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ANES 516B > Histamine and PONV > Flashcards

Histamine and PONV Flashcards

Exam 1

1
Q

What is an autocoid?

A

Biological factors that act like local hormones, have a brief duration, and act near the site of synthesis

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2
Q

Three defining characteristics of autocoid:

A

1) Act like local hormones
2) Brief duration
3) Act near site of synthesis

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3
Q

T/F: Autocoids act distal to the site of synthesis.

A

F: they act close to the site of synthesis.

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4
Q

T/F: Autocoids behave similarly to local hormones.

A

True.

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5
Q

T/F: Autocoids are characterized by a brief duration.

A

True.

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6
Q

What type of autocoid are we focusing on in this lecture specifically?

A

Histamines

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7
Q

What is the major difference between autocoids and hormones?

A

Autocoids can be synthesized by almost every cell, while hormones are only synthesized by specific tissues.

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8
Q

Is histamine a hormone?

A

No, it is an autocoid, though it behaves similarly to a hormone.

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9
Q

What type of autocoid is histamine?

A

Endogenous amine

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10
Q

T/F: Histamine is an endogenous amine.

A

True.

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11
Q

Histamine is a chemical mediator in what immune response?

A

Inflammatory response

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12
Q

What type of role does histamine play in the inflammatory response?

A

It is a chemical mediator in the inflammatory response.

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13
Q

What type of cells releases histamine?

A

Mast cells

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14
Q

Where can mast cells be found?

A

Skin, lungs, GI tract, basophils

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15
Q

What types of tissues are involved in histamine release? By what means?

A

Skin, lungs, GI tract, basophils via mast cell secretion

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16
Q

T/F: GI tract tissue releases histamine as part of inflammatory immunoresponse.

A

True.

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17
Q

Skin, lungs, GI tract, and basophils all secrete:

A

histamine.

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18
Q

Can histamine cross the blood-brain barrier? What about histamine blockers?

A

Histamine cannot cross the blood brain barrier, but histamine blockers can.

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19
Q

Histamine causes allergic reaction by what mechanism?

A

Antigen-antibody response

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20
Q

The antigen-antibody response of histamine causes what?

A

Allergic reaction

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21
Q

Allergic reactions are mediated by what autocoid?

A

Histamine (causes inflammation)

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22
Q

How many types of histamine receptors are there?

A

Three.

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23
Q

Which histamine receptor is involved in respiratory + GI smooth muscle contraction?

A

H1

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24
Q

Which histamine receptor is involved in increased GI secretion of H+?

A

H2

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25
Q

Which histamine receptor is involved in pruritis/sneezing?

A

H1

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26
Q

Which histamine receptor is involved in decreased histamine synthesis and release?

A

H3

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27
Q

Which histamine receptor is involved with increased HR/ contractility?

A

H2

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28
Q

Which histamine receptor is involved with nitric oxide release by vascular smooth muscle?

A

H1

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29
Q

Which muscles contract upon activation of H1 receptors?

A

GI and respiratory smooth muscle

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30
Q

H1 receptors are responsible for what three actions?

A

GI and respiratory smooth muscle contraction
Pruritis/ sneezing
Nitric oxide release by vascular smooth muscle

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31
Q

When H1 receptors are stimulated, what is released from vascular smooth muscle?

A

Nitric oxide

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32
Q

Nitric oxide is released from what when H1 receptors are stimulated?

A

Vascular smooth muscle

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33
Q

Which types of muscles are directly affected by stimulation of H1 receptors?

A

GI + respiratory smooth muscle (contracts)

Vascular smooth muscle (release nitric oxide)

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34
Q

Itchy, watery eyes are mediated by which histamine receptor?

A

H1 receptor

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35
Q

Bronchoconstriction during an asthma attack is caused by activation of which histamine receptor?

A

H1 receptor

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36
Q

Result of activation of H3 receptor?

A

Decreased histamine synthesis and release

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37
Q

T/F: activation of H1 receptors causes releases of nitrous oxide from vascular smooth muscle.

A

False: causes release of nitric oxide from vascular smooth muscle

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38
Q

Activation of H2 receptors cause:

A

Increased GI secretion of H+

Increased HR and contractility

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39
Q

T/F: activation of H3 receptor is a positive feedback loop that causes increased synthesis and release of histamine.

A

False; negative feedback loop that causes decreased release and synthesis of histamine

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40
Q

Activation of which receptor is responsible for increased HR during allergic reaction?

A

H2

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41
Q

Activation of which receptor is responsible for increased H+ secretion in GI tract?

A

H2 receptor

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42
Q

Which histamine receptors have a direct effect on GI tissues? What are those effects?

A

H1: increased smooth muscle constriction in GI tract
H2: increased H+ secretion in GI tract

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43
Q

If your patient has watery, itchy eyes and is coughing and sneezing, which histamine receptor is activated?

A

H1

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44
Q

What is the effect of NO release by vascular smooth muscle w/ activation of H1 receptors?

A

Vasodilation –> hypotension

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45
Q

Hypotension may occur with an allergic reaction because of:

A

NO release by vascular smooth muscle, caused by activation of H1 receptors

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46
Q

Of all three histamine receptors, we are mainly concerned with the effects of:

A

H1 + H2

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47
Q

What are the general cardiovascular effects of histamine release?

