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Critical Care/Hematology/Oncology > Week 4 > Flashcards

Week 4 Flashcards

1
Q

classes of chemo-induced N&V (CINV)

A

acute: occurring within first 24 hours after intiation of chemo

dealyed: occuring 24 hours to sevearl days 2-5) after chemo

breakthrough: occuring despite appropriate prohlyatic trtment

anticipatory: occuring before a treatment as a conditioned response to the occurence of CINV in previous cycle

refractory: recurring in subsequent cycles of therapy, excluding acticipatory CINV

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2
Q

patho of CINV

neuro transmitters associated w. CINV

A

neurotransmitters and receptors in cns and gi tract assocated w. CINV

Seretonin (5-HT3) and its receptor

substance P and the neurokinin-1 (NK-1) receptor

dopamine and its receptors

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3
Q

Patho of CNV

mchanisms of emetic response to chemo

A

Peripheral pathway
*5-HT3-mediated
*originates in GI tract
*activated in first 24hrs after chemo
*primarily associated w. acute emesis

Central pathway
*NK-1 receptor mediated
*occurs primarily in the brain
*thought to be predominantly involved in delayed CINV

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4
Q

principles of emesis control

A

Prevention is key

facots in choosing antiemetic
*emetic risk of therapy
*prior experience w. antiemetics
*pt factors

for chemo regimens w. multipk agents, anti emetic prophylaxis should be based on agent w. highest emetogenic risk

lifestyle measures may help alleviate CINV

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5
Q

Risk factors for developing CINV

A

age <50

emesis during pregnancy

history of cinv, prone to motion sickness

female sex

emetic potential of chemo theraoy

little or no previous alcohol use

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6
Q

trends for emetic risk of chemo meds

A

IV&raquo_space; oral

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7
Q

emesis prevention- high emetic risk parenteral anticancer agents

A

note: scheduled ATC regardless if pt is experiencing CINV or not
*need at least 3 antiemetics
*dexamethasone,nk1 ra, and 5-ht3 RA have synergistic effects

Option 1 preffered:
Day1:
*Olanzapine
*Dexamethasone
*NK1-RA
*5-HT3
Day 2-4
*Olanzapine
Dexamethasone
**Aprepitant (nk1 ra)
**note: if Aprepitant IV is used, only given x1 dose on day 1. if Aprepitant PO is given on day 1, then it is also given on days 2 and 3
* you should never see aprepitant used IV on days 2 and 3

Option 2:
Day 1:
*olanzapine
*dexamethasone
*Palonsetron
Day 2-4:
*Olanzapine

Option 3:
Day 1:
*dexamethasone
*nk1 RA
*5-ht3 RA
Day 2-4
*dexamethasone
**Aprepitant (only use dondays 2,3 as PO if aprepitant PO was used on day 1)

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8
Q

Emesis prevention- Moderateemetic risk Parenteral anticancer agents

A

*need 2 antiemetic agents of different pathways
*up to 3 days

Option 1:
Day 1:
*dexamethasone
*5HT3
Day 2-3
*dexamethasone OR 5-HT3 RA

Option 2:
Day 1:
*olanzapine
*dexamethasone
*palonosetron
Day 2-3
*olanzapine

Option 3:
Day 1:
NK1 RA
Dexamethasone
5-HT3-RA

Day 2-3
*can be nothing
*if pt was on aprepitant PO day 1, would continue on day 2-3
*+/- dexamethasone

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9
Q

Emetic Prevention - low emetic risk
Parenteral anticancer agents

A

option 1: dexamethasone

option 2: metoclopramide

Option 3: prochlorperazine

option 4: 5-HT3 RA

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10
Q

Emetic PRevention: miminimal emetic risk

A

no routine ppx (unless pt start experiencing SS)

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11
Q

Emesis prevention
oral anticancer agents

High-moderate emetic risk
Low-minimal emetic risk

A

high-mod emetic risk
*5HT3 RA

Low to minimal emetic risk
*PRN recommened

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12
Q

Break through emesis treatment

A

*add one agent from a different drug class to the current regimen

*counsider routine, ATC adinistration rather than prn dosing(ex for pts on oral anti-cancer agents)

*consider antacid therapy if pt has dyspepsia

*palonesetron not used for breakthorugh emesis due to long 1/2 life (~40 hrs)

ex:
Olanzapine
5-HT3 RA
Prochlorperazine
dexamethasone
metaclopramide
scopolamine
lorazepam
dronabinol

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13
Q

anticipatory emesis treatment

A

prevention is key

avoid stong smells that precipitate symptoms

lorazepam is useful in anticipatory anxiety-related emesis

acupuncture

behavioral therapy
*guided imagery
*relaxtion
*hypnosis
*cognitive distraction
*yoga
*biofeedback
*Progressive muscle relaxation
*guided imagery

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14
Q

antimetic agents

Dexamethasone

indications:
MOA: mechanism in CINV unkown

AE:
*insomnia -> admin in morniing
*dyspepsia-> take w. food. consider adding h2 RA or PPO as clinically indicated
*hyperglycemia
*HTN

DDI:–

Pearls/considerations:–

A
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15
Q

antiemetic agents

5-HT3 RA

exs:
indications:
MOA:
AE:
DDI:
Pearls/considerations:

A

antiemetic agents

exs: ondansetron (1st gen), palonosetron, granistron(1st gen)

indications:
MOA: blockvagal nerve terminals and centrally in the chemo receptor trigger zone (medulla) seretonin, both peripherally (GI tract) on

AE: HEadache, constipation, qtc prolongation

DDI:
Pearls/considerations:
*ondansetron, Granistron are short acting and most effective in preventing acute CINV

*palonesetron is a 2nd gen, longer t1/2 ~40 hrs). not used for breakthrough nausea. effectivein preventing acute and delayed CINV

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16
Q

antiemetic agents

NK1 RA

exs:
indications:
MOA:
AE:
DDI:
Pearls/considerations:

A

antiemetic agents

exs:
*aprepitant
*Fosaprepitant
*rolaprepitant
*fosnetupitant(available in combo w. palonesetron)
*netupitant (available in combo w. palonosetron)

indications: *prevention of CINV, not treatment of breathrough nausea. most useful in preventing delayed cinv

