Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHRM 864: Therapeutics IV > Hematologic Disease Leukemias > Flashcards

Hematologic Disease Leukemias Flashcards

1
Q

What is Chronic Myeloid Leukemia?

A
  • Unregulated Myeloid proliferation of excess mature neutrophil [cell grow and dont die]
  • Philadelphia chromosome = Bcr/Abl
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the Phiadelphia Chromosome in Chronic Myeloid Leukemia?

A
  • Break in chromosome 9 & 22 = Bcr/Abl
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A
  • No known risks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the presentation of Chronic Myeloid Leukemia?

A
  • Find out by accident
  • Fatigue, Sweating, Bone Pain, Weight Loss
  • Full Faster
  • Leukocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Leukocytosis?

A
  • MEDICAL EMERGENCY!!
  • 1,000,000 cells/mm3
  • Risk of Leukostasis = Thick Blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the Diagnosis for Chronic Myeloid Leukemia?

A
  • Bone Marrow Biopsy
  • FISH or PCR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is important to know about Imatinib?

A
  • Daily
  • 3A4
  • NAUSEA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is important to know about Dasatinib?

A
  • Daily [avoid acid reducers]
  • 3A4
  • Fluid retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is important about Nilotinib?

A
  • BID [Empty Stomach]
  • 3A4
  • QTc Prolongation, Metaboic Syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is important about Bosutinib?

A
  • Daily
  • 3A4
  • DIARRHEA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is important about Ponatinib?

A
  • Daily
  • 3A4
  • ISCHEMIC REACTIONS, HYPERTENSION
  • Works with T315I resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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`
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is Chronic Lymphoid Leukemia?

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?

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

What is the presentation for Chronic Lymphoid Leukemia?

A
  • Accidentally finding it
  • Maybe recurrent sinus infection
25
Q

What are we looking for in cytogenetics within Chronic Lymphoid Leukemia?

A
  • Del(11q) with organ failure [lymphadenopathy]
  • Del(17p) is bad = TP53 lost [no checkpoint in apoptosis]
26
Q

What is the Diagnosis of Chronic Lymphoid Leukemia?

A
  • Monoclonal B lymphocytes > 5x10^9
  • Look for CD19, CD20, CD5, CD23, CD10
27
Q

What is the treatment overview for Chronic Lymphoid Leukemia?

A
  • Treatment reserved for Stage III or IV; Organ Failure; clinical symptoms
  • DONT treatment a Number?
28
Q

What are some of the treatment options for Chronic Lymphoid Leukemia?

A
  • Acalabrutinib +/- Obinutuzumab
  • Venetoclax + Obinutuzumab
  • Zanubrutinib
29
Q

What are the BTK inhibitors that are use in Chronic Lymphoid Leukemia?

A
  • Ibrutinib, Zanubrutinib, Acalabrutinib
  • Stops phophorylation in B-Cells
30
Q

What did the trials for the BTK inhibitors show for Chronic Lympoid Leukemia?

A
  • That Ibrutinib had toxicities
  • ALPINE showed Zanubrutinib was better
31
Q

What is Venetoclax within Chronic Lymphoid Leukemia?>

A
  • Inhibits BCL-2 resulting in release of BIM and PUMA –> releases proapoptotic proteins
32
Q

What is important to know about Ventoclax in Chronic Lymphoid Leukemia?

A
  • PGP interactions: inhibits or induces
  • 3A4 interactions
33
Q

Give a brief summary of Chronic Lympoid Leukemia?-

A
  • Early Stage ONLY observe
  • Treatment is based on age, comorbidites, cytogenetics [Del(17p) is bad]
  • Lymphocytosis = BTK inihibitors and Idelalisb
34
Q

What is AML?

A
  • Arise from single leukemia cells that expand & acquire additional mutation causing proliferations resulting in monoclonal population of leukemic cells [single clone that expands]
35
Q

What are some of the risk factors for AML?

A
  • Unknown
  • from other diseases?
  • Genetics or Environmental?
36
Q

What is the presentation of AML?-

A
  • Pancytopenia: Anemia [fatigue, pallor, palpitations], Neutropenia [infections], Thrombocytopenia [bleeding]
  • Bone Pain
37
Q

What is the risk stratification/cytogenetics within AML?

A
  • Favorable [NPM1 & CEBPA]
  • Intermediate [NPM1+FLT3-ITD]
  • Unfavorable [FLT3-ITD (bad)]
38
Q

What is important to know about the FLT3 Mutation in AML?

A
  • Newly Diagnosed AML
  • Worse overall prognosis [more aggressive, lower remission]
  • TKIs: Midostaurin, Gilteritinib, Quiartinib
39
Q

What is the treatment goal for AML?

A
  • Induction of remission to cause consolidation [preventing relapse]
  • Consolidation: Favorable - Chemo; Unfavorable - transplant
40
Q

What is the treatment for AML?

A
  • 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
Q

What is Instensive Chemotherapy 7+3 in AML?

A
  • INDUCTION
  • Cytarabine x7d
  • Idarubicin or Daunorubicin x3d
42
Q

What is used for Consolidation in AML?

A
  • Cytarabine [HiDAC] - Dose depends on age
  • Cerebellar side effects & Conjunctivitis
43
Q

What do you use in FLT3+ Positive Disease in AML?

A
  • Midostaurin [QTc Prolongation & Nausea]
  • Gilterinib
44
Q

What is a brief summary of AML?

A
  • BONE MARROW BIOPSY
  • Treatment is induction and consolidation [induce remission then eradicate disease]
45
Q

What is ALL?

A
  • Arise from single leukemia cells that expand & acquire additional mutation causing proliferations resulting in monoclonal population of leukemic cells [single clone that expands]
46
Q

What are the risk factors for ALL?

A
  • Genetic, Radiation, EBV/HIV [because of lymphoid]
47
Q

What is the presentation of ALL?

A
  • Pancytopenia: Anemia [fatigue, pallor, palpitations], Neutropenia [infections], Thrombocytopenia [bleeding]
  • Bone Pain
  • Can go into brain
48
Q

What is the diagonsis of ALL?

A
  • BONE MARROW biopsy
49
Q

What is one thing we look for in ALL?

A
  • Philadelphia Chromosome [BCR-ABL] - both in myeloid & lymphoid
  • TKI added to Chemo
50
Q

What is the adult treatment overview for ALL?

A
  • 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
Q

What is main treatment for ALL?

A
  • HyperCVAD
52
Q

What is in HyperCVAD?

A
  • Hyper-Fractionated Cyclophosphamide
  • Vincristine
  • Doxorubicin
  • Dexamethasone
  • THEN: Methotrexate & Cytarabine
53
Q
A

PHRM 864: Therapeutics IV (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions