Hematology Week 3: Acute Lymphoblastic Leukemia/Lymphoma Flashcards
(62 cards)
1
Q
Question 1
A
D) The patient has neutropenia
2
Q
Question 2
A
B
3
Q
Question 3
A
sheets of blast taking over bone marrow
4
Q
A
CD19 positive
CD20 Negative
CD34 Positive
CD33 Negative
TDT Positive
5
Q
Immature markers
A
TDT
CD34
6
Q
B cell marker
A
CD19
7
Q
Myeloid marker
A
CD33
8
Q
Dx is?
A
B cell - ALL
9
Q
Acute Lymphoblastic Leukemia
&
Acute Lymphoblastic Lymphoma
A
10
Q
Where are
Acute Lymphoblastic Leukemia
&
Acute Lymphoblastic Leukemia
Found?
A
11
Q
B-ALL Normal Counterpart
A
Precursor B Lymphocyte
12
Q
B-ALL Key Markers
3 listed
A
- CD19
- CD34
- TdT
13
Q
B-ALL Predominant age
A
<10 years
14
Q
B-ALL Predominant Location
A
Blood and BM
15
Q
B-ALL Prognosis
A
~90%
16
Q
T-ALL Normal counterpart
A
Precursor T lymphocyte
17
Q
T-ALL Key Markers
3 listed
A
- CD3
- CD34
- TdT
18
Q
T-ALL Predominant Age
A
Adolescence
19
Q
T-ALL Predominant Location
A
Tissue (especially the thymus)
20
Q
T-ALL Prognosis
A
<80%
21
Q
ALL Symptoms
8 listed
A
- Fatigue (anemia)
- Fever, infections (neutropenia)
- Bleeding (thrombocytopenia)
- Bone pain (sometimes young children won’t walk or bear weight)
- Lymphadenopathy
- Hepatosplenomegaly
- Mediastinal compression (superior vena cava syndrome) in T-ALL
- CNS manifestations to meningeal involvement
22
Q
ALL onset Timeline
A
Abrupt “stormy” onset (days to weeks)
23
Q
ALL affects what age group
A
Usually children
24
Q
ALL survival
A
25
Simplified risk assessment in B-ALL
Philadelphia chromosome in B-ALL is very bad because of the different cell they are present in and cytogenetic context
26
Question 4
A. ETV6-RUNX1 is present
this fusion is associated with t(12;21)
27
t(12;21) on a karyotype
very difficult to see on karyotype and is called cryptic on karyotype
28
t(12;21)
CoreBindingFactorß+RUNX1 is a transcription factor which promotes genes necessary for maturation and differentiation
ETV6-RUNX1 fusion becomes a repressor instead of a Txn factor
29
Question 5
B NO
He is on the better risk side
30
Phases of Treatment of ALL
4 listed
* Remission induction - the goal is to induce remission
* Intensification/Consolidation - the goal is to eradicate disease below levels of detection
* Maintenance Therapy - the goal is to prevent relapse
* CNS Treatment
31
Anthracycline main toxicity
Cardiac toxicity
32
Only use anthracycline in?
Higher risk patients because of cardiac toxicity
33
Treatment of ALL phase timeline
* Remission Induction - 4-6 weeks
* Intensification/consolidation - 6-9 months
* Maintenance therapy - 2-3 years
* CNS Treatment - ALL has high propensity to go to CNS
34
Treatment of ALL Overview
Treatment of ALL Overview
35
Treatment of ALL Number and sequence of drugs
typically glucocorticoids and chemotherapy
36
Vincristine drug class
Vinca Alkaloids
37
Vincristine properties
38
Vincristine is metabolized in?
The liver so liver function is monitored
39
Vincristine main toxicity
peripheral neuropathy - numbness or tingling coldness in hands and feet
40
Vincristine metabolized by?
CYP3A4 in the liver
41
Does Vincristine cross the blood-brain barrier?
No
42
Vincristine MOA
Bind to tubulin and disrupt mitotic spindle and cause metaphase arrest
43
Methotrexate drug class
Antimetabolite
Folic acid analog - does not bind to DNA
44
Methotrexate MOA
* Folic acid analog - does not bind to DNA
* actively transported into cells in direct proportion to growth rates and polyglutamated
* in high dose can penetrate CNS
45
Methotrexate Toxicities
* Hepatotoxic
* Neprotoxic
46
Methotrexate Overview
47
Mercaptopurine Drug class
purine analogs
48
Mercaptopurine MOA
* Does not bind to DNA
* crosses blood-brain barrier
* inhibits de novo purine synthesis
49
Mercaptopurine toxicities
Hepatotoxicity
50
Mercaptopurine Overview
51
Cyclophosphamide drug class
Alkylating Agents
52
Cyclophosphamide MOA
Binds directly to DNA
53
Cyclophosphamide Toxicities
* Nausea
* Vomiting
* myelosuppression
* Hemorrhagic cystitis
* alopecia
* can cause late secondary leukemia
54
Aspariginase can cause?
Pancreatitis
55
Vincristine can cause
severe neuropathy that can affect GI motility and lead to constipation/ileus
56
Always give ______ with glucocorticoids
always give PPI inhibitor with any steroid
Proton pump inhibitor
57
Typhlitis AKA
Neutropenic Colitis
58
Asparaginase toxicities
* DIC
* Hyperglycemia
* Rare liver toxicity
59
Vincristine Toxicities
peripheral neuropathy
60
Glucocorticoids Toxicities
4 listed
* hyperglycemia
* Mood/psychosis
* Muscle wasting
* Ulcers
61
if patients arent already neutropenic the chemo will make them neutropenic
62
8 years later
avascular necrosis of hip is side effect of high dose glucocorticoids
