Final Exam Review Flashcards
1
Q
Anesthetic effect of immobility is decreased or lost if carbon atom chain length exceeds a distance of ___ or ___ carbon atoms
A
4 or 5 carbon atoms
2
Q
Modern inhaled anesthetics are ___; what inhalation agent is an exception to this rule?
A
Halogenated hydrocarbons; nitrous oxide is the exception to this rule
3
Q
Chemical structure of halothane
A
1 bromine, 1 chlorine, 3 fluorine
4
Q
How many fluorines does isoflurane have?
A
5
5
Q
How many fluorines does desflurane have?
A
6
6
Q
How many fluorines does sevoflurane have?
A
7
7
Q
Addition of fluorine, chlorine, bromine, or iodine to an inhalation agent is also called ___
A
Halogenation
8
Q
Halogenation affects what 4 things?
A
- Potency
- Arrhythmogenic properties
- Flammability
- Chemical stability
9
Q
Potency ___ (increases/decreases) with heavier halogens
A
Increases (bromine is heavier and more potent than fluorine)
10
Q
Increased halogen atoms ___ (increases/decreases) the occurrence of arrythmias
A
Increases
11
Q
More halogens ___ (increases/decreases) flammability
A
Decreases
12
Q
Chemical stability is ___ (increased/decreased) with more halogens
A
Increased
13
Q
Inhalation agents are very minimally metabolized—most are excreted from the ___
A
Lungs
14
Q
Inhalation agents are ___ acting
A
Rapid
15
Q
Of the inhaled anesthetics, only ___ and ___ are “true gases;” other potent agents are ___
A
Nitrous and oxygen are true gases; others are vapors of volatile liquids
16
Q
Even though all inhalation agents are technically not true gases, all are referred to as ___ because they are in the gas phase when administered to the lungs
A
Gases
17
Q
All gases are ___ (ionized or non-ionized)
A
Non-ionized
18
Q
Goal of inhalation anesthesia is to create a partial pressure of agent in the ___ that equilibrates in the ___
A
Partial pressure of agent in the lungs that equilibrates in the CNS
19
Q
General anesthesia is defined as a drug’s capacity to induce and sustain as needed, a state of (4 things):
A
- Unconsciousness
- Amnesia
- Analgesia
- Immobility
20
Q
What rule is this?—lipid solubility is directly proportional to potency
A
Meyer-Overton rule
21
Q
A reduction in body temperature ___ (increases/decreases) anesthetic requirement
A
Decreases
22
Q
Anesthetic sites of action include ___ and ___ structures
A
Supraspinal and spinal structures
23
Q
What structure in the nervous system specifically causes immobility to painful stimulus?
A
Spinal cord—GABA receptors
24
Q
What structures cause amnesia and immobility?
A
Supraspinal structures
25
Potency is directly related to ___
Lipid solubility
26
The potency of an anesthetic ___ (increases/decreases) as its liposolubility increases
Increases
27
Oil:gas partition coefficient provides a quantitative measure of ___
Lipid solubility
28
What is MAC?
Minimum alveolar concentration where 50% will not move in response to surgical stimuli
29
With regards to CNS depression that results from inhalation agents...inhalation agents “probably” work by enhancing ___ ion channels and blocking ___ channels
Enhancing inhibitory ion channels and blocking excitatory ion channels
30
Inhalation agents cause ___ of neurons
Hyperpolarization
31
Inhalation agents work at the ___ receptor
GABA
32
What occurs during hyperpolarization?— ___ enters neurons through ___ receptor, efflux of ___ out of neurons
Chloride enters neurons through GABA receptor, efflux of potassium out of neurons
33
1 MAC = ___% won’t respond to surgical stimuli
50%
34
MAC BAR = ___ MAC
1.3 MAC
35
1.3 MAC (MAC BAR) = ___% won’t respond to surgical stimuli
95%
36
Immobility from inhalation agents is ___ mediated
Spinal cord mediated—they inhibit nociceptive input in the dorsal horn of the spinal cord
37
How do we measure immobility?
MAC
38
The length of the anesthetic molecule is significant in that immobility is lost if carbon atom chain length exceeds a distance of ___ or ___ carbon atoms
4 or 5
39
How do we measure amnesia?
No reliable way to measure—BIS monitor?
40
Amnesic effects of anesthesia are generated from ___ structures such as ___ and ___ (both are part of the limbic system); and ___
Supraspinal structures such as amygdala and hippocampus; and cortex
41
How do we measure analgesia?
Cannot be measured
42
Intraoperative measures of pain suggest that inhaled anesthetics ___ (do/do not) suppress the perception of painful stimuli
Do NOT (i.e.: increased HR, increased systemic BP)
43
At equilibrium...___ partial pressure = ___ partial pressure = ___ partial pressure
CNS = blood = alveolar
44
Inhaled anesthetics are delivered from the ___ to ___ to ___
Lungs to blood to CNS
45
Plasma and tissues have a ___ (low/high) capacity to absorb inhaled anesthetics (relative to the amount delivered to the lungs), so they rapidly make their way to the CNS
Low capacity
46
The more blood soluble the agent, the ___ (faster/slower) the rise in blood partial pressure, and the ___ (faster/slower) the CNS uptake
Slower the rise in blood partial pressure; the slower the CNS uptake
47
The blood:gas solubility coefficient is an indicator of speed of ___
Uptake/elimination
48
The more blood soluble the drug, the ___ (slower/faster) the brain and spinal cord uptake and therefore the ___ (slower/faster) the anesthesia state achieved
Slower; slower
49
How can we combat high blood:gas solubility/slower induction?
Turn up the flow of the gas to speed up induction
50
It is easy to maintain blood/CNS concentrations of inhalation agents because a ___ (small/large) amount is removed by metabolism
Small
51
Equilibrium of agent is a result of 3 factors—1) inhaled anesthetics are delivered from ___ to ___ to ___
Lungs to blood to CNS
52
Equilibrium of agent is a result of 3 factors—2) Plasma and tissues have a ___ (high/low) capacity to absorb inhaled anesthetics (relative to the amount delivered to the lungs), so they rapidly make their way to the CNS
Low
53
Equilibrium of agent is a result of 3 factors—3) Easy to maintain blood/CNS concentrations of inhalation agents because a ___ (low/high) amount is removed by metabolism
Low
54
Volatile anesthetics are ___ at ambient temperature/pressure
Liquids
55
What is the pressure exerted by molecular collisions of gas molecules against container walls?
Vapor pressure
56
Vapor pressure is proportional to ___
Temperature
57
Increased temperature = ___ (increased/decreased) vapor pressure
Increases
58
As long as you have liquid in the container, the vapor pressure is independent of the ___ of the liquid
Volume
59
What law is this?—the sum of the partial pressures of each gas in a mixture equals the total pressure of the mixture
Dalton’s Law
60
Atmospheric pressure = ___ mm Hg
760
61
Gases equilibrate based on ___, not on concentration
Partial pressures
62
Solubility describes the tendency of a gas to ___ with a solution
Equilibrate
63
Henry’s Law—as solubility increases, ___ increases
Partial pressure increases
64
The lower the blood solubility, the ___ induction/emergence
Faster induction/emergence
65
Speed of uptake and elimination from the brain is inversely related to ____
Blood solubility
66
Uptake/elimination from the brain is ___ (slower/faster) with agents that are LESS blood soluble
Faster
67
The oil:gas coefficient provides a quantitative measure of ___
Lipid solubility
68
___ is directly related to lipid solubility
Potency
69
The concentration of a gas in a mixture depends on what two factors?
