A client's ankle is edematous after an ankle sprain. Which physiological mechanism is responsible for the swelling?

Histamine-mediated vascular permeability leading to fluid transudation.

Bradykinin cascade resulting in the accumulation of substance P.

Thromboxane A activation of chemical mediators.

Neutrophil migration secondary to chemotaxis.

Answer and Explanation

The Correct Answer is A

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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Correct Answer is B

Explanation

A) Nerve degeneration due to chronic gastric reflux:

Nerve degeneration due to chronic gastric reflux may lead to conditions such as gastroesophageal reflux disease (GERD) or esophagitis, but it is not directly related to the clinical presentation of intestinal obstruction. Symptoms of GERD or esophagitis typically include heartburn, regurgitation, and dysphagia rather than severe, colicky abdominal pain, nausea, vomiting, and abdominal distention.

B) Volvulus that occurred during an appendectomy:

Correct. Volvulus refers to the twisting of a segment of the intestine around its mesentery, leading to obstruction of the bowel lumen and compromising blood flow to the affected area. In this scenario, the client's clinical presentation of severe, colicky abdominal pain, nausea, vomiting, and abdominal distention is consistent with symptoms of intestinal obstruction, which can occur secondary to volvulus. Volvulus may result from various factors, including prior abdominal surgeries, such as an appendectomy, leading to abnormal positioning or adhesions within the abdomen.

C) Esophagitis due to reflux of gastric contents:

Esophagitis due to reflux of gastric contents can cause symptoms such as heartburn, chest pain, and difficulty swallowing, but it is not typically associated with severe, colicky abdominal pain, nausea, vomiting, and abdominal distention characteristic of intestinal obstruction.

D) A history of having Helicobacter pylori infection:

Helicobacter pylori infection is associated with conditions such as peptic ulcer disease and gastritis, but it is not directly related to the clinical presentation of intestinal obstruction. Symptoms of H. pylori infection may include abdominal pain, nausea, and vomiting, but they are not typically colicky and severe as those seen in intestinal obstruction.

A. Inflammation results from deposition of crystals in the synovial space of joints producing irritation. B. Inflammation is caused by immune complex and autoantibody deposition in connective tissue. C. Joint inflammation occurs when chondrocyte injury destroys joint cartilage, producing osteophytes. D. Joint destruction happens due to an autoimmune inflammation involving IgG response to an antigen.

Correct Answer is C

Explanation

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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A client's ankle is edematous after an ankle sprain. Which physiological mechanism is responsible for the swelling?

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