The document discusses the life and death of Helicobacter pylori in the stomach. It describes how H. pylori is able to survive the highly acidic conditions of the stomach through mechanisms like urease activity and acid adaptation. The urease produced by H. pylori helps neutralize gastric acid, allowing it to colonize the stomach. It discusses how H. pylori is able to regulate its internal pH and preferentially colonizes regions of the stomach with neutral or slightly acidic pH levels. The document also reviews current treatment regimens for eradicating H. pylori infections.
The document discusses sulfonamides, which were the first effective antimicrobial agents against bacterial infections. It describes the discovery of prontosil and sulfanilamide as the active component. While sulfonamides were widely used, resistance emerged and newer drugs became available. The mechanisms of action and classifications of sulfonamides are summarized. Cotrimoxazole, a combination of sulfamethoxazole and trimethoprim, produces a bactericidal effect and has a broader spectrum than either drug alone. Adverse effects and uses of sulfonamides and cotrimoxazole are briefly outlined. Sulfadoxine-pyrimethamine is also discussed as a synergistic combination used against malaria and
This document discusses the difference between sulfonamide antibiotics and sulfonylurea drugs used to treat diabetes. While sulfonamide antibiotics can cause allergic reactions, the literature suggests cross-reactivity with sulfonylureas is rare. Sulfonylureas are structurally distinct from antibiotics as they do not contain the arylamine group thought to be responsible for antibiotic allergies. Several studies reviewed found no evidence patients with sulfonamide antibiotic allergies experienced adverse effects from sulfonylureas. The document concludes sulfonylureas should not be contraindicated for diabetic patients with sulfonamide antibiotic allergies based on the low risk of cross-reactivity.
The document discusses anti-ulcer drugs and the physiology of the gastrointestinal tract. It provides details on:
1) The neuronal and hormonal control of the GI tract, including the enteric nervous system and hormones like gastrin and somatostatin.
2) The regulation of acid secretion by parietal cells and mediators like histamine, acetylcholine, and prostaglandins.
3) The pathophysiology of peptic ulcers involving an imbalance between aggressive factors like acid and protective mucosal defenses. Common causes include H. pylori infection and NSAID use.
4) Approaches for treating peptic ulcers including reducing acid with H2 blockers or
The document discusses anti-ulcer drugs. It begins by describing peptic ulcers and the imbalance between aggressive and defensive factors that can lead to their development. It then covers the classes of anti-ulcer drugs, including H2 blockers that reduce acid secretion, proton pump inhibitors, prostaglandin analogs, and antacids. Sucralfate and colloidal bismuth subcitrate are also covered as ulcer protective drugs. Diagnostic tests for ulcers like endoscopy and barium meal are mentioned. The goal of anti-ulcer treatment is outlined as relieving pain, promoting healing, preventing complications, and reducing relapse.
This document discusses sulfonamides, including their history, mechanisms of action, classifications, uses, and adverse effects. It specifically focuses on cotrimoxazole and sulfadoxine + pyrimethamine combinations. Cotrimoxazole is a fixed dose combination of sulfamethoxazole and trimethoprim that is bactericidal and has a wide spectrum of action. It is used for urinary tract, respiratory, and intestinal infections. Sulfadoxine + pyrimethamine is also a fixed dose combination that acts synergistically through sequential blockade of protozoal folic acid synthesis, making it effective against chloroquine resistant malaria and toxoplasmosis. Both combinations can cause hypersensitivity reactions and
Antibiotic Tetracyclines history,classification,mechanism of action and adver...Muhammad Amir Sohail
Tetracyclines are a class of broad-spectrum antibiotic drugs derived from soil actinomycetes. They work by inhibiting bacterial protein synthesis and have activity against many gram-positive and gram-negative bacteria. Common adverse effects include gastrointestinal upset, tooth discoloration in children, and risk of liver toxicity or nephrotoxicity in high doses. Tetracyclines have a wide range of clinical uses including treatment of respiratory infections, urinary tract infections, and certain other bacterial infections.
Sulfonamides were the first effective antimicrobial agents against bacterial infections but resistance has limited their use. They work by inhibiting the bacterial enzyme involved in folate synthesis. Sulfonamides are classified based on duration of action and include sulfadiazine and sulfamethoxazole. Resistance can develop via decreased drug uptake, decreased enzyme affinity, or increased PABA synthesis. Cotrimoxazole is a fixed dose combination of trimethoprim and sulfamethoxazole that has synergistic antibacterial effects and lower resistance due to sequential folate pathway inhibition. It is commonly used to treat urinary tract, respiratory, and gastrointestinal infections.
The document discusses sulfonamides, which were the first effective antimicrobial agents against bacterial infections. It describes the discovery of prontosil and sulfanilamide as the active component. While sulfonamides were widely used, resistance emerged and newer drugs became available. The mechanisms of action and classifications of sulfonamides are summarized. Cotrimoxazole, a combination of sulfamethoxazole and trimethoprim, produces a bactericidal effect and has a broader spectrum than either drug alone. Adverse effects and uses of sulfonamides and cotrimoxazole are briefly outlined. Sulfadoxine-pyrimethamine is also discussed as a synergistic combination used against malaria and
This document discusses the difference between sulfonamide antibiotics and sulfonylurea drugs used to treat diabetes. While sulfonamide antibiotics can cause allergic reactions, the literature suggests cross-reactivity with sulfonylureas is rare. Sulfonylureas are structurally distinct from antibiotics as they do not contain the arylamine group thought to be responsible for antibiotic allergies. Several studies reviewed found no evidence patients with sulfonamide antibiotic allergies experienced adverse effects from sulfonylureas. The document concludes sulfonylureas should not be contraindicated for diabetic patients with sulfonamide antibiotic allergies based on the low risk of cross-reactivity.
