Myelodysplasgic Syndromes And Acute Myeloid Leukemia Flashcards

1
Q

What is the result of MDS and AML?

A

Decreased production of one or more of the major hematopoitic lineages

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2
Q

What are clonal stem cell disorders?

A

Stem cells make same cells

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3
Q

What is the halmark ?

A

Bone marrow failure

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4
Q

What is MDS?

A

Heterogeneous hematopoisis and increased apoptosis with periferial cytopenia

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5
Q

What about MDS?

A

Recurrent genetic abnormailitis
Baraible increase in blast cell percenatge
Increase risk of developing acute myeloid leukemai pre leukemic
Mostly 70

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6
Q

What is the pathogensis of MDS ?

A

Genetic disorders in myeloid progenitor or in blast cells

That is why it can affect one type or many because progenitor

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7
Q

What is etiology ? Of MDS

A

Primary denovo

Secondary chemical benzene smoking chemotherapy radiation

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8
Q

How diagnose mds ?

A
Clinical features 
     Cytopenia and severity 
Laboratory features 
CBC 
Cytopenia 
Elevated MCV ( macrocytic the anemai ) 

Peripharal blood
Dysplastic feautres in one or more cell lines
+- circulating blast cells

Bone marrow
Dysplastic features in one or more cell lines
+- increased % of blasts cells

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9
Q

Define Acute myeloid leukemia ? AML

A

Uncontrolled clonal proliferation and accumulation of immmature myeloid ( myeloblasts ) in bone marrow also blood or tissue skin lung u name causing bone marrow failure

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10
Q

Aml is

A

Hetergenous depend on type some form we can cure others we cant

20% of childhood less than 15 years acute leukemia

In adults 80 myloid ans rest lymphoid in adults more than 15

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11
Q

What cause acute myeloid leukemia ?

A

Ionizing radiation

Chemicals benzene and other petroleum derivatives

Chemotherapy
Alkylating ( secondary AML )

Germline predisposition
Inheried or de nove grnetic defects like down syndroem

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12
Q

What is the pathogensis ?

A

Two hit model of leukemigesis ?

  1. Loss of function of transcription needed for differentiation
    Lack of differntiation ( loss of function
2. Gain of function mutation of tyrosine kineses 
Will cause enzyme active ( tyrosine important for phosphorylation leading to abnormal proliferation 
Enhanced proliferation ( gain of function
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13
Q

What is the clinical presentation of AML ?

A

Due to bone marrow replacement failure related cytopenia

Due to extramedullary infilteration
Hepatospleenomegaly
Skin lesions
Gum hypertrophy

Due to release of procoagulanta or profibrinolytic substance s
DIC
Excessive firinoluis

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14
Q

How to diagnose ?

A

Morphology
Amust
Bone marrow aspirate smears
Identifiction of a variety of blast cellls
Auer rods ( in acute leukemia for sure acute myeold anmie but not see it ok )
Should find more than 20 percent blast cells in the bone marrow

Immunophenotyping immune antibodies to identify which type
Flow cytometric analysis using monoclonal antobodies
Rapid and sensitive
Detect specific cellular antigens surface or intracellur
Not on linlinage but also which one ehich origen
Cytogenetic and genotyping

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