E2 Supp Care I Flashcards
what are the 5 types of N/V?
Anticipatory
Acute
Delayed
Breakthrough
Refractory
Type of N/V that is considered a “learned response” and has had hypnosis be successful (lol)
Anticipatory
Type of N/V that usually occurs within 24 hours of receiving chemo
acute
type of N/V occuring >24 hours after chemo
delayed
type of N/V that occurs even if on scheduled anti-emetics prior to chemo
Breakthrough
Type of N/V that persists after failing other therapies
refractory
what does the chemo trigger zone (CTC) stimulate?
the vomiting center (located in nucleus tractus solitarii)
Nausea -> followed by _________ -> finally emesis
wretching
what is wretching
labored movement of abdominal and thoracic muscles before puking
5 neurotransmitters implicated in CINV
dopamine
histamine
ach
serotonin
substance p
she said the last two were the important ones for us tho
T or F
Level 1 and 2 agents do not contribute to the emetogenicity of the regimen
True
T or F:
younger patients are a bigger risk factor for CINV than old asses
true somehow
what can be protective for CINV?
chronic ethanol loll
what is prophylaxis for acute N/V based on?
emetogenic potential of chemotherapy
How many different drug classes do we use when pt is classified as highly emetogenic (regimen A). what are they?
- NK-1 antagonist
Steroid
5-HT3 antagonist
Atypical Antipsychotics
what do the NK-1 antagonists end with?
-repitant
what is the steroid used for emetogenic pts
dexamethasone
what 2 classes do we ALWAYS use in emetogenic regimens? (unsure if this is specifically highly or not at the time of making this card)
5-HT3 antag and steroid
what do the 5-HT3 antags end with>
-setron
what atypical antipsychotic do we use for emetogenic shit
olanzapine
what random ass drug can be added on to highly emetogenic regimen B and C?
lorazepam
what is the moderately emetogenic regimen A? (classes)
steroid and 5-HT3 antag
what is the moderately emetogenic regimen B? (classes)
5-HT3 antag and a steroid
what is the moderately emetogenic regimen C? (classes)
NK-1 antag
steroid
5-HT3 antag
T or F
Low emetogenic regimens require choosing both drug class options
false, only one needed between steroid and 5-HT3 antag
name some of the classes included in breakthrough N/V regimen (theres a lot)
dopamine receptor antag
phenothiazines
antipsychotic
benzo
cannabinoid
serotonin agonist
steroids
anticholinergics
delayed N/V typically involves use of one of the following:
________
________
________
dexamethasone
NK-1 antag
Olanzapine
4 actions for anticipatory NV
prevention
behavioral
acupuncture
lorazepam
prevention guidelines for high to moderate emetogenic risk with oral chemo
5-Ht3 antag before chemo and continue daily
prevention guidelines for low to minimal emetogenic risk with oral chemo (3)
metoclopramide
prochlorperazine
5-HT3 antag
prevention guidelines for radiation induced emesis
5-HT3 antag po with or without dexa
are the common toxicities across classes that important for us to know?
please someone let me know
T or F:
emetogenicity is additive
true, adding two agents can make it worse
when are anti-emetics most effective? (not a time)
when given for prophylaxis
T or F
GI mucosa is comprised of epithelial cells and has a slow turnover rate
false, rapid turnover rate
4 things that can be used as pain management for chemo induced mucositis
topical anesthetics
oral cryotherapy
sucralfate
opioids
what weird thing can you do before receiving 5-FU to decrease mucositis incidence and severity
ice chips 30 min before
what is the most common dose-limiting toxicity of chemo?
neutropenia
what is the nadir?
(absolute neutrophil count or ANC) is the lowest value the blood counts fall to during a cycle of chemo
someone tell me what to know from slide 54
please
what kind of neutropenia is this?
ANC < 0.5 x 103/µL
severe
what kind of neutropenia is this?
ANC < 0.5 x 103/µL and a single oral temperature > 101F (> 38.3C) or > 100.4F (> 38.0C) for at
least an hour
febrile
If the patient is to receive a chemotherapy regimen that is expected to cause > 20% incidence of febrile neutropenia
A. Primary prophylaxis
B. Secondary prophylaxis
A. primary
The patient experienced a neutropenic complication from a previous cycle of chemotherapy and now you want to prevent that again
A. Primary prophylaxis
B. Secondary prophylaxis
B. secondary
4 things colony stimulating factors decrease for prophylactic use
- incidence of febrile neutropenia
- length of hospitalization
- confirmed infections
- duration of antibiotics
what are the 3 CSF agents we have on the slides?
Filgrastim G-CSF
Pegfilgrastim
Sargramostim GM-CSF
Has non-linear PK and clearance
A. Filgrastim G-CSF
B. Pegfilgrastim
C. Sargramostim GM-CSF
B
Drop in WBC and neutrophil count after discontinuation
A. Filgrastim G-CSF
B. Pegfilgrastim
C. Sargramostim GM-CSF
A and C
Not considered a biosimilar
A. Tbo-Filgrastim (Granix)
B. Filgrastim-sndz (Zarxio)
C. Filgrastim-aafi (Nivestym)
D. Filgrastim-ayow (Releuko)
A
how long after completion of chemo do you start Filgrastim?