The document discusses anti-ulcer drugs and the physiology of the gastrointestinal tract. It provides details on:
1) The neuronal and hormonal control of the GI tract, including the enteric nervous system and hormones like gastrin and somatostatin.
2) The regulation of acid secretion by parietal cells and mediators like histamine, acetylcholine, and prostaglandins.
3) The pathophysiology of peptic ulcers involving an imbalance between aggressive factors like acid and protective mucosal defenses. Common causes include H. pylori infection and NSAID use.
4) Approaches for treating peptic ulcers including reducing acid with H2 blockers or
The document discusses anti-ulcer drugs. It begins by describing peptic ulcers and the imbalance between aggressive and defensive factors that can lead to their development. It then covers the classes of anti-ulcer drugs, including H2 blockers that reduce acid secretion, proton pump inhibitors, prostaglandin analogs, and antacids. Sucralfate and colloidal bismuth subcitrate are also covered as ulcer protective drugs. Diagnostic tests for ulcers like endoscopy and barium meal are mentioned. The goal of anti-ulcer treatment is outlined as relieving pain, promoting healing, preventing complications, and reducing relapse.
This document discusses sulfonamides, including their history, mechanisms of action, classifications, uses, and adverse effects. It specifically focuses on cotrimoxazole and sulfadoxine + pyrimethamine combinations. Cotrimoxazole is a fixed dose combination of sulfamethoxazole and trimethoprim that is bactericidal and has a wide spectrum of action. It is used for urinary tract, respiratory, and intestinal infections. Sulfadoxine + pyrimethamine is also a fixed dose combination that acts synergistically through sequential blockade of protozoal folic acid synthesis, making it effective against chloroquine resistant malaria and toxoplasmosis. Both combinations can cause hypersensitivity reactions and
Antibiotic Tetracyclines history,classification,mechanism of action and adver...Muhammad Amir Sohail
Tetracyclines are a class of broad-spectrum antibiotic drugs derived from soil actinomycetes. They work by inhibiting bacterial protein synthesis and have activity against many gram-positive and gram-negative bacteria. Common adverse effects include gastrointestinal upset, tooth discoloration in children, and risk of liver toxicity or nephrotoxicity in high doses. Tetracyclines have a wide range of clinical uses including treatment of respiratory infections, urinary tract infections, and certain other bacterial infections.
Sulfonamides were the first effective antimicrobial agents against bacterial infections but resistance has limited their use. They work by inhibiting the bacterial enzyme involved in folate synthesis. Sulfonamides are classified based on duration of action and include sulfadiazine and sulfamethoxazole. Resistance can develop via decreased drug uptake, decreased enzyme affinity, or increased PABA synthesis. Cotrimoxazole is a fixed dose combination of trimethoprim and sulfamethoxazole that has synergistic antibacterial effects and lower resistance due to sequential folate pathway inhibition. It is commonly used to treat urinary tract, respiratory, and gastrointestinal infections.
The document discusses probiotics, their history, functions, and food sources. It begins by defining probiotics as live microorganisms that provide health benefits when consumed in adequate amounts. The concept of probiotics was first proposed in the early 20th century by Elie Metchnikoff, who suggested certain bacteria in fermented milk could promote intestinal and overall health. The document then outlines the characteristics, mechanisms of action, advantages, and functions of probiotic consumption before providing examples of probiotic foods and the probiotic strains they contain.
This document discusses the role of probiotics in adult gastroenterology. It provides a brief history of probiotics dating back to Elie Metchnikof in 1908. Probiotics are defined as live microorganisms that provide health benefits when consumed. The gut microbiota plays an important role in health, and probiotics may help treat or prevent conditions caused by microbial imbalances like infectious diarrhea, irritable bowel syndrome, inflammatory bowel disease, obesity, and liver diseases. Probiotics have demonstrated benefits, but their effects tend to be strain-specific and more research is still needed, especially for conditions like Crohn's disease. Safety concerns also exist for certain at-risk populations.
This document provides an overview of probiotics and prebiotics. It discusses the history of probiotics beginning with Elie Metchnikoff's conceptualization in the early 20th century. Examples of commonly used probiotic bacteria like Bifidobacterium and Lactobacillus are provided. The mechanisms of action of probiotics and examples of prebiotics like inulin and fructooligosaccharides are summarized. Finally, clinical applications of probiotics and prebiotics in managing conditions like antibiotic-associated diarrhea, lactose intolerance, and hypercholesterolemia are briefly described.
This document provides an overview of probiotics, focusing on the bacteria Lactobacillus and Bifidobacterium. It discusses the history of probiotics, why they are important for human health, examples of foods containing probiotics, and their mechanisms of action. The document also covers commercial probiotic strains, genetically engineered probiotics, prebiotics, and Indian probiotic manufacturers.
