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Blood & Lymph > Leukemia Clinical Care 1 > Flashcards

Leukemia Clinical Care 1 Flashcards

1
Q

Leukemias are a primary bone marrow malignancy which 2 categories _______.

A
  1. acute vs. chronic
  2. myeloid vs. lymphoid
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2
Q

MC types of cancer

A
  1. Breast
  2. Lung

(leukemia cases a year ~ 60K)

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3
Q

Myeloblasts give rise to _______ which terminal cells

A

granulocytes

(all blood components come from myeloid stem cells)

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4
Q

Feather’s edge allows you to look at

A

a zone of morphology: gives you a view of different cell types

(important for dx)

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5
Q
A
  • A: RBC
  • B: lymphocyte (granules)
  • C & E: neutrophil (kidney beans)
  • D: Eosinophil (kidney beans w/orange granules)
  • F: monocyte (tissue MF)
  • G: plt
  • J: basophil
  • H: lymphocyte (B or T: dark nucleus w/little cytoplasm)
  • I: band cell (baby neutrophil, no segmentation yet)
  • J: basophil (dark purple granules
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6
Q
A

smudge cells: fragile cells → CLL

(obtained by putting coverslip on it; CLL will also have large lymphoblasts w/little cytoplasm)

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7
Q

MC Leukemia

A

CLL

(AML>CML>ALL)

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8
Q

CLL affects which age group?

A

men >70 yo

(~ 9 year survival rate)

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9
Q

CLL distinguishing sx (3)

A
  1. cytopenia: bone marrow infiltration
  2. Auto-Immune AIHA, ITP (Igs attack)
  3. anorexia

(50% asymptomatic, other sx: lymphadenopathy, hepatosplenomegaly)

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10
Q

Diagnosis of CLL, shows a lymphocytosis > _____/uL via flow cytometry.

A

5,000

(also look for CD5+)

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11
Q

______ is a precursor to CLL

A

MBL: monoclonal B-cell lymphocytosis (1% chance of progressing to CLL)

(CLL phenotype but ALC<5000/uL)

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12
Q

30% of patients with MBL have _____ (disease).

A

hepatitis C

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13
Q

How is Small Lymphocytic Lymphoma different than CLL?

A

same; the difference is location. SLL is in the lymph nodes (>1.5cm)

(ALC<5000)

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14
Q

Lymphocytosis may be caused by other diseases. It must be categorically ______ to be considered cancer.

A

clonal

(may be viral or stress that causes the WBC to increase)

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15
Q

Rai Staging of CLL

A
  • 0 Lymphocytosis only
  • 1: lymphadenopathy
  • 2: hepatosplenomegaly
  • 3: anemia (bone marrow involved)
  • 4: thrombocytopenia

(all have lymphocytosis. Bone marrow involved)

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16
Q

Binet Staging System for CLL :

A

A: <2 lymph areas enlarged

B: 3+ lymph areas + organomegaly

C: anemia or thrombocytopenia

(there is also an international workshop staging system that combines Rai and Binet)

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17
Q

The majority of leukemia depends on their cytogenetic molecular abnormalities. Which ones are associated with poor prognosis? Good prognosis?

A

Poor:

  1. TP53 gene on 17p13.1
  2. ATM gene on 11q22.3

Good:

  1. RB1 gene on 13q14.3

(identifying these is extremely important for survival estimates)

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18
Q

When is CLL treated (7)?

A
  1. massive lymphadenopathy
  2. massive splenomegaly
  3. constitutional: fever, weight loss, fatigue
  4. recurrent infections
  5. bone marrow failure: anemia
  6. autoimmune cytopenias
  7. rapid doubling time
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19
Q

Rituximab

A

anti-CD20 mAb → complement activation & phagocytosis

(type 1, the new one is Obinituzimab)

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20
Q

New generation CD-20 mAb

A

Obinituzumab

21
Q

New generation CD-20 mAb? Why is it better than Rituximab?

