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KLowe Pharmacology 1 > Final Exam Review > Flashcards

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

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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

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3
Q

Chemical structure of halothane

A

1 bromine, 1 chlorine, 3 fluorine

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4
Q

How many fluorines does isoflurane have?

A

5

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5
Q

How many fluorines does desflurane have?

A

6

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6
Q

How many fluorines does sevoflurane have?

A

7

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7
Q

Addition of fluorine, chlorine, bromine, or iodine to an inhalation agent is also called ___

A

Halogenation

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8
Q

Halogenation affects what 4 things?

A
  • Potency
  • Arrhythmogenic properties
  • Flammability
  • Chemical stability
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9
Q

Potency ___ (increases/decreases) with heavier halogens

A

Increases (bromine is heavier and more potent than fluorine)

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10
Q

Increased halogen atoms ___ (increases/decreases) the occurrence of arrythmias

A

Increases

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11
Q

More halogens ___ (increases/decreases) flammability

A

Decreases

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12
Q

Chemical stability is ___ (increased/decreased) with more halogens

A

Increased

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13
Q

Inhalation agents are very minimally metabolized—most are excreted from the ___

A

Lungs

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14
Q

Inhalation agents are ___ acting

A

Rapid

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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

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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

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17
Q

All gases are ___ (ionized or non-ionized)

A

Non-ionized

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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

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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
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20
Q

What rule is this?—lipid solubility is directly proportional to potency

A

Meyer-Overton rule

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21
Q

A reduction in body temperature ___ (increases/decreases) anesthetic requirement

A

Decreases

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22
Q

Anesthetic sites of action include ___ and ___ structures

A

Supraspinal and spinal structures

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23
Q

What structure in the nervous system specifically causes immobility to painful stimulus?

A

Spinal cord—GABA receptors

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24
Q

What structures cause amnesia and immobility?

A

Supraspinal structures

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25
Q

Potency is directly related to ___

A

Lipid solubility

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26
Q

The potency of an anesthetic ___ (increases/decreases) as its liposolubility increases

A

Increases

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27
Q

Oil:gas partition coefficient provides a quantitative measure of ___

A

Lipid solubility

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28
Q

What is MAC?

A

Minimum alveolar concentration where 50% will not move in response to surgical stimuli

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29
Q

With regards to CNS depression that results from inhalation agents…inhalation agents “probably” work by enhancing ___ ion channels and blocking ___ channels

A

Enhancing inhibitory ion channels and blocking excitatory ion channels

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30
Q

Inhalation agents cause ___ of neurons

A

Hyperpolarization

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31
Q

Inhalation agents work at the ___ receptor

A

GABA

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32
Q

What occurs during hyperpolarization?— ___ enters neurons through ___ receptor, efflux of ___ out of neurons

A

Chloride enters neurons through GABA receptor, efflux of potassium out of neurons

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33
Q

1 MAC = ___% won’t respond to surgical stimuli

A

50%

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34
Q

MAC BAR = ___ MAC

A

1.3 MAC

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35
Q

1.3 MAC (MAC BAR) = ___% won’t respond to surgical stimuli

A

95%

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36
Q

Immobility from inhalation agents is ___ mediated

A

Spinal cord mediated—they inhibit nociceptive input in the dorsal horn of the spinal cord

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37
Q

How do we measure immobility?

A

MAC

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38
Q

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

A

4 or 5

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39
Q

How do we measure amnesia?

A

No reliable way to measure—BIS monitor?

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40
Q

Amnesic effects of anesthesia are generated from ___ structures such as ___ and ___ (both are part of the limbic system); and ___

A

Supraspinal structures such as amygdala and hippocampus; and cortex

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41
Q

How do we measure analgesia?

A

Cannot be measured

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42
Q

Intraoperative measures of pain suggest that inhaled anesthetics ___ (do/do not) suppress the perception of painful stimuli

A

Do NOT (i.e.: increased HR, increased systemic BP)

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43
Q

At equilibrium…___ partial pressure = ___ partial pressure = ___ partial pressure

A

CNS = blood = alveolar

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44
Q

Inhaled anesthetics are delivered from the ___ to ___ to ___

A

Lungs to blood to CNS

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45
Q

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

A

Low capacity

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46
Q

The more blood soluble the agent, the ___ (faster/slower) the rise in blood partial pressure, and the ___ (faster/slower) the CNS uptake

A

Slower the rise in blood partial pressure; the slower the CNS uptake

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47
Q

The blood:gas solubility coefficient is an indicator of speed of ___

A

Uptake/elimination

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48
Q

The more blood soluble the drug, the ___ (slower/faster) the brain and spinal cord uptake and therefore the ___ (slower/faster) the anesthesia state achieved

A

Slower; slower

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49
Q

How can we combat high blood:gas solubility/slower induction?

A

Turn up the flow of the gas to speed up induction

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50
Q

It is easy to maintain blood/CNS concentrations of inhalation agents because a ___ (small/large) amount is removed by metabolism

A

Small

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51
Q

Equilibrium of agent is a result of 3 factors—1) inhaled anesthetics are delivered from ___ to ___ to ___

A

Lungs to blood to CNS

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52
Q

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

A

Low

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53
Q

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

A

Low

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54
Q

Volatile anesthetics are ___ at ambient temperature/pressure

A

Liquids

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55
Q

What is the pressure exerted by molecular collisions of gas molecules against container walls?

A

Vapor pressure

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56
Q

Vapor pressure is proportional to ___

A

Temperature

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57
Q

Increased temperature = ___ (increased/decreased) vapor pressure

A

Increases

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58
Q

As long as you have liquid in the container, the vapor pressure is independent of the ___ of the liquid

A

Volume

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59
Q

What law is this?—the sum of the partial pressures of each gas in a mixture equals the total pressure of the mixture

A

Dalton’s Law

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60
Q

Atmospheric pressure = ___ mm Hg

A

760

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61
Q

Gases equilibrate based on ___, not on concentration

A

Partial pressures

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62
Q

Solubility describes the tendency of a gas to ___ with a solution

A

Equilibrate

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63
Q

Henry’s Law—as solubility increases, ___ increases

A

Partial pressure increases

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64
Q

The lower the blood solubility, the ___ induction/emergence

A

Faster induction/emergence

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65
Q

Speed of uptake and elimination from the brain is inversely related to ____

A

Blood solubility

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66
Q

Uptake/elimination from the brain is ___ (slower/faster) with agents that are LESS blood soluble

A

Faster

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67
Q

The oil:gas coefficient provides a quantitative measure of ___

A

Lipid solubility

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68
Q

___ is directly related to lipid solubility

A

Potency

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69
Q

The concentration of a gas in a mixture depends on what two factors?

A
  • Partial pressure

- Solubility

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70
Q

Is tissue solubility greater in fat or muscle tissue?

A

Fat > muscle

Anesthetics can linger in the fatty tissue; may take longer for a fat person to wake up

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71
Q

What tissue receives the greatest amount of cardiac output?

A

Vessel-rich group (75% CO, least % body mass)

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72
Q

What tissue receives the least amount of cardiac output?

A

Fat (6% CO)

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73
Q

Goal of anesthesia = produce and maintain a constant partial pressure of inhalation anesthetic in the ___

A

Brain

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74
Q

Develop an ___ anesthetic concentration&raquo_space; develop an ___ anesthetic concentration&raquo_space; develop a ___ anesthetic concentration&raquo_space; distribute anesthetic agent from ___ to ___

A

Inspired concentration&raquo_space; alveolar concentration&raquo_space; blood concentration&raquo_space; distribute from blood to tissue

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75
Q

What is a “wash in”?

