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.
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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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
A) Lipase:
Correct. Lipase is an enzyme produced by the pancreas that aids in the digestion of fats. Elevated levels of lipase in the blood can indicate pancreatic damage or inflammation, such as that which may occur due to trauma like a gunshot wound to the abdomen. Pancreatic injury can lead to leakage of enzymes into the bloodstream, resulting in elevated serum lipase levels. Monitoring lipase levels helps assess pancreatic function and detect injury or disease.
B) Myoglobinuria:
Myoglobinuria refers to the presence of myoglobin, a protein found in muscle cells, in the urine. It is often associated with muscle injury or breakdown, such as rhabdomyolysis. While abdominal trauma may result in muscle injury, myoglobinuria is not specific to pancreatic damage and is more indicative of muscle-related injury or conditions.
C) White blood count (WBC):
Elevated white blood cell count (WBC), or leukocytosis, is a non-specific marker of inflammation or infection. While it may occur in response to tissue injury, including pancreatic injury, it is not specific to pancreatic damage and can be elevated due to various other factors, such as surgical stress, infection, or inflammation.
D) Bilirubin:
Bilirubin is a pigment produced during the breakdown of red blood cells and is excreted by the liver. Elevated levels of bilirubin may indicate liver dysfunction or obstruction of the bile ducts, but they are not specific to pancreatic damage. While pancreatic injury can lead to obstruction of the bile ducts in some cases, monitoring bilirubin levels alone is not sufficient to diagnose pancreatic damage.
Correct Answer is C
Explanation
The ABG results indicate respiratory acidosis (pH 7.0, PaCO2 66 mmHg) with compensatory metabolic alkalosis (HCO3- 24 mEq/L). The low PaO2 (60 mmHg) suggests hypoxemia.
pH 7.0: The pH is below the normal range (7.35 to 7.45), indicating acidosis.
PaCO2 66 mmHg: The PaCO2 is elevated above the normal range (35 to 45 mmHg), indicating respiratory acidosis.
HCO3- 24 mEq/L: The bicarbonate level is within the normal range (21 to 28 mEq/L), indicating compensatory metabolic alkalosis.
PaO2 60 mmHg: The PaO2 is decreased below the normal range (80 to 100 mmHg), indicating hypoxemia.
These findings suggest that the client is experiencing respiratory failure, which is characterized by inadequate gas exchange resulting in hypoxemia and hypercapnia. In this case, the massive pulmonary embolus is causing ventilation-perfusion (V/Q) mismatch, leading to impaired gas exchange and respiratory compromise. Tachycardia, hypotension, and audible bilateral pulmonary crackles further support the diagnosis of respiratory failure in the context of a massive pulmonary embolus.
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