MOA:Inhibits substance P/neurokinin 1 (augments 5HT3-RA and dexamethasone antiemetic activity

AE: Fatigue, GI upset, headache, hiccups

DDI: INHIBITS CYP3A4 AND CYP2C9 (Decrease dexamethasone dose to 8mg dail on days 2-4) (except for rolapitant)

Pearls/considerations:
rolapitant has extended half life (7days) sould not be administered <2 week intervals
*for us of aprepitant TO PREVENT CINV, if IV formulation used, x1 dose onday 1. if PO formulation used, used on day 1 and then on days 2-3

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17
Q

antiemetic agents

Olanzapine

exs:
indications:
MOA:
AE:
DDI:
Pearls/considerations:

A

antiemetic agents

exs:
indications: useful in both prevention and treatment of cinv

MOA: blocks dopamine, 5HT3, muscarinic, and histmaine receptors

AE:
*SEDATION: -> admin at bedtime unless given as a premedication. consider lower dosing for elderly

*hyperglycemia

*fatigue

*qtc prolongation

DDI:

Pearls/considerations:

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18
Q

antiemetic agents

Dopamine antagonists

exs:
indications:
MOA:
AE:
DDI:
Pearls/considerations:

A

antiemetic agents

exs: proclorperazine
metoclopramide
promethazine

indications: most useful for breakthrough cinv

MOA: antagonizes dopamine in the chemoreceptor region

AE:
(phenothiazines)Prochlorperazine, Promethazine
*rowsiness
*constipation
*prochlorperazine( least chance of qtc prolongation

metoclopramide
*benzamines
*drowsiness
*diarrhea
*qtc prolongation
*tardive dyskinesia (avoid >12 weeks)

DDI:

Pearls/considerations:
*procloperazine has less risk fo rqtc prolongation

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19
Q

antiemetic agents

benzodiazepines

exs:
indications:
MOA:
AE:
DDI:
Pearls/considerations:

A

antiemetic agents

exs: LORZEPAM, ALPRAZOLAM

indications: most useful for anticiptaory CINV that has an anxiety component

MOA: anxiolyic

AE: sedation, dizziness

DDI:

Pearls/considerations:
*administer at night before or the morning of chemotherapy or both

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20
Q

antiemetic agents

Cannabinoids

exs:
indications:
MOA:
AE:
DDI:
Pearls/considerations:

A

antiemetic agents

Cannbinoids

exs: Dronabinol
indications: rarely used, only indicated in refractor disease
MOA: CB1 agonism supresses vomiting
*indirect activation of 5HT1A in raphe nucleus

AE:
sedation
euphoria, hallucinations
palpitation
flushing
cough

DDI:
Pearls/considerations:
*PO

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21
Q

antiemetic agents

scopolamine

exs:
indications:
MOA:
AE:
DDI:
Pearls/considerations:

A

antiemetic agents

exs:
indications:
MOA: anticholinergic

AE:
dry mouth
somnolence
blurred vision

DDI:
Pearls/considerations:

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22
Q

Cancer treatment induced diarrhea

A

incidence as high as 50-80%

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23
Q

most common offenders of cancer treatment induced diarrhea

A

fluorouracil

capecitadine

irinotecan

pertuzumab

abemaciclib

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24
Q

assessment of ctid

A

hx of citd

volume and duration of diarrhea

added risk factors
*fever
*orthostatic symptoms(dizziness)
*abdominal pain/cramping
*weakness

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25
Q

Irinotecan-induced diarrhea

A

can cause acute or delayed diarrhea

acute: due to cholinergic stimulation
*mean duration of symptoms is 30 min
*usually respond rapidly to atropine

delayed diarrhea: due to GI mucosal damage secondary to SN-38
*usually occur more than 24 hours after amdinistration
*noncumulative and occurs at all dose levels

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26
Q

mgt of CTID

A

non phar:
Iavoid foods that would aggravate the diarrhea

aggresive oral rehydration w. fluids that contain water, salt, and sugar

Pharm measures:
*loperamide-first line (4mg followed by 2 mg q4h or after every unformed stool . (not to exceed 16mg/d for CTID, MDD in regular circumstances is 8mg/d)

*diphenoxylate-atropine
*1-2 tabs q6hrs until control achieved (not to exceed 8 tablets/day

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27
Q

refractory CTID treatment options

A

octreotide

tincture of opium

probiotics

rule of C. diff and infection collitis

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28
Q

mucositis

SS
Complications

A

symptom: typically occurs within 5-14 days

complications:
decreased oral intake (poor nutritional status,
grade 3: severe oral pain
grade 4: requires parenteral or enteral nutrition

increase infection risk(gram+ oral flora, candida or fungal infections)

pain (may require opioids and pca administration)

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29
Q

mucositis vs stomatitis

A

mucositis: erythematous and ulcerative lesions of the mucose observed in pts treated w. chemo

can occur anywhere in gi tract

stomatitis: mucositis limited to the oral cavity

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30
Q

patho of chemo induced mucositis

A

five stage model of oral mucosisits

initiation- cellular damaged induced, reactive oxygen species formulations

primary damage resoinse
*activiation of p53 and nf-kb

sgnal aplifiation

ulceration- high risk for bacterial colonization

healing cessation from ongoing tissue damage

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31
Q

Risk factors for chemo induced mucositis

A

chemo
* melphalan
cisplastin+radiation
*high dose methotrexae
doxorubicin
busulfan
5-FU

pt factors:
smoking
poor oral hygeine
oral lesions at baseline
female sex
pretreamtent nutritional status

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32
Q

prevention of chemo induced mucositis

A

oral hygeine:
*avoid acidic or spicy foods
*burhs w. soft toothbrush twice daily; fossin gdaily
*swithc tabs to solutions o iv if hospitalized
*use nonalcoholic mouthwashes at least 4 times day
(ex NS or salt and soda

cryotherapy:
moa: local vasocinstriction-> less drug delivered to the oral mucose
*hold ice chips in their mouth for 30min before and/or during chemo