- Partial pressure
| - Solubility
70
Is tissue solubility greater in fat or muscle tissue?
Fat > muscle
Anesthetics can linger in the fatty tissue; may take longer for a fat person to wake up
71
What tissue receives the greatest amount of cardiac output?
Vessel-rich group (75% CO, least % body mass)
72
What tissue receives the least amount of cardiac output?
Fat (6% CO)
73
Goal of anesthesia = produce and maintain a constant partial pressure of inhalation anesthetic in the ___
Brain
74
Develop an ___ anesthetic concentration >> develop an ___ anesthetic concentration >> develop a ___ anesthetic concentration >> distribute anesthetic agent from ___ to ___
Inspired concentration >> alveolar concentration >> blood concentration >> distribute from blood to tissue
75
What is a “wash in”?
Using high gas flows (5-10L/min range) to increase the partial pressure of an anesthetic agent
76
Fi =
Inspired gas
77
What effect is this?—by turning up the concentration of the gas, patient will go to sleep faster (because higher partial pressure of gas is generated from higher flows, leading to a rapid induction of anesthesia)
Concentration effect
78
For kids, do a pure ___ anesthetic
Inhaled
79
The rate at which the alveolar partial pressure of the anesthetic agent rises is determined by what 2 factors?
- Inspired concentration
| - Alveolar ventilation
80
When alveolar ventilation is high, partial pressure of anesthetic in the alveoli ___
Increases rapidly
81
What law is associated with the second gas effect?
Fick’s law
82
What effect is this?—when first gas (usually N2O) is used, it is picked up rapidly from the alveoli by the blood; rapid crossing of N2O into the blood tends to pull the second gas along with it, so that the arterial partial pressure of the second gas rises more rapidly than it would if it were alone in the alveoli
Second gas effect
83
Three factors determine how rapidly anesthetics pass from inspired gases to the blood: ___ of the agent; rate of ___ through the lungs; ___ of the agents in arterial/venous blood
- Solubility of the agent
- Rate of blood flow through the lungs (CO)
- Partial pressure of the agents in arterial/venous blood
84
Lower CO = ___ (faster/slower) induction
Faster
Box car gets fuller, so more gas goes into the bloodstream and then to the brain
85
Higher CO = ___ induction
Slower
Box car gets less full because the train is moving faster, so less gas goes into the bloodstream/to the brain
86
Blood:gas partition coefficient = solubility of agent in ___
Blood
87
The higher the blood solubility coefficient, the ___ it takes to anesthetize the patient
Longer
88
IV anesthesia—normal CO, drugs go to their site of action ___
Relatively quickly
89
IV anesthesia—low CO, drugs go to their site of action ___
Slowly
90
Inhaled agents—low CO—as blood goes to the lungs, will pick up ___ (more/less) agent
More
91
Inhaled agents—high CO—as blood goes to the lungs, will pick up ___ (more/less) agent
Less
92
Tissue groups/order of greatest to least effect of inhalation agents:
Vessel rich: brain, heart, liver, kidney, endocrine
Fat: adipose tissue
Muscle: skin and muscle
Vessel poor: bone, ligaments, teeth, hair, cartilage
93
Majority of inhalation agents work in the ___ group
Vessel rich
94
What are the 4 stages of anesthesia?
Stage 1–stage of analgesia
Stage 2–stage of delirium or excitement
Stage 3–stage of anesthesia
Stage 4–stage of depression
95
Stage 1–stage of analgesia begins with ___ and ends with ___
Begins with administration of anesthesia, ends with loss of consciousness
96
Stage 2–stage of delirium or excitement—what can occur?
Laryngospasm!!!
97
During stage 2, patient is in a more ___ state
Hyperreflexive—increased muscle tone/rigidity; irregular breathing, tachypnea; HR elevated, BP up; pupils dilate
98
Stage 2 lasts from ___ to ___
Loss of consciousness to surgical anesthesia
99
Stage 3–stage of anesthesia—what is no longer a risk?
Laryngospasm is not a risk—excitement subsides
100
Stage 3–there is a return of ___ and pupils are ___
Return of regular respiration; pupils are centered
101
Stage 3–cough, gag, and eyelid reflexes are ___
Absent
102
Stage 4–stage of depression
Respiratory/cardiac depression
103
MAC =
Minimum alveolar concentration
104
MAC is the partial pressure of an inhalation anesthetic at 1 atm that prevents skeletal muscle movement in response to a surgical skin incision in ___% of the patient population
50%
105
MAC is a reliable indicator of dose and potency of an anesthetic—T/F?
TRUE
106
The lower the MAC, the ___ (less/more) potent the agent and the ___ (lower/higher) the blood:gas partition coefficient (blood solubility)
More potent; higher the blood:gas partition coefficient
107
How does pregnancy affect MAC?
Decreases
108
Infants/young kids have ___ MAC
Higher MAC d/t higher metabolic rate
109
Intoxicated person has ___ MAC
Lower
110
Chronic alcoholic has ___ MAC
Higher
111
Hypothermic patients have ___ MAC
Decreased MAC d/t decreased metabolic rate
112
Hyperthermia causes ___ MAC d/t ___ metabolic rate; higher MAC up to ___ degrees C, then MAC ___ again
Higher MAC d/t higher metabolic rate; higher MAC up to 42 degrees C, then MAC decreases again
113
How do hypoxia, anemia, and hypotension affect MAC?
Decreases
114
Elderly have ___ MAC
Decreased
115
Infants have ___ MAC
Increased
116
MAC is usually greatest in ___ d/t their high basal metabolic rate
Newborn
117
Hyperthermia ___ MAC
Increases
118
Chronic drug use—alcohol, barbiturates, narcotics— ___ MAC
Increase
119
Hyper/hypothyroid ___ MAC
Has NO EFFECT ON MAC
120
Blood pressure—MAP < ___ mm Hg decreases MAC
40
121
Hypercalcemia ___ MAC
Decreases
122
Hypernatremia ___ MAC
Increases
123
Hyponatremia ___ MAC
Decreases
124
Cocaine ___ MAC d/t higher BP/HR
Increases
125
Local anesthetics ___ MAC
Decreases
126
All drugs decrease MAC except ___
Sympathomimetics—amphetamine, cocaine, ephedrine all INCREASE MAC
127
Acute use of sympathomimetics ___ MAC
Increases
128
Chronic use of sympathomimetics ___ MAC
Decreases
129
Potency is directly related to ___
Lipid solubility
130
MAC is inversely related to ___
Potency
131
More potent agent = ___ MAC
Lower
132
Standard deviation in MAC is ~___%, so ___% of patients should not move at 1.2 MAC and ___% of patients should not move at 1.3 MAC
10%; 95%; 99%
133
What type of MAC is this?—MAC at which 50% of subjects will respond to the command “open your eyes”
MAC-awake
134
What type of MAC is this?—blocks the adrenergic response to skin incision
MAC-BAR or 1.2 MACS
135
What type of MAC is this?—similar to MAC-BAR in that its values exceed the anesthetic requirements for surgical skin incision
MAC intubation
136
MAC of iso
1–(most potent out of the agents we typically use)
137
MAC of sevo
2
138
MAC of des
6–(least potent out of agents we use)
139
MAC values for different inhaled anesthetics are ___
Additive
0.5 MAC of nitrous oxide + 0.5 MAC of isoflurane has the same effect as 1 MAC of any single inhaled anesthetic
140
3 factors that determine the input of inhaled anesthetic into the alveoli: ___ partial pressure; ___ ventilation; ___ of the breathing system
Inspired partial pressure; alveolar ventilation; characteristics of the breathing system
141
High inspired partial pressure = ___ induction; what effect is this?
