This document summarizes information about allopurinol, a medication used to treat gout. It discusses how allopurinol works by inhibiting the enzyme xanthine oxidase, which is involved in the production of uric acid in the body. Common uses and side effects of allopurinol are described, as well as monitoring requirements and cautions when taking it. The mechanism of action and uses of indomethacin, a nonsteroidal anti-inflammatory drug, and probenecid, a uricosuric medication, are also briefly covered.
This document discusses drugs used to treat gout, including colchicine, NSAIDs, corticosteroids, uricosuric agents like probenecid and sulfinpyrazone, and the uric acid synthesis inhibitor allopurinol. It provides details on the pathophysiology of gout, mechanisms of action, pharmacokinetics, indications, dosages and adverse effects of these drugs for both acute gout attacks and long-term treatment of chronic gout and hyperuricemia.
This document discusses the pathophysiology, treatment, and pharmacology of gout. It covers the following key points:
1) Gout is caused by the buildup of uric acid crystals in the joints due to high levels of uric acid in the blood. It discusses the biochemical pathway involved in uric acid production.
2) Treatment involves managing acute gout attacks with NSAIDs or colchicine, and lowering uric acid levels long-term with xanthine oxidase inhibitors like allopurinol and febuxostat, or uricosuric drugs like probenecid.
3) Colchicine provides rapid relief of gout attacks but has gastrointestinal side
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This document discusses the pathophysiology and treatment of gout. It notes that gout results from urate crystal precipitation due to hyperuricemia. Treatment involves decreasing acute attack symptoms with NSAIDs, colchicine or glucocorticoids. Chronic treatment aims to lower urate levels using uricosuric drugs like probenecid or allopurinol which inhibits urate synthesis. Newer drugs like febuxostat, pegloticase and canakinumab that target different urate pathways are also discussed for treating refractory cases. The document provides details on the mechanisms, uses, interactions and side effects of these pharmaceutical agents for gout management.
Dr. Faraz Farishta is a consultant endocrinologist and president of the Diabetes Awareness Foundation. The document discusses hyperuricemia (high levels of uric acid in the blood) and its treatment. It notes that hyperuricemia can be caused by increased uric acid production or decreased excretion. Febuxostat is introduced as a selective xanthine oxidase inhibitor drug that is more effective than allopurinol at lowering uric acid levels. It has advantages over allopurinol such as being safer for use in patients with renal impairment and not requiring dose adjustment in mild to moderate cases.
Dr. Faraz Farishta is a consultant endocrinologist and president of the Diabetes Awareness Foundation. The document discusses hyperuricemia (high levels of uric acid in the blood) and its treatment. It describes that uric acid is produced from the breakdown of purine compounds and excreted primarily by the kidneys. Hyperuricemia can be caused by increased uric acid production or decreased excretion and is a risk factor for gout. The document evaluates treatments for hyperuricemia including medications like allopurinol and febuxostat, a newer xanthine oxidase inhibitor. It finds that febuxostat more effectively lowers uric acid levels and is
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Uric acid is produced when the body breaks down purines. Febuxostat is a new drug for treating hyperuricemia and gout that works by selectively inhibiting the enzyme xanthine oxidase, unlike allopurinol which non-selectively inhibits several enzymes. Febuxostat has been shown to effectively lower uric acid levels at recommended doses without needing dose adjustments for mild to moderate kidney or liver dysfunction, as opposed to allopurinol which requires dosage adjustments for renal impairment. Management of gout focuses on long-term urate-lowering therapy to maintain uric acid levels below target thresholds to prevent further crystal formation and promote crystal dissolution.
1) Peptic ulcers are caused by an imbalance between aggressive factors like gastric acid and protective factors in the stomach and duodenum.
2) Anti-ulcer drugs work by decreasing gastric acid secretion, enhancing mucosal protection, or eradicating the H. pylori bacteria responsible for many ulcers.
