Diuretics | Definition | Mechanism of Action | Classes of DrugsChetan Prakash
This presentation provides knowledge about Diuretics,Role of sodium, types of urine output, General mechanism of action, Normal Physiolofy of urine formation, GFR Formation, Classes of Diuretics, diuretics abuse and recent discovery. An assignment for the subject, Advanced Pharmacology-I, 1st year M.Pharm, 1st semester.
The kidneys lie on the posterior abdominal wall, one on each side of the vertebral column, behind the peritoneum and below the diaphragm
The nephron consists of a tubule closed at one end, the other end opening into a collecting tubule
Continuing from the glomerular capsule the remainder of the nephron is about 3 cm long and is described in three parts:
the proximal convoluted tubule
the medullary loop (loop of Henle)
the distal convoluted tubule, leading into a collecting duct
High efficacy diuretics (Inhibitors of Na-+K+-2Cl¯ cotransport)
Sulphamoyl derivatives : Furosemide, Bumetanide, Torasemide
2. Medium efficacy diuretics (Inhibitors of Na+-Cl¯ symport)
Benzothiadiazines (thiazides) Hydrochlorothiazide, Benzthiazide, Hydroflumethiazide, Bendroflumethiazide
Thiazide like (related heterocyclics) Chlorthalidone, Metolazone, Xipamide, Indapamide, Clopamide
3. Weak or adjunctive diuretics
(a) Carbonic anhydrase inhibitors : Acetazolamide
(b) Potassium sparing diuretics
Aldosterone antagonist: Spironolactone, Eplerenone
Inhibitors of renal epithelial Na+ channel: Triamterene, Amiloride.
(c) Osmotic diuretics :Mannitol, Isosorbide, Glycerol
Diuretics | Definition | Mechanism of Action | Classes of DrugsChetan Prakash
This presentation provides knowledge about Diuretics,Role of sodium, types of urine output, General mechanism of action, Normal Physiolofy of urine formation, GFR Formation, Classes of Diuretics, diuretics abuse and recent discovery. An assignment for the subject, Advanced Pharmacology-I, 1st year M.Pharm, 1st semester.
The kidneys lie on the posterior abdominal wall, one on each side of the vertebral column, behind the peritoneum and below the diaphragm
The nephron consists of a tubule closed at one end, the other end opening into a collecting tubule
Continuing from the glomerular capsule the remainder of the nephron is about 3 cm long and is described in three parts:
the proximal convoluted tubule
the medullary loop (loop of Henle)
the distal convoluted tubule, leading into a collecting duct
High efficacy diuretics (Inhibitors of Na-+K+-2Cl¯ cotransport)
Sulphamoyl derivatives : Furosemide, Bumetanide, Torasemide
2. Medium efficacy diuretics (Inhibitors of Na+-Cl¯ symport)
Benzothiadiazines (thiazides) Hydrochlorothiazide, Benzthiazide, Hydroflumethiazide, Bendroflumethiazide
Thiazide like (related heterocyclics) Chlorthalidone, Metolazone, Xipamide, Indapamide, Clopamide
3. Weak or adjunctive diuretics
(a) Carbonic anhydrase inhibitors : Acetazolamide
(b) Potassium sparing diuretics
Aldosterone antagonist: Spironolactone, Eplerenone
Inhibitors of renal epithelial Na+ channel: Triamterene, Amiloride.
(c) Osmotic diuretics :Mannitol, Isosorbide, Glycerol
This slide talks about the different pharmacological properties of Antihypertensive Drugs. The classification and examples of these drugs are also given in detail.
Diuretics enhances the urine output. It is mainly used in treatment of hypertension, hypervolumia, edema, congestive cardiac failure, electrolyte imbalances etc. They have some adverse reactions like hypotension, dehydration, hypovolumia, etc.
Chemistry of Anti Anginal Drugs by Professor BeubenzProfessor Beubenz
This presentation will give you an idea about the chemistry of Anti-anginal drugs along with its classification, mechanism of action & Structural Activity Relationship.
#Professor_Beubenz
For more such videos do
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https://www.youtube.com/watch?v=-7yjQm4zzX8&t=1183s
Hypolipidemic agents, also known as cholesterol-lowering drugs or antihyperlipidemic agents, are a diverse group of pharmaceuticals that are used in the treatment of high levels of fats (lipids), such as cholesterol, in the blood (hyperlipidemia). They are also called lipid-lowering drugs.
