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PHRM 864: Therapeutics IV > Hematologic Disease Leukemias > Flashcards

Hematologic Disease Leukemias Flashcards

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1
Q

What is Chronic Myeloid Leukemia?

A
  • Unregulated Myeloid proliferation of excess mature neutrophil [cell grow and dont die]
  • Philadelphia chromosome = Bcr/Abl
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2
Q

What is the Phiadelphia Chromosome in Chronic Myeloid Leukemia?

A
  • Break in chromosome 9 & 22 = Bcr/Abl
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3
Q

What are some of the risk factors in Chronic Myeloid Leukemia?

A
  • No known risks
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4
Q

What is the presentation of Chronic Myeloid Leukemia?

A
  • Find out by accident
  • Fatigue, Sweating, Bone Pain, Weight Loss
  • Full Faster
  • Leukocytosis
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5
Q

What is Leukocytosis?

A
  • MEDICAL EMERGENCY!!
  • 1,000,000 cells/mm3
  • Risk of Leukostasis = Thick Blood
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6
Q

What is the Diagnosis for Chronic Myeloid Leukemia?

A
  • Bone Marrow Biopsy
  • FISH or PCR
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7
Q

What is the difference between FISH and PCR in Chronic Myeloid Leukemia ?

A
  • PCR = selected segment [more sensitive]
  • FISH = detects a specific DNA sequence
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8
Q

What are the phases of Chronic Myeloid Leukemia?

A
  • Chronic Phase: <10% blasts [immature cells]
  • Accelerated Phase: 10-19% blasts
  • Blast Crisis: >20% blasts; terminal stage
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9
Q

What is the treatment for Chronic Myeloid Leukemia?

A
  • NO TREATMENT; FATAL IN 5 YEARS
  • Goal: lower leukemic clone with Tyrosine Kinase Inhibitors
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10
Q

What is important to know about the Treatment Response Criteria for Chronic Myeloid Leukemia?

A
  • Want the molecular response to be DEEP: BCR-ABL < 0.01%
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11
Q

What is the main TKI that is used in Chronic Myeloid Leukemia and what trial showed it effetiveness?

A
  • Imatinib
  • IRIS trial [everyone was either on or swtiched to it]
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12
Q

What is important to know about the Adverse effects from Imatinib within Chronic Myeloid Leukemia?

A
  • Neutropenia, Thrombocytopenia, Anemia [all subside within 4 years]
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13
Q

What are the 2nd generation TKIs that are used in Chronic Myeloid Leukemia?

A
  • Dasatinib, Nilotinib, Bosutinib
  • Approved as 1st line
  • Really only used when Imatinib cant be used
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14
Q

What is important to know about Imatinib?

A
  • Daily
  • 3A4
  • NAUSEA
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15
Q

What is important to know about Dasatinib?

A
  • Daily [avoid acid reducers]
  • 3A4
  • Fluid retention
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16
Q

What is important about Nilotinib?

A
  • BID [Empty Stomach]
  • 3A4
  • QTc Prolongation, Metaboic Syndrome
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17
Q

What is important about Bosutinib?

A
  • Daily
  • 3A4
  • DIARRHEA
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18
Q

What is important about Ponatinib?

A
  • Daily
  • 3A4
  • ISCHEMIC REACTIONS, HYPERTENSION
  • Works with T315I resistance
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19
Q

What is the most common resistance that is found in Chronic Myeloid Leukemia and how is it formed?

A
  • T315I
  • Overexpression; Mutated kinase domains; gene alterations`
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20
Q

What is the treatment summary of Chronic Myeloid Leukemia?

A
  • Start: Imatinib
  • Then: Dasatinib, Niloinib, Bosutinib
  • T315I: Ponatinib, Asciminib [NEW]
  • NO mutation: Stem Cell Transplant
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21
Q

Give a brief summary for Chronic Myeloid Leukemia?

A
  • Caused by BCR-ABL [Philadelphia Chromosome; 9 & 22]
  • Three Phases: Chronic, Accelerated, Blast Crisis
  • TKIs!!!! based on patient and resistanceq
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22
Q

What is Chronic Lymphoid Leukemia?

Study These Flashcards
A
  • Monoclonal B lymphocytes transform, causing expansion [NO apoptosis], then Lymphocyte accumulation
  • Possible Richter’s transformation
23
Q

What are some of the risk factors for Chronic Lymphoid Leukemia?

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A
  • Family Hx: 1st Degree
  • Male
  • White
  • Old
    :(
24
Q

What is the presentation for Chronic Lymphoid Leukemia?