Faster induction—concentration effect
142
Hyperventilation = ___ (slower/faster) induction
Faster
143
Hypoventilation = ___ (slow/fast) induction
Slow
144
Factors that affect uptake of inhaled anesthetic into pulmonary arterial blood: ___ of gas; ___ output; ___ partial pressure difference
Solubility of gas; cardiac output; arterial to venous partial pressure difference
145
High CO = ___ induction
Slow
146
Low CO = ___ induction
Fast
147
Factors affecting transfer of inhaled anesthetic from arterial blood to brain: ___ partition coefficient; ___ blood flow; ___ partial pressure difference
Brain-blood partition coefficient; cerebral blood flow; arterial to venous partial pressure difference
148
Agents in order of increasing potency:
Nitrous << Des << Sevo << Iso << Halo
149
As you go up on gas in a patient in an anesthetize state who is spontaneously breathing, a patient’s tidal volume will go ___ as a negative feedback protective mechanism
Down
So that they don’t deepen their anesthesia to the point where they stop breathing
150
For emergence in a patient with an LMA spontaneously breathing—tidal volume will go ___ as you go down on gas
Up
151
Which agent should be used for fat patients and why?
Des!!! Because it binds the least to the fatty tissue out of all other agents
152
Which agent is most irritating to the lungs?
Des—patients will cough after
153
___ comes off fastest, then ___, ___
Des; sevo; iso
154
What type of shunt does this describe?—blood shunts past the lungs...so blood doesn’t pick up agent, goes to the left side (with no agent), catches up with blood that did pick up agent, agent becomes diluted, slower induction
Right-to-left shunt
155
Is a left-to-right shunt clinically significant?
No
156
Emergence from anesthesia = the rate at which alveolar gas partial pressure ___ (increases/decreases) with time
Decreases
157
Higher partial pressure at ___ during emergence; lower partial pressure in the ___
Brain/bloodstream; lower partial pressure in the lungs because gas is shut off
158
During emergence, gas moves out from ___ to ___ to ___ to be exhaled
Brain to blood to lungs
159
Hypoventilation/low fresh gas flows result in ___ of anesthetic
Rebreathing of anesthetic—will have transfer of anesthetic back into tissues and delayed wake up
160
What can occur if nitrous was used during the case and it is abruptly discontinued for emergence?
Diffusion hypoxia
161
What should you do to prevent diffusion hypoxia?
Turn up O2 to 100% for 5-10 minutes after N2O has been discontinued
162
MAP ___ (increases/decreases) with increases in concentration of des, sevo, and iso (in a dose dependent manner)
Decreases
163
Least decrease in MAP with ___ (which agent?)
Sevo
164
Decrease in MAP from inhaled anesthetics reflects a decrease in ___
SVR
165
Exceptions—halothane decreases MAP by decreasing ___, not SVR
CO
166
N2O causes ___ or ___ MAP
Unchanged or mildly increased MAP—activates SNS and increases SVR
167
Substituting N2O for a portion of the volatile anesthetic decreases the magnitude of BP decrease—T/F?
TRUE—because nitrous adds sympathetic stimulus, so BP doesn’t fall as dramatically
168
Inhaled agents typically ___ (increase/decrease) heart rate
Increase—response occurs at unique concentrations for each agent
169
Des causes minimal increase in HR at concentrations ___; at concentrations ___, a linear, dose dependent increase in HR is observed
< 1 MAC; > 1 MAC
170
With sevo, HR does not increase until concentrations ___
> 1.5 MAC...really won’t see 1.5 MAC with sevo, so won’t really see HR increases with sevo
171
What agent produces a minor increase in EF, which is part of the reason why CV surgeries use it on the bypass machine?
DES
172
Are dysrythmia problems common with newer agents?
No d/t their halogenation
173
What agent sensitizes the heart to PVCs?
Halothane
174
Inhaled anesthetics prolong ___
QT interval
175
Avoid what agent in patients with known congenital long QT syndrome?
Sevo
176
Volatile anesthetics exert a protective effect on the heart, limiting the area of myocardial injury and preserving function after exposure to ischemic insult—T/F?
True
177
How do volatile anesthetics protect the heart?
Coronary steal—blood is taken from the poor ischemic areas of the heart and given to the rich
178
What does the following describe?—exposure to a single or multiple brief episodes of ischemia can confer a protective effect on the myocardium against reversible or irreversible injury with subsequent prolonged ischemic insult
Ischemic preconditioning
179
As anesthetic concentration increases, there is ___ respiratory rate, ___ tidal volume
Increased respiratory rate, decreased tidal volume
180
Gas exchange becomes ___ (more/less) efficient as anesthetic depth increases
Less
181
PaCO2 ___ (increases/decreases) with deeper anesthesia
Increases—pt is not breathing and blowing off CO2; can increase tidal volume and/or RR to blow off more CO2
182
As patient starts to wake up (emergence), tidal volume ___ (increases/decreases)
Increases
183
Natural response to CO2 is ___ by volatile anesthetics
Blunted
Volatile anesthetics cause a dose related blunting of respiratory response to increased CO2
184
ETCO2 is ___ (higher/lower) than PaCO2 on ABG
Lower (2-5 mm Hg lower)
185
Inhaled anesthetics reduce what respiratory capacity?
FRC
186
Inhaled anesthetics cause ___ in the dependent areas of the lung; occurs to a greater extent with ___ ventilation
Atelectasis; spontaneous ventilation
187
What agent is pungent and irritates the airway?
Des
188
All inhaled anesthetics decrease CMRO2 except for ___
Nitrous—increases CMRO2, causes cerebral vasodilation—not the best gas to use in neuro cases
189
Volatile anesthetics produce a dose dependent ___ (increase/decrease) in cerebral blood flow
Increase
Higher concentrations > 1 MAC increase cerebral blood flow; lower concentrations < 0.5 MAC do not significantly change cerebral blood flow
190
___ventilate patients with increased ICP to keep CO2 at 35 mm Hg
Hyperventilate
191
ICP ___ (increases/decreases) with all volatile anesthetics at doses > 1 MAC
Increases
192
At 1 MAC or greater, the volatile anesthetic will inhibit the body’s normal mechanisms of autoregulation—T/F?
True
193
Volatile anesthetics and nitrous oxide ___ (increase/decrease) the amplitude and ___ (increase/decrease) the latency of SSEP in a dose dependent matter
Decrease the amplitude; increase the latency of SSEP
194
SSEP = ___—evaluate the integrity of the ___ and ___
Somatosensory evoked potentials—evaluate the integrity of the brain and spinal cord
195
Evoked potentials may be abolished at ___ MAC
1
196
What agent is associated with epileptiform activity on the EEG, especially at high concentrations?
