Helicobacter pylori was first observed in 1983 infecting human stomachs and causing gastritis. It is a unique, fastidious bacterium that colonizes the gastric mucosa and is highly adapted to survive the acidic stomach environment. H. pylori infection is strongly associated with peptic ulcer disease, gastric cancer, and gastric MALT lymphoma. Successful treatment requires combination antibiotic therapy alongside proton pump inhibitors or bismuth compounds to eradicate the infection.
H. pylori resistance to antibiotics is a growing problem. Clarithromycin resistance occurs via point mutations and decreases the efficacy of standard triple therapy by 66%. Sequential therapy and bismuth-based quadruple therapy are recommended alternatives with success rates over 70%. Levofloxacin resistance is also emerging, though data is limited. Screening for clarithromycin resistance is advised if prevalence is over 20%. Reinfection can occur but is less than 14% after one year. Vaccines show promise but challenges remain developing effective options.
Warren and Marshall revolutionized the understanding of gastroduodenal diseases by discovering Helicobacter pylori in the stomachs of patients with gastric inflammation in 1982. They found the bacterium was present in almost all patients with gastric inflammation, duodenal ulcers, and gastric ulcers. Barry Marshall later inoculated himself with H. pylori to prove it causes infection. H. pylori infects the lower stomach and causes inflammation (gastritis), which can lead to duodenal and gastric ulcers. Diagnosis involves noninvasive breath tests or invasive endoscopy with biopsy and culture. Treatment combines antibiotics and acid-lowering drugs to eliminate the bacteria. Prolonged H. pylor
This document discusses Helicobacter pylori, including its characteristics, mechanisms of pathogenesis, diagnosis, treatment, and antibiotic resistance patterns. Some key points:
- H. pylori is a gram-negative bacterium that colonizes the stomach and is the primary cause of peptic ulcer disease and gastric cancer. It produces urease and adheres to gastric epithelial cells.
- Virulence factors like the cag pathogenicity island and vacuolating cytotoxin A are associated with more severe disease outcomes. Persistent inflammation driven by H. pylori infection increases cancer risks.
- Diagnosis involves invasive tests like biopsy and culture or non-invasive breath, stool, and blood tests.
How Helicobacter Pylori can cause gastric ulcerations and how this can lead t...Pırıl Erel
Analysis and disccusion of how Helicobacter Pylori (H.pylori) developed genetically and physically as a bacterium to be effective in affecting host cells. It has successfully affected 50% of host cells within the human population. Retrospective research of genomic advances and interactions of H.pylori migration between old and new world.
Helicobacter pylori is a spiral-shaped bacteria that lives in the stomach. It was originally considered that bacteria could not survive in the acidic stomach. Marshall and Warren first cultured H. pylori from human stomachs and showed it was associated with gastric inflammation. H. pylori infection can cause dyspepsia, peptic ulcers, gastric cancer, and other diseases. Testing and treating H. pylori infections can help prevent future illness.
Extra gastric & extra intestinal manifestations of h.pyloriahmed mosaad
The document discusses various extragastric and extra intestinal manifestations that have been associated with H. pylori infection based on epidemiological and clinical studies, finding positive associations with diseases of the gastrointestinal tract like inflammatory bowel disease, gallstones, and liver diseases like NAFLD and hepatocellular carcinoma, as well as hematological, dermatological, endocrinal, cardiovascular, neurological, and allergic conditions. However, it notes that for some conditions like the relationship between H. pylori and hepatocarcinogenesis, more research is still needed to confirm potential correlations.
Role of helicobacter pylori in gastric cancerOmid Yeganeh
Helicobacter pylori (H. pylori) infection occurs when a type of bacteria called Helicobacter pylori (H. pylori) infects your stomach. This usually happens during childhood. A common cause of peptic ulcers, H. pylori infection may be present in more than half the people in the world.Infection with H. pylori causes chronic inflammation and significantly increases the risk of developing duodenal and gastric ulcer disease and gastric cancer. Infection with H. pylori is the strongest known risk factor for gastric cancer, which is the second leading cause of cancer-related deaths worldwide.H. pylori is truly an “opportunistic” bacterium that uses various well defined virulence factors as tool for attachment and persistent colonization of human gastric mucosa.
