This document discusses drugs used to treat peptic ulcer. It categorizes the drugs into three groups: 1) drugs affecting gastric acid like antacids, H2 blockers, and proton pump inhibitors, 2) mucosal protective agents like sucralfate, and 3) drugs that eradicate H. pylori like triple therapy and quadruple therapy. It provides details on the pharmacokinetics, mechanisms of action, uses, and side effects of representative drugs in each category. The document explains that peptic ulcer is caused by an imbalance between protective and damaging factors in the stomach and duodenum.
This document summarizes various drugs used to treat peptic ulcers caused by excess stomach acid and Helicobacter pylori infection. It discusses histamine antagonists like cimetidine that block acid production. Proton pump inhibitors like omeprazole irreversibly block the acid pump. Sucralfate forms a protective barrier over ulcers. Antibiotics can eliminate H. pylori infections. Lifestyle changes and antacids are also mentioned.
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
This document discusses pharmacotherapy for peptic ulcer disease. It outlines the physiology of gastric acid secretion stimulated by various phases. Peptic ulcer disease is defined as an erosion of the gastrointestinal tract exposed to acid and pepsin. Causes include Helicobacter pylori, NSAIDs, alcohol, stress, and steroids. Therapies aim to enhance defenses or eliminate aggressive factors like H. pylori. Drug classes discussed are antacids, H2 receptor antagonists, prostaglandin analogues, and antibiotics for H. pylori.
The document discusses non-steroidal anti-inflammatory drugs (NSAIDs). It covers their classification, mechanisms of action, uses, and adverse effects. NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes and subsequent prostaglandin production. They are effective for pain, fever, and inflammation but can cause gastrointestinal, renal, hepatic, and bleeding side effects. The document focuses on specific NSAIDs including aspirin, ibuprofen, indomethacin, and mephenamic acid, outlining their pharmacology, dosing, and indications.
This document discusses drugs used to treat peptic ulcers and gastroesophageal reflux disease (GERD). It describes the mechanisms and uses of various classes of drugs including antacids, H2 receptor antagonists, proton pump inhibitors, mucosal protective drugs, and anti-Helicobacter pylori drugs. The main goals of antiulcer therapy are relief from pain, promotion of ulcer healing, prevention of complications and relapse. Proton pump inhibitors are now the most widely used drugs for peptic ulcers due to their strong acid suppression and excellent safety profile. Eradication of H. pylori infection is also important for ulcer treatment and prevention.
Peptic ulcers form in the esophagus, stomach, or duodenum due to excessive acid secretions, breakdown of mucosal protection, or H. pylori infection. Acid is secreted via vagus nerve stimulation or gastric distention stimulating gastrin and histamine release. Drugs to treat ulcers include antacids to reduce acidity, H2 blockers to inhibit histamine, and PPIs to further reduce acid secretion. Ulcer protection drugs form a protective lining, while combinations of omeprazole, clarithromycin, amoxicillin, or metronidazole are used to treat H. pylori infections.
This document discusses emetics, which induce vomiting, and antiemetics, which prevent vomiting. It describes the physiology of vomiting including the vomiting center and chemoreceptor trigger zone in the brain. It explains the mechanisms and sites of action of various classes of antiemetic drugs including antihistamines, 5-HT3 receptor antagonists, dopamine antagonists, cannabinoids, glucocorticoids, and others. It provides details on specific antiemetic drugs like metoclopramide, ondansetron, dexamethasone, and their indications, mechanisms, pharmacokinetics and adverse effects.
This document discusses anti-spasmodic drugs, which are smooth muscle relaxants used to prevent spasms in the gastrointestinal tract and urinary bladder. It describes two types - anticholinergics/antimuscarinics which block acetylcholine receptors, and non-anticholinergic smooth muscle relaxants. Specific drugs discussed include hyoscine butylbromide, dicyclomine, and drotaverine. These drugs are used to treat conditions involving smooth muscle spasms like irritable bowel syndrome, abdominal pain, and urinary incontinence. Their mechanisms of action and side effect profiles are also outlined.
This document summarizes various drugs used to treat peptic ulcers caused by excess stomach acid and Helicobacter pylori infection. It discusses histamine antagonists like cimetidine that block acid production. Proton pump inhibitors like omeprazole irreversibly block the acid pump. Sucralfate forms a protective barrier over ulcers. Antibiotics can eliminate H. pylori infections. Lifestyle changes and antacids are also mentioned.
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
This document discusses pharmacotherapy for peptic ulcer disease. It outlines the physiology of gastric acid secretion stimulated by various phases. Peptic ulcer disease is defined as an erosion of the gastrointestinal tract exposed to acid and pepsin. Causes include Helicobacter pylori, NSAIDs, alcohol, stress, and steroids. Therapies aim to enhance defenses or eliminate aggressive factors like H. pylori. Drug classes discussed are antacids, H2 receptor antagonists, prostaglandin analogues, and antibiotics for H. pylori.
