Therapeutics V Exam 2- Supportive Care Ii

Front 1

significance of infection when undergoing chemo

Back 1

Infection is a major cause of morbidity & mortality

Front 2

Fever during neutropenia may be the only sign of

Back 2

severe underlying infection- other signs of infection that normal people get might not happen because your wbc are fucked

Front 3

common sites for infection

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Areas of impaired or damaged host defenses are common sites of infection (mouth...and shit)

Front 4

high risk patients for febrile neutropenia (4)

Back 4

Prolonged (>7 days) & profound neutropenia (ANC <100 cells/mm3 post-chemo)

AND/OR

Clinically unstable (fucked up vitals)
Significant medical co-morbid conditions- contributing to current illness

requires hospitalization (REQUIRES not...just got admitted)

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Significant medical co-morbid conditions- contributing to current illness (4)

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Hypotension
Pneumonia,
New-onset abdominal pain,
Neurologic changes (altered mental status- old people-->get urine sample. wtf)

Front 6

low risk patients for febrile neutropenia (2)

candidates for what type of treatment

Back 6

Anticipated brief (<7 days duration) neutropenic periods
No or few co-morbidities
Candidates for oral empirical therapy in outpatient setting

Front 7

most important bacteria you want to kill for febrile neutropenia

why?

Back 7

pseudomonas!!!!!
gram (-) kills you faster than gram (+), even though gram (+) more common

Front 8

4 IV abx you want to give for high risk febrile neutropenia pt (IMPORTANT)

Back 8

cefapime
carbapenem (mirapenem)
ceftazidime
piperacillin/tazobactam (zosyn)

Front 9

do not take what for febrile neutropenia

Back 9

don't take stupid otc for fever

Front 10

drugs for febrile neutropenia low risk pt (2)

Back 10

oral cipro + augmentin (amox/clav)

Front 11

when to throw in the vanc for febril neutropenia

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don't use vanc until gram + suspected as causing issue, or soft tissue infection

Front 12

granulocyte colony stimulating factor moa (2)

Back 12

stimulates production, maturation, and activation of neutrophils

also activates neutrophils to increase migration and cytotoxicity

Front 13

pegfilgrastim vs. filgrastim
class of drug

Back 13

pegfilgrastim dosed once?? like...just once SQ after chemo i think

G-CSF

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macrophage colony stimulating factor (GM-CSF)

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stimulates proliferation, differentiation, and functional activity of neutrophils, eosinophils, monocytes & macrophages

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GM-CSF

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sargramostim

Front 16

Palifermin (Kepivance): what is it

used for what

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keratinocyte growth factor

for mucositis

Front 17

preferred route of admin for growth factors

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Subcutaneous administration is preferred route for G-CSF, ESA and Oprelvekin

Front 18

Reserve primary administration for

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pts with expected incidence (from literature regarding their chemo) of febrile neutropenia ≥ 20%

rare so usually just give chemo once then see what happens

Front 19

Avoid primary admin of growth factors in patients...

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receiving chemo & radiotherapy (like…together)

Front 20

Consider dose reduction in lieu of CSFs when? (2)

Back 20

after neutropenic fever or severe or prolonged neutropenia after the previous cycle of treatment (usually not if curative intent though)

Front 21

clinical factors predispose to increased complications from prolonged neutropenia (7)

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patient age greater than 65 years
poor performance status and/or nutritional status
previous episodes of FN
extensive prior treatment including large radiation ports or administration of combined chemoradiotherapy (fried out marrow)
cytopenias due to bone marrow involvement by tumor
presence of open wounds or active infections
more advanced cancer, as well as other serious comorbidities

Front 22

growth factor use in hospitalized pt with febrile neutropenia- use?

Back 22

Not routinely used as adjunctive treatment with antibiotic therapy for patients with fever and neutropenia

DONT USE IT IN THE HOSPITAL I GUESS JUST FOR SECONDARY PPX OF WHATEVER

Front 23

filgrastim- when to give

give until when

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Given 24 to 72 hours after chemotherapy & continued until reaching an absolute neutrophil count (ANC) of 2000 – 3000

Front 24

3 AE of filgrastim

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Bone pain (histamine mediated marrow swelling), pain at site of injection, fever or “flu-like” symptoms

Front 25

2 drugs that may help for filgrastim bone pain (anecdotal)

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NSAIDs & antihistamines have been used to decrease bone pain but have not been formally evaluated

Front 26

pegfilgrastim- not used for what

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mobilization of stem cells shit

Front 27

Fixed dose of pegfilgrastim should not be used in

Back 27

infants, children, and adolescents less than 45 kg

Front 28

sargramostim- used for what? not used for what?

Back 28

Usually used in BMT for stem cell mobilization, shorten time to neutrophil recovery, or myeloid reconstruction/marrow engraftment , not used really for febrile neutropenia ppx

Front 29

ESA used for whome?

DO NOT USE with what type of chemo?

Back 29

used for pt where intent of chemo is palliative. DO NOT USE if trying to cure or induce CR because ESAs can fuck up those people by helping with angiogenesis

Front 30

if you're using ESA you have to enroll in what?