H. pylori resistance to antibiotics is a growing problem. Clarithromycin resistance occurs via point mutations and decreases the efficacy of standard triple therapy by 66%. Sequential therapy and bismuth-based quadruple therapy are recommended alternatives with success rates over 70%. Levofloxacin resistance is also emerging, though data is limited. Screening for clarithromycin resistance is advised if prevalence is over 20%. Reinfection can occur but is less than 14% after one year. Vaccines show promise but challenges remain developing effective options.
Warren and Marshall revolutionized the understanding of gastroduodenal diseases by discovering Helicobacter pylori in the stomachs of patients with gastric inflammation in 1982. They found the bacterium was present in almost all patients with gastric inflammation, duodenal ulcers, and gastric ulcers. Barry Marshall later inoculated himself with H. pylori to prove it causes infection. H. pylori infects the lower stomach and causes inflammation (gastritis), which can lead to duodenal and gastric ulcers. Diagnosis involves noninvasive breath tests or invasive endoscopy with biopsy and culture. Treatment combines antibiotics and acid-lowering drugs to eliminate the bacteria. Prolonged H. pylor
This document discusses Helicobacter pylori, including its characteristics, mechanisms of pathogenesis, diagnosis, treatment, and antibiotic resistance patterns. Some key points:
- H. pylori is a gram-negative bacterium that colonizes the stomach and is the primary cause of peptic ulcer disease and gastric cancer. It produces urease and adheres to gastric epithelial cells.
- Virulence factors like the cag pathogenicity island and vacuolating cytotoxin A are associated with more severe disease outcomes. Persistent inflammation driven by H. pylori infection increases cancer risks.
- Diagnosis involves invasive tests like biopsy and culture or non-invasive breath, stool, and blood tests.
How Helicobacter Pylori can cause gastric ulcerations and how this can lead t...Pırıl Erel
Analysis and disccusion of how Helicobacter Pylori (H.pylori) developed genetically and physically as a bacterium to be effective in affecting host cells. It has successfully affected 50% of host cells within the human population. Retrospective research of genomic advances and interactions of H.pylori migration between old and new world.
Helicobacter pylori is a spiral-shaped bacteria that lives in the stomach. It was originally considered that bacteria could not survive in the acidic stomach. Marshall and Warren first cultured H. pylori from human stomachs and showed it was associated with gastric inflammation. H. pylori infection can cause dyspepsia, peptic ulcers, gastric cancer, and other diseases. Testing and treating H. pylori infections can help prevent future illness.
Extra gastric & extra intestinal manifestations of h.pyloriahmed mosaad
The document discusses various extragastric and extra intestinal manifestations that have been associated with H. pylori infection based on epidemiological and clinical studies, finding positive associations with diseases of the gastrointestinal tract like inflammatory bowel disease, gallstones, and liver diseases like NAFLD and hepatocellular carcinoma, as well as hematological, dermatological, endocrinal, cardiovascular, neurological, and allergic conditions. However, it notes that for some conditions like the relationship between H. pylori and hepatocarcinogenesis, more research is still needed to confirm potential correlations.
Role of helicobacter pylori in gastric cancerOmid Yeganeh
Helicobacter pylori (H. pylori) infection occurs when a type of bacteria called Helicobacter pylori (H. pylori) infects your stomach. This usually happens during childhood. A common cause of peptic ulcers, H. pylori infection may be present in more than half the people in the world.Infection with H. pylori causes chronic inflammation and significantly increases the risk of developing duodenal and gastric ulcer disease and gastric cancer. Infection with H. pylori is the strongest known risk factor for gastric cancer, which is the second leading cause of cancer-related deaths worldwide.H. pylori is truly an “opportunistic” bacterium that uses various well defined virulence factors as tool for attachment and persistent colonization of human gastric mucosa.