A

Using high gas flows (5-10L/min range) to increase the partial pressure of an anesthetic agent

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76
Q

Fi =

A

Inspired gas

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77
Q

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)

A

Concentration effect

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78
Q

For kids, do a pure ___ anesthetic

A

Inhaled

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79
Q

The rate at which the alveolar partial pressure of the anesthetic agent rises is determined by what 2 factors?

A
  • Inspired concentration

- Alveolar ventilation

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80
Q

When alveolar ventilation is high, partial pressure of anesthetic in the alveoli ___

A

Increases rapidly

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81
Q

What law is associated with the second gas effect?

A

Fick’s law

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82
Q

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

A

Second gas effect

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83
Q

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

A
  • Solubility of the agent
  • Rate of blood flow through the lungs (CO)
  • Partial pressure of the agents in arterial/venous blood
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84
Q

Lower CO = ___ (faster/slower) induction

A

Faster

Box car gets fuller, so more gas goes into the bloodstream and then to the brain

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85
Q

Higher CO = ___ induction

A

Slower

Box car gets less full because the train is moving faster, so less gas goes into the bloodstream/to the brain

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86
Q

Blood:gas partition coefficient = solubility of agent in ___

A

Blood

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87
Q

The higher the blood solubility coefficient, the ___ it takes to anesthetize the patient

A

Longer

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88
Q

IV anesthesia—normal CO, drugs go to their site of action ___

A

Relatively quickly

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89
Q

IV anesthesia—low CO, drugs go to their site of action ___

A

Slowly

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90
Q

Inhaled agents—low CO—as blood goes to the lungs, will pick up ___ (more/less) agent

A

More

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91
Q

Inhaled agents—high CO—as blood goes to the lungs, will pick up ___ (more/less) agent

A

Less

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92
Q

Tissue groups/order of greatest to least effect of inhalation agents:

A

Vessel rich: brain, heart, liver, kidney, endocrine
Fat: adipose tissue
Muscle: skin and muscle
Vessel poor: bone, ligaments, teeth, hair, cartilage

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93
Q

Majority of inhalation agents work in the ___ group

A

Vessel rich

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94
Q

What are the 4 stages of anesthesia?

A

Stage 1–stage of analgesia
Stage 2–stage of delirium or excitement
Stage 3–stage of anesthesia
Stage 4–stage of depression

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95
Q

Stage 1–stage of analgesia begins with ___ and ends with ___

A

Begins with administration of anesthesia, ends with loss of consciousness

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96
Q

Stage 2–stage of delirium or excitement—what can occur?

A

Laryngospasm!!!

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97
Q

During stage 2, patient is in a more ___ state

A

Hyperreflexive—increased muscle tone/rigidity; irregular breathing, tachypnea; HR elevated, BP up; pupils dilate

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98
Q

Stage 2 lasts from ___ to ___

A

Loss of consciousness to surgical anesthesia

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99
Q

Stage 3–stage of anesthesia—what is no longer a risk?

A

Laryngospasm is not a risk—excitement subsides

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100
Q

Stage 3–there is a return of ___ and pupils are ___

A

Return of regular respiration; pupils are centered

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101
Q

Stage 3–cough, gag, and eyelid reflexes are ___

A

Absent

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102
Q

Stage 4–stage of depression

A

Respiratory/cardiac depression

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103
Q

MAC =

A

Minimum alveolar concentration

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104
Q

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

A

50%

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105
Q

MAC is a reliable indicator of dose and potency of an anesthetic—T/F?

A

TRUE

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106
Q

The lower the MAC, the ___ (less/more) potent the agent and the ___ (lower/higher) the blood:gas partition coefficient (blood solubility)

A

More potent; higher the blood:gas partition coefficient

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107
Q

How does pregnancy affect MAC?

A

Decreases

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108
Q

Infants/young kids have ___ MAC

A

Higher MAC d/t higher metabolic rate

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109
Q

Intoxicated person has ___ MAC

A

Lower

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110
Q

Chronic alcoholic has ___ MAC

A

Higher

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111
Q

Hypothermic patients have ___ MAC

A

Decreased MAC d/t decreased metabolic rate

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112
Q

Hyperthermia causes ___ MAC d/t ___ metabolic rate; higher MAC up to ___ degrees C, then MAC ___ again

A

Higher MAC d/t higher metabolic rate; higher MAC up to 42 degrees C, then MAC decreases again

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113
Q

How do hypoxia, anemia, and hypotension affect MAC?

A

Decreases

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114
Q

Elderly have ___ MAC

A

Decreased

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115
Q

Infants have ___ MAC

A

Increased

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116
Q

MAC is usually greatest in ___ d/t their high basal metabolic rate

A

Newborn

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117
Q

Hyperthermia ___ MAC

A

Increases

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118
Q

Chronic drug use—alcohol, barbiturates, narcotics— ___ MAC

A

Increase

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119
Q

Hyper/hypothyroid ___ MAC

A

Has NO EFFECT ON MAC

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120
Q

Blood pressure—MAP < ___ mm Hg decreases MAC

A

40

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121
Q

Hypercalcemia ___ MAC

A

Decreases

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122
Q

Hypernatremia ___ MAC

A

Increases

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123
Q

Hyponatremia ___ MAC

A

Decreases

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124
Q

Cocaine ___ MAC d/t higher BP/HR

A

Increases

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125
Q

Local anesthetics ___ MAC

A

Decreases

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126
Q

All drugs decrease MAC except ___

A

Sympathomimetics—amphetamine, cocaine, ephedrine all INCREASE MAC

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127
Q

Acute use of sympathomimetics ___ MAC

A

Increases

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128
Q

Chronic use of sympathomimetics ___ MAC

A

Decreases

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129
Q

Potency is directly related to ___

A

Lipid solubility

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130
Q

MAC is inversely related to ___

A

Potency

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131
Q

More potent agent = ___ MAC

A

Lower

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132
Q

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

A

10%; 95%; 99%

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133
Q

What type of MAC is this?—MAC at which 50% of subjects will respond to the command “open your eyes”

A

MAC-awake

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134
Q

What type of MAC is this?—blocks the adrenergic response to skin incision

A

MAC-BAR or 1.2 MACS

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135
Q

What type of MAC is this?—similar to MAC-BAR in that its values exceed the anesthetic requirements for surgical skin incision

A

MAC intubation

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136
Q

MAC of iso

A

1–(most potent out of the agents we typically use)

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137
Q

MAC of sevo

A

2

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138
Q

MAC of des

A

6–(least potent out of agents we use)

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139
Q

MAC values for different inhaled anesthetics are ___

A

Additive

0.5 MAC of nitrous oxide + 0.5 MAC of isoflurane has the same effect as 1 MAC of any single inhaled anesthetic

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140
Q

3 factors that determine the input of inhaled anesthetic into the alveoli: ___ partial pressure; ___ ventilation; ___ of the breathing system

A

Inspired partial pressure; alveolar ventilation; characteristics of the breathing system

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141
Q

High inspired partial pressure = ___ induction; what effect is this?

