Nursing practice questions with comprehensive rationales
NurseDive Free Nursing Practice Question
Prednisone is an oral corticosteroid that has less mineralocorticoid activity than other oral steroids. What does the nurse expect when giving this medication?
A. It will cause less extreme hyperglycemia
Prednisone causes hyperglycemia by increasing gluconeogenesis and insulin resistance, similar to other corticosteroids. Its lower mineralocorticoid activity does not significantly reduce this effect compared to other steroids. This statement is inaccurate, as prednisone’s glycemic impact is comparable, not less extreme, than other corticosteroids.
B. It will cause less sodium and water retention
Prednisone has minimal mineralocorticoid activity compared to steroids like hydrocortisone, resulting in less sodium and water retention. Mineralocorticoids promote renal sodium reabsorption, causing fluid retention. Prednisone’s glucocorticoid dominance reduces these effects, making this statement accurate for expected nursing observations during administration.
C. It will cause more sodium retention and less water retention
Prednisone’s low mineralocorticoid activity leads to less, not more, sodium retention. It does not disproportionately affect water retention independently of sodium. This statement is inaccurate, as prednisone’s profile minimizes both sodium and water retention compared to steroids with higher mineralocorticoid effects.
D. It will cause more extreme hyperglycemia
Prednisone causes hyperglycemia, but its effect is not more extreme than other corticosteroids like dexamethasone. Its glucocorticoid activity drives gluconeogenesis similarly across the class. This statement is inaccurate, as prednisone’s hyperglycemic effects are standard, not uniquely severe, among oral corticosteroids.
This question is an excerpt from Nurse Dive's nursing test bank - Pathophamacology Proctored Exam (Examplify). Take the full exam now
Full Explanation
Choice A reason: Prednisone causes hyperglycemia by increasing gluconeogenesis and insulin resistance, similar to other corticosteroids. Its lower mineralocorticoid activity does not significantly reduce this effect compared to other steroids. This statement is inaccurate, as prednisone’s glycemic impact is comparable, not less extreme, than other corticosteroids.
Choice B reason: Prednisone has minimal mineralocorticoid activity compared to steroids like hydrocortisone, resulting in less sodium and water retention. Mineralocorticoids promote renal sodium reabsorption, causing fluid retention. Prednisone’s glucocorticoid dominance reduces these effects, making this statement accurate for expected nursing observations during administration.
Choice C reason: Prednisone’s low mineralocorticoid activity leads to less, not more, sodium retention. It does not disproportionately affect water retention independently of sodium. This statement is inaccurate, as prednisone’s profile minimizes both sodium and water retention compared to steroids with higher mineralocorticoid effects.
Choice D reason: Prednisone causes hyperglycemia, but its effect is not more extreme than other corticosteroids like dexamethasone. Its glucocorticoid activity drives gluconeogenesis similarly across the class. This statement is inaccurate, as prednisone’s hyperglycemic effects are standard, not uniquely severe, among oral corticosteroids.
Similar Questions
Which statement about phenazopyridine (Pyridium) is accurate?
A. It is used to relieve pain from urinary irritation
Phenazopyridine is a urinary analgesic that relieves pain, burning, and irritation in the urinary tract by exerting a topical anesthetic effect on the uroepithelium. It is commonly used for symptomatic relief in UTIs, making this statement accurate, as it directly addresses its therapeutic role in managing urinary discomfort.
B. It should be taken with an antibiotic until both medications are gone
Phenazopyridine is used short-term (typically 2 days) for symptom relief, not necessarily until an antibiotic course is completed. Antibiotics treat the underlying UTI, while phenazopyridine addresses symptoms. This statement is inaccurate, as their durations are independent, based on clinical need, not synchronized completion.
C. It is contraindicated for clients with urinary tract infection to use
Phenazopyridine is not contraindicated in UTIs; it is specifically indicated for symptomatic relief in these infections. It does not treat the infection but alleviates discomfort. This statement is inaccurate, as phenazopyridine is a standard adjunctive therapy in UTI management for pain relief.
D. The drug will relieve discomfort almost immediately
Phenazopyridine provides relief within hours, not almost immediately. Its onset requires absorption and distribution to the urinary tract, typically taking 1-2 hours. This statement is inaccurate, as the relief, while rapid, is not instantaneous, and patients should be informed of the expected timeframe.
Full Explanation
Choice A reason: Phenazopyridine is a urinary analgesic that relieves pain, burning, and irritation in the urinary tract by exerting a topical anesthetic effect on the uroepithelium. It is commonly used for symptomatic relief in UTIs, making this statement accurate, as it directly addresses its therapeutic role in managing urinary discomfort.
Choice B reason: Phenazopyridine is used short-term (typically 2 days) for symptom relief, not necessarily until an antibiotic course is completed. Antibiotics treat the underlying UTI, while phenazopyridine addresses symptoms. This statement is inaccurate, as their durations are independent, based on clinical need, not synchronized completion.
Choice C reason: Phenazopyridine is not contraindicated in UTIs; it is specifically indicated for symptomatic relief in these infections. It does not treat the infection but alleviates discomfort. This statement is inaccurate, as phenazopyridine is a standard adjunctive therapy in UTI management for pain relief.
Choice D reason: Phenazopyridine provides relief within hours, not almost immediately. Its onset requires absorption and distribution to the urinary tract, typically taking 1-2 hours. This statement is inaccurate, as the relief, while rapid, is not instantaneous, and patients should be informed of the expected timeframe.
