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FLUID & ELECTROLYTE BALANCE, diuretics

An introduction to pharmacy

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FLUID & ELECTROLYTE BALANCE, diuretics

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  1. DRUGS FOR FLUID & ELECTROLYTE BALANCECONTINUED Dr. Kenneth Orimma B.Sc., M.Sc., M.B.B.S, D.I.R, D.M(Doctor of Medicine) Psychiatry

  2. DIURETICS:

  3. DIURETICS: Thiazide Thiazide Diuretics: Not as powerful as Loop Diuretics but are still Potassium-Wasting) Site of Action: o Distal Convoluted Tubules Mechanism of Action: o Inhibiting the Na/Cl transporter in the DCT o → prevents Na+ Resorption into Interstitium (Therefore Prevents H2O Resorption) o Maintains a High Filtrate Osmolarity → Retaining Water in the Tubule Indications: o Uncomplicated Hypertension – (One of the 1st lines of treatment for hypertension) o Severe Resistant Oedema o Mild Heart Failure o Ascites (due to hepatic cirrhosis) o Renal Failure

  4. DIURETICS: Thiazide Side Effects of Thiazides: o Hypovolemia & Hypotension o Hypokalemia: § May require Potassium Supplements, Or coupling with K+-Sparing Diuretics o Hyponatremia: Can be Fatal o Hypomagnesaemia o Hypercalcemia o Metabolic Alkalosis (Due to reverse dilatation effect of H2O loss, but no HCO3 Loss) o Hyperuricemia → Gout o Hyperglycemia o Reversible Erectile Dysfunction

  5. DIURETICS: Thiazide Classical Agents: o Chlorothiazide o Chlortalidone

  6. DIURETICS:

  7. DIURETICS:K+ Sparing Diuretics K+ Sparing Diuretics: o Site of Action: Collecting Ducts o Indications: § Used in Pts where K+ Loss is Hazardous – (Eg: Pts on Digoxin or Amiodarone) § Heart Failure § Hyperaldosteronism § Resistant Essential Hypertension § Ascites (Due to Hepatic Cirrhosis)

  8. DIURETICS:K+ Sparing Diuretics K+ Sparing Diuretics: subgroups This is based on their mechanisms of actions 1: Epithelial Na+ Channel Inhibitors 2: Aldosterone Antagonists:

  9. DIURETICS:K+ Sparing Diuretics Epithelial Na+ Channel Inhibitors Mechanism of Action: • Directly Inhibits the Aldosterone-Activated Na+ Channels in walls of Collecting Ducts:→ Inhibits H2O Resorption • K+ Sparing Effect comes from a Loss of Na+-Concentration Gradient which normallypowers a Secondary-Active Na/K-Symporter on Basal Membrane Classical Agents: • Amiloride • Triamterene Side Effects: • Hyperkalaemia – (Potentially Fatal) o Avoid in Pts with Renal Failure/ACE-Inhibitors/K+ Supplements • Avoid NSAID Use – (Possible drug interaction)

  10. DIURETICS:K+ Sparing Diuretics Aldosterone Antagonists Mechanism of Action of Aldosterone Antagonists: • Prevents Aldosterone from binding to its Nuclear Receptor → Prevents Expressionof the Protein aldosterone leading → ↓Na+ Channel Proteins → ↓Na+ Resorption → Inhibits H2O Resorption → ↓TCA Enzymes → ↓ATP → ↓Na+ Pump Function → ↓Na+ Resorption then Ultimately → ↓ H2O Resorption • Works only when Renin-Angiotensin System is Active • The K+ Sparing Effect comes from a Loss of Na+-Concentration Gradient which normallypowers a Secondary-Active Na/K-Symporter on Basal Membrane

  11. DIURETICS:K+ Sparing Diuretics Classical Aldosterone Antagonists • Spironolactone Side Effects: • Hyperkalemia – (Potentially Fatal) O Avoid in Pts with Renal Failure/ACE-Inhibitors/K+ Supplements • GI Upset • Gynecomastia • Menstrual Disorders • Testicular Atrophy

  12. DIURETICS:Osmotic Diuretic Drugs: Osmotic Diuretic Drugs: Site of Action: § Filtered in the Glomerulus § Affects Any Nephron that is Freely Permeable to Water Mechanism of Action: § Inert Substances (Eg: Sugars) that are filtered by the Kidneys, but not reabsorbed →Increases Filtrate Osmolarity to: o →Inhibit Passive Water Reabsorption o →Facilitate Passive Water Excretion Indications: § Acute Renal Failure – Prevent kidneys from drying out § Cerebral Oedema & Intraocular Pressure: • Simply by increasing Plasma Osmolarity • Relieves such pressures via osmosis

  13. DIURETICS:Osmotic Diuretic Drugs Classical Osmotic diuretic Agents: § Mannitol § Isosorbide § Glycerin Side Effects: § Transient Hypervolaemia (Ie: ↑Extracellular Fluid – due to ↑Plasma Osmolarity) • Can →Dilution Hyponatraemia • Can →Heart Failure • Can →Pulmonary Oedema § Headache, Nausea & Vomiting

  14. DIURETICS:Acetazolamide Acetazolamide Mechanism of Action: • A potent carbonic anhydrase inhibitor • The diuretic effect of acetazolamide is due to its action in the kidney on the reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. • The result is renal loss of bicarbonate (HCO3 ion), which carries out sodium, water, and potassium. • Alkalinization of the urine and promotion of diuresis are the end result. • Alteration in ammonia metabolism occurs due to increased reabsorption of ammonia by the renal tubules as a result of urinary alkalinization.

