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Thiazides, such as hydrochlorothiazide, cause the body to lose water (diuretics). They prevent Na+/Cl- reabsorption from the kidney's distal convoluted tubules. Thiazides also cause potassium loss and a rise in serum uric acid levels. Although thiazides are commonly used to treat hypertension, their hypotensive effects are not always related to diuretic activity. Although the mechanism is unknown, thiazides have been demonstrated to reduce hypertension-related morbidity and death. Thiazides promote vasodilation in vascular smooth muscles by activating calcium-activated potassium channels (large conductance) and blocking different carbonic anhydrases in vascular tissue.
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Potentiation of orthostatic hypotension may occur when using alcohol, barbiturates, or narcotics.
Thiazides can compromise the regulation of diabetes mellitus by diet and antidiabetic drugs (oral medicines and insulin). Antihypertensive Medications: Potentiation or additive impact.
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Patients with anuria and those who are hypersensitive to hydrochlorothiazide or other sulfonamide-derived medications should avoid taking it. In diabetic mellitus, therapy should not be started.
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Hydrochlorothiazide is generally well tolerated. However, weakness, restlessness, dizziness, headache, fever, diarrhea, vomiting, sialadenitis, cramps, constipation, stomach irritation, nausea, anorexia, and hypotension are all possible adverse effects. Hyperglycemia, glycosuria, hyperuricemia, and muscular spasm may occur in rare cases.
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Although there is evidence of fetal danger with hydrochlorothiazide medication, it is recommended if the benefits outweigh the risks. When edema is caused by a pathologic condition, thiazides should be used during pregnancy.
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Thiazides should be used with caution in patients with severe renal disease, impaired hepatic function or progressive liver disease and gout.
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Store between 15-30°C. Protect from light, moisture and freezing.
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