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Duke Pharmacology- Hannah > Anti-emetics > Flashcards

Anti-emetics Flashcards

1
Q

What is the most common complication observed in PACU?

A

PONV

also most common reason (along with pain) for hospitalization following ambulatory surgery

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2
Q

What are the pathways in which antiemetics can prevent and treat PONV?

A

centrally acting
peripherally acting
combination therapies

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3
Q

What do at risk patients benefit from?

A

one or more prophylactic measures

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4
Q

What are the types of risk factors for PONV?

A

surgical, anesthetic, and individual

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5
Q

What are the patient risk factors for PONV?

A

Female gender (overall strongest predictor), history of PONV or motion sickness, non-smoker, age (risk decreases by 10% per decade), apprehension (r/t swallowed air and abdominal distension), gastroparesis, recent food ingestion

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6
Q

What are the surgical risk factors for PONV?

A 
increased duration of anesthetic/surgery (each 30 min increase in duration increases PONV risk by 60%)
surgical type (laparoscopy, ENT, T&A, breast, GU/GYN)
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7
Q

What are the anesthesia risk factors for PONV?

A

preop administered opioid analgesics, inhalational induction, volatile anesthetic agents, nitrous oxide

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8
Q

What induction agent is found to result in less postoperative vomiting?

A

Propofol

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9
Q

What are the post-anesthetic related risk factors for PONV?

A

ambulation, postural hypotension, uncontrolled pain, postoperative opioid administration, early PO intake, lower FiO2 concentration, reversal agents (specifically neostigmine)

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10
Q

According to the SAMBA guidelines when would we give prophylaxis?

A

Moderate risk- give one or two prophylactic measures

High risk- multiple interventions

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11
Q

The risk factors included in the Apfel score are:

A

female gender, nonsmoker, history of PONV, postoperative opioids

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12
Q

How can vomiting be triggered directly?

A

noxious stimuli, toxins, drugs, irritants

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13
Q

How can vomiting be triggered indirectly?

A

stimulation of the vomiting center in the medulla oblongata

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14
Q

What makes up the vomiting center in the brain?

A

located in the medulla oblongata: cerebral cortex/thalamus, vestibular apparatus, vagal afferent GI tracts, chemoreceptor trigger zone*** important part of the pathway

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15
Q

What is the goal of combination therapy?

A 
targets multiple receptors, provides rapid onset agent and longer duration of action, benefits patients at high risk, treat with different pharmacological agent class if prophylactic treatment did not work
consider combo therapy for certain surgical procedures: gastric, esophageal, plastics, eye, mandibular jaw wiring, increased ICP
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16
Q

What are the receptors involved in the vomiting pathway?

A

histamine, muscarinic, opioid, dopamine (D2), 5-hydroxytryptamine (serotonin)

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17
Q

What specific serotonin receptor mediates vomiting?

A

5-HT3 receptor mediates vomiting and is found in GI tract and brain (CTZ & NTS)

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18
Q

How are the effects of 5-HT3 receptor mediated?

A

via ion channel receptors (gated Na+/K+ channels)

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19
Q

What is the trigger zone of serotonin activated by?

A

anesthetics and opioids

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20
Q

What does serotonin do to the respiratory system?

A

causes increased airway resistance

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21
Q

What does serotonin do to the GI system?

A

release of Ach increases peristalsis

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22
Q

What does serotonin do to the CV system?

A

powerful vasoconstrictor (except in the heart/skeletal muscle), vasodilation in the heart

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23
Q

What are the serotonin receptor antagonists and what is their action?

A

ondansetron, palonosetron, dolasetron

inhibit central and peripheral stimulation of 5-HT3 receptors

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24
Q

What are the side effects of serotonin receptor antagonists?

A

headache, prolonged QT interval

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25
Q

When are serotonin receptor antagonists?

A

administered at the end of surgery

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26
Q

What are benefits of serotonin receptor antagonists?