Sevo
197
Inhalation agents produce a dose dependent skeletal muscle ___ and ___ the activity of neuromuscular blocking drugs
Skeletal muscle relaxation; enhance/potentiate the activity of neuromuscular blocking drugs
198
Immune mediated liver injury from inhaled anesthetics is ___
Rare
199
Mild liver injury may occur with what inhalation anesthetic?
Halothane (because 45% of it gets metabolized by the liver); known as halothane hepatitis
200
What gas forms compound A? What organ does compound A affect?
Sevo; affects the kidneys (nephrotoxic)
201
Compound A is formed after prolonged sevoflurane administration at ___ low/high fresh gas flows
Low (1L/min)
202
Package insert for sevo states that low fresh gas flow <2L/min must be limited to less than ___ MAC hours of sevo anesthesia
Less than 2 MAC hours
203
What triggers MH?
- Succs (depolarizing agent)
| - All halogenated agents—halothane > forane > sevo > des
204
What is the earliest and most sensitive sign of MH?
Increased ETCO2
205
Other signs of MH:
- Fever
- Tachycardia
- Cyanosis
- Rigidity
- Trismus—failure of the masseter muscle to relax
206
Treatment of MH
Dantrolene 2.5 mg/kg IV every 5 minutes; max dose = 10 mg/kg
207
Don’t use nitrous in patients with ___, ___
Pneumo, retinal repair—N2O enters air filled cavities easily and can expand these areas
208
Soda lime is 94% ___ hydroxide; 5% ___ hydroxide; 1% ___ hydroxide
94% Calcium hydroxide (Ca[OH]2); 5% sodium hydroxide (NaOH); 1% potassium hydroxide (KOH)
209
___ reaction with CO2 absorbent
Exothermic reaction
210
Fire can occur from soda lime, especially with ___
Sevo
211
___ (high/low) fresh gas flow rates accelerate the desiccation of CO2 absorbents
High
212
Compound A can cause ___
Nephrotoxicity
213
Compound A/nephrotoxicity is caused by which agent?
Sevo at low fresh gas flows
214
To prevent nephrotoxicity from compound A, want to maintain fresh gas flows of sevo at ___L/min or ___
2L/min or greater
Also want to use fresh/hydrated soda lime to minimize the risk
215
If a vaporizer tipped over, should you use it?
No!!! Can overdose patient with volatile anesthetic (higher concentration of gas will get to the patient)
216
Vapor pressure is a function of ___
Temperature
217
Adding volatile agent to the wrong vaporizer—if a high vapor pressure agent is placed in a vaporizer designed for a lower vapor pressure agent, the concentration of the agent delivered to the patient will be ___ (lower/higher) than the dial setting
HIGHER
HLH—high, low, high
218
Adding volatile agent to the wrong vaporizer—if a low vapor pressure agent is placed in a vaporizer designed for a higher vapor pressure agent, the concentration of the agent delivered to the patient will be ___ (lower/higher) than the dial setting
LOWER
LHL—low, high, low
219
Which agent has the highest vapor pressure?
Des—669 mm Hg; has to be heated to 2 atm of pressure
220
Sevo vapor pressure
170 mm Hg (lowest out of agents we use)
221
Iso vapor pressure
240 mm Hg
222
Halo vapor pressure
244 mm Hg
223
Agents in order of increasing vapor pressure
Sevo < Iso < Halo < Des
224
At high altitudes, the partial pressure of desflurane will be ___ (higher/lower) and output concentration will be ___ (higher/lower), leading to ___(over/under)dosing if no adjustments are made to account for higher altitude
Lower; lower; underdosing
225
Have to use ___ (lower/higher) doses at ___ (lower/higher) altitudes
Higher doses at higher altitudes
226
ACH binds to ___ receptor (nitrogen portion binds to BOTH alpha subunits), causes influx of ___
Nicotinic receptor, causes influx of sodium
227
NMBs cause ___ only; need to give ___ medication
Paralysis only; need to give sedation/pain medication
228
___% suppression of single twitch response is adequate for surgery
90% suppression
229
Succs is a ___polarizing agent
Depolarizing
230
Succs can bind to one or both ___ receptors, causes ___ influx and keeps cell in a ___ state (cannot return to resting membrane potential); this prevents ___ from binding and exerting its effect
Nicotinic receptors; causes Na influx and keeps cell in a depolarized state (cannot return to resting membrane potential); this prevents ACH from binding and exerting its effect
231
Non-depolarizing = ___ antagonism at the ___ receptor; blocks ___ from binding to receptors
Competitive antagonism at the nicotinic receptor; blocks ACH from binding to receptors
232
ACH binds to ___ alpha subunits of the nicotinic receptor; depolarizing/non-depolarizing NMBs bind to ___ alpha subunits
ACH binds to BOTH (has to bind to both subunits to exert its effect); NMBs bind to one or both subunits
233
Tracheal intubation dose for NMBs = ___x ED 95 dose
2x ED 95 dose
234
___ is a poor predictor of laryngeal relaxation compared to ___
Adductor pollicis muscle ... compared to orbicularis oculi
235
___ (small/large) muscles are blocked first; ___ blocked last
Small muscles are blocked first (i.e.: eyes/fingers); diaphragm is blocked last
236
Reversal of NMB— ___ affected last by NMB, but they recover first d/t blood flow
Diaphragm/abdomen are affected last, but they recover first d/t blood flow
237
___ to ___ for onset of action; ___ to ___ for recovery
Small to large for onset of action; large to small for recovery
238
What two non-depolarizing NMBs cause histamine release with the benzyl group?
- Atracurium
| - Mivacurium
239
All NMBs are highly ___ (nonionized/ionized) and ___ soluble
Highly ionized and water soluble—stay in the body fluid, don’t deposit into fatty tissue
240
Can you give NMBs orally?
No—because they are highly ionized and water soluble
241
Are NMBS highly protein bound?
No
242
What NMB is highly protein bound?
Atracurium
243
Aminosteroid NMBs end in ___
-curonium
244
Benzyl NMBs end in ___
-curium
245
Hyperkalemia with succs is caused by ___ influx into the cell
Na+
246
Phase I blockade with succs = __polarizing; ___ at onset
Depolarizing; twitches at onset—won’t have continuous muscle movement afterwards because further impulses are blocked
247
Phase II blockade with succs = ___polarizing because further impulses are blocked
Non-depolarizing
248
What breaks down succs?
Plasma cholinesterase
So anything that reduces plasma cholinesterase causes prolonged NMB with succs (i.e.: liver disease, neostigmine, high estrogen levels)
249
Obese patients have ___ (low/high) plasma cholinesterase—may need ___ (lower/higher) dose of succs
High plasma cholinesterase—may need higher dose of succs
250
How do you test for atypical cholinesterase?
Dibucaine test
251
Giving succs with a baby dose of non-depolarizer may reduce some of the myalgia/increased pressure side effects seen with succs (but will NOT reduce Hyperkalemia risk)—T/F
True
252
Dysrythmias (bradycardia, junctional, sinus arrest) with succs are increased if you give a second dose within ___ minutes of giving the first dose
Within 5 minutes; atropine helps
253
Patients with muscular dystrophy, third degree burns, atrophy, severe trauma, upper motor neuron lesions should NOT receive with NMB? Why?