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33
Q

mgt of chemo induced mucositis

A

oral decontamination: bland mouthwash or oncology m outhwash. dexamethasone mouthwash for everolimus induced mucositis

pain control: 2% iscous lidocaine swish and spit, systemi opioids

palliation of dry mouth: artificial salive products or chewing gum to increase saliva production

nutritional supports: liquid or soft diet; tpn

oral candidiasis trt: nystatin oral solution or clotrimazole lozenge
*flucanozole 200 mg po x1 dose, then 100mg daily x 21 days

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34
Q

NEutropenia

A

neutropenia: absolute neutrophil count (ANC)<500 cells/mm3 or expected to decrease to <500 cells/mm3 in 48 hours

proound neutropenia: anc<100 CELLS/MM3

PROLONGED NEUTROPENIA: LASTIN LONGER THan 10 days

febrile neutropenia:
*single temp:>38.3 C orall or >38C over 1 hours
AND
ANC<500 cells/mm3 or expected to decrease to <500 cells/mm3 in 48 hours

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35
Q

consequences of neutropenia

A

dose reduction or treatment delayes

compromise clinical outcomes

longer hospital stays

increased treatment costs

decreased QOL

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36
Q

risk factors for febrile neutropenia

A

prior chemo or radiation

persistent neutropenia

bone marrow involvement by tumor

recent surgery and or open wounds

liver dysfunction (bilirubin >2.0 mg/dL)

renal dysfunction (Crcl <50 ml/min)

age> 64 years recieving ful chemo dos eintensity

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37
Q

primary prevention for febrile neutropenia

A

overall risk for neutropenia

High –>(regardless of pt risk factors) G-CSF recommended

intermediate risk (+>/1 risk factor) consider GCSF

Low (+>2 risk factors). GCSFs may be considered

note: G-CSF=granulocyte colony stimulating factor

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38
Q

pharm options for primary prevention for febril neutropenia

Filgastrim (category 1)

A

short -acting g-csf

start the next day or up to 3-4 days after completion of chemo

given daily until ANC recovery

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39
Q

pharm options for primary prevention for febril neutropenia

pegfilgastrim (category 1)

A

long acting g-csf

admin up to 3-4 days AFTER completion of chemo

singe administration!!

allow >/12 days between the dose of pegfilgastrim and the next cycle of chemotherapy

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40
Q

pharm options for primary prevention for febril neutropenia

Eflapegfilgastrim-xnst

(category 2A)

A

long acting c-csf

admin ~24hr after completion of chemo

single administration

do not admin 14 days before and 24 hrs after admin of chemo

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41
Q

treatment of febrile neutropenia

A

did pt recieve ppx g-csf? and which?

recieved filgastrim: continue filgastrim

recieved pegfilgastrim or eflapegfilgrastrim ppx: no additional g-csfs needed

if did not recieve ppx g-csf-> assess risk factors for infection-associated complication

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42
Q

risk factors for infection associated complications in establisehd febrile neutropenia

A

sepsis syndorme

age>65

ANC<100

neutropenia expected to be >10 days in duration

pneumonia or other clinically documented infctions

invasive fungal infection

hospitalization at the time of fever

prior episode of febrile neutropenia

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43
Q

secondary prevention for febrile neutropenia

A

(pt has hx of febrile neutropenia or dose limiting neutropenic event)

if pt has hz of prior use of g-csf-> consider chemo dose reduction or change in treatment regimen

if pt has no prior use of g-csf-> consider gcsf

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44
Q

Leukemia

A

Disease of bon marrow-> cancer of blood cells

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45
Q

acute vs chronic leukemia

A

acute
rapid onser
symptomatic (bleeding)
rapidly fatal if untreated
immature cells (blasts)
usually leukemia

chornic
*slowly progressive
*mos asymptomatic
*some survive years without trtment
*immature and matue cells

leukocystosis can occur in both phases

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46
Q

Histology differentiation of types of leukemia

A

Cancer can occur in the myeloid or the lymphoid white blood cells

when it occurs in the myeloid cells , it is called myelogenous leukemia

when it occurs in the lymphocytes , it is called lymphocytic leukemia

myeloid cells include granulocytes ( basophils, neutrophils, eosinophils), also platelets, and erythrocytes

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47
Q

Acute myeloid Lymphoma (AML) epidemiology

A

most common in adults aged 65-74. average age 68

most deadly leukemia in the US

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48
Q

risk factors for AML

A

increasing age

prior chemo= therapy related AML (t-AML)
ex: anthracyclines, alkylators (ex: cyclophosphamide, melhalan), topoisomerase inhibitors (etoposide)

prior pelvic radiation

cigarette smoking

radiation exposure

benzene exposure

pesticide exposure

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49
Q

Signs and sYmptons of AML

A

Anemia (fatigue and sob)

THOMBOCYTOPENIA (BLEEDING RISK)

NEUTROPENIA
ANC <500 or <1000 w. anticipated decrease to <500 w.in 48 hr

spontanous tumor lysis syndrome (TLS)

cns involvement rre(<3%) (somnolecense, headaches, consfusion

WBC count: 1/3 pts present w. pancytopenia, 1/3 w. wbc in normal limits, 1/3 w. elevated wbc

hyperleukocytosis: elevated wbc >/100,000/mcl
*poor prognosis
*increases risk of cns involvement
*very high risk of Tumor lysis syndrome

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50
Q

Patho of leukemia

A

hypercellular bone marrow
*immature blasts “outgrow” all other cells
*crowding results in cytopenias
* does not allow room for other cell lineages to grow

normal cellularity in marrow: 30-40%
sometimes these pts ca have 90-95% cellularity

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51
Q

hyperleukocytosis

A

oncologic emergency

8hyperviscosity syndrome (blood sludging)
*stumor, sob, vision changes
*can cause stroke, respiratory failure, cardiac ischemia, renal failure, retinal hemorrhage

management: hyroxyurea (hydrea)
*oral ribonucleitide reductase inhibitor
*used for count control
*used until clinically stable and ready to start induction chemo

*leukopheresis

dosing: package insert 50-100mg/kg/day
dosing heavily physician/pt specific

AE: nvd, risk for tumor lysis syndrome

LONG TERM: CUTANEOUS VASCULITIC ULCERATIONS
MUCOSITIS
ALOPECIA, HYPERIGMENTATION

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52
Q

diagnostic criteria of aml

A

WHO definition

> /20% blasts isolated on bone marrow biopsy (bmbx) or peripheral blood

cytogenitically definition: detection of cytogenetic abnormalities known to indicate AML, regardless of blast % on bmbx

