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PHRM 864 EXAM 2 > Supportive care > Flashcards

Supportive care Flashcards

1
Q

Potential causes of N/V in cancer patients

A

Therapy related - chemo, radiation, post-surgical
gastrointestinal
neurologic - severe pain, metastases
metabolic - hypercalcemia, hyperglycemia, uremia
Drugs - opioids, anesthetics, ethanol
Psychophysiologic - anxiety, anticipatory N/V

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2
Q

Anticipatory N/V

A

can be provoked by sight, sound, or smell
Non-pharm treatments like hypnosis have shown to be successful

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3
Q

Acute N/V

A

usually withing 24 hours of receiving chemo

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4
Q

Delayed N/V

A

related to chemo occuring after 24 hours following completion of chemotherapy

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5
Q

Breakthrough N/V

A

this is N/V that occurs even if on scheduled anti-emetics prior to chemotherapy
Meaning we know the patients chemo regimen will cause N/V so we give them the proper tx to take before hand and even with that patient experience N/V after recieivng their chemo

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6
Q

Refractory N/V

A

nausea and vomiting that persists despite appropriate anti-emetics

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7
Q

Pathophysiology

A

Chemotherapy induces damage to the epithelial cells lining the GI
Enterochromaffin cells lining the GI tract will release massive emounts of serotonin when exposed to chemo

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8
Q

Progression of N/V

A

nausea –> wretching –> finally emesis

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9
Q

Neurotransmitters implicated in CINV

A

Dopamine
Histamine
Acetylcholine
Serotonin
Substance P

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10
Q

Risk factors for CINV

A

Women are higher risk

younger patients are more at risk
prior history of motion sickness

previous history of morning sickness
previous CINV tend to do worse

anxiety/ high pretreatment anticipatory nausea

Chronic ethanol can be protective

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11
Q

Highly emetogenic regimen A

A

NK-1 antagonist
Dexamethasone - steroid
5-HT3 antagonist - ondansetron (all end in tron)
Olanzapine - atypical antipyschotic

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12
Q

Highly emetogenic regimen B

A

Olanazpine - atypical antipsychotic
Palonestron -5-HT3 antagonis
Dexamethasone - steroid
+/- lorazepam PO or IV
+/- H2 blocker or proton pump inhibitor

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13
Q

Highly emetogenic regimen C

A

Nk-1 antagonist
Dexamethasone
ondansetron - 5-HT3 antagonist

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14
Q

Moderately emetogenic regimen A

A

dexamethasone
Ondansetrone
+/- lorazepam PO or IV
+/- H2 blocker or proton pump inhibitor

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15
Q

Moderately emetogenic regimen B

A

Olanzapine
Palonosetron
Dexamethasone
+/- lorazepam PO or IV
+/- H2 blocker or proton pump inhibitor

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16
Q

Moderately emetogenic regimen C

A

NK-1 antagonist
dexamethasone
Ondansetron - 5-HT3 antagonist

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17
Q

Low emetogenic regimens

A

Pick any of the following agents. Only 1 needed
Dexamethasone, metoclopramide, prochlorprerazine
5HT3 antagonist - ondansetron, dolasetron, granisetron
+/- lorazepam PO or IV
+/- H2 blocker or proton pump inhibitor

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18
Q

Breakthrough Nausea and vomiting treatment

A

dopamine receptor antagonists - haloperidol, metoclopramide
Phenothiazines - Prochloperazine, promethazine
Antipsychotic - olanzapine
Depending on the severity of the nausea/vomiting, you can schedule these agents

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19
Q

Delayed N/V treatment

A

Typically involves use of one of the
following:
Dexamethasone
NK-1 antagonist
Olanzapine

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20
Q

Anticipatory N/V treatment

A

preventative care, behavioral treatment- yoga, relaxation exercises, music therapy
Acupuncture/ acupressure, lorazepam

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21
Q

other prevention guidelines

A

Hight to moderate emetogenic risk
- start before chemotherapy and continue daily
- 5-HT3 antagonists

Low to minimal emetogenic risk
- start before chemotherapy and maybe given daily as needed
- Metoclopramide, prochlorperazine, 5HT3 antagonists

Radiation induced emesis
- radiation therapy to the upper abdomen/ localized sites
-total body irradiation
- start pretreatment for each day of radiation therapy
- granisetron PO +/- dexamehtasone
- ondansetron PO +/- dexamethasone

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22
Q

Common toxicities for 5-HT3 antagonists

A

Headaches, asyptomatic and transient EKG changes (max doses), constipation, increased transaminases