Hypolipidemic drug, also called lipid-lowering drug, any agent the reduces the level of lipids and lipoproteins (lipid-protein complexes) in the blood.
In this slide contains definition, pharmacology, classification, mechanism of action, uses, side effects of various diuretics drugs.
Presented by: MARY VISHALI BOREDDY (Department of pharmacology).
RIPER, anantapur
the detail study of diuretics which include their drugs, use,classification of diuretics, side effect, mechanism of action, metabolism, synthesis etc. this all things are cover in this presentation.
This slide talks about the different pharmacological properties of Antihypertensive Drugs. The classification and examples of these drugs are also given in detail.
Diuretics enhances the urine output. It is mainly used in treatment of hypertension, hypervolumia, edema, congestive cardiac failure, electrolyte imbalances etc. They have some adverse reactions like hypotension, dehydration, hypovolumia, etc.
Chemistry of Anti Anginal Drugs by Professor BeubenzProfessor Beubenz
This presentation will give you an idea about the chemistry of Anti-anginal drugs along with its classification, mechanism of action & Structural Activity Relationship.
#Professor_Beubenz
For more such videos do
#Subscribe
#Share
#Like
to the Channel Professor Beubenz
Thank You.
https://www.youtube.com/watch?v=-7yjQm4zzX8&t=1183s
Hypolipidemic agents, also known as cholesterol-lowering drugs or antihyperlipidemic agents, are a diverse group of pharmaceuticals that are used in the treatment of high levels of fats (lipids), such as cholesterol, in the blood (hyperlipidemia). They are also called lipid-lowering drugs.
Hypolipidemic drug, also called lipid-lowering drug, any agent the reduces the level of lipids and lipoproteins (lipid-protein complexes) in the blood.
In this slide contains definition, pharmacology, classification, mechanism of action, uses, side effects of various diuretics drugs.
Presented by: MARY VISHALI BOREDDY (Department of pharmacology).
RIPER, anantapur
the detail study of diuretics which include their drugs, use,classification of diuretics, side effect, mechanism of action, metabolism, synthesis etc. this all things are cover in this presentation.
This ppt tells us about the topics diuretics and antidiuretics.
It also indicates us about their classification, mechanism of action, side effects and many more.
Hello friends. In this PPT I am talking about diuretics. If you like it, please do let me know in the comments section. A single word of appreciation from you will encourage me to make more of such videos. Thanks. Enjoy and welcome to the beautiful world of pharmacology where pharmacology comes to life. This video is intended for MBBS, BDS, paramedical and any person who wishes to have a basic understanding of the subject in the simplest way.
A detailed information about the diuretics - classification of drugs, mechanism of action, side effects, dosage and indications.
Classification based on the efficacy of the diuretics.
1. High
2. Moderate
3. Weak
A brief introduction given about the nephron structure and its indications.
Pharmacology of drugs acting on Renal System.pdfAFFIFA HUSSAIN
Diuretics also known as water pills increases the excretion of water and electrolytes (Na+) in
urine.
Natriuresis – large amount of sodium excreted in urine due to the action of kidneys.
Promoted by – ventricular and atrial natriuretic as well as calcitonin.
Inhibited by chemicals such as aldosterone. The drugs which increases sodium excretion are
known as natriuretic.
Diuresis – increased or excessive production of urine. The drugs which enhances the excretion
of water without loss of electrolyte is called as aquaretic.
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
2. Definition
• Diuretics are medications that increase the amount of urine
excreted.
• The majority of diuretic drugs inhibit renal ion transporters,
which reduces the reabsorption of Na+ at various locations
throughout the nephron.
• In order to keep the osmotic balance, water is passively
transported into the urine together with Na+ and other ions like
Cl- in higher than usual proportions.
• Diuretics thereby increase the amount of urine produced and
frequently alter its pH as well as the ionic content of both the
urine and the blood.
3.
4. How could urine output be increased?
• Increase GFR Vs Decrease Tubular reabsorption (the most
important clinically)
• If you increase the glomerular filtration increase tubular
reabsorption ( so you cannot use glomerular filtration).