C:\Documents And Settings\Louay Labban Uok\Desktop\All\Powerpoints\Helicopact...Prof.Louay Labban
This document discusses Helicobacter pylori, a common bacterium found in the stomach that can cause various gastrointestinal issues. It is present in about half of the world's population. While most infected individuals do not experience symptoms, H. pylori is linked to ulcers, gastritis, and in rare cases, stomach cancer. The document outlines risk factors for infection, potential symptoms, diagnostic tests including blood tests and breath tests, and recommendations for who should be tested.
Helicobacter pylori is a type of bacteria that infects the stomach and is the most common cause of gastritis and peptic ulcers worldwide. Infection is very common and increases with age. H. pylori bacteria can be transmitted through direct contact with infected feces or vomit, or through contaminated food or water. While most infected people never show symptoms, potential symptoms include abdominal pain, nausea, loss of appetite, and weight loss. Diagnosis involves tests of the blood, breath, or stool to detect H. pylori. Treatment consists of antibiotics along with medication to reduce stomach acid in order to kill the bacteria and allow the stomach lining to heal.
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.
The 14C-urea breath test is used to assess the effectiveness of treatment for Helicobacter pylori (H. pylori) infection. The test involves swallowing a capsule containing 14C-labeled urea, which is metabolized by any remaining H. pylori bacteria into 14CO2 that is exhaled and can be detected. A result over 200 cpm indicates H. pylori is still present, while under 50 cpm indicates treatment was effective in eradicating the infection. The test provides accurate results one month after treatment completion to verify treatment success or failure.
Helicobacter pylori is a bacteria that causes peptic ulcers and is linked to gastric cancer. There are invasive and non-invasive tests to diagnose H. pylori infection. Invasive tests include histology, culture, and rapid urease test, while non-invasive options are urea breath test, stool antigen test, and serology. Molecular techniques like PCR are also used and can identify specific genes or antibiotic resistance. The accuracy of diagnostic tests may be affected in cases of bleeding or partial gastrectomy. Post-treatment tests like urea breath test are recommended to confirm eradication success.
H. pylori is a gram-negative, microaerophilic bacterium that colonizes the stomach and is associated with gastritis, peptic ulcers, and gastric cancer. It is spiral-shaped with multiple sheathed flagella that enable movement. H. pylori infection is transmitted orally and causes inflammation and damage to the gastric mucosa through virulence factors like urease and cytotoxin. Diagnosis involves invasive tests on gastric biopsy or non-invasive breath, stool, and blood tests. Eradication of H. pylori can cure peptic ulcers.
Inflammation of the intestinal mucosa caused by H. pyloriNasreddine Saidi
1. The document discusses the mucosal immune response to pathogens like H. pylori in the intestinal tract.
2. It describes the innate and adaptive immune effectors in the epithelium, lamina propria, and Peyer's patches that respond to these pathogens.
3. The normal response of the mucosal immune system is tolerance to food antigens to avoid inflammation, but it mounts a strong response to pathogens through IgA antibodies, T cells, and other effectors.
H. pylori is a gram-negative bacterium found in the stomach that can cause several diseases if left untreated. It is acquired in childhood and persists indefinitely without treatment. H. pylori infection is associated with peptic ulcer disease, gastric cancer, and gastric MALT lymphoma. Eradicating H. pylori infection cures most cases of peptic ulcer disease and gastric MALT lymphoma and may reduce the risk of gastric cancer progression. However, most infected individuals do not develop clinically significant complications from H. pylori.
H. pylori is a common human pathogen that causes peptic ulcer disease and gastric cancer by infecting the stomach and causing inflammation. It is transmitted through poor sanitation and hygiene. Over time, the inflammation can lead to cell damage in the stomach lining and increase cancer risk. Treating H. pylori infections with antibiotics can eliminate gastric cancer risk by eradicating the bacteria. The risk level depends on how much damage has already occurred, so follow up after treatment may be needed to check cancer risk in areas where it is more common.