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23
Q

Common toxicities for Corticosteroids

A

Short term use: anxiety, euphoria, insomnia, hyperglycemia, increased appetite

24
Q

Common toxicities for Substance P antagonists

A

hiccups, worry about drug interactions

25
Q

Common toxicities for Dopamine antagonists

A

Extrapyramidal side effects, diarrhea, sedation

26
Q

Common toxicities for olanzapine

A

Dystonic reation, sedation

27
Q

Common toxicities for Phenothiazines (prochlorperazine, promethazine)

A

Sedation, akathesia, dystonia, IV promethazine = tissue damage

28
Q

Common toxicities for Cannibanoids (dronabinol)

A

Drowsiness, dizziness, euphoria, mood changes, hallucinations, increased appetite

29
Q

Common toxicities for benzodiazepines (lorazepam)

A

Sedation, hypotension, urinary incontinence, hallucinations

30
Q

Common toxicities for Anticholinergic (scopolamine patch)

A

cant see, cant hear, cant spit, cant shit, cant piss

31
Q

Important Principles for
Prevention and Management

A

emetogenicity is additive so if a patient is on two agents that are each moderately ematogenic that makes it a highly emetogenic regimen

anti-emetics should be tailored accordingly for patients on multiple day chemotherapeies do to different emetogenic levels (higher on day one and moderate on day 2 and 3)

anti-emetics are more effective when given 5 to 30 minutes prior to chemotherapy

32
Q

Pathopysiology of Mucositis

A

The pathopysiology is still missunderstood but can be described as initiation, upregulation with generation of messengers, ulceration, healing
May range from mild inflamation to bleeding ulceration
can affect the entire GI tract from mouth all the way down

33
Q

risk factors associated with mucositis

A

pre-existing oral lesions, poor dental hygiene or ill fitting dentures, combined modality treatment (chemo and radiation)

34
Q

Prevention and treatment for mucositis

A

avoid foods that are spicy, salty, and/ or acidic fruit
mainly eating soft liquid foods soft cheese, eggs, purees, custards
avoid smoking and alcohol

35
Q

General mouth care recommendations for mucositis

A

pre treatment dental screening, especially in patients receiving radiation therapy to the oral mucosa or those receiving high dose chemotherapy
Baking soda rinses - twice - four times daily
soft bristle toothbrush
saliva substitue for radiation induced xerostomia

36
Q

Pain management for mucositis

A

Topical anesthetics - lidocaine in them
sucking on ice cubes during treatment
sucralfate - forms a protective barrier
oral and parenteral opioid analgesics - Patient controlled analgesia pump is common

37
Q

Neutropenia backround

A
  • white blood cells normal range 4.8-10.8 x 10^3/ul
    Decreased WBC = neutropenia <0.5 x 10^3/ul
    bone marrow suppression is the most common dose limiting toxicity of chemotherapy
    Nadir is known as the lowest neutrophil cound or ANC and is used to describe the lowest level the blood count falls to during a cycle of chemotherapy
    usually drop happens 10-14 days into chemo and will return to normal after 3 to 4 weeks after chemo
38
Q

ANC count calculation and guidelines neutropenia

A

ANC = WBC x % granulocytes (neutrophils + bands)
- patients counts should always be assessed before chemo administration
WBC > 3 x 10^3/ul or ANC of > 1.5x10^3/ul AND platelet count greater than or equal to 100 x 10^3/ul

39
Q

Severe Neutropenia ANC count

A

< 0.5 x 10^3/ul

40
Q

Febrile neutropenia ANC count and temp

A

ANC < 0.5 x 10^3/ul and a single oral temperature > 101 degrees F or greater than or equal to 100.4 degrees F for at LEAST an hour

41
Q

Guidelines primary prohylaxis and secondary prohylaxis for neutropenia

A

PRIMARY
- if pt is on regimen that is excpected to cause greater than or equal to 20% incidence of febrile neutropenia
High risk pts are defined as: preexcisting neutropenia due to disease, extensive prior chemotherapy, previous irradiation to the pelvis or any area with large amount of bone marrow

Secondary
- when a patient that has had previous neutropenia troubles on a previous cycle and now we want to prevent that again
use a CSF preventively with next cycle of chemotherapy

42
Q

Treatment for neutropenic fever

A

Filgrastim G-CSF - regulats production and function of neutrophil cell lines, dont abrublty D/C as can see rapid drop in neutrophil count if you do

Pegfilgrastim (Neulasta) - Has a non-linera pharmacokinestics and clearence - the drug is removed more rapidly with patients who have increasing neutrophil count

