Thiazides can cause: (DNB Dec 2010)
|A||Hypokalaemic metabolic alkalosis|
5. Thiazides are slowly acting diuretics.
6. Mechanism of action includes binding to Na+2cl- in early part of distal convoluted tubules.
7. There is natreuresis and this is accompanied by volume loss. Inhibition of reabsoption of sodium in DCT is accompanied by loss of potassium and hydrogen ions. This can cause metabiolic alkalosis.
8. These drugs, typified by hydrochlorthiazide are well absorbeD.
9. HCT absorption is increased by fooD.
10. Indapamide and metolazone are eliminated by bile; rests of thiazides are eliminated in urine.
11. Cutoff limits of administration of thiazides is <35ml/minutes.
12. Thiazides are drugs of choice for: hypertensison, nephrogenic diabetes insipidous, essential hypercalciuria and primary hyperparathyroidism.
13. Main side effects include: hypokalemia, hypomagnsemia, hypercalcemia, hyperglyecemia, hyperlipidemia and hyperuricemiA. Impotence occurs.
14. Metabolic alkalosis means the pH of body fluids have gone beyond the physiological limits (i.e. 7.35 to 7.45). It can occur due to decrease H+ concentrations or increased HCO3- concentrations or both.
15. Vomiting can cause loss of H+ ions and can induce this situation.
16. Loss of water, poor in bicarbonates can also cause this situation.
17. That is seen typically with thiazides and loop diuretics. It can be corrected by acetazolamide that can cause bicarbonate dieresis. Importance too can be a side effect of thiazides that perhaps occur due to volume contraction. However, it is not common.
(Mnemonics: Loop diuretic looses calcium wherase thiazide retain calcium in the body)