The document discusses non-steroidal anti-inflammatory drugs (NSAIDs). It covers their classification, mechanisms of action, uses, and adverse effects. NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes and subsequent prostaglandin production. They are effective for pain, fever, and inflammation but can cause gastrointestinal, renal, hepatic, and bleeding side effects. The document focuses on specific NSAIDs including aspirin, ibuprofen, indomethacin, and mephenamic acid, outlining their pharmacology, dosing, and indications.
This document discusses drugs used to treat peptic ulcers and gastroesophageal reflux disease (GERD). It describes the mechanisms and uses of various classes of drugs including antacids, H2 receptor antagonists, proton pump inhibitors, mucosal protective drugs, and anti-Helicobacter pylori drugs. The main goals of antiulcer therapy are relief from pain, promotion of ulcer healing, prevention of complications and relapse. Proton pump inhibitors are now the most widely used drugs for peptic ulcers due to their strong acid suppression and excellent safety profile. Eradication of H. pylori infection is also important for ulcer treatment and prevention.
Peptic ulcers form in the esophagus, stomach, or duodenum due to excessive acid secretions, breakdown of mucosal protection, or H. pylori infection. Acid is secreted via vagus nerve stimulation or gastric distention stimulating gastrin and histamine release. Drugs to treat ulcers include antacids to reduce acidity, H2 blockers to inhibit histamine, and PPIs to further reduce acid secretion. Ulcer protection drugs form a protective lining, while combinations of omeprazole, clarithromycin, amoxicillin, or metronidazole are used to treat H. pylori infections.
This document discusses emetics, which induce vomiting, and antiemetics, which prevent vomiting. It describes the physiology of vomiting including the vomiting center and chemoreceptor trigger zone in the brain. It explains the mechanisms and sites of action of various classes of antiemetic drugs including antihistamines, 5-HT3 receptor antagonists, dopamine antagonists, cannabinoids, glucocorticoids, and others. It provides details on specific antiemetic drugs like metoclopramide, ondansetron, dexamethasone, and their indications, mechanisms, pharmacokinetics and adverse effects.
This document discusses anti-spasmodic drugs, which are smooth muscle relaxants used to prevent spasms in the gastrointestinal tract and urinary bladder. It describes two types - anticholinergics/antimuscarinics which block acetylcholine receptors, and non-anticholinergic smooth muscle relaxants. Specific drugs discussed include hyoscine butylbromide, dicyclomine, and drotaverine. These drugs are used to treat conditions involving smooth muscle spasms like irritable bowel syndrome, abdominal pain, and urinary incontinence. Their mechanisms of action and side effect profiles are also outlined.
This document discusses drugs used to treat gout. It begins by classifying the objectives and associated drugs for treating gout, including relieving inflammation/pain with NSAIDs and colchicine, and preventing attacks by inhibiting uric acid formation with allopurinol and febuxostat or augmenting excretion with probenecid. It then provides details on the mechanisms, pharmacokinetics, indications, interactions and adverse effects of various drugs including colchicine, probenecid, allopurinol, febuxostat, NSAIDs and corticosteroids. It concludes by recommending NSAIDs as first line for acute gout and allopurinol as first line for chronic g
This document discusses macrolide antibiotics. It begins by introducing macrolides as a class of antibiotics characterized by a macrocyclic lactone ring to which sugars are attached. It then focuses on individual macrolides including erythromycin, clarithromycin, azithromycin, roxithromycin, and spiramycin. The document discusses the mechanism of action, spectrum of activity, resistance, pharmacokinetics, uses, interactions, and adverse effects of macrolide antibiotics.
Centrally acting skeletal muscle relaxants such as baclofen, tizanidine and diazepam decrease muscle tone by acting in the central nervous system without affecting motor function. They selectively depress polysynaptic reflexes involved in muscle tone regulation. Peripherally acting neuromuscular blockers like succinylcholine and tubocurarine act at the neuromuscular junction, competing for acetylcholine receptors to cause paralysis. Succinylcholine is used for short procedures due to its rapid onset and offset of action but can cause prolonged apnea in some patients due to abnormal pseudocholinesterase metabolism. Dantrolene acts directly on the muscle to inhibit calcium release and contraction.
This document discusses drugs that act on the digestive system, specifically those used to treat conditions related to acid production and motility in the gastrointestinal tract. It covers antacids, H2 receptor blockers, and proton pump inhibitors which are used to reduce acid in conditions like GERD and peptic ulcers. It also discusses laxatives and antidiarrheal drugs used to treat constipation and diarrhea respectively. Finally, it outlines the pathways of vomiting and the sites of action of various antiemetic drugs like antihistamines, anticholinergics, and serotonin blockers.
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.