A

they do not cause sedation and are generally well tolerated

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27
Q

What is the typical dosage of ondansetron?

A

PO: 4 or 8 mg or for PONV prophylaxis 16 mg PO dose x 1 one hour before induction of anesthesia
4 mg single dose IV or 0.1 mg/kg if <40 kg

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28
Q

What is the half-life and onset of ondansetron?

A

half-life: 4 hours
onset: 30 minutes
peak plasma is almost immediate

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29
Q

Where is zofran metabolized?

A

liver by hydroxylation and conjugation CYP-450
severe hepatic impairment will decrease clearance so dose adjustment needed
no dose adjustment for kidneys

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30
Q

Side effects for ondansetron include:

A

headache, dizziness, diarrhea, constipation, QTc prolongation

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31
Q

When is ondansetron most effective?

A

when administered at the end of the surgical procedure

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32
Q

What anti-emetic is effective for chemotherapy induced N/V?

A

palonosetron

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33
Q

What is the half-life of palonosetron?

A

40 hours

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34
Q

Palonosetron should not be given to

A

pediatric patients

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35
Q

The dosing of palonosetron is

A

0.75 mg

no dosage adjustments needed for elderly, renal, hepatic patients

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36
Q

What is the mechanism of action of dolasetron?

A

reduce activity of the vagus nerve to limit activation of the vomiting center in the medulla oblongata

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37
Q

What is the dosage of dolasetron?

A

12.5 mg IV

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38
Q

What is the duration of action of dolasetron?

A

4-9 hours

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39
Q

How is dolasetron eliminated?

A

liver via CYP450 and the kidneys

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40
Q

What is the onset of action of dolasetron?

A

immediate- very fast acting

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41
Q

When should dolasetron (anzemet) be administered?

A

within 15 minutes before the end of anesthesia

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42
Q

What dosage of dolasetron is given?

A

PO dose 100 mg 1-2 hours preop or 50 mg IV

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43
Q

What are the adverse effects of dolasetron?

A

headache, dizziness, constipation, QT prolongation

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44
Q

How is dolasetron excreted?

A

in the urine/feces

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45
Q

Which serotonin antagonist has an active metabolite and what is it?

A

dolasetron

active metabolite: hydrodolasetron

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46
Q

What is the mechanism of action of droperiol?

A

blocks dopamine receptors that contribute to development of PONV

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47
Q

What properties does droperiol possess?

A

anxiolytic, sedative, hypnotic and antiemetic properites

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48
Q

What class is droperiol a part of?

A

butyrophenone/dopamine receptor antagonist

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49
Q

What is the dose of droperidol?

A

0.625-1.25 mg IV (slow) or IM

50
Q

What is the onset of droperidol?

A

3 to 10 minutes

51
Q

How is droperidol metabolized?

A

in the liver

52
Q

What is a concern when administering droperidol?

A

QT interval prolongation

patients need to be monitored for 2-3 ours w/ EKG after giving drug

53
Q

What is the peak onset of droperidol?

A

30 minutes

54
Q

What is the duration of action?

A

2-4 hours

55
Q

A dosage of 20 mcg/kg of droperidol

A

can cause prolonged sedation (increased PACU LOS)

56
Q

A high dose of droperidol can cause

A

high dose (50-75 mcg/kg) can cause increased side effects such as anxiety, dizziness, drowsiness, hypotension, and extrapyramidal side effects

57
Q

Prochlorperazine (compazine) is considered a

A

antipsychotic/antiemetic

58
Q

What is the mechanism of action of prochlorperazine?

A

affects multiple receptors: histaminergic, dopaminergic (D2 blockade), muscarinic

59
Q

What is the dosage of prochlorperazine?

A

5-10 mg IM/IV before induction

60
Q

Prochloperazine has high levels of

A

protein binding (91-99%)

61
Q

The duration of action of prochlorperazine is?

A

3-4 hours with a peak of 2-4 hours

62
Q

Prochlorperazine is metabolized by

A

the liver

63
Q

What are the side effects of greatest concern of prochlorperazine?

