Propaedeutics of Internal Diseases · MU Plovdiv

75. Chronic myeloleukosis and Chronic lympholeukosis

Inside: 19 sections · 8 labelled pictures · 30 flashcards · 5 min

Topic 75 of 100 in the MU Plovdiv syllabus for Propaedeutics of Internal Diseases (Medicine, Year 3). The free AceMed note covers it in 12 sections, about 706 words (5 min of reading), with 30 flashcards.

In this note

  1. Chronic Myeloid Leukemia (CML)
  2. Definition:
  3. Classification (Phases of CML):
  4. Etiology:
  5. Pathogenesis:
  6. Symptoms:
  7. Diagnosis:
  8. Laboratory Tests:
  9. Treatment:
  10. Prognosis:
  11. Chronic Lymphoid Leukemia (CLL)
  12. Physical Examination:

Definition:

Chronic myeloid leukemia (CML) is a clonal myeloproliferative neoplasm characterized by:

  • Excessive proliferation of mature and maturing granulocytes (especially neutrophils, eosinophils, basophils)
  • Caused by a reciprocal translocation t(9;22) → Philadelphia chromosome, resulting in the BCR-ABL fusion gene, which encodes a constitutively active tyrosine kinase.
  • Accounts for ~15% of all leukemias, affecting mostly adults between 40–60 years.

Classification (Phases of CML):

  1. Chronic phase (CP):
  • Most patients present in this phase (often asymptomatic or mild symptoms)
  1. Accelerated phase (AP):
  • Worsening symptoms, increased blasts, cytopenias
  1. Blast crisis (BC):
  • Resembles acute leukemia (AML or ALL) with >20% blasts in blood/marrow

Etiology:

General Risk Factors:

  • Ionizing radiation: DNA damage to hematopoietic precursors
  • Chemical exposure: Benzene
  • Genetic predispositions
  • Viruses: HTLV-1 (more relevant to T-cell leukemia but mentioned as general risk)

Specific Etiology:

  • Philadelphia chromosome (t(9;22)):
  • ABL gene on chromosome 9 fuses with BCR gene on chromosome 22
  • Forms BCR-ABL fusion gene → constitutive activation of tyrosine kinase
  • Drives uncontrolled proliferation and resistance to apoptosis

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