Succs because they are at increased risk of severe hyperkalemia
254
Why are patients with muscular disorders at an increased risk of Hyperkalemia from succs administration?—d/t ___ of nicotinic receptors
D/t up regulation of nicotinic receptors in patients with muscular dystrophy
255
May not see hyperkalemia initially after succs administration—can develop within ___ hours and last up to ___ months or more
Can develop within 96 hours and last up to 6 months or more (up to 2 years)
256
Very high risk of hyperkalemia with succs = males with undiagnosed ___
Undiagnosed myopathy—will definitely get hyperkalemia from Succs
257
Myalgias with succs come from the ___ in the depolarizing phase (phase I)
Fasciculations
258
Is there a reversal agent for succs?
No—have to wait for it to wear off
259
Are there reversal agents for non-depolarizing agents?
Yes
260
Which two non-depolarizing NMBs cause histamine release?
Atracurium and mivacurium
261
Non-depolarizing NMBs can cause critical myopathy in intubated patients on long-term paralysis > ___ days
> 6 days
262
What two types of steroid NMBs are at highest risk for myopathy?
Aminosteroid and corticosteroids
263
Most anaphylactic reactions in the OR occur from the ___
Neuromuscular blocker
264
More nitrogens = ___ (more/less) risk for allergic reaction
More risk for allergic reaction
265
____ (men or women) are at greater risk of allergic reaction from NMB agents
Women—could be d/t higher estrogen levels inhibiting cholinesterase, leading to a build up of succs (7.3% women vs. 2% men)
266
How do Alzheimer’s/dementia medications affect NMBs?
Can lead to build up of NMB/prolonged neuromuscular blockade because they are acetylcholinesterase inhibitors
I.e.: aricept, excelon
267
Do aminoglycosides increase or decrease the effects of NMBs?
Increase the effects
I.e.: gentamicin
268
Do local anesthetics increase or decrease the effects of NMBs?
Increase
I.e.: lidocaine, quinidine
269
Do loop diuretics increase or decrease the effects of NMBs?
Increase
270
What NMB is best to use with phenytoin d/t its reduced effects?
Vecuronium
271
How does hypothermia affect NMB?
For every degree change from 36 C, can prolong duration of NMB for 10-15 minutes
272
Hypokalemia causes ___ to succs, ___ to non-depolarizing agents
Resistance to succs, sensitive to non-depolarizing
273
Hyperkalemia is ___ to succs, ___ to non-depolarizing
Sensitive to succs, resistant to non-depolarizing
274
Which NMB is bad in renal failure patients because 80% of the drug is eliminated via kidneys?
Pancuronium
275
Which drug has the most significant CV side effects—increased HR, MAP, CO?
Pancuronium
276
Pancuronium interacts with ___—more incidence of dysrhythmias
Digoxin
277
When broken down, pancuronium has an ___
Active metabolite—half as potent
278
Give roc ___x the ED95 dose to get similar onset to succs (1-2 mins or less)
3-4 x
279
What two NDNMBs undergo Hoffman elimination?
Atracurium and cisatracurium
280
Hoffman elimination results in ___ metabolite
Laudanosine metabolite
281
Laudanosine metabolite causes peripheral ___
Vasodilation
282
Laudanosine metabolite is safe in ___ patients
Renal/hepatic dysfunction patients
283
At 3x ED95 dose of atracurium, can see ___ HR, ___ MAP
Increase HR, decrease MAP
284
What (3) things cause the decrease in MAP when giving 3x ED95 dose of atracurium?
- Laudanosine metabolite causes peripheral vasodilation
- Histamine release with atracurium causes vasodilation
- Tachycardia relaxes vessels
285
What drugs should you use to combat the atracurium histamine release?
H1 and H2 blockers
286
Prolonged duration of action of ___ in obese patients d/t fluid shifts in ECF, not d/t increased fatty tissue
Cisatracurium
287
Does cisatracurium cause histamine release?
NO—only atracurium and mivacurium cause histamine release
288
What drug should not be used in patients with kidney/liver disease?
Vecuronium
289
Vecuronium is ___ (more/less) lipid soluble than other agents because it has only one nitrogen group
More lipid soluble
290
What is the only good thing about mivacurium?
Patient may not need a reversal agent
291
What is the enzyme that breaks down ACH?
Acetylcholinesterase
292
What are the two cholinergic receptors?
Nicotinic + muscarinic receptors—both are targets of ACH
293
Anticholinergic =
Antimuscarinic (they can be used interchangeably)
294
Acetylcholinesterase inhibitors = ___ effects
PNS/‘rest and digest’ effects
295
Anticholinesterase drugs =
Acetylcholinesterase inhibitors
296
What determines drug interactions at the enzyme acetylcholinesterase?
Positively charged nitrogen molecule
297
3+ =
Tertiary amines
298
What anticholinesterase drug is a tertiary amine?
Physostigmine
299
Tertiary amines are ___ (more/less) likely to enter the CNS because they are ___ (more/less) ionized and are ___ (more/less) lipophilic than quaternary ammoniums
More likely; less ionized; more lipophilic
300
4+ =
Quaternary ammonium
301
What are (3) quaternary ammonium drugs
- Edrophonium
- Neostigmine
- Pyridostigmine
302
Quaternary ammonium drugs do not enter the ___
CNS
303
All reversal agents work by inhibiting the enzyme ___; this increases the ___; does NOT increase ___
Acetylcholinesterase; this increases the available ACH in the body; does NOT increase the release of ACH
304
Reversal agents just prevent ___
ACH from being metabolized
305
Reversal agents cause ___ at the ___ receptor
Competitive antagonism at the nicotinic receptor—flood the receptor with ACH
306
ACH normally will bind to ___ and ___ receptors
BOTH nicotinic and muscarinic receptors...ACH must bind to BOTH receptors!
307
How reversal agent medications interact with acetylcholinesterase determines ___
Onset of action
308
Neostigmine, pyridostigmine, and physostigmine all bind to acetylcholinesterase and cause a ___ change in the enzyme
Conformational change (so the enzyme can’t break down ACH)
309
Edrophonium acts like a ___
Magnet—positive binds to negative portion of enzyme; NO chemical reaction; reversible binding; faster onset of action
310
Edrophonium has a ___ onset of action than neo/pyrido/physostigmine
Faster (because no chemical reaction occurs—it acts like a magnet)
311
If you give a reversal agent without a neuromuscular blocker, you will see...
Phase I—fasciculations
Phase II—block
Like what happens when you give succs—because you are overwhelming the nicotinic receptors with ACH
312
Interaction with enzyme (acetylcholinesterase) determines ___ of reversal agents
Onset of action
313
Edrophonium onset of action
1-2 minutes
314
Neostigmine onset of action
7-11 minutes
315
Pyridostigmine onset of action
Up to 16 minutes
316
DOA for reversal agents
All last for about 1-2 hours
317
With reversal agents, you have to wait until patient has ___
Spontaneous recovery
318
Can neostigmine reverse a deep blockade?
No
319
Is there a benefit to giving an additional dose of reversal agent? Why?
NO—once the enzyme is maximally inhibited, you’re not going to release more ACH by giving more reversal agent; have to wait for the patient to reverse on their own
320
How do antibiotics (aminoglycoside, fluoroquinolones, TCN) affect reversal?
All inhibit/slow down reversal
321
How does hypothermia affect reversal?