A

Faster induction—concentration effect

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142
Q

Hyperventilation = ___ (slower/faster) induction

A

Faster

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143
Q

Hypoventilation = ___ (slow/fast) induction

A

Slow

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144
Q

Factors that affect uptake of inhaled anesthetic into pulmonary arterial blood: ___ of gas; ___ output; ___ partial pressure difference

A

Solubility of gas; cardiac output; arterial to venous partial pressure difference

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145
Q

High CO = ___ induction

A

Slow

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146
Q

Low CO = ___ induction

A

Fast

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147
Q

Factors affecting transfer of inhaled anesthetic from arterial blood to brain: ___ partition coefficient; ___ blood flow; ___ partial pressure difference

A

Brain-blood partition coefficient; cerebral blood flow; arterial to venous partial pressure difference

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148
Q

Agents in order of increasing potency:

A

Nitrous &laquo_space;Des &laquo_space;Sevo &laquo_space;Iso &laquo_space;Halo

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149
Q

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

A

Down

So that they don’t deepen their anesthesia to the point where they stop breathing

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150
Q

For emergence in a patient with an LMA spontaneously breathing—tidal volume will go ___ as you go down on gas

A

Up

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151
Q

Which agent should be used for fat patients and why?

A

Des!!! Because it binds the least to the fatty tissue out of all other agents

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152
Q

Which agent is most irritating to the lungs?

A

Des—patients will cough after

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153
Q

___ comes off fastest, then ___, ___

A

Des; sevo; iso

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154
Q

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

A

Right-to-left shunt

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155
Q

Is a left-to-right shunt clinically significant?

A

No

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156
Q

Emergence from anesthesia = the rate at which alveolar gas partial pressure ___ (increases/decreases) with time

A

Decreases

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157
Q

Higher partial pressure at ___ during emergence; lower partial pressure in the ___

A

Brain/bloodstream; lower partial pressure in the lungs because gas is shut off

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158
Q

During emergence, gas moves out from ___ to ___ to ___ to be exhaled

A

Brain to blood to lungs

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159
Q

Hypoventilation/low fresh gas flows result in ___ of anesthetic

A

Rebreathing of anesthetic—will have transfer of anesthetic back into tissues and delayed wake up

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160
Q

What can occur if nitrous was used during the case and it is abruptly discontinued for emergence?

A

Diffusion hypoxia

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161
Q

What should you do to prevent diffusion hypoxia?

A

Turn up O2 to 100% for 5-10 minutes after N2O has been discontinued

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162
Q

MAP ___ (increases/decreases) with increases in concentration of des, sevo, and iso (in a dose dependent manner)

A

Decreases

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163
Q

Least decrease in MAP with ___ (which agent?)

A

Sevo

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164
Q

Decrease in MAP from inhaled anesthetics reflects a decrease in ___

A

SVR

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165
Q

Exceptions—halothane decreases MAP by decreasing ___, not SVR

A

CO

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166
Q

N2O causes ___ or ___ MAP

A

Unchanged or mildly increased MAP—activates SNS and increases SVR

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167
Q

Substituting N2O for a portion of the volatile anesthetic decreases the magnitude of BP decrease—T/F?

A

TRUE—because nitrous adds sympathetic stimulus, so BP doesn’t fall as dramatically

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168
Q

Inhaled agents typically ___ (increase/decrease) heart rate

A

Increase—response occurs at unique concentrations for each agent

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169
Q

Des causes minimal increase in HR at concentrations ___; at concentrations ___, a linear, dose dependent increase in HR is observed

A

< 1 MAC; > 1 MAC

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170
Q

With sevo, HR does not increase until concentrations ___

A

> 1.5 MAC…really won’t see 1.5 MAC with sevo, so won’t really see HR increases with sevo

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171
Q

What agent produces a minor increase in EF, which is part of the reason why CV surgeries use it on the bypass machine?

A

DES

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172
Q

Are dysrythmia problems common with newer agents?

A

No d/t their halogenation

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173
Q

What agent sensitizes the heart to PVCs?

A

Halothane

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174
Q

Inhaled anesthetics prolong ___

A

QT interval

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175
Q

Avoid what agent in patients with known congenital long QT syndrome?

A

Sevo

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176
Q

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?

A

True

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177
Q

How do volatile anesthetics protect the heart?

A

Coronary steal—blood is taken from the poor ischemic areas of the heart and given to the rich

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178
Q

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

A

Ischemic preconditioning

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179
Q

As anesthetic concentration increases, there is ___ respiratory rate, ___ tidal volume

A

Increased respiratory rate, decreased tidal volume

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180
Q

Gas exchange becomes ___ (more/less) efficient as anesthetic depth increases

A

Less

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181
Q

PaCO2 ___ (increases/decreases) with deeper anesthesia

A

Increases—pt is not breathing and blowing off CO2; can increase tidal volume and/or RR to blow off more CO2

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182
Q

As patient starts to wake up (emergence), tidal volume ___ (increases/decreases)

A

Increases

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183
Q

Natural response to CO2 is ___ by volatile anesthetics

A

Blunted

Volatile anesthetics cause a dose related blunting of respiratory response to increased CO2

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184
Q

ETCO2 is ___ (higher/lower) than PaCO2 on ABG

A

Lower (2-5 mm Hg lower)

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185
Q

Inhaled anesthetics reduce what respiratory capacity?

A

FRC

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186
Q

Inhaled anesthetics cause ___ in the dependent areas of the lung; occurs to a greater extent with ___ ventilation

A

Atelectasis; spontaneous ventilation

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187
Q

What agent is pungent and irritates the airway?

A

Des

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188
Q

All inhaled anesthetics decrease CMRO2 except for ___

A

Nitrous—increases CMRO2, causes cerebral vasodilation—not the best gas to use in neuro cases

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189
Q

Volatile anesthetics produce a dose dependent ___ (increase/decrease) in cerebral blood flow

A

Increase

Higher concentrations > 1 MAC increase cerebral blood flow; lower concentrations < 0.5 MAC do not significantly change cerebral blood flow

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190
Q

___ventilate patients with increased ICP to keep CO2 at 35 mm Hg

A

Hyperventilate

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191
Q

ICP ___ (increases/decreases) with all volatile anesthetics at doses > 1 MAC

A

Increases

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192
Q

At 1 MAC or greater, the volatile anesthetic will inhibit the body’s normal mechanisms of autoregulation—T/F?

A

True

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193
Q

Volatile anesthetics and nitrous oxide ___ (increase/decrease) the amplitude and ___ (increase/decrease) the latency of SSEP in a dose dependent matter

A

Decrease the amplitude; increase the latency of SSEP

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194
Q

SSEP = ___—evaluate the integrity of the ___ and ___

A

Somatosensory evoked potentials—evaluate the integrity of the brain and spinal cord

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195
Q

Evoked potentials may be abolished at ___ MAC

A

1

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196
Q

What agent is associated with epileptiform activity on the EEG, especially at high concentrations?

A

Sevo

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197
Q

Inhalation agents produce a dose dependent skeletal muscle ___ and ___ the activity of neuromuscular blocking drugs

A

Skeletal muscle relaxation; enhance/potentiate the activity of neuromuscular blocking drugs

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198
Q

Immune mediated liver injury from inhaled anesthetics is ___

A

Rare

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199
Q

Mild liver injury may occur with what inhalation anesthetic?