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53
Q

Prognostic Markers

A

cytogenetics!!!; predicts abilility to obtain remission w. induction chemo with persons chromosomal make up aka karyotype, risk of relapse, and overall survivial

moelcular abnormalities

age

primary vs secondary aml

performance status

availability of stem donor

wbc at diagnosis

extramedullary disease (disease not in marrow)

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54
Q

FMS-Like Tyrosine Kinase (FLT3) mutations and effects of mutations

A

two types
*internal tandem duplication (ITD)

*Tyrosine kinase domain(TKD) point mutations

promotes proliferation and blocks differentiation

associated w. worse prognosis, increased relapse rate and lower OS

associate w. leukocyosis and high percentage of blasts in bone marrow de novo AML
(ITD mutations associated w. worse survival/worse prognosis compared to tkd mutation)

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55
Q

Other molecular mutations for idh

A

ISOCITRATE dehydrogenase(IDH)

others being researched: RUNX1, TET2, spliceosome mutations

56
Q

Risk stratification based on cytogenetics and molecular mutations

A

favorable risk: low risk of relapse if we get them into remission

intermediate risk

poor risk

*intermediate and poor risk pts are taken to transplants once they get to remission

57
Q

AML treatment algorithm: agressive chemoTHERPAY

step 1: DETERMINE if pt is a candidate for aggresive chemo

(criteria for high-intensity induction chemo)

A

most pts<60

pts >/60 w.o significant co morbidities or end organ dysfunction (adeque renal, hepatic, and cardiac function
*adequate performance status

pts w. aggressive disease course (hyperleukocytosis, tumor lysis syndrome at presentation)

pts who are candidates for an allogenic stem cell transplant

58
Q

AML treatment algorithm: agressive chemoTHERPAY

Step 2 : if pt is candidate for aggressive chemo, what is/are the regimen of choice

A

Cytarabine +Anthracycline (7+3) based regimen

for pts <60 yo.
cytarabine 100mg/m^2 IV daily continuous infusion x7 days
+daunorubicin 60 mg/m^2 x 3days OR idarubicin 12mg/m2/dx 3 days

for pts >/60
cytarabine 100mg/m^2 IV daily continuous infusion x7 days
+daunorubicin 60 mg/m^2 x 3days OR idarubicin 12mg/m2/dx 3 days
**note: pts >/65 have <50% complete remission rate (CR)

59
Q

WBC phases oh 7+3 treatment for AML

A

days 1-7: chemo admin
*SE: n/v, GI, fatigue
WBC drop significantly

Days 8-24: cell count nadir and recovery
*side effects: fatigue, fevr/infection, high rbc and platelet transfusion requirmeent

days 25+ complete cell count recovery expected.
*d/c from hospital once ANC>500 and no longer platlet transfusion dependent

60
Q

Additional induction regimens for AML

A

7+3 based regimens
*additional chemos and or tyrosine kinase inhibitors added to backbone of 7+3

exs:
FLT3-ITD or FLT3TKD positive
*Midostaurin
*50 mg BID w. food on days 8-21 of each cours of chemo (induction and consolidation)
*can cause nausea

*favorable/intermediate cytogenetics
*gemtuzumab ozogamicin (GO)
3mg/m^2 (max 4.5 mg) on days 1,4, and 7 of induction and day 1 of consolidation courses
*antibody drug conjugate.
no increase in survival seen in poor risk pts

Liposomal Daunorubicin +cytaribine (vyxeos)
*indication: 1st line treatment of treatment related/ secondary AML
*liposomal formulations

61
Q

AML treatment algorithm: agressive chemoTHERPAY

Step 3: Analysis of treatment Response

A

Day 14 bmbx:
*Leukemia free state on day 14
Goal: <5-10% blasts, hypocellular (<10-20% cells)

complete remission/complete response n(CR) criteria: day 28+
*criteria for CR: <5% blasts and ANC>1000 ANDD platelets>100,000

complete remission w. incomplete count recovery (iCR)
*older pts w. prior MDS- residual dysplasia prevents full platelet recovery

62
Q

AML treatment algorithm: agressive chemoTHERPAY

Step 4: Await countrecovery +/- G-CSF

response criteria in AML

A

complete remission/complete response n(CR) criteria: day 28+
*criteria for CR: <5% blasts and ANC>1000 ANDD platelets>100,000

complete remission w. incomplete count recovery (iCR)
*older pts w. prior MDS- residual dysplasia prevents full platelet recovery

*repeat bmbx to document complete remission

63
Q

AML treatment algorithm: agressive chemoTHERPAY

Step5: Consolidation therapy

purpose:
favorable risk:
intermediate/poor risk

A

purpose: to eliminate remaining disease that was not eliminated during induction phase

favorable risk pts:
A) HiDAC: Hi dose cytarabine
*for those who recieved 7+3 based therapies
*gold standard consolidation therapy for AML
1.5-3 g/m^2 iv q12hrs x 6 doses q28 days x 3-4 cycles

b) other option: Liposomal daunorubicin+ cytarabine

Intermediate/poor risk
*stem cell transplant
*based on cytogenetics, molecular mutations
*usually, compete induction and 1+ cycle(s) if consolidation prior to transplant

64
Q

AML treatment algorithm: non-agressive chemoTHERPAY

step 1: if pt is not a candidate for agressive chemo, what is/are the regimen of choice

A

“low intensity” chemo

*reserved for those unfit for intensive chemo or those w. significant comorbidities

a) HYpomethylating Agents (hma)+Venetoclax

*Azacitidine (Vidoza) 75 mg/m^2/dayx7 days q28 days-> can be subq or iv
**standard of care
*Decitabine (Dacogen): 20 mg/m^2/day IVx5 days q28 days

b) Low dose cytarabine (LDAC) +venetoclax

c)Ivosidenib +Venetoclax
*both agents given continuously
*only in IDH1 mutated pts

d) LDAC+ Glasdegib

65
Q

Venetoclax interactions and dose reductions

A

immediatly when pt is on venetoclax, must consider other drugs pt is on to identify any DDI

HMA backbone dose: 400mg PO once daily
*strong cyp3a4 inhibitors (posiconazole/voriconazole): 100 mg once daily
*mod cyp3a4 inhibitors: isavuconazole, diltiazem, verapamil ) or pgp inhibiors (amiodarone, carvedilol) 200 mg once daily

LDAC backbone:
*strong cyp3a4 inhibitors (posiconazole/voriconazole): 150 mg once daily
*mod cyp3a4 inhibitors: isavuconazole, diltiazem, verapamil ) or pgp inhibiors (amiodarone, carvedilol) 300 mg once daily

66
Q

Options for relapsed or refractory AML disease

A

clinical trial

can repeat intial induction regimen if response lasted >12 months

etc.