This document provides information on Helicobacter pylori, including its scientific classification, history of discovery, morphology, culture characteristics, pathogenesis, clinical manifestations, and methods of laboratory diagnosis. Key points include that H. pylori was identified in 1982 as the cause of chronic gastritis and gastric ulcers, it is a gram-negative, microaerophilic, spiral bacterium that colonizes the stomach, and diagnostic tests include rapid urease test, histology, culture, PCR, serology, and urea breath test.
H. Pylori is commonly transmitted in childhood in crowded, poor living conditions through oral-oral or fecal-oral routes. It persists by mimicking human glycans to avoid immune responses. Around half the world is infected, with higher prevalence in developing regions. It colonizes the stomach using urease and vacuolating cytotoxin A (VacA) and CagA pathogenicity island virulence factors. Acute infection causes diarrhea and slowed growth while chronic infection leads to gastritis in most cases. H. Pylori is associated with diseases like gastric ulcers and cancer.
Helicobacter pylori has coexisted with humans for at least 60,000 years based on human migration patterns and findings in ancient mummies. H. pylori is a gram-negative, microaerophilic, spiral-shaped bacterium that typically resides in the stomach. It can cause peptic ulcers and gastritis, and may lead to gastric cancer or lymphoma. Diagnostic tests include breath, stool, biopsy, and serology tests. Immunohistochemistry provides reliable detection and is especially useful for visualizing coccoid forms, though it is more expensive than histochemical staining methods. A vaccine is in development that aims to prevent H. pylori's ability to inhibit host immune responses.
The document discusses a study design on molecular diagnosis and genotyping of Helicobacter pylori and its pathogenesis. The study aims to develop a multiplex PCR assay for definitive diagnosis of H. pylori directly from clinical samples. It also aims to analyze the prevalence of virulence factors like cagA, vacA among H. pylori strains and their impact on clinical conditions like gastric ulcer and cancer. Furthermore, the study will examine the effects of cagA positive and negative H. pylori strains on gastric epithelial cell lines, analyzing cell proliferation, apoptosis and cytokine production.
Helicobacter pylori is a gram-negative, spiral-shaped bacterium that infects the stomachs of approximately half of the world's population. It is the primary cause of peptic ulcers and is associated with chronic gastritis and gastric cancer. In Pakistan, a study found the prevalence of H. pylori infection to be 74.4%, with risk factors including presence of household animals and larger family size. H. pylori infection is usually treated with a combination of proton pump inhibitors, antibiotics, and bismuth to achieve eradication rates as high as 93%.
This document provides an overview of Helicobacter pylori, including its historical discovery in 1982 by Marshall and Warren which revolutionized ulcer treatment. It describes H. pylori's morphology as a spiral-shaped, flagellated, gram-negative bacterium that lives in the stomach mucus layer. The document discusses H. pylori's worldwide prevalence, routes of transmission, virulence factors, mechanisms of infection, associated diseases like ulcers and stomach cancer, and laboratory tests for diagnosis. In conclusion, H. pylori infection typically causes long-term gastritis in most cases, while clinical complications represent an imbalance in gastric homeostasis.
Helicobacter pylori is a gram-negative bacterium that infects the stomach of half of the human population, causing chronic gastric inflammation. Common symptoms include abdominal pain, nausea, and vomiting. Diagnosis can be made through stool, blood, or breath tests. Treatment typically involves a combination of amoxicillin, clarithromycin, and a proton pump inhibitor in a regimen known as triple therapy. The prescribed medications can be very expensive, so it is important to have health insurance coverage.
Laboratory diagnosis of H. Pylori infection, Ola ElgaddarOla Elgaddar
A short presentation for the different laboratory techniques used in diagnosing Helicobacter Pylori infection. A special focus is given for the diagnostic performance of every test.
