CINV Flashcards

1
Q

Per patient perceptions what is the number one severe side effects of chemo?

A

Fatigue

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2
Q

What are the CINV RFs?

A
Female
age < 50
H/o motion sickness
H/o N/V associated with pregnancy
EtOH consumption (< 10 drinks/week)
H/o CINV
GI radiation
Brain involvement
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3
Q

What is the definition of nausea?

A

Awareness of the urge to vomit

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4
Q

What is the definition retching?

A

Non-productive attempt to vomit

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5
Q

What is the definition of vomiting?

A

Forceful expulsion of GI contents

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6
Q

What is intractable nausea?

A

N/V not adequately controlled after multiple antiemetics are used in series and combinations

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7
Q

What is anticipatory nausea?

A

N/V occurring as a result of a conditioned response from previous treatment

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8
Q

What is acute CINV?

A

0-24 hours after chemotherapy

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9
Q

What is delayed CINV?

A

> 24 hours after chemotherapy

Often associated with highly emetogenic chemo agents, esp cisplatin regimens

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10
Q

What is non-pharm treatment of CINV?

A
Avoidance of strong odors
Eating small meals more frequently
Psychological relaxation techniques
Acupuncture/acupressure
P6 stimulation (relief band)
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11
Q

What is the pathophysiology of CINV?

A

Chemoreceptor trigger zone
Cerebral cortex
Peripheral pathways
Vestibular system

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12
Q

What is the Chemoreceptor trigger zone?

A

Exposure to toxins in the blood stream or CSF stimulates the vomiting center

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13
Q

How is the cerebral cortex involved in CINV?

A

Gains input from the senses, meningeal inrritation and increased ICP that activate vomiting centers

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14
Q

How are peripheral pathways involved in CINV?

A

GI and viscera mechano- and chemoreceptors transmit messages via the vagus and splanchnic serves, sympathetic ganglia and glossopharyngeal nerves

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15
Q

How is the vestibular system involved in CINV?

A

N/V triggered by motion

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16
Q

What is the incidence of CINV for high risk antineoplastic agents?

A

> 90%

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17
Q

What is the incidence of CINV for moderate risk antineoplastic agents?

A

30-90%

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18
Q

What is the incidence of CINV for low risk antineoplastic agents?

A

10-30%

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19
Q

What is the incidence of CINV for minimal risk antineoplastic agents?

A

< 10%

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20
Q

What are the two CINV high risk antineoplastic agents he circled?

A

Anthracycline/cyclophosphamide combination

Cisplatin

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21
Q

What drugs can be used as antiemetics?

A
Corticosteroids
Betyrophenones
Serotonin antagonists
Antimuscarinic
NK1 antagonists
Benzo
Phenothiazines &amp; dopamine antagonists
Cannabinoids
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22
Q

What is the MOA of dexamethasone in CINV?

A

Overall unknown
Inhibition of PG synthesis
Decreased BBB permeability of chemo agents
Inhibition of cortical input to vomiting center

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23
Q

What is the place in therapy of dexamethasone in CINV?

A

Brain tumor or CNS involvement
Malignant bowel obstruction
Chemotherapy incuded N/V

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24
Q

What are the serotonin antagonists?

A

Ondansetron
Granisetron
Palonosetron

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25
Q

What is the MOA of serotonin agonists?

A

Block serotonin receptors in the GI tract

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26
Q

When are serotonin antagonists effective at preventing acute emesis?

A

After chemo, radiation and anesthesia

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27
Q

What are AEs of serotonin antagonists?

A

HA

Constipation

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28
Q

What dose of ondansetron for high emetic risk?

A

PO: 24 mg
IV: 8 mg or 0.15 mg/kg

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29
Q

What is the dose of ondansetron for moderate emetic risk?

A

PO: 16 mg
IV: 8 mg or 0.15 mg/kg

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30
Q

What are the doses of high/ moderate emetic risk granesitron?

A

PO: 2 mg
IV: 1 mg or 0.01 mg/kg
SC: 10 mg qweekly

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31
Q

If dosed appropriately, can we consider all serotonin agonists equivalent?

A

Yes

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32
Q

What is the place in therapy for NK1 receptor antagonists?

A

For the prevention of acute and delayed N/V following highly emetogenic regimens

33
Q

What are the DDIs for NK1 receptor antagonists?

A

Warfarin

Dexmethasone

34
Q

What are the advantages of NK1 RAs?

A

Administration as an all-oral regimen
Single-dose schedule given on day of chemo
Possible dexamethasone sparing regimen

35
Q

What are the challenges of NK1 RAs?

A

Pts unable to tolerate PO

Cost, procurement, and reimbursement

36
Q

What does NEPA contain?

