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Hematology > Hematology Week 3: Acute Lymphoblastic Leukemia/Lymphoma > Flashcards

Hematology Week 3: Acute Lymphoblastic Leukemia/Lymphoma Flashcards

1
Q

Question 1

A

D) The patient has neutropenia

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2
Q

Question 2

A

B

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3
Q

Question 3

A

sheets of blast taking over bone marrow

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4
Q
A

CD19 positive

CD20 Negative

CD34 Positive

CD33 Negative

TDT Positive

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5
Q

Immature markers

A

TDT

CD34

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6
Q

B cell marker

A

CD19

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7
Q

Myeloid marker

A

CD33

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8
Q

Dx is?

A

B cell - ALL

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9
Q

Acute Lymphoblastic Leukemia

&

Acute Lymphoblastic Lymphoma

A
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10
Q

Where are

Acute Lymphoblastic Leukemia

&

Acute Lymphoblastic Leukemia

Found?

A
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11
Q

B-ALL Normal Counterpart

A

Precursor B Lymphocyte

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12
Q

B-ALL Key Markers

3 listed

A
  • CD19
  • CD34
  • TdT
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13
Q

B-ALL Predominant age

A

<10 years

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14
Q

B-ALL Predominant Location

A

Blood and BM

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15
Q

B-ALL Prognosis

A

~90%

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16
Q

T-ALL Normal counterpart

A

Precursor T lymphocyte

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17
Q

T-ALL Key Markers

3 listed

A
  • CD3
  • CD34
  • TdT
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18
Q

T-ALL Predominant Age

A

Adolescence

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19
Q

T-ALL Predominant Location

A

Tissue (especially the thymus)

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20
Q

T-ALL Prognosis

A

<80%

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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
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22
Q

ALL onset Timeline

A

Abrupt “stormy” onset (days to weeks)

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23
Q

ALL affects what age group

A

Usually children

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24
Q

ALL survival

A
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25
Q

Simplified risk assessment in B-ALL

A

Philadelphia chromosome in B-ALL is very bad because of the different cell they are present in and cytogenetic context

26
Q

Question 4

A

A. ETV6-RUNX1 is present

this fusion is associated with t(12;21)

27
Q

t(12;21) on a karyotype

A

very difficult to see on karyotype and is called cryptic on karyotype

28
Q

t(12;21)

A

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
Q

Question 5

A

B NO

He is on the better risk side

30
Q

Phases of Treatment of ALL

4 listed

A
  • 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
Q

Anthracycline main toxicity

A

Cardiac toxicity

32
Q

Only use anthracycline in?

A

Higher risk patients because of cardiac toxicity

33
Q

Treatment of ALL phase timeline

A
  • 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
Q

Treatment of ALL Overview

A

Treatment of ALL Overview

35
Q

Treatment of ALL Number and sequence of drugs

A

typically glucocorticoids and chemotherapy

36
Q

Vincristine drug class

A

Vinca Alkaloids

37
Q

Vincristine properties

A
38
Q

Vincristine is metabolized in?

A

The liver so liver function is monitored

39
Q

Vincristine main toxicity

A

peripheral neuropathy - numbness or tingling coldness in hands and feet

40
Q

Vincristine metabolized by?

A

CYP3A4 in the liver

41
Q

Does Vincristine cross the blood-brain barrier?

A

No

42
Q

Vincristine MOA

A

Bind to tubulin and disrupt mitotic spindle and cause metaphase arrest

43
Q

Methotrexate drug class

A

Antimetabolite

Folic acid analog - does not bind to DNA

44
Q

Methotrexate MOA

A
  • 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
Q

Methotrexate Toxicities

A
  • Hepatotoxic
  • Neprotoxic
46
Q

Methotrexate Overview

A
47
Q

Mercaptopurine Drug class

A

purine analogs

48
Q

Mercaptopurine MOA

A
  • Does not bind to DNA
  • crosses blood-brain barrier
  • inhibits de novo purine synthesis
49
Q

Mercaptopurine toxicities

A

Hepatotoxicity

50
Q

Mercaptopurine Overview

A
51
Q

Cyclophosphamide drug class

A

Alkylating Agents

52
Q

Cyclophosphamide MOA

A

Binds directly to DNA

53
Q

Cyclophosphamide Toxicities

A
  • Nausea
  • Vomiting
  • myelosuppression
  • Hemorrhagic cystitis
  • alopecia
  • can cause late secondary leukemia
54
Q

Aspariginase can cause?

A

Pancreatitis

55
Q

Vincristine can cause

A

severe neuropathy that can affect GI motility and lead to constipation/ileus

56
Q

Always give ______ with glucocorticoids

A

always give PPI inhibitor with any steroid

Proton pump inhibitor

57
Q

Typhlitis AKA

A

Neutropenic Colitis

58
Q

Asparaginase toxicities

A
  • DIC
  • Hyperglycemia
  • Rare liver toxicity
59
Q

Vincristine Toxicities

A

peripheral neuropathy

60
Q

Glucocorticoids Toxicities

4 listed

A
  • hyperglycemia
  • Mood/psychosis
  • Muscle wasting
  • Ulcers
61
Q

if patients arent already neutropenic the chemo will make them neutropenic

A
62
Q

8 years later

A

avascular necrosis of hip is side effect of high dose glucocorticoids

Hematology (26 decks)

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