The nurse is caring for a client with intestinal obstruction who presents with severe, colicky abdominal pain, nausea, vomiting, and abdominal distention. Which pathophysiologic mechanism supports the client's clinical presentation?

Tumor lysis syndrome (TLS) is a potentially life-threatening oncologic emergency characterized by the rapid release of intracellular contents into the bloodstream following the destruction of cancer cells. This release can lead to metabolic disturbances, including hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia. Here's how the child's laboratory results are indicative of tumor lysis syndrome:

A) Wilm's tumor:

Wilms tumor is a type of kidney cancer that primarily affects children. However, it typically does not cause the metabolic disturbances seen in tumor lysis syndrome. Laboratory abnormalities in Wilms tumor are generally related to renal dysfunction and may include hematuria and proteinuria.

B) Tumor lysis syndrome:

Correct. Tumor lysis syndrome occurs when chemotherapy or radiation therapy causes a rapid breakdown of cancer cells, leading to the release of intracellular contents such as potassium, phosphorus, and uric acid into the bloodstream. The elevated potassium and phosphorus levels seen in the child's laboratory results are consistent with tumor lysis syndrome. Hyperkalemia (elevated potassium) and hyperphosphatemia (elevated phosphorus) are common metabolic disturbances in tumor lysis syndrome.

C) Superior vena cava syndrome:

Superior vena cava syndrome occurs when the superior vena cava, a major vein that carries blood from the upper body to the heart, becomes partially or completely obstructed. This obstruction can lead to symptoms such as facial swelling, dyspnea, and dilated neck veins. While superior vena cava syndrome may occur in cancer patients, it does not typically cause the metabolic disturbances seen in the child's laboratory results.

D) Hyperleukocytosis:

Hyperleukocytosis refers to an extremely high white blood cell count, which can occur in leukemia. While leukemia can lead to metabolic abnormalities, the child's laboratory results, particularly the elevated potassium and phosphorus levels, are more indicative of tumor lysis syndrome than hyperleukocytosis.

Chronic osteoarthritis (OA) is a degenerative joint disease characterized by the breakdown of joint cartilage and underlying bone changes. The pathophysiological process of OA involves various factors contributing to joint pain and inflammation. Here's why option C is the correct choice:

A) Inflammation results from deposition of crystals in the synovial space of joints producing irritation:

This statement is more characteristic of crystal-induced arthritis, such as gout or pseudogout, where crystals (e.g., urate or calcium pyrophosphate crystals) deposit in the joints and cause acute inflammation and irritation. While inflammation may occur in OA, it is primarily a result of mechanical stress and cartilage degradation rather than crystal deposition.

B) Inflammation is caused by immune complex and autoantibody deposition in connective tissue:

This statement is more characteristic of autoimmune diseases such as rheumatoid arthritis (RA), where immune complex deposition and autoantibody production lead to chronic inflammation and joint damage. In OA, inflammation is not primarily mediated by immune complex deposition or autoantibodies.

C) Joint inflammation occurs when chondrocyte injury destroys joint cartilage, producing osteophytes:

Correct. In osteoarthritis, joint inflammation occurs as a result of chondrocyte injury and cartilage breakdown. Over time, the degenerative changes in the joint lead to the formation of osteophytes (bone spurs) at the joint margins. These changes can irritate surrounding tissues, including the synovium, ligaments, and tendons, contributing to joint pain and inflammation.

D) Joint destruction happens due to an autoimmune inflammation involving IgG response to an antigen:

This statement is more characteristic of autoimmune arthritis, such as rheumatoid arthritis (RA), where autoantibodies (e.g., rheumatoid factor, anti-citrullinated protein antibodies) target joint tissues, leading to chronic inflammation and joint destruction. In OA, joint destruction primarily results from mechanical stress and wear-and-tear on the joint structures rather than autoimmune mechanisms.