Diuresis diuretics
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This document discusses factors that regulate aldosterone secretion and recommends reading several chapters from Ganong that cover related topics such as diuresis, diuretics, and how most diuretics increase urinary excretion of electrolytes. It instructs the reader to learn about the factors that regulate aldosterone secretion by reading the relevant sections from the listed chapters.
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The document summarizes the process of hemoglobin degradation and bilirubin metabolism. It discusses how hemoglobin is broken down into globin, heme, and iron. Heme is further degraded into biliverdin and then bilirubin by heme oxygenase. Bilirubin is conjugated in the liver and secreted into bile. It is excreted in feces or reabsorbed and appears in urine. Conditions that interfere with bilirubin metabolism can cause jaundice. The document classifies types of jaundice and inherited disorders of bilirubin metabolism.
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Erythrocytes have a lifespan of 120 days before being removed from circulation and degraded by macrophages in the spleen and liver. Approximately 6 grams of hemoglobin is broken down per day in an adult human. Heme is broken down by the enzyme heme oxygenase into biliverdin, iron, and carbon monoxide. Biliverdin is further degraded by biliverdin reductase into bilirubin, which is transported bound to albumin in plasma and taken up by hepatocytes in the liver. In the liver, bilirubin is conjugated and excreted into bile as bilirubin diglucuronide.
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AMINO ACIDS.pptx
The principle sources of protein are pulses, cereals, peas, beans and nuts and principle animal sources are milk and its products, meat, fish, liver, eggs etc.
Primarily proteins are hydrolyzed from polypeptides to dipeptides and then finally they are converted in amino acids and absorbed in gut.
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Heme is degraded into bilirubin through several steps. Heme is degraded into biliverdin by heme oxygenase, then biliverdin is reduced to bilirubin. Bilirubin is transported bound to albumin and taken up by hepatocytes. In hepatocytes, bilirubin is conjugated by UDP-glucuronyltransferase and secreted into bile. In the intestines, bilirubin is deconjugated by bacteria and excreted in stool. Elevated bilirubin can cause jaundice, which is classified based on the site of pathology as prehepatic, hepatic, or posthepatic jaundice.
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Erythrocytes have a lifespan of 120 days before being removed from circulation and degraded by macrophages in the spleen and liver. Approximately 6 grams of hemoglobin is broken down per day in an adult human. Heme is broken down by the enzyme heme oxygenase into biliverdin, iron, and carbon monoxide. Biliverdin is further degraded by biliverdin reductase into bilirubin, which is transported bound to albumin in plasma and taken up by hepatocytes in the liver. In the liver, bilirubin is conjugated and excreted into bile as bilirubin diglucuronide.
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The kidney regulates electrolyte and fluid balance in the body through its main functions of filtering blood to form urine and reabsorbing necessary water and ions back into circulation. The functional unit of the kidney is the nephron, which contains a glomerulus for blood filtration and a tubule system for reabsorption and secretion. As fluid moves through the nephron's tubules, complex mechanisms involving countercurrent exchange and active transport work to concentrate urine by returning water to the blood while retaining waste products.
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The major points of heme catabolism and bilirubin metabolism are:
1. Heme is broken down to bilirubin in macrophages of the reticuloendothelial system, mainly in the liver and spleen.
2. Unconjugated bilirubin is transported to the liver bound to albumin and taken up by hepatocytes.
3. In hepatocytes, bilirubin is conjugated with glucuronic acid and secreted into bile.
4. In the intestines, bilirubin is converted to urobilinogen and a portion reabsorbed, becoming excreted in urine as urobilin, while the remainder is oxidized to st
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Edema is the accumulation of excessive body fluid in interstitial spaces or serous cavities due to diseases rather than being a disease itself. It can be classified based on its range (generalized vs local) or cause (renal, hepatic, cardiac, etc.). Edema develops due to an imbalance in fluid exchange between plasma and tissues or due to renal sodium and water retention. Causes include increased capillary pressure, decreased plasma proteins, obstructed lymphatics, increased capillary permeability, and renal issues. Edema fluid characteristics depend on capillary permeability and it can be pitting or recessive with distribution influenced by factors like gravity. Edema generally harms tissues but may help dilute toxins in
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1) Hemoglobin is broken down in red blood cells, producing bilirubin at a rate of approximately 250-350 mg per day.