A

Obinituzumab

ADCC & direct apoptosis

22
Q

Which medications are the most effective at controlling proliferation of B cells in CLL?

A
  1. BTK inhibitors
  2. PI3K inhibitors
23
Q

Venetoclax MOA

(treatment for CLL)

A

BCL-2 inhibitor

(BCL-2 = anti-apoptotic protein; CA upregulates its expression)

24
Q

CLL can transform to ______ (5)

A
  1. Richter’s: transformation to other lymphomas
  2. Prolymphocytic
  3. Hodgkin’s
  4. Acute lymphoblastic leukemia
  5. Multiple Myeloma
25
Q

Richter Syndrome is a transformation from CLL. The main finding is diffuse large B-cell lymphoma w/ rapidly _______.

A

enlarging nodule in lymph node or spleen

(prognosis < 1 yr)

26
Q

What elements of supportive care are provided to newly diagnosed CLL patients?

A
  1. Risk stratification
  2. Counseling
  3. Health Screening
  4. Vaccination/infection prevention
27
Q
A

Hairy cell leukemia

28
Q
A

Dry-tap: fibrosis

(hairy cell leukemia)

29
Q
A

Hairy cell leukemia

(“fried egg” appearance)

30
Q
A

TRAP +: acid phosphatase + cells

(Hairy cell leukemia)

31
Q

How do you identify Hairy Cell Leukemia by flow cytometry?

A
  1. CD11c : C = the 3rd letter of the alphabet
  2. CD25: 5-2 = 3
  3. CD103
  4. CD123

(mn: picture hairy cell w/3 projections)

32
Q

Which mutation is seen in 90% of hairy cell leukemia (HCL) patients?

A

BRAF V600E

(important to ID for medication)

33
Q

2 types of HCL & their differences

A
  1. classical: dry tap, BRAF V600 +
  2. variant: easy marrow tap, no BRAF mutation, no response to purine analogs
34
Q

HCL treatment options

35
Q

What is Agent Orange?

A

Used in Vietnam & Korea to defoliate jungle vegetation

(others were used. All predisposed Vietnam veterans to leukemia)

36
Q

What are the presumptive diagnoses for cancers caused by Agent Orange (5)?

A
  1. ALL
  2. Chronic B-cell Leukemia
  3. Hodgkin & NHL
  4. Multiple Myeloma
  5. Prostate, respiratory & soft tissue sarcomas
37
Q

What are the presumptive diagnoses for dermatologic conditions caused by Agent Orange (2)?

A
  1. Chloracne
  2. Porphyria Cutanea Tarda
38
Q

What are the presumptive diagnoses for Chronic diseases caused by Agent Orange (4)?

A
  1. DM
  2. Ischemic heart disease
  3. parkinson’s
  4. peripheral neuropathy
39
Q
A

“variety show” - multiple cells

(chronic myeloid leukemia)

40
Q

Normal bone marrow is ______% cells & _____% space. Erythroid:Myeloid?

A
  • 50%/50%
  • 1:3
41
Q
A

marrow completely replaced by cells

42
Q

Chronic myeloid leukemia (CML) account for 15% of leukemias and mostly affects which demographic?

A

60 yo

(M:F = 1:1)

43
Q

BCR-ABL (philidelphia chromosome) is found in which 2 diseases?

A
  1. CML
  2. B-cell ALL
44
Q

CML sx

A
  1. splenomegaly
  2. anemia, thrombocytopenia
  3. increased uric acid
45
Q

CML phases

46
Q

Imatinib indications

47
Q

Imatinib MOA

A

occupies ATP binding pocket of Abl kinase → blocks signaling & proliferation

48
Q

How is CML response to Imatinib evaluated?

A

% of cells in the metaphase that were Ph+

49
Q

What is the goal of CML treatment?

A

Deep molecular response

Blood & Lymph (29 decks)

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