A 
Decreased BP (d/t NO release, H1) 
Increased HR (H2)
Increased capillary permeability (H1)
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48
Q

T/F: histamine release may result in increased HR and decreased BP.

A

True

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49
Q

T/F: histamine release decreases capillary permeability.

A

False; increases capillary permeability.

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50
Q

How does histamine release affect thee respiratory system? Via which histamine receptor?

A

It constricts respiratory smooth muscle to cause bronchoconstriction via the H1 receptor.

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51
Q

Which receptor is responsible for labored breathing during an allergic reaction?

A

H1

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52
Q

What is the dermal reaction to histamine release?

A

Classic flare and wheal response

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53
Q

The flare and wheal response is what system’s reaction to histamine release?

A

Derma

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54
Q

How does NO production (H1) affect the vasculature?

A

It causes local vasodilation and increased permeability.

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55
Q

Which action of histamine release causes local vasodilation?

A

NO production by vascular smooth muscle

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56
Q

What is the immunological affect of histamine release?

A

Histamine is a mediator of Type I hypersensitive reaction.

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57
Q

Histamine is a mediator of what reaction?

A

Type I hypersensitive

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58
Q

Which hypersensitive reaction does histamine mediate?

A

Type I hypersensitive reaction

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59
Q

How does histamine release affect peak airway pressure?

A

It increases peak airway pressure.

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60
Q

If your patient displayed a decreased blood pressure, an increased HR, and high peak pressures, what might you expect?

A

An allergic reaction–symptoms are caused by histamine release.

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61
Q

What four facts must you know about H1 activation?

A

Occurs at lower concentrations of histamine
Decreased AV node conduction
Coronary artery vasoconstriction
Bronchial smooth muscle constriction

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62
Q

What is the effect of H1 activation on bronchial smooth muscle?

A

Bronchial smooth muscle constriction

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63
Q

What is the effect of H1 activation on AV node conduction?

A

Causes decreased AV node conduction.

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64
Q

T/F: Activation of H1 receptors increased conduction at the AV node.

A

False; it decreases conduction at the AV node.

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65
Q

Activation of H1 receptors decreases conduction at what node?

A

AV node

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66
Q

Conduction of AV node is reduced when which histamine receptors are activated?

A

H1 receptors

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67
Q

How does activation of H1 receptors affect the coronary artery?

A

It causes coronary artery vasoconstriction.

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68
Q

Activation of H1 receptors causes constriction of what major blood vessel group?

A

Coronary arteries

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69
Q

Coronary arteries vasoconstrict upon the activation of what histamine receptor?

A

H1

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70
Q

T/F: Activation of H1 receptors occurs at lower concentrations of histamine.

A

True.

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71
Q

How does concentration level of histamine affect H1 receptors?

A

H1 receptors are activated at lower concentrations of histamine.

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72
Q

Which histamine receptor causes CV effects?

A

H2 receptor

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73
Q

Main effects of H2 activation:

A

CV effects
Catecholamine release
Coronary artery vasodilation
Increased gastric H+ secretion by parietal cells in the stomach

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74
Q

What CV effects does activation of H2 receptors have?

A

Increased HR/ contractility

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75
Q

Effect of activation of H2 receptors on coronary artery?

A

Coronary artery vasodilation

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76
Q

Activation of which receptor causes coronary artery vasoconstriction?
Activation of which receptor causes coronary artery vasodilation?

A

H1

H2

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77
Q

Activation of which histamine receptors results in catecholamine release?

A

H2

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78
Q

What is the main effect of activation of H2 receptors?

A

Increased gastric H+ secretion by parietal cells in the stomach

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79
Q

By what mechanism does activation of H2 receptors cause catecholamine release?

A

Adrenal gland stimulation

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80
Q

H2 activation increases secretion of what by the stomach?

A

Increases secretion of H+ by parietal cells in stomach.

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81
Q

T/F: H2 receptors increase secretion of H+ by parietal cells in the stomach.

A

True.

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82
Q

What is the mechanism behind the skin response to histamine release?

A

Dilated capillaries in affected area
Edema d/t increased capillary permeability
“Wheal” d/t dilated arterioles around edema

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83
Q

Classic mosquito bite/ hives reaction seen in histamine release is d/t what?

A

Dilated arterioles around edema

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84
Q

What causes edema in histamine release?

A

Increased capillary permeability

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85
Q

Effect of histamine release on capillaries?

A

Causes dilated capillaries w/ increased capillary permeability

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86
Q

Dilated arterioles around edema cause what?

A

Wheals

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87
Q

Increased capillary permeability and dilated capillaries cause what?

A

Edema

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88
Q

What two things cause edema in a histamine release reaction?

A

Dilated capillaries

Increased capillary permeability

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89
Q

Histamine antagonists: what will they block?

A

Edema + pruitis

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90
Q

T/F: histamine antagonists block edema + pruitis.

A

True.

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91
Q

Histamine antagonists: what won’t they block? How should you treat instead?

A

Hypotension d/t NO release in vascular smooth muscle; treat via vasoconstriction

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92
Q

T/F: histamine agonists will block edema and pruitis.

A

False; histamine antagonists block edema + pruitis.

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93
Q

T/F: histamine antagonists will not block hypotension d/t release of NO by vascular smooth muscle cells

A

True.

