Low Efficacy Diuretics. Potassium sparing diuretics. Carbonic anhydrase inhibitors. Osmotic diuretics. Miscellaneous
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1 University of Al Qadisiyah College of Pharmacy Dr. Bassim I Mohammad, MBChB, MSc, Ph.D Low Efficacy Diuretics 1. Potassium sparing diuretics 2. Carbonic anhydrase inhibitors 3. Osmotic diuretics 4. Miscellaneous Potassium sparing diuretics 1. Aldosterone antagonists Spironolactone Eplerenone 2. Renal epithelial Na+ channel inhibitors Triamterene Amiloride Carbonic anhydrase inhibitors Acetazolamide Dichloro Ethaxazolamide Osmotic diuretics Mannitol Glucose Miscellaneous CCBs ARBs Dopamine Adenosin Receptor Antagonists
2 Potassium sparing diuretics Spironolactone: It acts by competitive inhibition with aldosterone for specific intracellular receptors on DCT leading to NaCl loss and decrease K excretion. It increases calcium excretion by direct action on the tubules Action is dependent on aldosterone PKs Spironolactone : oral bioavailability ~75 % Converted into metabolite (canrenone). Delayed onset of action (max. diuretic effect 4 days) Uses 1. It is a weak diuretic 2. More useful in refractory edema which is associated with hyperaldosteronism in cases of liver cirrhosis, CHF and nephrotic syndrome. 3. Resistant HT 4. It is used (as K-sparing) to counteract the K+ loss due to thiazides or loop diuretics 5. Hyperkalemia especially in patient with renal diseases or co-therapy with ACIs, ARBs or with NSAIDs and B-blockers (reduced renin). 6. Gynaecomastia 7. Menstrual irregularities 8. Impotence 9. Metabolic acidosis 10. GI upset, confusion and skin rash Side Effects Hyperkalemia especially in patient with renal diseases or co-therapy with ACIs, ARBs or with NSAIDs and B-blockers (reduced renin). Gynaecomastia Menstrual irregularities Impotence Metabolic acidosis GI upset, confusion and skin rash
3 Eplerenone Eplerenone is the first of a new class of drugs known as selective aldosterone receptor antagonists (SARA), which selectively block the aldosterone receptor with minimal effect at other steroid receptors. like spironolactone, is a competitive antagonist of the aldosterone receptor. Oral eplerenone is approved for use in patients with LV systolic dysfunction following MI. PKs It is 50% - 75% as potent as spironolactone It is cleared primarily via metabolism by CYP3A4 to inactive metabolites, with an elimination half-life of 4 to 6 hours Side Effects Hyperkalemia and sex hormone related side effects appear to be lower than with spironolactone. Mild dose dependent increases in cholesterol Elevated serum transaminases and Thyroid-stimulating hormone was reported Drug/Drug interaction with hepatic enzyme inducers/inhibitors Eplerenone vs. Spironolactone Parameter Eplerenone Spironolactone Receptor Selectivity SARA Non-SARA Potency Less More metabolite inactive active Duration of action shorter longer Side effect profile Less high Hepatic enzyme inducer/inhibitors I Yes No
4 Renal epithelial Na+ channel inhibitors Triamterene and Amiloride They non-aldosterone antagonists Both are used in conjunction with thiazides and loop diuretics Hyperkalemia is potential risk Triamterene Half life ~ 4 hrs Leg cramps, renal stone, impaired glucose tolerance and photosensitivity are noted side effects Amiloride Its structurally related to but 10 times more potent than the triamterene It decreases calcium excretion and increases urate excretion (uricosuric effect) Half life ~ 15 hrs Blocks entry of lithium into renal cells and mitigate DI caused by lithium As aerosol symptomatic improvement in cystic fibrosis by increasing fluidity of respiratory secretions Carbonic anhydrase inhibitors CA is an enzyme which catalyzes the reversible reaction H20 +CO2 « » H2CO3. Carbonic acid ionizes into HCO3 and H+, thus helps in the transport of CO2 and H+ secretion. The CA enzyme is present in the renal tubular cells, gastric mucosa, pancreas, ciliary body and RBC. Acetazolamide The net effect is inhibition of HCO3 reabsorption in PCT. The secretion of H+ is inhibited. The distal Na+ is exchanged with K. So K+ loss in urine. The urine produced is rich in bicarbonate -- alkaline urine depletes body of HCO3---- producing acidosis.
5 Extra renal actions: Lowering of IOP due to decreased formation of aqueous humor. Decreased gastric acid and bicarbonate secretion. Raised levels of CO2 in brain and lowering of ph raising seizure threshold and sedation Uses Very weak diuretic Glaucoma To alkalinize urine (salycilate poisoning) Epilepsy Acute mountain sickness Side effects Drowsiness, Parasthesia and Headache Acidosis Hypokalemia Crystalurea and stone formation Contraindicated in liver disease interfere with elimination of ammonia Osmotic diuretics Mannitol It is a non-electrolyte pharmacologically inert Not metabolized, freely filtered in the glomerulus, undergoes no (limited) reabsorption Inhibits water and electrolyte reabsorption Expands extracellular fluid and increases GFR Increases renal blood flow - salt reabsorption is reduced Primary action is to increase urinary volume Not absorbed orally given I.V Side effects Headache, Nausea, Vomiting and allergy
6 Miscellaneous CCBs (DHPs group) have direct (intrinsic) diuretic effect. For ex. Nefidipine increase urine volume and Na excretion and may inhibit aldosterone release. ARBs and ACEIs, as they have antialdosterone effect, they act as K-retaining agent. They should not be combined with other K-retainers especially in patients with renal impairment Dopamine: Indirect diuretic action: improvement in COP and cardiac function, so increase renal perfusion. Direct effect: in case of fluid retention, stimulation of DA1 receptor on renal tubular cells which appose the effect of ADH. Adenosin receptor antagoinsts: They act by afferent arteriolar dilatation and increase GFR. Special problems with diuretics 1. Overdiuresis 2. Resistance 3. Hyponatremia Overdiuresis Overdiuresis: overvigrous duiresis is common and may reduce intravascular volume and ventricular filling so that COP dropped thus tissue underperfusion occurs Overdiuresis is seen during hospital setting when rigid policy is carried out. Some time the addition of ACEIs and ARBs enhance the risk of overdiuresis Diuretic Resistance 1. Compensatory Mechanisms (RAAS, SNS) 2. Failure to reach tubular site of action a - Decreased G.I. absorption b - Decreased secretion into tubular lumen (e.g. uremia, decreased kidney perfusion) c - Decreased availability in tubular lumen (e.g. nephrotic syndrome) 3. Interference by other drugs (e.g. NSAID s) 4. Tubular adaptation (ex chronic Loop diuretic use) (hypertrophy of distal nephron cells as a result of aldosterone induced growth,) Can Use Combination of Diuretics to Induce a Synergistic Effect (SNB) Hyponatremia Hyponatremia may occur especially in HF (elderly patients): Predominant H2O retention caused by: In appropriate release of ADH Increase activity of Ag II
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