67
Q

targeted therapies in AML

A

FLT3 mutations (FLT3 ITD, FLT3 TKD)
A)FDA approved
*Midostaurin (Rydapt)->only used frontline. not used in refractory disease/relapse
*Gliteritinib-> only fda approved for relapsed/refractory flt3+ AML

IDH inhibitors:
a)FDA approved
*IVOSIDENIB-targets idh1- approved for newly diagnosed and relapsed/refractory disease
*ENASIDENIB- TARGETS idh2->approved for refractory/relapsed disease

68
Q

Supportive care in AML

A

A)transfusions
*rbc transfusion if hgb<8g/dL
*plt transfusion if plt<10,000 mcL

b)infection ppx while neutropenic

I. Antiviral: HSV/VZV-acyclovir 400mg BID

II. antibacterial: ciprofloxacin 500mg BID or levofloxacin 500mg qd

III. invasive fungal(Asperigillus & mold (mucomycosis)
*posaconazole (covers mucoid)
*voriconazole (covers mold as well)

69
Q

Tumor lysis syndrome

A

oncologic emergency

rapid tumor breakdown following chemotherapy

sudden release of intracellular potassium, phosphorous , uric acid

onset: 12-72 hrs post chemo

risk factors:
renal insufficiency
elevated uric acid, phosphorous, lactate dehydrogenase
dehydration

common tumor types: hematologic malignancies

associated w. large tumor burden, higher cell turnover, etc.

70
Q

presentation of tls

A

metabolic disturbances hyperuricemia-> can crystalize and lead to irreversible kidney damage

hyperphosphatemia:calcium phophate precipitate inkidneys

hyperkalemia

hypocalceima

clinical manifestations:
**acute renal failure
*NVD
*hematuria
*CHF, cardiac dysrhtmias
syncope
seizures
death

71
Q

TLS PPX

A

A)allopurinol
inhibits formulation of uric acid
dose: 300-600 mg/day

renal adjustment:
crcl 10-30: 200 mg/day
crcl: <10: 100 mg/dau

hydration

Rasburicase-> breaks down uric acid( usually used for treatment, not for ppx)

72
Q

TLS management

A

Hyperuricemia
*IV hydration
maintain urine output >2.5L
*furosemide if unable to maintain urine output alone
*Rasburicase: 1.5-6 mg as single dose. can repeat q12-24hrs on repeat levels
*roswell dosing: 1.5 mg if pt<60kg, 3 if pt>60kg
*rasburicase can cause anemia in pts w. g6pd deficiency.

Hyperkalemia
*EKG-rule out active arrythmia
Sodium polystyrene sulfonate (kayexalate)
*insulin and glucose
*dialysis

Hyperphosphatemia
*phosphate binders (sevelamer, calcium acetate)
*dialysis

Hypocalcemia
*do not treat

73
Q

Clinical pearls of chemo used in leukemia

A

Anthracyclines( daunorubicin, idarubicin, mitoxantrone)
*red in color: ink-light reddish urine
mitoxantrone: blue in color->blue green urine, sclera
*AE: myelosupression
cardiotoxicity

Cytarabine:
AE with HiDAC: neurotoxicity
*NEURO CHECKS REQUIRED pior to each dose
conjunctivitis

Gemtuzumab+Otogamicin (GO):
*mab-> infusion reactions( premedicate w. APAP, diphenhydramine, and methylprednisolone
hepatotoxic
BBW: VENO OCCLUSIVE DISEASE-> fatal disease that causes obstruction of blood veseels that lead into liver
*monitor LFTs, bilirubin, ascites, weight gain, hepatomegaly, amdominal pain

Low Intensity Chemo
*HMA backbones (Azacitidine)
AE: constipation-> standing bowel meds
low-mod emetogenicity, premedicate w. ondansetron
*Venetoclaax: AE: myelosupression

74
Q

Myeloid Growth Factors

A

Granulocyte-colony stimulating Factor (G-CSF): Filgrastrim (Neupogen), filgastrim-sndz(Zarxio)

Granulocyte macrophage colony stimulating factor (GM-CSF): Sargramostim

indication in leukemia: may be used for severe infections in setting of neutropenia (i.e severe sepsis)

AE: bone pain (up to 50%)-> recommend loratidine ((due to histamine release of bone, causing the pain) or hydroxyzine
*feevr

75
Q

Chronic Myeloid leukemia

etiology/pathogenesis

A

driven by acquired mutation that affects hemotopeitic stem cells
*philidlphia chromosome (Ph+) mutation creating MCR-ABL fusion onco gene, contains an active tyrosine kinase region which is responsible for cell proliferation, cell growth and survival

76
Q

risk factors for cml

A

ionizing radiation

77
Q

SS of CML

A

up to 50% of pts are asymptomatic

*splenomegaly >50% are present due to elevated platelets

anorexia

bone pain

purpura

unexplained weightloss

fatigue

78
Q

Lab findings for cml

A

LEKOCYTOSIS - WBC>25 X 10^9/L

bone marrow findings
*hypercellularity(74-90%)
*increased erythropoeisis
*increased megakaryocytes
*minimal dysplasia
blasts<10%

*Ph+ chromosome

79
Q

Phases of CML

A

chronic blast phase(CP): <10% blasts
etc.
goal: delay progression to AP/BP, eradicate philidelphia chromosome

Accelerated Phase: 10-19% blasts in peripheral blood and/or marrow
etc.
Goal: control wbs, bring back to CP an avoid progressin to BP

blast phase (BP): >.20% blasts in peripheral or in bone marrow
Goal : survive induction, bridge to allogeneic stem cell transplant