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94
Q

Principle effects of H2 receptor activation?

A

Increased H+ secretion in stomach

Increased HR/contractility

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95
Q

Summarize the actions of histamine antagonists:

A

They will block pruitis and edema caused by histamine release, but they will not treat the hypotension caused by NO release.

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96
Q

T/F: to stop a histamine reaction, you must block histamine receptors.

A

False; it will help the reaction, but it will not stop it.

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97
Q

At what receptors do histamine antagonists act?

A

H1 + H2

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98
Q

At what receptors do histamine antagonists not act?

A

H3

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99
Q

What type of antagonists are histamine antagonists?

A

Competitive inhibitors

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100
Q

T/F: histamine antagonists primarily work at H1 + H2 receptors.

A

True.

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101
Q

How do histamine antagonists work?

A

They do not block the release of histamine. Instead, histamine is still present and an allergic reaction still occurs, but the histamine antagonists block the bad side effects.

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102
Q

T/F: histamine antagonists prevent the secretion of histamine.

A

False.

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103
Q

T/F: histamine antagonists aid in diminishing an allergic reaction by blunting the bad side effects of histamine release.

A

True

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104
Q

Do histamine antagonists inhibit the release of histamine?

A

No.

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105
Q

What do histamine antagonists block?

A

Bad side effects caused by histamine release and activation.

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106
Q

By what means do histamine antagonists prevent the bad side effects of histamine release?

A

Competitive inhibition

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107
Q

T/F: histamine antagonists are well absorbed orally.

A

True

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108
Q

Histamine antagonists are especially absorbed when adminisitered in what form?

A

Oral

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109
Q

T/F: histamine receptors work primarily on H1 + H3 receptors.

A

False: work primarily in H1 and H2 receptors

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110
Q

What are the two types of H1 blockers?

A

First generation + second generation

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111
Q

What is the primary difference between first generation and second generation H1 blockers?

A

H1 receptors blocker tend to cross the BBB more easily.

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112
Q

Which type of H1 blocker tends to cross the BBB more readily?

A

First gen H1

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113
Q

T/F: Second generation H1 receptor blockers are falling out of favor because they tend to cross the BBB.

A

False: first generation

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114
Q

Besides H1 receptors, what other receptors do H1 receptor blockers activate?

A

Muscarinic cholinergic
Serotonin
Alpha

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115
Q

Muscarinic cholinergic
Serotonin
Alpha
H1 receptor blockers

What do they have in common?

A

All blocked by first generation H1 blockers

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116
Q

Which type of blocker causes significant sedation?

A

First generation H1 receptor blocker

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117
Q

T/F: First generation H1 receptor blockers cause signficant sedation.

A

True

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118
Q

What receptors do second generation H1 receptor blocker bind w/?

A

H1 only; no muscarinic cholinergic, alpha, or serotonin

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119
Q

At higher doses, second generation H1 receptor blockers are:

A

non-competitive

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120
Q

What is the primary benefit to using second generation H1 receptor blockers instead of first generation?

A

Much less sedative effect

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121
Q

Which type of H1 receptor blockers is non-competitive at higher doses?

A

Second generation

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122
Q

Which type of histamine receptor blocker only affects H1 receptors?

A

Second generation

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123
Q

What are the three first generation H1 receptor blockers you are expected to know?

A

Diphenhydramine
Dramamine
Promethazine

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124
Q

Diphenhydramine is a:

A

First generation H1 receptor blocker

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125
Q

Dramamine is a:

A

First generation H1 receptor blocker

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126
Q

Promethazine is a:

A

First generation H1 receptor blocker

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127
Q

T/F: Diphenhydramine is a second generation H1 receptor blocker.

A

False: first generation

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128
Q

T/F: Dramamine is a first generation H1 receptor blocker.

A

True.

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129
Q

T/F: Promethazine is the same type of H1 receptor blocker as diphenhydramine.

A

True.

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130
Q

Name the second generation H1 receptor blockers that you should know.

A

Loratadine (Claritin)

Fexofenadine (Allegra)

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131
Q

Another name for Claritin?

A

Loratadine

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132
Q

Another name for Fexofenadine?

A

Allegra

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133
Q

Another name for Loratadine?

A

Claritin

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134
Q

Another name for Allegra?

A

Fexofenadine

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135
Q

Fexofenadine is what type of H1 receptor blocker?

A

Second generation

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136
Q

Loratadine is what type of H1 receptor blocker?

A

Second generation

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137
Q

Which medication tends to cause drowsiness, promethazine or loratadine?

A

Promethazine

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138
Q

Which medication acts on nothing but H1 receptors, Dramamine or Fexofenadine?

A

Fexofenadine

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139
Q

Which medication acts on seratonin receptors, Dramamine or Loratadine?

A

Dramamine

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140
Q

Which antihistamine medications are non-competitive at higher doses?

A

Loratadine

Fexofenadine

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141
Q

Which antihistamines cause sedation?

A

Diphenhydramine
Dramamine
Promethazine

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142
Q

Promethazine is used to treat what symptoms?

A

Nausea/ vomiting

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143
Q

Which drug is primarily used to treat motion sickness or motion-induced nausea?

A

Dramamine

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144
Q

What is the primary concern w/ second generation antihistamines?

A

They can prolong QT intervals at high doses.

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145
Q

Which has more side effects, first generation or second generation antihistamines? Why?

