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Phar 509 > Chemotherapy-Induced Nausea and Vomiting and Mucositis > Flashcards

Chemotherapy-Induced Nausea and Vomiting and Mucositis Flashcards

1
Q

What percentage of oncology patients experience some type of nausea or vomiting

A

90%

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2
Q

What the three main areas of the body involved in CINV

A

Central nervous system, peripheral nervous system, and the GI tract

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3
Q

What are the two key reigons of the brainstem involved in CINV, what is the flow between the two

A

Chemoreceptor trigger zone and Vomitting center, CTZ stimulates the VC

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4
Q

What are the two pathways of the CTZ

A

Peripheral: chemotherapy directly irritating cells in the GI tract releasing serotonin stimulating the CTZ leading to stimulating VC (Acute CINV)
Central: Substance P binds to NK-1 receptors and dopamine is stimulated by CTZ (Delayed CINV)

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5
Q

Which patient risk factors increase the likelihood of CINV

A

Being female, age less than 50, history of motion sickness, previous CINV, N/V with past pregnancies, low alcohol use, Anxiety

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6
Q

T/F: Alcohol use makes it more likely a patient will have CINV

A

False: Alcohol use is actually PROTECTIVE against CINV

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7
Q

What are treatment related risk factors of CINV

A

Drug, dose, route, schedule, radiation, surgery

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8
Q

What are autonomic symptoms of nausea, what receptors are involved

A

Pallor, tachycardia, diaphoresis, salivation/ dopamine, serotonin, muscarinic, and histamine

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9
Q

T/F: Grade 1 and 2 in CINV can be resolved with outpatient care while Grade 3 and 4 may require hospitalization

A

True

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10
Q

What are the types of CINV

A

Acute. delayed, breakthrough, anticipatory, refractory

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11
Q

What causes acute CINV, when does it occur, peaks and resolves, mediated by

A

ANY CHEMOTHERAPY, within first 24 hours following chemotherapy, peaks after 5 hours to 6 hours and resolves in 24 hours, mediated by serotonin

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12
Q

What causes delayed CINV, when does it occur, peaks and resolves

A

Associated with platinum, anthracyclines, and nitrogen mustards/ 24 hours after chemotherapy, peaks at 48 hours to 72 hours and can last from 5 to 7 days, mediated by dopamine and NK-1 more than serotonin

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13
Q

What is breakthrough CINV, incidence, solution

A

Occurs despite prophylactic treatment and requires rescue with antiemetics, 10-40%, rescue antiemetics should utilize a different MOA

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14
Q

What is refractory CINV, solution

A

Occurs during subsequent cycles due to inadequate control in the previous cycles so patients have poor responses to multiple antiemetics

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15
Q

What is anticipatory CINV, triggers

A

Occurs before patient recieve their next chemotherapy cycle (mostly nausea)/ sight, smell, taste, sounds, thoughts, or anxiety associated with chemo

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16
Q

What is the corticosteroid used in CINV, what is it indicated in, MOA

A

Dexamethasone/ acute, delayed, breakthrough, refractory/ interaction with serotonin receptors, activation of glucocorticoid receptors, interaction with CTZ

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17
Q

T/F: Dexamtheasone has slow onset and low bioavailability

A

False: Dexamethasone has FAST onset and HIGH bioavailability

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18
Q

What are adverse effects of dexamethasone

A

Insomnia (take before 4 pm), GI upset (take with food), appetite stimulant (eat), anxiety, hypertension

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19
Q

What are the 1st generation 5HT-3 antagonists, which CINV is most affected

A

Ondansetron, Dolasetron, Granisetron/ prevention of acute and breakthrough

20
Q

Which 1st generation 5HT-3 antagonist is most geared toward acute and delayed CINV

A

Granisetron

21
Q

What are the 2nd generation 5HT-3 antagonist, which CINV is most effected, what makes it most different

A

Palonestron, acute and delayed, 100X higher affinity with a 40 hour half life

22
Q

What are the adverse effects of 5-HT3 antagonists

A

Headache, constipation, fatigue, QTc prolongation (more common with IV)

23
Q

When should 5-HT3 antagonist be given for chemotherapy

A

At least 30 mins to an hour

24
Q

What are the three NK-1 inhibitors, what CINV do they block, which have IV formulations, which does not have drug interactions and why

A

Aprepitant, Fosaprepitant, Rolapitant/ Acute and Delayed/ Aprepitant and Fosaprepitant/ Rolapitant because it does not interact with CYP3A4 and CYP2C9