Peptic ulcers are caused by a loss of gastric or duodenal mucosa leading to ulcer formation. Drugs used to treat peptic ulcers work by reducing acid secretion, neutralizing acid, protecting the ulcer, or eradicating Helicobacter pylori infection. Common classes of drugs include H2 receptor antagonists, proton pump inhibitors, antacids, sucralfate, bismuth subcitrate, and multi-drug regimens for H. pylori. The document provides details on the mechanisms, uses, and side effects of these various drug classes.
Anti-spasmodic drugs are used to treat symptoms of irritable bowel syndrome like pain and spasms. There are two main classes - antimuscarinic drugs which block cholinergic transmission and relax smooth muscle, and direct smooth muscle relaxants like mebeverine which directly affect colonic muscle activity. These drugs work by reducing contractions of the intestines which helps relieve IBS symptoms like pain and bloating. Common anti-spasmodics discussed include hyoscine butylbromide, dicyclomine, and drotaverine.
NSAIDs are a group of drugs that relieve pain, fever, and inflammation by inhibiting prostaglandin synthesis. They can be classified based on their action on COX enzymes or their chemical structure. Their mechanism of action involves blocking COX pathways to prevent the formation of prostaglandins. Common adverse effects include gastric irritation and impaired healing. NSAIDs should be used cautiously in patients with conditions like peptic ulcer or impaired kidney function.
Drug acting on inflammatory bowel diseaseAlisha Talwar
This document discusses drugs used to treat inflammatory bowel disease (IBD). It describes several classes of drugs including 5-aminosalicylic acid (mesalamine), corticosteroids, immunomodulating drugs like azathioprine and mercaptopurine, and biologic agents. For each drug class or individual drug, it provides information on mechanism of action, indications, contraindications, dosing, side effects, and nursing considerations. The document aims to comprehensively cover the pharmacological management of IBD.
Pharmacology of Gastrointestinal Disorders dineshmeena53
This power point presentation will be helpful for Pharmacy, Medical and paramedical students. it consists of" what are the common GIT disorders and their pharmacological management "
H2-receptor antagonists like cimetidine, ranitidine, famotidine, and nizatidine are rapidly absorbed from the intestine and undergo hepatic metabolism, reducing their bioavailability. They exhibit competitive inhibition at the H2 receptor on parietal cells, suppressing both basal and meal-stimulated acid secretion in a dose-dependent manner. H2 antagonists are effective for conditions like GERD, peptic ulcer disease, and stress-related bleeding by increasing gastric pH and inhibiting acid secretion. However, they can cause adverse effects like diarrhea, headaches, and drug interactions by inhibiting hepatic cytochrome P450 pathways.
Classification
Mechanism of action
Duration of action
Absorption and distribution
Mode of action
Theories of action of L.A
Pharmacokinetics of local anaesthetics
Routes of administration
Metabolism or biotransformation
Individual agents
Vasoconstrictors
Systemic effects
Toxicity
Advantages
Disadvantages
Maximum allowable dose
Local anaesthetics in community trust services
This document discusses the pharmacotherapy of peptic ulcer disease. It begins by describing the physiology of gastric acid secretion and the factors that regulate it. It then discusses peptic ulcer disease itself, including its epidemiology, symptoms, and pathophysiology. The main part of the document covers the various drugs used to treat peptic ulcers, including proton pump inhibitors, H2 receptor antagonists, prostaglandin analogues, anticholinergics, antacids, and ulcer protectives. It also discusses antimicrobial drugs for H. pylori eradication, commonly used combination therapies, and treatments for resistant H. pylori infections.
Prokinetics are the type of drugs which enhances gastrointestinal motility/transit by
increasing the frequency or strength of contractions.
They speed up gastric emptying by enhancing coordinated propulsive motility.
Treat Gastrointestinal symptoms : Abdominal discomfort, Bloating, constipation,
Heart burn, nausea and vomiting. And few gastrointestinal disorders : irritable bowel
Syndrome, gastritis, gastroparesis and functional dyspepsia.
Increases gastric emptying
Relief of gastric stasis
Decreases reflux esophagitis/heart burn
Decreases regurgitation of gastric contents& emesis
This document discusses the causes, treatment, and management of diarrhea. It begins by defining diarrhea as three or more loose stools in a 24 hour period. The causes of diarrhea include osmotic, secretory, motility issues, altered morphology, allergies, drugs, and certain cancers. Treatment involves rehydration either orally or intravenously. Oral rehydration solutions contain sodium, potassium, citrate, and glucose. Antimicrobial therapy may be used for certain infectious causes. Probiotics can help with antibiotic-associated diarrhea. Management of inflammatory bowel disease is also discussed.