Purpose of Diuretics use:
• To maintain urine volume (e.g.: renal failure)
• To mobilize edema fluid (e.g.: Heart failure, Liver failure,
nephrotic syndrome)
• To control high blood pressure.
5. • Diagrammatic representation of nephron showing the four sites of solute reabsorption. The thick ascending limb of loop
of Henle (TAL) is impermeable to water
• Glu.—Glucose; A.A.—Amino acid; Org. An.—Organic anions.
6. Major locations of ion and water exchange in the nephron, showing sites of
action of the diuretic drugs.
8. THIAZIDES DIURETICS
The thiazides are the most widely used diuretics. They are sulfonamide derivatives. All
thiazides affect the distal convoluted tubule, and all have equal maximum diuretic effects,
differing only in potency. Thiazides are sometimes called “low ceiling diuretics,” because
increasing the dose above normal therapeutic doses does not promote further diuretic
response.
Ex:
• Chlorothiazide DIURIL, SODIUM DIURIL
• Chlorthalidone THALITONE
• Hydrochlorothiazide (HCTZ) MICROZIDE
• Indapamide
• Metolazone ZAROXOLYN
9. Mechanism of Action
• Increased excretion of Na+ and Cl-
• Loss of K+: (Because thiazides increase Na+ in the filt ate arriving at the distal tubule, more K+ is also
exchanged for Na+, resulting in a continual loss of K+ from the body with prolonged use of these drugs.)
• Loss of Mg2+ : (Magnesium deficiency requiring supplementation can occur with chronic use of thiazide
diuretics, particularly in elderly patients. The mechanism for the magnesuria is not understood.)
• Decreased Urinary Calcium excretion
• Reduced peripheral vascular resistance: (An initial reduction in blood pressure results from a decrease
in blood volume and, therefore, a decrease in cardiac output. With continued therapy, volume recovery occurs.
However, there are continued antihypertensive effects, resulting from reduced peripheral vascular resistance
caused by relaxation of arteriolar smooth muscle. How these agents induce vasodilation is unknown.)
10. Pharmacokinetics
• Orally administered
• Poor absorption
• Onset of action in ~ 1 hour
• Wide range of t ½ amongst different
thiazides, longer than loop diuretics
• Free drug enters tubules by filtration
and by organic acid secretion
11. Therapeutic Uses
• Hypertension
• Heart failure
• Hypercalciuria: prevent excess Ca2+
excretion to form stones in ducts
• Osteoporosis
• Treatment of Li+ toxicity
• Diabetes insipidus
12. Side Effects/ Adverse Effects
• Potassium depletion: Hypokalemia is the most frequent problem with
the thiazide diuretics, and it can predispose patients who are taking
digoxin to ventricular arrhythmias. Thiazides decrease the intravascular
volume, resulting in activation of the renin–angiotensin–aldosterone
system. Low-sodium diets blunt the potassium depletion caused by
thiazide diuretics.
• Hyponatremia
• Hyperuricemia
• Volume depletion: This can cause orthostatic hypotension or light-
headedness.
• Hypercalcemia
• Hyperglycemia: Therapy with thiazides can lead to glucose
intolerance, possibly due to impaired release of insulin and tissue uptake
of glucose. New-onset diabetes has been reported more often with
thiazides than with other antihypertensive agents.
13. LOOP/ HIGH-CEILING DIURETICS
• (Inhibitors of Na+-K+-2Cl¯ Cotransport)
• The major site of action is the thick ascending limb of Loop of Henle
(TAL), therefore, called loop diuretics.
Ex:
• Bumetanide
• Ethacrynic acid EDECRIN
• Furosemide LASIX
• Torsemide DEMADEX
14. Mechanism of action
• Loop diuretics inhibit the cotransport of Na+/K+/2Cl− in the luminal membrane in the
ascending limb of the loop of Henle.
• Therefore, reabsorption of these ions is decreased.
• The loop diuretics may increase renal blood flow, possibly by enhancing prostaglandin
synthesis.
• NSAIDs inhibit renal prostaglandin synthesis and can reduce the diuretic action of loop
diuretics.
[Note: Unlike thiazides, loop diuretics increase the Ca2+ content of urine. In patients with
normal serum Ca2+ concentrations, hypocalcemia does not result, because Ca2+ is
reabsorbed in the distal convoluted tubule.]