Inhibits
322
Respiratory acidosis ___ reversal
Inhibits
323
Hypokalemia/metabolic acidosis ___ reversal
Inhibits
324
Reversal agents act at the nicotinic, muscarinic, or both receptors?
Muscarinic receptor
325
Reversal agents binding to the muscarinic receptor = ___ effects—___cardia, broncho___, ___ pupils, ___peristalsis
PNS effects—rest and digest
- Bradycardia
- Bronchoconstriction
- Tiny pupils (miosis)
- Hyperperistalsis (gut starts moving)
326
Hyperperistalsis increases the risk of ___, especially with ___
PONV, especially with neostigmine
327
We give atropine, glycopyrrolate, and scopolamine to limit the ___ effects of reversal agents
Muscarinic effects
328
Is there a risk of prolonging the neuromuscular blockade when giving atropine, glycopyrrolate, or scopolamine with the reversal agent?
No—because these drugs act at the MUSCARINIC receptor, not at nicotinic receptors
329
You should have the anticholinergic/antimuscarinic medication on board ___ (before or after) giving the reversal agent (anticholinesterase) to limit some of the muscarinic side effects
BEFORE giving the reversal agent
330
Physostigmine is a ___
Tertiary amine—crosses BBB
331
If you accidentally give an additional dose of reversal agent (OD of ACHase inhibitors), what occurs?
Muscarinic/nicotinic overdose—too much ACH
Some signs:
- Difficulty seeing
- Salivation
- Bronchoconstriction—trouble breathing
- Bradycardia*** significant drops in HR
- Abdominal cramps
- Loss of bowel/bladder control
- Muscle weakness —> paralysis
- CNS depression
332
Treatment of ACHase inhibitor (reversal agent) OD— ___ to treat the decreased HR
Atropine
333
Treatment of ACHase inhibitor (reversal agent) OD—pralidoxime
Acetylcholinesterase reactivator—kicks reversal agents off of receptor (competitive antagonism)
334
Parlidoxime would only work for NMBs that are ___
Reversible (non-depolarizing NMBs)—so would NOT work on succs
335
Above all, treatment for ACHase inhibitor (reversal agent) OD is mostly ___
Supportive measures—have to wait for the body to make more acetylcholinesterase (could take months)
336
Anticholinergic drugs have no effect on ___
Acetylcholinesterase
337
Anticholinergic drugs work at the ___ receptor to block effects of ___
Muscarinic receptor; block effects of ACH
338
What two drugs are tertiary amines? Where do they enter?
-Atropine
-Scopolamine
^ enter the CNS
339
Quaternary ammoniums do not enter the ___
CNS—i.e.: glycopyrrolate
340
No risk of prolonged blockade with anticholinergics because they act at the ___ receptor, NOT ___ receptor
Muscarinic receptor, NOT nicotinic receptor
341
Anticholinergics cause ___ at the muscarinic receptor
Competitive antagonism
342
M1-M5–odd = ___ effects; ___ coupled; increase ___
Stimulatory effects; G-protein coupled; increase Ca
343
M1-M5–even = ___ effects; decrease ___; decrease ___; decrease ___
Inhibitory effects; decrease adenylyl cyclase; decrease cAMP; decrease Ca
Agonist with inhibitory effects
344
Which receptor is most sensitive to effects of anticholinergics? (AKA the least dose of anticholinergic is required to see these effects)
M3 receptor—respiratory effects
345
M2 receptor affects the ___
Heart—higher doses of anticholinergic required to see these effects
346
M1 receptors affects the ___
CNS—higher doses required to see these effects
347
Can give anticholinergics pre- or post-op—given with ACHase inhibitors to block some of the ___ effects
Muscarinic (PNS) effects
348
You would give what type of anticholinergic pre-op for the sedative effects?
A tertiary amine because these drugs can cross the CNS (i.e.: atropine, scopolamine)
349
For sedative effects— ___ is 100x more potent than ___; has ___ effects too
Scopolamine is 100x more potent than atropine; has amnesic effects too
350
You would not give a ___ pre-op. Why?
Quaternary ammonium (i.e.: glycopyrrolate) because it has NO CNS effects (cannot cross the BBB, won’t cause sedation)
351
Neo with atropine or glycopyrrolate has become a favorable post-op cocktail d/t lack of CNS effects
Neo with glyco—because glyco = quaternary ammonium, cannot cross BBB into the CNS, so won’t see delayed arousal post-op from prolonged sedative effects (like you would see with atropine)
352
Atropine is really used for ___ effects
CV
353
What can occur from anticholinergics in children/elderly? Why?
Restlessness/somnolence—d/t not fully formed BBB in kids and failing BBB in elderly; the rush of ACH that occurs with anticholinergic medications is highly activating in these patients
354
What are (4) examples of anticholinergic medications that can cause restlessness/somnolence in children/elderly?
- Bladder control medications
- Benadryl
- Atropine
- Scopolamine
355
Use anticholinergics with caution in patients with ___
Glaucoma—can increase intraocular pressure (IOP)
356
Antisalivation effects— ___ 3x potent; ___ 2x potent (longer DOA); ___ 1x
Scopolamine 3x potent; glycopyrrolate 2x potent with longer DOA; atropine 1x
357
Scopolamine patch targets CN ___ to reduce motion sickness
CN VIII (Trigeminal)
358
Scopolamine patch—may see ___ on the side where the patch is placed
Pupil dilation
359
When should you put on scopolamine patch?—takes at least ___ hours to see benefits, leave on for ___ hours
Pre-op—takes at least 4 hours to see benefits, leave on for 24 hours
360
Treatment for OD on anticholinergic (i.e.: scopolamine and atropine—tertiary amines that enter the CNS)
Physostigmine—repeat doses as needed because it is metabolized quickly
361
Physostigmine is a ___
Tertiary amine ACHase inhibitor
362
Effects from OD on anticholinergic—CNS effects
Restlessness > hallucinations > somnolence > unconsciousness
363
Other effects from OD on anticholinergic— ___ mouth, ___ vision; photo___; ___cardia; ___ body temperature; skeletal muscle ___; ___stasis; GI effects
- Dry you out—dry mouth, blurred vision (d/t pupil dilation and dry eyes)
- Photophobia
- Tachycardia
- Increased body temperature
- Skeletal muscle weakness
- Orthostasis
- Constipation/urinary retention
364
OD on anticholinergic medication can be ___
Fatal
365
Biggest issue with ACHase inhibitor (reversal agent) + anticholinergic (used to prevent muscarinic effects) = ___
Incomplete reversal when patient arrives to PACU
366
Sugammadex is approved for ___ and ___ reversal only in the US
Roc and vec reversal
367
Sugammadex is ___ shape— ___ center
Donut shape—lipophilic/hydrophobic center
368
Sugammadex takes the lipophilic/steroidal NMB and sucks it up to be eliminated through ___
Kidney
369
Sugammadex can reverse ___
Deeper blockades with higher doses
370
Adverse effects of sugammadex— ___ aPTT
Increased aPTT—for an hour, no actual increased bleeding seen
371
Adverse effects of sugammadex—HR
Brady up to arrest—rare; happens in minutes after sugammadex administration; give atropine to treat
372
Adverse effects of sugammadex—N/V
1/2 as bad as neostigmine
373
Sugammadex is not recommended for use in ___
Severe renal impairment—CrCl < 30 ml/min
374
1/2 life of sugammadex is ___ hours
2 hours
375
More than ___% of sugammadex is eliminated in the first 24 hours
90%
376
1/2 life of sugammadex increases with ___
Renal impairment
377
Reduced efficacy of ___ after sugammadex administration because...