This document discusses probiotics, including their history, definition, commonly used strains, properties, established health effects, mechanisms of action, advantages, effects in livestock, synergistic use with prebiotics, and the market size. Probiotics are live microorganisms that, when consumed in adequate amounts, confer health benefits. Commonly used probiotic strains include Lactobacillus and Bifidobacterium. Probiotics can help treat conditions like antibiotic-associated diarrhea, cancer, and high cholesterol, and provide benefits to livestock. Prebiotics feed beneficial bacteria to create synbiotic combinations with probiotics. The global probiotics market was estimated at $15.9 billion in 2008 and is projected to reach $
Gasbarrini A. Microbiota, Antibiotici e Probiotici in Gastroenterologia. ASMa...Gianfranco Tammaro
PROF. ANTONIO GASBARRINI - 3° Giornata Master ECM in Gastroenterologia 2016 (25/11/2016) - Fondazione Santa Lucia - Sala Congressi - Roma
Sito: www.asmad.net
Canale Youtube: https://youtu.be/ouYcXg_ZtJM
Probiotics are living microorganisms that provide health benefits when consumed in adequate amounts. They help maintain a healthy balance of bacteria in the gut and can aid in digestion, strengthen the immune system, and reduce risks of certain diseases. Common probiotic strains include Lactobacillus and Bifidobacterium species. Probiotics are available in foods like yogurt as well as supplements. Prebiotics are non-digestible fibers that feed beneficial bacteria in the gut. Synbiotics combine probiotics and prebiotics to support a healthy microbiome.
Ringkasan dokumen tersebut adalah:
1. Dokumen tersebut membahas tentang sejarah Mesir kuno mulai dari letak geografis, seni bangunan, pertanian, sistem pemerintahan, ilmu pengetahuan dan teknologi yang dimiliki peradaban Mesir kuno.
2. Peradaban Mesir kuno berkembang selama hampir 3 milenium SM dan mencapai puncak kejayaannya pada Zaman Mesir Baru.
3. Masyarakat Mesir kuno memiliki pen
Probiotics are live microorganisms that resemble beneficial bacteria naturally found in the gut. They provide health benefits such as improving digestion and nutrient absorption, protecting against harmful bacteria, and strengthening the immune system. Common sources of probiotics include yogurt, kefir, kimchi, and supplements. While generally safe, potential side effects can include mild digestive issues like bloating or gas.
Probiotics for the Gut - A Guide for Primary Care PhysiciansJarrod Lee
Probiotics have been shown to be of benefit in several gut disorders. Today, probiotics are a multibillion dollar industry, with a myriad of options that can be confusing. This presentation introduces the fundamentals of probiotics to primary care doctors for use in their daily practice.
Probiotics are live microorganisms that provide health benefits when consumed. Probiotics like certain Lactobacillus and Bifidobacterium species may help treat periodontal disease by inhibiting pathogenic bacteria, reducing inflammation, and strengthening the immune system. While more research is still needed, some studies have found probiotics can decrease gingivitis and periodontal pocket depth when consumed as lozenges or gum to allow colonization of the oral cavity. Prebiotics may also help probiotics thrive in the mouth, but their role in oral health is still unclear. Overall, probiotics show promise for periodontal disease but are still in the early stages of research and validation through large clinical trials is required.
The document discusses probiotics, which are live microorganisms that provide health benefits when consumed. It defines probiotics and lists common types including various Lactobacillus and Bifidobacterium bacteria. The document then outlines uses of probiotics for humans, cattle/poultry, and aquaculture. It provides a table of commercial probiotic strains and discusses specific probiotic supplements including Bio-K+, Bio-K+ Fruity, Bio-K+ Dairy Free, and Bio-Kaps Regular Strength.
This document discusses prebiotics and probiotics and their effects on gut health. It defines prebiotics as fibers that feed the good bacteria in our digestive systems. Probiotics are live active cultures that can positively change our gut microbiome when consumed daily, such as in yogurt. The document encourages eating a diet high in prebiotics like fruits and vegetables, and probiotic sources like yogurt, to support digestive and immune health.
Scientific Validation Of Polydextrose As A Fibre AndGeoffreyOsullivan
Presents an overview of the scientific evidence and methods used to prove polydextrose is a safe and effective soluble prebiotic fibre with high toleration
The document summarizes an annual probiotic symposium held in Chennai, India in December 2016. It includes the following:
- An agenda for the symposium that covers definitions of probiotics, prebiotics, and synbiotics; the history of probiotics; the role of probiotics in gastrointestinal diseases; their functions and mechanisms of action; clinical applications in gastroenterology; dosage and safety issues; and conclusions.
- Presentations on the topics of probiotics in gastrointestinal diseases, their equilibrium in nature and the human body, and the gut flora.
- Evidence that certain probiotic strains like Lactobacillus and Bifidobacterium can reduce disease activity and symptoms
Probiotics are live microorganisms that when consumed in adequate amounts may provide health benefits. They include bacteria like Lactobacillus and Bifidobacterium. Probiotics can affect the intestinal flora, are promoted as food supplements, and have potential health claims, though many remain unproven. Prebiotics are nondigestible fibers that promote the growth of probiotic bacteria. Together, probiotics and prebiotics can modify the gut microflora and are thought to protect against pathogens and stimulate immune function, though their effects depend on the specific strains and more research is still needed to substantiate all claims.
Probiotics and prebiotics can modify the composition and activities of gut microflora. Probiotics include bacteria like Lactobacillus, Bifidobacterium, Enterococcus, and yeasts. They are found naturally in foods like yogurt and kimchi. Prebiotics are non-digestible fibers that feed beneficial bacteria in the gut. Sources include onions, garlic, chicory root and asparagus. Both probiotics and prebiotics help maintain a healthy gut microbiome and provide various health benefits such as treating diarrhea, aiding digestion, and boosting immunity."
This document summarizes microbial responses to acid stress. It discusses how bacteria like E. coli, Salmonella, and Helicobacter pylori have developed mechanisms to regulate internal pH and withstand acidic environments. These include proton pumps, amino acid decarboxylases, and the urease enzyme system. Regulatory systems like sigma factors and two-component systems help induce acid shock proteins and responses during acid exposure. Gram-positive bacteria like streptococci take a more flexible approach by allowing internal pH to decrease along with external pH.