Emetics and antiemetics are used to induce or prevent vomiting. Emetics work centrally in the medulla, peripherally in the stomach, or both. Common emetics include apomorphine, mustard, and ipecacuanha. Antiemetics have various mechanisms of action and include anticholinergics, antihistamines, neuroleptics, prokinetic drugs, 5-HT3 antagonists, and adjuvant medications. Common antiemetics are hyoscine, promethazine, metoclopramide, ondansetron, and corticosteroids. These drugs are used to treat nausea and vomiting from different causes like motion sickness, chemotherapy,
This document discusses drugs used to treat peptic ulcers. It begins by outlining common indications for treatment and classifying drugs into those that inhibit acid secretion, neutralize acid, protect ulcers, and treat H. pylori infections. Key drugs discussed include H2 receptor blockers like cimetidine and ranitidine, proton pump inhibitors like omeprazole and pantoprazole, antacids, and combinations used to eradicate H. pylori. Nursing responsibilities are identified like administering antacids appropriately and avoiding drug interactions.
The document discusses drugs used to treat peptic ulcers, gastroesophageal reflux disease, diarrhea, and constipation. It describes the causes of peptic ulcers including H. pylori infection and NSAID use. Treatment involves eradicating H. pylori, reducing gastric acid with H2 blockers or proton pump inhibitors, and protecting the gastric mucosa. Various classes of drugs are covered that act on these mechanisms including antimicrobials, H2 blockers, proton pump inhibitors, prostaglandins, and antacids.
1) The document discusses drugs used in the treatment of constipation, including laxatives, which are classified based on their mechanism and intensity of action.
2) Bulk forming agents like fiber, psyllium, and methylcellulose work by absorbing water in the intestines and forming a gel, which softens stool and increases stool mass. Stool softeners like docusates and liquid paraffin work by a detergent action that softens stool.
3) Stimulant purgatives like bisacodyl and senna irritate the intestinal mucosa, increasing motility and fluid accumulation in the intestines. They have more potent effects than bulk formers or softeners.
This document discusses peptic ulcers. It defines peptic ulcers as breaks in the gastrointestinal mucosa exposed to acid and pepsin. The pathophysiology involves an imbalance between defensive and aggressive factors on the gastroduodenal mucosa. Common causes of ulcers include Helicobacter pylori infection, NSAIDs, smoking, alcohol, and acid hypersecretion. Management involves lifestyle modifications, medications to reduce acid secretion, antibiotics to treat H. pylori, and surgery for complications or treatment failures.
The document discusses peptic ulcers, which are sores in the lining of the stomach or duodenum caused by an imbalance between defensive and damaging factors. Key points include: Helicobacter pylori bacteria and NSAIDs are major causes of ulcers. Symptoms include abdominal pain relieved by food or antacids. Complications can include bleeding, perforation, or obstruction if not treated. Treatment involves antibiotics to eliminate H. pylori, acid reducers to promote healing, and lifestyle changes like quitting smoking.
This document discusses drugs used to treat gout. It begins by classifying the objectives and associated drugs for treating gout, including relieving inflammation/pain with NSAIDs and colchicine, and preventing attacks by inhibiting uric acid formation with allopurinol and febuxostat or augmenting excretion with probenecid. It then provides details on the mechanisms, pharmacokinetics, indications, interactions and adverse effects of various drugs including colchicine, probenecid, allopurinol, febuxostat, NSAIDs and corticosteroids. It concludes by recommending NSAIDs as first line for acute gout and allopurinol as first line for chronic g
This document discusses macrolide antibiotics. It begins by introducing macrolides as a class of antibiotics characterized by a macrocyclic lactone ring to which sugars are attached. It then focuses on individual macrolides including erythromycin, clarithromycin, azithromycin, roxithromycin, and spiramycin. The document discusses the mechanism of action, spectrum of activity, resistance, pharmacokinetics, uses, interactions, and adverse effects of macrolide antibiotics.
Centrally acting skeletal muscle relaxants such as baclofen, tizanidine and diazepam decrease muscle tone by acting in the central nervous system without affecting motor function. They selectively depress polysynaptic reflexes involved in muscle tone regulation. Peripherally acting neuromuscular blockers like succinylcholine and tubocurarine act at the neuromuscular junction, competing for acetylcholine receptors to cause paralysis. Succinylcholine is used for short procedures due to its rapid onset and offset of action but can cause prolonged apnea in some patients due to abnormal pseudocholinesterase metabolism. Dantrolene acts directly on the muscle to inhibit calcium release and contraction.
This document discusses drugs that act on the digestive system, specifically those used to treat conditions related to acid production and motility in the gastrointestinal tract. It covers antacids, H2 receptor blockers, and proton pump inhibitors which are used to reduce acid in conditions like GERD and peptic ulcers. It also discusses laxatives and antidiarrheal drugs used to treat constipation and diarrhea respectively. Finally, it outlines the pathways of vomiting and the sites of action of various antiemetic drugs like antihistamines, anticholinergics, and serotonin blockers.
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.
