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8 Cards in this Set
- Front
- Back
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Types of Myeloid Malignancies (3)
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1. Acute myeloid leukemia: failure to differentiate
2. Myeloproliferative disorders: overproduction of mature cells 3. Myelodysplastic syndromes: ineffective maturation |
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Acute Myeloid Leukemia: Causes, Clinical Features, Diagnosis, Outcome, Treatment
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1. Causes: Primary (denovo/unkown), Secondary (toxins, transformation from other myeloid neoplasms)
2. Clinical Features: Anemia (fatigue), Thrombocytopenia (bleeding), Neutropenia (infections), Tumour Lysis Syndrome (increased uric acid/phosphate/LDH, renal failure), Leukostasis (hemorrhage,hypoxia), DIC 3. Diagnosis: Morphology (large blasts +/- Auer rods), Myeloid Granules, Immunologic Markers, Cytogenetics Outcome: fatal in days/weeks (untreated), complete remission (70%), relapse (20-40%) Treatment: Intensive Chemo + Supportive Therapy (antibiotics, RBC, platelets), Bone Marrow Transplantation (autologous,allogeneic) |
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Chronic Myeloproliferative Disorders: Types, Common Features, Prognosis
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1. Types: Chronic Myeloid Leukemia, Polycythemia Rubra Vera, Essential Thrombocythemia, Primary Myelofibrosis
2. Common Features: Splenomegaly, Increased Uric Acid, Basophilia/Eosinophilia, Transformation to Acute Leukemia or Myelofibrotic Stage 3. Prognosis: Years of Survival |
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Chronic Myeloid Leukemia: Clinical Presentation, Diagnosis, Natural History, Treatment
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1. Clinical Presentation: Increased granulocytes with huge left shift, splenomegaly, no acute illness
2. Diagnosis: Philadelphia Chromosome (t(9;22) Bcr-Abl) in blood and marrow 3. Natural History: Chronic Phase (+/- 4years, few symptoms, easy to control), Accelerated Phase (more difficult to control), Blast Crisis (Acute Leukemia, Rapidly Fatal) 4. Treatment: Oral chemotherapy, Bcr-Abl tyrosine kinase inhibitors (prolongs survival), Bone Marrow Transplant (possibly curative) |
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Polycythemia Rubra Vera: Pathogenesis, Clinical Presentation, Lab Findings, Complications, Diagnosis, Treatment, Prognosis
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1. Pathogenesis: RBCs produced independent of EPO due to mutation in signalling protein (JAK-2), results in overproduction of RBCs and increased blood viscosity
2. Clinical Presentation: headache, visual disturbances, mucosal bleeding, generalized pruritis, facial rubor, bloodshot eyes, red extremities, splenomegaly 3. Lab Findings: high Hb/Hct/RBC/neutrophils/basophiles/platelets, decreased iron/MCV 4. Complications: Thrombosis (DVT,TIA,stroke,digital ischemia),mucosal bleeding 5. Diagnosis: Exclude dehydration and secondary polycythemia, splenomegaly, JAK-2 mutation (PCR) 6. Treatment: phlebotomy, oral chemotherapy, antiplatelet agent (ASA), JAK-2 inhibitor 7. Prognosis: Survive Decades |
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Essential Thrombocytopenia: Clinical Presentation, Diagnosis, Treatment
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1. Clinical Presentation: asymptomatic (most), thrombosis, hemorrhage, splenomegaly
2. Diagnosis: exclude reactive thrombocytosis, JAK-2 mutation (50%) 3. Treatment: observation (asymptomatic), lower platelet count + ASA (thrombosis), lower platelet count (hemorrhage) |
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Primary Myelofibrosis: Pathogenesis, Cause, Clinical Presentation, Diagnosis, Course, Treatment
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1. Pathogenesis: Marrow replaced by fibrosis due to abnormal megakaryocyte collagen deposition
2. Clinical Presentation: marked splenomegaly, blood produced in liver/spleen, increased followed by decreased blood counts 3. Cause: DeNovo or from PRV/ET 4. Diagnosis: abnormal blood counts, leukoerythroblastic blood film, BM fibrosis, JAK-2 mutation 5. Course: Steady deterioration (3-5 years), morbidity due to massive splenomegaly +/- low counts 6. Treatment: Transfusions (symptomatic), splenectomy (risky), bone marrow transplant (potentially curative), JAK-2 inhibitors |
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Myelodysplastic Syndromes: Clinical Features, Diagnosis, Prognosis, Treatment
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1. Clinical Features: older people, anemia+/-thrombocytopenia+/-neutropenia, bizarre looking blood cells, acquired cytogenetic abnormalities
2. Diagnosis: unexplained cytopenias (esp. macrocytic anemia), rule out B12/folate deficiency or other BM disorder, abnormal BM morphology, clonal cytogenetic abnormality 3. Prognosis: variable (2-5 years), can transform to AML 4. Treatment: transfusion/antibiotics (symptomatic), EPO, bone marrow transplant (possibly curative) |