Birth control because sugammadex binds up the birth control
378
Patients on birth control given sugammadex should use secondary contraception for ~___ after sugammadex administration
1 week
379
Sugammadex has greater ___ and ___ than neostigmine
Safety and efficacy
380
Goal with PONV is ___
Prevention! If we can prevent PONV, decreased discharge time, more satisfied patients
381
In the general population—___% experience vomiting, ___% experience nausea
30% experience vomiting, 50% experience nausea
382
High risk patients for PONV = ___ or more risk factors; have a ___% chance of occurrence
3 or more risk factors; have a 70-80% chance of occurrence
383
Nausea/vomiting is a ___ mechanism
Protective
384
If one nausea/vomiting med isn’t working, try one that works on a ___
Different pathway
385
Histamine antagonists, muscarinic antagonists, dopamine antagonists, and cannabinoids all work by intercepting the ___ and ___ in the medulla
Intercepting the CTZ and vomiting center in the medulla
386
Main target to prevent nausea/vomiting is the ___; stops the ___, not necessarily the ___
Chemoreceptor trigger zone (CTZ); stops the vomiting, not necessarily the nausea
387
PONV classified by time—early = ___ hours post-op
2-6 hours post-op
388
PONV classified by time—late = ___ hours post-op
6-24 hours post-op
389
PONV classified by time—delayed = ___ hours post-op
> 24 hours post-op
390
PONV classified by time—post discharge = ___ hours post-op
> 24 hours post d/c
391
If you have a patient with 3 or more risk factors for N/V, you should ___
Pre-treat
392
Top 3 risk factors for PONV:
- Female
- History of PONV (pre-op or chemo-induced)
- Non smoker
393
Risk for PONV— < ___ y/o
< 50 yo
394
Risk for PONV—general ___ (greater than or less than) regional; ___ anesthetics/N2O
General > regional; volatile anesthetics/N2O
395
Risk for PONV—opioids, use ___ instead
Tylenol
396
Risk for PONV—duration of procedure—every 30 minutes, increase risk for PONV by ___%
60%
397
What (3) types of procedures increase the risk of PONV?
- Cholecystectomy
- Gynecological
- Laparoscopic
398
Motion sickness ___ risk of PONV
Increases
399
One risk factor for PONV = ___% risk
20%
400
Two risk factors for PONV = ___% risk
40%
401
Three risk factors for PONV = ___% risk
60%
402
Four risk factors for PONV = ___% risk
80%
403
Even if you have ZERO risk factors, still have ___% risk
10% risk
404
Risk factors for children—age > ___ years; history of PONV or PONV in ___; procedure > ___ mins; ___ surgery
Age > 3 years
History of PONV or PONV in relatives
Procedure > 30 mins
Strabismus surgery
405
What induction drug is beneficial in reducing PONV? By what %?
Propofol; can reduce PONV by 20%
406
TIVA reduces PONV risk by ___%
25%
407
Regional anesthesia is ___x lower incidence of PONV
9x
408
Should use ___ instead of opioids to reduce risk of PONV
NSAIDs i.e.: Tylenol—good pain control, less PONV
409
(6) pretreatment options for PONV:
- Dexamethasone
- Serotonin antagonists
- H1 blockers
- Scopolamine patch
- NK1 antagonists
- Droperidol
410
Does hydration help reduce PONV?
Not so much
411
There is not much data to support the use of reglan, oxygen, ginger root, and cannabinoids to reduce PONV—T/F
True
412
Serotonin antagonists (5HT3), D2 blockers, reglan, and H1 blockers are all ___ medications
Rescue medications
413
Post-discharge nausea vomiting occurs in ___ of patients
1/3 of patients
414
Patients at high risk for post-discharge nausea vomiting should be given ___, ___ patch, ___, and ___ meds (i.e.: zofran, phenergan, scopolamine patch)
Dexamethasone, scopolamine patch, education, and rescue meds
415
Med that lasts long ___
Dexamethasone
416
Shorter acting medication ___
Zofran
417
Most nausea/vomiting meds are given at the ___ of the procedure, except for ___, ___, and ___
END of the procedure, except for scop patch, arepitant, Dexamethasone
418
Which med is most effective—zofran, droperidol, or Dexamethasone?
All are equally effective in reducing PONV by 25%
Ask patient if they’ve had any before
419
5HT3 antagonists are aka as ___
Serotonin antagonists
420
5HT3 antagonists end in ___
Setron (i.e.: ondansetron, dolasetron, granisetron, palonosetron)
421
5HT3 antagonists work at ___
Vagal afferents
422
Which two 5HT3 antagonists are used in chemo patients and why?
-Dolasetron
-Palonosetron
Both are longer acting
423
Zofran half-life is ___ hours; palonsetron half-life is ___ hours
4 hours; 40 hours
424
Dolasetron is a ___; requires CYP2D6 to metabolize active metabolite ___
Pro-drug; hydrodolasetron
425
Side effects of 5HT3 antagonists are generally ___; low risk of ___ (especially if patient is taking ___)
Mild; low risk of serotonin syndrome (especially if patient is taking SSRIs)
426
Risk of QT prolongation/torsades from 5HT3 antagonists
Study showed that the dose given was 32 mg IV—we use nowhere near this dose
427
Dexamethasone is a ___
Corticosteroid
428
Dexamethasone should be given ___ (before/after) induction
BEFORE
429
Dexamethasone does not have ___ effects
Mineralocorticoid effects
430
Side effects of dexamethasone—most side effects seen are associated with ___ use
Long-term use—i.e.: impaired wound healing, infection
431
Single use of dexamethasone for post-op nausea/vomiting usually has a ___ risk of side effects
Low
432
Droperidol is an ___ (D2) drug; very similar to ___
Anti-dopaminergic drug; very similar to haloperidol
433
Droperidol is used for ___, ___, and ___
Sedation, agitation, and nausea/vomiting
434
Droperidol targets the ___
CTZ
435
Older, first generation antipsychotics were used for nausea/vomiting because of their ___
D2 effects
436
Side effects of droperidol—___ symptoms or ___
Extrapyramidal symptoms (EPS) or tardive dyskinesias (TD)
437
Examples of EPS:
- Shuffling
- Lip smacking
- Neck turning
- Whole body twists
438
If extrapyramidal symptoms are not identified early, they can become ___
Permanent
439
Do not give droperidol to patients who have ___ disease or ___ disorders
Parkinson’s disease or movement disorders
440
Black box warning for QT prolongation/sudden cardiac death with droperidol—risk is ___
Risk is VERY RARE; doses to see this side effect are so high, so most people do not see this side effect; the FDA refused to pull the black box warning
441
Two examples of phenothiazines:
- Promethazine (phenergan)
| - Prochlorperzine (compazine)
442
Phenothiazines are ___ receptor antagonists
D2
443
Phenothiazines are highly anti___
Antihistaminergic
444
(2) side effects of phenothiazines:
- Sedation
| - EPS
445
Phenothiazines have a very ___ (high or low) risk of QT prolongation
LOW
446
Amisulpride (Barhemsys) is a ___ antagonist
D2 antagonist—newer medication on the market
447
Only indication for amisulpride (barhemsys) is for ___
Post-op nausea/vomiting
448
Administer amisulpride (barhemsys) ___ (before or after) induction
Before
449
Side effects of amisulpride (barhemsys)—elevated ___; ___ prolongation; postural ___; ___kalemia; abdominal ___
