hema Flashcards
What is leukemia?
A neoplastic proliferation of abnormal WBCs that interfere with normal blood cell production, leading to anemia and thrombocytopenia.
How is leukemia classified?
By type of WBC affected: Myelogenous leukemia (granulocytes or monocytes affected), Lymphocytic leukemia (lymphocytes affected). By disease progression: Acute leukemia (rapid, affects immature cells), Chronic leukemia (slow, affects mature cells).
What is the difference between acute and chronic leukemia?
Acute leukemia: Circulation of immature cells (blasts). Chronic leukemia: Circulation of mature cells.
What is the pathogenesis of ALL?
Mutation in precursor T/B lymphocytes leading to maturation arrest due to: Enhanced tyrosine kinase activity → increased blast proliferation, Inactivation of tumor suppressor genes, Activation of proto-oncogenes.
What are the epidemiological features of ALL?
Most common childhood malignancy (peak age <6 years), More common in males, Higher risk in Down syndrome.
What are the symptoms of ALL?
Systemic: Infections, fever, fatigue, weight loss. Lymphoid involvement: Lymphadenopathy, testicular enlargement, splenomegaly. Bone marrow failure: Anemia, thrombocytopenia. CNS involvement: Headache, nausea, vomiting, visual symptoms (especially in relapse cases).
What laboratory findings are seen in ALL?
Increased leukocytes (>10x10⁹/L in 50% of cases), Neutropenia, Anemia, Thrombocytopenia.
How is ALL diagnosed?
Immunophenotyping: B-cell ALL: CD19, CD20, CD10, Tdt+. T-cell ALL: CD3, CD5, CD7, Tdt+. Cytogenetics: Philadelphia chromosome (t9;22) in ~25% of adult cases. Bone marrow biopsy: Presence of lymphoblasts. Periodic acid-Schiff (PAS) positivity.
What is the treatment approach for ALL?
Induction chemotherapy (removes blasts, restores normal hematopoiesis), Consolidation/intensification chemotherapy (eliminates residual leukemic cells), Maintenance chemotherapy (prevents recurrence, lasts 2-3 years), Intrathecal methotrexate (CNS prophylaxis), Stem cell transplantation (for high-risk or relapsed cases).
What is the genetic hallmark of CML?
Philadelphia chromosome (t9;22), leading to BCR-ABL fusion gene → constitutive tyrosine kinase activation.
What are the clinical phases of CML?
Chronic phase: Asymptomatic/mild symptoms, <10% blasts. Accelerated phase: Progressive splenomegaly, >20% basophils, 10-19% blasts. Blast phase: >20% blasts, transforms into AML (2/3 cases) or ALL (1/3 cases).
How is CML diagnosed?
Peripheral smear: Leukocytosis, basophilia (universal finding), eosinophilia. Bone marrow biopsy: Hypercellular marrow, left shift. Cytogenetics: Philadelphia chromosome detected via FISH/karyotyping.
What is the first-line treatment for CML?
Tyrosine kinase inhibitors (TKIs): 1st gen: Imatinib, 2nd gen: Dasatinib, Nilotinib.
How is treatment response monitored in CML?
Via quantitative PCR (Q-PCR) for BCR-ABL transcripts.
What is the most common type of leukemia?
Chronic lymphocytic leukemia (CLL).
What is the typical patient demographic for CLL?
Elderly (>60 years), median age 65, more common in males.
What is the characteristic finding on a peripheral smear in CLL?
Smudge cells (fragile leukemic cells that rupture during smear preparation).
How is CLL diagnosed?
Flow cytometry: CD19, CD20 (weak), CD5, CD23+. CBC: Lymphocytosis (>5 x 10⁹/L), anemia, thrombocytopenia. Bone marrow biopsy (not essential).
What complications can arise from CLL?
Autoimmune hemolytic anemia (AIHA, positive Coombs test), Hypogammaglobulinemia → recurrent infections, Richter’s transformation (to diffuse large B-cell lymphoma).
What is the first-line treatment for symptomatic CLL?
FCR regimen (Fludarabine, Cyclophosphamide, Rituximab).