A

extrapyramidal and anticholinergic side effects

64
Q

What are the adverse effects of prochlorperazine?

A

sedation, blurred vision, hypotension, dizziness, neuroleptic malignant syndrome, restlessness, dystonia

65
Q

Metoclopramide (reglan) is considered

A

a dopamine antagonists

66
Q

What is the mechanism of action of metoclopramide?

A

centrally acting as dopamine receptor antagonist in CTZ/vomit center
peripherally acting as cholinomimetic in GI tract (facilitates Ach transmission at muscarinic receptors)

67
Q

Metoclopramide should not be given rapidly because

A

it can cause anxiety and abdominal cramping

give slowly over 1-2 minutes

68
Q

What is the dosage of reglan?

A

10 mg IV

69
Q

What can reglan be used for?

A

gastroparesis, GERD, aspiration pneumonia prophylaxis

used as gastric aspiration prophylaxis for high risk patients

70
Q

Metoclopramide is ineffective at

A

doses lower than 10 mg IV unless used in combination with other antiemetics

71
Q

One advantage of reglan is

A

it’s lack of sedative properties

should be used with another agent for PONV not as effective without it

72
Q

Where is reglan metabolized?

A

in the liver and excreted by the kidneys so must be modified for impaired renal function

73
Q

What are the adverse effects of metoclopramide?

A

may cause extrapyramidal side effects in higher doses; contraindicated in Parkinson’s disease, seizure, GI obstruuction

74
Q

Metoclopramide should be avoided in

A

pheochromocytoma cases as it can cause HTN crisis by releasing catecholamines from tumor

75
Q

What is the onset of action of metoclopramide?

A

3 to 5 minutes

76
Q

What is the peak of action and duration of action for metoclopramide?

A

1-2 hours

77
Q

Where is aprepitant metabolized?

A

in the liver

78
Q

What patients does aprepitant need dose adjustment for?

A

it doesn’t; no need for dose adjustment in renal failure patients

79
Q

What is the dosage of aprepitant?

A

40-80 mg PO preop

80
Q

Aprepitant is recommended for

A

high-risk non-pregnant patients

81
Q

What is the class and mechanism of action of aprepitant?

A

neurokinin-1 receptor antagonist; inhibits Substance P at central and peripheral receptors

82
Q

Aprepitant increases the activity of

A

serotonin receptor antagonists like ondansetron so we would want to decrease the dosage of ondansetron

83
Q

What are the adverse effects of aprepitant?

A

fatigue, dizziness, hypoesthesia, disorientation, N/D, anorexia, constipation, diarrhea, dyspepsia, heartburn, abdominal pain, gastritis, perforating duodenal ulcer, hiccups

84
Q

If giving aprepitant with dexamethasone

A

reduce dose by half to maintain dexamethasone plasma concentrations

85
Q

Females should be warned that

A

aprepitant will make hormonal contraceptives non-effective for 28 days

86
Q

What is the mechanism of action of dexamethasone?

A

long-acting corticosteroid and it is unknown its action as antiemetic

87
Q

What is the metabolism of dexamethasone?

A

liver- no adjustment for hepatic/renal failure

88
Q

What is the dosage of dexamethasone?

A

4-10 mg IV

peds 0.2-0.5 mg/kg IV

89
Q

What is the half-life, peak, and onset?

A

half-life: 1-5 hours
Peak: 5-10 minutes
Onset: 2 hours

90
Q

When should dexamethasone be administered?

A

at the beginning of the case

91
Q

Dexamethasone side effects include:

A

perineal pruiritis if patient is awake

92
Q

What are the absolute contraindications of decadron?

A

uncontrolled infections, known hypersensitivity, cerebral malaria, systemic fungal infection, concurrent treatment with live virus vaccine

93
Q

Dimenhydrinate (dramamine) is considered a

A

histamine receptor antagonists

94
Q

What is the mechanism of action of dimenhydrinate?

