The nurse assesses the client for which clinical manifestation associated with a bone fracture?

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.

Choice A reason: Chronic kidney disease (CKD) does not primarily cause anemia by leaking red blood cells (RBCs) into urine. While hematuria may occur in some renal conditions, anemia in CKD results mainly from reduced erythropoietin production, not RBC loss. This statement is inaccurate, as it misrepresents the primary mechanism of anemia in CKD.

Choice B reason: Inflammation in CKD may contribute to anemia by suppressing erythropoiesis through cytokine release, but it does not directly attack RBCs. The primary cause is erythropoietin deficiency due to impaired renal function. This statement is inaccurate, as it overstates inflammation’s role and ignores the key hormonal mechanism in CKD-related anemia.

Choice C reason: High vascular pressure in CKD can damage kidneys but does not directly cause RBCs to burst (hemolysis). Anemia in CKD stems from reduced erythropoietin, not mechanical RBC destruction. This statement is inaccurate, as it incorrectly links hypertension’s renal effects to direct RBC damage, misrepresenting the anemia’s cause.

Choice D reason: CKD causes anemia due to reduced erythropoietin synthesis by damaged kidneys. Erythropoietin stimulates RBC production in bone marrow. In CKD, impaired renal function decreases erythropoietin, leading to anemia. This statement is accurate, as it correctly identifies the hormonal deficiency as the primary cause of low RBC counts in CKD.