Peptic ulcers are caused by a loss of gastric or duodenal mucosa leading to ulcer formation. Drugs used to treat peptic ulcers work by reducing acid secretion, neutralizing acid, protecting the ulcer, or eradicating Helicobacter pylori infection. Common classes of drugs include H2 receptor antagonists, proton pump inhibitors, antacids, sucralfate, bismuth subcitrate, and multi-drug regimens for H. pylori. The document provides details on the mechanisms, uses, and side effects of these various drug classes.
Anti-spasmodic drugs are used to treat symptoms of irritable bowel syndrome like pain and spasms. There are two main classes - antimuscarinic drugs which block cholinergic transmission and relax smooth muscle, and direct smooth muscle relaxants like mebeverine which directly affect colonic muscle activity. These drugs work by reducing contractions of the intestines which helps relieve IBS symptoms like pain and bloating. Common anti-spasmodics discussed include hyoscine butylbromide, dicyclomine, and drotaverine.
NSAIDs are a group of drugs that relieve pain, fever, and inflammation by inhibiting prostaglandin synthesis. They can be classified based on their action on COX enzymes or their chemical structure. Their mechanism of action involves blocking COX pathways to prevent the formation of prostaglandins. Common adverse effects include gastric irritation and impaired healing. NSAIDs should be used cautiously in patients with conditions like peptic ulcer or impaired kidney function.
Drug acting on inflammatory bowel diseaseAlisha Talwar
This document discusses drugs used to treat inflammatory bowel disease (IBD). It describes several classes of drugs including 5-aminosalicylic acid (mesalamine), corticosteroids, immunomodulating drugs like azathioprine and mercaptopurine, and biologic agents. For each drug class or individual drug, it provides information on mechanism of action, indications, contraindications, dosing, side effects, and nursing considerations. The document aims to comprehensively cover the pharmacological management of IBD.
Pharmacology of Gastrointestinal Disorders dineshmeena53
This power point presentation will be helpful for Pharmacy, Medical and paramedical students. it consists of" what are the common GIT disorders and their pharmacological management "
H2-receptor antagonists like cimetidine, ranitidine, famotidine, and nizatidine are rapidly absorbed from the intestine and undergo hepatic metabolism, reducing their bioavailability. They exhibit competitive inhibition at the H2 receptor on parietal cells, suppressing both basal and meal-stimulated acid secretion in a dose-dependent manner. H2 antagonists are effective for conditions like GERD, peptic ulcer disease, and stress-related bleeding by increasing gastric pH and inhibiting acid secretion. However, they can cause adverse effects like diarrhea, headaches, and drug interactions by inhibiting hepatic cytochrome P450 pathways.
Classification
Mechanism of action
Duration of action
Absorption and distribution
Mode of action
Theories of action of L.A
Pharmacokinetics of local anaesthetics
Routes of administration
Metabolism or biotransformation
Individual agents
Vasoconstrictors
Systemic effects
Toxicity
Advantages
Disadvantages
Maximum allowable dose
Local anaesthetics in community trust services
This document discusses the pharmacotherapy of peptic ulcer disease. It begins by describing the physiology of gastric acid secretion and the factors that regulate it. It then discusses peptic ulcer disease itself, including its epidemiology, symptoms, and pathophysiology. The main part of the document covers the various drugs used to treat peptic ulcers, including proton pump inhibitors, H2 receptor antagonists, prostaglandin analogues, anticholinergics, antacids, and ulcer protectives. It also discusses antimicrobial drugs for H. pylori eradication, commonly used combination therapies, and treatments for resistant H. pylori infections.
Prokinetics are the type of drugs which enhances gastrointestinal motility/transit by
increasing the frequency or strength of contractions.
They speed up gastric emptying by enhancing coordinated propulsive motility.
Treat Gastrointestinal symptoms : Abdominal discomfort, Bloating, constipation,
Heart burn, nausea and vomiting. And few gastrointestinal disorders : irritable bowel
Syndrome, gastritis, gastroparesis and functional dyspepsia.
Increases gastric emptying
Relief of gastric stasis
Decreases reflux esophagitis/heart burn
Decreases regurgitation of gastric contents& emesis
This document discusses the causes, treatment, and management of diarrhea. It begins by defining diarrhea as three or more loose stools in a 24 hour period. The causes of diarrhea include osmotic, secretory, motility issues, altered morphology, allergies, drugs, and certain cancers. Treatment involves rehydration either orally or intravenously. Oral rehydration solutions contain sodium, potassium, citrate, and glucose. Antimicrobial therapy may be used for certain infectious causes. Probiotics can help with antibiotic-associated diarrhea. Management of inflammatory bowel disease is also discussed.
