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Thera IX > 21 Leukemia Chow > Flashcards

21 Leukemia Chow Flashcards

1
Q

What is Leukemia?

A

A group of malignant diseases of the bone marrow and blood resulting from uncontrolled proliferation of myeloid or lymphoid cells

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2
Q

What is AML?

A

Acute Myelogenous Leukemia

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3
Q

What is CML?

A

Chronic Myelogenous Leukemia

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4
Q

What is ALL?

A

Acute Lymphocytic Leukemia

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5
Q

What is CLL?

A

Chronic Lymphocytic Leukemia

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6
Q

What is Acute Leukemia?

A

Impaired differentiation and proliferation of immature cells (blasts). Sudden onset and rapid progression. Survival: weeks to months without treatment

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7
Q

What is Chronic Leukemia?

A

Proliferation of relatively mature cells. Slow onset, often asymptomatic. Survival: years with supportive care

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8
Q

What is the average age at diagnosis for AML?

A

67

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9
Q

What is the pathogenesis of AML?

A

Leukemic blast cells: 1) have limited ability to differentiate normally, 2) crowd out other cells and inhibit normal hematopoiesis in bone marrow, 3) May affect one or more myeloid lineages, 4) “leak” into peripheral blood

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10
Q

What is the clinical presentation of AML?

A

Neutropenia (frequent infection, fever). Thrombocytopenia (easy bruising and bleeding). Anemia (fatigue, pale mucous membranes). Lab abnormalities (increased LDH, uric acid, serum creatinine, etc)

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11
Q

What is the treatment overview for AML?

A

AML progresses rapidly –> treatment should be initiated ASAP. Treat with CURATIVE intent for most patients. Choice of therapy depends on age, comorbidities, performance status, and cytogenetics. Chemotherapy

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12
Q

What are the treatment phases for AML?

A

Induction (achieve disease remission (normal blood count, no bone marrow disease)). Consolidation (eradicate residual disease and reduce risk of relapse). Maintenance (destroy any remaining leukemic cells to maintain disease-free state)

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13
Q

What is the standard therapy for AML Induction (< 60 yo)?

A

Combination of cytarabine and an anthracycline (1-2 cycles). “7+3”: Cytarabine on days 1-7, and Idarubicin or Daunorubicin on days 1-3

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14
Q

What is an alternative to the “7+3” treatment for AML induction (< 60 yo)?

A

HiDAC = High Dose Ara-C (1 cycle). Cytarabine (high dose) and Ibarubicin or Daunorubicin on days 1-3

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15
Q

What is the treatment of AML Induction (> 60 yo) like?

A

High frequency of unfavorable cytogenetics, secondary AML, and comorbidities. Choice of treatment depends on performance status and cytogenetics: Standard induction (7+3), Low intensity chemotherapy (who can’t handle 7+3). Intermediate intensity chemotherapy. Best supportive care

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16
Q

What are the ADRs with Idarubicin (Idamycin)?

A

Cumulative cardiotoxicity (>150mg/m2), as with most anthracyclines. Myelosuppression, alopecia, increased LFTs, urine discoloration. VESICANT

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17
Q

What is the emetogenicity like for Idarubicin?

A

Moderate

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18
Q

What are the ADRs with Cytarabine (Ara-C)?

A

Myelosuppression, fever, rash, tumor lysis syndrome

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19
Q

What is the Emetogenicity with Cytarabine (Ara-C)?

A

Low to moderate

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20
Q

What is the problem with HIGH DOSE Cytarabine (Ara-C)?

A

Myelosuppression. Cerebellar toxicity (watch for tremors,slurred speech, etc). Conjunctivitis

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21
Q

What is Clofarabine (Clolar) used for?

A

Relapsed pediatric ALL. In elderly patients with AML with poor prognostic factors

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22
Q

What are the ADRs with Clofarabine (Clolar)?

A

Myelosuppression! Capillary leak syndrome, hepatotoxicity

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23
Q

What is the Emetogenicity like for Clofarabine (Clolar)?