Sargamostim GM-CSF - effects phagocytic accessory cells, dont abruptly D/C as it will cause rapid drop in WBC and Neutrophils

43
Q

Filgrastim dosing and AEs

A

5mcg/kg/day
- start up to 3-4 days after completion of chemotherapy and continue until post nadir ANC recovery to normal or near normal levels
AEs - flu like symptoms, bone and joint pain, DVT

44
Q

Pegfilgrastim dosing and AEs

A

6mg SQ x 1 dose (has onpro body injector to iliminate the need for patients to come back for doing after first day of chemo)
- start at least 24 hours after chemotherapy and can be given up to 3-4 days after chemotherapy (14 day inbetween cycle)
AEs - flu like symptoms, bone and joint pain, DVT

45
Q

Thrombocytopenia definition and platelet count

A

usually defined as platelet count < 100 x 10^3/ul, however increased risk of bleeding occurs when platelet count is less than or equal to 20 x 10^3/ul may require transfusion
- transfusions usually will not occur unless patient is symptomatic (ecchymosis, petechiae, hemoptysis, hematemesis)

46
Q

thrombocytopemia treatment

A

Blood transfusion
usually 40-50 x 10^3 ul for major invasive procedures
or
greater than 20 x 10^3/ul for other minor procedures

47
Q

causes of Anemia and why its significant in cancer

A

Decreased red blood cell production, decreased erythropoietin production, decreased body stores of vitamin B12, iron, or folic acid, blood loss
low hemoglobin levels have been correlated with poor performance status which has been correlated with decreased survival

48
Q

Chemotherapy induced anemia

A

patient with Hgb less than or equal to 11 g/dL or greater than or equal to 2g/dL drop from baseline should undergo a workup

49
Q

Chemotherapy induced anemia treatment

A

assess patients symptoms, institutional guidelines, published guidelines and give transfusion if indicated

consider ESA treatment if the patients is untreatable in the long run, patients without other identifiable causes, cancer and chronic kidney disease

50
Q

ESA - Epoetin alfa

A

Dose should be adjusted to maintain the lowest Hgb level

51
Q

ESA - Darbepoetin (Aranesp)

A

stimulated erythropoiesis
indicated for anemia in patient with non-myeloid malignancies where anemia is caused by chemotherapy

52
Q

Iron in anemic cancer patients with ESA

A

All patients with ESA treatment should have baseline iron studies performed
if patient is iron deficient a work up should be done
LMW iron dextran - first choice IV infusion
Iron sucrose (venofer) - IV injection and infusion
Ferric gluconate - IV injection and infusion

53
Q

Acute type I chemotherapy related cardiac dysfunction

A
  • Occurs immediately after a single dose or course
    of therapy with an anthracycline
  • Uncommon and transient
  • May involve abnormal ECG findings, including
    QT-interval prolongation, ST-T wave changes,
    and arrhythmias
  • Rarely, congestive heart failure (CHF) and/or
    pericarditis are observed
  • Not related to cumulative dose and is uncommon
54
Q

Chronic type I chemotherapy related cardiac dysfunction

A
  • Onset usually within a year of receiving
    anthracycline therapy
  • Rapid onset and progression
  • Common and life threatening
  • Related to cumulative dose patient received
  • Symptoms include tachycardia, tachypnea,
    exercise intolerance, pulmonary and venous
    congestion, ventricular dilatation, poor perfusion,
    and pleural effusion
55
Q

Late-onset type I chemotherapy related cardiac dysfunction

A
  • Develops several years or even decades after
    therapy
  • Manifests as ventricular dysfunction, CHF,
    conduction disturbances, and arrhythmias
  • Occurs more often in childhood / adolescence
    cancer survivors who received anthracyclines
56
Q

Type II Chemotherapy Related
Cardiac Dysfunction

A

Trastuzumab
– Does note appear to be dose related or occur
in all patients
– Ranges widely in severity
– Has not been associated with cardiac damage
– Mechanism involves EGFR pathway which
normally blunts the effects of stress signaling
pathways (a stunning effect) that are required
to maintain cardiac function, structure, and
contractility

57
Q

Type II Chemotherapy Related
Cardiac Dysfunction

A
  • Trastuzumab
    – Appears to be largely reversible and short lived
    – Incidence is ~ 3% in non-anthracycline treated
    patients and increases to 5% in those who have
    received previous anthracyclines
    – If trastuzumab is given concurrently with
    anthracycline, the incidence can increase up to
    27% cardiac toxicity (NYHA class III/IV)

PHRM 864 EXAM 2 (9 decks)

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