Why is there hyperuricemia in tumor lysis syndrome?

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.

How does tumor lysis cause hyperuricemia?

When cancer cells break down quickly in the body, levels of uric acid, potassium, and phosphorus rise faster than the kidneys can remove them. This causes TLS. Excess phosphorus can “sop up” calcium, leading to low levels of calcium in the blood.

What causes hyperuricemia in TLS?

Catabolism of the nucleic acids to uric acid leads to hyperuricemia; the marked increase in uric acid excretion can result in the precipitation of uric acid in the renal tubules and renal vasoconstriction, impaired autoregulation, decreased renal flow, oxidation, and inflammation, resulting in acute kidney injury.

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Why is there acidosis in tumor lysis syndrome?

Patients with high-risk disease may be prone to lactic acidosis from massive tumor cell necrosis. Because acidosis inhibits uric acid excretion (43), prompt recognition and correct of acidosis may prevent or ameliorate uric acid nephropathy.

Why is there hyperphosphatemia in tumor lysis syndrome?

Hyperphosphatemia is another electrolyte imbalance associated with tumor lysis syndrome. The nucleic acid has a phosphate group, and the breakdown of the tumorous cell will lead to the release of a significant amount of phosphorus into the bloodstream. Most of the phosphorus is renally excreted.

Why does hypocalcemia occur in tumor lysis syndrome?

Hyperphosphatemia causes acute kidney failure 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.

Why is there hyperkalemia in tumor lysis syndrome?

Hyperkalemia and hyperphosphatemia result directly from rapid cell lysis. Hypocalcemia is a consequence of acute hyperphosphatemia with subsequent precipitation of calcium phosphate in soft tissues. In acute kidney injury, decreased calcitriol levels also cause hypocalcemia.

What is the pathophysiology of Tumour lysis syndrome?

The pathophysiology involves massive tumor cell lysis resulting in the release of large amounts of potassium, phosphate, and uric acid. Deposition of uric acid and calcium phosphate crystals in the renal tubules may lead to acute renal failure, which is often exacerbated by concomitant intravascular volume depletion.

How does allopurinol work in tumor lysis syndrome?

Medications can be adjusted after the start of chemotherapy in response to the level of tumor lysis and/or metabolic disturbances. Allopurinol, a xanthine oxidase inhibitor, reduces the conversion of nucleic acid byproducts to uric acid, in this way preventing urate nephropathy and subsequent oliguric renal failure.

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Does radiation cause tumor lysis syndrome?

In the literature, radiation has been rarely reported as a cause of TLS. Most reported cases are associated with hematological pathologies and splenic radiation is the most often related scenario [8].

What is Rasburicase and what is its role in the mitigation of TLS?

Rasburicase, a recombinant urate oxidase enzyme, is a new agent indicated in the treatment or prophylaxis of hyperuricemia in pediatric patients with cancer who are at high risk for TLS.

What labs indicate tumor lysis syndrome?

Most patients with tumor lysis syndrome have laboratory derangements in lactate dehydrogenase, potassium, phosphate, calcium, and uric acid, as well as abnormal renal functions, occurring 1-3 days after chemotherapy initiation. Hyperkalemia is often the first life-threatening abnormality.

What is tumor lysis syndrome TLS?

Tumor lysis syndrome (TLS) is an oncologic emergency that is caused by massive tumor cell lysis with the release of large amounts of potassium, phosphate, and nucleic acids into the systemic circulation.

How is hyperphosphatemia treated in tumor lysis syndrome?

Treatment options of hyperkalemia include sodium polystyrene sulfonate, hypertonic glucose and insulin, loop diuretics, and bicarbonate. Treatment of hyperphosphatemia reduces dietary phosphate intake and includes phosphate binders such as aluminum hydroxide and aluminum carbonate.

What is prevention of tumor lysis syndrome?

The most important treatment for TLS is prevention. The mainstays of TLS prevention include aggressive hydration, control of hyperuricemia with allopurinol and rasburicase treatment, and close monitoring of electrolyte abnormalities.

What oncology nurses need to know about tumor lysis syndrome?

Tumor lysis syndrome (TLS) is an oncologic emergency caused by massive tumor cell death with the release of large amounts of potassium, phosphate, and nucleic acids into systemic circulation. Nucleic acids break down to uric acid, leading to hyperuricemia in patients.

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