The document discusses clinical biochemistry of gastrointestinal diseases. It covers topics like peptic ulcer disease, gastric ulcer, duodenal ulcer, Zollinger-Ellison syndrome, gastritis, and acute pancreatitis. For peptic ulcer disease, it describes causes such as H. pylori infection and NSAID use, signs and symptoms, characteristics of gastric versus duodenal ulcers, and methods of diagnosis. It also provides details on Zollinger-Ellison syndrome, including causes, signs, diagnosis, and treatment. For gastritis, it discusses definitions, classifications, and histopathology of acute and chronic forms.
The document discusses the physiology of acid secretion in the gastrointestinal tract and the pathophysiology of peptic ulcers. It covers the anatomy of the stomach and types of cells that secrete acid and other substances. Risk factors for peptic ulcers include H. pylori infection and NSAID use. Diagnosis involves endoscopy, urea breath test, and stool antigen test. Treatment includes lifestyle modifications, antacids, H2 receptor antagonists, proton pump inhibitors, and anticholinergics. Surgery may be required in some cases.
This document provides an overview of peptic ulcer disease. It begins with definitions of acid peptic disease and what constitutes a peptic ulcer. It then discusses the epidemiology of peptic ulcers and covers the etiology and pathophysiology, including factors that damage the stomach lining like excess acid secretion, NSAIDs, and Helicobacter pylori infection. The document reviews the history of drug development for peptic ulcers and describes various drug classes used for treatment, including antacids, H2 receptor antagonists, and proton pump inhibitors. It also discusses testing and treatment for H. pylori infection, as well as principles of medical management of peptic ulcers.
This document discusses peptic ulcers and their treatment. It begins by defining a peptic ulcer as a disruption of the stomach or duodenal mucosa caused by acid and pepsin exposure. Risk factors include H. pylori infection, NSAID use, smoking, stress, and excess acid secretion. Symptoms can include epigastric pain, nausea, vomiting, weight loss, and bleeding. Treatment aims to eradicate H. pylori, relieve symptoms, heal ulcers, and prevent recurrence. The standard first-line treatment is a proton pump inhibitor combined with two antibiotics for 14 days.
Disorders of Lower GIT system Ppt (3).pptAbdiWakjira2
This document provides information on the management of various gastrointestinal disorders. It begins with an overview of the gastrointestinal tract and then discusses gastroesophageal reflux disease (GERD) in detail, including causes, complications, clinical manifestations, diagnosis, and management. It also briefly covers gastritis, peptic ulcer disease, and the differences between gastric and duodenal ulcers. The document is intended to describe the features, diagnosis, and management of common gastrointestinal disorders for medical learning purposes.
This document outlines a lecture on peptic ulcer disease (PUD). It begins with definitions of PUD and ulcers, noting the typical burning pain exacerbated by fasting and relieved by eating. It then discusses gastric physiology including the mucosal defense system and role of prostaglandins. Key causes of ulcers are described as H. pylori bacteria and NSAID use. Clinical features, complications, differential diagnosis, diagnostic tests, and treatment approaches are summarized. The role of H. pylori and NSAIDs in duodenal and gastric ulcers is emphasized throughout.
- Gastric and duodenal disorders like gastritis and peptic ulcers are common gastrointestinal problems that can be caused by factors like H. pylori infection, NSAID use, stress, and diet. Chronic gastritis and ulcers require long-term management like antibiotics, proton pump inhibitors, and lifestyle modifications.
- Peptic ulcers form in the stomach or duodenum due to an imbalance between gastric acid and the mucosal protective factors. Duodenal ulcers are more common than gastric ulcers and have distinguishing clinical features. Treatment aims to eliminate H. pylori and reduce acid with medications, surgery if needed.
- Morbid obesity is defined as being over 100 pounds
This document summarizes a seminar on peptic ulcer disease. It defines peptic ulcers, classifies them as acute or chronic, and discusses their etiology, including H. pylori infection and stress factors. It covers the pathogenesis of ulcers, clinical features, diagnosis including tests for H. pylori, and treatment using proton pump inhibitors, H2 receptor antagonists, and antibiotics. It also discusses complications, factors affecting treatment success, adverse drug reactions, drug interactions, and patient counseling.
The document discusses the physiology of acid secretion in the gastrointestinal tract and the pathophysiology of peptic ulcers. It covers the anatomy of the stomach and types of cells that secrete acid and other substances. Risk factors for peptic ulcers include H. pylori infection and NSAID use. Diagnosis involves endoscopy, urea breath test, and stool antigen test. Treatment includes lifestyle modifications, antacids, H2 receptor antagonists, proton pump inhibitors, and anticholinergics. Surgery may be required in some cases.
This document provides an overview of peptic ulcer disease. It begins with definitions of acid peptic disease and what constitutes a peptic ulcer. It then discusses the epidemiology of peptic ulcers and covers the etiology and pathophysiology, including factors that damage the stomach lining like excess acid secretion, NSAIDs, and Helicobacter pylori infection. The document reviews the history of drug development for peptic ulcers and describes various drug classes used for treatment, including antacids, H2 receptor antagonists, and proton pump inhibitors. It also discusses testing and treatment for H. pylori infection, as well as principles of medical management of peptic ulcers.
This document discusses peptic ulcers and their treatment. It begins by defining a peptic ulcer as a disruption of the stomach or duodenal mucosa caused by acid and pepsin exposure. Risk factors include H. pylori infection, NSAID use, smoking, stress, and excess acid secretion. Symptoms can include epigastric pain, nausea, vomiting, weight loss, and bleeding. Treatment aims to eradicate H. pylori, relieve symptoms, heal ulcers, and prevent recurrence. The standard first-line treatment is a proton pump inhibitor combined with two antibiotics for 14 days.
Disorders of Lower GIT system Ppt (3).pptAbdiWakjira2
This document provides information on the management of various gastrointestinal disorders. It begins with an overview of the gastrointestinal tract and then discusses gastroesophageal reflux disease (GERD) in detail, including causes, complications, clinical manifestations, diagnosis, and management. It also briefly covers gastritis, peptic ulcer disease, and the differences between gastric and duodenal ulcers. The document is intended to describe the features, diagnosis, and management of common gastrointestinal disorders for medical learning purposes.
This document outlines a lecture on peptic ulcer disease (PUD). It begins with definitions of PUD and ulcers, noting the typical burning pain exacerbated by fasting and relieved by eating. It then discusses gastric physiology including the mucosal defense system and role of prostaglandins. Key causes of ulcers are described as H. pylori bacteria and NSAID use. Clinical features, complications, differential diagnosis, diagnostic tests, and treatment approaches are summarized. The role of H. pylori and NSAIDs in duodenal and gastric ulcers is emphasized throughout.
- Gastric and duodenal disorders like gastritis and peptic ulcers are common gastrointestinal problems that can be caused by factors like H. pylori infection, NSAID use, stress, and diet. Chronic gastritis and ulcers require long-term management like antibiotics, proton pump inhibitors, and lifestyle modifications.
- Peptic ulcers form in the stomach or duodenum due to an imbalance between gastric acid and the mucosal protective factors. Duodenal ulcers are more common than gastric ulcers and have distinguishing clinical features. Treatment aims to eliminate H. pylori and reduce acid with medications, surgery if needed.
