A client with chronic osteoarthritis is troubled by knee pain. Which pathophysiological process is contributing to the pain?
Inflammation results from deposition of crystals in the synovial space of joints producing irritation.
Inflammation is caused by immune complex and autoantibody deposition in connective tissue.
Joint inflammation occurs when chondrocyte injury destroys joint cartilage, producing osteophytes.
Joint destruction happens due to an autoimmune inflammation involving IgG response to an antigen.
The Correct Answer is C
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.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
A) Histamine-mediated vascular permeability leading to fluid transudation:
Correct. Ankle edema following an ankle sprain is often due to inflammation and increased vascular permeability. Histamine, released from mast cells and basophils during the inflammatory response, causes vasodilation and increases vascular permeability. This leads to the leakage of fluid from the blood vessels into the surrounding tissues, resulting in edema.
B) Bradykinin cascade resulting in the accumulation of substance P:
While bradykinin is involved in the inflammatory response and can contribute to pain and vasodilation, it does not directly cause fluid transudation leading to edema in the context of an ankle sprain.
C) Thromboxane A activation of chemical mediators:
Thromboxane A is involved in platelet aggregation and vasoconstriction rather than increasing vascular permeability and edema formation.
D) Neutrophil migration secondary to chemotaxis:
Neutrophil migration is part of the inflammatory response and can contribute to tissue damage and inflammation, but it is not the primary mechanism responsible for the development of edema following an ankle sprain.
Correct Answer is A
Explanation
A) The usual types of reactions are mediated by antibodies:
Correct. Types I, II, and III hypersensitivity reactions are mediated by antibodies (IgE, IgG, or IgM) that bind to antigens and trigger immune responses. In contrast, Type IV hypersensitivity reactions are T-cell mediated and do not involve antibodies.
B) B-lymphocytes produce the offending substances:
This statement is incorrect. B-lymphocytes are involved in antibody-mediated immune responses (types I, II, and III hypersensitivity reactions), not Type IV hypersensitivity reactions, which are primarily mediated by T-lymphocytes.
C) They typically occur with the first exposure to an antigen:
This statement is incorrect. Type IV hypersensitivity reactions usually require sensitization upon initial exposure to an antigen, and subsequent exposures elicit the delayed hypersensitivity response. This is similar to types I, II, and III hypersensitivity reactions, which also involve sensitization upon initial exposure.
D) Delayed reactions are characterized by cytokine release:
This statement is partially correct. Type IV hypersensitivity reactions are characterized by a delayed onset (typically 24 to 72 hours after exposure) and involve the release of cytokines from activated T-lymphocytes, leading to inflammation and tissue damage. However, other types of hypersensitivity reactions may also involve cytokine release, so this feature alone does not differentiate Type IV from other types of reactions.
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