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A
  • Accidentally finding it
  • Maybe recurrent sinus infection
25
What are we looking for in cytogenetics within Chronic Lymphoid Leukemia?
- Del(11q) with organ failure [lymphadenopathy] - Del(17p) is bad = TP53 lost [no checkpoint in apoptosis]
26
What is the Diagnosis of Chronic Lymphoid Leukemia?
- Monoclonal B lymphocytes > 5x10^9 - Look for CD19, CD20, CD5, CD23, CD10
27
What is the treatment overview for Chronic Lymphoid Leukemia?
- Treatment reserved for Stage III or IV; Organ Failure; clinical symptoms - DONT treatment a Number?
28
What are some of the treatment options for Chronic Lymphoid Leukemia?
- Acalabrutinib +/- Obinutuzumab - Venetoclax + Obinutuzumab - Zanubrutinib
29
What are the BTK inhibitors that are use in Chronic Lymphoid Leukemia?
- Ibrutinib, Zanubrutinib, Acalabrutinib - Stops phophorylation in B-Cells
30
What did the trials for the BTK inhibitors show for Chronic Lympoid Leukemia?
- That Ibrutinib had toxicities - ALPINE showed Zanubrutinib was better
31
What is Venetoclax within Chronic Lymphoid Leukemia?>
- Inhibits BCL-2 resulting in release of BIM and PUMA --> releases proapoptotic proteins
32
What is important to know about Ventoclax in Chronic Lymphoid Leukemia?
- PGP interactions: inhibits or induces - 3A4 interactions
33
Give a brief summary of Chronic Lympoid Leukemia?-
- Early Stage ONLY observe - Treatment is based on age, comorbidites, cytogenetics [Del(17p) is bad] - Lymphocytosis = BTK inihibitors and Idelalisb
34
What is AML?
- Arise from single leukemia cells that expand & acquire additional mutation causing proliferations resulting in monoclonal population of leukemic cells [single clone that expands]
35
What are some of the risk factors for AML?
- Unknown - from other diseases? - Genetics or Environmental?
36
What is the presentation of AML?-
- Pancytopenia: Anemia [fatigue, pallor, palpitations], Neutropenia [infections], Thrombocytopenia [bleeding] - Bone Pain
37
What is the risk stratification/cytogenetics within AML?
- Favorable [NPM1 & CEBPA] - Intermediate [NPM1+FLT3-ITD] - Unfavorable [FLT3-ITD (bad)]
38
What is important to know about the FLT3 Mutation in AML?
- Newly Diagnosed AML - Worse overall prognosis [more aggressive, lower remission] - TKIs: Midostaurin, Gilteritinib, Quiartinib
39
What is the treatment goal for AML?
- Induction of remission to cause consolidation [preventing relapse] - Consolidation: Favorable - Chemo; Unfavorable - transplant
40
What is the treatment for AML?
- Intensive: Cytarabine + Anthracycline 7+3 - Low to Moderate: Venetoclax + Hypo-methylating agent - Low-Intensity: Hypo-methylating agents; low does chemo - Supportive Care: Blood products
41
What is Instensive Chemotherapy 7+3 in AML?
- INDUCTION - Cytarabine x7d - Idarubicin or Daunorubicin x3d
42
What is used for Consolidation in AML?
- Cytarabine [HiDAC] - Dose depends on age - Cerebellar side effects & Conjunctivitis
43
What do you use in FLT3+ Positive Disease in AML?
- Midostaurin [QTc Prolongation & Nausea] - Gilterinib
44
What is a brief summary of AML?
- BONE MARROW BIOPSY - Treatment is induction and consolidation [induce remission then eradicate disease]
45
What is ALL?
- Arise from single leukemia cells that expand & acquire additional mutation causing proliferations resulting in monoclonal population of leukemic cells [single clone that expands]
46
What are the risk factors for ALL?
- Genetic, Radiation, EBV/HIV [because of lymphoid]
47
What is the presentation of ALL?
- Pancytopenia: Anemia [fatigue, pallor, palpitations], Neutropenia [infections], Thrombocytopenia [bleeding] - Bone Pain - Can go into brain
48
What is the diagonsis of ALL?
- BONE MARROW biopsy
49
What is one thing we look for in ALL?
- Philadelphia Chromosome [BCR-ABL] - both in myeloid & lymphoid - TKI added to Chemo
50
What is the adult treatment overview for ALL?
- Induction to cause remission then consolidate with eradicating the disease follwoed by maintenace to prevent relapse - CAN HIDE IN BRAIN AND TESTES [intrathecal chemo]
51
What is main treatment for ALL?
- HyperCVAD
52
What is in HyperCVAD?
- Hyper-Fractionated Cyclophosphamide - Vincristine - Doxorubicin - Dexamethasone - THEN: Methotrexate & Cytarabine
53

PHRM 864: Therapeutics IV (28 decks)

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