3) Common classes of anti-ulcer medications include H2 receptor antagonists, proton pump inhibitors, antacids, and anti-H. pylori drugs. H2 receptor antagonists and proton pump inhibitors reduce acid by blocking histamine and the proton pump, while antacids neutralize existing acid.
Allopurinol and febuxostat are uric acid synthesis inhibitors used to treat chronic gout and hyperuricaemia. Allopurinol inhibits the enzyme xanthine oxidase to decrease uric acid production, while febuxostat selectively inhibits xanthine oxidase. Both drugs aim to lower uric acid levels in the blood long-term to prevent recurrent gout attacks. Common side effects include nausea, abdominal pain, liver enzyme elevations, and allergic reactions. Drug interactions can occur when taken with other medications that are metabolized by the liver or kidneys.
This document discusses the pharmacotherapy of peptic ulcers. It begins by classifying the main drugs used: 1) those that inhibit gastric acid secretion like H2 blockers and proton pump inhibitors, 2) antacids that neutralize acid, 3) ulcer protectives like sucralfate, and 4) anti-H. pylori drugs for eradication. It then goes into detail about the mechanisms, uses, and side effects of the major drug classes. H2 blockers competitively block H2 receptors to suppress acid secretion. Proton pump inhibitors irreversibly inactivate the H+/K+ ATPase pump for prolonged acid inhibition. Antacids chemically neutralize acid. Sucralfate
The all the content in this profile is completed by the teachers, students as well as other health care peoples.
thank you, all the respected peoples, for giving the information to complete this presentation.
this information is free to use by anyone.
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This document discusses drugs used for acid peptic disease. It begins by introducing acid peptic disorders and describing the imbalance between aggressive and defensive factors in the gastrointestinal tract that can lead to conditions like peptic ulcers. The document then examines the pathogenesis of these conditions and various drug therapies used to enhance defensive factors or eliminate aggressive ones. It provides detailed descriptions of different drug classes, including H2 receptor antagonists, proton pump inhibitors, anticholinergics, prostaglandin agonists, mucosal protective agents, and ulcer healing drugs. For each class, it discusses mechanisms of action, pharmacokinetics, clinical uses, and adverse effects.
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Presentation on Antacids and antiulcer drugs. Introduction to ulcers, classification of antiulcer drugs, their pharmacological actions, uses and adverse effects.
Peptic ulcers are open sores that develop on the inside lining of esophagus, stomach and/or the upper portion of small intestine. Peptic ulcer occur mainly due to imbalance between aggressive and defensive factors in the stomach.
This document discusses drugs used to treat peptic ulcers and gastroesophageal reflux disease (GERD). It begins by defining peptic ulcers and their causes, including an imbalance between aggressive and defensive factors in the gastrointestinal tract. It then covers the different types of ulcers and regulators of gastric acid secretion. The document categorizes and describes the mechanisms and uses of several classes of drugs: H2 antagonists like cimetidine and ranitidine; proton pump inhibitors like omeprazole; prostaglandin analogues like misoprostol; antacids; and anti-H. pylori drugs. It discusses the interactions, adverse effects, and treatment of peptic ulcers, G
This document discusses gout (monosodium urate arthropathy). It begins by defining gout as a disorder of purine metabolism seen in middle-aged males and post-menopausal women that results from hyperuricemia and deposition of monosodium urate crystals in joints. It then covers the pathophysiology of purine metabolism and uric acid production, classification of primary and secondary gout, clinical features including podagra, and diagnostic tests including synovial fluid analysis. It concludes by outlining treatment approaches for acute gout attacks and chronic gout prevention including NSAIDs, colchicine, corticosteroids, allopurinol, febuxostat, probenecid,
This document summarizes anti-ulcer drugs. It discusses the causes of ulcers including H. pylori infections and NSAID use. The main types of ulcers are described along with signs and symptoms. Treatment includes eradicating H. pylori, decreasing acid secretion through proton pump inhibitors or H2 receptor blockers, and protecting the stomach lining with drugs like misoprostol or sucralfate. Proton pump inhibitors are now the most potent way to decrease acid production and promote ulcer healing.