Elevated prolactin (gynecomastia); QT prolongation; postural hypotension; hypokalemia; abdominal distention
450
Metoclopramide (Reglan) is a ___ antagonist
Dopamine antagonists—antagonizes dopamine’s effect on the CTZ
451
Reglan accelerates the rate of gastric ___
Gastric emptying
452
Reglan does NOT alter ___ ion concentration
Hydrogen ion concentration
453
Reglan ___ (increases/decreases lower esophageal tone), which can prevent the kickback of GI contents that make people feel nauseous
Increases
454
Reglan can reduce ___ risk because it increases gastric emptying
Aspiration
455
Renal impairment requires a ___ in reglan dose
Decrease because its eliminated through the kidneys
456
Reglan readily crosses the ___ and ___; is excreted in ___
BBB and placenta; is excreted in breast milk
457
Reglan side effects—can see lots of abdominal ___; feeling of ___ or ___ with one time dose; ___ symptoms
Abdominal cramping; feeling of unease or restlessness with one time dose (AKA akathisia); extrapyramidal symptoms (with chronic use)
458
Reglan has an inhibitory effect on ___; may increase sedative actions of CNS depressants, EPS
Plasma cholinesterase
459
Avoid giving reglan with ___ or ___
Phenothiazines or butyrophenones
460
Avoid administering reglan to patients who have a history of ___ or preexisting ___ symptoms
History of seizures or preexisting extrapyramidal symptoms
461
Avoid reglan with ___ obstruction
Mechanical gastric outlet obstruction
462
Reglan is great to give ___ minutes pre-op if you want to reduce ___ risk
30 minutes pre-op if you want to reduce aspiration risk
463
Reglan ___ (increases/decreases) gastric fluid volume; ___ (does or does not) alter gastric pH; faster administration can cause ___
Decreases gastric fluid volume; does not alter gastric pH; faster administration can cause cramping
464
If reglan doesn’t help, ___ (do or do not) use another dopamine antagonist drug
Do NOT use another dopamine antagonist drug—it won’t work
465
Two H1 antagonists:
- Dimenhydrinate (Dramamine)
| - Diphenhydramine (Benadryl)
466
H1 antagonists release ___, are highly ___, and have ___ side effects
Release histamine, are highly sedating, and have anticholinergic side effects
467
If you give H1 antagonists with phenergan (promethazine) you will ___
Knock your patient out
468
Scopolamine patch is a ___ medication; place at least ___ hours prior to surgery
Anticholinergic medication; place at least 4 hours prior to surgery
469
Arepitant (Emend) is a ___ receptor antagonist
Neurokinin 1 receptor antagonist
470
How does arepitant (emend) work?—substance ___ is being blocked from NK1 receptor to send feelings of ___
Substance P is being blocked; send feelings of nausea
471
Arepitant (emend) is only approved for treatment of ___
Post-op nausea/vomiting
472
You should administer arepitant (emend) ___ hours prior to induction
3 hours
473
Arepitant (emend) may reduce effectiveness of birth control pills for up to ___ weeks
4 weeks
474
Arepitant may increase INR for ___ days when given in conjunction with warfarin
7-10 days
475
Arepitant (emend) is highly ___ bound
Protein
476
Dronabinol (marinol) is a ___, effective for ___
Cannabinoid, effective for chemo-induced nausea/vomiting
Not much data on this one
477
H2 receptor antagonists = ___ reducers
Acid reducers
478
(3) H2 receptor antagonists:
- Famotidine (Pepcid)
- Ranitidine (Zantac—taken off market 04/2020)
- Cimetidine (Tagamet)
479
Why was ranitidine (Zantac) taken off the market in 04/2020?
Found NMDA—cancer causing molecule
The older the Zantac was or the more heat it was exposed to, the more NMDA that was found
480
MOA of H2 receptor antagonists—UNDER NORMAL CONDITIONS...histamine activates ___ by binding to the H2 receptors on the parietal cells; this increases ___; activates ___ pump to secrete ___ ions against a large concentration gradient in exchange for ___...H2 receptor antagonists BLOCK this whole mechanism by inhibiting the binding of ___ to H2 receptors
Adenylyl cyclase; increases cAMP; activates proton pump to secrete H+ ions in exchange for K+
H2 receptor antagonists inhibit the binding of histamine to H2 receptors
481
Which H2 receptor antagonist is most potent? Least potent?
Most potent = famotidine
Least potent = cimetidine
482
H2 receptor antagonists and PPIs ___ (increase/decrease) ventilator associated pneumonias—because they ___ pH
INCREASE—because they change the pH, increasing the pH so bacteria can actually grow
483
H2 receptor antagonists change the ___
pH
484
H2 receptor antagonists have NO influence on the pH of the gastric fluid that is ___
Already in the stomach!
485
H2 receptor antagonists are great pre-op prophylaxis for patients with ___ history or patients undergoing procedures with ___
Allergic history; patients undergoing procedures with IV contrast
486
Drug-induced histamine release ___ (is/is not) prevented by H1 and H2 receptor antagonist pre-treatment; ___ response is less, but you have to give ___
Is NOT prevented by H1/H2 receptor antagonist pre-treatment; hypotensive response is less, but you have to give both H1 and H2 receptor antagonists to see an effect (if you only use H2 receptor antagonist, effects can actually be exaggerated)
487
What is a rare but serious complication of H2 receptor antagonist therapy?
Thrombocytopenia—only seen with megadose or long-term use
488
Cimetidine (Tagamet) can cause ___ in elderly
Confusion
489
H2 antagonists decrease ___; ___cardia and ___tension are generally associated with rapid IV push
CAMP; bradycardia and hypotension are generally associated with rapid IV push
490
Cimetidine (and ranitidine) inhibit CYP450, slowing metabolism/increasing risk of toxicity from what (4) drugs?
- Diazepam
- Propanolol
- Meperidine
- Lidocaine
491
H2 receptor antagonists can ___ absorption of some drugs by ___ gastric pH
Alter absorption; increasing gastric pH
492
H2 receptor antagonists can ___ (increase/decrease) absorption of ketoconazole, iron products, calcium carbonate, magnesium, and B12, because they need a more ___ environment to be properly absorbed
Decrease absorption because they need a more acidic environment to be properly absorbed
493
Proton pump inhibitors end in “-___”
-prazole
I.e.: omeprazole, pantoprazole, lansoprazole
494
Proton pump inhibitors are used to treat moderate to severe ___; ___ disease; ___ disorders
Moderate to severe GERD; peptic ulcer disease; hypersecretory disorders
495
Using PPIs PRN ___ (is/is not) very effective; ___ (longer/shorter) duration of action
Is not; longer duration of action
496
Should administer proton pump inhibitors ___ hours prior to surgery (ideally, administer ___)
3 hours before; ideally administer the night before
497
Pantoprazole with ranitidine 1 hour prior to surgery decreases gastric ___ and ___
Fluid and pH
498
Main adverse reaction with PPIs = ___
C. Dif because you’re changing the pH
499
What is much more effective than PPIs to control GERD?
Dietary changes