The document summarizes the anatomy and physiology of acid production in the stomach. It discusses how parietal cells in the gastric glands secrete acid via proton pumps activated by histamine and other factors. Mucosal defenses protect the stomach from acid. Peptic ulcers result from an imbalance between these factors. Common ulcer treatments target proton pumps using proton pump inhibitors or histamine receptors using H2 blockers. The document then provides details on the structure and mechanism of action of proton pumps and how different drug classes inhibit acid secretion.
This document discusses anti-ulcer agents. It defines peptic ulcers as erosions in the stomach or duodenum lining caused by an imbalance between aggressive factors like acid and protective factors. Common causes of ulcers include H. pylori, NSAIDs, and stress. Treatment approaches aim to reduce acid secretion using H2 blockers, proton pump inhibitors, anticholinergics, and prostaglandins. Other approaches neutralize acid with antacids, protect the ulcer with sucralfate or bismuth, and eradicate H. pylori with antibiotic combinations.
This document provides an overview of colon specific drug delivery systems. It discusses the advantages of targeting drug delivery to the colon which includes reduced dosing, lower side effects, and improved patient compliance. It also reviews some limitations such as multiple manufacturing steps and potential for drug degradation by colonic microflora. The document then examines the anatomy and physiology of the colon, factors that influence colonic drug delivery such as pH and transit time, and how drugs are absorbed in the colon. It concludes by outlining several approaches to colon specific drug delivery including pH dependent coatings, time release systems, prodrugs activated by colonic bacteria, and the use of carriers degraded by colonic microflora.
The document discusses probiotics, their history, functions, and food sources. It begins by defining probiotics as live microorganisms that provide health benefits when consumed in adequate amounts. The concept of probiotics was first proposed in the early 20th century by Elie Metchnikoff, who suggested certain bacteria in fermented milk could promote intestinal and overall health. The document then outlines the characteristics, mechanisms of action, advantages, and functions of probiotic consumption before providing examples of probiotic foods and the probiotic strains they contain.
This document discusses the role of probiotics in adult gastroenterology. It provides a brief history of probiotics dating back to Elie Metchnikof in 1908. Probiotics are defined as live microorganisms that provide health benefits when consumed. The gut microbiota plays an important role in health, and probiotics may help treat or prevent conditions caused by microbial imbalances like infectious diarrhea, irritable bowel syndrome, inflammatory bowel disease, obesity, and liver diseases. Probiotics have demonstrated benefits, but their effects tend to be strain-specific and more research is still needed, especially for conditions like Crohn's disease. Safety concerns also exist for certain at-risk populations.
This document provides an overview of probiotics and prebiotics. It discusses the history of probiotics beginning with Elie Metchnikoff's conceptualization in the early 20th century. Examples of commonly used probiotic bacteria like Bifidobacterium and Lactobacillus are provided. The mechanisms of action of probiotics and examples of prebiotics like inulin and fructooligosaccharides are summarized. Finally, clinical applications of probiotics and prebiotics in managing conditions like antibiotic-associated diarrhea, lactose intolerance, and hypercholesterolemia are briefly described.
This document provides an overview of probiotics, focusing on the bacteria Lactobacillus and Bifidobacterium. It discusses the history of probiotics, why they are important for human health, examples of foods containing probiotics, and their mechanisms of action. The document also covers commercial probiotic strains, genetically engineered probiotics, prebiotics, and Indian probiotic manufacturers.
This document discusses probiotics, including their history, definition, commonly used strains, properties, established health effects, mechanisms of action, advantages, effects in livestock, synergistic use with prebiotics, and the market size. Probiotics are live microorganisms that, when consumed in adequate amounts, confer health benefits. Commonly used probiotic strains include Lactobacillus and Bifidobacterium. Probiotics can help treat conditions like antibiotic-associated diarrhea, cancer, and high cholesterol, and provide benefits to livestock. Prebiotics feed beneficial bacteria to create synbiotic combinations with probiotics. The global probiotics market was estimated at $15.9 billion in 2008 and is projected to reach $
Gasbarrini A. Microbiota, Antibiotici e Probiotici in Gastroenterologia. ASMa...Gianfranco Tammaro
PROF. ANTONIO GASBARRINI - 3° Giornata Master ECM in Gastroenterologia 2016 (25/11/2016) - Fondazione Santa Lucia - Sala Congressi - Roma
Sito: www.asmad.net
Canale Youtube: https://youtu.be/ouYcXg_ZtJM
Probiotics are living microorganisms that provide health benefits when consumed in adequate amounts. They help maintain a healthy balance of bacteria in the gut and can aid in digestion, strengthen the immune system, and reduce risks of certain diseases. Common probiotic strains include Lactobacillus and Bifidobacterium species. Probiotics are available in foods like yogurt as well as supplements. Prebiotics are non-digestible fibers that feed beneficial bacteria in the gut. Synbiotics combine probiotics and prebiotics to support a healthy microbiome.
Ringkasan dokumen tersebut adalah:
1. Dokumen tersebut membahas tentang sejarah Mesir kuno mulai dari letak geografis, seni bangunan, pertanian, sistem pemerintahan, ilmu pengetahuan dan teknologi yang dimiliki peradaban Mesir kuno.
2. Peradaban Mesir kuno berkembang selama hampir 3 milenium SM dan mencapai puncak kejayaannya pada Zaman Mesir Baru.
3. Masyarakat Mesir kuno memiliki pen
Probiotics are live microorganisms that resemble beneficial bacteria naturally found in the gut. They provide health benefits such as improving digestion and nutrient absorption, protecting against harmful bacteria, and strengthening the immune system. Common sources of probiotics include yogurt, kefir, kimchi, and supplements. While generally safe, potential side effects can include mild digestive issues like bloating or gas.