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Heme is broken down through catabolism into bile pigments like bilirubin and biliverdin. This occurs mainly in the liver, spleen, and bone marrow. Heme is obtained from senescent red blood cells and other heme-containing proteins. It is degraded at a rate of 6 grams per day. Heme is broken down into biliverdin by heme oxygenase, and biliverdin is further converted to bilirubin. Bilirubin is taken up by the liver and conjugated with glucuronic acid before being secreted into bile or forming urobilins to be excreted in urine and feces. Normal plasma bilirubin levels are 0.2-0
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Jaundice, or yellowing of the skin and eyes, occurs when bilirubin levels are elevated. It is classified based on the type of bilirubin elevated (conjugated vs unconjugated) and the site of the underlying disease (prehepatic, hepatic, or posthepatic). Prehepatic jaundice results from excessive bilirubin production, hepatic jaundice can involve either conjugated or unconjugated bilirubin depending on the specific liver disease, and posthepatic jaundice occurs when conjugated bilirubin backs up due to biliary obstruction. Common causes are then outlined for each category.
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Arteriosclerosis and atherosclerosis are diseases that cause hardening and narrowing of arteries. Arteriosclerosis is thickening of arterial walls while atherosclerosis involves plaque buildup within artery walls from accumulation of lipids, calcium, and other substances. Major risk factors for atherosclerosis include age, smoking, diet, hypertension, diabetes, and stress. The formation of fatty streaks and plaques within artery walls can progress over decades and lead to complications when plaques rupture and form blood clots. Prevention focuses on lifestyle modifications like quitting smoking, regular exercise, healthy diet, weight control, and stress management.
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Diuretics are recommended as first-line therapy for hypertension. The document discusses various classes of diuretics including loop diuretics, thiazides, thiazide-like agents, and potassium sparing agents. It provides examples of drugs in each class, their mechanisms of action, and sites of action. The document summarizes evidence from clinical trials showing that thiazide diuretics like chlorthalidone are more effective than hydrochlorothiazide at reducing cardiovascular events in hypertension. Indapamide is discussed as an alternative to hydrochlorothiazide with similar efficacy and fewer metabolic side effects. Combinations of ACE inhibitors or calcium channel blockers with diuretics are also effective antihy
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Books referred: https://www.amazon.in/Biochemistry-2019-Satyanarayana-Satyanarayana-Author/dp/B07WGHCTKZ/ref=sr_1_1?dchild=1&qid=1592209115&refinements=p_27%3AU+Satyanarayana&s=books&sr=1-1
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This document discusses lactose intolerance, including its causes, symptoms, and diagnosis. Lactose intolerance is caused by a deficiency of the enzyme lactase, which breaks down lactose in the small intestine. Undigested lactose passes to the colon, where bacteria ferment it causing symptoms like bloating, diarrhea and nausea. The H2 breath test is an accurate way to diagnose lactose intolerance by measuring increased hydrogen levels in breath after ingesting lactose. Management involves taking lactase supplements, using lactose-reduced products, or limiting dairy.
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The document summarizes the catabolism of heme. Heme is degraded in reticuloendothelial cells of the liver, spleen, and bone marrow. It is broken down into biliverdin by heme oxygenase and then into bilirubin by biliverdin reductase. Bilirubin binds to albumin and is taken up by hepatocytes in the liver. In the liver, bilirubin is conjugated with glucuronic acid and excreted into bile. It is further broken down in the intestines into urobilinogen and stercobilinogen and excreted in urine and feces. Normal plasma bilirubin is 0.2-0.8
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Appendicitis is an inflammation of the appendix, a finger-shaped pouch that projects from your colon on the lower right side of your abdomen.
