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  • Hematology Pathology - 004) Acute Myelogenous Leukemia (AML) (Illustrations - Key)

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    Acute myeloid leukemia (AML) results from increased myeloblasts in the bone marrow that crowd out normal hematopoiesis. This leads to decreased red blood cells, platelets, and normal white blood cells. Increased myeloblasts also expand into the bone marrow, causing bone pain, and can spread to the blood and tissues, causing organ dysfunction. AML is diagnosed through blood tests showing low blood counts and elevated myeloblasts, as well as bone marrow biopsy demonstrating over 20% myeloblasts. Treatment involves chemotherapy to induce remission by promoting myeloblast differentiation into mature cells.

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    11630040 - Hematology Pathology - 004 ] Acute Myelogenous Leukemia (AML) [Illustrations - key]

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    Acute myeloid leukemia (AML) results from increased myeloblasts in the bone marrow that crowd out normal hematopoiesis. This leads to decreased red blood cells, platelets, and normal white blood cells. Increased myeloblasts also expand into the bone marrow, causing bone pain, and can spread to the blood and tissues, causing organ dysfunction. AML is diagnosed through blood tests showing low blood counts and elevated myeloblasts, as well as bone marrow biopsy demonstrating over 20% myeloblasts. Treatment involves chemotherapy to induce remission by promoting myeloblast differentiation into mature cells.

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    6 views1 page

    Hematology Pathology - 004) Acute Myelogenous Leukemia (AML) (Illustrations - Key)

    Uploaded by

    hasanatiya41
    Acute myeloid leukemia (AML) results from increased myeloblasts in the bone marrow that crowd out normal hematopoiesis. This leads to decreased red blood cells, platelets, and normal white blood cells. Increased myeloblasts also expand into the bone marrow, causing bone pain, and can spread to the blood and tissues, causing organ dysfunction. AML is diagnosed through blood tests showing low blood counts and elevated myeloblasts, as well as bone marrow biopsy demonstrating over 20% myeloblasts. Treatment involves chemotherapy to induce remission by promoting myeloblast differentiation into mature cells.

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    of 1

    PATHOPHYSIOLOGY DIAGNOSTIC APPROACH

    Hematopoiesis Pathway Effects of ↑↑ Myeloblasts in Bone Marrow CBC w/ P.B.S. Immunophenotyping

    ↓↓RBC’s Myeloperoxidase
    ↑↑ Myeloblasts (2/2 ↓Space) M.P.O.
    Hemocytoblast ↓↓PLTs
    ↓↓Functional WBC’s
    ↑↑Risk of Infections ↑ Immunohistochemistry Flow Cytometry
    PNA pneumonia Variable WBC’s
    myeloid lymphoid ↓
    stem cells stem cells ↑↑Mortality
    M.S.C. L.S.C.
    RBC
    ↑↑Myeloblasts M.P.O. (+) → AML N/A
    ↓↓ Anemia (↓Space)

    ↑↑↑
    ↑↑↑
    P.B.S. Auer rods (APL)
    Fatigue, Pallor, Dyspnea
    TREATMENT
    peripheral blood smear
    PLT
    ↓↓ Thrombocytopenia (↓Space) UTI
    RBC PLT Myeloblast ↑↑ Lymphoblast Bone Marrow Biopsy
    Bruising, Bleeding
    Definitive Diagnosis Chemotherapy: AML (non APL Subtype)
    promyelocyte ↑↑Myeloblasts
    Expands Bone Marrow
    P.M.C. B-lymphocytes Induction → Consolidation → Maintenance
    T-lymphocytes Bone Pain Cellulitis
    >20% Myeloblasts Agents

    Auer rods (APL) Cytarabine


    Ida/daunorubicin
    Neutrophils Eosinophils Basophils
    Effects of ↑↑ Myeloblasts in Blood and Tissues

    Tests of Complications Chemotherapy: AML (APL Subtype)


    Granulocytes

    Promote Differentiation
    (≥100K) Disseminated intravascular coagulation DIC
    Causes of ↑↑ Myeloblasts Myeloblast → P.M.C. → Granulocyte
    Leukostasis Cutaneous/Mucosal DIC (APL)
    Agents
    ATRA
    1 AML ALL Leukemia Cutis
    Chemoradiation (M/C) Tissue ± Arsenic Trioxide
    H.C.B. Gingival Hyperplasia plasminogen
    activator ↑PIT ↑INR ↓Fibrinogen ↑D-Dimer ↓PLTs ↓RBC’s
    ↑↑DNA H/A ↑TPA ↑Tissue
    Factor Bone Marrow Transplant
    Mutation Replication TIA Tumor Lysis Syndrome
    ↑↑Fibrinolysis (III) T.L.S.
    CVA ↑↑K+ AML (Poor prognostic findings)
    M.S.C. L.S.C.
    2 AKI
    M/C ↑↑Bleeding ↑↑Clotting
    Genetic Dx
    3-
    ↑↑PO4 + Ca2+ ↑Cr AML (Failed chemotherapy)
    • 2/2 Chemotherapy Risk Crystals
    ↓↓Clotting ↑↑Uric Acid ↑BUN
    Down Syndrome Dyspnea L/C
    (Trisomy 21) • Spontaneous Factors ↓↓Ca 2+ Complications
    Myeloblast ↑↑
    acute promyelocytic leukemia Hypoxemia 2/2 ↑↑ Tumor Burden
    (2/2 Consumption)
    AML Subtype (APL)
    (↑↑Myeloblasts )
    15;17 translocation Leukostasis Tumor Lysis Syndrome
    PML-RAR-α
    Genetic Studies
    ICH inter cerbral
    P.M.C. Vision Ca2+ Cytoreduction
    hemorrhage

    Changes ↑K+
    3 Cytogenetics PCR
    3 IVF
    Bone Marrow Disorder ↑PO
    3- Hydroxyurea
    Vision Loss 4

    ↑Uric Acid Crystals Pulmonary Leukapheresis * ↑Purines 1


    MDS →→→ AML Hemorrhage
    AKI Allopurinol
    Chemotherapy
    acute kidney injury
    CML →→→ 15;17 ↓Uric Acid
    ↓UOP ↓AKI
    Granulocytes chronic myeloid 2 (toxic)
    leukemia ↑Cr Bruising Rasburicase
    Bleeding 15;17 translocation (+) PML-RAR-α (+)
    ↑BUN ↑Allantoin
    myelodysplastic syndrome (non-toxic)
    APL APL

    ACUT E MYELOGENOUS LEUKEMIA

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