A

Halothane (because 45% of it gets metabolized by the liver); known as halothane hepatitis

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200
Q

What gas forms compound A? What organ does compound A affect?

A

Sevo; affects the kidneys (nephrotoxic)

201
Q

Compound A is formed after prolonged sevoflurane administration at ___ low/high fresh gas flows

A

Low (1L/min)

202
Q

Package insert for sevo states that low fresh gas flow <2L/min must be limited to less than ___ MAC hours of sevo anesthesia

A

Less than 2 MAC hours

203
Q

What triggers MH?

A
  • Succs (depolarizing agent)

- All halogenated agents—halothane > forane > sevo > des

204
Q

What is the earliest and most sensitive sign of MH?

A

Increased ETCO2

205
Q

Other signs of MH:

A
  • Fever
  • Tachycardia
  • Cyanosis
  • Rigidity
  • Trismus—failure of the masseter muscle to relax
206
Q

Treatment of MH

A

Dantrolene 2.5 mg/kg IV every 5 minutes; max dose = 10 mg/kg

207
Q

Don’t use nitrous in patients with ___, ___

A

Pneumo, retinal repair—N2O enters air filled cavities easily and can expand these areas

208
Q

Soda lime is 94% ___ hydroxide; 5% ___ hydroxide; 1% ___ hydroxide

A

94% Calcium hydroxide (Ca[OH]2); 5% sodium hydroxide (NaOH); 1% potassium hydroxide (KOH)

209
Q

___ reaction with CO2 absorbent

A

Exothermic reaction

210
Q

Fire can occur from soda lime, especially with ___

A

Sevo

211
Q

___ (high/low) fresh gas flow rates accelerate the desiccation of CO2 absorbents

A

High

212
Q

Compound A can cause ___

A

Nephrotoxicity

213
Q

Compound A/nephrotoxicity is caused by which agent?

A

Sevo at low fresh gas flows

214
Q

To prevent nephrotoxicity from compound A, want to maintain fresh gas flows of sevo at ___L/min or ___

A

2L/min or greater

Also want to use fresh/hydrated soda lime to minimize the risk

215
Q

If a vaporizer tipped over, should you use it?

A

No!!! Can overdose patient with volatile anesthetic (higher concentration of gas will get to the patient)

216
Q

Vapor pressure is a function of ___

A

Temperature

217
Q

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

A

HIGHER

HLH—high, low, high

218
Q

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

A

LOWER

LHL—low, high, low

219
Q

Which agent has the highest vapor pressure?

A

Des—669 mm Hg; has to be heated to 2 atm of pressure

220
Q

Sevo vapor pressure

A

170 mm Hg (lowest out of agents we use)

221
Q

Iso vapor pressure

A

240 mm Hg

222
Q

Halo vapor pressure

A

244 mm Hg

223
Q

Agents in order of increasing vapor pressure

A

Sevo < Iso < Halo < Des

224
Q

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

A

Lower; lower; underdosing

225
Q

Have to use ___ (lower/higher) doses at ___ (lower/higher) altitudes

A

Higher doses at higher altitudes

226
Q

ACH binds to ___ receptor (nitrogen portion binds to BOTH alpha subunits), causes influx of ___

A

Nicotinic receptor, causes influx of sodium

227
Q

NMBs cause ___ only; need to give ___ medication

A

Paralysis only; need to give sedation/pain medication

228
Q

___% suppression of single twitch response is adequate for surgery

A

90% suppression

229
Q

Succs is a ___polarizing agent

A

Depolarizing

230
Q

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

A

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
Q

Non-depolarizing = ___ antagonism at the ___ receptor; blocks ___ from binding to receptors

A

Competitive antagonism at the nicotinic receptor; blocks ACH from binding to receptors

232
Q

ACH binds to ___ alpha subunits of the nicotinic receptor; depolarizing/non-depolarizing NMBs bind to ___ alpha subunits

A

ACH binds to BOTH (has to bind to both subunits to exert its effect); NMBs bind to one or both subunits

233
Q

Tracheal intubation dose for NMBs = ___x ED 95 dose

A

2x ED 95 dose

234
Q

___ is a poor predictor of laryngeal relaxation compared to ___

A

Adductor pollicis muscle … compared to orbicularis oculi

235
Q

___ (small/large) muscles are blocked first; ___ blocked last

A

Small muscles are blocked first (i.e.: eyes/fingers); diaphragm is blocked last

236
Q

Reversal of NMB— ___ affected last by NMB, but they recover first d/t blood flow

A

Diaphragm/abdomen are affected last, but they recover first d/t blood flow

237
Q

___ to ___ for onset of action; ___ to ___ for recovery

A

Small to large for onset of action; large to small for recovery

238
Q

What two non-depolarizing NMBs cause histamine release with the benzyl group?

A
  • Atracurium

- Mivacurium

239
Q

All NMBs are highly ___ (nonionized/ionized) and ___ soluble

A

Highly ionized and water soluble—stay in the body fluid, don’t deposit into fatty tissue

240
Q

Can you give NMBs orally?

A

No—because they are highly ionized and water soluble

241
Q

Are NMBS highly protein bound?

A

No

242
Q

What NMB is highly protein bound?

A

Atracurium

243
Q

Aminosteroid NMBs end in ___

A

-curonium

244
Q

Benzyl NMBs end in ___

A

-curium

245
Q

Hyperkalemia with succs is caused by ___ influx into the cell

A

Na+

246
Q

Phase I blockade with succs = __polarizing; ___ at onset

A

Depolarizing; twitches at onset—won’t have continuous muscle movement afterwards because further impulses are blocked

247
Q

Phase II blockade with succs = ___polarizing because further impulses are blocked

A

Non-depolarizing

248
Q

What breaks down succs?

A

Plasma cholinesterase

So anything that reduces plasma cholinesterase causes prolonged NMB with succs (i.e.: liver disease, neostigmine, high estrogen levels)

249
Q

Obese patients have ___ (low/high) plasma cholinesterase—may need ___ (lower/higher) dose of succs

A

High plasma cholinesterase—may need higher dose of succs

250
Q

How do you test for atypical cholinesterase?

A

Dibucaine test

251
Q

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

A

True

252
Q

Dysrythmias (bradycardia, junctional, sinus arrest) with succs are increased if you give a second dose within ___ minutes of giving the first dose

A

Within 5 minutes; atropine helps

253
Q

Patients with muscular dystrophy, third degree burns, atrophy, severe trauma, upper motor neuron lesions should NOT receive with NMB? Why?

A

Succs because they are at increased risk of severe hyperkalemia

254
Q

Why are patients with muscular disorders at an increased risk of Hyperkalemia from succs administration?—d/t ___ of nicotinic receptors

A

D/t up regulation of nicotinic receptors in patients with muscular dystrophy

255
Q

May not see hyperkalemia initially after succs administration—can develop within ___ hours and last up to ___ months or more

A

Can develop within 96 hours and last up to 6 months or more (up to 2 years)

256
Q

Very high risk of hyperkalemia with succs = males with undiagnosed ___

A

Undiagnosed myopathy—will definitely get hyperkalemia from Succs

257
Q

Myalgias with succs come from the ___ in the depolarizing phase (phase I)

A

Fasciculations

258
Q

Is there a reversal agent for succs?

A

No—have to wait for it to wear off

259
Q

Are there reversal agents for non-depolarizing agents?

A

Yes

260
Q

Which two non-depolarizing NMBs cause histamine release?