80
Q

Treatment of CML

A

Targeted therapy-Tyrosine Kinase Inhibitors (TKIs)

1st gn: Imatinib (Gleevec)
2nd gen: Dasatinib (Sprycel), Nilotinib
3rd Gen: Bossutinib, Ponatinib

STAMP inhibitor: Asciminib, binds to a different place on TKI

oral admin

now condiered a chronic disease state managed w. TKI’s

81
Q

Responses to therapy in CML

A

hematologic response: looking at peripheral blood counts

cytogenic response: bmbx, number of Ph+ metaphases remaining

molecular response: how much kinase is in blood
*how we currently monitor response

82
Q

Tyrosine Kinase Inhibitors

Imatinib (Gleevac)

moa:
dose:
AE:
AE mgt:
Pearls/considerations:

A

Tyrosine Kinase Inhibitors

moa: selective inhibitor of bcr-abl TYROSINE KINASE
*also inhibits c-kit and plt derived growth factor receptor

dose:400 mg daily

AE: edema/ fluid retention, myalgias, hypophosphatemia, NVD
AE mgt: diuretics, supportive care. consider checking EF if pleaural/pericardiac. for myalgias, calcium supplementation

Pearls/considerations:
*high doses >400 mg not recommended as initial therapy
* developed resistance, lead to development of later gen TKIs

83
Q

Tyrosine Kinase Inhibitors

Dasatinib (Sprycel)

moa:
dose:
AE:
Pearls/considerations:

A

Tyrosine Kinase Inhibitors

Dasatinib

moa:
dose: 100 mg daily

AE:
*pleural/ pericardial effusions, bleeding risk, pulmonary arterial HTN

AE mgt:
*pulmonary htn: d/c
*fluid retention, edema, ascites: diuretics, supportive

Pearls/considerations:
*standard oc care
*second gen,
*cns penetration

84
Q

Tyrosine Kinase Inhibitors

Nilotinib

moa:
dose:
AE:
Pearls/considerations:

A

Tyrosine Kinase Inhibitors

moa:
dose: 300 mg

AE: elevated pancreatic enzymes, indirect hyperbilirubinemia, qtc prolongation, cv events
AE mgt:
*qtc prolongation: ecg@baseline, 7 days after intiation, and periodically. corect for hypokalemia and hypomagnesemia.
elevatd lft: consider dose reduction or d/c
*peripheral arterial occlusive disease: d/c

Pearls/considerations:
*qtc prolongation
*2nd gen mgt

85
Q

Tyrosine Kinase Inhibitors

Bosutinib

moa:
dose:
AE:
Pearls/considerations:

A

Tyrosine Kinase Inhibitors

moa:
dose:
AE:
*Diarrhea manageable w. loperamide, hepatotoxicity, headache, rash
AE mgt:
*hepatotoxicity: hold until recovery, then dose reduce or d/c
*diarrhea: hold until recover, loperamide

Pearls/considerations:
*3rd gen

86
Q

How to choose which tki to use

A

SoKal score: calculates relative risk calculation

intermediate-high risk
Category 1 recommendation: *2nd or 3rd gen TKI

low risk:
*Imatinib or 2nd gen

87
Q

monitoring cml

A

color chart:
red: tki resistance disease
*evaluate pt compliance and ddi.
*CONSIDER MUTATIONAL ANALYSIS
recommendation: switch to alternate tki and evaluate for allogenic hct

yellow: possible tki resistance
recommendation: switch to alternate tki, continue same tki (other than imatinib) or increase imatinib dose to max of 800mg and ocnsider evaluation for allognic hct

light green: tki sensitive disease
recommendation: if optimal, continue same tki, if not optimal, share decision making w. pt

green: continue same tki

88
Q

mutation profiles for CML clinical pearl

A

Asciminib and Ponatinib are only tki that cover BCR-ABL T315I mutation

T315I mutation is resistant to other TKIs.

89
Q

Tyrosine Kinase Inhibitors

Ponatinib

moa:
dose:
AE:
Pearls/considerations:

A

Tyrosine Kinase Inhibitors

moa:
dose:
AE: elevated pancreatic enzymes, HTN, skin toxicity, thrombotic events

AE mgt:
hepatotoxicity: hold until recover, then dose reduce or d/c
*ischemic reactions: d/c
elevated lft: hold until recovery

Pearls/considerations:
*3rd gen
*reserved for pts who failed atleast 2 tki, or have T315I mutation
*BBW: vascular occlusion, hepatotoxicity, HF

90
Q

Tyrosine Kinase Inhibitors

Asciminib

moa:
dose:
AE:
Pearls/considerations:

A

Tyrosine Kinase Inhibitors

moa: STAMP inhibitor
dose:
AE:
Pearls/considerations:
trt of pts who have previously recieved 2+ tkis or have T31FI mutaion

91
Q

TKI common class side effects

A

myelosupression
transminitis
hepatotoxicity
electrolyte changes
CV events

92
Q

TKI DDI

A

imatinib-cyp3a4 substrate and inhibitor

Dasatinib, bosutinib, poatinib-cyp3a4 substrate

nilotinib: cyp3a4 substrate and inhibitor, also 2cb, 2c9, and 2d6

93
Q

TKI food drug interactions

A

dasitinib- needs acidic environment for absorption (no ppis or h2 blockers)

nilotinib and asciminib: admin on empty stomach. 2 hrs before eating or 1 hr after

94
Q

tki dose adjustment for organ impairment

A

imatinib: dose adjust for renal and hepatic

nilotinib, bosutinib, ponatinib- dose adjust for hepatic

95
Q

Acclerated phase/blast crisis treatment

A

Goal: return pt to chronic phase

all tkis have been shown to induce favorable response rates

current recommendations:
Dasatinib, niltinib, or bosutinib
omacetaxine can be considered in cass of disease progression

blast crisis:
TKI +/- chemo followed by allogenic HSCT
*chemo chosen on subtype of the disease

96
Q

what s the prostate

A

surrounds urethra

produces seminal fluid that nourishes and transports sperm

composed of acinar secretory calles arranges in a radial shape surrounded by a foundation of supporting tissue

