* Hyperkalemia. Potassium is mainly an intracellular ion. High turnover of tumor cells leads to spill of potassium into the blood. Symptoms usually do not manifest until levels are high (> 6.5 mmol/L) normal 3.5–5.0 mmol/L and they include * palpitations, cardiac conduction abnormalities, and arrhythmias (can be fatal) * muscle weakness or paralysis * Hyperphosphatemia. Like potassium, phosphates are also predominantly intracellular. Hyperphosphatemia causes<unk>  kidney injury in tumor lysis syndrome, because of deposition of calcium phosphate crystals in the kidney parenchyma. * Hypocalcemia. Because of the hyperphosphatemia, calcium is precipitated to form calcium phosphate, leading to hypocalcemia. Symptoms of hypocalcemia include (but are not limited to): * tetany * paresthesias * muscle cramps * muscle weakness * sudden changes in mental status, including emotional lability * Parkinsonian (extrapyramidal) movement disorders * papilledema * Hyperuricemia and hyperuricosuria. Massive cell death and nuclear breakdown generates large quantities of nucleic acids. Of these, the purines (adenine and guanine) are converted to uric acid via the purine degradation pathway and excreted in the urine. However, at the high concentrations of uric acid generated by tumor lysis, uric acid is apt to precipitate as monosodium urate crystals.<unk>  uric acid nephropathy (AUAN) due to hyperuricosuria has been a dominant cause of<unk>  kidney failure but with the advent of effective treatments for hyperuricosuria, AUAN has become a less common cause than hyperphosphatemia. Two common conditions related to excess uric acid, gout and uric acid nephrolithiasis, are not features of tumor lysis syndrome. * Lactic acidosis. * Pretreatment spontaneous tumor lysis syndrome. This entity is associated with<unk>  kidney failure due to uric acid nephropathy prior to the institution of chemotherapy and is largely associated with lymphoma and<unk> . The important distinction between this syndrome and the post-chemotherapy syndrome is that spontaneous TLS is not associated with hyperphosphatemia. One suggestion for the reason of this is that the high cell turnover rate leads to high uric acid levels through nucleobase turnover but the tumor reuses the released phosphate for growth of new tumor cells. In post-chemotherapy TLS, tumor cells are destroyed and no new tumor cells are being synthesized. TLS is most common during cytotoxic treatment of hematologic neoplasms.
complications of Acute lymphoblastic leukemia
complications of Agranulocytosis
symptom of Acute myeloid leukemia
symptoms of Aplastic anemia
symptom of Aplastic anemia
types of Acute lymphoblastic leukemia
medical cause of Neutropenia
symptom of Myelodysplastic syndrome