Back 30

if you're using ESA you have to use REMS program

Front 31

palfermin- used for what? what is it?

Back 31

Synthetic version of keratinocyte growth factor aimed at decreasing horrible mucositis (prevention) (not used THAT much)

Front 32

why is prevention of mucositis important?

Back 32

in areas like the mouth mucositis can increase infective risk and that can spread to rest of body

Front 33

3 AE of palfermin

Back 33

skin toxicity (rash, edema, purities), oral toxicities (taste alterations), and pain

Front 34

EGFR-I “Rash”- pathophys
is it acne

Back 34

EGFR inhibition interferes with normal skin tissue function causing inflammation

NOT ACNE, but often called acneiform

Front 35

EGFR-inhibitor rash- most commonly affected areas (2 main ones)

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More commonly affected areas include nose, nasolabial folds, cheeks, chin & forehead (“T-zone”); upper chest and/or back

Front 36

EGFR inhibitor rash- dose dependency, what increases severity??

usually occurs when and peaks when

Back 36

Dose dependent, increased severity w/antibodies
Usually occurs within 7 – 10 days, peaks in 2 weeks

Front 37

non pharm options for EGFR inhibitor rash (2)

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MOISTURIZE! MOISTURIZE! MOISTURIZE!
Gentle cleansers, creams, low fragrance/alcohol
Minimize sun exposure & use sunscreen

Front 38

ppx for EGFR inhibitor rash (3)

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Begin prophylaxis with doxycycline 100 mg daily or minocycline 100 mg BID & low – potency topical steroid BID for first 6 weeks

Front 39

other options for EGFR inhibitor rash ppx (4)

Back 39

can also try retinoids, topical abx, oral steroids or dose reduction of chemo

Front 40

onset of hand/foot syndrome with traditional agents vs. tyrosine kinase inhibitors

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usu. develop from 2 – 12 days after starting traditional agents & 2 – 4 wks for multikinase inhibitors

Front 41

3 things in the pathophys of mucositis that are causing the dmg

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Process in which chemical cell damage, proinflammatory cytokines, and bacteria lead to mucosal cell damage & eventually ulceration

Front 42

mucositis 3 locations

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labial, buccal and soft‐palate mucosa; the floor of the mouth; & the ventral aspect of the tongue

Front 43

stepwise progression of mucositis (3)

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Asymptomatic erythema at 0 – 5 days post
Desquamation with white patches at 0 – 7 days post
Contiguous pseudomembranes at 6 – 12 days post

Front 44

mucositis- duration of therapy and effect on dmg

Back 44

Continuous infusions worse than short IV infusions (bolus better)

Front 45

4 non pharm for mucositis prevention/management

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Regular, systematic oral care hygiene, including brushing with a soft toothbrush, flossing, bland rinses, and moisturizers as part of a standardized oral protocol
Dental assessment & treatment prior to start of therapy for all patients, especially head & neck cancer patients
Avoid rough food, spices, salt and acidic fruit; avoid smoking and alcohol
Ice chips 30 minutes prior to therapy

Front 46

2 drugs used for mucositis

Back 46

Palifermin for patients receiving high‐dose chemo & total body irradiation followed by stem cell transplant
Around-the-clock pain management is a must

Front 47

2 causes of pathophys of hot flashes (affects men and women)

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Possibly due to dysfunction in the central thermoregulatory set point in hypothalamus as a result of decreased estrogen or gonadal steroid levels
Serotonin might also have an important role in thermoregulation

Front 48

using HRT to treat hot flashes

Back 48

dumb...if you have cancer that is based on hormones

Front 49

professor's rec for treating hot flashes (2 main drugs to use, which one preferred best)

why not use the other stuff?

Back 49

venlafaxine
then gabapentin next


other SSRI's not as robust, and DDI's that can fuck up endoxifen through CYP2C9 (go with SNRI before SSRI)

Front 50

non pharm modifications for hot flashes (4)

Back 50

sipping cold drinks, lowering room temp, loose fitted clothing, avoiding alcohol & spices in diet

Front 51

3 hot flash drugs that interact with tamoxifen

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paroxetine
sertraline
citalopram

Front 52

downside to gabapentin (3)

Back 52

weight gain
sedation
TID

Front 53

downside to pregabalin for hot flashes (2)

Back 53

expensive
BID - TID

Front 54

misc supplement for hot flashes

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vitamin E for mild

Front 55

what is an HSR? (2)

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Adverse rxn usually occurring within seconds to minutes of administration with features of an anaphylactic (antibody mediated) or anaphylactoid (not antibody mediated) reaction- usually anaphylactoid

Unexpected reaction not consistent with the drug’s known toxicities

Front 56

HSRs usually what type
exception

Back 56

type I rxn (allergic/histamine mediated), unless you are using mabs/methotrex then could be the others

Front 57

2 drugs at very high risk for HSR

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asparaginase
paclitaxel- also excipient in drug called "cremifore??" that people react to (double whammy)