15. Pharmacokinetics
• Orally administered
• Rapid absorption
• Rapid onset of action
• Bound to plasma proteins: displaced by warfarin and Clofibrate
• Duration of action is relatively brief (2 to 4 hours), allowing patients to predict the
window of diuresis.
• They are secreted into urine.
16. Therapeutic
uses
• The loop diuretics are the drugs of
choice for acute pulmonary edema &
Chronic peripheral edema caused from
heart failure or renal impairment.
• Chronic Renal failure or Nephrosis
• Hypertension
• Hypercalcemia
• Acute and chronic hyperkalemia
17. Adverse Effects
Ototoxicity: Reversible or permanent hearing loss may occur with loop diuretics,
particularly when used in conjunction with other ototoxic drugs (for example,
aminoglycoside antibiotics). Ethacrynic acid is the most likely to cause deafness.
Hyperuricemia: Furosemide and ethacrynic acid compete with uric acid for the
renal secretory systems, thus blocking its secretion and, in turn, causing or
exacerbating gouty attacks.
Acute hypovolemia: Loop diuretics can cause a severe and rapid reduction in
blood volume, with the possibility of hypotension, shock, and cardiac arrhythmias.
Potassium depletion: The heavy load of Na+ presented to the collecting tubule
results in increased exchange of tubular Na+ for K+, leading to the possibility of
hypokalemia. The loss of K+ from cells in exchange for H+ leads to hypokalemic
alkalosis. Use of potassium-sparing diuretics or supplementation with K+ can prevent
the development of hypokalemia.
Hypomagnesemia: Chronic use of loop diuretics combined with low dietary
intake of Mg2+ can lead to hypomagnesemia, particularly in the elderly. This can be
corrected by oral supplementation.
18. POTASSIUM-SPARING DIURETICS
• Potassium-sparing diuretics act in the collecting tubule to inhibit Na+
reabsorption and K+ excretion.
• These drugs should be avoided in patients with renal dysfunction because of
the increased risk of hyperkalemia. Within this class, there are drugs with
two distinct mechanisms of action: aldosterone antagonists and sodium
channel blockers.
Ex:
• Amiloride MIDAMOR
• Eplerenone INSPRA
• Spironolactone ALDACTONE
• Triamterene DYRENIUM
19. Mechanism of action
• Spironolactone is a synthetic steroid that
antagonizes aldosterone at intracellular
cytoplasmic receptor sites rendering the
spironolactone–receptor complex inactive.
• It prevents translocation of the receptor complex
into the nucleus of the target cell, ultimately
resulting in a failure to produce mediator proteins
that normally stimulate the Na+/K+-exchange sites
of the collecting tubule.
• Thus, a lack of mediator proteins prevents Na+
reabsorption and, therefore, K+ and H+ secretion.
Eplerenone is another aldosterone receptor
antagonist, which has actions comparable to those
of spironolactone, although it may have fewer
endocrine effects than spironolactone
20. Pharmacokinetics
• Both spironolactone and eplerenone are absorbed after oral administration and are
significantly bound to plasma proteins.
• Spironolactone is extensively metabolized and converted to several active
metabolites.
• The metabolites, along with the parent drug, are thought to be responsible for the
therapeutic effects.
• Spironolactone is a potent inhibitor of P-glycoprotein, and eplerenone is metabolized
by cytochrome P450 3A4.
22. Side effects/ Adverse effects
• Spironolactone can cause
Gastric upset.
Gynecomastia in male patients & Menstrual irregularities in female patients. Because
it chemically resembles some of the sex steroids.
Hyperkalemia,
Nausea
Lethargy
Mental confusion can occur.
Potassium-sparing diuretics should be used with caution with other medications that can
induce hyperkalemia, such as angiotensin-converting enzyme inhibitors and potassium
supplements.
23. CARBONIC ANHYDRASE INHIBITORS
• Acetazolamide and other carbonic anhydrase inhibitors are more often used for
their other pharmacologic actions than for their diuretic effect, because they are
much less efficacious than the thiazide or loop diuretics.
• Limited uses as diuretics
• Developed from sulfanilamide (caused metabolic acidosis and alkaline urine)
Ex:
• Acetazolamide DIAMOX
24. Mechanism of action
• Acetazolamide inhibits carbonic anhydrase located intracellularly (cytoplasm) and on the
apical membrane of the proximal tubular epithelium.
