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NurseDive Free Nursing Practice Question
Which patient below is at greatest risk for developing gout?
A. A 45-year-old male with a BMI of 40 taking hydrochlorothiazide and aspirin
Gout results from hyperuricemia, leading to urate crystal deposition in joints. A 45-year-old male with obesity (BMI 40) has increased purine turnover, elevating uric acid. Hydrochlorothiazide reduces urate excretion, and aspirin impairs renal uric acid clearance, significantly increasing gout risk, making this patient the most susceptible due to multiple risk factors.
B. A 39-year-old female hospitalized with bulimia that has a BMI of 24
Bulimia may cause electrolyte imbalances, but it is not strongly linked to hyperuricemia or gout. A BMI of 24 is normal, reducing obesity-related purine production. This 39-year-old female has fewer gout risk factors compared to an obese male on medications that elevate uric acid, making her less likely to develop gout.
C. A 27-year-old female with ulcerative colitis
Ulcerative colitis may cause systemic inflammation, but it is not a direct risk factor for gout. Hyperuricemia is not typically associated with inflammatory bowel diseases unless complicated by other factors like diuretic use. This 27-year-old female has a lower gout risk compared to the obese male with predisposing medications.
D. A 56-year-old male who limits consumption of smoked meat and some cheeses
Limiting purine-rich foods like smoked meat and cheeses reduces uric acid production, lowering gout risk. This 56-year-old male’s dietary habits mitigate hyperuricemia, making him the least likely to develop gout compared to the obese patient on medications that impair uric acid metabolism and excretion.
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Full Explanation
Choice A reason: Gout results from hyperuricemia, leading to urate crystal deposition in joints. A 45-year-old male with obesity (BMI 40) has increased purine turnover, elevating uric acid. Hydrochlorothiazide reduces urate excretion, and aspirin impairs renal uric acid clearance, significantly increasing gout risk, making this patient the most susceptible due to multiple risk factors.
Choice B reason: Bulimia may cause electrolyte imbalances, but it is not strongly linked to hyperuricemia or gout. A BMI of 24 is normal, reducing obesity-related purine production. This 39-year-old female has fewer gout risk factors compared to an obese male on medications that elevate uric acid, making her less likely to develop gout.
Choice C reason: Ulcerative colitis may cause systemic inflammation, but it is not a direct risk factor for gout. Hyperuricemia is not typically associated with inflammatory bowel diseases unless complicated by other factors like diuretic use. This 27-year-old female has a lower gout risk compared to the obese male with predisposing medications.
Choice D reason: Limiting purine-rich foods like smoked meat and cheeses reduces uric acid production, lowering gout risk. This 56-year-old male’s dietary habits mitigate hyperuricemia, making him the least likely to develop gout compared to the obese patient on medications that impair uric acid metabolism and excretion.
Similar Questions
What is the mechanism of action of sodium-glucose cotransporter 2 inhibitors (SGLT-2 inhibitors)?
A. Blocks glucose reabsorption by the kidneys and increases glucose excretion to lower blood sugar
SGLT-2 inhibitors, like empagliflozin, block sodium-glucose cotransporter 2 in the proximal tubule, preventing glucose reabsorption. This increases urinary glucose excretion, lowering blood sugar in type 2 diabetes. The mechanism is insulin-independent, reducing hyperglycemia and promoting weight loss, making this statement accurate for their primary action.
B. Interacts with the transcription factor that improves insulin sensitivity in the liver, skeletal muscle, and fat
SGLT-2 inhibitors do not interact with transcription factors to improve insulin sensitivity. This describes metformin’s action via AMPK activation in liver and muscle. SGLT-2 inhibitors act renally, not on transcription factors, making this statement inaccurate as it misattributes their mechanism to a different drug class.
C. Inhibits hepatic glucose production and increases insulin sensitivity in peripheral tissues
Inhibiting hepatic glucose production and increasing insulin sensitivity is metformin’s mechanism, not SGLT-2 inhibitors. SGLT-2 inhibitors work renally to excrete glucose, not by altering hepatic gluconeogenesis or peripheral insulin sensitivity. This statement is inaccurate, as it describes a different antidiabetic drug’s action.
D. Blocks ATP-sensitive K+ channels on membrane of beta cells to promote insulin secretion
Blocking ATP-sensitive K+ channels is the mechanism of sulfonylureas, like glipizide, which stimulate insulin secretion from beta cells. SGLT-2 inhibitors act on renal glucose reabsorption, not beta cell channels. This statement is inaccurate, as it incorrectly assigns a sulfonylurea mechanism to SGLT-2 inhibitors.
Full Explanation
Choice A reason: SGLT-2 inhibitors, like empagliflozin, block sodium-glucose cotransporter 2 in the proximal tubule, preventing glucose reabsorption. This increases urinary glucose excretion, lowering blood sugar in type 2 diabetes. The mechanism is insulin-independent, reducing hyperglycemia and promoting weight loss, making this statement accurate for their primary action.
Choice B reason: SGLT-2 inhibitors do not interact with transcription factors to improve insulin sensitivity. This describes metformin’s action via AMPK activation in liver and muscle. SGLT-2 inhibitors act renally, not on transcription factors, making this statement inaccurate as it misattributes their mechanism to a different drug class.
Choice C reason: Inhibiting hepatic glucose production and increasing insulin sensitivity is metformin’s mechanism, not SGLT-2 inhibitors. SGLT-2 inhibitors work renally to excrete glucose, not by altering hepatic gluconeogenesis or peripheral insulin sensitivity. This statement is inaccurate, as it describes a different antidiabetic drug’s action.
