Cancer Toxicities Flashcards
metabolic causes of N/V
hyperglycemia
hypercalcemia
hypoadernalism
uremia
hyponatremia
anticipatory
learned response from previous emetic reactions
provoked by sight, sound, or smell
acute N/V
within 24 hours of chemo
delayed N/V
after 24 hours
substance P and NK1 binding
breakthrough N/V
N/V despite being treated with anti-emetics before
refractory N/V
N/V that persists despite anti-emetics
failed other therapies
patho of N/V
GI tract is disrupted by chemo
enterochomaffin cells release large stores of serotonin
chemoreceptor trigger zone stimulates vomiting center
input to vomiting center from what sources
higher cortical centers
pharynx
GI tract
wretching is what
labored movement before vomiting
neurotransmitters involved in N/V
dopamine, histamine, acetylcholine, serotonin, substance P
chemo induced N/V most common drug
cisplatin
highly emetogenic percentage and level
> 90% level 5
moderately emetogenic percentages and level
> 30-90% level 3-4
low emetic risk percentage and level
10-30% level 2
minimal emetic risk percentage
<10% level 1
level 1 and 2 effect on emetogenicity
do not effect when combined
when combining with a level 3/4 agent how much do we increase emetogenicity
1 level per drug added
N/V prophylaxis required when
moderate-high emetic risk agents
>30%
CINV risk factors
women
younger
hx motion sick, morning sick, CINV
anxious
what is protective of CINV
chronic alcohol use
highly emetogenic classes that need to be given CINV
5HT3 antagonist
steroid
options for highly emetogenic regimen
4 - NK-1 antagonist, steroid, 5HT3, antipsych
3- dexamethasone, palonosetron, olanzapin
3 - NK-1 antagonist, steroid, 5-HT3 antag
options for moderately emetogenic regimen
3- dexamethasone, palonosetron, olanzapin
3 - NK-1 antagonist, steroid, 5-HT3 antag
2 - steroid and 5HT3 antagonist
low emetogenic regimen and drugs
pick a drug
5HT3 antagonists
dexamethasone
metoclopramide
prochorperazine