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The major points of heme catabolism and bilirubin metabolism are:
1. Heme is broken down to bilirubin in macrophages of the reticuloendothelial system, mainly in the liver and spleen.
2. Unconjugated bilirubin is transported to the liver bound to albumin and taken up by hepatocytes.
3. In hepatocytes, bilirubin is conjugated with glucuronic acid and secreted into bile.
4. In the intestines, bilirubin is converted to urobilinogen and a portion reabsorbed, becoming excreted in urine as urobilin, while the remainder is oxidized to st
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Edema is the accumulation of excessive body fluid in interstitial spaces or serous cavities due to diseases rather than being a disease itself. It can be classified based on its range (generalized vs local) or cause (renal, hepatic, cardiac, etc.). Edema develops due to an imbalance in fluid exchange between plasma and tissues or due to renal sodium and water retention. Causes include increased capillary pressure, decreased plasma proteins, obstructed lymphatics, increased capillary permeability, and renal issues. Edema fluid characteristics depend on capillary permeability and it can be pitting or recessive with distribution influenced by factors like gravity. Edema generally harms tissues but may help dilute toxins in
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Vasopressin, also known as anti diuretic hormone (ADH), is secreted by the hypothalamus and stored and released by the posterior pituitary gland. It acts to conserve water in the body by increasing the permeability of collecting tubules and ducts in the kidneys to water absorption. ADH also causes vasoconstriction which increases blood pressure. Its secretion is regulated by factors like sodium concentration, blood volume, and blood pressure in order to maintain fluid homeostasis. Disorders of ADH secretion can cause diabetes insipidus, characterized by excessive urine production and thirst.
Pathology of Peptic Ulcer
This document provides information about peptic ulcers, including their types, causes, symptoms, and treatment. It discusses the different types of peptic ulcers that can occur in the stomach, duodenum, and esophagus. The main causes of peptic ulcers are infection with Helicobacter pylori bacteria and use of non-steroidal anti-inflammatory drugs. Common symptoms include abdominal pain, nausea, vomiting, and weight loss. Treatment involves lifestyle changes, medications to reduce acid production or treat H. pylori, and sometimes surgery for complications.
Heme catabolism and jaundice
1) Hemoglobin is broken down in red blood cells, producing bilirubin at a rate of approximately 250-350 mg per day.
2) Bilirubin binds to albumin and is transported to the liver, where it is conjugated and secreted into bile ducts.
3) Jaundice occurs when there is excessive bilirubin that cannot be processed by the liver, resulting in a buildup that discolors the skin and eyes. It can be caused by hemolytic anemia, liver disease, or bile duct obstruction.
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The document provides information about the liver, including its functional anatomy, blood supply, bile secretion, and functions. Some key points:
- The liver is the largest exocrine gland, located in the upper right abdomen below the diaphragm. It has both secretory and excretory functions.
- The liver receives the majority of its blood supply from the hepatic portal vein and hepatic artery. It filters blood from the intestines through the enterohepatic circulation.
- Bile is secreted by hepatocytes and emptied into bile canaliculi. It is modified as it passes through ducts and is either released directly into the intestines or stored in the gallbladder.
- The liver
Peptic ulcer
Peptic ulcers are breaks in the stomach or duodenal lining caused by an imbalance between gastric acid and the mucosal defenses. Duodenal ulcers are more common than gastric ulcers and usually occur between ages 30-50 in men. Common symptoms include abdominal pain relieved by eating. Helicobacter pylori infection and NSAID use are major causes. Treatment involves antibiotics to eradicate H. pylori, acid suppressants, and lifestyle modifications to prevent recurrence and complications like bleeding.
Disorders of lipid metabolism
Lipid storage disorders are inherited metabolic disorders where harmful amounts of lipids accumulate in cells and tissues due to deficiencies or issues with lipid metabolizing enzymes. Over time, excess lipid storage can damage the brain, nerves, liver, spleen, and bone marrow. These disorders can be inherited autosomally recessively or x-linked recessively. Specific disorders discussed include cholelithiasis, obesity, fatty liver, and atherosclerosis.
