The nurse is caring for a client who experienced multiple invasive trauma from a motor vehicle collision and has developed systemic inflammatory response syndrome (SIRS). Which pathophysiological process is most likely associated with the development of SIRS in this client?
Multiple organ dysfunction.
Acute kidney injury.
Intestinal obstruction.
Sepsis.
The Correct Answer is A
A) Multiple organ dysfunction:
Correct. Systemic inflammatory response syndrome (SIRS) is a widespread inflammatory response to a variety of severe clinical insults, including trauma, infection, burns, or other sources of tissue injury. In the context of trauma from a motor vehicle collision, the body may mount a systemic inflammatory response involving multiple organ systems. This can progress to multiple organ dysfunction syndrome (MODS), where there is progressive dysfunction of two or more organ systems.
B) Acute kidney injury:
Acute kidney injury (AKI) can certainly occur in the context of severe trauma and systemic inflammation, such as in SIRS. However, AKI is a specific manifestation rather than the overarching pathophysiological process associated with the development of SIRS.
C) Intestinal obstruction:
Intestinal obstruction is a mechanical obstruction of the intestines and is not typically associated with the development of SIRS unless there is associated ischemia or perforation leading to systemic inflammation.
D) Sepsis:
Sepsis is a severe infection that has spread throughout the body and triggers a systemic inflammatory response. While sepsis can lead to SIRS, it is not the only cause. In this scenario, trauma from a motor vehicle collision is the primary cause of the systemic inflammatory response, rather than infection.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
DKA is a serious complication of diabetes mellitus characterized by hyperglycemia, ketosis, and metabolic acidosis. The laboratory results consistent with DKA include:
Elevated blood glucose level: A blood glucose level of 525 mg/dL (28 mmol/L) is significantly elevated and consistent with DKA.
Low arterial blood pH: A decreased arterial blood pH indicates acidosis, which is characteristic of DKA. Normal arterial blood pH ranges from 7.35 to 7.45.
Low bicarbonate (HCO3-) level: A low bicarbonate level indicates metabolic acidosis, which is also characteristic of DKA. Normal bicarbonate levels range from 21 to 28 mEq/L (21 to 28 mmol/L).
Among the options provided:
A) Arterial blood pH 7.5 and bicarbonate level 32 mEq/L (32 mmol/L):
This pH and bicarbonate level are indicative of alkalosis, which is not consistent with DKA.
B) Arterial blood pH 7.42 and bicarbonate level 18 mEq/L (18 mmol/L):
This pH is within the normal range, and the bicarbonate level is slightly decreased but not indicative of metabolic acidosis consistent with DKA.
C) Arterial blood pH 7.25 and bicarbonate level 10 mEq/L (10 mmol/L):
Correct. This pH is decreased, indicating acidosis, and the bicarbonate level is significantly below the normal range, consistent with metabolic acidosis characteristic of DKA.
D) Arterial blood pH 7.38 and bicarbonate level 29 mEq/L (29 mmol/L):
While the pH is within the normal range, the bicarbonate level is elevated, which is not consistent with metabolic acidosis seen in DKA.
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.
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