A

H1 antagonist- competes with histamine at H1 receptor sites in the GI tract, blood vessels and respiratory tract; blocks CTZ, depresses labyrinthine function, and vestibular stimulation

95
Q

What is the dosage of dimenhydrinate?

A

50-100 mg IV/IM q4 hour

96
Q

What is the onset and duration of dimenhydrinate?

A

onset: immediate
duration: 4-6 hours

97
Q

What is the metabolism of dimenydrinate?

A

liver; no dosage adjustment for hepatic/renal failure

98
Q

What are the adverse effects of dimenhydrinate?

A

drowsiness, urinary retention, dry mouth, blurred vision, extrapyramidal effects, commonly causes sedation

99
Q

What is the mechanism of action of promethazine (phenergan)?

A

antihistamine (H1 antagonist) and anticholinergic/muscarinic-blocking effects responsible for antiemetic activity

100
Q

What is the dosage of promethazine?

A

12.5-25 mg q4-q6 hours

IM route is preferred (onset 20 minutes)

101
Q

What is the duration of action promethazine?

A

4-6 hours

102
Q

How is promethazine metabolized?

A

hepatic (glucuronidation and sulfoxidation)

no dosage adjustment needed for renal impairment

103
Q

What are the common side effects of promethazine?

A

confusion, drowsiness, dry mouth, constipation (avoid in patients >65 years)
risk of significant sedation (esp with opioids)- limited utility

104
Q

Promethazine of 5-10 mg IV is recommended for

A

prophylaxis/rescue due to antihistamine properties

105
Q

Scopolamine is a

A

anticholinergic and acts as a muscarinic antagonist

inhibits the action of Ach at parasympathetic sites in smooth muscle, CNS, and secretory glands

106
Q

Scopolamine acts through

A

blocking the communication between nerves of the vestibule and vomit center in brain (may also directly block vomiting center)

107
Q

Scopolamine competitively blocks

A

the binding of Ach

108
Q

Anticholinergic poisoning causes

A

agitation, delirium, dry mouth, tachycardia, impaired vision, hallucinations, unconsciousness
physostigmine can be given

109
Q

Scopolamine should be avoided in patients with

A

closed-angle glaucoma and elderly over 65

110
Q

Scopolamine can cause

A

many CNS side effects and can cause cerebral depression, sedation, and amnesia
dry mouth, increased thirst, dry skin, constipation, drowsiness, dizziness, blurred vision, dilated pupils, & light sensitivity

111
Q

the dosage of scopolamine is

A

1.5 mg topical patch behind the ear the evening before surgery
keep on for 24 hours postop

112
Q

Scopolamine is metabolized

A

in the liver

113
Q

The onset of action of scopolamine is

A

2-4 hours (transdermal)
DOA: 72 hours
Elimination half-life: 4-5 hours

114
Q

Ephedrine is considered

A

an indirect-acting sympathomimetic agent

115
Q

The dosage of ephedrine is

A

10-25 mg IV recommended for N/V associated with postural hypotension in PACU

116
Q

Midazolam can be given to treat PONV with

A

2 mg IV given as a premedication, intraoperatively, or as a rescue therapy

117
Q

For pediatric patients undergoing strabismus surgery

A

midazolam and dexamethasone causes ZERO incidence of PONV

118
Q

The mechanism of action for midazolam

A

is related to GABA receptor antagonism, inhibition of dopamine release and anxiolytic effects

119
Q

Reduction of baseline risk factors for PONV include:

A

avoid general anesthesia with Inhalational Volatile agent, minimize opioid use, preferential use of propofol infusion, avoid nitrous oxide, adequate hydration

120
Q

The goal of pain management is to

A

decrease postop analgesic requirements, reduce pain scores, and decrease PONV

121
Q

Uncontrolled postoperative pain causes triggering of stress response–>

A

catecholamine release, increased oxygen consumption, increased cardiac workload and tachycardia

Duke Pharmacology- Hannah (14 decks)

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