A

Netupitant/palonosetron

37
Q

What is netupitant?

A

Highly selective substance P/NK 1 receptor

38
Q

What is olanzapine?

A

5-HT2 and DA antagonist for antiemetic activity

39
Q

What are the SEs of olanzapine?

A

Drowsiness
Akathisia
Pseudoparkinsonism

40
Q

What are DDIs for olanzapine?

A

Metoclopramide/kaloperidol

Increased risk of extrapyramidal SE

41
Q

What are the phenothiazines?

A

Prochloroperazine
Promethazine
Thiethylperizine
Perphenazine

42
Q

What is the MOA for phenothiazines?

A

Block DA receptors in the chemoreceptor trigger zone

43
Q

What is the place in therapy for phenothiazines?

A

Opioid induced n/v

Delayed nausea d/t chemotherapy

44
Q

What are the AEs of phenothiazines?

A

Sedation
EPS
Akathesia

45
Q

How are phenothiazines usually incorporated into antiemetic plans?

A

PRN

46
Q

What is a concern with promethazine use?

A

Extravasation

47
Q

What are butyrophenones?

A

Haloperidol

Droperidol

48
Q

What is the MOA of btyrophenones?

A

Block DA receptors in chemoreceptor trigger zone

49
Q

When can butyrophenones be used?

A

Potential use in breakthrough and/or refractory N/V after trying other agents

50
Q

What are AEs of butyrophenones?

A

Sedation
Dystonia
Akasthesia

51
Q

What is droperidol’s BBW?

A

QT prolongation

52
Q

What is the MOA of metoclopramide at low doses?

A

DA D2 antagonist

53
Q

What is the MOA of metoclopramide at high dises?

A

Some 5HT2 antagonism

54
Q

What is the place in therapy for metoclopramide?

A

Opioid induced N/V
Malignant bowel obstruction
Impaired GI motility
Refractory CINV

55
Q

What are the AEs of metoclopramide?

A

Diarrhea
Dystonic reactions
Akathesia
Sedation

56
Q

What was an AE of HD metoclopramide?

A

Tardive dyskinesia

57
Q

Why are benzos used as antiemetics?

A

Combined with 5HT3 antagonists and dexamethasone for anxiolytic and amnestic effects
Mitigates metoclopramide-induced agitation

58
Q

What are effective as an adjunctive agent?

A

Cannabinoids

59
Q

What two receptors do cannabinoids work on?

A

CB1 and CB2

60
Q

What are CB1 receptors located?

A

Throughout the CNS

61
Q

Where are CB2 receptors located?

A

On the brain stem neurons, most concentrated in periphery

62
Q

How does cannabinoid prevent CINV?

A

Acting at central CB receptors by preventing proemetic effects of endogenous compounds

63
Q

What are the AEs of cannabinoids?

A

Sedation
Dizziness
Hypotension
Dysphoria

64
Q

What is a 4-drug combination used for high emetogenic risk?

A

NK1 receptor antagonist
5HT3 receptor antagonist
Dexamethasone
Olanzapine

65
Q

When do we use a 3 drug combination?

A

Carboplatin AUC 4+

66
Q

What is the 3 drug combination?

A

NK1 RA
5-HT3 RA
Dexamethasone

67
Q

When do we ues a 2 drug combination?

A

Moderate-emetic-risk agents, excluding carbo

68
Q

What is the 2 drug regimen?

A

5-HT3 receptor antagonist

Dexamethasone

69
Q

If a pt is low emetogenic risk what do we give?

A

5-HT3 or dexamethasone

70
Q

If the patient has not had olanzapine previously and has N/V despite adequate prophylaxis?

A

Add olanzapine to the regimen

71
Q

If the patient is having breakthrough nausea/vomiting, what can be added to the standard regimen?

A

Anti-emetic with alternative mechanism

72
Q

When is refractory n/v common?

A

Regimens containing multiple alkylating agents and stem cell transplants

73
Q

If a patient has intractable n/v, how are the medications dosed?

A

Scheduled around the clock

74
Q

What medications are used for intractable n/v?

A

Mirtazepine
Cannabinoids
Olanzapine
ODTs, IV or rectal formulations may be required

75
Q

What are the DOCs for opioid induced n/v?

A

Metoclopramide
Prochloroperazine
Haloperidol

76
Q

What is the most common causes of N/V in patients with end-stage cancer?

A

Constipation

77
Q

How does constipation cause n/v?

A

Slowing of intestinal persitalsis
Increased ab pressure and distention of bowel
Activation of gut neurotransmitters

78
Q

What cancers are bowel obstruction common in?

A

Ovarian

Colorectal