A

First generation because they act on muscarinic receptors

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146
Q

Common side effects of first generation antihistamines?

A 
Somnolence 
Decreased alertness
Slowed reaction time
Dry mouth 
Blurred vision 
Urinary retention 
Impotence 
Tachycardia 
Dysrhythmias
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147
Q

Which symptoms of fist generation antihistamines are primarily d/t their actions on muscarinic receptors?

A 
Impotence
Tachycardia
Urinary retention
Dysrhythmias
Dry mouth 
Blurred vision
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148
Q

What are four uses of H1 blockers?

A

They are primarily used to treat anaphylaxis and anaphylactoid reactions, but they also treat rhinoconjunctivitis, bronchospasm,
and motion sickness.

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149
Q

Motion Sickness is treated by what type of histamine receptor blocker?

A

H1 receptor blocker

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150
Q

What should you give a patient to treat rhinoconjunctivitis?

A

H1 receptor blocker

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151
Q

By what means do H1 receptor blockers treat motion sickness?

A

They decrease vestibular and visual input from the brain.

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152
Q

Decreasing vestibular and visual input from the brain assists in treating what issue?

A

Motion sickness

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153
Q

Which histamine receptor blocker treats motion sickness by decreasing vestibular and visual input from the brain?

A

H1 receptor blocker

154
Q

Any drug that ends in -tidine is what type of histamine receptor blocker?

A

H2 receptor blocker

155
Q

How can you identify an H2 receptor blocker?

A

Look for the ending “tidine”

156
Q

What is the main effect of H2 receptor blockers?

A

They decrease gastric acid secretion.

157
Q

What is the most widely used H2 receptor blocker?

A

Famotidine (Pepcid)

158
Q

T/F: H2 receptor blockers aid in emptying the gut of gastric acid.

A

False; they only prevent production of new gastric acid. They do nothing to clear any acid that is already present in the gut.

159
Q

Rank H2 receptor blockers in terms of potency.

A

C < R = N < F

160
Q

What is the relative potency of cimetidine?

A

Potency = 1

161
Q

What is the relative potency of famotidine?

A

Potency = 50

162
Q

What is the relative potency of nizatidine?

A

Potency = 10

163
Q

What is the relative potency of ranitidine?

A

Potency = 10

164
Q

T/F: Nizatidine is more potent than ranitidine.

A

False; they are equally potent.

165
Q

T/F: Cimetidine is less potent than Nizatidine.

A

True

166
Q

T/F: Ranitidine is more potent than Famotidine.

A

False; famotidine is the most potent H2 receptor blocker.

167
Q

What is the least potent H2 receptor blocker?

A

Cimetidine

168
Q

Which type of antihistamine is characterized by extensive first pass metabolism in the liver?

A

H2 receptor blockers

169
Q

Do H2 antihistamine drugs cross the BBB? What about the placenta?

A

They cross both; they are not teratogenic, though.

170
Q

T/F: H2 antihistamines are teratogenic.

A

False.

171
Q

What is the consensus on giving renal failure patients H2 antihistamines?

A

They are not contraindicated because there are no truly bad side effects, but renal failure will increased the elimination time of these drugs.

172
Q

How does an increase in age affect H2 antihistamine metabolism?

A

Increasing age doubles half-life.

173
Q

T/F: antihistamines last longer in an elderly patient than a young patient.

A

True.

174
Q

How are H2 antihistamines best absorbed?

A

Rapid oral absorption

175
Q

T/F: H2 antihistamines boast rapid oral absorption.

A

True.

176
Q

What are some reasons to use H2 antihistamines?

A

Treatment of duodenal ulcers
Allergy prophylaxis
Preop medication (gray area)

177
Q

Which antihistamine is useful for the treatment of duodenal ulcers?

A

H2 receptor blockers

178
Q

Can you use H2 antihistamines as allergy prophylaxis?

A

Yes.

179
Q

Effects of H2 receptor blockers on gastric acid already present in belly?

A

No effect; only prevents new acid secretion

180
Q

Why might you use caution in administering H2 receptor blockers to the elderly?

A

They cross the BBB, so they may cause confusion at times.

181
Q

What is the issue with long term use of H2 receptor blockers?

A

They weaken the gastric barrier to bacteria, causing H. pylori to proliferate and weakening the barrier.

182
Q

They stomach is at risk for proliferation of what bacteria under chronic use of H2 receptor blockers?

A

H. pylori

183
Q

What is a cross reaction that you should keep in mind when administering cimetidine?

A

Cimetidine inhibits cytochrome p450, resulting in a prolonged duration of propanolol, diazepam, and lidocaine.

184
Q

Cimetidine can prolong duration of propanolol, diazepam, and lidocaine via:

A

inhibition of cytochrome P450.

185
Q

What H2 receptor blocker may inhibit cytochrome P450 w/ chronic use?

A

Cimetidine

186
Q

Cimetidine inhibits what w/ chronic use?

A

Cytochrome p450

187
Q

T/F: Inhibition of cytochrome p450 is a possibility w/ all H2 receptor blockers.

A

False, only cimetidine

188
Q

H2 antihistamines may interact w/ cerebral H2 receptors, causing what side effects?

A

Headache
Somnolence
Confusion

189
Q

H2 antihistamines may interact w/ cardiac H2 receptors, causing what side effects?

