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.
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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 B
Explanation
Acute leukemia, including acute myeloid leukemia (AML), involves the proliferation of abnormal myeloblasts (immature white blood cells) in the bone marrow, leading to decreased production of normal blood cells. Here's the breakdown of the pathophysiology contributing to bruising in acute leukemia:
A) Oxyhemoglobin provides less oxygen to tissues:
Oxyhemoglobin refers to hemoglobin bound to oxygen, and its role is in oxygen transport, not in the process of bruising. Therefore, this option is not directly related to the pathophysiology of bruising in acute leukemia.
B) Insufficient platelets delay the clotting process:
Correct. Thrombocytopenia, or low platelet count, is a common complication of acute leukemia due to the replacement of normal bone marrow cells with leukemia cells, leading to inadequate production of platelets. Platelets play a crucial role in hemostasis and clot formation. Insufficient platelets result in delayed clotting, leading to easy bruising and bleeding tendencies in patients with acute leukemia.
C) Phagocytic cells are inadequate in fighting infection:
Leukopenia, or low white blood cell count, can occur in acute leukemia due to suppression of normal hematopoiesis by leukemia cells in the bone marrow. While leukopenia predisposes patients to infections due to impaired immune function, it is not directly related to the pathophysiology of bruising.
D) Lack of iron causes hypochromic blood cells:
Iron deficiency anemia can result in hypochromic red blood cells, but this is not typically associated with the pathophysiology of bruising in acute leukemia. Anemia may contribute to other symptoms such as fatigue and pallor, but bruising primarily results from thrombocytopenia-induced clotting abnormalities.
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