Probiotics for the Gut - A Guide for Primary Care PhysiciansJarrod Lee
Probiotics have been shown to be of benefit in several gut disorders. Today, probiotics are a multibillion dollar industry, with a myriad of options that can be confusing. This presentation introduces the fundamentals of probiotics to primary care doctors for use in their daily practice.
Probiotics are live microorganisms that provide health benefits when consumed. Probiotics like certain Lactobacillus and Bifidobacterium species may help treat periodontal disease by inhibiting pathogenic bacteria, reducing inflammation, and strengthening the immune system. While more research is still needed, some studies have found probiotics can decrease gingivitis and periodontal pocket depth when consumed as lozenges or gum to allow colonization of the oral cavity. Prebiotics may also help probiotics thrive in the mouth, but their role in oral health is still unclear. Overall, probiotics show promise for periodontal disease but are still in the early stages of research and validation through large clinical trials is required.
The document discusses probiotics, which are live microorganisms that provide health benefits when consumed. It defines probiotics and lists common types including various Lactobacillus and Bifidobacterium bacteria. The document then outlines uses of probiotics for humans, cattle/poultry, and aquaculture. It provides a table of commercial probiotic strains and discusses specific probiotic supplements including Bio-K+, Bio-K+ Fruity, Bio-K+ Dairy Free, and Bio-Kaps Regular Strength.
This document discusses prebiotics and probiotics and their effects on gut health. It defines prebiotics as fibers that feed the good bacteria in our digestive systems. Probiotics are live active cultures that can positively change our gut microbiome when consumed daily, such as in yogurt. The document encourages eating a diet high in prebiotics like fruits and vegetables, and probiotic sources like yogurt, to support digestive and immune health.
Scientific Validation Of Polydextrose As A Fibre AndGeoffreyOsullivan
Presents an overview of the scientific evidence and methods used to prove polydextrose is a safe and effective soluble prebiotic fibre with high toleration
The document summarizes an annual probiotic symposium held in Chennai, India in December 2016. It includes the following:
- An agenda for the symposium that covers definitions of probiotics, prebiotics, and synbiotics; the history of probiotics; the role of probiotics in gastrointestinal diseases; their functions and mechanisms of action; clinical applications in gastroenterology; dosage and safety issues; and conclusions.
- Presentations on the topics of probiotics in gastrointestinal diseases, their equilibrium in nature and the human body, and the gut flora.
- Evidence that certain probiotic strains like Lactobacillus and Bifidobacterium can reduce disease activity and symptoms
Probiotics are live microorganisms that when consumed in adequate amounts may provide health benefits. They include bacteria like Lactobacillus and Bifidobacterium. Probiotics can affect the intestinal flora, are promoted as food supplements, and have potential health claims, though many remain unproven. Prebiotics are nondigestible fibers that promote the growth of probiotic bacteria. Together, probiotics and prebiotics can modify the gut microflora and are thought to protect against pathogens and stimulate immune function, though their effects depend on the specific strains and more research is still needed to substantiate all claims.
Probiotics and prebiotics can modify the composition and activities of gut microflora. Probiotics include bacteria like Lactobacillus, Bifidobacterium, Enterococcus, and yeasts. They are found naturally in foods like yogurt and kimchi. Prebiotics are non-digestible fibers that feed beneficial bacteria in the gut. Sources include onions, garlic, chicory root and asparagus. Both probiotics and prebiotics help maintain a healthy gut microbiome and provide various health benefits such as treating diarrhea, aiding digestion, and boosting immunity."
This document summarizes microbial responses to acid stress. It discusses how bacteria like E. coli, Salmonella, and Helicobacter pylori have developed mechanisms to regulate internal pH and withstand acidic environments. These include proton pumps, amino acid decarboxylases, and the urease enzyme system. Regulatory systems like sigma factors and two-component systems help induce acid shock proteins and responses during acid exposure. Gram-positive bacteria like streptococci take a more flexible approach by allowing internal pH to decrease along with external pH.
The document summarizes the anatomy and physiology of acid production in the stomach. It discusses how parietal cells in the gastric glands secrete acid via proton pumps activated by histamine and other factors. Mucosal defenses protect the stomach from acid. Peptic ulcers result from an imbalance between these factors. Common ulcer treatments target proton pumps using proton pump inhibitors or histamine receptors using H2 blockers. The document then provides details on the structure and mechanism of action of proton pumps and how different drug classes inhibit acid secretion.
This document discusses anti-ulcer agents. It defines peptic ulcers as erosions in the stomach or duodenum lining caused by an imbalance between aggressive factors like acid and protective factors. Common causes of ulcers include H. pylori, NSAIDs, and stress. Treatment approaches aim to reduce acid secretion using H2 blockers, proton pump inhibitors, anticholinergics, and prostaglandins. Other approaches neutralize acid with antacids, protect the ulcer with sucralfate or bismuth, and eradicate H. pylori with antibiotic combinations.
This document provides an overview of colon specific drug delivery systems. It discusses the advantages of targeting drug delivery to the colon which includes reduced dosing, lower side effects, and improved patient compliance. It also reviews some limitations such as multiple manufacturing steps and potential for drug degradation by colonic microflora. The document then examines the anatomy and physiology of the colon, factors that influence colonic drug delivery such as pH and transit time, and how drugs are absorbed in the colon. It concludes by outlining several approaches to colon specific drug delivery including pH dependent coatings, time release systems, prodrugs activated by colonic bacteria, and the use of carriers degraded by colonic microflora.