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Precise guide for DGNM, B.Sc Nursing & M.Sc Nursing Students .. regarding Edema, and its management. Highly recommended for II B.Sc Nursing Students.
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Atherosclerosis is a condition where arteries become narrowed and hardened due to plaque buildup on their walls. It develops gradually over time due to risk factors like high blood pressure, high cholesterol, smoking, and family history. Early on, it causes no symptoms but can eventually lead to chest pain, leg pain, heart attack, or stroke depending on which arteries are affected. Treatment involves lifestyle changes like a healthy diet and exercise as well as medications to lower cholesterol and blood pressure. Surgery may be needed for severe cases.
Inflammation(mak) part 1
Inflammation is the protective response of tissues to harmful stimuli and involves the immune system, blood vessels, and proteins. It eliminates the initial injurious agent, damaged tissue, and initiates repair. Acute inflammation occurs rapidly and is short-lived, involving fluid accumulation and neutrophil migration. Chronic inflammation lasts longer with lymphocyte and macrophage involvement, scarring and vascular proliferation. The classical signs of inflammation are heat, redness, swelling and pain. Inflammation is normally a tightly regulated process but can cause harm if uncontrolled.
Catabolism of heme
Heme is broken down through catabolism into bile pigments like bilirubin and biliverdin. This occurs mainly in the liver, spleen, and bone marrow. Heme is obtained from senescent red blood cells and other heme-containing proteins. It is degraded at a rate of 6 grams per day. Heme is broken down into biliverdin by heme oxygenase, and biliverdin is further converted to bilirubin. Bilirubin is taken up by the liver and conjugated with glucuronic acid before being secreted into bile or forming urobilins to be excreted in urine and feces. Normal plasma bilirubin levels are 0.2-0
HEMOSTASIS & COAGULATION.pptx
Normal haemostasis involves platelet plug formation, coagulation cascade, and fibrin clot formation to stop bleeding at the site of vascular injury. It is regulated by the endothelium, platelets, and coagulation factors. The coagulation cascade can be initiated through the intrinsic or extrinsic pathway, both leading to thrombin generation and fibrin clot formation. Counter-regulatory mechanisms like fibrinolysis and natural anticoagulants limit clot formation to the site of injury. Laboratory tests monitor components of the coagulation cascade like platelet count and function, prothrombin time, activated partial thromboplastin time, and fibrinogen levels.
Jaundice (pathophysiology)
Jaundice, or yellowing of the skin and eyes, occurs when bilirubin levels are elevated. It is classified based on the type of bilirubin elevated (conjugated vs unconjugated) and the site of the underlying disease (prehepatic, hepatic, or posthepatic). Prehepatic jaundice results from excessive bilirubin production, hepatic jaundice can involve either conjugated or unconjugated bilirubin depending on the specific liver disease, and posthepatic jaundice occurs when conjugated bilirubin backs up due to biliary obstruction. Common causes are then outlined for each category.
Atherosclerosis
Arteriosclerosis and atherosclerosis are diseases that cause hardening and narrowing of arteries. Arteriosclerosis is thickening of arterial walls while atherosclerosis involves plaque buildup within artery walls from accumulation of lipids, calcium, and other substances. Major risk factors for atherosclerosis include age, smoking, diet, hypertension, diabetes, and stress. The formation of fatty streaks and plaques within artery walls can progress over decades and lead to complications when plaques rupture and form blood clots. Prevention focuses on lifestyle modifications like quitting smoking, regular exercise, healthy diet, weight control, and stress management.
Jaundice
Jaundice is a yellow discoloration caused by increased bilirubin in the blood, which is a sign of liver disease or damage. It can be caused by hepatocellular issues within the liver, hemolytic anemia where red blood cells are destroyed too quickly, or obstructive issues where the bile duct is blocked. Symptoms include yellow skin and eyes, light stool, dark urine, itching, and nausea. Diagnosis involves blood and imaging tests to determine the cause and severity. Treatment depends on the underlying condition but may include medications, fluids, blood transfusions, or procedures to clear the bile duct. Lifestyle changes like eating fruits and vegetables and avoiding risk factors can help prevent jaundice.
