Supportive Care Flashcards
CINV
increases morbidity
negatively effects patients QOL
non-adherence to chemo +/- dose reductions
weakness, dehydration, electrolyte imbalance, esophageal tears, decline in behavioral & mental status
acute CINV
occurring within first 24 hours
delayed CINV
24 hours to several days (2-5 days) after chemo
breakthrough CINV
occurs despite prophylactic treatment
anticipatory CINV
before treatment as a conditioned response to the occurrence in previous cycles
refractory CINV
recurring in subsequent cycles of therapy, excluding anticipatory CINV
peripheral emetic response pathway
5HT3 mediated
originates in GI tract
activated in first 24 hours after chemo
associated with acute emesis
central emetic response pathway
NK1 receptor mediated
primarily in the brain
involved in delayed CINV
general principles of emesis control
prevention!
choosing antiemetic agents: emetic risk, prior experience with antiemetics, patient factors
prophylaxis based on agent with the highest emetogenic risk
lifestyle management: smaller more frequent meals, healthier meals, room temperature food
risk factors of CINV
<50 yo
emesis during pregnancy
history of CINV, prone to motion sickness
female sex
little/no previous alcohol use
anxiety/ high pretreatment expectations of nausea
high IV emetogenic potential
AC ( anthracycline + cyclophosphamide)
carboplatin >4
Carmustine
Cisplatin
Cyclophosphamide
Dacarbazine
Doxorubicin
Epirubicin
Fam-trastuzumab deruxtecan
Ifosfamide
Mechlorethamine
Melphalan
Sacituzumab
Streotozocin
oral agents prophylaxis required on days of chemo admin
azacitidine
busulfan
certinib
cyclophosphamide
fedratinib
lomustine
midostaurin
mitotane
selinexor
temozolomide
breakthrough emesis treatment
add one agent from a different drug class
consider routine admin vs PRN
antacid therapy if patient has dyspepsia
*olanzapine, lorazepam, dronabinol, 5HT3 RA, prochloperazine, dexamethasone, metoclopramide, scopolamine
anticipatory emesis treatment
prevention!
avoid strong smells
Lorazepam useful
acupuncture
behavioral therapy: guided imagery, relaxation, hypnosis, cognitive distraction, yoga, biofeedback, progressive muscle relaxation,
Dexamethasone
MOA unknown
ADEs:
Insomnia- admin in morning
dyspepsia: take with food, consider H2 antagonist or PPI
Hyperglycemia
Hypertension
5HT3 RA (ondansetron, palonosetron, granisetron)
MOA: blocks serotonin peripherally (GI tract) on vagal nerve terminals and centrally in the chemoreceptor trigger zone (medulla)
1st gen: ondansetron, granisetron
-most effective for acute
-short acting
2nd gen: palonosetron
-effective in acute & delayed
-long acting
ADES:
headache
constipation
QTc prolongation
NK1 RA (aprepitant, fosaprepitant, rolapitant, fosnetupitant/palonestron, netupitant/ palonestron)
MOA: inhibits the substance P/ neurokinin 1
-augments 5HT3 & dexamethasone antiemetic activity
Only for prevention not treatment
-most useful delayed CINV
Drug interactions (except rolapitant)
-inhibition of CYP3A4 and CYP2C9 (decrease dexamethasone dose on days 2-4)
ADEs: fatigue, GI upset, headache, hiccups
Rolapitant has extended half life should not admin <2 wk intervals
Olanzapine
MOA: blocks dopamine, 5HT3, muscarinic and histamine receptors
Useful in prevention and breakthrough
ADES;
sedation: admin at bedtime, consider low dose for elderly
Hyperglycemia
Fatigue
QTc prolongation
Dopamine antagonists (prochlorperazine, metoclopramide, promethazine)
MOA: antagonize dopamine in the chemoreceptor trigger zone
Breakthrough CINV
Prochlorperazine, Promethazine
-phenothiazines
-drowsiness
-constipation
Metoclopramide
-benzamines
-drowsiness
-diarrhea
-QTc prolongation
-tardive dyskinesia (avoid >12wks)
Benzodiazepines (lorazepam)
MOA: anxiolytic
Useful for anticipatory or breakthrough with anxiety component
ADMIN either night before, morning of or both
ADES;
sedation
dizziness
Cannabinoids
MOA: CB1 agonism suppresses vomiting
indirect activation of 5HT1a in raphe nucleus
Only for refractory disease
ADEs: sedation, euphoria, hallucinations, palpitations, flushing, cough