A

Bradycardia
Hypotension
Heart block

190
Q

T/F: H2 antihistamines can potentiate throbocytopenia.

A

True.

191
Q

What type of drug is cromolyn?

A

Mast cell stablizer

192
Q

Name an example of a mast cell stabilizer.

A

Cromolyn

193
Q

Action of cromolyn?

A

inhibits antigen-induced release of histamine from mast cells

194
Q

What drug inhibits antigen-induced release of histamine from mast cells?

A

Cromolyn, a mast cell stabilizer

195
Q

How is cromolyn administered?

A

Via inhalation

196
Q

What drug is used as prophylaxis for bronchial asthma?

A

Cromolyn

197
Q

Cromolyn is used as prophylaxis for:

A

bronchial asthma

198
Q

What type of asthma might you use cromolyn for? How does it help?

A

Bronchial asthma: prevents histamine release from mast cells, decrease occurance of bronchial smooth muscle constriction (H1-mediated reaction to histamine release)

199
Q

Name three proton pump inhibitors.

A

Omeprazole
Protonix
Prevacid

200
Q

Omeprazole is what type of drug?

A

Proton pump inhibitor

201
Q

Protonix is what type of drug?

A

Proton pump inhibitor

202
Q

Prevacid is what type of drug?

A

Proton pump inhibitor

203
Q

What do proton pump inhibitors do?

A

They prolong inhibition of gastric acid secretion for up to 24 hours.

204
Q

How long do PPIs prolong inhibition of gastric acid secretion?

A

Up to 24 hours

205
Q

Mechanism of action of Omeprazole?

A

Prolong inhibition of gastric acid secretion for up to 24 hours

206
Q

Which is more effective in preventing further secretion of gastric acid, H2 receptor blockers or PPIs?

A

PPIs

207
Q

Mechanism of action of Protonix?

A

Prolongs inhibition of gastric acid secretion for up to 24 hours

208
Q

Which is more effective in preventing gastric acid secretion, Prevacid or Famotidine?

A

Prevacid

209
Q

What are the benefits to PPIs as a preoperative medicine?

A

They can increase gastric fluid pH.
They can decrease gastric fluid volume.
They must be given > 3 hours prior to surgery.

210
Q

Effect of PPIs on gastric fluid if given preoperatively?

A

They can increase gastric pH and decrease gastric volume.

211
Q

In order to be effective, when must PPIs be administered?

A

> 3 hours prior to surgery

212
Q

What medication class is especially effective at preventing aspiration?

A

PPIs

213
Q

Why are PPIs given in the ICU to intubated patients?

A

Patients are NPO for many hours, if not days, but their stomachs continue to produce acid. Without any food to mitigate the acid, it can cause GI ulcers and bleeding.

214
Q

Is serotonin a hormone?

A

No; like histamine, it is an autocoid, but it has behaviors that are similar to hormones.

215
Q

Serotonin is an:

A

autocoid

216
Q

Serotonin is oxidized by:

A

liver and lungs

217
Q

Role of liver and lungs in serotonin levels?

A

Serotonin is oxidized by the liver and lungs.

218
Q

What part of the body is involved in uptake of serotonin?

A

Platelets

219
Q

Platelets and serotonin:

A

Platelets uptake serotonin

220
Q

In addition to being characterized as an autocoid, serotonin is also:

A

a neurotransmitter in the CNS

221
Q

Where is 90% of serotonin found?

A

In enterochromaffin cells of the GI tract.

222
Q

Where is 10% of serotonin found?

A

In CNS and platelets.

223
Q

The majority of serotonin is found in the:

A

gut.

224
Q

Where are enterochromaffin cells located?

A

In the GI tract

225
Q

What cells in the GI tract contain the majority of the body’s serotonin stores?

A

Enterochromaffin cells

226
Q

What do enterochromaffin cells store in the gut?

A

Serotonin

227
Q

How much of serotonin stores are located in the CNS and platelets?

A

10%

228
Q

What are the sites of action of serotonin?

A

GI tract
Platelets
CV system

229
Q

Where does serotonin work in the GI tract? What are its effects?

A

5-HT4 receptor: gastrokinetic effects

5-HT3 receptor: drug-induced N/V

230
Q

Which neurotransmitter mediates the N/V reaction to drugs?

A

Serotonin

231
Q

Via what receptor does serotonin mediate the N/V reaction to drugs?

A

5-HT3 receptor

232
Q

Via what receptor does serotonin cause gastrokinetic effects?

A

5-HT4 receptor

233
Q

Serotonin activates the 5-HT4 receptor to cause what effects?

A

Gastrokinetic effects

234
Q

Serotonin activates the 5-HT3 receptor to cause what effects?

A

Drug-induced N/V

235
Q

Where are 5-HT3 and 5-HT4 receptors located in the body?

A

GI tract

236
Q

Serotonin has how many sites of action in the CNS?

A

15

237
Q

Serotonin mediates what aspects of the CNS?

A 
Appetite
Sleep
Cognition
Sensory perception
Motor activity 
Temperature regulation
Nociception 
Sexual behavior 
Hormone secretion
238
Q

Appetite, sexual behavior, nociception, temperature regulation, motor activity, hormone secretion, sensory perception, sleep, and cognition are all affected by:

A

CNS action of serotonin

239
Q

Where are 5HT1 receptors located?