- Morbid obesity is defined as being over 100 pounds
This document summarizes a seminar on peptic ulcer disease. It defines peptic ulcers, classifies them as acute or chronic, and discusses their etiology, including H. pylori infection and stress factors. It covers the pathogenesis of ulcers, clinical features, diagnosis including tests for H. pylori, and treatment using proton pump inhibitors, H2 receptor antagonists, and antibiotics. It also discusses complications, factors affecting treatment success, adverse drug reactions, drug interactions, and patient counseling.
This document discusses perforated peptic ulcers. It first covers the surgical anatomy and blood supply of the stomach and duodenum. It then discusses the epidemiology, pathophysiology, risk factors, presentation, diagnosis, and treatment of perforated peptic ulcers. Key points include that perforations are more common in duodenal versus gastric ulcers and have a higher mortality rate for gastric ulcers. Risk factors include H. pylori infection, NSAID use, smoking, and Zollinger-Ellison syndrome. Patients typically present with sudden severe abdominal pain. Diagnosis involves upright chest x-rays showing free air. Treatment is surgical repair of the perforation.
Peptic ulcer disease is a break in the gastrointestinal mucosa caused by aggressive acid-peptic juices. Common sites are the stomach and duodenum. H. pylori infection and NSAID use are major causes. Clinical features include abdominal pain, nausea, and vomiting. Diagnosis involves endoscopy, biopsy, and H. pylori testing. Treatment includes lifestyle modifications, medications like PPIs, and H. pylori eradication therapy. Surgery is considered if complications develop or medical management fails. Proper counseling helps patients understand diet and medication.
The document provides information on inflammatory bowel disease (IBD), including its classification into ulcerative colitis and Crohn's disease. It discusses the epidemiology, etiology, pathophysiology, clinical manifestations, diagnosis, treatment goals, and pharmacological and non-pharmacological treatment approaches for IBD. The major drug therapy types used for IBD include aminosalicylates, corticosteroids, immunosuppressants, TNF inhibitors, and antimicrobials. Surgery may be required for severe cases or complications that do not respond to medical management.
The document provides information on inflammatory bowel disease (IBD), including its classification into ulcerative colitis and Crohn's disease. It discusses the epidemiology, etiology, pathophysiology, clinical manifestations, diagnosis, treatment goals, and pharmacological and non-pharmacological treatment approaches for IBD. The major drug therapy types used for IBD include aminosalicylates, corticosteroids, immunosuppressants, TNF inhibitors, and antimicrobials. Surgery may be required for severe cases or complications that do not respond to medical management.
Peptic ulcers are lesions that occur in the stomach or duodenum due to exposure to gastric acid and pepsin. They typically result from an imbalance between aggressive factors like acid and pepsin and defensive mucosal factors. The most common causes are Helicobacter pylori infection and use of nonsteroidal anti-inflammatory drugs. Treatment involves eradicating H. pylori if present, reducing acid secretion with proton pump inhibitors, and protecting the mucosa with drugs like sucralfate or misoprostol.
Gastritis is an inflammation of the stomach lining that can be either acute or chronic. Acute gastritis is short-term and caused by factors like NSAIDs, alcohol, bile reflux, or radiation/chemotherapy. Chronic gastritis is long-term inflammation that can result from repeated acute episodes or be caused by H. pylori bacteria or chemical irritants. Symptoms include epigastric pain, nausea, vomiting, and bleeding. Treatment involves antacids, H2 blockers, PPIs, and antibiotics for H. pylori. Nursing care focuses on pain relief, nutrition, fluid balance, education, and symptom management.
Peptic ulcer disease and GERD are common digestive disorders caused by an imbalance between gastric acid and the stomach's protective mechanisms. Peptic ulcers form when the stomach or duodenal lining is broken down, typically due to H. pylori infection or long-term NSAID use. GERD occurs when stomach acid backs up into the esophagus, often due to a weak lower esophageal sphincter. Both are treated using proton pump inhibitors to reduce acid production along with antibiotics for H. pylori if present. Lifestyle changes like sleeping upright and smaller meals can help prevent acid reflux.
Talking about gastritis & peptic ulcer disease ( definetions , clinical picture , diagnosis & treatment , complications ) , all informations are Up tu date of 2017
This document discusses peptic ulcers, including their definition, classification, causes, symptoms, diagnosis, and treatment. Peptic ulcers are caused by an imbalance between gastric acid and pepsin damaging the stomach and duodenal lining and the mucosal defenses that normally protect it. Key points covered include that Helicobacter pylori infection and NSAID use are the primary causes of peptic ulcers. Symptoms include abdominal pain and bleeding. Treatment involves eradicating H. pylori, reducing acid production, and managing pain and risk of complications.
This document provides information on the causes, diagnosis, and management of peptic ulcer disease and gastric outlet obstruction. It discusses that peptic ulcers are caused by an imbalance between aggressive factors like acid secretion and defensive factors. Infection with H. pylori is a key cause. Diagnosis involves endoscopy with biopsy. Management focuses on treating H. pylori infection and using antisecretory drugs. Surgery is reserved for complications or refractory cases. Gastric outlet obstruction is usually due to peptic ulcer disease but can also be caused by malignancy, inflammation, or other conditions.
The document summarizes gastrointestinal agents and gastric acid secretion. It discusses the gastrointestinal tract and its role in digestion. It describes the three phases of gastric secretion and the factors that stimulate and inhibit acid production. Common gastrointestinal disorders are outlined along with agents used to treat them, including antacids, H2 receptor antagonists, and proton pump inhibitors. The inhibition of gastric acid secretion is an important therapeutic target for conditions like ulcers and GERD.
Toxic megacolon is an acute form of colonic distension characterized by a very dilated colon accompanied by abdominal distension and sometimes fever, abdominal pain, or shock. It occurs in 1-2.5% of patients with colon diseases like ulcerative colitis and has a high mortality risk if not treated promptly. Diagnostic criteria include radiographic evidence of large colon diameter and symptoms of fever, rapid heart rate, high white blood cell count, or low blood pressure.
Inflammatory bowel disease (IBD) represents a group of chronic disorders that cause prolonged inflammation of the digestive tract. The two main types are ulcerative colitis, which causes inflammation and ulcers in the lining of the large intestine, and Crohn's disease, which is a chronic inflammatory disease that can affect any part of the gastrointestinal tract from mouth to anus. IBD is treated through a combination of medications, dietary changes, and sometimes surgery, with the goals of inducing and maintaining remission of symptoms, preventing complications, and avoiding surgery if possible. Treatments include aminosalicylates, corticosteroids, immunosuppressants, biologics that target tumor necrosis factor, and antimicrobial agents.
This document discusses peptic ulcer disease (PUD), including its causes, types, symptoms, diagnosis, and treatment. PUD is characterized by erosion of the GI mucosa from stomach acid and pepsin. It commonly affects the lower esophagus, stomach, and duodenum. The two main types are gastric and duodenal ulcers. Symptoms include abdominal pain, nausea, and vomiting. Diagnosis involves endoscopy and tests for H. pylori bacteria. Treatment focuses on reducing stomach acid with PPIs or H2 blockers, eradicating H. pylori, and protecting the mucosa. Complications can include bleeding, perforation, and obstruction if not properly treated.
