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Duke Pharmacology- Hannah > Anti-emetics > Flashcards

Anti-emetics Flashcards

(121 cards)

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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
When are serotonin receptor antagonists?
administered at the end of surgery
26
What are benefits of serotonin receptor antagonists?
they do not cause sedation and are generally well tolerated
27
What is the typical dosage of ondansetron?
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
28
What is the half-life and onset of ondansetron?
half-life: 4 hours onset: 30 minutes peak plasma is almost immediate
29
Where is zofran metabolized?
liver by hydroxylation and conjugation CYP-450 severe hepatic impairment will decrease clearance so dose adjustment needed no dose adjustment for kidneys
30
Side effects for ondansetron include:
headache, dizziness, diarrhea, constipation, QTc prolongation
31
When is ondansetron most effective?
when administered at the end of the surgical procedure
32
What anti-emetic is effective for chemotherapy induced N/V?
palonosetron
33
What is the half-life of palonosetron?
40 hours
34
Palonosetron should not be given to
pediatric patients
35
The dosing of palonosetron is
0.75 mg | no dosage adjustments needed for elderly, renal, hepatic patients
36
What is the mechanism of action of dolasetron?
reduce activity of the vagus nerve to limit activation of the vomiting center in the medulla oblongata
37
What is the dosage of dolasetron?
12.5 mg IV
38
What is the duration of action of dolasetron?
4-9 hours
39
How is dolasetron eliminated?
liver via CYP450 and the kidneys
40
What is the onset of action of dolasetron?
immediate- very fast acting
41
When should dolasetron (anzemet) be administered?
within 15 minutes before the end of anesthesia
42
What dosage of dolasetron is given?
PO dose 100 mg 1-2 hours preop or 50 mg IV
43
What are the adverse effects of dolasetron?
headache, dizziness, constipation, QT prolongation
44
How is dolasetron excreted?
in the urine/feces
45
Which serotonin antagonist has an active metabolite and what is it?
dolasetron | active metabolite: hydrodolasetron
46
What is the mechanism of action of droperiol?
blocks dopamine receptors that contribute to development of PONV
47
What properties does droperiol possess?
anxiolytic, sedative, hypnotic and antiemetic properites
48
What class is droperiol a part of?
butyrophenone/dopamine receptor antagonist
49
What is the dose of droperidol?
0.625-1.25 mg IV (slow) or IM
50
What is the onset of droperidol?
3 to 10 minutes
51
How is droperidol metabolized?
in the liver
52
What is a concern when administering droperidol?
QT interval prolongation | patients need to be monitored for 2-3 ours w/ EKG after giving drug
53
What is the peak onset of droperidol?
30 minutes
54
What is the duration of action?
2-4 hours
55
A dosage of 20 mcg/kg of droperidol
can cause prolonged sedation (increased PACU LOS)
56
A high dose of droperidol can cause
high dose (50-75 mcg/kg) can cause increased side effects such as anxiety, dizziness, drowsiness, hypotension, and extrapyramidal side effects
57
Prochlorperazine (compazine) is considered a
antipsychotic/antiemetic
58
What is the mechanism of action of prochlorperazine?
affects multiple receptors: histaminergic, dopaminergic (D2 blockade), muscarinic
59
What is the dosage of prochlorperazine?
5-10 mg IM/IV before induction
60
Prochloperazine has high levels of
protein binding (91-99%)
61
The duration of action of prochlorperazine is?
3-4 hours with a peak of 2-4 hours
62
Prochlorperazine is metabolized by
the liver
63
What are the side effects of greatest concern of prochlorperazine?
extrapyramidal and anticholinergic side effects
64
What are the adverse effects of prochlorperazine?
sedation, blurred vision, hypotension, dizziness, neuroleptic malignant syndrome, restlessness, dystonia
65
Metoclopramide (reglan) is considered
a dopamine antagonists
66
What is the mechanism of action of metoclopramide?
centrally acting as dopamine receptor antagonist in CTZ/vomit center peripherally acting as cholinomimetic in GI tract (facilitates Ach transmission at muscarinic receptors)
67
Metoclopramide should not be given rapidly because
it can cause anxiety and abdominal cramping | give slowly over 1-2 minutes
68
What is the dosage of reglan?
10 mg IV
69
What can reglan be used for?
gastroparesis, GERD, aspiration pneumonia prophylaxis | used as gastric aspiration prophylaxis for high risk patients
70
Metoclopramide is ineffective at
doses lower than 10 mg IV unless used in combination with other antiemetics
71
One advantage of reglan is
it's lack of sedative properties | should be used with another agent for PONV not as effective without it
72
Where is reglan metabolized?
in the liver and excreted by the kidneys so must be modified for impaired renal function
73
What are the adverse effects of metoclopramide?
may cause extrapyramidal side effects in higher doses; contraindicated in Parkinson's disease, seizure, GI obstruuction
74
Metoclopramide should be avoided in
pheochromocytoma cases as it can cause HTN crisis by releasing catecholamines from tumor
75
What is the onset of action of metoclopramide?
3 to 5 minutes
76
