Loop and Thiazide Diuretics Quiz

Mechanism of Action and Effects of Loop and Thiazide Diuretics

• Blocking the Na+ 2K+ 22Cl2 symport leads to 25% of filtered sodium not being reabsorbed, causing natriuresis, hyponatremia, and possibly hypokalemia, hypocalcemia, and hypomagnesemia.
• Loop diuretics like furosemide and bumetanide block the Na+ 2K+ 22Cl2 symport, leading to potent natriuretic effects and are also known as "high ceiling" and "high efficiency" diuretics.
• Loop diuretics are derived from various chemical backgrounds and can cause ototoxicity due to their action on the chloride channel in the inner ear.
• Mutations in the gene for the Na+ 2K+ 22Cl2 co-transporter result in Bartter's syndrome, which presents similar symptoms to those seen in patients taking loop diuretics.
• Thiazide diuretics inhibit sodium and chloride reabsorption at the cortical portion of the ascending loop of Henlé and the distal convoluted tubule, leading to moderate natriuretic effects.
• Thiazides competitively bind to the chloride binding site of the Na+ 2Cl2 symporter and inhibit the Na+ 2Cl2 symporter by binding to the chloride binding site.
• Thiazides can increase potassium and hydrogen ion exchange for sodium in the distal convoluted tubule, leading to increased excretion of potassium and hydrogen ions.
• Mutations in the Na+ 2Cl2 symporter lead to Gitelman's syndrome, a form of inherited hypokalemic alkalosis.
• Thiazides also increase calcium reabsorption in the distal convoluted tubule, opposite to the effect of loop diuretics in their respective operational segment.
• Loop diuretics block the region of the nephron with the capacity to reabsorb the most sodium, while thiazides inhibit sodium and chloride reabsorption at a different site in the nephron.
• Loop diuretics lead to substantial natriuresis and are the most potent and effective natriuretic compounds, while thiazides are conspicuously less potent, inhibiting at most 3–5% of filtered sodium.
• Loop diuretics block the Na+ 2K+ 22Cl2 symport, while thiazides inhibit the electroneutral Na+ 2Cl2 symport located at a different site in the nephron.