Gastroparesis in Chronic Kidney DiseaseVishal Bagchi
· Identify the common causes of gastroparesis in CKD · Overview of gut physiology
· Differentiate gastroparesis vs. other GI issues and their symptoms "· Provide comparison of gastroparesis & other common GI issues in CKD
· Testing and findings"
· Compare and contrast various evidence-based treatments for gastroparesis "· Review efficacy of current treatments in CKD for gastroparesis
· Cite what providers can safely advise patients to reduce symptoms"
Gastritis is inflammation of the stomach lining that can be acute (sudden) or chronic (long-lasting). The most common causes are infection with Helicobacter pylori bacteria and long-term use of nonsteroidal anti-inflammatory drugs. While many people with gastritis do not have symptoms, some experience upper abdominal pain, nausea, or vomiting. Treatment involves medications to reduce stomach acid and antibiotics to treat H. pylori infections. Left untreated, chronic gastritis caused by H. pylori can increase the risk of ulcers and stomach cancer.
Peptic ulcer is caused mainly by infection with Helicobacter pylori bacteria or use of nonsteroidal anti-inflammatory drugs like aspirin. Symptoms include abdominal pain and discomfort. Risk factors include smoking, alcohol, family history, and certain illnesses. Complications can include internal bleeding, perforation of the stomach wall, or gastric outlet obstruction. Treatment involves eradicating H. pylori with antibiotics if present, reducing NSAID use, and medications to reduce acid production and promote healing. Prevention focuses on healthy lifestyle habits and protecting against infections.
Ulcerative colitis causes inflammation and ulcers in the lining of the rectum and colon. Common symptoms include bloody diarrhea, abdominal pain, fatigue, and weight loss. Tests used to diagnose include physical exam, medical history, blood tests, and stool samples. While the specific cause is unknown, genetic and environmental factors may play a role. Treatment often involves medications like mesalazine which reduce inflammation. The disease course varies depending on extent of involvement, with limited disease usually having a milder course.
1-1-Computing and Pharmaceutical Numeracy.pdfMuungoLungwani
This document provides a summary of a lecture on pharmaceutical numeracy and calculations. It covers topics such as fractions, decimals, dosage forms, weights and measures, dilution, concentration, and calculations for reducing/enlarging formulas and percentage preparations. Study questions are also provided to help reinforce concepts related to quantitative pharmaceutical procedures and calculations.
The document discusses states of matter and pharmaceutical materials. It begins by comparing gases, liquids, and solids, noting that solids have molecules in close contact that do not move. It then discusses intermolecular forces, ideal gas laws, liquefaction of gases, and the solid state including crystals, unit cells, polymorphism, and amorphous solids. It notes that polymorphism can impact properties like solubility, melting point, and bioavailability which are important for pharmaceutical processes and drug performance.
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Similar to PMY 6110_2-2-Gastrointestinal Diseases.pdf
This document discusses perforated peptic ulcers. It first covers the surgical anatomy and blood supply of the stomach and duodenum. It then discusses the epidemiology, pathophysiology, risk factors, presentation, diagnosis, and treatment of perforated peptic ulcers. Key points include that perforations are more common in duodenal versus gastric ulcers and have a higher mortality rate for gastric ulcers. Risk factors include H. pylori infection, NSAID use, smoking, and Zollinger-Ellison syndrome. Patients typically present with sudden severe abdominal pain. Diagnosis involves upright chest x-rays showing free air. Treatment is surgical repair of the perforation.
Peptic ulcer disease is a break in the gastrointestinal mucosa caused by aggressive acid-peptic juices. Common sites are the stomach and duodenum. H. pylori infection and NSAID use are major causes. Clinical features include abdominal pain, nausea, and vomiting. Diagnosis involves endoscopy, biopsy, and H. pylori testing. Treatment includes lifestyle modifications, medications like PPIs, and H. pylori eradication therapy. Surgery is considered if complications develop or medical management fails. Proper counseling helps patients understand diet and medication.
The document provides information on inflammatory bowel disease (IBD), including its classification into ulcerative colitis and Crohn's disease. It discusses the epidemiology, etiology, pathophysiology, clinical manifestations, diagnosis, treatment goals, and pharmacological and non-pharmacological treatment approaches for IBD. The major drug therapy types used for IBD include aminosalicylates, corticosteroids, immunosuppressants, TNF inhibitors, and antimicrobials. Surgery may be required for severe cases or complications that do not respond to medical management.
The document provides information on inflammatory bowel disease (IBD), including its classification into ulcerative colitis and Crohn's disease. It discusses the epidemiology, etiology, pathophysiology, clinical manifestations, diagnosis, treatment goals, and pharmacological and non-pharmacological treatment approaches for IBD. The major drug therapy types used for IBD include aminosalicylates, corticosteroids, immunosuppressants, TNF inhibitors, and antimicrobials. Surgery may be required for severe cases or complications that do not respond to medical management.
Peptic ulcers are lesions that occur in the stomach or duodenum due to exposure to gastric acid and pepsin. They typically result from an imbalance between aggressive factors like acid and pepsin and defensive mucosal factors. The most common causes are Helicobacter pylori infection and use of nonsteroidal anti-inflammatory drugs. Treatment involves eradicating H. pylori if present, reducing acid secretion with proton pump inhibitors, and protecting the mucosa with drugs like sucralfate or misoprostol.
Gastritis is an inflammation of the stomach lining that can be either acute or chronic. Acute gastritis is short-term and caused by factors like NSAIDs, alcohol, bile reflux, or radiation/chemotherapy. Chronic gastritis is long-term inflammation that can result from repeated acute episodes or be caused by H. pylori bacteria or chemical irritants. Symptoms include epigastric pain, nausea, vomiting, and bleeding. Treatment involves antacids, H2 blockers, PPIs, and antibiotics for H. pylori. Nursing care focuses on pain relief, nutrition, fluid balance, education, and symptom management.
Peptic ulcer disease and GERD are common digestive disorders caused by an imbalance between gastric acid and the stomach's protective mechanisms. Peptic ulcers form when the stomach or duodenal lining is broken down, typically due to H. pylori infection or long-term NSAID use. GERD occurs when stomach acid backs up into the esophagus, often due to a weak lower esophageal sphincter. Both are treated using proton pump inhibitors to reduce acid production along with antibiotics for H. pylori if present. Lifestyle changes like sleeping upright and smaller meals can help prevent acid reflux.
Talking about gastritis & peptic ulcer disease ( definetions , clinical picture , diagnosis & treatment , complications ) , all informations are Up tu date of 2017
This document discusses peptic ulcers, including their definition, classification, causes, symptoms, diagnosis, and treatment. Peptic ulcers are caused by an imbalance between gastric acid and pepsin damaging the stomach and duodenal lining and the mucosal defenses that normally protect it. Key points covered include that Helicobacter pylori infection and NSAID use are the primary causes of peptic ulcers. Symptoms include abdominal pain and bleeding. Treatment involves eradicating H. pylori, reducing acid production, and managing pain and risk of complications.
This document provides information on the causes, diagnosis, and management of peptic ulcer disease and gastric outlet obstruction. It discusses that peptic ulcers are caused by an imbalance between aggressive factors like acid secretion and defensive factors. Infection with H. pylori is a key cause. Diagnosis involves endoscopy with biopsy. Management focuses on treating H. pylori infection and using antisecretory drugs. Surgery is reserved for complications or refractory cases. Gastric outlet obstruction is usually due to peptic ulcer disease but can also be caused by malignancy, inflammation, or other conditions.
