Acute Leukemia Flashcards
1
Q
Initial Presentation
A
- Pancytopenia => pallor, fatigue, anorexia, bleeding, infection
- Febrile neutropenia
- Pancytopenia requires transfusions and won’t stop until remission occurs
- Hyperuricemia, before or soon after first treatment
2
Q
Hyperuricemia Treatment
A
- Allopurinol 300 mg with IV hydration including sodium bicarbonate
- Start a few days before first chemo to prevent tumor lysis syndrome
- Use rasburicase in those with significant uric acid elevations, renal dysfunction, or high WBC
3
Q
Acute Lymphoblastic Leukemia Treatment
A
- Combination chemo
- 3 phases: remission induction, consolidation, and maintenance phases
4
Q
Induction Phase
A
- Given regardless of ANC and platelet counts
- Prednisone or Dexamethasone, vincristine, L-asparaginase, +/- daunorubicin
- Duration ~4 weeks
- 2nd inductions used
- Adults and high risk children often have 2nd induction
5
Q
CNS Preventative Therapy
A
- Present in most patients and undetectable
- Caused relapse in CNS and then bone marrow
- IT chemo is used with methotrexate +/- cytarabine and hydrocortisone (PF saline)
- Begins in induction phase and continues through each phase
- Methotrexate dosing varies by age
6
Q
Induction Agent AE
A
- Vincristine: neurotoxicity (fatal IT), give with laxatives
- Prednisone/Dexamethasone: behavioral changes, increased appetite
- Asparaginase: allergic rxn, rare clotting/bleeding or pancreatitis
- Daunorubicin/Doxorubicin: N/V, myelosuppression, cardiotox, vesicant injury
- Methotrexate: N/V
7
Q
Consolidation Phase
A
- Intensification/Re-intensification
- Decreases risk of developing resistance
- ~25 weeks generally
- CSF agents not usually employed during ALL treatment
- Antiemetic support is often needed
- Higher dose methotrexate is sometimes employed but the regimen is generally based on specific types of ALL
8
Q
Possible Consolidation Regimen Options
A
- Cyclophosphamide
- Cytarabine
- Mercaptopurine
- Methotrexate
- Vincristine
- PEG asparaginase
- Doxorubicin
- Dexamethasone
9
Q
Maintenance
A
- AKA Continuation Therapy
- ~100 weeks, excluding mature B-cell ALL
- Most would relapse without this therapy
- Methotrexate + mercaptopurine + VP pulses
- Vincristine + Prednisone (sometimes dexa instead) shown to improve outcome in all patients
- IT chemo approx every 12-16 weeks
- AE: low level myelosuppression, hepatic enzyme elevations
10
Q
Dose Adjusting Maintenance Therapy
A
- Based on WBC monitoring QW or QoW
- Maintain ANC in target range on 500-1500
- Adjust dosing based on a 6 week period
- Alternating dose increases of methotrexate or mercaptopurine by ~25% with at least 6-8 weeks between increases
- Impact of steroids on ANC elevation needs to be considered when deciding on methotrexate/mercaptopurine increases
11
Q
Treatment of Relapse
A
- Bone marrow relapse is most common
- Relapses during maintenance have worse prognosis for maintaining remission
- 4-drug induction regimen recommended: vincristine, prednisone, asparaginase, and daunorubicin
- Need another CNS prevention course and 2-3 years of more intensive consolidation/maintenance phases
- Some may be able to get bone marrow transplant
12
Q
Testicular Relapse?
A
- Testicular radiation therapy with 2400cGy +
- Chemotherapy listed for normal relapse patients
13
Q
Pharmacological Issues with ALL
A
- IDMTX: better remission rates but worse neurotoxicity
- Imatinib can be used for CML and BCR/AML+ ALL
- Late effects in life: cardiotox, skeletal morbidity (esp with dexamethasone), neurotoxicity
14
Q
AML
A
- Acute Myeogenous Leukemia
- Chemo approach depends on age, performance status, and genetics
- Standard chemo components: daunorubicin OR idarubicin + cytarabine
- Courses repeated 2-4 times based on risk status, response, and tolerance
- Severe myelosuppression, N/V, and mucositis
- CNS treatment with systemic chemo
- Post-remission therapy done after initial chemo and can include same agents with different dosing/schedules/etc
- Genetics is big determiner in resistance
15
Q
APML
A
- Acute Promyelocytic Leukemia
- Subtype of AML, 10% of AML
- Binding of retinoids leads to cell differentiations
- Has its own induction and consolidation phase