Emetics and antiemetics are used to induce or prevent vomiting. Emetics work centrally in the medulla, peripherally in the stomach, or both. Common emetics include apomorphine, mustard, and ipecacuanha. Antiemetics have various mechanisms of action and include anticholinergics, antihistamines, neuroleptics, prokinetic drugs, 5-HT3 antagonists, and adjuvant medications. Common antiemetics are hyoscine, promethazine, metoclopramide, ondansetron, and corticosteroids. These drugs are used to treat nausea and vomiting from different causes like motion sickness, chemotherapy,
This document discusses drugs used to treat peptic ulcers. It begins by outlining common indications for treatment and classifying drugs into those that inhibit acid secretion, neutralize acid, protect ulcers, and treat H. pylori infections. Key drugs discussed include H2 receptor blockers like cimetidine and ranitidine, proton pump inhibitors like omeprazole and pantoprazole, antacids, and combinations used to eradicate H. pylori. Nursing responsibilities are identified like administering antacids appropriately and avoiding drug interactions.
The document discusses drugs used to treat peptic ulcers, gastroesophageal reflux disease, diarrhea, and constipation. It describes the causes of peptic ulcers including H. pylori infection and NSAID use. Treatment involves eradicating H. pylori, reducing gastric acid with H2 blockers or proton pump inhibitors, and protecting the gastric mucosa. Various classes of drugs are covered that act on these mechanisms including antimicrobials, H2 blockers, proton pump inhibitors, prostaglandins, and antacids.
1) The document discusses drugs used in the treatment of constipation, including laxatives, which are classified based on their mechanism and intensity of action.
2) Bulk forming agents like fiber, psyllium, and methylcellulose work by absorbing water in the intestines and forming a gel, which softens stool and increases stool mass. Stool softeners like docusates and liquid paraffin work by a detergent action that softens stool.
3) Stimulant purgatives like bisacodyl and senna irritate the intestinal mucosa, increasing motility and fluid accumulation in the intestines. They have more potent effects than bulk formers or softeners.
This document discusses peptic ulcers. It defines peptic ulcers as breaks in the gastrointestinal mucosa exposed to acid and pepsin. The pathophysiology involves an imbalance between defensive and aggressive factors on the gastroduodenal mucosa. Common causes of ulcers include Helicobacter pylori infection, NSAIDs, smoking, alcohol, and acid hypersecretion. Management involves lifestyle modifications, medications to reduce acid secretion, antibiotics to treat H. pylori, and surgery for complications or treatment failures.
The document discusses peptic ulcers, which are sores in the lining of the stomach or duodenum caused by an imbalance between defensive and damaging factors. Key points include: Helicobacter pylori bacteria and NSAIDs are major causes of ulcers. Symptoms include abdominal pain relieved by food or antacids. Complications can include bleeding, perforation, or obstruction if not treated. Treatment involves antibiotics to eliminate H. pylori, acid reducers to promote healing, and lifestyle changes like quitting smoking.
This document discusses peptic ulcers, including their causes, symptoms, diagnosis, and treatment. Peptic ulcers are abnormalities in the gastrointestinal tract caused by damage from stomach acid. The most common causes are infection with Helicobacter pylori bacteria and long-term use of nonsteroidal anti-inflammatory drugs. Common symptoms include abdominal pain, nausea, and vomiting of blood. Diagnosis involves tests to detect H. pylori infection and endoscopy to view the ulcers. Treatment focuses on eradicating H. pylori with antibiotics, reducing stomach acid with proton pump inhibitors or H2 blockers, and protecting the lining with sucralfate.
This document provides information on the management of peptic ulcer disease. It discusses the physiology of gastric acid secretion, introduces peptic ulcer disease, and outlines various drugs used to treat PUD. Key drugs mentioned include proton pump inhibitors like omeprazole, H2 receptor antagonists like ranitidine, prostaglandin analogues like misoprostol, antacids, and combinations used to eradicate Helicobacter pylori.
This document discusses peptic ulcer disease (PUD), including risk factors, pathophysiology, diagnosis, and treatment. Some key points:
- H. pylori infection and NSAID use are the leading causes of PUD. H. pylori infection is present in 60% of Americans over age 60.
- Diagnosis involves testing for H. pylori (stool antigen, urea breath, serology), and endoscopy if high risk or symptoms persist after treatment.
- Treatment for H. pylori-associated PUD is triple therapy (PPI plus two antibiotics) for 14 days. NSAID-associated PUD is treated with PPIs and prostag
The document outlines the treatment and management of peptic ulcer disease. For H. pylori-positive patients, it recommends triple therapy with a proton pump inhibitor, clarithromycin, and metronidazole or amoxicillin for 14 days. For H. pylori-negative patients, it recommends treatment with proton pump inhibitors or H2 receptor antagonists along with antacids. It describes surgical interventions for complications or treatment failure and recommends lifestyle changes and prophylactic treatment for high-risk patients to prevent ulcers.