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DIURETICS PNA---PDF
This document discusses different classes of diuretic drugs, including their mechanisms of action and sites of action in the kidney. It covers carbonic anhydrase inhibitors which act in the proximal convoluted tubule, loop diuretics which act in the loop of Henle, thiazide diuretics which act in the distal convoluted tubule, and potassium-sparing diuretics which act in the cortical collecting duct. Adverse effects are discussed for each class. The key functions of the kidney in filtration, reabsorption and regulation of water and electrolytes are also summarized.
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Diuretics are recommended as first-line therapy for hypertension. The document discusses various classes of diuretics including loop diuretics, thiazides, thiazide-like agents, and potassium sparing agents. It provides examples of drugs in each class, their mechanisms of action, and sites of action. The document summarizes evidence from clinical trials showing that thiazide diuretics like chlorthalidone are more effective than hydrochlorothiazide at reducing cardiovascular events in hypertension. Indapamide is discussed as an alternative to hydrochlorothiazide with similar efficacy and fewer metabolic side effects. Combinations of ACE inhibitors or calcium channel blockers with diuretics are also effective antihy
Diuretics by P.Ravisankar
Introduction to diuretics.
Therapeutic approaches.
Normal physiology of urine formation.
Classification of drugs .
Mechanism of action of Acetazolamide.
Mechanism of action of Thiazides.
Mechanism of action of Loop diuretics.
Mechanism of action of potassium sparing diuretics &aldosterone antagonists.
Diuretics
This document discusses different classes of diuretic drugs, including their sites of action in the nephron, mechanisms of action, therapeutic uses, and side effects. It covers osmotic diuretics, carbonic anhydrase inhibitors, thiazide diuretics, loop diuretics, and potassium-sparing diuretics. The main points are that diuretics work by inhibiting transport in different parts of the nephron like the proximal tubule, loop of Henle, or distal convoluted tubule. They are used to treat conditions like edema, hypertension, and heart failure. Common side effects among the classes include electrolyte imbalances and metabolic alterations.
Diuretics
This document discusses different types of diuretic drugs, which cause increased urination by reducing sodium and water reabsorption in the kidneys. It describes carbonic anhydrase inhibitors which act in the proximal tubule; osmotic diuretics like glycerin and mannitol which act in the loop of Henle; high-ceiling diuretics like furosemide that inhibit sodium reabsorption in the thick ascending limb; thiazide diuretics which inhibit sodium-chloride symporters in the distal tubule; potassium-sparing diuretics like amiloride that inhibit sodium channels in the late distal tube and collecting duct; and mineralocorticoid receptor antagonists like
Diuretics & Their Mechanism.PPT
This document discusses the classification and mechanisms of different types of diuretic drugs. It describes high efficacy diuretics that inhibit sodium-potassium-chloride cotransport, medium efficacy diuretics that inhibit sodium-chloride symport like thiazide diuretics, and weak diuretics including carbonic anhydrase inhibitors, potassium sparing diuretics, and osmotic diuretics. It also covers the sites of action and transport mechanisms affected by these diuretic classes in different parts of the nephron like the thick ascending limb of Henle's loop and distal convoluted tubule.
Diuretics
Diuretics are chemicals that increase urine formation by increasing sodium and chloride ion excretion. There are several classes of diuretics that act at different sites along the nephron. Loop diuretics act in the ascending loop of Henle by inhibiting sodium-potassium-chloride transport. Thiazides act in the distal convoluted tubule by inhibiting sodium and chloride transport. Carbonic anhydrase inhibitors act in the proximal tubule by inhibiting the enzyme carbonic anhydrase. Potassium-sparing diuretics act in the collecting duct and do not promote potassium secretion. Osmotic diuretics act by increasing osmotic pressure in the proximal tubule and loop of Henle to prevent water
Diuretics
The document discusses different classes of diuretic drugs, including their mechanisms and effects. It describes loop diuretics like furosemide that inhibit sodium chloride reabsorption in the thick ascending limb of Henle's loop, increasing excretion of sodium and chloride in urine. It also discusses thiazide diuretics that act in the early distal tubule by inhibiting carbonic anhydrase and enhancing excretion of magnesium and potassium while inhibiting calcium and uric acid excretion. Finally, it mentions osmotic diuretics like mannitol that cause water retention in the proximal tubule through osmotic effects, resulting in water diuresis.
