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Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic. Patients with severe liver disease or cirrhosis are very susceptible to thiazide-induced hypokalemic hypochloremic alkalosis.
Blood ammonia concentrations may be further increased in patients with previously elevated concentrations. Hepatic encephalopathy and death have occurred secondary to the electrolyte alterations accompanying diuretic use.
Therapy with thiazide diuretics should be administered cautiously in patients with impaired hepatic function or progressive liver disease, and discontinued promptly if signs of impending hepatic coma appear e.
The use of thiazide diuretics has been reported to possibly exacerbate or activate systemic lupus erythematosus. Reported cases have generally been associated with chlorothiazide and hydrochlorothiazide. Therapy with thiazide diuretics should be administered cautiously in patients with a history or risk of SLE.
In addition, thiazide diuretics decrease the GFR and may precipitate azotemia in renal disease. Cumulative effects may also develop because most of these drugs are excreted unchanged in the urine by glomerular filtration and active tubular secretion.
Therapy with thiazide diuretics should be administered cautiously at reduced dosages in patients with renal impairment. If renal function becomes progressively worse, as indicated by rising BUN or serum creatinine levels, an interruption or discontinuation of thiazide therapy should be considered. Thiazide diuretics should be used with caution in patients with history of bronchial asthma as sensitivity reactions may occur.
Moderate Potential Hazard, Moderate plausibility. Diabetes Mellitus, Abnormal Glucose Tolerance. Thiazide diuretics may cause hyperglycemia and glycosuria in patients with diabetes. They may also precipitate diabetes in prediabetic patients. These effects are usually reversible following discontinuation of the drugs. Therapy with thiazide diuretics should be administered cautiously in patients with diabetes mellitus, glucose intolerance, or a predisposition to hyperglycemia. Patients with diabetes mellitus should be monitored more closely during thiazide therapy, and their antidiabetic regimen adjusted accordingly.
Whether these effects are dose-related and sustained during chronic therapy are unknown. Patients with preexisting hyperlipidemia may require closer monitoring during thiazide therapy, and adjustments made accordingly in their lipid-lowering regimen.
Urinary calcium excretion is decreased by thiazide diuretics during chronic administration. Pathologic changes in the parathyroid gland with hypercalcemia and hypophosphatemia have been reported during prolonged therapy. However, the common complications of hyperparathyroidism such as renal lithiasis, bone resorption, and peptic ulceration have not been seen. Clinicians should be cognizant of these effects when prescribing or administering thiazide therapy to patients with hyperparathyroidism.
These drugs should be discontinued before carrying out tests for parathyroid function. Thiazide diuretics decrease the rate of uric acid excretion.
Hyperuricemia occurs frequently but is usually asymptomatic and rarely leads to clinical gout except in patients with a history of gout or chronic renal failure. Therapy with thiazide diuretics should be administered cautiously in such patients. Thiazide diuretics may decrease serum PBI protein-bound iodine levels without associated thyroid disturbance. Clinicians should be cognizant of this effect when prescribing or administering thiazide therapy to patients with thyroid disorders.
There are drug interactions with bendroflumethiazide. Do not stop taking any medications without consulting your healthcare provider. Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.
High Blood Pressure amlodipine , lisinopril , losartan , furosemide , hydrochlorothiazide , metoprolol , atenolol , Lasix , Norvasc , valsartan , More Edema furosemide , hydrochlorothiazide , Lasix , spironolactone , chlorthalidone , torsemide , bumetanide , Aldactone , metolazone , triamterene , Bumex , indapamide , More By clicking Subscribe, I agree to the Drugs.
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To view content sources and attributions, please refer to our editorial policy. We comply with the HONcode standard for trustworthy health information - verify here. View all 9 references. Gudbrandsson T, Hansson L "Combination therapy with saluretics and atenolol in essential hypertension. After his examination, he was referred to a cardiologist because of a murmur on cardiac oscultation. On oscultation of the heart, there was a grade 3—4 systolic murmur at the third to fourth right intercostal sternal border.
The rest of the physical examination was unremarkable. Chest x-ray showed increased diameter of the right heart, and electrocardiogram showed right axis deviation and right bundle branch block. On magnetic resonance imaging of the brain, there was corticomedullary infarction in the left cerebellar hemisphere Figure 1. Transthoracic two-dimensional echocardiography showed an apical displacement of both the septal and the posterior tricuspid leaflets, and an intervening zone that was anatomically ventricular but functionally right atrial atrialized right ventricle Figure 2.
Colour-Doppler echocardiography showed severe tricuspid valve regurgitation Figure 3 and secundum atrial septal defect Figure 4. Transesophageal echocardiography verified the echocardiographic findings. Magnetic resonance image of the corticomedullary infarct in the left cerebellar hemisphere in a year-old man one month after stroke.
Apical four-chamber colour flow echocardiogram showing severe tricuspid regurgitation TR in systole. Apical four-chamber colour flow echocardiogram showing secundum atrial septal defect ASD in diastole. Tricuspid valve tissue is dysplastic, and a variable portion of the septal and inferior cusps adheres to the right ventricular wall some distance away from the atrioventricular junction.
Because of the abnormally situated tricuspid orifice, a portion of the right ventricle lies between the atrioventricular ring and the origin of the valve, which is continuous with the right atrial chamber.
This proximal segment is atrialized, and a distal, functionally small ventricular chamber exists. The degree of impairment of right ventricular function depends primarily on the extent to which the right ventricular inflow portion is atrialized and on the magnitude of tricuspid valve regurgitation 2. The principal echocardiographic findings observed in patients with this anomaly, as well as in those with other forms of right ventricular volume overload, are an increase in right ventricular dimension, paradoxical ventricular septal motion, an increase in tricuspid valve excursion and an abnormal closing velocity of the tricuspid valve.
Specific diagnosis requires identification, usually from an apical four-chamber view, of displacement of the septal tricuspid leaflet. Tricuspid regurgitation, if present, is detected by Doppler examination 2. Associated cardiac anomalies are patent foramen ovale or atrial septal defect, right ventricular outflow tract obstruction and Wolff-Parkinson-White syndrome. Long term prognosis depends on the severity of tricuspid regurgitation, the presence of right ventricular failure, and the presence and degree of cyanosis due to shunting from right to left.
Complications such as right ventricular failure, infective endocarditis and paradoxical embolism can occur 2. Emboli arising in systemic veins may pass directly to the systemic circulation because right to left intracardiac shunts allow venous blood to bypass the normal filtering action of the lungs.
The shunt may be a consequence of congenital heart disease but can also occur across a patent foramen ovale if pressure in the right atrium exceeds that in the left.
Avoid combinations; the risk of the interaction outweighs the benefit.
Therapy with thiazide diuretics should be administered cautiously in patients with a history or risk of SLE.