The document discusses various enzyme inhibitors including xanthine oxidase inhibitors, cytochrome P450 inhibitors, DHFR inhibitors, and gastric proton pump inhibitors. It provides details on the mechanisms of several specific inhibitors such as allopurinol, ciprofloxacin, trimethoprim, and omeprazole. The document was presented by Sanjay Gopi to Dr. S.D. Joshi of the Department of Pharmaceutical Chemistry at SET's College of Pharmacy in Dharwad, India.
Vonoprazan is a novel potassium-competitive acid blocker (PCAB) that provides more potent and sustained acid suppression compared to proton pump inhibitors (PPIs). Studies show Vonoprazan achieves faster and higher gastric pH control from the first dose. It is also effective for Helicobacter pylori eradication, achieving higher eradication rates than PPI-based triple therapies. Vonoprazan has also shown non-inferiority to lansoprazole for healing erosive esophagitis with higher cure rates.
Peptic ulcer disease is caused by a disturbance in the mucosal barrier that protects the stomach and duodenum from acid and pepsin. This allows acid and pepsin to damage the lining and cause ulcers. Treatment involves reducing acid production through proton pump inhibitors or H2 blockers. Additional treatments include antacids to neutralize acid, ulcer protectives like sucralfate to form a protective barrier, and multi-drug regimens to eliminate the bacteria H. pylori when present. Lifestyle changes and avoidance of NSAIDs and smoking are also important parts of treatment and management.
Helicobacter pylori is a spiral-shaped bacterium that can cause peptic ulcer disease and is associated with gastric cancer. It colonizes the stomach and causes a chronic inflammatory response. Several bacterial virulence factors like the cag pathogenicity island, vacuolating cytotoxin, and urease contribute to pathogenesis. H. pylori infection typically results in chronic gastritis and in some cases can lead to more severe outcomes like peptic ulcers, gastric atrophy, intestinal metaplasia, and cancer. Diagnosis involves endoscopy with biopsy to detect the bacteria through histology or other tests. Treatment aims to eradicate the infection through antibiotic therapy combined with proton pump inhibitors.
This document provides information about peptic ulcer disease (PUD) and its treatment with Omeprazole. PUD is caused by an imbalance between gastric acid and the stomach's protective mechanisms. Helicobacter pylori infection is responsible for most cases of PUD. Omeprazole is a proton pump inhibitor that suppresses gastric acid production by inhibiting the hydrogen-potassium ATPase enzyme in parietal cells. It has high bioavailability, is well-tolerated though some patients report side effects like headache and diarrhea. Omeprazole is effective for treating PUD and in combination with antibiotics can help eradicate H. pylori infections. It provides effective relief of symptoms from conditions
This document provides an overview of peptic ulcer disease including the anatomy and physiology of the stomach and duodenum, pathophysiology of peptic ulcers, types of gastric ulcers, symptoms, etiology, complications, diagnosis, and treatment. It discusses topics like the role of Helicobacter pylori infection in peptic ulcers, tests to diagnose H. pylori, and treatments which aim to eliminate H. pylori, reduce acid production, and promote healing. Common medications mentioned are proton pump inhibitors, H2 receptor blockers, antibiotics, and sucralfate.
Proton pump inhibitors (PPIs) block the gastric H,K-ATPase, inhibiting gastric acid secretion. This effect enables healing of peptic ulcers, gastroesophageal reflux disease (GERD), Barrett's esophagus, and Zollinger-Ellison syndrome, as well as the eradication of Helicobacter pylori as part of combination regimens.Proton-pump inhibitors (PPIs) are a class of medications that cause a profound and prolonged reduction of stomach acid production. They do so by irreversibly inhibiting the stomach's H+/K+ ATPase proton pump.[1]
They are the most potent inhibitors of acid secretion available.[2] Proton-pump inhibitors have largely superseded the H2-receptor antagonists, a group of medications with similar effects but a different mode of action, and antacids.[3]
PPIs are among the most widely sold medications in the world. The class of proton-pump inhibitor medications is on the World Health Organization's List of Essential Medicines.[4][5] Omeprazole is the specific listed example.[4][5]
Mechanism of action
The activation of PPIs
Proton pump inhibitors act by irreversibly blocking the hydrogen/potassium adenosine triphosphatase enzyme system (the H+/K+ ATPase, or, more commonly, the gastric proton pump) of the gastric parietal cells.[71] The proton pump is the terminal stage in gastric acid secretion, being directly responsible for secreting H+ ions into the gastric lumen, making it an ideal target for inhibiting acid secretion.[citation needed]Because the H,K-ATPase is the final step of acid secretion, an inhibitor of this enzyme is more effective than receptor antagonists in suppressing gastric acid secretion.[72] All of these drugs inhibit the gastric H,K-ATPase by covalent binding, so the duration of their effect is longer than expected from their levels in the blood.[73]
Targeting the terminal step in acid production, as well as the irreversible nature of the inhibition, results in a class of medications that are significantly more effective than H2 antagonists and reduce gastric acid secretion by up to 99%.[2
This document discusses gastric proton pump inhibitors (PPIs), which are a class of medications that powerfully reduce stomach acid production by irreversibly inhibiting the proton pump in the stomach. It describes the mechanism of action of PPIs, including how they are activated in acidic environments to covalently bind to and deactivate the proton pump. Four common PPI medications - omeprazole, lansoprazole, rabeprazole, and pantoprazole - are profiled, outlining their chemical properties, bioavailability, uses in treating acid-related gastrointestinal conditions, and potential side effects.
