A febrile client admitted for pneumonia becomes diaphoretic and flushed. What pathophysiological process does the nurse suspect?
The client’s core body temperature reached the new thermoregulatory set point and the body is trying to prevent overheating
An exogenous pyrogen is directly resetting the client’s thermoregulatory set point in the anterior pituitary
The client is experiencing hyperthermia and the body’s mechanisms to control heat are no longer working effectively
An endogenous pyrogen is stimulating the production of leukotrienes to increase the thermoregulatory set point of the hypothalamus
The Correct Answer is A
Choice A reason: In fever, pyrogens reset the hypothalamic thermoregulatory set point, causing the body to raise core temperature via shivering and vasoconstriction. Once reached, diaphoresis and flushing occur to dissipate heat, preventing overheating. This statement accurately describes the body’s response to achieving the fever’s set point in pneumonia.
Choice B reason: Exogenous pyrogens (e.g., bacterial toxins) act via endogenous pyrogens (cytokines) to reset the hypothalamic, not anterior pituitary, set point. The pituitary regulates hormones, not thermoregulation. This statement is inaccurate, as it misidentifies the anatomical site and mechanism of fever induction.
Choice C reason: Hyperthermia involves uncontrolled heat gain (e.g., heat stroke), not a regulated fever like in pneumonia. The client’s diaphoresis and flushing indicate intact heat loss mechanisms, not failure. This statement is inaccurate, as fever, not hyperthermia, drives the observed symptoms in this scenario.
Choice D reason: Endogenous pyrogens (e.g., IL-1, IL-6) stimulate prostaglandins, not leukotrienes, to reset the hypothalamic set point in fever. Leukotrienes are involved in allergic responses, not thermoregulation. This statement is inaccurate, as it misattributes the biochemical mediator of fever in pneumonia.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
Choice A reason: Ascites results from increased permeability of peritoneal capillaries, often due to inflammatory molecules like cytokines in conditions such as liver cirrhosis or portal hypertension. This allows plasma proteins and fluid to leak into the peritoneal cavity, causing fluid accumulation. This statement accurately describes the pathophysiology of ascites in liver-related disorders.
Choice B reason: Low aldosterone levels do not cause ascites; instead, high aldosterone in liver disease (e.g., cirrhosis) promotes sodium and water retention, exacerbating fluid accumulation. This statement is inaccurate, as secondary hyperaldosteronism due to reduced liver metabolism of aldosterone is a key factor in ascites development.
Choice C reason: The liver’s failure to produce clotting factors can lead to bleeding tendencies, like variceal hemorrhage, but this does not directly cause ascites. Ascites is driven by fluid leakage from capillaries, not bleeding. This statement is inaccurate, as clotting factor deficiency is unrelated to peritoneal fluid accumulation.
Choice D reason: While fluid imbalance contributes to ascites, the primary mechanism involves portal hypertension and capillary permeability, not just osmotic pressure changes. This statement is overly vague and less accurate than the specific role of inflammatory molecules increasing capillary leakage in the peritoneal cavity.
Correct Answer is C
Explanation
Choice A reason: A 30-year-old male with occasional alcohol use and normal BMI (25) has minimal osteoporosis risk. Alcohol in moderation and normal weight do not significantly reduce bone density. Peak bone mass is typically preserved at this age, making him less at risk compared to glucocorticoid users.
Choice B reason: A 22-year-old female post-pregnancy may experience temporary bone density loss due to calcium demands during pregnancy and lactation, but young age and ongoing bone remodeling reduce long-term osteoporosis risk. Recovery is likely with adequate nutrition, making her less at risk than the glucocorticoid-treated patient.
Choice C reason: Glucocorticoids, used for inflammatory bowel disease, significantly increase osteoporosis risk by inhibiting osteoblast activity, reducing calcium absorption, and increasing bone resorption. This 40-year-old male faces accelerated bone loss, especially with chronic use, making him the highest risk among the options due to medication-induced bone density reduction.
Choice D reason: A 35-year-old female running marathons engages in weight-bearing exercise, which promotes bone density through mechanical stress and osteoblast stimulation. This reduces osteoporosis risk compared to glucocorticoid use, as exercise enhances bone remodeling and strength, making her less likely to develop osteoporosis than the male on steroids.
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