The document summarizes gastrointestinal agents and gastric acid secretion. It discusses the gastrointestinal tract and its role in digestion. It describes the three phases of gastric secretion and the factors that stimulate and inhibit acid production. Common gastrointestinal disorders are outlined along with agents used to treat them, including antacids, H2 receptor antagonists, and proton pump inhibitors. The inhibition of gastric acid secretion is an important therapeutic target for conditions like ulcers and GERD.
Toxic megacolon is an acute form of colonic distension characterized by a very dilated colon accompanied by abdominal distension and sometimes fever, abdominal pain, or shock. It occurs in 1-2.5% of patients with colon diseases like ulcerative colitis and has a high mortality risk if not treated promptly. Diagnostic criteria include radiographic evidence of large colon diameter and symptoms of fever, rapid heart rate, high white blood cell count, or low blood pressure.
Inflammatory bowel disease (IBD) represents a group of chronic disorders that cause prolonged inflammation of the digestive tract. The two main types are ulcerative colitis, which causes inflammation and ulcers in the lining of the large intestine, and Crohn's disease, which is a chronic inflammatory disease that can affect any part of the gastrointestinal tract from mouth to anus. IBD is treated through a combination of medications, dietary changes, and sometimes surgery, with the goals of inducing and maintaining remission of symptoms, preventing complications, and avoiding surgery if possible. Treatments include aminosalicylates, corticosteroids, immunosuppressants, biologics that target tumor necrosis factor, and antimicrobial agents.
This document discusses peptic ulcer disease (PUD), including its causes, types, symptoms, diagnosis, and treatment. PUD is characterized by erosion of the GI mucosa from stomach acid and pepsin. It commonly affects the lower esophagus, stomach, and duodenum. The two main types are gastric and duodenal ulcers. Symptoms include abdominal pain, nausea, and vomiting. Diagnosis involves endoscopy and tests for H. pylori bacteria. Treatment focuses on reducing stomach acid with PPIs or H2 blockers, eradicating H. pylori, and protecting the mucosa. Complications can include bleeding, perforation, and obstruction if not properly treated.
Gastroparesis in Chronic Kidney DiseaseVishal Bagchi
· Identify the common causes of gastroparesis in CKD · Overview of gut physiology
· Differentiate gastroparesis vs. other GI issues and their symptoms "· Provide comparison of gastroparesis & other common GI issues in CKD
· Testing and findings"
· Compare and contrast various evidence-based treatments for gastroparesis "· Review efficacy of current treatments in CKD for gastroparesis
· Cite what providers can safely advise patients to reduce symptoms"
Gastritis is inflammation of the stomach lining that can be acute (sudden) or chronic (long-lasting). The most common causes are infection with Helicobacter pylori bacteria and long-term use of nonsteroidal anti-inflammatory drugs. While many people with gastritis do not have symptoms, some experience upper abdominal pain, nausea, or vomiting. Treatment involves medications to reduce stomach acid and antibiotics to treat H. pylori infections. Left untreated, chronic gastritis caused by H. pylori can increase the risk of ulcers and stomach cancer.
Peptic ulcer is caused mainly by infection with Helicobacter pylori bacteria or use of nonsteroidal anti-inflammatory drugs like aspirin. Symptoms include abdominal pain and discomfort. Risk factors include smoking, alcohol, family history, and certain illnesses. Complications can include internal bleeding, perforation of the stomach wall, or gastric outlet obstruction. Treatment involves eradicating H. pylori with antibiotics if present, reducing NSAID use, and medications to reduce acid production and promote healing. Prevention focuses on healthy lifestyle habits and protecting against infections.
Ulcerative colitis causes inflammation and ulcers in the lining of the rectum and colon. Common symptoms include bloody diarrhea, abdominal pain, fatigue, and weight loss. Tests used to diagnose include physical exam, medical history, blood tests, and stool samples. While the specific cause is unknown, genetic and environmental factors may play a role. Treatment often involves medications like mesalazine which reduce inflammation. The disease course varies depending on extent of involvement, with limited disease usually having a milder course.
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This document provides a summary of a lecture on pharmaceutical numeracy and calculations. It covers topics such as fractions, decimals, dosage forms, weights and measures, dilution, concentration, and calculations for reducing/enlarging formulas and percentage preparations. Study questions are also provided to help reinforce concepts related to quantitative pharmaceutical procedures and calculations.
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I understand you're going through a difficult time with the loss of your husband. While sleep aids can help in the short term, depression often requires longer term treatment. Let me see if I can arrange for you to speak with one of the counselors here - they may be able to provide support that will help you cope and feel better over time. There are also medications and therapies that a doctor can recommend specifically for depression if needed. How does that sound? I'm here if you need anything else.
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The document discusses preformulation characterization of new drug candidates. It covers assessing key physical properties like crystallinity, polymorphism, hygroscopicity, particle size and shape, bulk density, and flow properties which influence formulation development, stability, and bioavailability. Solubility analysis including determining pKa, pH solubility profiles, and effects of temperature are also important to understand for formulation. Together, preformulation studies provide essential information to guide development of a stable, safe and effective dosage form with optimal bioavailability.
PMY 6120_1-2-Pharmaceutical Formulation Systems_Compound and Dispensing Proce...MuungoLungwani
This document discusses a course on pharmaceutical compounding and dispensing. The course covers background topics, dispensing and patient care, and extemporaneous dispensing. It aims to help students understand the roles of compounding pharmacists, resolve problems in making specific preparations, apply techniques to administrative and clinical aspects of drug delivery, determine dosages based on patient conditions, and apply principles of good pharmacy practice. Extemporaneous dispensing involves considerations for the intended use, safety, formula calculation, preparation method, container choice, and labeling for compounded products.
This document contains course information from Dr. L.T.M. Muungo on various pharmaceutical topics:
1. The document outlines several courses on formulation systems, pharmaceutical calculations, dispensing, manufacturing, compounding, clinical pharmacy practice, and other related topics.
2. Many of the courses discuss dosage forms, drug delivery systems, pharmaceutical ingredients, sterile and non-sterile processing, and other areas of pharmaceutics.
3. The document also provides information on clinical pharmacy year attachments, case studies, health systems, rational drug use, and research processes including proposal writing, data collection, analysis, and publication.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
3. June 26, 2012 Total slide. 126 3
Clinical Biochemistry Gastrointestinal Disease
Gastrointestinal disease
Peptic ulcer disease
Chronic duodenal ulcer
Chronic benign gastric ulcer
Zollinger-Ellison syndrome
Gastritis
Gastric cancer
Post gastrectomy syndrome
Acute pancreatitis
Chronic pancreatitis
Insulinoma
Glucagonoma
Somatostatinoma
4. June 26, 2012 Total slide. 126 4
Clinical Biochemistry Gastrointestinal Disease
5. June 26, 2012 Total slide. 126 5
Clinical Biochemistry Gastrointestinal Disease
Peptic Ulcer Disease (PUD)
What is it?
Group of chronic disorders characterized by ulcerating
mucosal lesions in upper GI tract
chronic inflammatory condition
common forms are duodenal and gastric ulceration
Where does it occur?
Stomach, duodenum
What causes PUD?