A

Atracurium and mivacurium

261
Q

Non-depolarizing NMBs can cause critical myopathy in intubated patients on long-term paralysis > ___ days

A

> 6 days

262
Q

What two types of steroid NMBs are at highest risk for myopathy?

A

Aminosteroid and corticosteroids

263
Q

Most anaphylactic reactions in the OR occur from the ___

A

Neuromuscular blocker

264
Q

More nitrogens = ___ (more/less) risk for allergic reaction

A

More risk for allergic reaction

265
Q

____ (men or women) are at greater risk of allergic reaction from NMB agents

A

Women—could be d/t higher estrogen levels inhibiting cholinesterase, leading to a build up of succs (7.3% women vs. 2% men)

266
Q

How do Alzheimer’s/dementia medications affect NMBs?

A

Can lead to build up of NMB/prolonged neuromuscular blockade because they are acetylcholinesterase inhibitors

I.e.: aricept, excelon

267
Q

Do aminoglycosides increase or decrease the effects of NMBs?

A

Increase the effects

I.e.: gentamicin

268
Q

Do local anesthetics increase or decrease the effects of NMBs?

A

Increase

I.e.: lidocaine, quinidine

269
Q

Do loop diuretics increase or decrease the effects of NMBs?

A

Increase

270
Q

What NMB is best to use with phenytoin d/t its reduced effects?

A

Vecuronium

271
Q

How does hypothermia affect NMB?

A

For every degree change from 36 C, can prolong duration of NMB for 10-15 minutes

272
Q

Hypokalemia causes ___ to succs, ___ to non-depolarizing agents

A

Resistance to succs, sensitive to non-depolarizing

273
Q

Hyperkalemia is ___ to succs, ___ to non-depolarizing

A

Sensitive to succs, resistant to non-depolarizing

274
Q

Which NMB is bad in renal failure patients because 80% of the drug is eliminated via kidneys?

A

Pancuronium

275
Q

Which drug has the most significant CV side effects—increased HR, MAP, CO?

A

Pancuronium

276
Q

Pancuronium interacts with ___—more incidence of dysrhythmias

A

Digoxin

277
Q

When broken down, pancuronium has an ___

A

Active metabolite—half as potent

278
Q

Give roc ___x the ED95 dose to get similar onset to succs (1-2 mins or less)

A

3-4 x

279
Q

What two NDNMBs undergo Hoffman elimination?

A

Atracurium and cisatracurium

280
Q

Hoffman elimination results in ___ metabolite

A

Laudanosine metabolite

281
Q

Laudanosine metabolite causes peripheral ___

A

Vasodilation

282
Q

Laudanosine metabolite is safe in ___ patients

A

Renal/hepatic dysfunction patients

283
Q

At 3x ED95 dose of atracurium, can see ___ HR, ___ MAP

A

Increase HR, decrease MAP

284
Q

What (3) things cause the decrease in MAP when giving 3x ED95 dose of atracurium?

A
  • Laudanosine metabolite causes peripheral vasodilation
  • Histamine release with atracurium causes vasodilation
  • Tachycardia relaxes vessels
285
Q

What drugs should you use to combat the atracurium histamine release?

A

H1 and H2 blockers

286
Q

Prolonged duration of action of ___ in obese patients d/t fluid shifts in ECF, not d/t increased fatty tissue

A

Cisatracurium

287
Q

Does cisatracurium cause histamine release?

A

NO—only atracurium and mivacurium cause histamine release

288
Q

What drug should not be used in patients with kidney/liver disease?

A

Vecuronium

289
Q

Vecuronium is ___ (more/less) lipid soluble than other agents because it has only one nitrogen group

A

More lipid soluble

290
Q

What is the only good thing about mivacurium?

A

Patient may not need a reversal agent

291
Q

What is the enzyme that breaks down ACH?

A

Acetylcholinesterase

292
Q

What are the two cholinergic receptors?

A

Nicotinic + muscarinic receptors—both are targets of ACH

293
Q

Anticholinergic =

A

Antimuscarinic (they can be used interchangeably)

294
Q

Acetylcholinesterase inhibitors = ___ effects

A

PNS/‘rest and digest’ effects

295
Q

Anticholinesterase drugs =

A

Acetylcholinesterase inhibitors

296
Q

What determines drug interactions at the enzyme acetylcholinesterase?

A

Positively charged nitrogen molecule

297
Q

3+ =

A

Tertiary amines

298
Q

What anticholinesterase drug is a tertiary amine?

A

Physostigmine

299
Q

Tertiary amines are ___ (more/less) likely to enter the CNS because they are ___ (more/less) ionized and are ___ (more/less) lipophilic than quaternary ammoniums

A

More likely; less ionized; more lipophilic

300
Q

4+ =

A

Quaternary ammonium

301
Q

What are (3) quaternary ammonium drugs

A
  • Edrophonium
  • Neostigmine
  • Pyridostigmine
302
Q

Quaternary ammonium drugs do not enter the ___

A

CNS

303
Q

All reversal agents work by inhibiting the enzyme ___; this increases the ___; does NOT increase ___

A

Acetylcholinesterase; this increases the available ACH in the body; does NOT increase the release of ACH

304
Q

Reversal agents just prevent ___

A

ACH from being metabolized

305
Q

Reversal agents cause ___ at the ___ receptor

A

Competitive antagonism at the nicotinic receptor—flood the receptor with ACH

306
Q

ACH normally will bind to ___ and ___ receptors

A

BOTH nicotinic and muscarinic receptors…ACH must bind to BOTH receptors!

307
Q

How reversal agent medications interact with acetylcholinesterase determines ___

A

Onset of action

308
Q

Neostigmine, pyridostigmine, and physostigmine all bind to acetylcholinesterase and cause a ___ change in the enzyme

A

Conformational change (so the enzyme can’t break down ACH)

309
Q

Edrophonium acts like a ___

A

Magnet—positive binds to negative portion of enzyme; NO chemical reaction; reversible binding; faster onset of action

310
Q

Edrophonium has a ___ onset of action than neo/pyrido/physostigmine

A

Faster (because no chemical reaction occurs—it acts like a magnet)

311
Q

If you give a reversal agent without a neuromuscular blocker, you will see…

A

Phase I—fasciculations
Phase II—block

Like what happens when you give succs—because you are overwhelming the nicotinic receptors with ACH

312
Q

Interaction with enzyme (acetylcholinesterase) determines ___ of reversal agents

A

Onset of action

313
Q

Edrophonium onset of action

A

1-2 minutes

314
Q

Neostigmine onset of action

A

7-11 minutes

315
Q

Pyridostigmine onset of action

A

Up to 16 minutes

316
Q

DOA for reversal agents

A

All last for about 1-2 hours

317
Q

With reversal agents, you have to wait until patient has ___

A

Spontaneous recovery

318
Q

Can neostigmine reverse a deep blockade?

A

No

319
Q

Is there a benefit to giving an additional dose of reversal agent? Why?

A

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
Q

How do antibiotics (aminoglycoside, fluoroquinolones, TCN) affect reversal?

A

All inhibit/slow down reversal

321
Q

How does hypothermia affect reversal?

A

Inhibits

322
Q

Respiratory acidosis ___ reversal

A

Inhibits

323
Q

Hypokalemia/metabolic acidosis ___ reversal

A

Inhibits

324
Q

Reversal agents act at the nicotinic, muscarinic, or both receptors?