95% of prostate cancer cases are caused by adenocarcinoma

97
Q

epidemiology of prostate cancer

A

most diagnosed cancer in males

2nd most common diagnosed cancer in US

5 year relative survivial from 2012-2018: 96.8%

for most pts. prostate cancer is a slow growing or indolent disease

98
Q

risk factors for prostate cancer

A

Race: african amerians more common, less common in asians. incidence higher in US and scandanavian countries

Age:most ppl dagnosed 65-74. Median age of diagnosis: 67

Family hx: increase in men w. family hx of prostate cancer
*familial predisposition
*BRCA-2 mutations a.w 2-6 fold increase in risk
*lynch syndrome 2-5.8 fold increase in risk

Lifetime risk of prostate cancer
*16% of one first degree raltive vs 8% if no family hx

99
Q

screning for prostate cancer

A

different organizations have different screening protocols

usually involves prostate -specific antigen
often determined by pts age and life expectancy

100
Q

clinical presentation of prostate cancer

A

localized
*asymptomatic generally

locally invasisive
*urrerteral dysfunction
*urinary frequency
*urinary hesitancy
*dribbling or decreased urinary stream
*incomplete bladder emptying

advanced disease
*back pain
cord compression
lower-extremeity edema
pthologic factors
anemia
weightloss

101
Q

prognostic factors

PSA

A

A)protate specific antigen
*gycoprotein produced by prostate epithelial cells

*specific for prostate, not for cancer
(if pt ha bph, psa can be high)
*can be reduced by 5-alpha reductase inhibitors)

normal range </4, some pts with psa 2.5-4 still develop prostate cancer

PSA velocity may be another predictor of prostate cancer risk

102
Q

general prognostic factors of prostate cancer

A

prostate specific antigen (PSA)

tumor size and extent of primary tumor

histologic grade(gleason score)

103
Q

Prognostic factors

tumor size and extent of primary tumor

A

localized tumore: excellent long term prognosis

locally advanced cancer: 5 year survival is very good

metastatic disease: not curable, median survival shortened

104
Q

staging system for prostate cancer

A

TNM: tumor, node, metastasis

Tumor (T): clinical staging to determine size
Node (N): presence and extent of regional lymph node involvement
Metastasis: presence and extent of metastasis

105
Q

Prognostic factors

Histologic grade-Gleason score

A

gleason score
*describes how cancer cells look under a microscope

pathologist gets biopsy of tissue and assigns a score to 1st and second most predominnant tissue

score ranges 1-5
closest to 1: low grade tumor cells; looks similar to normal cells
closest to 5: high grade tumor cells; mutated so much they barely look like normal cells

both numbers are added, to give a score. total score between 2-10.

106
Q

Gleason score group

A

gleason scores 2-4 tend to be less agressive,

gleason scores 7-10 tend to be more agressive

107
Q

Goals of therapy for prostate cancer

A

localized disease:
cure
control disease and symptoms
decrease morbidity and mortality

advanced/ metastatic disease
*palliation
*improved qol
*prolong survival

108
Q

factors to consider for prostate cancer treatment

A

pt comorbidities

pt symptoms

recurrence risk

pt life expectancy (expected survivial

disease stage
** for localized and regional disease, treatment approach is based on RISK STRATIFICATION rther than stage

109
Q

Local prostate cancer disease recurrence risk stratification

A

Recurrance Risk: Very low
expected survival
1) <10 years
* initial therapy: observation
2) 10-20 years
*initial therapy: Active surveillance
3) >/20 years
*initial therapy:

110
Q

Prostate cancer treatment

A

gold standard: Androgen Deprivation therapy (ADT) for advanced prostate cancer

testosterone is the driving force of prostate cancer

surgical castration: bilateral orchiectomy
!!!Medical Castration:
*LHRH agonists+/- antiandrogen
*LHRH antagonist

intent is to lower levels of testosterone

111
Q

prostate cancer treatment

LHRH agonists

A

moa: mimics endogenous LHRH, causing sustained release of LH and FSH. release of lh and fsh would normally cause production of testosterone. howevere, sustained release causes negative feedback loop, decreasing the amount of testosterone produced.

ex: Leuprolide (Trelstar), Goserelin (Zoladex)

112
Q

LHRH agonist adverse effects

A

acute: tumor flare (due to short term increase in testosterone due to LH an FSH), hot flashes, erectile dysfunction, edema, gynecomastia, injection site reaction

Long term: osteoporosis, clinical fracture, insulin resistance, increased risk of diabetes, CV events, alteration in diabetes

113
Q

moa of initial tumor flare in prostate cancer

A

cause by a surge in lh/fsh release, causing increased testosterone production.

SS: increased bone pain (if metastatic) or increased urinary SS
resolves after 2 weeks
starting a first gen anti androgen before admin of LHRH agonist and continuing for 2-4 weeks frequently used to mitigate tumor flare.

baseline bone mineral density test bfore starting longterm ADT (calcium and vit. D supplementation

114
Q

LHRH antagonists

A

moa: binds to GnRH receptors in on cells in pituitary gland, dramatically reducing LH/FSH resulting reduced production of testosterone to castrate levels

ex:Degarelix
Relugolix

advantage: much faster drop in testosterone levels
castration levels seen in 7 days or less compared to 28 days w. lhrh agonists. no tumor flare and thus no antiandrogen needed

cons: less flexible indosing schedule, high cost

115
Q

anti androgens in prostate cancer

A

moa: inhibits anrogen uptke and/orbinding in target tissues. specifcally, a competitice inhibitor for the binding of DHT and testtosterone

first gen:
bicalutamide
flutamide
nilutamise

second gen:
apalutamide
enzalutimaide
darolutamide

2nd gen more potent

ade: diarrhea, gynecomastia, elevated lft, hot fashes
monitoring: lfts monthly

116
Q

combined androgen blockade in prostate cancer

A

lhrh agonist or antagonist +anti androgen

contraversial
associated w. more ADE

117
Q

Castration sensitive prostate cancer therapy options

A

ADT+ abiraterone or Apalutamide or Enzalutamide

ADT w. docetaxel x6 cycles +abiraterone or darolutmidde
*use din high volume castration sensitive metastatic prostate cancer

choice of regimen invoes discussion w. pt about potential toxicities of abiraterone and docetaxel as well as cost of treatment

