The client has been diagnosed with type 1 diabetes mellitus and has been prescribed Humulin R insulin. The patient will take the dose at 0900. When should the client be sure to have a snack or meal?
0900-0930
1100-1130
1400-1430
1700-1730
The Correct Answer is B
Choice A reason: Humulin R (regular insulin) has an onset of 30-60 minutes and peaks at 2-3 hours. Taking a snack at 0900-0930, immediately after injection, is too early, as insulin action is minimal, and glucose from the meal may cause hyperglycemia before insulin peaks, making this timing inappropriate.
Choice B reason: Humulin R peaks at 2-3 hours (1100-1200 for a 0900 dose), when hypoglycemia risk is highest due to maximum glucose uptake. A snack or meal at 1100-1130 provides glucose to counter insulin’s peak effect, preventing low blood sugar, making this the most appropriate timing.
Choice C reason: By 1400-1430, Humulin R’s effect (duration 5-8 hours) is waning, reducing hypoglycemia risk. A snack at this time is less critical, as insulin’s glucose-lowering action is declining. This timing is less effective for preventing hypoglycemia compared to the peak action period at 1100-1130.
Choice D reason: At 1700-1730, Humulin R’s effect is nearly gone (duration 5-8 hours), making hypoglycemia unlikely from the 0900 dose. A snack this late is irrelevant to the insulin’s action, as glucose levels are stabilized, making this timing inappropriate for preventing hypoglycemia.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
Choice A reason: Lithium toxicity is a concern but not inevitable. It occurs with levels above 1.5 mEq/L, often due to dehydration or drug interactions, common in trauma settings. However, routine monitoring of levels is a more immediate nursing priority than assuming toxicity, as early detection prevents severe outcomes like seizures or renal damage.
Choice B reason: Lithium is primarily excreted by the kidneys, not metabolized by the liver. Liver function tests are not indicated for lithium monitoring, as it does not undergo hepatic metabolism. This statement is inaccurate, as renal function tests are critical to assess lithium clearance and prevent toxicity in trauma patients.
Choice C reason: Stress does not directly increase lithium requirements. Trauma-related dehydration or renal impairment can elevate lithium levels, risking toxicity, but this is due to reduced clearance, not increased need. This statement is inaccurate, as dosing adjustments should be based on serum levels, not stress alone.
Choice D reason: Lithium has a narrow therapeutic range (0.6-1.2 mEq/L), and trauma-related factors like dehydration or medications can alter levels, risking toxicity or subtherapeutic effects. Regular serum level monitoring is critical, especially in acute settings, to ensure safety and efficacy, making this statement accurate and a priority nursing concern.
Correct Answer is B
Explanation
Choice A reason: Excessive bile acid absorption, often due to ileal dysfunction, reduces bile acid availability in the gallbladder, promoting cholesterol supersaturation and gallstone formation. This contributes to cholelithiasis, particularly cholesterol gallstones, by altering bile composition, making this condition a significant risk factor, not the least likely.
Choice B reason: Elevated serum calcium (hypercalcemia) is not directly linked to cholelithiasis. While hypercalcemia can cause kidney stones, gallstone formation is driven by bile composition changes, like cholesterol or bile acid imbalances, not serum calcium levels. This makes it the least likely contributor to gallstone development.
Choice C reason: Elevated dietary cholesterol increases hepatic cholesterol secretion into bile, leading to supersaturation and cholesterol gallstone formation. This is a well-established risk factor for cholelithiasis, as excess cholesterol overwhelms bile acid and phospholipid solubilization, promoting crystal formation, making it a significant contributor, not the least likely.
Choice D reason: Inflammation of epithelial tissue, such as in chronic cholecystitis, promotes gallstone formation by altering gallbladder motility and bile stasis. Inflammatory changes disrupt bile acid metabolism and increase mucin production, facilitating stone nucleation. This condition is a known risk factor for cholelithiasis, not the least likely contributor.
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