A

Moderate

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24
Q

What is Azacitidine (Vidaza)?

A

DNA Hypomethylator

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25
Q

What is Azacitidine (Vidaza) used for?

A

Myelodysplasic syndrome (MDS). In elderly patients with AML with low blast count (20-30%)

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26
Q

What are the ADRs with Azacitidine (Vidaza)?

A

Myelosuppression! N/V

27
Q

What is the Emetogenicity like with Azacitidine (Vidaza)?

A

Moderate

28
Q

What is Decitabine (Dacogen)?

A

Similar to Azacitidine. Approved for MDS and in elderly patients with AML

29
Q

What are the ADRs with Decitabine (Dacogen)?

A

Myelosuppression, fatigue

30
Q

What is the Emetogenicity with Decitabine (Dacogen)?

A

Minimal

31
Q

What is Laboratory Tumor Lysis Syndrome (TLS)?

A

Two or more of the following within 3 days before or 7 days after chemotherapy: Hyper K > 6 (or 25% increase), Hyper phos > 4.5 (or 25% increase), Hypo Ca < 7 (or 25% decrease), Hyperuricemia > 8 (or 25% increase)

32
Q

What is Clinical TLS?

A

Laboratory TLS + one or more of the following: SCr > 1.5 xULN. Seizure. Cardiac arrhythmia/sudden death

33
Q

What is the Clinical presentation of TLS?

A

Renal failure. Hyperuricemia (N/V, lethargy, gout exacerbation). Hyperkalemia (muscle weakness). Hyperphosphotemia. Hypocalcemia (muscle cramps, seizures, tetany)

34
Q

What are the risk factors for TLS?

A

High tumor burden (WBC > 25k, LDH > 1500). High proliferation rate. High chemo-sensitivity. Pre-existing renal insufficiency. Patient risk factors: baseline hyperuricemia, acidic urine, dehydration, age, medications

35
Q

What is the prevention and management of TLS?

A

Begin 24-48 hrs prior to cytotoxic treatment. Hydration +/- diuresis. Urine alkalinization. Allopurinol. Rasburicase

36
Q

What is Pathogenesis of CML?

A

(+) Philadelphia chromosome: t(9;22) resulting in BCR-ABL fusion gene, a constitutively active tyrosine kinase. Uncontrolled proliferation of mature appearing granulocytes in the bone marrow. Increase of immature and mature granulocytes in peripheral blood

37
Q

What is the average age of Chronic Myelogenous Leukemia (CML)?

A

65 yo

38
Q

What are the different phases of CML?

A

Chronic, Accelerated, Blast

39
Q

What is Chronic Phase of CML?

A

Duration: 3-6 years. Indolent course characterizes of increase in WBC. Minor, nonspecific symptoms. < 5% blast

40
Q

What is Accelerated Phase of CML?

A

Duration: 6-9 months. Worsening myeloid differentiation and maturation. Leukocytosis, bone pain, anemia, bleeding, thrombo-cytosis/-penia

41
Q

What is Blast Crisis?

A

Duration: 3-6 months survival. Transformation of acute leukemia. > 20% blasts

42
Q

What are the treatment principles of CML?

A

Immediate treatment is required for severe leukocytosis (severe leukocytosis (WBC > 100k) can lead to leukostasis, with WBC infiltrating tissues of major organs). Control WBC in chronic phase and delay progression to accelerated/blast phases. Treat accelerated/blast phase CML with induction chemotherapy to return to 2nd chronic phase. Allogeneic stem cell transplant is the only curative therapy

43
Q

What is the 1st line treatment for Chronic Phase CML?

A

Tyrosine Kinase Inhibitors: Imatinib (Gleevec), Dasatinib (Sprycel), Nilotinib (Tasigna)

44
Q

What are the common ADRs with Imatinib (Gleevec)?

A

N/V, GI irritation (take with food, may disperse tablet in water or apple juice, stir until dissolved and use immediately)! Myalgias, muscle cramps, arthralgia!