  15. DIURETICS:Acetazolamide Indications: • treatment of chronic simple glaucoma (a major indication) • Also used to treat secondary glaucoma, and pre-operatively in acute angle-closure glaucoma where delay of surgery is desired in order to lower intraocular pressure. • edema due to congestive heart failure or drug-induced edema (as an adjunctive treatment - limited by its low efficacy) • centrencephalic epilepsies (petit mal, unlocalized seizures), but its usefulness for treatment of epilepsy is limited by the rapid development of tolerance due to upregulation of carbonic anhydrase in neuronal tissue • acute mountain sickness (prevention or amelioration of symptoms associated with) in climbers attempting rapid ascent and in those who are very susceptible to acute mountain sickness despite gradual ascent

  16. DIURETICS:Acetazolamide Contraindications: • Situations in which sodium and/or potassium blood serum levels are depressed, • Cases of marked kidney and liver disease or dysfunction, • Suprarenal gland failure • Hyperchloremic acidosis • Cirrhosis - because of the risk of development of hepatic encephaiopathy • Long-term administration of acetazolamide is contraindicated in patients with chronic noncongestive angle-closure glaucoma 

  17. DIURETICS:Acetazolamide Side Effects: • long-term usefulness of carbonic anyhydrase inhibitors is commonly compromised by the development of a metabolic acidosis, which requires discontinuation of treatment. • electrolyte imbalances • hearing dysfunction or tinnitus • loss of appetite, taste alteration and gastrointestinal disturbances such as nausea, vomiting and diarrhea • Polyuria • occasional instances of drowsiness and confusion

  18. DRUGS ALTERING THE pH URINE: Clinical Significance of drugs altering urine PH The pH of the Urine affects the Excretion Rates of different Drugs (Depending if drug is acidic or basic) Urine Alkalinisation: purposes o Excretion: § Increases the Excretion of Weak-Acid Drugs (Eg: Salicylates/Aspirin & Barbiturates) this is why Bicarbonate is sometimes used to treat Overdoses of salicylates, aspirin & barbiturates § Decreases the Excretion of Weak-Base Drugs o Precipitation: § Can prevent Weak-Acid Drugs from Precipitating in the Urine (↓kidney stones) § Also decreases Precipitation of Uric Acid Crystals in the Urine (↓kidney stones)

  19. DRUGS ALTERING THE pH URINE: Clinical Significance of drugs altering urine PH Urine Acidification – (Rarely Ever Used): purposes o Excretion: § Increases the Excretion of Weak-Base Drugs § Decreases the Excretion of Weak-Acid Drugs (Eg: Salicylates & Barbiturates) o Precipitation: § Can prevent Weak-Base Drugs from Precipitating in the Urine (↓kidney stones)

  20. DRUGS ALTERING THE pH URINE: Urinary Alkalizers: Carbonic Anhydrase Inhibitors: o Mechanism of Action: § Blocks Bicarbonate Reabsorption → Alkaline Urine (but Metabolic Acidosis) Oral Citrate: o Mechanism of Action: § Metabolised via TCA-Cycle → Produces Bicarbonate as a by-product Urinary Acidifiers – (Rarely Ever Used): Ammonium Chloride: o Only Used Clinically for an oral Acid-Loading test to Diagnose Renal Tubular Acidosis

  21. FLUID REPLACEMENT THERAPY: Crystalloid Vs Colloid Solution: Crystalloids: o Aqueous Solutions of Mineral Salts or other water-soluble molecules o Crystalloids have a Low Osmotic-Pressure in Blood due to Haemodilution Colloids: o Mixtures of Larger Insoluble Molecules (Note: Blood itself is a colloid) o Colloids Preserve a High Colloid-Osmotic Pressure in the Blood

  22. Crystalloid Vs Colloid Solution

  23. FLUID REPLACEMENT THERAPY: Crystalloid Solutions: Saline: o The Most Commonly used Crystalloid Advantage • Is Isotonic → Does not cause dangerous fluid shifts Disadvantage • Failure/Oedema Indication • o Used for General Extracellular Fluid Replacement Dextrose: • o Saline with 5% Dextrose – Used if Pt is at risk of Hypoglycaemia; or Hypernatraemia • o Note: Becomes Hypotonic when Glucose is Metabolised → Can cause fluid overload

  24. FLUID REPLACEMENT THERAPY: Crystalloid Solutions: Lactated Ringer’s/Hartmann’s Solution: o A Solution of Multiple Electrolytes: § Sodium § Chloride § Lactate § Potassium § Calcium o Used in Pts with Hemorrhage, Trauma, Surgery or Burns o Also used to Buffer Acidosis

  25. FLUID REPLACEMENT THERAPY: Colloid Solutions: Albumin: o Albumin 40g/100ml - Used in Liver Disease, Severe Sepsis, or Extensive Surgery o Albumin 200g/100ml – Used in Hemorrhage/Plasma loss due to Burns/Crush Injury/Peritonitis/Pancreatitis; or Hypoproteinemia; or Hemodialysis Polygeline (Haemaccel): o Gelatin Cross-linked with urea o Used in Dehydration due to GI Upsets (Vom/Diarrhoea)

  26. FLUID REPLACEMENT THERAPY: THE END THANK YOU VERY MUCH

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