25
Q

What are the adverse effects of NK-1 inhibitors

A

Fatigue, GI upset, headache, and HICCUPS

26
Q

T/F: NK-1 inhibitors are NOT used in monotherapy and only used in HEC and MEC regimens

A

True

27
Q

What are the two types of dopamine antagonists

A

Phenthiazines and substituted benzamine

28
Q

What are the phenothiazines for dopamine antagonists, MOA, adverse effects

A

Prochloperazine and promethazine, antagonizes dopamine receptors in CTZ (can be used rectally)/ drowsines, EPS at high doses, CONSTIPATION, QT-c prolongation

29
Q

What are the substituted benzamines for dopamine antagonists, MOA, adverse effects

A

Metoclperamide,Antagonizes dopamine receptors in CTZ and 5HT-3 receptors in the GI tract while also enhancing GI motility with more emptying/ DIARRHEA, EPS at high doses, QT-c prolongation

30
Q

What antipsychotic can also be used for CINV, which CINV is it used for, receptors involved, Adverse events

A

Olanzapine/ Acute, Delayed, Breakthrough, Refractory/ Both serotonin, dopamine/ SEDATION, dry mouth, hyperglycemia and QT-c prolongation

31
Q

What can used for anticipatory CINV, when should they take it

A

Lorazepam and Alprazolam, the night before or morning of chemotherapy

32
Q

What are other antiemtics and what are they used for

A

Anticholinergics: Scopolamine, H1 blockers: meclizine or diphenhydramine, H2 blockers or PPIs: Ranitidine, famotidine, omeprazole or lasoprazole/ Refractory and Breakthrough CINV

33
Q

What are synthetic THC products approved by the FDA

A

Dronabinol and Nabilone

34
Q

What is the antiemetic backbone

A

Dexamethasone, 5-HT3 antagonist, NK-1 inhibitor

35
Q

What are the HEC drugs

A

cisplatin, carboplatin (AUC greater than or equal to 4), doxorubicin greater than or equal to 60 mg/m2, epirubicin greater than 90 mg/m2, doxorubicin PLUS cyclophosamide, ifosamide greater than 2 grams/m2

36
Q

What are the MEC drugs

A

Carboplatin (AUC greater than carboplatin), oxaplatin, doxorubicin less than 60 mg/m2, danorubicin, cyclophosamide, irinotecan and methotrexate at a high dose

37
Q

T/F: HEC gets a 3-4 antiemetic regimen, MEC gets a 2-3 antiemetic regimen, Low gets one BUT if the patient has any type of Nausea/Vomitting regardless of regimen they get something

A

True

38
Q

For HEC what drugs does the patient get on day 1, days 2-4 (take home meds)

A

5-HT3 therapy PLUS NK-1 inhibitor PLUS Dexamethasone 12 mg/ IF APREPITANT is used day 1 give 80 mg by mouth days 2-3 PLUS dexamethasone 8 mg daily days 2-4 regardless

39
Q

For MEC what drugs does the patient get on day 1, days 2-3

take home meds

A

5HT3 (plonosetron or granisetron preferred) PLUS dexamethsone PLUS MAYBE an NK-1 inhibitor/ Aprepitant 80 mg by mouth days 2-3 if used PLUS dexamethasone 8 mg daily 2-4 regardless

40
Q

What drug is used for a 4 drug regimen, what would it replace

A

Olanzapine, NK-1 antagonists

41
Q

What drugs are given for low emetic risk

A

Dexamethasone 12 mg OR metoclopramide 10-40 mg OR Prochloperazine OR 5-HT3 antagonist (not long acting)

42
Q

What is mucositis, pathophysiology, onset, resolution

A

Red ulcer and lesions that is present in the mucosa of the GI tract due to chemotherapy, initial tissue damage that cause reactive oxygen species that damages tissues causing inflammation and infection, 4-5 days post chemotherapy and 2 to 3 weeks after radiation, 2-4 weeks after chemotherapy

43
Q

Grading for Mucositis

A

Grade 1: Minimal symptoms and normal diet
Grade 2: Symptomatic but can eat and swallow modified diet ( DOES NOT interfere with daily life)
Grade 3: Symptomatic and can take LIQUIDS ONLY
Grade 4: Sympotmatic and NEED TPN/ENTERAL FEEDING

44
Q

What drugs are msot known to cause mucositis

A

Melphalan, Busulfan, high dose methotrexate, doxorubicin, epirubicin, sunitinib

45
Q

What can be given for prevention of mucositis

A

Palifermin

Phar 509 (22 decks)

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