45
Q

What are the serious ADRs with Imatinib (Gleevec)?

A

Fluid retention, edema, weight gain! Myelosuppression! Hepatotoxicity. Rare cardiotoxicity

46
Q

What are the DDIs like with Imatinib (Gleevec)?

A

Major substrate and strong inhibitor of CYP 3A4

47
Q

What is resistance to Imatinib (Gleevec) like?

A

To overcome resistance: increase dose of Imatinib (better response rate, but also more ADRs), New TKI with better binding affinity to BCR-ABL

48
Q

What is good about Dasatinib (Sprycel)?

A

Active in binding site-mutations that cofer resistance to Imatinib (except for T315I)

49
Q

What is patient education for Dasatinib (Sprycel)?

A

Take with or without food. Do not crush or chew tabs. Separate antacids by at least 2hrs, avoid H2RA/PPI

50
Q

What are the ADRs of Dasatinib (Sprycel)?

A

Myelosuppression. Bleeding. Fluid retention. QT prolongation

51
Q

What are the DDIs with Dasatinib (Sprycel)?

A

Substrate and Inhibitor of CYP 3A4. Similar to drug interactions as Imatinib

52
Q

What is good about Nilotinib (Tasigna)?

A

Active in binding site-mutations that confer resistance to Imatinib (except for T315I). 3-7x more potent in Imatinib-sensitive cell lines (20-50x more potent in Imatinib-resistant cell lines). NOT approved for patients in blast crisis

53
Q

What is patient education for Nilotinib (Tasigna)?

A

Take on EMPTY stomach. Do not open capsule; swallow capsule whole

54
Q

What are the ADRs with Nilotinib (Tasigna)?

A

Myelosuppression (hold for ANC < 1 or platelet < 50k)! QT prolongation! Hepatotoxicity. Endocrine: hyperglycemia, increased lipase. Less fluid retention vs. Imatinib and Dasatinib

55
Q

What is the DDI like with Nilotinib (Tasigna)?

A

Substrate and strong inhibitor of CYP 3A4

56
Q

In the study, what is the efficacy of Dasatinib and Nilotinib as 1st line treatments?

A

Shows that Dasatinib and Nilotinib were more efficacious than Imatinib

57
Q

How does Bosutinib (Bosulif) work?

A

Active in binding site-mutations that confer resistance to Imatinib (except for T315I and V229L). May also be active in patients with certain BCR-ABL mutations resistant to Dasatinib (e.g. F317L) and Nilotinib (e.g. Y253H)

58
Q

What is the FDA indication for Bosutinib (Bosulif)?

A

Chronic/accelerated/blast phase Ph+ CML with resistance or intolerance to prior therapy (Not approved as 1st line treatment of CML)

59
Q

What is patient education for Bosutinib (Bosulif)?

A

Take with food. Do not crush or chew tablet. Separate antacids by at least 2 hrs, avoid H2RA/PPI

60
Q

What are the ADRs with Bosutinib (Bosulif)?

A

GI disturbances (diarrhea, N/V, rash)! Myelosuppression! Transaminitis. Less fluid retention that other TKIs, rare QT prolongation

61
Q

What is Omacetaxine (Synribo)?

A

A cephalotaxine alkaloid that reduces BCR-ABL protein synthesis, independent of direct BCR-ABL binding. Active in multiple CML cell lines, including T315I mutation

62
Q

What is Omacetaxine (Synribo) approved for?

A

Patients in chronic or accelerated phase CML, who are intolerant to or have failed 2 or more prior TKI therapies (Not approved for patients in blast crisis)

63
Q

What are the ADRs with Omacetaxine (Synribo)?

A

Myelosuppression! Common: Diarrhea, Nausea. Hyperglycemia

64
Q

What are the DDIs like with Omacetaxine (Synribo)?

A

NOT a substrate of CYP450 enzymes

Thera IX (29 decks)

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