This document discusses the treatment of epilepsy with anti-epileptic drugs. It lists both older and newer drugs used to treat partial seizures, generalized seizures, and other types of seizures. The drugs are divided based on their mechanism of action, such as blocking or altering sodium channels, inhibiting neurotransmitter release, or altering membrane permeability. Common side effects of anti-epileptic drugs include nausea, vomiting, sedation, and neurological issues; some drugs also have potential for serious side effects like agranulocytosis or fetal abnormalities if taken during pregnancy.
This document discusses different classes of anti-depressant drugs, including:
1) Amine Re-uptake Inhibitors (ARI) such as tricyclic antidepressants (TCAs) and heterocyclic antidepressants that work by inhibiting the reuptake of neurotransmitters like serotonin and norepinephrine.
2) Selective Serotonin Reuptake Inhibitors (SSRIs) that more selectively inhibit the reuptake of serotonin.
3) Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs) like venlafaxine that inhibit the reuptake of both serotonin and norepinephrine.
4) Monoamine
This document discusses drugs used to treat migraines. It separates drugs into those for acute attacks and those for prophylaxis. For acute attacks, it lists NSAIDs, anti-emetics, prokinetics, triptans, ergotamine, and opioids. For prophylaxis, it discusses beta-blockers, calcium channel blockers, antidepressants, and other drugs that act on serotonin receptors or have other mechanisms of action. It provides information on the pharmacokinetics, mechanisms of action, uses, and side effects of several representative drugs in each category.
This document summarizes peptic ulcers, which are ulcers that can form in the esophagus, stomach, or duodenum. Peptic ulcers are commonly caused by H. pylori infections or NSAID use. H. pylori infections are usually treated with a combination of antibiotics and proton pump inhibitors. Treatment aims to eliminate H. pylori and reduce stomach acid levels to allow ulcers to heal. Surgery may be needed for complications like bleeding or perforation. Maintaining a healthy lifestyle can help prevent ulcer recurrence.
This document discusses various drugs used to treat gastric acid-related disorders. It describes antacids that neutralize acid in the stomach, including aluminum and magnesium compounds, calcium carbonate, and sodium bicarbonate. It also discusses H2 receptor antagonists, proton pump inhibitors, and other drugs that reduce acid secretion. The document provides details on the mechanisms of action, pharmacokinetics, therapeutic uses and potential side effects of these different drug classes.
The document summarizes different types of antacids and drugs used to treat peptic ulcers and eradicate Helicobacter pylori infections. It describes proton pump inhibitors as the most effective antiulcer drugs that irreversibly inhibit the proton pump. It also discusses histamine-2 receptor antagonists, prostaglandin analogs, mucosal protective agents, and triple and quadruple drug therapies used to eradicate H. pylori infections.
Surgical treatment for peptic ulcer diseaseBashir BnYunus
This document discusses surgical treatments for peptic ulcer disease. It outlines relevant anatomy and physiology, classifications of PUD, indications for surgery, and various surgical options including vagotomy, gastrectomy, Graham's omental patch, and suture ligation of the gastroduodenal artery. Complications are also reviewed. The prognosis is generally satisfactory with operative procedures, though complications can include bleeding, leakage, obstruction, and recurrent ulceration. Delayed treatment increases morbidity and mortality risks.
Peptic ulcer disease involves breaks in the mucosal lining of the stomach or duodenum that penetrate through the muscular layer. The most common causes are infection with H. pylori bacteria and use of non-steroidal anti-inflammatory drugs (NSAIDs). Symptoms include abdominal pain, nausea, and weight loss. Diagnosis involves endoscopy to visualize the ulcers. Treatment involves antibiotics to eradicate H. pylori, proton pump inhibitors to reduce acid secretion, and avoidance of NSAIDs. Surgery is reserved for complications or treatment failure.
Peptic ulcer disease is caused by gastric or duodenal ulcers that form lesions in the stomach or duodenal mucosa. Risk factors include H. pylori infection, smoking, NSAID use, and genetic factors. Symptoms include epigastric pain relieved by food and antacids. Treatment aims to relieve pain, eradicate H. pylori infection, heal ulcers, and prevent recurrence through lifestyle changes and medication like PPIs or H2 blockers. Surgery was more common historically but is now rare due to H. pylori treatments, though it may be used for complications like perforation.
The document discusses various drugs used to treat peptic ulcers. It begins by describing peptic ulcers and their pathogenesis. It then covers several classes of anti-ulcer drugs that work by reducing acid secretion, such as H2 blockers like cimetidine and proton pump inhibitors like omeprazole. Other drug approaches discussed include agents that enhance mucosal defense like misoprostol, and antacids that neutralize gastric acid. The role of Helicobacter pylori infection in ulcers is also summarized.
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CHUYÊN ĐỀ ÔN TẬP VÀ PHÁT TRIỂN CÂU HỎI TRONG ĐỀ MINH HỌA THI TỐT NGHIỆP THPT ...
