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Zorluk: KolayEndocrinology and Metabolism

Match each antihyperglycemic medication with its primary mechanism of action.

  • MetforminDecreases hepatic gluconeogenesis and improves peripheral insulin sensitivity
  • EmpagliflozinIncreases urinary glucose excretion by blocking proximal renal tubule reabsorption
  • SemaglutideEnhances glucose-dependent insulin secretion and delays gastric emptying
  • GlimepirideBinds to ATP-sensitive potassium channels on beta cells to stimulate insulin release

Cevap

Metformin decreases hepatic gluconeogenesis; Empagliflozin blocks proximal tubule glucose reabsorption; Semaglutide enhances glucose-dependent insulin secretion; Glimepiride stimulates ATP-sensitive potassium channels on beta cells.
Each listed medication represents a distinct class of antidiabetic drugs with a unique physiological target. Metformin (a biguanide) acts on the liver to reduce glucose output. Empagliflozin (an SGLT2 inhibitor) acts on the kidneys to induce glycosuria. Semaglutide (a GLP-1 agonist) mimics incretin hormones to enhance glucose-dependent insulin release. Glimepiride (a sulfonylurea) functions as an insulin secretagogue by binding to potassium channels on beta cells.

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1
Identify the pharmacologic class for each listed antihyperglycemic agent.
Metformin is a biguanide, empagliflozin is an SGLT2 inhibitor, semaglutide is a GLP-1 agonist, and glimepiride is a sulfonylurea.
Knowing the drug class is the foundational step in recalling its mechanism of action.
2
Correlate each identified drug class with its specific physiological target.
Biguanides target the liver (gluconeogenesis), SGLT2 inhibitors target the kidneys (proximal tubule), GLP-1 agonists target the incretin pathway, and sulfonylureas target pancreatic beta cells.
This confirms the correct pairing between the medication and the mechanism.

Anahtar Kavram

Pharmacotherapy for Type 2 Diabetes Mellitus
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Konular

Endocrinology and Metabolism

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