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SRI VENKATESHWARA UNIERSITY
Presented by
A Sreedhar Reddy
M pharmacy
INTRODUCTION
1)THIAZIDE DIURETICS:
• Chlorthiazide.
• Chlorthalidone.
• Hydrochlorothiazide
• Indapamide.
• Metolazone.
2) LOOP DIURETICS:
• Bumetanide.
• Ethacrynic acid
• Furosemide.
• Torsemide.
3) POTASSIUM-SPARING DIURETICS
a) Aldosterone antagonist
• Eplerenone
• Spironolactone
b)Inhibitors of renal epithelial Na+ Channel
• Amiloride.
• Triamterene
4)CARBONIC ANHYDRASE INHIBITORS
Acetazolamide
5) OSMOTIC DIURETICS
• Mannitol.
• Urea
NORMAL REGULATION OF FLUIDS AND
ELECTROLYTES BY THE KIDNEY
• Approximately 16% to 20% of the blood plasma entering the kidneys is
filtered from the Glomerular capillaries into Bowman’s capsule.
• The filtrate, although normally free of proteins and blood cells,
contains most of the low molecular weight plasma components in
concentrations similar to that in the plasma.
• The kidney regulates the ionic composition and volume of urine by
active reabsorption or secretion of ions and passive reabsorption of
water at five functional zones along the nephron:
• 1) the proximal convoluted tubule,
• 2) the descending loop of Henle,
• 3) the ascending loop of Henle,
• 4) the distal convoluted tubule, and
• 5) the collecting tubule and duct
A. Proximal convoluted tubule
• all the glucose, bicarbonate, amino acids, and other metabolites are
reabsorbed here.
• Approximately two-thirds of the Na+ is also reabsorbed.
• Chloride enters the lumen of the tubule in exchange for an anion, such
as oxalate.
• The proximal tubule is the site of the organic acid and base secretory
systems
• The organic acid secretory system secretes a variety of organic acids,
such as uric acid, some antibiotics, and diuretics, from the bloodstream
into the proximal tubular lumen.
• The organic acid secretory system is saturable, and diuretic drugs in
the bloodstream compete for transfer with endogenous organic acids
such as uric acid.
B. Descending loop of Henle
• The remaining filtrate, which is isotonic, next enters the
descending limb of the loop of Henle and passes into the
medulla of the kidney.
• The osmolarity increases along the descending portion of
the loop of Henle because of the countercurrent
mechanism that is responsible for water reabsorption.
• This results in a tubular fluid with a threefold increase in
salt concentration.
• Osmotic diuretics exert part of their action in this region.
C. Ascending loop of Henle
• The cells of the ascending tubular epithelium are unique in being
impermeable to water.
• Active reabsorption of Na+, K+, and Cl− occur here
• Approximately 25% to 30% of the tubular sodium chloride returns to
the interstitial fluid
D. Distal convoluted tubule
E. Collecting tubule and duct
Hypertension
Heart failure
Hypercalciuria
4. Diabetes Insipidus
Potassium depletion
Hyponatremia
Hyperuricemia
Volume depletion
Hypercalcemia
Hyperglycemia
• These compounds lack the thiazide structure, but, like the
thiazides, they have the unsubstituted sulfonamide group and,
therefore, share their mechanism of action.
• The therapeutic uses and adverse effect profiles are similar to
those of the thiazides.
• They include:
1. Chlorthalidone
2. Metolazone
3. Indapamide
• Bumetanide ,furosemide ,torsemide, and ethacrynic acid have their
major diuretic action on the ascending limb of the loop of Henle .
• Furosemide is the most commonly used of these drugs.
• Bumetanide and torsemide are much more potent than furosemide, and
the use of these agents is increasing.
• Ethacrynic acid is used infrequently due to its adverse effect profile.