Pharmacology.. Treatment of Peptic Ulcer
1. P H R M A C O L O G Y - NOTE 3 - Treatment of Peptic Ulcer
DRUGS FOR PEPTIC ULCER
Drugs Affecting Mucosal Drugs erdicate
HCL Protictive Agents H. Pylori
Colloidal Bismuth Quadruple
Antacids H2 Blocker Sucralfate Misoprostol Triple Therapy
compounds Therapy
Omeprazole OR Omeprazole OR
Bismuth
AL(OH)3 Cimetidine Lansoprazole Lansoprazole
Subsalycilate
(PPI) (PPI)
Bismuth Bismuth
Mg(OH)2 Ranitidine Clarithromycin
Sobcitrate Subsalycilate
Amoxycillin OR
Famotidine Metronidazole
Metronidazole
Proton Pump
Anti-muscarinic Tetracycline
Inhibitors
Omeprazole Pirenzepine
(GU & DU)
Peptic Ulcer
• It is caused by imbalance between:
• Protective Factors
Lansoprazole • (Mucus & Bicharbonate).
• Dameging Factors 8
• (HCL & pepsin).
• So, it is caused by either DF or PF.
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2. P H R M A C O L O G Y - NOTE 3 - Treatment of Peptic Ulcer
Drugs Affecting Gastric (HCL) Acid
DRUGS PHARMACOKINETIC ACTION USES SIDE EFFECT
AL(OH)3 Weak bases (-OH). 1) Neutralize Slowly Used for symptomatic Constipation.
Taken 30 min in empty stomach. already relife of dyspepsia In renal failure,
Taken 2 hrs after meal. secreted acid. Aluminum toxicity
Antacid
Relieve heart burn immediatly. 2) Inhibit Encephalopathy
MG(OH)2 If it take with other drugs, formation of Fast Diarrhoea
It form insoluble com;ex that adsorb on pepsin
Combination Fast & Constipation + Diarrhoea = nothing
GIT wall not absorb. sustained
So, it take 2 hrs after or before other druds
Simethicone They are added to antacid either it combined or surface tension Anti-flatulent.
Additives
no. So, reduce buble To prevent reflux.
formation.
Alginates Form a layer of foam on the Reduce reflux
top of gastric content.
H2 Potency T1/2 Duration Inhibition of Cyto-450 is an enzyme that H2 antagonist cross placenta & are
antagonist (hrs) Cyto-450 metabolizes drugs. also secreted in breast milk.
(blokers) Cimetidine 1 1.5 – 6 1 Not used by elderly Gynecomastia.
2.3 male because it is anti- Galactorrhea.
Extremly androgenic Inhibition of Cyto-450
save drugs So, conc. of Theophyline &
Warfine.
Ranitidine 5 -10 1– 2.4 8 0.1
Famotidine 32 2.5 - 4 12 0
Omeprazole Average T1/2= 1.5 hrs. Irreversible inhibitors for
+ +
Lansoprazole Need acidic media, So H /K ATPase
PPI
Taken 1 hr befor meal.
Don’t take with other acid suppressing
agent.
Pirenzepine Inhibit gastric acid by blocking M3 Used in refractory
receptor cases that is not
muscarinic
responding to other
Anti-
drugs.
Used in nocturnal
pain.
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3. P H R M A C O L O G Y - NOTE 3 - Treatment of Peptic Ulcer
Muocosal protective Agents
DRUGS PHARMACOKINETIC ACTION USES SIDE EFFECT
Sucralfate It is salt of ( socrose + AL(OH)3 ). 1) In acidic pH, it become
Taken 1 hr befor meal. viscous gell & protect ulcer.
Work in acidic pH 2) Stimulate PG production.
Not used with antacid or H 2 antagonist.
Misoprostol It is a PGE1 analogue 1) Gastric acid inhibition. Used with NSAID to Diarrhoea
2) Stimulate secretion of prevent peptic ulcer Abdominal pain.
mucus & bicarbonate. Abortion?
3) Enhance mucusal blood
flow.
Bismuth subsalicylate 1) Coat the ulcer Stain stools & tongue with black
2) stimulate secretion of color.
Bismuth sobcitrate mucus & bicarbonate. Cause bismuth toxicity with long
3) PG synthesis. used.
Drugs erdicate Helicobacter pylori
DRUGS PHARMACOKINETIC ACTION USES SIDE EFFECT
Omeprazole It is combination of ONE acid suppressant + 2
Or antibiotics.
Lansoprazole (PPI) Given for 14 days.
Triple Therapy
Clarithromycin Then, followed by PPI for 4 - 6 wks.
Amoxycillin
or
Metronidazole
Omeprazole It is combination of ONE acid suppressant + 3
Or antibiotics.
Lansoprazole (PPI) Given when triple therapy fails.
Quadruple Therapy
Bismuth Subsalicylate
Metronidazole
Tetracycline
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