Cancer-induced N/V (CINV) EXAM 2 Flashcards
What are the factors that determine the likelihood of N/V?
-specific drugs are more likely to cause emeses (Cisplatin)
-dose
-if you use multiple drugs
-IVP or CI
Which moderate emetic risk drugs are known to have a high risk for Emesis when given together?
Anthracycline + Cyclophosphamide combination
not true for every combination
What is the emetic risk for most monoclonal antibodies used in cancer treatment?
low or minimal emergetic
What is the definition of acute emesis?
within 24h (peak = 4-6h)
What is the definition of delayed emesis?
after 1-5 days (peaks 2-3d)
caused by
-Cisplatin
-Carboplatin
-Oxoplatin
-Cyclophosphamide
-Ifosfamide
-doxorubicin (also other anthracyclines, daunorubicin etc.)
What is the best way to treat Anticipatory emesis?
anxiolytics
-bc they had poor anti-emetic control at the first time, now the anxiety causes the nausea
What is breakthrough emesis?
emesis despite optimal CINV prophylaxis
-> need to add Mr drugs
Risk factors for CINV
prior emetic control
-anxiety, depression
-women > men
-children> adults
-EtOH abuse are less likely to have CINV
What is the pathophysiology of vomiting induced by chemotherapy?
-peripheral release of 5-HT3 and NK-1
-stimulation of 5-HT3 and NK-1 receptors in the brain (CTZ and brain stem)
-autonomic response -> Vomiting
Which cells in the GI release 5-HT3 during cancer treatment?
enterochromaffin cells
What is the primary mediator in acute CINV?
-Serotonin
-also NK-1
Blocking serotonin helps with acute N/B but not delayed vomiting
Which mediator is improtant for delayed vomiting in cancer therapy?
NK-1
also works for acute emesis
What are the common 5-HT3 and NK-1 antagonists used for CINV?
5-HT3 antagonist: Ondansetron
NK-1 antagonist: Aprepitant
What are the main antiemetic drugs?
-Corticosteroids
-5HT3 antagonists
-Dopamine antagonists
-Olanzapine (D2 antagonist and serotonin antagonist)
-NK-1 inhibitors
What is a common side effect of 5-HT3 antagonists?
-headache
-ECG changes (QT prolongation) higher risk with > 8 mg given IVP
for 8 mg we give continuous infusion over 15 min
-no QTc with Palonosetron
Where in the body do 5-HT3 antagonists work?
-Peripheral (GI): blocking 5-HT3 release from enterochromaffin cells
-central (brain): blocking 5-HT3 receptors in the medulla
How is Ondansetron metabolized?
CYP 2D6
will not work well with ultra metabolizer -> change to Palonosetron (Aloxi)
What is the brand name of Ondanstron?
Zofran