Dr. T.V. Rao provides an overview of Helicobacter pylori (H. pylori), the bacterium associated with peptic ulcer disease and gastric cancer. Some key points:
- H. pylori was discovered in 1983 by Warren and Marshall and linked to gastritis and ulcers. They received the 2005 Nobel Prize in Physiology or Medicine.
- H. pylori colonizes the stomach of about half of individuals worldwide. It is a gram-negative, spiral-shaped bacterium that lives in the mucus layer of the stomach.
- H. pylori infection can cause chronic gastritis, peptic ulcers, and in rare
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1. The life and death of
Helicobacter pylori
in stomach
Davoud azadi
2. Introduction
• Colonisation of the normal stomach has been achieved only
by Helicobacter spp., such as H.pylori, H. felis or H.
mustelae
• Gram negative, motile, microaerophilic, spiral shaped
organisms that dwell on the gastric surface and within the
gastric mucus
• They are found more frequently in the antrum than in the
fundus and often within antral glands
• grow between pH 6.0 and 8.5 and survive between pH 4.0
and 8.5 in the absence of urea
3. The gastric environment
• The pH of the gastric lumen:
median pH is 1.4 .The pH can fall to below 1.0 with acid
secretion at night
The pH at the gastric surface(neutral) is thought to be
significantly higher than in the lumen(pH:2)
The pH of the lumen of the fundic glands, is much lower, The
pH on the antral surface likely to be higher
HCO3 secretion is able to neutralise 10% of maximal acid
secretion.( gastric surface pH:6)
4. Microbial acid adaptation
• pH of periplasmic space, that is important for their survival or
growth.
• Neutrophiles bacteria like HP that can only survive but not grow in
acid are acid resistant
• Neutrophiles bacteria grow best at neutral pH but are able to survive
and grow in acidity and to increase their periplasmic pH
5. 1. All are designed to maintain a tolerable electrochemical
gradient of H+ across the inner membrane of these bacteria.
This can be achieved by alterations in transmembrane potential
lead to reducing the effective gradient
2. Acid tolerance can be achieved by the generation of neutralising
buffers either inside the cell or in the periplasmic space.
3. Many bacteria respond to acidity by changes in gene expression
of specialised proteins.
7. STRUCTURAL ASPECTS OF MEMBRANE PROTEINS
• The outer membrane of Gram negative
containing a variety of proteins
• some membrane spanning, porins are
able to mediate the flux of various small
molecules across the outer membrane.
• some associated with only one face(LPS)
8. STRUCTURAL ASPECTS OF MEMBRANE PROTEINS
• A means of acid protection would be to alter the isoelectric point
of these proteins as a means of reducing the transport of protons
across the bilayer.
• Helicobacteria porins and some inner membrane proteins have an
isoelectric point significantly more alkaline than that of bacteria
rarely exposed to acid thereby retarding flux of protons into the
periplasmic space
• In H pylori the c subunit of the F1F0ATP synthase. loss of four
carboxylic amino acids in the sequence of the compared with that
of E coli or B subtilis.
9. • increase in isoelectric point suggests that both the outer and inner
membrane of the organism can be exposed to high acidity
• increase in numbers of positively charged amino acids or
decrease in the number of carboxylic acids in the membrane
proteins
• Helicobacter pylori use of this adaptive mechanism is acid
resistance when is exposed directly to luminal acidity.
• This mechanism provide transient protection. Thus other
mechanisms must be present to allow both long term survival
and growth in the gastric environment.
10. ATP SYNTHESIS AND MEDIUM pH
• The survival of aerobic bacteria depends on their ability to
synthesise ATP, by hydronium flux inward across the F1F0
ATPase driven by an inwardly oriented electrochemical
gradient of H3O+
• The gradient related to pH gradient and the transmembrane
potential difference (PMF)
In E coli, in a medium of pH 7.0, the cytoplasmic pH is about
7.5 to 7.8 and the transmembrane potential is −160 mV, to
give an PMV: −200 mV.
H pylori in the absence of urea at pH 7.0 gave a value of
−131 mV and an internal pH of 8.4(lower proton
permeability of the membranes of this organism) PMV: −220
mV.
11. • H.pylori is able to maintain a membrane potential between
pH 4.0 and 8.5. If the pH was outside these limits there was
a relatively rapid and irreversible loss of the membrane
potential
• The addition of urea restored the membrane potential
within about pH 3.5.
• Addition of urea at neutral pH in the absence of buffer
resulted in medium alkalinisation to a pH > 8.5
• Urease activity is a two edged sword for H pylori, enabling
survival in acid, preventing survival in the absence of acid
12. REGULATION OF PERIPLASMIC pH IN
ACID•
Above mechanism that used by H pylori would not
ensure its survival in the stomach
• this organism is synthesis of a neutral pH with urease at
high concentrations.
• 15% of the protein synthesis is devoted to the production
of ure A or ure B.and active urease enzyme need Ni2−
13. Urease activity
• H pylori has a prokaryotic carbonic anhydrase in its genomic
sequence, hence the eventual effect of urease activity at a pH less
than the pKa of NH3 (9.5) and greater than 4.8 therefore is able to
alkalinise the environment of the urease
• urease activity rapidly showed was organism either in solution or
bound to the cell surface.
