrophonium
bronchoconstriction, salivation, increased bowel motility, urination, severe bradycardia
146
Edrophonium should be given to
reverse NMBD but only non-depolarizers
147
Edrophonium should be given with
atropine
148
The mechanism of action neostigmine is
acetylcholinesterase inhibitor
| allows for buildup of Ach at the NMJ and accelerates recovery from NMBD
149
Neostigmine should be given with
glycopyrolate to avoid effects such as bradycardia, increased bowel motility
150
The mechanism of action of atropine is
anti-cholinergic drug
| blocks mACHr
151
The onset of edrophonium and neostigmine is
5-10 minutes
152
The half-life of edrophonium is
110 minutes
153
The half-life of neostigmine is
70-80 minutes
154
The side effects of anticholinergic drugs (atropine & glycopyrolate) include
dry mouth, mydriasis, difficulty swallowing, tachycardia, dry skin, flushed, increased body temperature
155
The mechanism of action of glycopyrrolate is
anti-cholinergic
156
The mechanism of action of scopolamine is
anti-cholinergic
157
Scopolamine can be used for
preoperative sedation, PONV
158
Scopolamine can cause
amnesia and sedation, adverse effects include dry mouth, increased thirst, dry skin, constipation, drowsiness, dizziness, blurred vision, dilated pupils, light sensitivty
159
Scopolamine is metabolized by
the liver
160
The elimination half-life of scopolamine is
4.5 hours
161
The MOA of succinylcholine is
depolarizing neuromuscular blocking drug
162
The duration of action of succinylcholine is short
14 minutes due to rapid hydrolysis
163
How is succinylcholine metabolized
via pseudocholinesterase or butrylcholinesterase in the blood
164
How quickly does succinylcholine create intubating conditions?
60 seconds
165
The Dibucaine number can be used to indicate
the level of butylcholinsterase in the blood which will indicate how prolonged the block of succinylcholine is
166
What is the reversal for succinylcholine?
there is none because it is metabolized so quickly in the blood
167
Side effects of succinylcholine include:
hyperkalemia, myoglobinuria, bradycardia, dysrthymias, increased intraocular pressure, increased intracranial pressure, myalgias, & masseter spasm
168
Succinylcholine should not be given to
patients < 5 years old b/c it is contraindicated in patients with duchene muscular dystrophy, and cardiac arrest from hyperkalemia can occur
169
succinylcholine lasts for
9 to 13 minutes
170
Atricurium's MOA is
non-depolarizing muscular blocking drug
| specifically a benzylisoquinolium
171
What limits the usage of atricurium?
Histamine release
172
How is atricurium eliminated?
through ester hydrolysis and spontaneous degradation
| Hoffman elimination
173
What is the MOA of ciastricurium?
non-depolarizing muscular blocking drug
| specifically a benzylisoquinolium
174
Atricurium has an active metabolite
known as Laudanosine and it is implicated in convulsions although not seen in a typical anesthesia dose
175
Atricurium and cisatricurium have (onset)
an intermediate onset
176
Cisatricurium is metabolized by
Hoffman elimination
177
Cisatricurium is different from atricurium in that
it does not cause histamine release
178
What is the volume of distribution of NMBDs?
small
179
The steroidal compounds of NMBDs include:
pancuronium, vecuronium, and rocuronium
180
Pancuronium is a
long acting NMBD
181
The onset time to maximum block of pancuronium is
2.9 minutes
182
Pancuronium is cleared by
the kidney
183
Pancuronium is used during
cardiac surgeries because it has vagolytic inhibiting properties to help maintain HR & BP
184
Vecuronium is a
intermediate-acting neuromuscular blocking drug
185
The onset time to maximum block of vecuronium is
2.4 minutes
186
Vecuronium is different from pancuronium in that
there is a slight decrease in potency and loss of vagolytic properties
187
Vecuronium is metabolized in
the liver
188
The relationship between potency and onset with NMBDs
increased potency= slower onset
189
List the factors that increase the potency of NMBDs
antibiotics- clindamycin, hypothermia, magnesium sulfate, local anesthetics, quinidine, inhalational agents
190
Rocuronium is an
intermediate-acting neuromuscular blocker
191
The time to maximum block for rocuronium is
1.7 miutes
192
Rocuronium is primarily metabolized
in the liver
193
Adverse effects of NMBDs include:
can have bradycardia and hypotension, histamine release can cause lots of issues
194
Which of the NMBDs has the highest potential for allergic reactions?
rocuronium (because it is given so frequently)
195
Neostigmine has
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
To ensure adequate reversal we want to see
TOF >0.9 with qualitative monitoring
only true objective monitoring
(it will not give you a number until you've had 4 twitches)
197
Sugammedex can be used
to reverse steroidal agents
198
Sugammedex side effects
possible allergic reactions and bleeding, can make pulmonary hypertension in peds worse, and can cause oral contraceptives to be ineffective
199
Sugammedex works by
encapsulating and deactivating NMBDs
| it is a modified gamma cylcodextrin
200
Toradol should not
be given to patients with impaired renal function
201
Non-selective NSAIDs usage is limited in preop because
causes GI toxicity, platelet dysfunction, and delayed bone healing (safe in the setting of primary bone healing)
202
Celebrex is
the only available cox-2 inhibitor
has less GI toxicity
increased CV risk
203
Risk factors for the development of GI complications due to NSAIDs include
elderly, H. pylori infection, hx. of previous ulcer, concomitant use of aspirin, anticoagulants, or corticosteroids
204
Celebrex is associated with
increased risks of MI, HF, and HTN
205
In patients with CV risks,
naproxen is NSAID of choice
206
Hypersensitivity with NSAIDs can be seen with a combination of
allergic rhinitis, nasal polyps, and asthma
207
Lidocaine is used for
multimodal pain management plan to supplement general anesthesia
208
The mechanism of action for lidocaine is
uncertain; may involve sodium channels or block priming of polymorphonuclear granulocytes
209
What drugs undergo first pass extraction in the lungs?