A

CNS

240
Q

How many 5HT1 receptor subtypes does serotonin act on?

A

5: 5HT1a-f

241
Q

Serotonin acts on 5HT1 receptors to cause

A

cerebral vasoconstriction

242
Q

By what means does serotonin cause cerebral vasoconstriction?

A

It acts on 5HT1 receptors in the brain.

243
Q

What serotonin agonist reverses middle cerebral artery vasodilation to improve migraine and cluster headaches?

A

Sumatriptan

244
Q

Sumatriptan is what type of drug?

A

Serotonin agonist

245
Q

Action of sumatriptan?

A

Reverses middle cerebral artery vasodilation to improve migraine and cluster headaches.

246
Q

What type of headaches does sumatriptan relieve?

A

Migraines and cluster headaches

247
Q

Why does reversal of vasodilation in the middle cerebral artery improve headaches?

A

A reduction of BF in the head reduces ICP, and that reduces headache incidence.

248
Q

Sumatriptan is related to what receptor in the brain?

A

5HT1

249
Q

Serotonin activates 5HT3 receptors in the gut to cause:

A

N/V, appetite, addiction, pain and anxiety

250
Q

N/V, appetite, addiction, pain and anxiety are all mediated by what receptor in the gut?

A

5HT3 receptors

251
Q

The “setrons” are antagonists to what type of serotonin-mediated receptor?

A

5-HT3 receptors in the gut

252
Q

T/F: Ondansetron is an antagonist to 5-HT3 receptors in the gut.

A

True.

253
Q

5-HT3 receptors mediate what type of symptoms?

A

N/V
Pain and anxiety
Appetite
Addiction

254
Q

First clinical use of Ondansetron?

A

Treatment of chemo-induced nausea

255
Q

T/F: Ondansetron is structurally related to serotonin.

A

True.

256
Q

Major side effects of ondansetron include:

A

Headaches, diarrhea, and increased liver enyzmes

257
Q

Your patient arrives to POHA complaining of nausea. Will ondansetron help you?

A

It is of little assistance in the midst of nausea–more effective as prophylaxis.

258
Q

Options for Ondansetron administration:

A

Sublingual
PO
IV

259
Q

T/F: Zofran is not approved for morning sickness.

A

False; Zofran is effective as a prophylactic measure against morning sickness.

260
Q

Action of antacids?

A

Neutralized or remove acid from gastric contents

261
Q

Which class of medication neutralizes or removes acid from gastric contents?

A

Antacids

262
Q

How do antacids neutralize or remove acid from gastric contents?

A

They increase the pH of the stomach to inactivate pepsin and increase gastric motility

263
Q

At what pH is gastrin inactivated?

A

pH > 5

264
Q

At what pH is gastric motility increased?

A

pH > 5

265
Q

When antacids increase the pH of the stomach to >5, what is the result?

A

Pepsin is inactivated and gastric motility increases.

266
Q

T/F: gastric motility is higher with lower pH.

A

False; gastric motility is higher with higher pH.

267
Q

What are the main benefits to using antacids prophylactically?

A

They are inexpensive, they promote healing, and they are fast-acting.

268
Q

Name some types of antacids.

A

Sodium bicarbonate (Tums)
Magnesium hydroxide
Calcium Carbonate
Aluminum Hydroxide

269
Q

What is the overall structural pattern of an antacid?

A

Metal + neutralizing base

270
Q

Benefits to sodium bicarbonate include:

A

Highly soluble
Rapid action in stomach
Brief duration

271
Q

How do we administer sodium bicarbonate to our patients? Why?

A

30 mL shot SB; we don’t have our patients chew TUMS prior to surgery for the fact that they could aspirate on the chewed particles.

272
Q

What antacids can cause metabolic alkalosis?

A

Sodium bicarbonate

Calcium carbonate

273
Q

Milk of Magnesia is also known as:

A

Magnesium hydroxide

274
Q

Which antacid may have a laxative effect?

A

Magnesium hydroxide

275
Q

What is the problem with giving high doses of magnesium hydroxide?

A

It may cause hypermagnesemia.

276
Q

What is the major benefit of giving magnesium hydroxide to your patient as opposed to other antacids?

A

No acid rebound

277
Q

Which antacid has a risk list that includes hypercalcemia, acid rebound, and metabolic alkalosis w/ chronic use?

A

Calcium carbonate

278
Q

What are the defining characteristics of aluminum hydroxide?

A

Minimal absorption
Phosphate depletion
Decreased gastric emptying

279
Q

Name two major drug interactions of antacids:

A

Increases delivery of PO drugs

Decreases bioavailability

280
Q

The drug effects of antacids depends on the drug’s specific:

A

pKA

281
Q

Why might administration of sodium citrate give you pause?

A

It may cause an increase of citric acid in the stomach.

282
Q

What is sucralfate?

A

It is a stomach coat that treats duodenal or gastric ulcers by protecting them from stomach acid

283
Q

What drug is known as a viscous suspension?

A

Sucralfate

284
Q

What drug protects the stomach lining from inflammatory effects of gastric acid?

A

Sucralfate

285
Q

What are the effects of prokinetics?

A

They increase LES tone.
They increase peristalsis.
They increase gastric emptying.