H. pylori or drug induced (most commonly by chronic NSAID
use)
6. June 26, 2012 Total slide. 126 6
Clinical Biochemistry Gastrointestinal Disease
Drugs that can cause PUD
methotrexate
cyclophosphamide
azathioprine
erythromycin
iron
corticosteriods
potassium chloride
NSAIDS
7. June 26, 2012 Total slide. 126 7
Clinical Biochemistry Gastrointestinal Disease
Signs and Symptoms of PUD
Can be symptomatic
anorexia, nausea, vomiting, belching, bloating, heartburn,
epigastric pain (pain in the upper abdomen)
awakened at night (usu. around 3am,)
duodenal ulcers
epigastric pain, tenderness, burning, aching between xiphoid
process and belly button
relieved with food intake or antacids
gastric ulcer
diffuse pain over midepigastrium (midstomach)
worsened by food
8. June 26, 2012 Total slide. 126 8
Clinical Biochemistry Gastrointestinal Disease
Characteristics and Comparisons
Between Gastric and Duodenal Ulcers
Gastric ulcer formation involves inflammatory
involvement of acid-producing cells but usually occurs
with low acid secretion.
Duodenal ulcers are associated with high acid and low
bicarbonate secretion.
Increased mortality and hemorrhage are associated with
gastric ulcers.
10. June 26, 2012 Total slide. 126 10
Clinical Biochemistry Gastrointestinal Disease
Normal Stomach
11. June 26, 2012 Total slide. 126 11
Clinical Biochemistry Gastrointestinal Disease
Esophagus & Stomach Normal
12. June 26, 2012 Total slide. 126 12
Clinical Biochemistry Gastrointestinal Disease
Definition:
Ulceration (breach in mucosa) due to acid & pepsin
attack – peptic ulcer.
Deeper than just mucosa
Single, punched out, clean base
14. June 26, 2012 Total slide. 126 14
Clinical Biochemistry Gastrointestinal Disease
H. Pylori organisms- silver st.
15. June 26, 2012 Total slide. 126 15
Clinical Biochemistry Gastrointestinal Disease
Pathogenesis:
Helicobacter pylori infection
Colonization of gastric mucous
Urease ammonia neutralization of acid Rebound
acid production.
Protease – Mucous break down.
Weak mucosal resistance
Acid & Pepsin digestion of mucosa
Chronic Ulceration
16. June 26, 2012 Total slide. 126 16
Clinical Biochemistry Gastrointestinal Disease
Normal
Increased Attack
Hyperacidity
Weak defense
Helicobacter pylori
Stress, drugs, smoking
Etiology of PUD
17. June 26, 2012 Total slide. 126 17
Clinical Biochemistry Gastrointestinal Disease
Helicobacter pylori:
Most common infection in the world (20%)
10% of men, 4% women develop PUD
Positive in 70-100% of PUD patients.
H.pylori related disorders:
Chronic gastritis – 90%
Peptic ulcer disease – 95-100%
Gastric carcinoma – 70%
Gastric lymphoma
Reflux Oesophagitis.
Non ulcer dyspepsia
18. June 26, 2012 Total slide. 126 18
Clinical Biochemistry Gastrointestinal Disease
Peptic Ulcer Morphology:
90% ulcers in first portion of duodenum or
lesser curvature of stomach
80 to 90% cases single ulcer. Round Small
ulcers with sharply punched out edges
Small <2cm, clean base.
Microscopy: 4 zones.
Superficial necrotic layer.
Inflammatory cells zone.
Granulation tissue zone
Collagenous scar layer.
19. June 26, 2012 Total slide. 126 19
Clinical Biochemistry Gastrointestinal Disease
20. June 26, 2012 Total slide. 126 20
Clinical Biochemistry Gastrointestinal Disease
21. June 26, 2012 Total slide. 126 21
Clinical Biochemistry Gastrointestinal Disease
Gastric peptic ulcer
22. June 26, 2012 Total slide. 126 22
Clinical Biochemistry Gastrointestinal Disease
Gastric peptic ulcer:
23. June 26, 2012 Total slide. 126 23
Clinical Biochemistry Gastrointestinal Disease
Gastric Ulcer
Gastric ulcer:
24. June 26, 2012 Total slide. 126 24
Clinical Biochemistry Gastrointestinal Disease
Duodenal Peptic Ulcer
25. June 26, 2012 Total slide. 126 25
Clinical Biochemistry Gastrointestinal Disease
Peptic ulcer - Endoscopy
26. June 26, 2012 Total slide. 126 26
Clinical Biochemistry Gastrointestinal Disease
Gastric Ulcer
27. June 26, 2012 Total slide. 126 27
Clinical Biochemistry Gastrointestinal Disease
Gastric Ulcer
28. June 26, 2012 Total slide. 126 28
Clinical Biochemistry Gastrointestinal Disease
Gastric Ulcer
Punched out ulcer
Clean base
Small single
Radiating mucosal folds.
Benign ulcer.
No tumor.
29. June 26, 2012 Total slide. 126 29
Clinical Biochemistry Gastrointestinal Disease
Peptic Ulcer
30. June 26, 2012 Total slide. 126 30
Clinical Biochemistry Gastrointestinal Disease
Peptic Ulcer Microscopy:
32. June 26, 2012 Total slide. 126 32
Clinical Biochemistry Gastrointestinal Disease
CDU Camplications
Hemorrhage
Due to the ulcer’s eroding a blood vessel
Perforation
Through the anterior wall of the duodenal cap
Causing peritonitis
Penetration of the ulcer into the adjacent structures
Such as pancrease , biliary tract , liver, colon, abdominal wall, or
even long
Luminal abstruction
Caused by the gradual contraction of the ulser scar
33. June 26, 2012 Total slide. 126 33
Clinical Biochemistry Gastrointestinal Disease
Gastric Ulcer
34. June 26, 2012 Total slide. 126 34
Clinical Biochemistry Gastrointestinal Disease
Points to Remember:
A peptic ulcer is a sore in the lining of the
stomach or duodenum due to attack by acid &
Pepsin.
The major cause - H. pylori bacterium. Others
are NSAIDs. spicy food, stress are risk factors.
H. pylori can be transmitted from person to
person through close contact
A combination of antibiotics and H pump
inhibitors is the most effective treatment.
35. June 26, 2012 Total slide. 126 35
Clinical Biochemistry Gastrointestinal Disease
Helecobacter pylori
36. June 26, 2012 Total slide. 126 36
Clinical Biochemistry Gastrointestinal Disease
Toludine Blue stain – H pylori
37. June 26, 2012 Total slide. 126 37
Clinical Biochemistry Gastrointestinal Disease
Urease production test
40. June 26, 2012 Total slide. 126 40
Clinical Biochemistry Gastrointestinal Disease
41. June 26, 2012 Total slide. 126 41
Clinical Biochemistry Gastrointestinal Disease
Zollinger-Ellison syndrome
Increased numbers of
Increased numbers of
parietal cells with no
parietal cells with no
change in surface and
change in surface and
foveolar mucous cells.
foveolar mucous cells.