The client with type 2 diabetes mellitus is prescribed semaglutide. The client knows that this medication is used for diabetes but that it is also popular for weight loss. What is the mechanism of action of this drug?
A. This drug is safe for the client who is pregnant
Semaglutide, a GLP-1 receptor agonist, is not considered safe in pregnancy due to limited data and potential fetal risks. Animal studies suggest possible teratogenicity, and it is typically avoided in pregnant patients with type 2 diabetes, making this statement inaccurate and irrelevant to its mechanism.
B. The drug impacts many factors including the natural hormone GLP-1 to increase insulin production
Semaglutide mimics GLP-1, enhancing glucose-dependent insulin secretion, suppressing glucagon release, slowing gastric emptying, and promoting satiety. These actions lower blood glucose and support weight loss in type 2 diabetes. This statement is accurate, as GLP-1-mediated insulin production is central to its mechanism of action.
C. The drug is used for type 1 diabetes mellitus most of the time
Semaglutide is primarily used for type 2 diabetes, not type 1, as it relies on functional beta cells to enhance insulin secretion. Type 1 diabetes involves absolute insulin deficiency, rendering GLP-1 agonists ineffective. This statement is inaccurate, as semaglutide is not indicated for type 1 diabetes.
D. The blood sugar does not need to be monitored as closely as other medication
Semaglutide requires regular blood sugar monitoring, as hypoglycemia can occur, especially with concomitant insulin or sulfonylureas. Its glucose-lowering effects necessitate careful management to prevent adverse events. This statement is inaccurate, as monitoring remains critical to ensure safe and effective diabetes control.
Full Explanation
Choice A reason: Semaglutide, a GLP-1 receptor agonist, is not considered safe in pregnancy due to limited data and potential fetal risks. Animal studies suggest possible teratogenicity, and it is typically avoided in pregnant patients with type 2 diabetes, making this statement inaccurate and irrelevant to its mechanism.
Choice B reason: Semaglutide mimics GLP-1, enhancing glucose-dependent insulin secretion, suppressing glucagon release, slowing gastric emptying, and promoting satiety. These actions lower blood glucose and support weight loss in type 2 diabetes. This statement is accurate, as GLP-1-mediated insulin production is central to its mechanism of action.
Choice C reason: Semaglutide is primarily used for type 2 diabetes, not type 1, as it relies on functional beta cells to enhance insulin secretion. Type 1 diabetes involves absolute insulin deficiency, rendering GLP-1 agonists ineffective. This statement is inaccurate, as semaglutide is not indicated for type 1 diabetes.
Choice D reason: Semaglutide requires regular blood sugar monitoring, as hypoglycemia can occur, especially with concomitant insulin or sulfonylureas. Its glucose-lowering effects necessitate careful management to prevent adverse events. This statement is inaccurate, as monitoring remains critical to ensure safe and effective diabetes control.
The client’s blood glucose level is 220 mg/dL. The client is about to eat breakfast. The prescribed sliding scale indicates that 4 units of insulin lispro (Humalog) be given subcutaneously at 7:30 am. At what time is the client most at risk for hypoglycemia?
A. Today at 8:30 am
Insulin lispro, a rapid-acting insulin, peaks 1-2 hours after administration (around 8:30-9:30 am for a 7:30 am dose). This peak coincides with maximum glucose-lowering effect, increasing hypoglycemia risk, especially if breakfast is inadequate or delayed. This time is the most likely for low blood sugar due to insulin’s pharmacodynamics.
B. Today at 7:45 am
At 7:45 am, insulin lispro is just beginning to act (onset 15-30 minutes), and breakfast is likely being consumed, providing glucose to counter insulin’s effect. Hypoglycemia risk is lower than at peak action (1-2 hours), making this time less critical for hypoglycemia monitoring.
C. Today at 12:30 pm
By 12:30 pm, insulin lispro’s effect (duration 3-5 hours) is waning, and glucose from breakfast is metabolized. Hypoglycemia risk is lower unless additional insulin or activity occurs. This time is less likely for hypoglycemia compared to the peak action period around 8:30 am.
D. Tomorrow at 6:30 am
Tomorrow at 6:30 am is beyond insulin lispro’s duration of action (3-5 hours). Hypoglycemia risk from the 7:30 am dose is negligible 23 hours later, as insulin is cleared. This time is irrelevant to the dose’s effect, making it the least likely for hypoglycemia.
Full Explanation
Choice A reason: Insulin lispro, a rapid-acting insulin, peaks 1-2 hours after administration (around 8:30-9:30 am for a 7:30 am dose). This peak coincides with maximum glucose-lowering effect, increasing hypoglycemia risk, especially if breakfast is inadequate or delayed. This time is the most likely for low blood sugar due to insulin’s pharmacodynamics.
Choice B reason: At 7:45 am, insulin lispro is just beginning to act (onset 15-30 minutes), and breakfast is likely being consumed, providing glucose to counter insulin’s effect. Hypoglycemia risk is lower than at peak action (1-2 hours), making this time less critical for hypoglycemia monitoring.
Choice C reason: By 12:30 pm, insulin lispro’s effect (duration 3-5 hours) is waning, and glucose from breakfast is metabolized. Hypoglycemia risk is lower unless additional insulin or activity occurs. This time is less likely for hypoglycemia compared to the peak action period around 8:30 am.
Choice D reason: Tomorrow at 6:30 am is beyond insulin lispro’s duration of action (3-5 hours). Hypoglycemia risk from the 7:30 am dose is negligible 23 hours later, as insulin is cleared. This time is irrelevant to the dose’s effect, making it the least likely for hypoglycemia.