Diuretics
1) Diuretics are drugs that cause net loss of sodium and water in urine. They are classified as loop diuretics, thiazide diuretics, potassium-sparing diuretics, carbonic anhydrase inhibitors, and osmotic diuretics.
2) Loop diuretics like furosemide work by inhibiting sodium-potassium-chloride reabsorption in the loop of Henle, while thiazide diuretics inhibit sodium-chloride reabsorption in the distal tubule.
3) Diuretics are used to treat conditions like edema, hypertension, heart failure, nephrotic syndrome, and cerebral edema. Common side effects include
Class diuretics
This document provides information on diuretic drugs, including their mechanisms and sites of action, indications for use, and adverse effects. It discusses loop diuretics like furosemide and bumetanide that act in the thick ascending loop of Henle, thiazide diuretics like hydrochlorothiazide that act in the distal tubule, and potassium-sparing diuretics like amiloride and spironolactone that act in the collecting ducts. It also covers carbonic anhydrase inhibitors and osmotic diuretics. Non-diuretic uses and combinations with other drugs are mentioned. Resistance, interactions, and specific adverse effects are summarized for each drug class.
Diuretics by Dr. Sookun Rajeev Kumar M.D
Diuretics work by inhibiting reabsorption of sodium and water in the kidneys, increasing urine output. There are several types of diuretics that act in different parts of the kidney: loop diuretics act in the ascending limb of Henle's loop, thiazide diuretics act in the distal convoluted tubule, and potassium-sparing diuretics act in the cortical collecting tubule. Diuretics are used to treat conditions like heart failure, liver failure, renal failure, and hypertension by mobilizing edema fluid and maintaining urine volume. Common side effects include hypokalemia, hyperglycemia, and increased uric acid levels.
Diuretics : Dr Renuka Joshi MD,DNB, (FNB )
This document discusses different classes of diuretic drugs, including their mechanisms of action, examples, effects, dosages, and interactions. It covers loop diuretics like furosemide and bumetanide that act in the thick ascending loop of Henle; thiazide diuretics like hydrochlorothiazide that act in the distal convoluted tubule; and potassium-sparing diuretics like spironolactone and amiloride that act in the collecting duct. It provides recommendations for diuretic use and combinations in the treatment of heart failure and fluid overload.
Diuretics in CKD
Diuretics are commonly used to treat hypertension in patients with chronic kidney disease (CKD). The ALLHAT trial found thiazide-type diuretics were superior to other antihypertensives in preventing cardiovascular disease and were less expensive. In CKD, loop diuretics are recommended for patients with a GFR <30 mL/min, while thiazide diuretics can be used for those with a GFR ≥30 mL/min. Combination diuretic therapy may be needed to overcome diuretic resistance seen in CKD. Close monitoring is required due to risks of electrolyte abnormalities and dehydration.
CARBONIC ANHYDRASE INHIBITOR: DIURETICS ACT ON PCT(proximal convoluted tubule)
Diuretics are substances that promote urine production and are used to treat various medical conditions like heart failure, liver cirrhosis, high blood pressure, water poisoning, and certain kidney diseases. Some diuretics, such as acetazolamide, help make urine more alkaline and aid in excreting substances like aspirin in case of overdose by inhibiting carbonic anhydrase, decreasing hydrogen ion formation and sodium-hydrogen antiport in the kidney, increasing sodium and bicarbonate in the urine and promoting diuresis. Side effects may include acidosis, kidney stones, and drowsiness.
