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The thiazides act in the distal tubule to decrease sodium reabsorption (inhibits Na/Cl transporter).
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As a result of decreased sodium and chloride reabsorption, a hyperosmolar diuresis ensues.
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Delivery of more sodium to the distal tubule results in potassium loss by an exchange mechanism.
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Thiazides also promote calcium reabsorption, in contrast to loop diuretics.
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The initial decrease in blood volume followed by a longer-termed reduction in vascular resistance appear to account for the hypotensive effects of the thiazides.
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Adverse Effects
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Potassium depletion is a potentially serious side-effect that may require potassium supplementation and/or concurrent use of potassium-sparing diuretics.
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Hyperuricemia may occur precipitating gout.
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The increase in systemic uric acid is due to a decrease in the effectiveness of the organic acid secretory system.
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Diabetic patient may have difficulty in maintaining proper blood sugar levels.
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Category: Pharmacology Notes
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