A

Muscarinic receptor

325
Q

Reversal agents binding to the muscarinic receptor = ___ effects—___cardia, broncho___, ___ pupils, ___peristalsis

A

PNS effects—rest and digest

  • Bradycardia
  • Bronchoconstriction
  • Tiny pupils (miosis)
  • Hyperperistalsis (gut starts moving)
326
Q

Hyperperistalsis increases the risk of ___, especially with ___

A

PONV, especially with neostigmine

327
Q

We give atropine, glycopyrrolate, and scopolamine to limit the ___ effects of reversal agents

A

Muscarinic effects

328
Q

Is there a risk of prolonging the neuromuscular blockade when giving atropine, glycopyrrolate, or scopolamine with the reversal agent?

A

No—because these drugs act at the MUSCARINIC receptor, not at nicotinic receptors

329
Q

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

A

BEFORE giving the reversal agent

330
Q

Physostigmine is a ___

A

Tertiary amine—crosses BBB

331
Q

If you accidentally give an additional dose of reversal agent (OD of ACHase inhibitors), what occurs?

A

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
Q

Treatment of ACHase inhibitor (reversal agent) OD— ___ to treat the decreased HR

A

Atropine

333
Q

Treatment of ACHase inhibitor (reversal agent) OD—pralidoxime

A

Acetylcholinesterase reactivator—kicks reversal agents off of receptor (competitive antagonism)

334
Q

Parlidoxime would only work for NMBs that are ___

A

Reversible (non-depolarizing NMBs)—so would NOT work on succs

335
Q

Above all, treatment for ACHase inhibitor (reversal agent) OD is mostly ___

A

Supportive measures—have to wait for the body to make more acetylcholinesterase (could take months)

336
Q

Anticholinergic drugs have no effect on ___

A

Acetylcholinesterase

337
Q

Anticholinergic drugs work at the ___ receptor to block effects of ___

A

Muscarinic receptor; block effects of ACH

338
Q

What two drugs are tertiary amines? Where do they enter?

A

-Atropine
-Scopolamine
^ enter the CNS

339
Q

Quaternary ammoniums do not enter the ___

A

CNS—i.e.: glycopyrrolate

340
Q

No risk of prolonged blockade with anticholinergics because they act at the ___ receptor, NOT ___ receptor

A

Muscarinic receptor, NOT nicotinic receptor

341
Q

Anticholinergics cause ___ at the muscarinic receptor

A

Competitive antagonism

342
Q

M1-M5–odd = ___ effects; ___ coupled; increase ___

A

Stimulatory effects; G-protein coupled; increase Ca

343
Q

M1-M5–even = ___ effects; decrease ___; decrease ___; decrease ___

A

Inhibitory effects; decrease adenylyl cyclase; decrease cAMP; decrease Ca

Agonist with inhibitory effects

344
Q

Which receptor is most sensitive to effects of anticholinergics? (AKA the least dose of anticholinergic is required to see these effects)

A

M3 receptor—respiratory effects

345
Q

M2 receptor affects the ___

A

Heart—higher doses of anticholinergic required to see these effects

346
Q

M1 receptors affects the ___

A

CNS—higher doses required to see these effects

347
Q

Can give anticholinergics pre- or post-op—given with ACHase inhibitors to block some of the ___ effects

A

Muscarinic (PNS) effects

348
Q

You would give what type of anticholinergic pre-op for the sedative effects?

A

A tertiary amine because these drugs can cross the CNS (i.e.: atropine, scopolamine)

349
Q

For sedative effects— ___ is 100x more potent than ___; has ___ effects too

A

Scopolamine is 100x more potent than atropine; has amnesic effects too

350
Q

You would not give a ___ pre-op. Why?

A

Quaternary ammonium (i.e.: glycopyrrolate) because it has NO CNS effects (cannot cross the BBB, won’t cause sedation)

351
Q

Neo with atropine or glycopyrrolate has become a favorable post-op cocktail d/t lack of CNS effects

A

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
Q

Atropine is really used for ___ effects

A

CV

353
Q

What can occur from anticholinergics in children/elderly? Why?

A

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
Q

What are (4) examples of anticholinergic medications that can cause restlessness/somnolence in children/elderly?

A
  • Bladder control medications
  • Benadryl
  • Atropine
  • Scopolamine
355
Q

Use anticholinergics with caution in patients with ___

A

Glaucoma—can increase intraocular pressure (IOP)

356
Q

Antisalivation effects— ___ 3x potent; ___ 2x potent (longer DOA); ___ 1x

A

Scopolamine 3x potent; glycopyrrolate 2x potent with longer DOA; atropine 1x

357
Q

Scopolamine patch targets CN ___ to reduce motion sickness

A

CN VIII (Trigeminal)

358
Q

Scopolamine patch—may see ___ on the side where the patch is placed

A

Pupil dilation

359
Q

When should you put on scopolamine patch?—takes at least ___ hours to see benefits, leave on for ___ hours

A

Pre-op—takes at least 4 hours to see benefits, leave on for 24 hours

360
Q

Treatment for OD on anticholinergic (i.e.: scopolamine and atropine—tertiary amines that enter the CNS)

A

Physostigmine—repeat doses as needed because it is metabolized quickly

361
Q

Physostigmine is a ___

A

Tertiary amine ACHase inhibitor

362
Q

Effects from OD on anticholinergic—CNS effects

A

Restlessness > hallucinations > somnolence > unconsciousness

363
Q

Other effects from OD on anticholinergic— ___ mouth, ___ vision; photo___; ___cardia; ___ body temperature; skeletal muscle ___; ___stasis; GI effects

A
  • 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
Q

OD on anticholinergic medication can be ___

A

Fatal

365
Q

Biggest issue with ACHase inhibitor (reversal agent) + anticholinergic (used to prevent muscarinic effects) = ___

A

Incomplete reversal when patient arrives to PACU

366
Q

Sugammadex is approved for ___ and ___ reversal only in the US

A

Roc and vec reversal

367
Q

Sugammadex is ___ shape— ___ center

A

Donut shape—lipophilic/hydrophobic center

368
Q

Sugammadex takes the lipophilic/steroidal NMB and sucks it up to be eliminated through ___

A

Kidney

369
Q

Sugammadex can reverse ___

A

Deeper blockades with higher doses

370
Q

Adverse effects of sugammadex— ___ aPTT

A

Increased aPTT—for an hour, no actual increased bleeding seen

371
Q

Adverse effects of sugammadex—HR

A

Brady up to arrest—rare; happens in minutes after sugammadex administration; give atropine to treat

372
Q

Adverse effects of sugammadex—N/V

A

1/2 as bad as neostigmine

373
Q

Sugammadex is not recommended for use in ___

A

Severe renal impairment—CrCl < 30 ml/min

374
Q

1/2 life of sugammadex is ___ hours

A

2 hours

375
Q

More than ___% of sugammadex is eliminated in the first 24 hours

A

90%

376
Q

1/2 life of sugammadex increases with ___

A

Renal impairment

377
Q

Reduced efficacy of ___ after sugammadex administration because…

A

Birth control because sugammadex binds up the birth control

378
Q

Patients on birth control given sugammadex should use secondary contraception for ~___ after sugammadex administration

