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