Diuretics ppt for BAMS students

This ppt incorporate a brief note on diuretic drugs

1. Dept of drvyaguna DIURETICS& ANTIDIURETICS

2. HUMAN RENAL PHYSIOLOGY Four Main Processes: Filtration Reabsorbtion Secretion Excretion

3. HUMAN RENAL PHYSIOLOGY Functions of the Kidney: Filtration: First step in urine formation Bulk transport of fluid from blood to kidney tubule Isosmotic filtrate Blood cells and proteins don ’ t filter Result of hydraulic pressure GFR = 180 L/day

4. HUMAN RENAL PHYSIOLOGY Functions of the Kidney: Reabsorbtion: Process of returning filtered material to bloodstream 99% of what is filtered May involve transport protein(s) Normally glucose is totally reabsorbed

5. HUMAN RENAL PHYSIOLOGY Functions of the Kidney: Secretion: Material added to lumen of kidney from blood Active transport (usually) of toxins and foreign substances Saccharine Penicillin

6. HUMAN RENAL PHYSIOLOGY Functions of the Kidney: Excretion: Loss of fluid from body in form of urine Amount = Amount + Amount -- Amount of Solute Filtered Secreted Reabsorbed Excreted

7. Functions of the Nephron Filtration Reabsorption Secretion Excretion

8. Diuretics are medicines that aid the elimination of sodium ( salt ) and water from the body. The oral forms of these drugs are sometimes referred to as "water pills."

9. Diuretics act by increasing the excretion by the kidneys of sodium in the urine. When the kidneys excrete sodium, they excrete water from the blood along with it. That decreases the amount of fluid flowing through the blood vessels, which reduces pressure on the walls of the arteries.

10. Diuretics in general lower the amount of salt and water in the body. Urine flow usually increases within hours of the first dose, but diuretics may take several weeks to treat conditions like high blood pressure . Mechanisms of action & types of diuretics depend on anatomical site.

11. LOOP DIURETICS Inhibits Na reabsorption (in tissue) by direct action on ascending Loop of Henle . Onset of action of 30-45 minutes Side Effects: hyponatremia , hypokalemia . Loop diuretics, such as furosemide ( Lasix ) reduce the ability of the body to reabsorb sodium at the ascending loop part of the nephron which leads to water retention in urine as water Used to control edematous states & hypercalcemia .

12. POTASSIUM SPARING DIURETICS Inhibits Na reabsorption in the collecting ducts and distal convoluted tubules. Common Medications: Spironolactone ( Aldactone ). Side Effects: hyponatremia , hyperkalemia

13. HIGH CEILING DIURETICS High ceiling diuretics producing the greatest diuresis Used when pts can't tolerate thiazides or have impaired renal function. More expensive with shorter duration of 1-4 hr. NSAIDs can adversely affect antihypertensive effect

14. OSMOTIC DIURETIC Causes a shift in fluid to move into the renal tubules from the surrounding tissue. High osmolality of agents reduces reabsorption of water Produces greatest amount of urine output. Common Medications: Mannitol ( Osmitrol ) Side Effects: Circulatory overload Fluid &electrolyte imbalance. Drug retained in EC space causes expansion of ECF. Pulmonary congestion, thirst, blurry vision, convulsion, Toxicity dependent on amount used.

15. THIAZIDE DIURETIC Inhibits Na, K & Cl resorption in the distal convoluted tubule Common Medication: hydrochlorothiazide ( HydroDIURIL ) Commonly used; least expensive. Frequent urination occurs due to elevated loss of water that has not been retained from the body as a result of a relationship with sodium loss Side Effects: hypokalemia , hypercalcemia , hyperlipidemia , hyperglycemia & hyperuricemia Thiazide diuretics are considered to be "potassium-wasting"

16. Carbonic Anhydrase Inhibitors Inhibit the enzyme named carbonic anhydrase which is seen in the proximal convoluted tubule part of the nephron . This results in the several effects including bicarbonate retention, potassium retention in urine and decreased absorption of sodium. Eg , acetazolamide and methazolamide

17. SIDE EFFECTS Common side effects of diuretic drug therapy: Orthostatic hypotension Hypokalemia (exception: K+ sparing diuretics such as spironolactone ) Hyponatremia

18. ANTIDIURETICS An antidiuretic is an agent or drug that, administered to an organism, helps control body water balance by reducing urination, opposing diuresis . Antidiuretic hormones : ADH/Vasopressin: A hormone secreted by the posterior lobe of the pituitary gland that constricts blood vessels, raises blood pressure, and reduces excretion of urine. Also called antidiuretic hormon

19. ADH increases water permeability in the last part of DCT and collecting duct . ADH stimulates the production of aquaporin 2 – water channel proteins at the time of demand .

20. SYNTHETIC ADH Desmopressin "; Desmopressin (5) (trade names: DDAVP, Stimate , Minirin ) is a synthetic replacement for the hormone vasopressin, the hormone which reduces the urine production. It may be taken nasallyiv form or as a tablet. Most frequently forthe treatment of diabetes insipidus (7) or nocturnal enuresis

21. LYTHOTRIPTICS The drugs which are used for the dissolution of calculus in the bladder or kidneys Eg , Bergenia ligulata , Boerrhaevia diffusa etc

22. Hepatoprotection Hepatoprotection or antihepatotoxicity is the ability to prevent damage to the liver . The liver plays a central role in transforming and clearing chemicals and is susceptible to the toxicity from these agents. Certain medicinal agents, when taken in overdoses and sometimes even when introduced within therapeutic ranges , may injure the organ. More than 900 drugs have been implicated in causing liver injury [1] and it is the most common reason for a drug to be withdrawn from the market.

23. HEPATOTOXICITY . Several mechanisms are responsible for either inducing hepatic injury or worsening the damage process. Many chemicals damage mitochondria , an intracellular organelle that produce energy. Its dysfunction releases excessive amount of oxidants that, in turn, injure hepatic cells. Activation of some enzymes in the cytochrome P-450 system such as CYP2E1 also lead to oxidative stress. [12] Injury to hepatocyte and bile duct cells lead to accumulation of bile acid inside the liver . This promotes further liver damage. [13] Non- parenchymal cells such as Kupffer cells , fat storing stellate cells , and leukocytes (i.e. neutrophil and monocyte ) also have a role in the mechanism.