Front 58

Only one drug class has never been reported to cause HSRs

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nitrosoureas (mustines)

Front 59

Overall reported incidence of HSR for all chemo (2) may be worse due to

Back 59

5 to 15% of patients
rates vary from drug to drug
may be worse due to under-reporting

Front 60

no proven risk factors but possible ones for HSR- (6)

Back 60

history of seasonal, food, general allergies
history of other drug allergies
prior exposure to the drug
dose of drug
tumor burden or type
patients receiving drugs with HSR history

Front 61

2 drugs that react (HSR) completely differently and how

Back 61

carboplatin- delayed HSR- can take up to 8 doses

paclitaxel- immediate HSR within 1-2 doses- can re-treat usually

Front 62

5 management strats for HSR

Back 62

Stop the infusion
Access and utilize support measures
premedicate
Multiple-day premeds(didn't discuss these much)
Desensitization: serial dilution dose titration

Front 63

drug of choice for HSR- other drug you can use to control rxn

can you restart chemo after rxn is managed?

Back 63

Diphenhydramine (drug of choice) or steroids for urticaria/rash- usually limited to one reaction and can restart drug

Front 64

4 other support meds/items for HSR

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Epinephrine, albuterol, O2 for shortness of breath
IV fluids or colloid replacement for hypotension

Front 65

4 things to premed with for HSR

Back 65

diphenhydramine, H2RA, acetaminophen &/or steroid

Front 66

most common cancers for hypercalcemia (3)

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lung, breast & multiple myeloma most common- bone mets

Front 67

sx of hypercalcemia (7)

Back 67

lethargy, confusion, anorexia, nausea, constipation, polyuria & polydipsia

Front 68

3 pharm steps for managing hypercalcemia

Back 68

saline- lots of fluids- hydrate and increase urine loss of calcium (adjust based on cv status) 250-500 ml/h if depleted, then 100-150 mL


then furosemide after volume correction

pamidronate or zoledronic acid (IV)- i'm pretty sure you put this in the saline

Front 69

alternatives to managing hypercalcemia

Back 69

glucocorticoids- i think this is just for like...shrinking tumors

calcitonin- transient

mithramycin
gallium nitrate

Front 70

eliminate what if hypercalcemic?

2 things to d/c

Back 70

Eliminate sources of calcium and discontinue medications that may increase calcium such as thiazides and Vitamin D

Front 71

tumor lysis syndrome due to...

Back 71

Due to massive release of intracellular contents after tumor cell death

Front 72

tumor lysis most commonly seen with...(2)

Back 72

hematologic & kinetically active solid tumors

Front 73

tumor lysis- treatable?

Back 73

NO. preventable only

Front 74

5 lab abnormalties that dx tumor lysis

Back 74

Labs show elevated uric acid (>8 mg/dL)
phosphorus (>1.45 mmol/L), potassium (>6 mg/dL)***
LDH (> 2x ULN)
low calcium

Front 75

clinical signs for tumor lysis (4)

Back 75

Scr ≥ 1.5x’s ULN, arrhythmia, seizure or sudden death (from potassium...)

Front 76

cancers at high risk for tumor lysis (3) and why

Back 76

agressive hematological malignancies (leukemia/lymphoma Burkitt (high grade), ALL, AMC- you have cancer cells EVERYWHERE and are highly chemosensitive)

Front 77

moderate risk for TLS (4)

Back 77

solid: SCLC- highly sensitive to chemo, some breast cancers


low grade lymphomas
seminoma

Front 78

thing that causes most of the problems with TLS and why

Back 78

uric acid (from DNA)- big deal- crystallizes in kidney and blocks elimination of all other elecrolytes and shit- so we target this for treatment

Front 79

2 drugs for TLS

Back 79

allopurinol-takes a while to work- give 2-3 days before chemo

rasburicase?- use if you want more immediate effects or "treatment" ; converts uric acid to allantoin

Front 80

4 other things you have to watch with TLS

Back 80

hyperkalemia
low calcium
hyperphos
cardiac monitoring

Front 81

6 things to manage hyperkalemia

Back 81

sodium polystyrene sulfonate, insulin, dextrose, sodium bicarb (if acidotic, but avoid because it fucks with rasburicase), albuterol, dialysis (if unresponsive to above)

Front 82

drug of choice for VTE and when to give when to stop

Back 82

GIVE TO EVERYONE HOSPITALIZED EVEN IF THEY ARE AMBULATORY in the absence of bleeding or other contraindications

then stop on discharge unless they had an event
LMWH

Front 83

cancer drug with very high rates of VTE

Back 83

bevacizumab (duh it fucks with VEGF)

Front 84

is route VTE ppx recommended for outpatients?

Back 84

Routine prophylaxis of ambulatory (not in hospital) cancer pts is not recommended, with the exception of pts receiving thalidomide or lenalidomide

Front 85

cancer pt undergoing what process should be considered for pharmacologic thromboppx?

Back 85

Pts undergoing major surgery for malignant disease should be considered for pharmacologic thromboprophylaxis