Mechanism of action:
pulmonary edema peripheral
edema
hypercalcemia
hyperkalemia
1. Ototoxicity
Hyperuricemia
3. Acute hypovolemia
Potassium depletion
Hypomagnesemia
POTASSIUM-SPARING DIURETICS
• Mechanism of action:
Acetazolamide and othercarbonicanhydraseInhibitors are used for
theirother pharmacologicactionsthanfortheirdiureticeffect
,becausetheyaremuchlessefficaciousthanthethiazideorloopdiuretics.
• Class • Adverse side effect • Drug interactions
• Thiazide • Hypokalemia
• Metabolic alkalosis
• Dehydration (hypovolemia),
leading to hypotension
• Hyponatremia
• Hyperglycemia in diabetics
• Hypercholesterolemia;
hypertriglyceridemia
• Increased low-density lipoproteins
• Hyperuricemia (at low doses)
• Azotemia (in renal disease patients)
• Hypokalemia potentiates digitalis
toxicity
• Non-steroidal anti-inflammatory
drugs: reduced diuretic efficacy
• Beta-blockers: potentiate
hyperglycemia, hyperlipidemias
• Corticosteroids: enhance
hypokalemia
• Loop • Hypokalemia
• Metabolic alkalosis
• Hypomagnesemia
• Hyperuricemia
• Dehydration (hypovolemia),
leading to hypotension
• Dose-related hearing loss
(ototoxicity)
• Hypokalemia potentiates digitalis
toxicity
• Non-steroidal anti-inflammatory
drugs: reduced diuretic efficacy
• Corticosteroids: enhance
hypokalemia
• Aminoglycosides: enhance
ototoxicity, nephrotoxicity
• K+ - sparing • Hyperkalemia
• Metabolic acidosis
• Gynecomastia (aldosterone
antagonists)
• ACE inhibitors: potentiate
hyperkalemia
• Non-steroidal anti-inflammatory
drugs: reduced diuretic efficacy
Reference.
Cardiovascular Pharmacology Concepts by Richard E. Klabunde,
Ph.D.
KD Tripathi Essential Medical pharmacology 8th edition
Padmaja Uday kumar Pharmacology

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diuretic drugs

  • 1. SRI VENKATESHWARA UNIERSITY Presented by A Sreedhar Reddy M pharmacy
  • 3.
  • 4. 1)THIAZIDE DIURETICS: • Chlorthiazide. • Chlorthalidone. • Hydrochlorothiazide • Indapamide. • Metolazone. 2) LOOP DIURETICS: • Bumetanide. • Ethacrynic acid • Furosemide. • Torsemide.
  • 5. 3) POTASSIUM-SPARING DIURETICS a) Aldosterone antagonist • Eplerenone • Spironolactone b)Inhibitors of renal epithelial Na+ Channel • Amiloride. • Triamterene 4)CARBONIC ANHYDRASE INHIBITORS Acetazolamide 5) OSMOTIC DIURETICS • Mannitol. • Urea
  • 6. NORMAL REGULATION OF FLUIDS AND ELECTROLYTES BY THE KIDNEY • Approximately 16% to 20% of the blood plasma entering the kidneys is filtered from the Glomerular capillaries into Bowman’s capsule. • The filtrate, although normally free of proteins and blood cells, contains most of the low molecular weight plasma components in concentrations similar to that in the plasma. • The kidney regulates the ionic composition and volume of urine by active reabsorption or secretion of ions and passive reabsorption of water at five functional zones along the nephron: • 1) the proximal convoluted tubule, • 2) the descending loop of Henle, • 3) the ascending loop of Henle, • 4) the distal convoluted tubule, and • 5) the collecting tubule and duct
  • 7.
  • 8. A. Proximal convoluted tubule • all the glucose, bicarbonate, amino acids, and other metabolites are reabsorbed here. • Approximately two-thirds of the Na+ is also reabsorbed. • Chloride enters the lumen of the tubule in exchange for an anion, such as oxalate. • The proximal tubule is the site of the organic acid and base secretory systems • The organic acid secretory system secretes a variety of organic acids, such as uric acid, some antibiotics, and diuretics, from the bloodstream into the proximal tubular lumen. • The organic acid secretory system is saturable, and diuretic drugs in the bloodstream compete for transfer with endogenous organic acids such as uric acid.
