What is the mechanism of action of sodium-glucose cotransporter 2 inhibitors (SGLT-2 inhibitors)?
Blocks glucose reabsorption by the kidneys and increases glucose excretion to lower blood sugar
Interacts with the transcription factor that improves insulin sensitivity in the liver, skeletal muscle, and fat
Inhibits hepatic glucose production and increases insulin sensitivity in peripheral tissues
Blocks ATP-sensitive K+ channels on membrane of beta cells to promote insulin secretion
The Correct Answer is A
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.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
Choice A reason: Trimethoprim/sulfamethoxazole does not require extended sun exposure. In fact, it causes photosensitivity, increasing sunburn risk, so patients should avoid prolonged sunlight. Vitamin D synthesis is unrelated to this antibiotic’s mechanism or side effects, making this statement inaccurate and potentially harmful for patient safety.
Choice B reason: Trimethoprim/sulfamethoxazole does not typically cause brown urine. Brown urine may indicate hematuria or other conditions, but it is not a common side effect of this drug. The medication may cause gastrointestinal upset or rash, but urine discoloration is not expected, making this statement inaccurate.
Choice C reason: Follow-up with a healthcare provider is necessary to ensure UTI resolution and monitor for side effects like rash, renal impairment, or rare hematologic effects. This statement is inaccurate, as lack of follow-up could miss treatment failure or complications, undermining effective management of the infection.
Choice D reason: Trimethoprim/sulfamethoxazole can cause bone marrow suppression, leading to anemia, particularly in patients with folate deficiency or prolonged use. Monitoring complete blood counts is critical to detect hemolytic anemia or other hematologic toxicities, making this statement accurate and essential for safe patient management during treatment.
Correct Answer is B
Explanation
Choice A reason: Calcium levels in plasma are primarily regulated by parathyroid hormone and vitamin D, not insulin. Insulin has minimal direct effect on calcium transport into cells. Calcium is critical for bone health and muscle function, but its movement is not significantly influenced by insulin’s action on cellular membranes.
Choice B reason: Insulin promotes potassium uptake into cells by activating the sodium-potassium ATPase pump, particularly in muscle and liver cells. This shifts potassium from plasma to intracellular spaces, lowering serum levels. This mechanism is critical in managing hyperkalemia, as insulin facilitates potassium movement alongside glucose, stabilizing membrane potentials.
Choice C reason: Magnesium is regulated by renal and gastrointestinal mechanisms, not directly by insulin. While insulin may indirectly influence magnesium via metabolic effects, it does not actively drive magnesium into cells like potassium. Magnesium is essential for enzymatic reactions, but its plasma levels are not significantly altered by insulin.
Choice D reason: Sodium is primarily regulated by aldosterone and the renin-angiotensin system, not insulin. Insulin does not directly force sodium into cells but may influence sodium-potassium ATPase indirectly. Sodium’s extracellular role in fluid balance is distinct from insulin’s intracellular potassium transport, making it an incorrect choice.
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