Cancer Tx-Related Tox - N/V Flashcards

1
Q

Most common AEs of chemotx?

A

N/V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How should N/V tx be approached?

A

It should be prevented before it actually happens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What’s acute CINV?

A

occurs ≤ 24h post-chemo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What’s delayed CINV?

A

occurs > 24h post-chemo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What’s anticipatory CINV?

A

Occurs as a conditioned response due to past neg experience BEFORE receiving next tx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What’s breakthrough CINV?

A

Occurs despite N/V prophylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

NTs involved in CINV?

A

5-HT3, Substance P

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does chemotx-induced release of serotonin bring about CINV?

A

It causes release of SEROTONIN in the GIT (peripherally) and via vagus nerve stimulation of the vomiting centre (centrally)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is substance P involved in CINV?

A

It stimulates NK-1 receptors in the CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What type of CINV is usually assoc w/ substance P and its stimulation of NK-1 receptors?

A

Delayed CINV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does EtOH intake affect the CTZ?

A

It makes the CTZ LESS sensitive > less likely to vomit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is a biphasic pattern of emesis?

A

When there’s one early and large episode of acute vomiting, then a second prolonged, less intense peak of vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What’s a monophasic pattern of emesis?

A

When there’s a long interval of moderately intense emesis ~6h post-tx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

4 emetic risk gps:

A

HIGH: risk in > 90% of pts

MOD: risk in 30-90% of pts

LOW: risk in 10-30% of pts

MINIMAL: risk in < 10% of pts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Serotonin receptor (5-HT3) antagonist drugs:

A

ondansetron, granisetron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MOA of 5-HT3 antagonists

A

bind to 5-HT receptors in CTZ and in vagal afferent fibres from the upper GIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is the efficacy of 5HT3 antagonists usually improved?

A

by adding a CS (usually dexamethasone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

AEs of 5-HT3 receptor antagonist

A

h/a, constipation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What kind of emesis is tx’ed by 5-HT3 receptor antagonists?

A

acute CINV

20
Q

Risks assoc w/ higher doses of 5-HT3 receptor antagonists?

A

QT prolongation

21
Q

Preferrend 5-HT3 receptor antagonist?

A

Palonosetron (longer half life, single dose, less concern w/ QT prolongation)

22
Q

MOA of neurokinin-1 (NK-1) receptor antagonists?

A

blocks substance P from binding to NK-1 receptors in the CNS

23
Q

When are neurokinin-1 (NK-1) receptor antagonists given?

A

Day 1 BEFORE chemotx

24
Q

What should be kept in mind when giving neurokinin-1 (NK-1) receptor antagonists with dexamethasone?

A

Dexa dose should be reduced 50% due to CYP interactions (CYP3A4 and CYP 2C9)

25
Q

T or F: The action of neurokinin-1 (NK-1) receptor antagonists is canceled out when given concurrently with 5-HT3 receptor antagonists like ondansetron

A

F

They work synergistically, actually

26
Q

neurokinin-1 (NK-1) receptor antagonists can be used for which types of CINV?

A

Acute and delayed

27
Q

Wrt CINV, CS monotx is used for…

A

low emetogenic chemo

28
Q

Wrt CINV, how are CS’s used for highly emetic and moderately emetic chemo?

A

CS is combined w/ a 5-HT3 receptor antagonist +/- NK1 receptor antagonist or olanzapine

29
Q

What kind of CINV is prophylaxed w/ CSs?

A

acute and delayed CINV

30
Q

MOA of CS for CINV?

A

Not sure (perhaps prostaglandin inhibition plays a role)

31
Q

Steroid of choice for CINV?

A

Dexamethasone

32
Q

How’re dopamine antagonists used in CINV?

A

Mainly for breakthrough CINV

33
Q

Risk of domperidone (dopamine antagonist)?

A

QT prolongation

34
Q

What’s used for preventing anticipatory emesis?

A

benzos

35
Q

T or F: BZDs are not great as antiemetics

A

T

36
Q

Olanzapine MOA in CINV?

A

acts on several receptors: DA, 5-HT3, histamine, ACh, and muscarinic

37
Q

Olanzapine is effective in preventing this.

A

Delayed N (nausea only)

38
Q

How is olanzapine used in high and mod emetogenic chemotx?

A

In combo w/ 5-HT3 receptor antagonist and dexamethasone (+/- NK1 receptor antagonist)

39
Q

dimenhydrinate MOA

A

Histamine antagonist

40
Q

Dimenhydrinate place in tx for CINV?

A

PRN for acute sx ctrl

41
Q

Cannabinoids/medical marijuana place in tx for CINV?

A

Refractory N/V only

42
Q

Efficacy of cannabinoids in CINV?

A

Not v. effective

43
Q

T or F: Immediate antiemetic regimen alteration should take place if breakthrough N/V is occurring

A

F

Must exclude other dz and med-related causes for emesis first

44
Q

When should you refer a CINV pt?

A

prolonged N/V, sig. wt loss, sx’s of dehydration, fever, abdominal pain, blood or “coffee grounds” in vomitus, altered consciousness

45
Q

Non-pharm approaches for CINV

A

eat small, freq meals, bland foods (no spicy or acidic foods), calorie-dense foods, eat foods at rm temp