  • 9. B. Descending loop of Henle • The remaining filtrate, which is isotonic, next enters the descending limb of the loop of Henle and passes into the medulla of the kidney. • The osmolarity increases along the descending portion of the loop of Henle because of the countercurrent mechanism that is responsible for water reabsorption. • This results in a tubular fluid with a threefold increase in salt concentration. • Osmotic diuretics exert part of their action in this region.
  • 10. C. Ascending loop of Henle • The cells of the ascending tubular epithelium are unique in being impermeable to water. • Active reabsorption of Na+, K+, and Cl− occur here • Approximately 25% to 30% of the tubular sodium chloride returns to the interstitial fluid D. Distal convoluted tubule
  • 12.
  • 13.
  • 14.
  • 15.
  • 17.
  • 19. • These compounds lack the thiazide structure, but, like the thiazides, they have the unsubstituted sulfonamide group and, therefore, share their mechanism of action. • The therapeutic uses and adverse effect profiles are similar to those of the thiazides. • They include: 1. Chlorthalidone 2. Metolazone 3. Indapamide
  • 20.
  • 21. • Bumetanide ,furosemide ,torsemide, and ethacrynic acid have their major diuretic action on the ascending limb of the loop of Henle . • Furosemide is the most commonly used of these drugs. • Bumetanide and torsemide are much more potent than furosemide, and the use of these agents is increasing. • Ethacrynic acid is used infrequently due to its adverse effect profile. Mechanism of action:
  • 22.
  • 23.
  • 25.
  • 26. 1. Ototoxicity Hyperuricemia 3. Acute hypovolemia Potassium depletion Hypomagnesemia
  • 28.
  • 29. • Mechanism of action:
  • 30.
  • 31.
  • 32.
  • 33.
  • 34. Acetazolamide and othercarbonicanhydraseInhibitors are used for theirother pharmacologicactionsthanfortheirdiureticeffect ,becausetheyaremuchlessefficaciousthanthethiazideorloopdiuretics.
  • 35.
  • 36.
  • 37.
  • 38.
  • 39.
  • 40.
  • 41. • Class • Adverse side effect • Drug interactions • Thiazide • Hypokalemia • Metabolic alkalosis • Dehydration (hypovolemia), leading to hypotension • Hyponatremia • Hyperglycemia in diabetics • Hypercholesterolemia; hypertriglyceridemia • Increased low-density lipoproteins • Hyperuricemia (at low doses) • Azotemia (in renal disease patients) • Hypokalemia potentiates digitalis toxicity • Non-steroidal anti-inflammatory drugs: reduced diuretic efficacy • Beta-blockers: potentiate hyperglycemia, hyperlipidemias • Corticosteroids: enhance hypokalemia • Loop • Hypokalemia • Metabolic alkalosis • Hypomagnesemia • Hyperuricemia • Dehydration (hypovolemia), leading to hypotension • Dose-related hearing loss (ototoxicity) • Hypokalemia potentiates digitalis toxicity • Non-steroidal anti-inflammatory drugs: reduced diuretic efficacy • Corticosteroids: enhance hypokalemia • Aminoglycosides: enhance ototoxicity, nephrotoxicity • K+ - sparing • Hyperkalemia • Metabolic acidosis • Gynecomastia (aldosterone antagonists) • ACE inhibitors: potentiate hyperkalemia • Non-steroidal anti-inflammatory drugs: reduced diuretic efficacy
  • 42. Reference. Cardiovascular Pharmacology Concepts by Richard E. Klabunde, Ph.D. KD Tripathi Essential Medical pharmacology 8th edition Padmaja Uday kumar Pharmacology