Mechanism of Action:
A thiazide diuretic inhibits sodium and chloride ion co-transporter in the cortical thick ascending limb and early distal tubule. It has a milder diuretic action than the loop diuretics because this nephron site reabsorbs less sodium ion than the thick ascending limb. This then allows a bit more sodium to arrive in the late distal tubule and collecting duct where there is aldosterone-stimulated sodium reabsorption in exchange for potassium and hydrogen ion excretion. This underlies the important metabolic adverse effects of hypokalaemia and alkalosis. Other metabolic effects stem from the increase in urate and calcium reabsorption in the proximal tubule.
Lecture and CAL materials:
- What are diuretics? (Video 23:07)
- What are thiazide diuretics? (Video 08:20)
- Which drugs affect renal function? (Video 11:32)
- Which drugs have adverse effects on renal function? (Video 11:48)
- How is blood pressure regulated? (Video 13:51)
- How is blood volume regulated? (Video 11:06)
- What is the renin-angiotensin system? (Video 04:37)
- What are the functions of the cardiovascular system? (Video 14:10)
- Diuretics pharmacology (16 mins YouTube, Armando Hasudungan) and antihypertensives (24 mins, same source)
- Diuretics pharmacology (18 mins YouTube, Speed Pharmacology) and antihypertensives, (15 mins, same source)
Drug specifics
| Alternative drug name | Bendrofluazide |
| Effects | Bendroflumethiazide is a thiazide diuretic that acts on the distal tubule. It reduces the reabsorption of electrolytes from the renal tubles therefore increasing sodium and chloride ion loss, and subsequently water loss. |
| Adverse actions | Common predictable side effects are hypokalaemia, alkalosis, dehydration, hyperuricaemia (precipitating acute gout), hypomagnesaemia, reduced calcium excretion and precipitation of latent diabetes (hyperglycaemia). Biochemistry should be monitored regularly. For more information please refer to EMC. |
| Dose | 2.5 mg oral once daily. For more information see EMC |
| Interactions | Important interactions are with other antihypertensives to cause hypotension, NSAIDs which antagonise the natriuretic effect, antidiabetic drugs (oral agents and insulin) are antagonised since thiazides may elevate blood glucose levels, calcium salts with increased serum calcium levels due to decreased excretion, digoxin with increased toxicity associated with hypokalemia, and lithium salts with enhance lithium toxicity due to reduced renal clearance. For more information please refer to EMC. |
| Contraindications | Should be avoided in hypercalcaemia, hyponatraemia, symptomatic hyperuricaemia and Addison's disease. Should also be avoided in severe renal insufficiency (eGFR < 30mL/minute/1.73m^2) and severe hepatic impairment. For more information see EMC. |
| Comments | Others thiazides include chlortalidone, indapamide and hydrochlorothiazide. Thiazides are less powerful than loop diuretics. Thiazides affect the renal tubular mechanism of electrolyte reabsorption. At maximal therapeutic dosage all thiazides are approximately equal in their diuretic potency. Thiazides increase excretion of sodium and chloride in approximately equivalent amounts. Natriuresis causes a secondary loss of potassium and bicarbonate. The mechanism of the antihypertensive effect of thiazides is unknown. Onset of action of thiazides occurs in two hours and the peak effect at about four hours. Duration of action persists for approximately six to 12 hours. Thiazides are eliminated rapidly by the kidney. |
| Contributors | Last updated by Madeleine Goudie, 15th March 2017 Reviewed by Jin Hah, 8th June 2017 |
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