Choice D reason: Blocking ATP-sensitive K+ channels is the mechanism of sulfonylureas, like glipizide, which stimulate insulin secretion from beta cells. SGLT-2 inhibitors act on renal glucose reabsorption, not beta cell channels. This statement is inaccurate, as it incorrectly assigns a sulfonylurea mechanism to SGLT-2 inhibitors.
A client who has been diagnosed with bladder cancer is scheduled for an ileal conduit. Which statement by the nurse to the client accurately describes the ileal conduit?
A. This is always a temporary procedure that can always be reversed later
An ileal conduit is typically a permanent procedure for bladder cancer after cystectomy, as the bladder is removed. Reversibility is rare and depends on specific circumstances, not guaranteed. This statement is inaccurate, as it falsely suggests that ileal conduits are always temporary and reversible.
B. Urine is diverted into the sigmoid colon, where it is expelled through the rectum
Diverting urine to the sigmoid colon describes a ureterosigmoidostomy, not an ileal conduit. In an ileal conduit, urine is diverted through an ileal segment to an abdominal stoma, not the rectum. This statement is inaccurate, as it describes a different urinary diversion procedure.
C. Urine is diverted from the ureters to a stoma opening on the abdomen
An ileal conduit involves diverting urine from the ureters through a segment of ileum to a stoma on the abdomen, where urine is collected in an external pouch. This is the standard procedure for bladder cancer post-cystectomy, making this statement accurate and descriptive of the ileal conduit.
D. The diversion creates an opening in the bladder for urine to be eliminated
An ileal conduit does not create an opening in the bladder; the bladder is often removed in bladder cancer. Urine is diverted from the ureters to a stoma, bypassing the bladder. This statement is inaccurate, as it misrepresents the anatomical changes in an ileal conduit.
Full Explanation
Choice A reason: An ileal conduit is typically a permanent procedure for bladder cancer after cystectomy, as the bladder is removed. Reversibility is rare and depends on specific circumstances, not guaranteed. This statement is inaccurate, as it falsely suggests that ileal conduits are always temporary and reversible.
Choice B reason: Diverting urine to the sigmoid colon describes a ureterosigmoidostomy, not an ileal conduit. In an ileal conduit, urine is diverted through an ileal segment to an abdominal stoma, not the rectum. This statement is inaccurate, as it describes a different urinary diversion procedure.
Choice C reason: An ileal conduit involves diverting urine from the ureters through a segment of ileum to a stoma on the abdomen, where urine is collected in an external pouch. This is the standard procedure for bladder cancer post-cystectomy, making this statement accurate and descriptive of the ileal conduit.
Choice D reason: An ileal conduit does not create an opening in the bladder; the bladder is often removed in bladder cancer. Urine is diverted from the ureters to a stoma, bypassing the bladder. This statement is inaccurate, as it misrepresents the anatomical changes in an ileal conduit.
A client with type 2 diabetes is prescribed glipizide, a sulfonylurea. The nurse should monitor the client for which of the following potential adverse effects?
A. Hypoglycemia
Glipizide, a sulfonylurea, stimulates insulin release from pancreatic beta cells by blocking ATP-sensitive potassium channels, increasing insulin secretion. This can cause hypoglycemia, especially if meals are skipped or with excessive dosing. Monitoring blood glucose is critical, as hypoglycemia can lead to symptoms like sweating, shakiness, or confusion, making this the primary adverse effect.
B. Hyperkalemia
Glipizide does not significantly affect potassium levels. Hyperkalemia is more associated with drugs like ACE inhibitors or potassium-sparing diuretics. Sulfonylureas primarily impact glucose metabolism, not electrolyte balance, making this an inaccurate adverse effect to monitor in patients taking glipizide.
C. Weight loss
Glipizide often causes weight gain, not weight loss, due to increased insulin levels promoting glucose uptake and fat storage. Weight loss is more associated with drugs like metformin or SGLT-2 inhibitors. This statement is inaccurate, as weight gain is a more likely concern with sulfonylureas.
D. Hypertension
Hypertension is not a common adverse effect of glipizide. Sulfonylureas primarily affect glucose metabolism, not blood pressure. While diabetes increases cardiovascular risk, glipizide does not directly cause hypertension, making this an inaccurate adverse effect to prioritize in monitoring for this medication.
Full Explanation
Choice A reason: Glipizide, a sulfonylurea, stimulates insulin release from pancreatic beta cells by blocking ATP-sensitive potassium channels, increasing insulin secretion. This can cause hypoglycemia, especially if meals are skipped or with excessive dosing. Monitoring blood glucose is critical, as hypoglycemia can lead to symptoms like sweating, shakiness, or confusion, making this the primary adverse effect.
Choice B reason: Glipizide does not significantly affect potassium levels. Hyperkalemia is more associated with drugs like ACE inhibitors or potassium-sparing diuretics. Sulfonylureas primarily impact glucose metabolism, not electrolyte balance, making this an inaccurate adverse effect to monitor in patients taking glipizide.
Choice C reason: Glipizide often causes weight gain, not weight loss, due to increased insulin levels promoting glucose uptake and fat storage. Weight loss is more associated with drugs like metformin or SGLT-2 inhibitors. This statement is inaccurate, as weight gain is a more likely concern with sulfonylureas.
Choice D reason: Hypertension is not a common adverse effect of glipizide. Sulfonylureas primarily affect glucose metabolism, not blood pressure. While diabetes increases cardiovascular risk, glipizide does not directly cause hypertension, making this an inaccurate adverse effect to prioritize in monitoring for this medication.