SEARCH RESULTS FOR: Acute-Lymphoblastic-Leukemia

Acute Lymphoblastic Leukemia

Acute Lymphoblastic Leukemia (ALL): Pathogenesis and Clinical Presentation Authors: Yan Yu, Katie Lin Reviewers: Crystal Liu, Kara Hawker, Jennifer Au, Lynn Savoie* * MD at time of initial publication Note: ALL is much rarer than AML and is usually seen in children Accumulation of genetic abnormalities in immature lymphoid precursor cells (B/T cell precursors) Neoplastic lymphoid precursor cells (“blasts”) divide and accumulate in bone marrow Abundance of blasts displaces other blood precursors from marrow, inhibiting their development/differentiati on After neoplastic blasts fill up bone marrow, they spill out into blood High turnover of these cancerous cells Multifactorial causes, most with unclear mechanisms Expanding marrow pushing on bone Pancytopenia on CBC 20% of marrow is blasts (on bone marrow aspirate and/or biopsy) Neoplastic blasts continue to divide and accumulate in lymph nodes and spleen (can occur, but not that common) Blasts detected as white blood cells on CBC High rate of cell lysis Weight loss, malaise, fever/chills, night sweats Bone pain (worse than that felt in AML, especially in children) ↓ in neutrophils ↓ in RBCs ↓ in platelets, reduced blood clotting ability Lymphadenopathy Splenomegaly May cause leukocytosis, despite pancytopenia Release of intracellular contents (uric acid, K+, LDH) into plasma Greater chances of infection Anemia Fatigue, shortness of breath, pallor Easy bruising and petechiae on skin Hyperuricemia Hyperkalemia High [LDH] Tumor lysis syndrome Acute kidney injury Gout Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Re-Published May 5, 2019 on www.thecalgaryguide.com