A client newly diagnosed with diabetes mellitus is experiencing increased thirst. Which physiologic mechanism must take place to control this manifestation?
Maintain a normal amount of circulating antidiuretic hormone.
Increase the client’s serum osmolarity.
Increase the excretion of acetone in the client’s urine.
Control the client’s blood glucose levels.
The Correct Answer is D
Choice A reason: Normal antidiuretic hormone levels regulate water balance but do not address thirst in diabetes mellitus, which is caused by hyperglycemia-induced osmotic diuresis. Controlling blood glucose corrects the osmotic imbalance driving thirst, making ADH maintenance less relevant and incorrect for this manifestation’s control.
Choice B reason: Increasing serum osmolarity would worsen thirst, as high osmolarity from hyperglycemia causes dehydration and polydipsia. The goal is to reduce osmolarity by controlling blood glucose, which mitigates osmotic diuresis. This choice is incorrect, as it exacerbates the mechanism driving the client’s symptom.
Choice C reason: Increased acetone excretion occurs in diabetic ketoacidosis, not directly related to thirst in new diabetes mellitus. Thirst results from hyperglycemia causing osmotic diuresis. Controlling glucose levels addresses the root cause, making acetone excretion irrelevant and incorrect for managing polydipsia in this client.
Choice D reason: Increased thirst in diabetes mellitus results from hyperglycemia causing osmotic diuresis, leading to dehydration. Controlling blood glucose levels reduces serum osmolarity, preventing fluid loss and alleviating thirst. This is the primary physiologic mechanism, supported by endocrinology evidence for managing diabetes-related polydipsia effectively.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
Choice A reason: Decreased histamine production does not occur during inflammation; histamine release increases, promoting vasodilation and permeability. Inflammation triggers immune responses, including histamine-mediated vascular changes to deliver immune cells. This choice is incorrect, as reduced histamine contradicts the immune system’s proinflammatory response to an inflammatory stimulus.
Choice B reason: Vasoconstriction reduces blood flow, counteracting inflammation’s goal of delivering immune cells to the site. Inflammation causes vasodilation to enhance blood flow and permeability. Vasoconstriction is not a primary immune response to inflammation, making this an incorrect choice for the body’s reaction to an inflammatory source.
Choice C reason: Increased vascular permeability is a hallmark of inflammation, allowing plasma, immune cells, and proteins to reach the affected site. Histamine and cytokines trigger this response, facilitating immune defense and tissue repair. This aligns with the immune system’s proinflammatory mechanism, making it the correct response to inflammation.
Choice D reason: Activation of exocytosis involves cellular vesicle release, not a primary inflammatory response. While immune cells may use exocytosis to release mediators, increased vascular permeability is the direct immune reaction to inflammation, enabling immune access. This choice is less specific, making it incorrect for the primary response.
Correct Answer is ["B","D","E"]
Explanation
Choice A reason: Fibrosis and calcification occur in chronic pancreatitis, not acute pancreatitis, which is characterized by sudden inflammation. Alcohol-induced acute pancreatitis involves duct obstruction and enzyme autodigestion, causing pain. Fibrosis is a long-term consequence, not a primary driver of the acute pain in this client’s recent alcohol binge.
Choice B reason: Inflammation from an obstructed pancreatic duct is a key cause of acute pancreatitis pain. Alcohol can trigger duct blockage, leading to enzyme backup, inflammation, and tissue irritation. This process causes severe upper abdominal pain radiating to the back, aligning with the client’s symptoms and elevated amylase/lipase levels.
Choice C reason: Bleeding gastric ulcers cause epigastric pain but are unrelated to pancreatitis, which involves pancreatic inflammation. Elevated amylase and lipase confirm pancreatitis, not ulcer disease. Ulcers do not radiate pain to the back or stem from alcohol binges, making this incorrect for the client’s diagnosis.
Choice D reason: Spasms of the sphincter of Oddi, often alcohol-induced, block pancreatic secretions, causing enzyme backup and inflammation. This contributes to the severe pain of acute pancreatitis, as obstructed flow exacerbates tissue irritation. This process aligns with the client’s symptoms and laboratory findings, supporting its role in pain causation.
Choice E reason: Autodigestion by pancreatic enzymes, activated prematurely due to duct obstruction, causes tissue damage and severe pain in acute pancreatitis. Alcohol triggers this process, leading to inflammation and necrosis. This is a primary pathophysiological mechanism, explaining the client’s pain and elevated amylase/lipase, per evidence-based pancreatitis pathology.
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