118
Q

castration resistant prostate cancer

A

serum testosterone <50 ng and disease progression

nccn recommendation: continue adt and maintain castrate levels while adding therapies

therapy base don whether pt has non metastatic m0 or metastatic m1 disease

119
Q

treatment for nometastatic m0 CRPC

A

M0-> continue AT to maintain castrate tstosterone

if PROSTATE DOUBLES >10 MONTHS
A) MONITOR or
2) other secondary hormone therapy

id prostate doubles <10 months
a) apalutamide
b)enzalutamide

120
Q

secondary hormone therapies for castration resistant prostate cancer CRPC

A

continue ADT to maintain castarte levels of testosterone and add:

2nd gen antiandrogen
*apalutamide for m0 and PSADT </10 months
darolutamide for m0 and PSADT </10 months
enzalutamide for m0 and PSADT </10 months and M1

androgen metabolism inhibitor
abiraterone w. prednisone or methylprednisolone

etc.

121
Q

Second generation antiandrogen therapies

Apalutamide (Erleada)

moa
dosing
ADE
considertions/pearls

A

Second generation antiandrogen therapies

moa: nonsteroidal androgen receptor inhibitor, binds dirctly to androgen receptor preventing androgen translocation, dna binding, and transcription. causes decreased prolifration of tumor cells and increased apoptosis leading to decreased tumor volume

dosing 240 mg once daily w. or w.o food

ADE: fatigue, htn

considertions/pearls
*ci in pts w. seizures

122
Q

Second generation antiandrogen therapies

Darolutamide

moa
dosing
ADE
considertions/pearls

A

Second generation antiandrogen therapies

moa
dosing
ADE
considertions/pearls
no increase risk in seizures
renal dosing

123
Q

Second generation antiandrogen therapies

Enzalutamide

moa
dosing
ADE
considertions/pearls

A

Second generation antiandrogen therapies

moa
dosing
ADE
considertions/pearls
*increased risk of seizures

124
Q

treatment of m1 CRPC

no prior docetaxel/ no prior hormone therapy

A

MOST PROSTATE CANCERS ARE ADENOCARCINOMAS. IF HISTOLOGY IS UNKOWN, TREAT AS IF ADENOCARCINMOMA.

no prior docetaxel/ no prior hormone therapy

preffered regimens
*abiraterone
docetaxel
enzalutamide

cirtain circumstances:
radium 223 for symptomatic bone metas.
sipuleacual

125
Q

treatment of m1 CRPC

prior hormone therapy/no prior docetaxel/

A

preferred: docetaxel

126
Q

treatment of m1 CRPC

prior docetaxel/ no prior hormone therpay

A

preferred: abiraterone
cabazitaxel
enzalutamide

127
Q

treatment of m1 CRPC

prior docetaxel and prior novel hormone therapy

A

preferred regimend:
docetaxel rechallange, cabazitaxel

128
Q

summary of treatment of m1 crpc 1st line

A

if pt has viseral metas (liver, lung, adrenal, peritoneum,brain (consider docetaxel if pt has not recieved it and pt is fit for chemo

no viseral metas.: treat based on prior therapy

symptomatic bone metas: radium 223

asymptomatic or minimally symptomatic, no liver metas, life expectancy> 6 months.. consider sipuleucal-T

129
Q

chemo therapy agents for m1 prostate cancer

Docetaxel

moa:
dose:
ade:
considerations/ pearls

A

chemo therapy agents for prostate cancer

moa:microtubule inhibitot

dose: dose+prednisone

ade:
*alopecia, myelosupression, peripheral neuropathy, hypersensitivity reaction (premidcate before)

considerations/ pearls:
cause hepatic impairment

130
Q

chemo therapy agents for m1 prostate cancer

Abiraterone (Zytiga)

moa:
dose:
ade:
considerations/ pearls

A

chemo therapy agents for prostate cancer

moa: inhibits CYP17. responsible for androgen biosynthesis in many diff tissues, inhibits formtion of testosterone precursors

dose:

ade:hypokalemia, diarrhea, edma, htn, hepatotoxicity

considerations/ pearls:
give w. steroids to prevent hypokalemia due to mineralcorticoid excesscaused by drug long term.
prednisone can increase glucose
*monitor lft, K+, po4, bp on monthly basis

131
Q

chemo therapy agents for m1 prostate cancer

Abiraterone

moa:
dose:
ade:
considerations/ pearls

A

chemo therapy agents for prostate cancer

moa:
dose:
ade:
considerations/ pearls:
*pt must always recieve w. steroid

132
Q

therapy agents for m1 prostate cancer

radium-223

moa:
dose:
ade:
considerations/ pearls

A

chemo therapy agents for prostate cancer

moa:
dose:
ade:
considerations/ pearls
only used in pt w. bone metas. ONLY and no visceral metas.
not used in combo w. chemo

133
Q

chemo therapy agents for prostate cancer

Sipulecual T (provenge)

moa:
dose:
ade:
considerations/ pearls

A

chemo therapy agents for prostate cancer

moa: dendritic cell vaccine designed to enhance t cell immune response to prostatic acid phosphatase

cells exposed to PAP fused with GM-CSF).
dose:
ade:infusion reactions
considerations/ pearls
$100,000 per dose

134
Q

second line therpiaes for m1 pc

A

if prir chemo, consider hormone therpay
*cabazitaxel
cabazitxel/ carboplatin
LU-177-PSMA-617

other trtments
*pembralizumab
radium 223 bone metastesis
etc.

135
Q

chemo therapy agents for prostate cancer

cabazitaxel

moa:
dose:
ade:
considerations/ pearls

A

chemo therapy agents for prostate cancer

moa: microtubule inhibitor
dose:
ade:*febrine neutropenia
considerations/ pearls
2nd line if pt still has disease progression
*pt must be on prednisone

136
Q

supportive care in prostate cancer

A

adt associted w. increase risk of bone fracture
*baseline dexa scans
*calcium 1000-1200 mg daily and vit. 400-800 iu

bone metas.: must give bone modifying agents
*Zolendronic acid, denosumab (at doses didfferent than in osteoporosis

Critical Care/Hematology/Oncology (4 decks)

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