42. June 26, 2012 Total slide. 126 42
Clinical Biochemistry Gastrointestinal Disease
Zollinger Ellison Syndrome
Tumour Location
Symptoms
Pancreas 50-60%
Duodenum 40-50%
20-25% Related to MEN-1
50-70% Malignant (lymphnode
metastases)
Gastrinoma Triangle 80%
Gastritis
Recurrent ulcers
Diarrhea (malabsorption)
43. June 26, 2012 Total slide. 126 43
Clinical Biochemistry Gastrointestinal Disease
Zollinger-Ellison syndrome
0.1 to 1 percent of patients with peptic ulcer disease .
Underestimation!
symptoms similar to typical peptic ulcer .
symptoms may be controlled by standard doses of an
antisecretory drug
patients may not be tested for hypergastrinemia
Gastrinomas can be either sporadic (80 percent) or
associated with multiple endocrine neoplasia type 1
44. June 26, 2012 Total slide. 126 44
Clinical Biochemistry Gastrointestinal Disease
Signs of ZES
Multiple ulcers
Diarrhea
ulcer in atypical site
resistant ulcer
enlarged folds
severe esophagirtis
45. June 26, 2012 Total slide. 126 45
Clinical Biochemistry Gastrointestinal Disease
Diarrhea in ZES
The high rate of acid volume load that cannot be
absorbed by the intestine
The excess acid exceeds the neutralizing capacity of
pancreatic bicarbonate . The exceptionally low pH of the
intestinal contents inactivates pancreatic digestive
enzymes, interferes with the emulsification of fat by bile
acids, and damages intestinal epithelial cells and villi.
The extremely high serum gastrin concentrations may
inhibit absorption of sodium and water by the small
intestine,
46. June 26, 2012 Total slide. 126 46
Clinical Biochemistry Gastrointestinal Disease
ZES diagnosis
Exclude hyperacidity!
>100mM/L in 12 hour overnight
secretion of HCl
Check gastrin,
if >1000=ZES.
<1000 but abnormal secretin
test to be performed
+200 pg/ml is ZES
Secretin chalenge test
47. June 26, 2012 Total slide. 126 47
Clinical Biochemistry Gastrointestinal Disease
ZES treatment
any patient with a sporadic gastrinoma and
without evidence of metastatic spread of disease
should be offered exploratory laparotomy with
curative intent
laparotomy is not routinely recommended for
patients with ZES as part of MEN 1 since the
multifocal nature of the tumors in this disorder
almost uniformly precludes cure of gastrin
hypersecretion
48. June 26, 2012 Total slide. 126 48
Clinical Biochemistry Gastrointestinal Disease
49. June 26, 2012 Total slide. 126 49
Clinical Biochemistry Gastrointestinal Disease
Definition
The term gastritis is used to denote
inflammation associated with mucosal injury
Gastritis is mostly a histological term that needs
biopsy to be confirmed
Gastritis is usually due to infectious agents
(such as Helicobacter pylori) and autoimmune
and hypersensitivity reactions.
50. June 26, 2012 Total slide. 126 50
Clinical Biochemistry Gastrointestinal Disease
Definition
Epithelial cell damage and regeneration without
associated inflammation is properly referred to
as “gastropathy”.
Gastropathy may be referred without histological
evidence and just according to gross
appearance in endoscopy or radiology
Gastropathy is usually caused by irritants such
as drugs (eg, nonsteroidal antiinflammatory
agents and alcohol), bile reflux, hypovolemia,
and chronic congestion.
51. June 26, 2012 Total slide. 126 51
Clinical Biochemistry Gastrointestinal Disease
Acute Esophagitis & Gastritis
52. June 26, 2012 Total slide. 126 52
Clinical Biochemistry Gastrointestinal Disease
Gross–histologic correlation?
53. June 26, 2012 Total slide. 126 53
Clinical Biochemistry Gastrointestinal Disease
CLASSIFICATION
GASTRITIS
ACUTE COMMON CHRONIC
EMAG
AMAG
BILE HP
STRESS
NSAID
54. June 26, 2012 Total slide. 126 54
Clinical Biochemistry Gastrointestinal Disease
CLASSIFICATION
Acute vs. chronic
Acute refers to short term inflammation
Acute refering to neurophilic infiltrate
Chronic referring to long standing forms
Chronic referring to mononuclear cell infiltrate
especially lymphocyte and maccrophages
56. June 26, 2012 Total slide. 126 56
Clinical Biochemistry Gastrointestinal Disease
Acute hemorrhagic erosive
hemorrhagic and erosive lesions shortly after
exposure of the gastric mucosa to various
injurious substances or a substantial reduction in
mucosal blood flow
57. June 26, 2012 Total slide. 126 57
Clinical Biochemistry Gastrointestinal Disease
Acute hemorrhagic erosive
nonsteroidal antiinflammatory drugs [NSAIDs],
alcohol, or bile acids) or to mucosal hypoxia
(such as in trauma, burns [Curling's ulcers] or
sepsis) or to a combination of factors such as
with antineoplastic chemotherapy
58. June 26, 2012 Total slide. 126 58
Clinical Biochemistry Gastrointestinal Disease
Acute hemorrhagic erosive
Gastric and duodenal ulceroinflammatory ulcers
occurring during severe damage to the central
nervous system (Cushing's ulcers) are often
considered in this group
59. June 26, 2012 Total slide. 126 59
Clinical Biochemistry Gastrointestinal Disease
Acute hemorrhagic erosive
specific pathogenetic factor in NSAID-induced
acute hemorrhagic and erosive gastropathy is
the inhibition of prostaglandin production.
Prostaglandins, especially those of the E class,
protect against acute mucosal injury due to
NSAIDs and other injurious substances by
several mechanisms, including the stimulation of
mucus and bicarbonate secretion, and
maintenance of mucosal blood flow
60. June 26, 2012 Total slide. 126 60
Clinical Biochemistry Gastrointestinal Disease
Acute hemorrhagic erosive
Hemorrhagic or erosive gastropathy may be
associated with the development of gastric or
duodenal ulcers. Acute ulceration is most likely
to occur in relation to shock-induced
hemodynamic instability (ie, the stress ulcer
syndrome).
61. June 26, 2012 Total slide. 126 61
Clinical Biochemistry Gastrointestinal Disease
Risk factors
Prior history of an adverse GI event (ulcer,
hemorrhage) increases risk four to fivefold
Age >60 increases risk five to sixfold
High (more than twice normal) dosage of a
NSAID increases risk 10-fold
Concurrent use of glucocorticoids increases risk
four to fivefold
Concurrent use of anticoagulants increases risk
10- to 15-fold
62. June 26, 2012 Total slide. 126 62
Clinical Biochemistry Gastrointestinal Disease
HP and NSAID
Patients with a history of uncomplicated or
complicated peptic ulcers (gastric, duodenal)
should be tested for H. pylori prior to beginning a
NSAID or low dose aspirin. If present, H. pylori
should be treated with appropriate therapy, even
if it is believed that the prior ulcer was due to
NSAIDs
63. June 26, 2012 Total slide. 126 63
Clinical Biochemistry Gastrointestinal Disease
Helicobacter pylori
Helicobacter pylori is a
spiral shaped, gram
negative bacterium
measuring
approximately 3.5
microns in length and
0.5 microns in width
64. June 26, 2012 Total slide. 126 64
Clinical Biochemistry Gastrointestinal Disease
Helicobacter pylori
Urease appears to be
vital for its survival
and colonization; it is
produced in
abundance, making
up more than 5
percent of the
organism's total
protein weight.