What is the peak of action and duration of action for metoclopramide?
1-2 hours
77
Where is aprepitant metabolized?
in the liver
78
What patients does aprepitant need dose adjustment for?
it doesn't; no need for dose adjustment in renal failure patients
79
What is the dosage of aprepitant?
40-80 mg PO preop
80
Aprepitant is recommended for
high-risk non-pregnant patients
81
What is the class and mechanism of action of aprepitant?
neurokinin-1 receptor antagonist; inhibits Substance P at central and peripheral receptors
82
Aprepitant increases the activity of
serotonin receptor antagonists like ondansetron so we would want to decrease the dosage of ondansetron
83
What are the adverse effects of aprepitant?
fatigue, dizziness, hypoesthesia, disorientation, N/D, anorexia, constipation, diarrhea, dyspepsia, heartburn, abdominal pain, gastritis, perforating duodenal ulcer, hiccups
84
If giving aprepitant with dexamethasone
reduce dose by half to maintain dexamethasone plasma concentrations
85
Females should be warned that
aprepitant will make hormonal contraceptives non-effective for 28 days
86
What is the mechanism of action of dexamethasone?
long-acting corticosteroid and it is unknown its action as antiemetic
87
What is the metabolism of dexamethasone?
liver- no adjustment for hepatic/renal failure
88
What is the dosage of dexamethasone?
4-10 mg IV | peds 0.2-0.5 mg/kg IV
89
What is the half-life, peak, and onset?
half-life: 1-5 hours Peak: 5-10 minutes Onset: 2 hours
90
When should dexamethasone be administered?
at the beginning of the case
91
Dexamethasone side effects include:
perineal pruiritis if patient is awake
92
What are the absolute contraindications of decadron?
uncontrolled infections, known hypersensitivity, cerebral malaria, systemic fungal infection, concurrent treatment with live virus vaccine
93
Dimenhydrinate (dramamine) is considered a
histamine receptor antagonists
94
What is the mechanism of action of dimenhydrinate?
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
What is the dosage of dimenhydrinate?
50-100 mg IV/IM q4 hour
96
What is the onset and duration of dimenhydrinate?
onset: immediate duration: 4-6 hours
97
What is the metabolism of dimenydrinate?
liver; no dosage adjustment for hepatic/renal failure
98
What are the adverse effects of dimenhydrinate?
drowsiness, urinary retention, dry mouth, blurred vision, extrapyramidal effects, commonly causes sedation
99
What is the mechanism of action of promethazine (phenergan)?
antihistamine (H1 antagonist) and anticholinergic/muscarinic-blocking effects responsible for antiemetic activity
100
What is the dosage of promethazine?
12.5-25 mg q4-q6 hours | IM route is preferred (onset 20 minutes)
101
What is the duration of action promethazine?
4-6 hours
102
How is promethazine metabolized?
hepatic (glucuronidation and sulfoxidation) | no dosage adjustment needed for renal impairment
103
What are the common side effects of promethazine?
confusion, drowsiness, dry mouth, constipation (avoid in patients >65 years) risk of significant sedation (esp with opioids)- limited utility
104
Promethazine of 5-10 mg IV is recommended for
prophylaxis/rescue due to antihistamine properties
105
Scopolamine is a
anticholinergic and acts as a muscarinic antagonist | inhibits the action of Ach at parasympathetic sites in smooth muscle, CNS, and secretory glands
106
Scopolamine acts through
blocking the communication between nerves of the vestibule and vomit center in brain (may also directly block vomiting center)
107
Scopolamine competitively blocks
the binding of Ach
108
Anticholinergic poisoning causes
agitation, delirium, dry mouth, tachycardia, impaired vision, hallucinations, unconsciousness physostigmine can be given
109
Scopolamine should be avoided in patients with
closed-angle glaucoma and elderly over 65
110
Scopolamine can cause
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
the dosage of scopolamine is
1.5 mg topical patch behind the ear the evening before surgery keep on for 24 hours postop
112
Scopolamine is metabolized
in the liver
113
The onset of action of scopolamine is
2-4 hours (transdermal) DOA: 72 hours Elimination half-life: 4-5 hours
114
Ephedrine is considered
an indirect-acting sympathomimetic agent
115
The dosage of ephedrine is
10-25 mg IV recommended for N/V associated with postural hypotension in PACU
116
Midazolam can be given to treat PONV with
2 mg IV given as a premedication, intraoperatively, or as a rescue therapy
117
For pediatric patients undergoing strabismus surgery
midazolam and dexamethasone causes ZERO incidence of PONV
118
The mechanism of action for midazolam
is related to GABA receptor antagonism, inhibition of dopamine release and anxiolytic effects
119
Reduction of baseline risk factors for PONV include:
avoid general anesthesia with Inhalational Volatile agent, minimize opioid use, preferential use of propofol infusion, avoid nitrous oxide, adequate hydration
120
The goal of pain management is to
decrease postop analgesic requirements, reduce pain scores, and decrease PONV
121
Uncontrolled postoperative pain causes triggering of stress response-->
catecholamine release, increased oxygen consumption, increased cardiac workload and tachycardia

Duke Pharmacology- Hannah (14 decks)

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