• surface urease activity reduces the acidity of the microenvironment
of the organism below the mucus layer of the gastric mucosa
14. • H. pylori have two urease :internal urease and surface urease
• This microenvironment located external to the organism or in the
periplasmic space
• Internal urease was designated as the responsible urease
compartment, it was neutralisation of the external
microenvironment
15. Urease activity
• External urease activity low at pH > 6.5 At pH < 6.5, there is a
notable increase in urease activity(about 10-fold) reaching maximum
at pH 5.5 and remaining steady until pH 3.0
• internal urease is activated at a pH < 6.5 and cytoplasmic pH
remains steady
• 95% of the urease is found inside and not on the surface or outside
majority of the protein is found in the cytoplasm thus inaccessible
for immune system elements
16. • internal urease is responsible for acid protection
• The inner membrane potential of H pylori at fixed medium pH
between 3.0 and 6.0 rose to −105 mV with the addition of 5mM
urea,
• internal urease activity was responsible to periplasmic pH was
elevated to pH 6.2
• Addition of urea also enabled protein synthesis at a fixed medium
pH of 3.0 to 6.0 where normally no protein synthesis is found.
17. RESPONSE TO ELEVATED pH
• external urease is toxic at neutral pH
• ureas elevates medium pH to 8.5 or greater
resultant irreversible loss of membrane potential
and death
• This latter effect may explain the absence of H
pylori infection in pernicious anaemia
• H.pylori show no Internal urease activity at a pH >
6.5 prevents alkalinisation in the absence of acid.
18. • In summary, internal urease is active at a gastric
pH of < 6.5 and enables survival and growth at pH
between perhaps 2.0 and 6.0 depending on the
gastric urea concentration
• urea concentrations for effective internal enzyme
activity is about 1 mM
• External urease does not function as a
gastroprotective mechanism but reducing the
immune response in the gut
19.
20. Detoxification
• H. pylori microaerophilic and able to protect themselves from the
toxic products of oxygen metabolism
• H. pylori possess a superoxide dismutase and a catalase
• H. pylori has two genes encoding peroxidases (JHP991/HP0390 and
JHP1471/HP1563) located adjacent to the superoxide dismutase
gene
• Theability to isolate catalase-negative mutants of H. pylori suggests
that at least one of the peroxidases can function as a catalase
21.
22. The ecological niche of H pylori
• pH 6-8 Optimum for H.pylori growth(growth or
protein synthesis)
• for effective colonisation, the periplasmic pH
must be kept within those pH 6-8
• H pylori would inhabit only those regions of
the gastric mucosal surface that remain largely
within this pH range
• population of Fundus of stomach is sparse but
population of is high Antral(absence of acid
secretion and the presence of HCO3)
23. • The organism is motile but pH not affect on chemotaxis of
Helicobacteria
• If the gastric pH is changed, intragastric population would tend
to redistribute on the gastric surface
• the ability of the bacteria to colonise the gastric surface where
the pH is between 3.0 and 6.0
• Hence with proton pump inhibition the antrum would tend to
lose organisms but the fundus would tend to acquire organisms
where the surface pH would exceed 3.0
24. Chemotaxis
• H. pylori motile bacteri and have chemotaxi like
other motile bacteria
• Three homologues of the chemotaxis pathway in
E. coli (CheW, CheA, and CheY)
• four methyl-accepting chemotaxis proteins
(MCPs), which mediate specificity for
ligands,sens environment conditions
27. 2013 regimens
• Triple therapy:
• proton pump inhibitor (PPI) (lansoprazole 30 mg twice daily,
omeprazole 20 mg twice daily, pantoprazole 40 mg twice daily,
rabeprazole 20 mg twice daily, or esomeprazole 40 mg once daily),
amoxicillin (1 g twice daily), and clarithromycin (500 mg twice
daily) for 7 to 14 days. We suggest treatment for 10 days to two
weeks.
• Quadruple therapy
• bismuth (525 mg four times daily) and two antibiotics (eg,
metronidazole 250 mg four times daily and tetracycline 500 mg
four times daily) given for 10 to 14 days. Quadruple therapy is
appropriate as initial therapy in areas in which the prevalence of
resistance to clarithromycin or metronidazole is ≥15 percent, or in
patients with recent or repeated exposure to clarithromycin or
metronidazole [18]. If tetracycline is not available, doxycycline
(100 mg twice daily) may be substituted
28. 1. PETER DOIG,1* BOUDEWIJN L. DE JONGE,1 RICHARD
A. ALM.et al. Helicobacter pylori Physiology Predicted from
Genomic Comparison of Two Strains. MICROBIOLOGY AND
MOLECULAR BIOLOGY REVIEWS, Sept. 2006, p. 675–707
2. David j. KellyThe Physiology and Metabolism of the Human
Gastric PathogenHelicobacter pylori. Advances in Microbial
Physiology. Volume 40 .1998, Pages 137–189
3. D Scott, D Weeks, K Melchers, et al. The life and death of
helicobacter pylori . Gut 1998;43(suppl 1):S56–S60
4. Marco Romano, and Antonio Cuomo. Eradication of
Helicobacter pylori: A Clinical Update.
MedGenMed. 2004; 6(1): 19.
5. Sheila E Crowe. Treatment regimens for Helicobacter pylori.
Gut2013 . : 19,
Editor's Notes
Thus these proteins are more positively
charged in acid than those of neutralophiles
such as Escherichia coli, thereby retarding flux
of protons into the periplasmic space
This inner membrane proteolipid is
responsible for the proton flow across the
membrane enabling ATP synthesis
provides a degree of resistance
to acid present on the outer surface and
perhaps occasionally on the outer face of the
inner membrane of H pylori.
Thus, the finding that H pylori is killed within a
few minutes by pH &lt; 4.0 in vitro in the absence
of urea provides evidence for the presence of
other mechanisms enabling acid tolerance.
H pylori survive between pH 4.0 and 8.2.
as would happen with
treatment with proton pump inhibitors