286
Q

T/F: prokinetics increase gastric emptying.

A

True.

287
Q

T/F: prokinetics serve to relax the LES.

A

False; they increase the LES tone.

288
Q

What is the most clinically useful prokinetic?

A

Metoclopramide

289
Q

What parts of the GI tract does Metoclopramide relax? When?

A

It relaxes the pylorus and the duodenum when the stomach contracts.

290
Q

Major effects of Metoclopramide?

A

Increased gastric emptying
Increased LES
Relaxes pylorus and duodenum when the stomach contracts

291
Q

In addition to being a prokinetic, what type of antagonist is metoclopramide?

A

Dopamine antagonist

292
Q

What are some side effects of metoclopramide as a dopamine antagonsit?

A

May cause sedation, agitation, and dysphoria

293
Q

What drug may cause dysphoria, agitation, and sedation when it interacts with dopamine receptors?

A

Metoclopramide

294
Q

In what patient population shoudl you avoid giving Metoclopramide?

A

Parkinsons patients

295
Q

Parkinsons patients should not receive what prokinetic? Why?

A

Parkinsons is caused by a depletion of dopamine in the brain, and metoclopramide is a dopamine antagonist that will exacerbate the situation.

296
Q

How should you administer metoclopramide?

A

Administer slowly to avoid dysphoria and agitation in patients.

297
Q

If you adminsiter Metoclopramide to quickly, what can occur?

A

It can cause dysphoria and agitation in patients.

298
Q

How is metoclopramide absorbed?

A

Oral absorption

299
Q

How is metoclopramide eliminated?

A

Renal elimination

300
Q

What organs eliminate metoclopramide from the body?

A

Kidneys

301
Q

What is the dosage of metoclopramide as a preop adjunct?

A

10-20 mg over 3-5 minutes, 15-30 minutes prior to induction

302
Q

When should you give metoclopramide in a preop setting?

A

15-30 minutes prior to induction

303
Q

Over what time period should you give metoclopramide?

A

Over 3-5 minutes

304
Q

How much is an appropriate preoperative dose of Metoclopramide?

A

10-20 mg

305
Q

Does Metoclopramide alter gastric pH?

A

No.

306
Q

T/F: Metoclopramide lowers gastric pH.

A

False; it increases LES tone, increases gastric emptying, and relaxes the pylorus and duodenum upon contraction of stomach.

307
Q

T/F: Reglan is a powerful anti-emetic.

A

False; there is no data to show that.

308
Q

Metoclopramide is used chronically to treat:

A

Gastroparesis and GERD

309
Q

What patients should receive metoclopramide prior to surgery?

A 
Trauma
Full Stomach
Obese
Diabetic
Pregnant
310
Q

Besides trauma and emergency patients that come in with a full stomach, what population groups are known for decreased gastric emptying that would benefit from Metoclopramide prior to surgery?

A

Obese
Diabetic
Pregnant

311
Q

The fact that metoclopramide is a dopamine antagonist doesn’t only affect Parkinson’s patients. What is a negative effect seen across patient pouplations?

A

Dysrhythmias: extrapyramidal effect

312
Q

Main side effects of Metoclopramide?

A

Abdominal cramping
Dysrhythmias
Dry mouth

313
Q

Rare side effects of chronic metoclopramide therapy include:

A

Hirsuitism

Maculopapular rash

314
Q

What kind of rash may occur on patients that are tacking metoclopramide chronically?

A

Maculopapular rash, a raised and red rash that occurs all over the body

315
Q

What type of prokinetic may cause hyperprolactinemia? What are the effects?

A

Metoclopramide

Can cause breast enlargement and menstrual irregularities

316
Q

Why might chronic metoclopramide use cause breast enlargement and irregular menstrual cycles?

A

Can cause hyperprolactinemia

317
Q

What are the fetal effects of Reglan?

A

No real effects

318
Q

Besides dopamine-depleted patients, what patients should not receive Metoclopramide?

A

Patients with GI obstruction because the blockage prevents the forward movement of food

319
Q

If your patient has a GI obstruction, avoid giving them:

A

Metoclopramide

320
Q

What type of drug is domperidone?

A

Prokinetic

321
Q

Domperidone is a

A

Prokinetic

322
Q

Main effects of domperidone as a prokinetic?

A

Increases peristalsis
Increases LES tone
Increases stomach emptying

323
Q

Is domperiodone a dopamine antagonist?

A

Yes.

324
Q

How does domperidone differ from metoclopramide in terms of side effects?

A

Domperidone doesn’t have cholinergic or central effects.

325
Q

T/F: domperidone has widespread cholinergic effects.

A

False; no cholinergic activity

326
Q

Does domperidone have central effects?

A

No, but metoclopramide does.

327
Q

What type of drug is cisapride?

A

Prokinetic

328
Q

Cisapride is a

A

Prokinetic

329
Q

Are all prokinetics dopamine antagonists?

A

No, cisapride is not a dopamine antagonist.

330
Q

Name a prokinetic that is not a dopamine antagonist.

A

Cisapride

331
Q

How does cisapride work?

A

It increases Ach in the gut to increase parasympathetic drive and increase gastric emptying.

332
Q

What prokinetic increases Ach in the gut to increase parasympathetic drive and therefore increases gastric emptying?

A

Cisapride

333
Q

What type of drug is dexamethasone?

