Cancer Tx-Related Tox - N/V Flashcards
Most common AEs of chemotx?
N/V
How should N/V tx be approached?
It should be prevented before it actually happens
What’s acute CINV?
occurs ≤ 24h post-chemo
What’s delayed CINV?
occurs > 24h post-chemo
What’s anticipatory CINV?
Occurs as a conditioned response due to past neg experience BEFORE receiving next tx
What’s breakthrough CINV?
Occurs despite N/V prophylaxis
NTs involved in CINV?
5-HT3, Substance P
How does chemotx-induced release of serotonin bring about CINV?
It causes release of SEROTONIN in the GIT (peripherally) and via vagus nerve stimulation of the vomiting centre (centrally)
How is substance P involved in CINV?
It stimulates NK-1 receptors in the CNS
What type of CINV is usually assoc w/ substance P and its stimulation of NK-1 receptors?
Delayed CINV
How does EtOH intake affect the CTZ?
It makes the CTZ LESS sensitive > less likely to vomit
What is a biphasic pattern of emesis?
When there’s one early and large episode of acute vomiting, then a second prolonged, less intense peak of vomiting
What’s a monophasic pattern of emesis?
When there’s a long interval of moderately intense emesis ~6h post-tx
4 emetic risk gps:
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
Serotonin receptor (5-HT3) antagonist drugs:
ondansetron, granisetron
MOA of 5-HT3 antagonists
bind to 5-HT receptors in CTZ and in vagal afferent fibres from the upper GIT
How is the efficacy of 5HT3 antagonists usually improved?
by adding a CS (usually dexamethasone)
AEs of 5-HT3 receptor antagonist
h/a, constipation