LEUKEMIAS DR BANSURI

Overview of Leukemias

Definition: Disorders characterized by accumulation of malignant white cells in the bone marrow and blood.

Types: Classified based on cell lineage and clinical course:

  • Acute: Rapid onset, aggressive.

  • Chronic: Insidious onset, less aggressive.

  • Lineage: Lymphoid or Myeloid.

Classification of Leukemias

Major Categories:

  • Myeloid (Acute/Chronic)

  • Lymphoid (Acute/Chronic)

  • Mixed lineage leukemias.

Acute vs Chronic Leukemia

Acute Leukemia

  • Characteristics: Rapid onset; aggressive, mostly poorly differentiated cells (> 20% blasts).

  • Examples: Acute Myeloid Leukemia (AML), Acute Lymphoblastic Leukemia (ALL).

Chronic Leukemia

  • Characteristics: Insidious onset; less aggressive with mature, differentiated cells.

  • Examples: Chronic Myeloid Leukemia (CML), Chronic Lymphocytic Leukemia (CLL).

Causes of Leukemia

Somatic Mutations: Activation of oncogenes and/or inactivation of tumor suppressor genes. Risk Factors:

  • Ionizing radiation.

  • Viruses: e.g., Human T-lymphotropic virus (HTLV-1).

  • Chemicals: Benzene, chemotherapy agents.

  • Smoking: Slight increase in incidence.

  • Genetic predisposition: e.g., Down syndrome, Fanconi anemia.

Hematopoiesis and Cell Lineages

Hematopoietic Stem Cell differentiates into:

  • Myeloid Line: Red Blood Cells, Granulocytes (Neutrophils, Eosinophils, Basophils), Monocytes, Platelets.

  • Lymphoid Line: B-lymphocytes and T-lymphocytes.

Pathophysiology of Acute Leukemias

  • Aggressive Disease: Malignant transformation in hemopoietic stem cells or early progenitors.

  • Genetic Abnormalities: Leads to increased proliferation, reduced apoptosis, and accumulation of blast cells.

Characterization

  • Blast Count: >20% in bone marrow indicates leukemia.

  • Diagnosis Techniques: Morphology, cytochemistry, immunophenotyping, and cytogenetics.

Etiology of Acute Leukemias

Inherited Factors: Increased incidence in genetic disorders (e.g., Down syndrome 20-30 fold, Fanconi anemia). Environmental Influences:

  • Chemicals: Benzene linked to bone marrow issues.

  • Drugs and Radiation: Alkylating agents and epipodophyllotoxins.

Classification of Acute Myeloid Leukemias (AML)

FAB Classification:

  • M0: Undifferentiated

  • M1: Without maturation

  • M2: With maturation; t(8;21)

  • M3: Acute promyelocytic; t(15;17)

  • M4: Myelomonocytic; inv(16)

  • M5: Monoblastic

  • M6: Erythroleukemia

  • M7: Megakaryoblastic

Diagnosis of AML

  • Diagnostic Studies: CBC for anemia/thrombocytopenia, coagulation studies for AML M3 (DIC), bone marrow examination (>20% blasts), cytogenetics for mutations.

Key Morphological Features

  • Myeloblasts: Delicate nucleus, purplish-red staining, moderate cytoplasm.

  • Auer Rods: Definitive evidence of AML.

Clinical Presentation of Leukemia

Common Symptoms:

  • Systemic: Weight loss, fever, fatigue, frequent infections.

  • Lymphoid: Swelling of lymph nodes, splenomegaly, hepatomegaly.

  • Hematological: Anemia, bruising, bleeding.

Prognosis for AML

Favorable Factors: Younger age (<60), high WBC counts, specific chromosomal abnormalities (e.g., del(5), del(7)).

Summary of Acute and Chronic Leukemias

  • Acute Leukemias: Clonal disorders; mutations in oncogenes are common.

  • Chronic Myeloid Leukemia: Characterized by Philadelphia chromosome; often asymptomatic early on.

  • Diagnosis: Relies on lab findings and genetic analysis to dictate treatment and prognosis.

Note: Continue exploring hematological disorders as knowledge evolves.