3-4 days and continue until post-nadir ANC is normal
how long after chemo do you start pegfilgrastim? also a unique thing too
at least 24 hours after chemo and give up to 3-4 days after.
at least 14 days should elapse between dose and the next cycle of chemo
3 adverse effects with. filgrastim
flu like sxs
bone + joint pain
DVT
what can the adverse effect of bone+musculoskeletal pain from CSF be attributed to?
rapid proliferation of bone marrow myeloid cells
what are 3 agents we can use for bone/musculoskeletal pain from CSFs
acetaminophen
non opioids
loratidine? weird and niche
what organ is affected in a rare adverse effect from CSF?
spleen
Usually defined as a platelet count
< 100 x 10^3/µL
thrombocytopenia
ASCO guideline recommends a threshold for platelet transfusion of 10 x 103/µL
thrombocytopenia
think of the number 10 i guess
4 general causes of anemia
decreased RBC prod
decreased erythropoietin prod
decreased b12, iron, folic
blood loss
Chemotherapy Induced Anemia:
Patients with a Hgb ≤ __ g/dL or ≥ __ g/dL drop
from baseline should undergo a work-up
11, 2
what is ESA?
erythropoietic stimulating agents
T or F:
ESAs increase risk of death, MI, stroke, VTE, make cancer worse, cause CKD, and something about perisurgery
true lol
ESAs are not recommended:
- In patients receiving ___________ ____________with curative intent
- In patients with cancer not receiving __________
- In patients receiving non-myelosuppressive chemo
- myelosuppressive chemotherapy
- chemotherapy
epoetin alfa:
_________ which stimulates RBC production
glycoprotein
Epoetin alfa:
stimulates _______ and ________ of committed erythroid progenitors in the bone marrow
division
differentiation
Epoetin:
Produced in the _______
kidney
Epoetin alfa:
________ production regulated by level of tissue oxygenation
endogenous
Darbepoetin:
stimulates erythropoiesis by binding to the ______ receptor like erythropoietin
epoetin
Darbepoetin:
Biochemically distinct from epoetin alfa by the addition of a _______ _______ -> prolonged half life (2 - 3 x longer than epoetin)
sialic acid
Darbepoetin:
indications ->
- anemia in patients with _________ ____________ where anemia is caused by chem o
non-myeloid malignancies
All oncology patients who are prescribed ESA therapy should have baseline _________ _________ performed
iron studies
Chemo toxicities:
tx for myalgias/arthralgias (2)
Nsaids
pt may need opioids
Chemo toxicities:
tx of hemorrhagic cystitis (2)
hydration
mesna
Chemo toxicities:
tx of heart failure (3) (1 is a med other 2 are not)
monitor cumulative dose
assess for risk factors
dexrazoxane
Chemo toxicities:
tx of Peripheral neuropathy (2) (1 med 1 not)
Change infusion rates (paclitaxel specific)
Adjunct pain meds (gabapentin/amitryptiline)
Chemo toxicities:
tx of pulmonary toxicity
(1)
corticosteroids (no good tx once it happens really)
Type I Chemotherapy Related Cardiac Dysfunction:
Occurs immediately after a single dose or course of therapy with an anthracycline
A. Acute
B. Chronic
C. Delayed
A
Type I Chemotherapy Related Cardiac Dysfunction:
Uncommon and transient
A. Acute
B. Chronic
C. Delayed
A
Type I Chemotherapy Related Cardiac Dysfunction:
May involve abnormal ECG findings, including QT-interval prolongation, ST-T wave changes, and arrhythmias
A. Acute
B. Chronic
C. Delayed
A
Type I Chemotherapy Related Cardiac Dysfunction:
Onset usually within a year of receiving anthracycline therapy
A. Acute
B. Chronic
C. Delayed
B
Type I Chemotherapy Related Cardiac Dysfunction:
- Rapid onset and progression
- Common and life threatening
A. Acute
B. Chronic
C. Delayed
B
Type I Chemotherapy Related Cardiac Dysfunction:
Symptoms include tachycardia, tachypnea, exercise intolerance, pulmonary and venous congestion, ventricular dilatation, poor perfusion, and pleural effusion
A. Acute
B. Chronic
C. Delayed
B
Type I Chemotherapy Related Cardiac Dysfunction:
Manifests as ventricular dysfunction, CHF, conduction disturbances, and arrhythmias
A. Acute
B. Chronic
C. Delayed
C
Type I Chemotherapy Related Cardiac Dysfunction:
Occurs more often in childhood / adolescence cancer survivors who received anthracyclines
A. Acute
B. Chronic
C. Delayed
C
Type II Chemotherapy Related Cardiac Dysfunction:
appears to be largely reversible and short-lived
trastuzumab