NurseReview.Org - Diuretics Updates (pharmacology worksheets)
Diuretic agents work by increasing urine output and sodium excretion. There are several classes of diuretics including carbonic anhydrase inhibitors, loop diuretics, osmotic diuretics, potassium-sparing diuretics, and thiazide diuretics. Nursing care involves monitoring for therapeutic and adverse effects such as hypokalemia, hypotension, and fluid imbalance.
Basic Pharmacology of Diuretics
The document discusses various classes of diuretic drugs, including their mechanisms of action, therapeutic uses, and adverse effects. It focuses on loop diuretics, which act on the thick ascending limb of the loop of Henle to inhibit sodium and chloride reabsorption, resulting in increased urinary excretion of sodium, chloride, potassium, magnesium, and calcium. Loop diuretics are potent and commonly used to treat edema associated with congestive heart failure or liver/kidney disease but can cause electrolyte imbalances and other adverse effects if not carefully monitored.
Diuretics
Diuretics
Pharmacology
Katzung
Abnormalities in fluid volume and electrolyte composition are common and important clinical disorders. Drugs that block specific transport functions of the renal tubules are valuable clinical tools in the treatment of these disorders. Although various agents that increase urine volume (diuretics) have been described since antiquity, it was not until 1937 that carbonic anhydrase inhibitors were first described and not until 1957 that a much more useful and powerful diuretic agent (chlorothiazide) became available. Technically, a “diuretic” is an agent that increases urine volume, whereas a “natriuretic” causes an increase in renal sodium excretion and an “aquaretic” increases excretion of solute-free water. Because natriuretics almost always also increase water excretion, they are usually called diuretics. Osmotic diuretics and antidiuretic hormone antagonists (see Agents That Alter Water Excretion) are aquaretics that are not directly natriuretic.
Diuretics2
Loop diuretics, thiazides, and other diuretic classes are summarized. Loop diuretics act in the thick ascending limb of Henle's loop by inhibiting the Na-K-2Cl transporter. Thiazides act in the distal convoluted tubule by blocking coupled Na and Cl reabsorption. Carbonic anhydrase inhibitors inhibit bicarbonate absorption in the proximal tubule. Osmotic diuretics like mannitol are filtered but not reabsorbed, drawing water out of cells. Potassium-sparing diuretics like amiloride act late in the distal nephron to inhibit Na reabsorption. Diuretic combinations can have synergistic effects.
Diuretics
A diuretic is a chemical that increases urine production by inhibiting sodium reabsorption in the nephron at four major sites. The primary sites are the proximal tubule, thick ascending limb of Henle's loop, distal convoluted tubule, and connecting tubule/cortical collecting tubule. Diuretics work by blocking sodium transport mechanisms like cotransporters at these sites, causing increased excretion of sodium and water. The specific transport mechanisms and diuretic drug targets vary between nephron segments.
Diuretics
This document provides information on loop diuretics and potassium sparing diuretics. It begins with an overview of normal urine formation and sites of renal reabsorption. It then classifies diuretics and discusses the mechanisms and sites of action of loop diuretics like furosemide and torsemide as well as potassium sparing diuretics like spironolactone and amiloride. It notes their therapeutic uses, interactions, and resistance. In recent years, new loop diuretic compounds like CRE 10904 have been developed.
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Diuretics in hypertension 2015 by Dr Abhishek Rathore
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CARBONIC ANHYDRASE INHIBITOR: DIURETICS ACT ON PCT(proximal convoluted tubule)
CARBONIC ANHYDRASE INHIBITOR: DIURETICS ACT ON PCT(proximal convoluted tubule)
NurseReview.Org - Diuretics Updates (pharmacology worksheets)
NurseReview.Org - Diuretics Updates (pharmacology worksheets)
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Diuresis diuretics
- 1. Read about the ‘ Factors that regulate Aldosterone secretion’ Please READ * Chapter 38 in Ganong * relevant sections in Chapter 14 Chapter 20 Chapter 24 Chapter 39
- 2. Diuresis – Markedly increased output of urine volume Diuretics – Substances that increase the rate of urine volume output Most ‘diuretics’ also increase urinary excretion of electrolytes.