lidocaine & propofol
210
Lidocaine is metabolize in
the liver
211
Morphine is a
naturally occurring opiate
212
In appropriate doses, opioid agonists
produce analgesia; do not cause loss of touch, loss of proprioception, and loss of consciousness
213
The mechanism of action of opioids
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
Opioids do not
block nerve impulses or alter responsiveness of afferent nerve endings to noxious stimulation
215
Opioid receptors are primarily found
in the brain and spinal cord
216
All opioids are metabolized in
the liver except for remifentanil
217
A common CV side effect of opioid administration is
bradycardia with sustained BP, orthostatic hypotension, cardiac protectant effect
218
Common respiratory side effects of opioids include
slow and deep
decreased responsiveness to CO2
dose-dependent depression of ventilation
increase airway resistance
219
Common CNS side effects of opioids include
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
Morphine causes sedation
that precedes analgesia
221
In the biliary tract
opioids cause spasm of biliary smooth muscle and the sphincter of Oddi
morphine can contract pancreatic ducts and mimic acute pancreatitis
222
Opioids exert effects on the GI tract including
constipation, decreased GI motility, and N/V
223
GU effects of opioids include
urinary retention
224
Morphine is the biggest culprit in
cutaneous changes- causes histamine release and lots of itching
225
The overdose triad includes
miosis, hypoventilation, and coma
226
Morphine side effects include
nausea, body warmth, pruritis (nose), dry mouth, and extremity heaviness
227
The onset of action of morphine is
15-30 minutes
228
Morphine has significant
renal metabolism and metabolism in the liver phase 2
229
Morphine has a long half-life due to
active metabolite
230
Meperidine MOA
MU-receptor agonist
| anti-shivering is d/t stimulation of kappa receptors
231
Meperdine is (potency)
1/10th as potent as morphine
232
the duration of action of meperdine is
2-4 hours
233
Meperdine is metabolized in
the liver
234
Meperdine should not
be given to patients with decreased kidney function because it will result in accumulation
235
Meperedine should not be given to patients taking
MAOI or fluoxetine because it may cause serotonin syndrome
236
Side effects of meperedine include
increase in heart rate, mydriasis, delirium and seizures
237
Fentanyl structure
phenylpiperdine ring
238
With fentanyl, the lungs have
a large first pass uptake
239
Fentanyl's pKa is
8.4 but it is highly lipid soluble
240
Morphine's pKa is
7.9
241
Fentanyl has a large
volume of distribution
242
The elimination half-time of fentanyl
is longer than that of morphine
243
The context sensitive half-time of fentanyl
increases with infusion >2 hours
244
What enzyme is inhibited by etomidate
11 beta hydroxylase
245
Side effects of fentanyl include
"secondary peaks" d/t release from pulmonary uptake, bradycardia, myoclonus, associated with modest increases in ICP, synergism with propofol and versed
246
The side effect commonly dissociated with agonist-antagonist opioids include
dysphoria d/t kappa agonism
247
The potency of phenylpiperdines is
sufentanil, fentanyl, remifentanil, and alfentanil
248
Sufentanil is known to produce
longer analgesia and less respiratory depression than fentanyl
249
Doses required for intubation with sufentanil
can cause chest wall rigidity
250
Lidocaine can cause
sedation
251
Phenylpiperdines that have high protein binding
sufentanil and alfentanil have extensive alpha 1 glycoprotein
252
Sufentanil has a significant
first pass pulmonary uptake
253
Sufentanil is metabolized by
phase 1 in the liver
254
For sufentanil clearance is dependent on
hepatic blood flow; clearance should be greater than 0.7
255
Alfentanil has a
rapid onset of action
| pKa is 6.5
256
Most to least ionized phenylpiperdines
fentanyl, sufentanil, alfentanil, and remifentanil
257
Volume of distribution of the phenylpiperdines:
fentanyl, sufentanil, remifentanil, and alfentanil
258
Alfentanil is metabolized in
the liver
259
Side effects of alfentanil include
more significant decrease in BP, acute dystonia- don't give to Parkinson's patients
260
Remifentanil MOA
selective mu agonist
261
Remifentanil is structurally significant in that
it has an ester linkage which allows for it to be metabolized by plasma esterases in the blood so allows for quick metabolism
262
Remifentanil Vd
small Vd
263
The context sensitive half-time of remifentanil is
4 minutes
264
Side effects of remifentanil:
important to administer a longer acting opioid for postop analgesia; can induce "seizure like" activity, N/V, depress ventilation/ decrease systemic BP
265
Butorphanol MOA
agonist-antagonist on opioid receptors
low affinity for mu receptors (antagonism)
moderate affinity for kappa receptors (analgesia and anti-shivering)
266
Butorphanol pearls:
limited intraop use
| metabolized in the liver
267
Side effects of butorphanol:
dysphoria, sedation, nausea, diaphoresis, depression of ventilation
268
Nalbuphine MOA:
agonist antagonist- chemically related to oxymorphone and naloxone
269
Nalbuphine is metabolized in
the liver
270
Antagonist effects of nalbuphine
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
Nalbuphine has less
dysphoria than butorphanol
| sedation most common
272
Naloxone half-life
30-45 minutes (shorter than most opioids so needs to be redosed)
273
Naloxone is metabolized
by the liver (phase II)
274
The dose of naloxone is
1-4 mcg/kg IV
275
Side effects of naloxone administration:
increased sympathetic nervous system activity, sudden onset of pain, tachycardia, hypertension, pulmonary edema, N/V, reversal of analesia
