A client with a sudden onset of big toe joint pain and swelling is diagnosed with gout. Which pathophysiologic process is producing the symptoms of gout?

Deposition of crystals in the synovial space of the joints produces inflammation and irritation.

Chondrocyte injury destroys joint cartilage, producing osteophytes and joint inflammation.

An immune complex and autoantibody deposition in connective tissue results in inflammation.

An autoimmune inflammation involving IgG response to an antigen causes joint destruction.

Answer and Explanation

The Correct Answer is A

Gout is a type of inflammatory arthritis caused by the deposition of monosodium urate crystals in the joints and surrounding tissues. Here's an explanation of the pathophysiological process producing the symptoms of gout:

A) Deposition of crystals in the synovial space of the joints produces inflammation and irritation:

Correct. In gout, elevated levels of uric acid in the blood lead to the formation and deposition of monosodium urate crystals in the synovial fluid of joints, particularly in the big toe joint (first metatarsophalangeal joint) in many cases. These crystals trigger an inflammatory response, activating immune cells and causing swelling, redness, warmth, and severe pain in the affected joint. The inflammation and irritation result from the body's immune response to the presence of these crystals.

B) Chondrocyte injury destroys joint cartilage, producing osteophytes and joint inflammation:

This option describes a process more characteristic of osteoarthritis, where degeneration of joint cartilage leads to the formation of osteophytes (bone spurs) and joint inflammation. Gout involves the deposition of urate crystals rather than direct chondrocyte injury.

C) An immune complex and autoantibody deposition in connective tissue results in inflammation:

This process describes the pathophysiology of autoimmune diseases such as rheumatoid arthritis, where immune complexes and autoantibodies contribute to inflammation and tissue damage. In gout, the inflammation is primarily triggered by the deposition of urate crystals rather than immune complex deposition.

D) An autoimmune inflammation involving IgG response to an antigen causes joint destruction:

This option describes the autoimmune process seen in diseases like rheumatoid arthritis, where antibodies target specific antigens, leading to joint destruction. Gout is not an autoimmune disease, and joint destruction in gout is primarily due to inflammation caused by urate crystal deposition rather than autoimmune mechanisms.

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Correct Answer is A,D,C,E,B

Explanation

This sequence starts with an injury to the arterial endothelium, leading to inflammation. Macrophages then consume LDL, forming foam cells. These foam cells release growth factors that stimulate the growth of smooth muscle cells. The smooth muscle cells grow over the fatty streaks, creating fibrous plaques. Finally, as these plaques grow, they narrow the vessel, which can result in ischemia. This is a simplified explanation of a complex process that involves many other factors and steps. It’s also important to note that this process can take many years to develop.

A. Histamine-mediated vascular permeability leading to fluid transudation. B. Bradykinin cascade resulting in the accumulation of substance P. C. Thromboxane A activation of chemical mediators. D. Neutrophil migration secondary to chemotaxis.

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.

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A client with a sudden onset of big toe joint pain and swelling is diagnosed with gout. Which pathophysiologic process is producing the symptoms of gout?

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Explanation

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