A

1 week

379
Q

Sugammadex has greater ___ and ___ than neostigmine

A

Safety and efficacy

380
Q

Goal with PONV is ___

A

Prevention! If we can prevent PONV, decreased discharge time, more satisfied patients

381
Q

In the general population—___% experience vomiting, ___% experience nausea

A

30% experience vomiting, 50% experience nausea

382
Q

High risk patients for PONV = ___ or more risk factors; have a ___% chance of occurrence

A

3 or more risk factors; have a 70-80% chance of occurrence

383
Q

Nausea/vomiting is a ___ mechanism

A

Protective

384
Q

If one nausea/vomiting med isn’t working, try one that works on a ___

A

Different pathway

385
Q

Histamine antagonists, muscarinic antagonists, dopamine antagonists, and cannabinoids all work by intercepting the ___ and ___ in the medulla

A

Intercepting the CTZ and vomiting center in the medulla

386
Q

Main target to prevent nausea/vomiting is the ___; stops the ___, not necessarily the ___

A

Chemoreceptor trigger zone (CTZ); stops the vomiting, not necessarily the nausea

387
Q

PONV classified by time—early = ___ hours post-op

A

2-6 hours post-op

388
Q

PONV classified by time—late = ___ hours post-op

A

6-24 hours post-op

389
Q

PONV classified by time—delayed = ___ hours post-op

A

> 24 hours post-op

390
Q

PONV classified by time—post discharge = ___ hours post-op

A

> 24 hours post d/c

391
Q

If you have a patient with 3 or more risk factors for N/V, you should ___

A

Pre-treat

392
Q

Top 3 risk factors for PONV:

A
  • Female
  • History of PONV (pre-op or chemo-induced)
  • Non smoker
393
Q

Risk for PONV— < ___ y/o

A

< 50 yo

394
Q

Risk for PONV—general ___ (greater than or less than) regional; ___ anesthetics/N2O

A

General > regional; volatile anesthetics/N2O

395
Q

Risk for PONV—opioids, use ___ instead

A

Tylenol

396
Q

Risk for PONV—duration of procedure—every 30 minutes, increase risk for PONV by ___%

A

60%

397
Q

What (3) types of procedures increase the risk of PONV?

A
  • Cholecystectomy
  • Gynecological
  • Laparoscopic
398
Q

Motion sickness ___ risk of PONV

A

Increases

399
Q

One risk factor for PONV = ___% risk

A

20%

400
Q

Two risk factors for PONV = ___% risk

A

40%

401
Q

Three risk factors for PONV = ___% risk

A

60%

402
Q

Four risk factors for PONV = ___% risk

A

80%

403
Q

Even if you have ZERO risk factors, still have ___% risk

A

10% risk

404
Q

Risk factors for children—age > ___ years; history of PONV or PONV in ___; procedure > ___ mins; ___ surgery

A

Age > 3 years
History of PONV or PONV in relatives
Procedure > 30 mins
Strabismus surgery

405
Q

What induction drug is beneficial in reducing PONV? By what %?

A

Propofol; can reduce PONV by 20%

406
Q

TIVA reduces PONV risk by ___%

A

25%

407
Q

Regional anesthesia is ___x lower incidence of PONV

A

9x

408
Q

Should use ___ instead of opioids to reduce risk of PONV

A

NSAIDs i.e.: Tylenol—good pain control, less PONV

409
Q

(6) pretreatment options for PONV:

A
  • Dexamethasone
  • Serotonin antagonists
  • H1 blockers
  • Scopolamine patch
  • NK1 antagonists
  • Droperidol
410
Q

Does hydration help reduce PONV?

A

Not so much

411
Q

There is not much data to support the use of reglan, oxygen, ginger root, and cannabinoids to reduce PONV—T/F

A

True

412
Q

Serotonin antagonists (5HT3), D2 blockers, reglan, and H1 blockers are all ___ medications

A

Rescue medications

413
Q

Post-discharge nausea vomiting occurs in ___ of patients

A

1/3 of patients

414
Q

Patients at high risk for post-discharge nausea vomiting should be given ___, ___ patch, ___, and ___ meds (i.e.: zofran, phenergan, scopolamine patch)

A

Dexamethasone, scopolamine patch, education, and rescue meds

415
Q

Med that lasts long ___

A

Dexamethasone

416
Q

Shorter acting medication ___

A

Zofran

417
Q

Most nausea/vomiting meds are given at the ___ of the procedure, except for ___, ___, and ___

A

END of the procedure, except for scop patch, arepitant, Dexamethasone

418
Q

Which med is most effective—zofran, droperidol, or Dexamethasone?

A

All are equally effective in reducing PONV by 25%

Ask patient if they’ve had any before

419
Q

5HT3 antagonists are aka as ___

A

Serotonin antagonists

420
Q

5HT3 antagonists end in ___

A

Setron (i.e.: ondansetron, dolasetron, granisetron, palonosetron)

421
Q

5HT3 antagonists work at ___

A

Vagal afferents

422
Q

Which two 5HT3 antagonists are used in chemo patients and why?

A

-Dolasetron
-Palonosetron
Both are longer acting

423
Q

Zofran half-life is ___ hours; palonsetron half-life is ___ hours

A

4 hours; 40 hours

424
Q

Dolasetron is a ___; requires CYP2D6 to metabolize active metabolite ___

A

Pro-drug; hydrodolasetron

425
Q

Side effects of 5HT3 antagonists are generally ___; low risk of ___ (especially if patient is taking ___)

A

Mild; low risk of serotonin syndrome (especially if patient is taking SSRIs)

426
Q

Risk of QT prolongation/torsades from 5HT3 antagonists

A

Study showed that the dose given was 32 mg IV—we use nowhere near this dose

427
Q

Dexamethasone is a ___

A

Corticosteroid

428
Q

Dexamethasone should be given ___ (before/after) induction

A

BEFORE

429
Q

Dexamethasone does not have ___ effects

A

Mineralocorticoid effects

430
Q

Side effects of dexamethasone—most side effects seen are associated with ___ use

A

Long-term use—i.e.: impaired wound healing, infection

431
Q

Single use of dexamethasone for post-op nausea/vomiting usually has a ___ risk of side effects

A

Low

432
Q

Droperidol is an ___ (D2) drug; very similar to ___

A

Anti-dopaminergic drug; very similar to haloperidol

433
Q

Droperidol is used for ___, ___, and ___

A

Sedation, agitation, and nausea/vomiting

434
Q

Droperidol targets the ___

A

CTZ

435
Q

Older, first generation antipsychotics were used for nausea/vomiting because of their ___

A

D2 effects

436
Q

Side effects of droperidol—___ symptoms or ___

A

Extrapyramidal symptoms (EPS) or tardive dyskinesias (TD)

437
Q

Examples of EPS:

A
  • Shuffling
  • Lip smacking
  • Neck turning
  • Whole body twists
438
Q

If extrapyramidal symptoms are not identified early, they can become ___

A

Permanent

439
Q

Do not give droperidol to patients who have ___ disease or ___ disorders

A

Parkinson’s disease or movement disorders

440
Q

Black box warning for QT prolongation/sudden cardiac death with droperidol—risk is ___

A

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
Q

Two examples of phenothiazines:

A
  • Promethazine (phenergan)

- Prochlorperzine (compazine)

442
Q

Phenothiazines are ___ receptor antagonists

A

D2

443
Q

Phenothiazines are highly anti___

A

Antihistaminergic

444
Q

(2) side effects of phenothiazines:

