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 B
Explanation
Polycystic kidney disease (PKD) is a genetic disorder characterized by the formation of multiple fluid-filled cysts in the kidneys. One of the complications associated with PKD is hypertension, which often occurs due to activation of the renin-angiotensin-aldosterone system (RAAS). Here's how the pathophysiological process of the RAAS contributes to the client's elevated blood pressure:
A) Intravascular fluid deficit:
In polycystic kidney disease, the development of multiple cysts in the kidneys can impair renal function and lead to decreased filtration and reabsorption capacity. However, this impairment typically leads to fluid retention rather than intravascular fluid deficit, contributing to hypertension rather than hypotension.
B) Renin angiotensin mechanism:
Correct. In PKD, the cysts disrupt normal kidney architecture and function, leading to activation of the renin-angiotensin-aldosterone system (RAAS). Reduced renal blood flow and glomerular filtration rate (GFR) stimulate the release of renin from the juxtaglomerular cells of the kidneys. Renin acts on angiotensinogen to convert it into angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor that increases peripheral vascular resistance, leading to elevated blood pressure. Additionally, angiotensin II stimulates the secretion of aldosterone, which promotes sodium and water retention, further contributing to hypertension.
C) Inflammatory process of bladder mucosa:
This option is not directly related to the pathophysiological process of hypertension in polycystic kidney disease. Flank pain and hematuria in PKD are often associated with cyst rupture or hemorrhage within the cysts rather than an inflammatory process of the bladder mucosa.
D) Mineral precipitation in urine:
Mineral precipitation in urine, such as the formation of kidney stones, can occur in polycystic kidney disease but is not directly associated with hypertension. Kidney stones may contribute to flank pain and hematuria but do not typically cause systemic hypertension.
Correct Answer is B
Explanation
Tumor lysis syndrome (TLS) is a potentially life-threatening oncologic emergency characterized by the rapid release of intracellular contents into the bloodstream following the destruction of cancer cells. This release can lead to metabolic disturbances, including hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia. Here's how the child's laboratory results are indicative of tumor lysis syndrome:
A) Wilm's tumor:
Wilms tumor is a type of kidney cancer that primarily affects children. However, it typically does not cause the metabolic disturbances seen in tumor lysis syndrome. Laboratory abnormalities in Wilms tumor are generally related to renal dysfunction and may include hematuria and proteinuria.
B) Tumor lysis syndrome:
Correct. Tumor lysis syndrome occurs when chemotherapy or radiation therapy causes a rapid breakdown of cancer cells, leading to the release of intracellular contents such as potassium, phosphorus, and uric acid into the bloodstream. The elevated potassium and phosphorus levels seen in the child's laboratory results are consistent with tumor lysis syndrome. Hyperkalemia (elevated potassium) and hyperphosphatemia (elevated phosphorus) are common metabolic disturbances in tumor lysis syndrome.
C) Superior vena cava syndrome:
Superior vena cava syndrome occurs when the superior vena cava, a major vein that carries blood from the upper body to the heart, becomes partially or completely obstructed. This obstruction can lead to symptoms such as facial swelling, dyspnea, and dilated neck veins. While superior vena cava syndrome may occur in cancer patients, it does not typically cause the metabolic disturbances seen in the child's laboratory results.
D) Hyperleukocytosis:
Hyperleukocytosis refers to an extremely high white blood cell count, which can occur in leukemia. While leukemia can lead to metabolic abnormalities, the child's laboratory results, particularly the elevated potassium and phosphorus levels, are more indicative of tumor lysis syndrome than hyperleukocytosis.
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