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?

A. Myocardial infarction:

Myocardial infarction (MI) typically presents with severe and prolonged chest pain or discomfort that is not relieved by rest or nitroglycerin. MI is characterized by myocardial necrosis due to prolonged ischemia, often resulting from the occlusion of a coronary artery by a thrombus or plaque rupture. While chest pressure and breathlessness are symptoms commonly associated with MI, the transient nature of the symptoms described by the client, as well as their relief after rest, is more indicative of stable angina rather than MI.

B. Unstable angina:

Unstable angina is characterized by new-onset angina, increasing frequency, or worsening intensity of angina symptoms. It is considered a medical emergency as it may precede a myocardial infarction. However, unstable angina typically presents with symptoms at rest or with minimal exertion and is not usually relieved by rest or nitroglycerin. The client's symptoms, which are relieved by rest, are more consistent with stable angina.

C. Stable angina:

Stable angina is characterized by predictable chest pain or discomfort that occurs with exertion or stress and is relieved by rest or nitroglycerin. The symptoms described by the client, including chest pressure and breathlessness that improve with rest, are consistent with stable angina. Stable angina occurs due to transient myocardial ischemia caused by an imbalance between myocardial oxygen supply and demand, often related to coronary artery disease.

D. Prinzmetal angina:

Prinzmetal angina, also known as variant angina, is characterized by chest pain or discomfort that occurs at rest, often in the early morning hours, and is typically caused by coronary artery spasm rather than fixed atherosclerotic lesions. While Prinzmetal angina can present with transient symptoms similar to those described by the client, it is less common than stable angina and is often associated with transient ST-segment elevation on electrocardiogram (ECG), which is not mentioned in the scenario.

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.