A

Glucocorticoid

334
Q

How is dexamethasone effective as an antiemetic?

A

It is a glucocorticoid that inhibits prostaglandin synthesi.

335
Q

What drug acts as an anti-emetic by inhibiting prostaglandin synthesis?

A

Dexamethasone

336
Q

When is dexamethasone administered?

A

At induction

337
Q

Effective dose of dexamethasone?

A

4 mg

338
Q

What is the half-life of dexamethasone? Why is that significant?

A

Half-life is 36 hours, making it a good choice for outpatient procedures.

339
Q

Why should you avoid high doses of dexamethasone?

A

At high doses, dexamethasone will increase sugar production in diabetics without increasing anti-emetic benefit.

340
Q

What type of drug is droperidol?

A

Butyrophenone

341
Q

Which antiemetics are a butyrophenone?

A

Droperidol, haloperidol

342
Q

T/F: droperidol is a dopamine antagonist.

A

True.

343
Q

Besides metoclopramide and domperidone, name a dopamine antagonist.

A

Droperidol

344
Q

Why is droperidol rarely used anymore?

A

It has a black box warning because it can cause QT elongation, leading to Torsades de Pointes (ventricular dysrhythmia d/t anti-dopamine activity).

345
Q

How much droperidol must you give your patient to see QT-prolonging effects?
How much to provide effective anti-emesis?

A

QT prolongation seen at 12 mg doses

Anti-emetic dose = 0.625 mg

346
Q

What type of drug is haloperidol?

A

Butyrophenone

347
Q

If you see “-idol,” think:

A

Butyrophenone

348
Q

Does haloperidol have anti-dopamine effects?

A

Yes; affinity for D2 receptors

349
Q

When should you use haloperidol?

A

As a rescue drug for PONV

350
Q

Effective dose of haloperidol?

A

1 mg

351
Q

When is the optimal time to done a scopalamine patch?

A

Night before, but morning of will suffice

352
Q

What type of drug is scopolamine?

A

Anticholinergic

353
Q

A signficant side effect of scopolamine can be:

A

Dry mouth d/t anticholinergic effects

354
Q

Why should patients wash their hands after removing their scopolamine patch?

A

Scopolamine is very lipophilic, and it can get into eyes and cause pupil dilation d/t anticholinergic effects.

355
Q

Why should you use caution in giving scopolamine to elderly populations?

A

Can cause dysphoria or even a cholinergic crisis

356
Q

What is the dose of a scopolamine transdermal patch?

A

1.5 mg

357
Q

What is a rescue drug for patients who are already nauseous and vomiting?

A

Promethazine (Phenergan)

H2 antihistamine

358
Q

What two antihistamines are considered antiemetics?

A

Promethazine

Diphenhydramine

359
Q

What illegal drug is often used to treat nausea due to chemotherapy?

A

Cannaboids

360
Q

T/F: ephedrine has anti-emetic effects.

A

True.

361
Q

What type of drug is aprepitant?

A

NK1 antagonist

362
Q

Name an NK1 antagonist that is primarily used to treat N/V d/t chemotherapy.

A

Aprepitant

363
Q

What type of antagonist is aprepitant?

A

NK1 antagonist

364
Q

What is the main ligand of NK1 receptors? Where are they found?

A

Main ligand = substance P

Found in vomiting center of brain in high concentrations

365
Q

NK1 receptors are highly concentrated in which part of the brain?

A

Vomiting center of brain

366
Q

How should you administer Aprepitant as an anti-emetic?

A

Give preoperatively PO to prevent PONV.

367
Q

Why is aprepitant not widely used as an anti-emetic?

A

It is extremely expensive.

368
Q

What parts of the CNS are involved in PONV?

A

Cortex
Thalamus
Hypothalamus
Meninges

369
Q

Which receptors in the vestibular system are involved in PONV?

A

H1 receptors are possibly involved, and M1 receptors are definitely involved.

370
Q

What cranial nerve(s) controls input to the GI tract and heart?

A

CN IX and CN X

371
Q

What receptors in the GI tract and the heart are involved in PONV?

A

Mechanorecetpors
Chemoreceptors
5-HT3 receptor

372
Q

Where is the vomiting center of the brain located?

A

Medulla oblongata

373
Q

What receptors are involved in the vomiting center of the brain?

A

H1 receptor
M1 receptor
NK1 receptor
5-HT3 receptor

374
Q

Where are D2 receptors located?

A

In the chemoreceptor trigger zone (area postrema)

375
Q

A 32 year old female prevents for first c-section. She feels very nauseated after epidural placement. What should you give her?

A

Give her fluids; she is nauseated after epidural placement because it caused hypotension.

376
Q

When you see “Heller myotomy,” you should automatically think:

A

Achalasia

377
Q

Effective dose of droperidol?

A

0.625 - 1.25 mg

378
Q

Effective dose of Zofran?

A

4 mg (0.1 mg/kg)

379
Q

Effective dose of graniestron?

A

0.01 mg/kg

380
Q

Effective dose of dolasetron?

A

12.5 mg (0.35 mg/kg)

381
Q

Effective dose of metoclopramide?

A

10 mg (0.15 mg/kg)

382
Q

Effective dose of dexamethasone?

A

4-10 mg (0.1 mg/kg)

ANES 516B (3 decks)

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