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2) Anti-ulcer drugs work by decreasing gastric acid secretion, enhancing mucosal protection, or eradicating the H. pylori bacteria responsible for many ulcers.
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Allopurinol and febuxostat are uric acid synthesis inhibitors used to treat chronic gout and hyperuricaemia. Allopurinol inhibits the enzyme xanthine oxidase to decrease uric acid production, while febuxostat selectively inhibits xanthine oxidase. Both drugs aim to lower uric acid levels in the blood long-term to prevent recurrent gout attacks. Common side effects include nausea, abdominal pain, liver enzyme elevations, and allergic reactions. Drug interactions can occur when taken with other medications that are metabolized by the liver or kidneys.
This document discusses the pharmacotherapy of peptic ulcers. It begins by classifying the main drugs used: 1) those that inhibit gastric acid secretion like H2 blockers and proton pump inhibitors, 2) antacids that neutralize acid, 3) ulcer protectives like sucralfate, and 4) anti-H. pylori drugs for eradication. It then goes into detail about the mechanisms, uses, and side effects of the major drug classes. H2 blockers competitively block H2 receptors to suppress acid secretion. Proton pump inhibitors irreversibly inactivate the H+/K+ ATPase pump for prolonged acid inhibition. Antacids chemically neutralize acid. Sucralfate
The all the content in this profile is completed by the teachers, students as well as other health care peoples.
thank you, all the respected peoples, for giving the information to complete this presentation.
this information is free to use by anyone.
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This document discusses drugs that affect the gastrointestinal system. It covers drugs that affect salivary secretion like gentian and nux vomica. It also discusses emetics that induce vomiting like ipecacuanha and apomorphine, as well as anti-emetics that prevent vomiting. Finally, it discusses drugs that affect appetite by stimulating or suppressing centers in the hypothalamus, including benzodiazepines, cyproheptadine, and glucocorticoids as appetite stimulants.
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1. Uric acid synthesis inhibitors
ALLOPURINOL
Presented By :
Lalith kumar.R
B.pharm,5-th sem
2. Definition :
Uric acid synthesis
inhibitors
Uric acid synthesis inhibitors are medications that
reduce the production of uric acid in the body by
inhibiting the enzyme xanthine oxidase.
1. Xanthine Oxidase
Inhibitors:
1. ALLOPURINOL 2. FEBUXOSTAT
Classification
:
2. Uricosuric
Agents:
1. PROBENECID 2. SULFINPYRAZONE
3. Allopurinol :
Definition
:
Allopurinol is a medication that belongs to the
class of xanthine oxidase inhibitors. It is
primarily used to manage hyperuricemia
associated with gout and certain types of kidney
stones.
5. Mechanism of
Action :
• Allopurinol works by inhibiting the enzyme
xanthine oxidase, which decreases the
production of uric acid from purines. As a
result, it lowers serum uric acid levels,
reducing the risk of gout flares and related
complications.
6. Pharmacokinetics
:
Absorption : Well absorbed from the GI tract.
Distribution : Found in body tissues like liver and kidneys.
Metabolism : Converted to oxypurinol in the liver.
Excretion : Primarily via kidneys; dosage adjustment needed
in renal impairment.
7. Dosage
:
Initial: 100 mg to 300 mg once daily.
Maintenance: Adjust based on serum uric acid levels; max 800
mg/day.
Renal Impairment: Dose adjustment required.
9. Adverse Drug Reactions
(ADRs) :
Skin Reactions: Rash (risk of severe conditions).
GI Issues: Nausea, vomiting, diarrhea.
Hematological Effects: Rare bone marrow
suppression.
Allergic Reactions: Hypersensitivity.
10. Uses
:
Gout Management: Treatment and prevention of flares.
Hyperuricemia: In chronic kidney disease.
Tumor Lysis Syndrome: Prevention of hyperuricemia
during chemotherapy.