65. June 26, 2012 Total slide. 126 65
Clinical Biochemistry Gastrointestinal Disease
Helicobacter pylori
urease forms
ammonia and
bicarbonate that
neutralize gastric acid
and form a protective
cloud around the
organism
66. June 26, 2012 Total slide. 126 66
Clinical Biochemistry Gastrointestinal Disease
Helicobacter pylori
spiral shape, flagella
facilitate its passage
through the mucus
layer
67. June 26, 2012 Total slide. 126 67
Clinical Biochemistry Gastrointestinal Disease
Helicobacter pylori
H. pylori then
attaches to gastric
epithelial cells by
means of specific
receptor-mediated
adhesion
68. June 26, 2012 Total slide. 126 68
Clinical Biochemistry Gastrointestinal Disease
Chemical gastritis (acute ・ chronic)
Alcoholic gastritis
Drug induced gastritis (e.g., NSAID)
Reflux ( due to duodenal juice or bile) gastritis
Other chemical gastritis
Radiation gastritis
Allergic gastritis
Autoimmune gastritis
Special forms of gastritis
Non HP gastritis
69. June 26, 2012 Total slide. 126 69
Clinical Biochemistry Gastrointestinal Disease
Stress ulcer pathophysiology
Hypersecretion of acid –head trauma.
Defects in gastric glycoprotein mucus –In
critically ill patients, increased concentrations of
refluxed bile salts or the presence of uremic
toxins can denude the glycoprotein mucous
barrier
Ischemia – Shock, sepsis, and trauma can lead
to impaired perfusion of the gut.
70. June 26, 2012 Total slide. 126 70
Clinical Biochemistry Gastrointestinal Disease
Stress ulcer risk factors
Shock
Sepsis
Hepatic failure
Renal failure
Multiple trauma
Burns over 35 percent of total body surface area
Organ transplant recipients
Head or spinal trauma
Prior history of peptic ulcer disease or upper GI
bleeding
71. June 26, 2012 Total slide. 126 71
Clinical Biochemistry Gastrointestinal Disease
73. June 26, 2012 Total slide. 126 73
Clinical Biochemistry Gastrointestinal Disease
WHO Classification
5 main categories
Adenocarcinoma, Adenosquamous cell carcinoma,
squamous cell carcinoma, undifferentiated carcinoma
and unclassified carcinoma
Adenocarcinoma – subdivided
Papillary, tubular, mucinous, signet ring
Further subdivided based on differentiation
74. June 26, 2012 Total slide. 126 74
Clinical Biochemistry Gastrointestinal Disease
Cancer of Stomach
1. Incidence
a. Worldwide common cancer, but less common in US
b. Incidence highest among Hispanics, African Americans,
Asian Americans, males twice as often as females
c. Older adults of lower socioeconomic groups higher risk
2. Pathophysiology
a. Adenocarcinoma most common form involving mucus-
producing cells of stomach in distal portion
b. Begins as localized lesion (in situ) progresses to
mucosa; spreads to lymph nodes and metastasizes early in
disease to liver, lungs, ovaries, peritoneum
75. June 26, 2012 Total slide. 126 75
Clinical Biochemistry Gastrointestinal Disease
Cancer of Stomach
3. Risk Factors
a. H. pylori infection
b. Genetic predisposition
c. Chronic gastritis, pernicious anemia, gastric polyps
d. Achlorhydria (lack of hydrochloric acid)
e. Diet high in smoked foods and nitrates
4. Manifestations
a. Disease often advanced with metastasis when diagnosed
b. Early symptoms are vague: early satiety, anorexia,
indigestion, vomiting, pain after meals not responding to
antacids
c. Later symptoms weight loss, cachexia (wasted away
appearance), abdominal mass, stool positive for occult blood
76. June 26, 2012 Total slide. 126 76
Clinical Biochemistry Gastrointestinal Disease
Cancer of Stomach
5. Collaborative Care
a. Support client through testing
b. Assist client to maintain adequate nutrition
6. Diagnostic Tests
a.CBC indicates anemia
b.Upper GI series, ultrasound identifies a mass
c.Upper endoscopy: visualization and tissue
biopsy of lesion
77. June 26, 2012 Total slide. 126 77
Clinical Biochemistry Gastrointestinal Disease
Cancer of Stomach
7. Treatment
a. Surgery, if diagnosis made prior to metastasis
1.Partial gastrectomy with anastomosis to
duodenum: Bilroth I or gastroduodenostomy
2.Partial gastrectomy with anastomosis to
jejunum: Bilroth II or gastrojejunostomy
3.Total gastrectomy (if cancer diffuse but limited
to stomach) with esophagojejunostomy
78. June 26, 2012 Total slide. 126 78
Clinical Biochemistry Gastrointestinal Disease
Fungating Carconoma
80. June 26, 2012 Total slide. 126 80
Clinical Biochemistry Gastrointestinal Disease
81. June 26, 2012 Total slide. 126 81
Clinical Biochemistry Gastrointestinal Disease
Post gastrectomy syndrome
b. Complications associated with gastric surgery
1. Dumping Syndrome
a.Occurs with partial gastrectomy; hypertonic, undigested
chyme bolus rapidly enters small intestine and pulls fluid into
intestine causing decrease in circulating blood volume and
increased intestinal peristalsis and motility
b.Manifestations 5 – 30 minutes after meal: nausea with
possible vomiting, epigastric pain and cramping, and diarrhea;
client becomes tachycardic, hypotensive, dizzy, flushed,
diaphoretic
c.Manifestations 2 – 3 hours after meal: symptoms of
hypoglycemia in response to excessive release of insulin that
occurred from rise in blood glucose when chyme entered
intestine
82. June 26, 2012 Total slide. 126 82
Clinical Biochemistry Gastrointestinal Disease
Post gastrectomy syndrome
Treatment: dietary pattern to delay gastric emptying
and allow smaller amounts of chyme to enter
intestine
Liquids and solids taken separately
Increased amounts of fat and protein
Carbohydrates, especially simple sugars, reduced
Client to rest recumbent or semi-recumbent 30 – 60
minutes after eating
Anticholinergics, sedatives, antispasmodic
medications may be added
Limit amount of food taken at one time
83. June 26, 2012 Total slide. 126 83
Clinical Biochemistry Gastrointestinal Disease
Post gastrectomy syndrome
Common post-op complications
Pneumonia
Anastomotic leak
Hemorrhage
Relux aspiration
Sepsis
Reflux gastritis
Paralytic ileus
Bowel obstruction
Wound infection
Dumping syndrome
84. June 26, 2012 Total slide. 126 84
Clinical Biochemistry Gastrointestinal Disease
Post gastrectomy syndrome
Nutritional problems related to rapid entry of food into the
bowel and the shortage of intrinsic factor
Anemia: iron deficiency and/or pernicious
Folic acid deficiency
Poor absorption of calcium, vitamin D
Radiation and/or chemotherapy to control metastasic spread
Palliative treatment including surgery, chemotherapy; client
may have gastrostomy or jejunostomy tube inserted
85. June 26, 2012 Total slide. 126 85
Clinical Biochemistry Gastrointestinal Disease
86. June 26, 2012 Total slide. 126 86
Clinical Biochemistry Gastrointestinal Disease
Pancreas
87. June 26, 2012 Total slide. 126 87
Clinical Biochemistry Gastrointestinal Disease
Function
Exocrine
precursor digestive enzymes
lipases
Endocrine
metabolic hormones
Insulin from β cells
Glucagon from α cells
88. June 26, 2012 Total slide. 126 88
Clinical Biochemistry Gastrointestinal Disease
Exocrine Pancreas
The final product of the exocrine pancreas is a
clear isotonic solution with a pH in the range of
8. The 2 distinct components of exocrine
secretion are enzyme secretion and
water+electrolyte secretion.
