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Fatigue, Genetic Mutation - Coggle Diagram

- - - - Chronic Myeloid Leukemia
        
        Chronic Phase
        
        Learning Issues
        
        Prevention & Education
        
        Prevention
        
        Physical Activity
        
        Early Detection
        
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        Avoid Hazards (chemical, radioactive)
        
        Education
        
        Raise Awareness
        
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        Prognosis & Complications
        
        Complications
        
        If Not Treated Well, May Lead to Blast Crisis (Low Chance of Survival)
        
        Prognosis
        
        Good as long as treated on time before disease progresses into the accelerated phase and/or the blast phase
        
        Risk Factors
        
        High radiation exposure
        
        Genetic Predisposition
        
        Prolonged chemical exposure
        
        Age
        
        Treatment & Management
        
        Initial Treatment
        
        Hydroxyurea
        
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        Referral
        
        Hematologist-Oncologist
        
        Confirmed CML: Chronic Phase
        
        Tyrosine Kinase Inhibitor
        
        Stem Cell Transplant
        
        Chemotherapy
        
        Splenectomy
        
        Pathophysiology
        
        Chemical exposure (15 years)
        
        Gene mutation
        
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        Accelerated Phase
        
        Blast Phase
      - CLL
        
        Requires lymphocytosis, not neutrophilia/myeloid precursors.
      - AML
        
        Requires >20% blasts; this case has 6% (consistent with CML chronic phase).
      - ALL
        
        Lymphoblasts are absent; myeloid lineage predominates
    - - Extreme leukocytosis and thrombocytosis are not features of nutritional anemia.
  - - - Extreme leukocytosis (115,700/μL) and myeloid predominance are inconsistent with HIV-related fatigue.
    - - No fever, night sweats, or respiratory symptoms, High WBC and thrombocytosis are atypical for TB.
  - - - No autoimmune markers (e.g., rash, arthritis, renal involvement).
  - - - No lymphadenopathy. Peripheral blood shows myeloid lineage cells, not lymphoid proliferation
  - - - Fatigue is accompanied by objective findings (hepatosplenomegaly, lab abnormalities). cannot be explained by psychiatric causes alone.
  - - - No symptoms of polyuria/polydipsia, Fasting blood glucose is normal (86 mg/dL)..
    - - No clinical signs of hypothyroidism (e.g., cold intolerance, dry skin). TSH level (2.29 uIU/mL) is within normal range (0.25–5.0)
- - - - Hb 8.7 g/dl (<13.5, low)
      - Blast cell 6% (<10%, chronic phase, normal none)
      - Thrombocyte 526k/uL (>450k, high)
      - Leukocyte 115.7k/uL (>>10k, Malignancy)
      - Erythrocyte 2.69 mil/uL (<4.5, low)
    - - Erythrocytes
        
        Normochromic, Normocytic Erythrocytes
        
        No significant RBC abnormalities
        
        Polychromasia & Erythroblasts (+)
        
        Suggests Increased RBC Production Due to Bone Marrow Stress
      - Leukocytes
        
        Increased Leukocytes
        
        Presence of Myeloblast to Segmented Neutrophils
        
        Hallmark of CML, Showing full Spectrum of Myeloid Maturation, From Early Precursors to Mature Neutrophils
        
        Aculte Leukemias (AML & ALL) would present with a predominance of blasts rather dance a mixture of different myeloid precursors
- - - - None
    - - None
    - - Works in a chemical factory for the past 15 years
- - - - Myeloid hyperproliferation
        
        Bone marrow over crowding
        
        Leukocyte spillage into the bloodstream
        
        Leukocytosis
        
        Infiltrate liver & spleen
        
        Hepato-splenomegaly
        
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        Myeloblast & Segmented Neutrophil (Tumor marker)
        
        CML
        
        Isufficient erythropoiesis space
        
        Anemia
        
        Immature erythrocyte (reticulocyte) spillage ti the blood stream
        
        Polychromatic (pbs)
        
        RNA & DNA spillage
        
        Breakdown into purine & guanine
        
        Uric Acid
        
        Thrombocytosis
        
        Macrothrombocyte & Clumping
        
        Increased ATP consumption
        
        Weightloss
        
        Leukocytosis & Thrombocytosis
    - - Thrombovytosis (macrothrombocyte & clumping)