• The decreased ability to exchange Na+ for H+ in the presence of acetazolamide results in
a mild diuresis. Additionally, HCO3− is retained in the lumen, with marked elevation in
urinary pH . The loss of HCO3− causes a hyperchloremic metabolic acidosis and
decreased diuretic efficacy following several days of therapy. Changes in the composition
of urinary electrolytes induced by acetazolamide. Phosphate excretion is increased by an
unknown mechanism.
[Note: Carbonic anhydrase catalyzes the reaction of CO2 and H2O, leading to H2CO3,
which spontaneously ionizes to H+ and HCO3− (bicarbonate).]
25. Pharmacokinetics
• Acetazolamide is well absorbed orally and excreted unchanged in
urine.
• Action of a single dose lasts 8–12 hours.
• It is approximately 90% protein bound and eliminated renally by both
active tubular secretion and passive reabsorption.
26. Therapeutic use
• Glaucoma: as adjuvant to other ocular hypotensive
• To alkalinize urine: for urinary tract infection or to promote excretion
of certain acidic drugs.
• Epilepsy: as adjuvant in absence seizures when primary drugs are not
fully effective; but tolerance to antiepileptic action develops.
• Mountain sickness
• Periodic paralysis.
27. Adverse Effects
• Metabolic acidosis (mild)
• Potassium depletion
• Renal stone formation
• Drowsiness
• Paresthesia may occur.
• The drug should be avoided in patients with hepatic cirrhosis, because it could lead to a
decreased excretion of NH4
+.
28. OSMOTIC DIURETICS
• A number of straightforward, hydrophilic chemical compounds that pass through the
glomerulus, like mannitol and urea, cause some degree of diuresis.
• A decrease in reabsorption from filtered compounds will result in a rise in urine output.
These compounds raise the osmolarity of the tubular fluid and stop more water from being
absorbed, which causes osmotic diuresis.
• Only a tiny bit of extra salt might also be excreted.
• Osmotic diuretics are ineffective for treating diseases where Na+ retention develops because
they are used to promote water excretion rather than Na+ excretion.
Ex:
• Mannitol OSMITROL
• Urea
[Note: Mannitol is not absorbed when given orally and should be given intravenously.]
29. Mechanism of action
• Osmotic diuretics are not reabsorbed.
• Increase osmotic pressure specifically in the proximal tubule and loop of Henle.
• Prevents passive reabsorption of H2O
• Increase H2O and Na+ excretion.
30. Therapeutic use
• Mannitol: Drug of choice, Non-toxic, freely filtered, non re-absorbable and non-
metabolized.
• Administered prophylactically for acute renal failure secondary to trauma, CVS disease,
surgery or nephrotoxic drugs.
• Short-term treatment of acute glaucoma.
• Infused to lower intracranial pressure
• Urea, Glycerol and Isosorbide are less efficient can penetrate cell membranes.
31. Side Effects
• Increase extracellular fluid volume
• Cardiac failure
• Pulmonary edema
• Hypernatremia
• Headache
• Nausea
• Hyperkalaemia secondary to diabetes or impaired renal function
32.
33.
34. References
• W. Karen, F. Richard, Panavelil Thomas A. “Chapter 18: Diuretics, Lippincott Illustrated
reviews: Pharmacology, Sixth Edition”, published by wolters kluwer Page- 241-253.
• Katzung Bertram G., “Chapter 15: Diuretic Agents, Basic & Clinical Pharmacology, 14th
Edition,” Published by Mc Graw Hill education, Page: 254- 275.
• Hall John E., Chapter 31: “Diuretics, Kidney diseases, Guyton and Hall Textbook of Medical
Physiology, 12th Edition,” published by Saunders Elsevier, Page: 397-409.
• Tripathi KD, “Chapter 42: Diuretics, Essentials of Medical Pharmacology, 8th Edition,”
published by The health sciences publisher, Page: 625-638.
• Tripathi KD, “Chapter 8: Drugs acting on Kidney, Pharmacological Classification of drugs
with doses and preparations, 5th edition,” published by Jaypee brothers medical publishers ltd,
Page: 102-103.