A
  • Sedation

- EPS

445
Q

Phenothiazines have a very ___ (high or low) risk of QT prolongation

A

LOW

446
Q

Amisulpride (Barhemsys) is a ___ antagonist

A

D2 antagonist—newer medication on the market

447
Q

Only indication for amisulpride (barhemsys) is for ___

A

Post-op nausea/vomiting

448
Q

Administer amisulpride (barhemsys) ___ (before or after) induction

A

Before

449
Q

Side effects of amisulpride (barhemsys)—elevated ___; ___ prolongation; postural ___; ___kalemia; abdominal ___

A

Elevated prolactin (gynecomastia); QT prolongation; postural hypotension; hypokalemia; abdominal distention

450
Q

Metoclopramide (Reglan) is a ___ antagonist

A

Dopamine antagonists—antagonizes dopamine’s effect on the CTZ

451
Q

Reglan accelerates the rate of gastric ___

A

Gastric emptying

452
Q

Reglan does NOT alter ___ ion concentration

A

Hydrogen ion concentration

453
Q

Reglan ___ (increases/decreases lower esophageal tone), which can prevent the kickback of GI contents that make people feel nauseous

A

Increases

454
Q

Reglan can reduce ___ risk because it increases gastric emptying

A

Aspiration

455
Q

Renal impairment requires a ___ in reglan dose

A

Decrease because its eliminated through the kidneys

456
Q

Reglan readily crosses the ___ and ___; is excreted in ___

A

BBB and placenta; is excreted in breast milk

457
Q

Reglan side effects—can see lots of abdominal ___; feeling of ___ or ___ with one time dose; ___ symptoms

A

Abdominal cramping; feeling of unease or restlessness with one time dose (AKA akathisia); extrapyramidal symptoms (with chronic use)

458
Q

Reglan has an inhibitory effect on ___; may increase sedative actions of CNS depressants, EPS

A

Plasma cholinesterase

459
Q

Avoid giving reglan with ___ or ___

A

Phenothiazines or butyrophenones

460
Q

Avoid administering reglan to patients who have a history of ___ or preexisting ___ symptoms

A

History of seizures or preexisting extrapyramidal symptoms

461
Q

Avoid reglan with ___ obstruction

A

Mechanical gastric outlet obstruction

462
Q

Reglan is great to give ___ minutes pre-op if you want to reduce ___ risk

A

30 minutes pre-op if you want to reduce aspiration risk

463
Q

Reglan ___ (increases/decreases) gastric fluid volume; ___ (does or does not) alter gastric pH; faster administration can cause ___

A

Decreases gastric fluid volume; does not alter gastric pH; faster administration can cause cramping

464
Q

If reglan doesn’t help, ___ (do or do not) use another dopamine antagonist drug

A

Do NOT use another dopamine antagonist drug—it won’t work

465
Q

Two H1 antagonists:

A
  • Dimenhydrinate (Dramamine)

- Diphenhydramine (Benadryl)

466
Q

H1 antagonists release ___, are highly ___, and have ___ side effects

A

Release histamine, are highly sedating, and have anticholinergic side effects

467
Q

If you give H1 antagonists with phenergan (promethazine) you will ___

A

Knock your patient out

468
Q

Scopolamine patch is a ___ medication; place at least ___ hours prior to surgery

A

Anticholinergic medication; place at least 4 hours prior to surgery

469
Q

Arepitant (Emend) is a ___ receptor antagonist

A

Neurokinin 1 receptor antagonist

470
Q

How does arepitant (emend) work?—substance ___ is being blocked from NK1 receptor to send feelings of ___

A

Substance P is being blocked; send feelings of nausea

471
Q

Arepitant (emend) is only approved for treatment of ___

A

Post-op nausea/vomiting

472
Q

You should administer arepitant (emend) ___ hours prior to induction

A

3 hours

473
Q

Arepitant (emend) may reduce effectiveness of birth control pills for up to ___ weeks

A

4 weeks

474
Q

Arepitant may increase INR for ___ days when given in conjunction with warfarin

A

7-10 days

475
Q

Arepitant (emend) is highly ___ bound

A

Protein

476
Q

Dronabinol (marinol) is a ___, effective for ___

A

Cannabinoid, effective for chemo-induced nausea/vomiting

Not much data on this one

477
Q

H2 receptor antagonists = ___ reducers

A

Acid reducers

478
Q

(3) H2 receptor antagonists:

A
  • Famotidine (Pepcid)
  • Ranitidine (Zantac—taken off market 04/2020)
  • Cimetidine (Tagamet)
479
Q

Why was ranitidine (Zantac) taken off the market in 04/2020?

A

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
Q

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

A

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
Q

Which H2 receptor antagonist is most potent? Least potent?

A

Most potent = famotidine

Least potent = cimetidine

482
Q

H2 receptor antagonists and PPIs ___ (increase/decrease) ventilator associated pneumonias—because they ___ pH

A

INCREASE—because they change the pH, increasing the pH so bacteria can actually grow

483
Q

H2 receptor antagonists change the ___

A

pH

484
Q

H2 receptor antagonists have NO influence on the pH of the gastric fluid that is ___

A

Already in the stomach!

485
Q

H2 receptor antagonists are great pre-op prophylaxis for patients with ___ history or patients undergoing procedures with ___

A

Allergic history; patients undergoing procedures with IV contrast

486
Q

Drug-induced histamine release ___ (is/is not) prevented by H1 and H2 receptor antagonist pre-treatment; ___ response is less, but you have to give ___

A

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
Q

What is a rare but serious complication of H2 receptor antagonist therapy?

A

Thrombocytopenia—only seen with megadose or long-term use

488
Q

Cimetidine (Tagamet) can cause ___ in elderly

A

Confusion

489
Q

H2 antagonists decrease ___; ___cardia and ___tension are generally associated with rapid IV push

A

CAMP; bradycardia and hypotension are generally associated with rapid IV push

490
Q

Cimetidine (and ranitidine) inhibit CYP450, slowing metabolism/increasing risk of toxicity from what (4) drugs?

A
  • Diazepam
  • Propanolol
  • Meperidine
  • Lidocaine
491
Q

H2 receptor antagonists can ___ absorption of some drugs by ___ gastric pH

A

Alter absorption; increasing gastric pH

492
Q

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

A

Decrease absorption because they need a more acidic environment to be properly absorbed

493
Q

Proton pump inhibitors end in “-___”

A

-prazole

I.e.: omeprazole, pantoprazole, lansoprazole

494
Q

Proton pump inhibitors are used to treat moderate to severe ___; ___ disease; ___ disorders

A

Moderate to severe GERD; peptic ulcer disease; hypersecretory disorders

495
Q

Using PPIs PRN ___ (is/is not) very effective; ___ (longer/shorter) duration of action

A

Is not; longer duration of action

496
Q

Should administer proton pump inhibitors ___ hours prior to surgery (ideally, administer ___)

A

3 hours before; ideally administer the night before

497
Q

Pantoprazole with ranitidine 1 hour prior to surgery decreases gastric ___ and ___

A

Fluid and pH

498
Q

Main adverse reaction with PPIs = ___

A

C. Dif because you’re changing the pH

499
Q

What is much more effective than PPIs to control GERD?

A

Dietary changes

KLowe Pharmacology 1 (2 decks)

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