Cholecystokinin is the most potent endogenous
hormone known to stimulate enzyme secretion.
Secretin is the most potent endogenous
stimulant of pancreatic electrolyte secretion.
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Clinical Biochemistry Gastrointestinal Disease
Endocrine Pancreas
The release of insulin into the portal blood is controlled
by the concentration of blood glucose, vagal
interactions, and local concentrations of somatostatin.
The major stimulus for glucagon release is a fall in
serum glucose.
Pancreatic polypeptide appears to function for
regulation of pancreatic exocrine secretion and biliary
tract motility.
Somatostatin has a broad inhibitory spectrum of
gastrointestinal activity
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Clinical Biochemistry Gastrointestinal Disease
Factors Leading to Pancreatitis
Alcohol intake – usually 5
to 10 years
Prior biliary disease
Abdominal surgery or
diagnostics
Trauma
Recent viral infections
Medications
Mostly middle aged men
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Clinical Biochemistry Gastrointestinal Disease
Pathophysiology
Inflammation from an insult or injury
Causes activation of pancreatic enzymes
Enzymes autodigest and cause fibrosis
Leads to thrombi and necrosis of tissue
Fat necrosis occurs
Fats bind to calcium
Results in hypocalcemia
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Clinical Biochemistry Gastrointestinal Disease
More Patho
Necrosis of blood vessels
Fibers in blood vessels and ducts are dissolved
Vasodilation starts due to vessel damage
Results in bleeding and hemorrhage
May be acute or chronic
May be mild to necrotizing
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Clinical Biochemistry Gastrointestinal Disease
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Clinical Biochemistry Gastrointestinal Disease
Acute Pancreatitis
Nonbacterial inflammatory disease caused by
activation, interstitial liberation, and
autodigestion of the pancreas by its own
enzymes.
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Clinical Biochemistry Gastrointestinal Disease
Acute Pancreatitis Aetiology
Gallstones and Alcohol account for 90%
Hyperlipidemia
Hypercalcemia
Familial
Pancreatic duct obstruction
Tumour
Pancreas divisum
Viral infection
Scorpion venom
Drugs
Idiopathic
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Clinical Biochemistry Gastrointestinal Disease
Acute Pancreatitis
Symptoms and signs
Midepigastric abdominal pain, radiating to
the back
Nausea and vomiting
Fever and tachycardia
Epigastric tenderness
Abdominal distention
Bluish discoloration in the flank (Grey
Turner’s sign)
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Clinical Biochemistry Gastrointestinal Disease
98. June 26, 2012 Total slide. 126 98
Clinical Biochemistry Gastrointestinal Disease
Acute Pancreatitis
Diagnosis
It is supported by appropriate laboratory
determinations and radiographic findings
Serum amylase is the most widely used lab
test
Hyperamylasemia is commonly observed
within 24 hrs. of the onset and gradually
returns to normal
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Clinical Biochemistry Gastrointestinal Disease
Acute Pancreatitis
Diagnosis
Elevated amylase levels may occur in other acute
abdominal conditions, though levels rarely exceed
500 IU/dL
Urinary amylase excretion is increased and this
may be very helpful in cases where the serum
amylase level has returned to normal.
Other lab. Findings
Moderate leukocytosis
Mild bilirubin elevation (<2mg/dL)
Raised Haematocrit
Hypocalcaemia (Calcium being complexed with fatty
acids)
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Clinical Biochemistry Gastrointestinal Disease
Acute Pancreatitis
Glasgow prognostic system
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Clinical Biochemistry Gastrointestinal Disease
Acute Pancreatitis
Treatment
Goals of medical treatment
Reduction of pancreatic secretory stimuli
Correction of fluid and electrolyte derangements
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Clinical Biochemistry Gastrointestinal Disease
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Clinical Biochemistry Gastrointestinal Disease
Chronic Pancreatitis
Is an entity encompassing recurrent or persistent
abdominal pain of pancreatic origin combined
with evidence of exocrine and endocrine
insufficiency and marked pathologically by
irreversible parenchymal destruction.
It is associated with alcohol abuse,
Hyperparathyroidism, congenital anomalies of
the pancreatic duct and pancreatic trauma. It
may also be idiopathic.
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Clinical Biochemistry Gastrointestinal Disease
Chronic Pancreatitis
Patients typically present in the fourth or fifth
decade with a history of alcohol abuse and with
epigastric or back pain.
Anorexia and weight loss may be present.
1/3 of pts. Have insulin-dependent diabetes
1/4 of pts have steatorrhea.
Narcotic abuse is common
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Clinical Biochemistry Gastrointestinal Disease
Chronic Pancreatitis
pancreatic calcifications in ~50%
pancreatic parenchymal nodularity,
calcifications and pancreatic ductal dilatation.
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Clinical Biochemistry Gastrointestinal Disease
Signs and Symptoms of
Chronic Pancreatitis
Abdominal pain: intense, burning,
Abdominal tenderness
Ascites
Steatorrhea
Jaundice
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Clinical Biochemistry Gastrointestinal Disease
More S & S of Chronic
Dark urine
Signs and symptoms of diabetes
Dyspnea
Orthopnea
Weight loss
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Clinical Biochemistry Gastrointestinal Disease
Diagnostics
Elevated amylase, lipase, and urine amylase
Elevated glucose, bilirubin, alkaline phosphatase
Elevated WBCs
Hypocalcemia
Hypomagnesia
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Clinical Biochemistry Gastrointestinal Disease
Chronic Pancreatitis
Medical Treatment
Control of abdominal pain
Treatment of endocrine and exocrine
insufficiency
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Clinical Biochemistry Gastrointestinal Disease
111. Clinical Biochemistry Gastrointestinal Disease
Insulinoma
•Characteristic clinical manifestation is fasting
hypoglycemia with symptoms
• insulinomas arise from cells of ductular/acinar
system of the pancreas
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Clinical Biochemistry Gastrointestinal Disease
Insulinoma
Incidence
0.4/100,000 person-yrs (4 cases/million/year)
So rare that few institutions have accrued
enough experience to provide data
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Clinical Biochemistry Gastrointestinal Disease
Insulinoma
Symptoms
Confusion, visual changes, unusual behavior
Sympathoadrenal symptoms include
palpitations, diaphoresis, and tremulousness
Amnesia as well
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Clinical Biochemistry Gastrointestinal Disease
Insulinoma
Information based on a collection of 224 patients
out of Olmsted County, Minnesota
Of those 224, 8% had MEN neoplasia
Tumor distribution:
87% had single benign lesions
7% benign tumors-multiple
6% had malignant insulinomas
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Clinical Biochemistry Gastrointestinal Disease
Insulinoma
Established by demonstrating inappropriately
high serum [insulin] during a spontaneous or
induced episode of hypoglycemia
Virtually all insulinomas are islet cell tumors
After diagnosis, imaging used to localize tumor