leukemias Flashcards

1
Q

acute leukemia main indication

A

blast/immature cells.

Bone aspirate smear is a must to confirm the diagnosis): >20% blasts in the bone marrow.

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2
Q

in myelogenous leukemia what cells are affected

A

granulocytes or monocytws

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3
Q

in lymphocytic leukemia what cells affected

A

lymphocytes are affected

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4
Q

how do u differ btwn chronic and acute leukemias

A

• By the maturity of cells affected and the rapidity of disease progression:

1-Acute leukemias are characterized by rapid progression and affect immature cells (i.e., immature cells proliferate before maturation)

2-Chronic leukemias progress slowly and affect mature cells

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5
Q

what is a symotom specific for AML

A

gingival hypertrophy

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6
Q

specific presentation more specific to ALL

A

testicular enlargement, lymphadenopathy, bone pain

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7
Q

what is the percentage in ppl of ost occurence in acute myeloid leukemia

A

80% of adult acute leukemias, 20% of childhood (<15 y/o) leukemias

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8
Q

risk factors of acute myeloid leukemia

A

o Exposure to ionizing radiaAon, previous chemotherapy e.g. alkylaAng agents (secondary AML), exposure to chemicals e.g. benzene o MyeloproliferaAve syndrome o Down syndrome o Viral infecAons

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9
Q

pathogenesis of AML

A

1.Loss of function of transcription factors needed for differentiation differentiation block.

2.Gain of function mutations of tyrosine kinases =enhanced proliferation

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10
Q

bone marrow biopsy in AML is a defenitive test would show

A

• >20% myeloid blasts confirms AML
• Checks for Auer rods (needle-like structures in blasts)

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11
Q

Chromosomal abnormaliAes in AML

A

o t (8;21) - AML1

o t (15;17) - PML/RARA

o Inversion 16 - MYH-11/Cbfb

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12
Q

acute promeolyctic leukemia

A

• A variant of AML (10-15% of cases) –> cytogeneAcs: t (15;17)

• May present with pancytopenia

• Associated with coagulopathy (DIC) is almost all cases, due to release of procoagulant/profibrinolytic factors from blast cells. (major cause of early death)

• All-trans-reAnoic acid (ATRA) must be combined to the treatment

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13
Q

tx of AML

A

Chemotherapy, targeted drugs, and bone marrow transplant in severe cases.

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14
Q

what are two main prognostic factors in AML

A

age
cytogenetics

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15
Q

gd prognostic factors in AML

A

o Favorable cytogeneAcs: T (15;17), t (8;21), inv (16)
o NPM1 mutaAon with normal FLT3
o De novo disease

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16
Q

poor prognostic factors in AML

A

o Adverse cytogenetics chromosome 5 del (5q), 7 del, or complex karyotype
o Minimal residual disease posiAvity after chemotherapy
o FLT3 mutation
o Secondary disease e.g. prior MDS or MPN
o Demographics: Age >60, male gender
o High WBC

17
Q

in lymphoid leukemia there is three types of lymphocytes

A
  1. B-cells
  2. T-cells
  3. NK cells
18
Q

what is the commonest type of leukemia in children more males and high risk in down syndrome

19
Q

what is the mutation in ALL

A

A genetic mutation causes uncontrolled growth of lymphoblasts (immature B or T cells).
• These blasts don’t mature or function properly, leading to low normal blood cells and leukemia symptoms.

20
Q

symptoms of ALL

A
  1. Patients present with infections, lymphadenopathy and testicular enlargement and splenomegaly due to extramedullary infiltration), bone pain and arthralgia
  2. May present with meningeal signs (headache, N/V, visual symptoms; especially in ALL relapse) > CNS disease
21
Q

ALL -> diagnosis depends on immunophenotyping:

A
  1. B-cell: CD19, CD20, CD10, Tdt (terminal deoxynucleo.de transferase)
  2. T-cell: CD3, CD5, CD7, Tdt

Note: Tdt is found in both B-cells and T-cells, help us to differentiate between myeloid & lymphoid leukemia, bcz Tdt is only found in lymphoblast cells

22
Q

in chest x ray of ALL

A

patients with ALL may have a mediastinal mass

23
Q

ALL prognosis

A

C. Achievement of first remission: 60-90%

D. Childhood ALL: 75% long-term remission (>5yr) -> better chemo tolerance, lower prevalence of
BCR- Abl fusion gene.

E. Adult ALL: 30-40% 5yr survival

24
Q

tx of ALL

A
  1. Intensive Chemotherapy (Induction Phase)
    • Goal: Destroy leukemia cells and achieve remission
    1. CNS Prophylaxis (Prevents Brain Relapse)
      • Intrathecal chemotherapy (Methotrexate) injected into spinal fluid
    2. Consolidation & Maintenance Therapy
      • Several months to years of lower-dose chemotherapy to prevent relapse
    3. Targeted Therapy (For Specific Mutations)
25
CLL
Chronic Lymphocytic Leukemia (CLL) is a slow-growing blood cancer where the bone marrow makes too many abnormal B-lymphocytes (B cells). These cancerous B cells don’t function properly and crowd out healthy blood cells over time. CLL is the most common leukemia in adults, especially in older people (>60 years).
26
why do CLL produce Hypogammaglobulinemia
B cells are important in production of immunoglobulins so if they are affected the level of Igs is lower than normal
27
what is chronic lymphoid leukemia associated with
CLL cells may process red blood cell antigens and act as antigen presenting cells, inducing a T-cell response and the formation of polyclonal antibodies by normal B cells, thus indirectly provoking autoimmune hemolytic anemia )
28
blood smear in CLL
• Smudge Cells (Fragile CLL cells that break during preparation)
29
bone marrow biopsy in CLL
Shows infiltration of CLL cells in the bone marrow
30
Immunophenotyping (flow cytometry): in CLL
Classical combination: CD19, CD20 (weak), CD5, CD23, CD79 (weak) with surface immunoglobulin (Kappa and Lambda light chains)
31
Cytogenetics/FISH: not essential for the diagnosis in CLL but have prognostic value. Karyotypic abnormalities include:
o 13q deletion: good prognosis and response to therapy o 11q or 17p (site of TP53) deletion or CD38+: poor prognosis.
32
hairy cell leukemia
• Subtype of CLL , occurs when BM makes too many B cells , also known as B lymphocytes • Chronic B cell malignancy; occurs primarily age >50, A/W BRAF muta.on
33
blood film in hairy cell leukemia
abnormal circulating lymphocytes with hairy cytoplasmic projection