Helicobacter pylori associated Peptic ulcer diseaseS M Ali Hasan
Helicobacter pylori is a common cause of peptic ulcer disease. It infects about half of the global population and transmission occurs through person-to-person contact or from infected instruments. Only 10-15% of infected individuals develop ulcers or other diseases. In Bangladesh, H. pylori infection rates are very high, ranging from 67-92% in studies. Treatment involves antibiotic regimens but resistance is a problem, with high rates of resistance to clarithromycin, metronidazole, and levofloxacin seen in Bangladesh. Management of peptic ulcers involves testing and treating H. pylori, endoscopic treatment for bleeding ulcers, and maintenance therapy to prevent
Helicobacter pylori es una bacteria espiral gramnegativa que infecta el estómago humano y causa gastritis y úlceras pépticas. Inicialmente se pensó que era una especie de Campylobacter, pero los estudios genómicos modernos demostraron que pertenece a un género diferente llamado Helicobacter. La infección por H. pylori puede ser asintomática o causar síntomas como dolor abdominal, y se transmite principalmente de persona a persona.
Este documento presenta información sobre Helicobacter pylori, una bacteria que coloniza el estómago y causa inflamación. Describe su historia, morfología, factores de riesgo, transmisión, patogenia, diagnóstico y tratamiento. El documento también analiza los efectos de H. pylori, incluida la gastritis crónica y su posible vínculo con el cáncer gástrico.
Helicobacter pylori es una bacteria gram-negativa que coloniza el estómago humano. Tiene forma de bacilo curvado y es microaerofílica. Coloniza el antro gástrico y las áreas de metaplasia, donde está protegida del ácido gástrico. Posee mecanismos de patogenicidad como la producción de ureasa, toxinas y enzimas que causan inflamación y daño al epitelio gástrico, contribuyendo al desarrollo de úlceras pépticas.
C:\Documents And Settings\Louay Labban Uok\Desktop\All\Powerpoints\Helicopact...Prof.Louay Labban
This document discusses Helicobacter pylori, a common bacterium found in the stomach that can cause various gastrointestinal issues. It is present in about half of the world's population. While most infected individuals do not experience symptoms, H. pylori is linked to ulcers, gastritis, and in rare cases, stomach cancer. The document outlines risk factors for infection, potential symptoms, diagnostic tests including blood tests and breath tests, and recommendations for who should be tested.
Helicobacter pylori is a type of bacteria that infects the stomach and is the most common cause of gastritis and peptic ulcers worldwide. Infection is very common and increases with age. H. pylori bacteria can be transmitted through direct contact with infected feces or vomit, or through contaminated food or water. While most infected people never show symptoms, potential symptoms include abdominal pain, nausea, loss of appetite, and weight loss. Diagnosis involves tests of the blood, breath, or stool to detect H. pylori. Treatment consists of antibiotics along with medication to reduce stomach acid in order to kill the bacteria and allow the stomach lining to heal.
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.
The 14C-urea breath test is used to assess the effectiveness of treatment for Helicobacter pylori (H. pylori) infection. The test involves swallowing a capsule containing 14C-labeled urea, which is metabolized by any remaining H. pylori bacteria into 14CO2 that is exhaled and can be detected. A result over 200 cpm indicates H. pylori is still present, while under 50 cpm indicates treatment was effective in eradicating the infection. The test provides accurate results one month after treatment completion to verify treatment success or failure.
Helicobacter pylori is a bacteria that causes peptic ulcers and is linked to gastric cancer. There are invasive and non-invasive tests to diagnose H. pylori infection. Invasive tests include histology, culture, and rapid urease test, while non-invasive options are urea breath test, stool antigen test, and serology. Molecular techniques like PCR are also used and can identify specific genes or antibiotic resistance. The accuracy of diagnostic tests may be affected in cases of bleeding or partial gastrectomy. Post-treatment tests like urea breath test are recommended to confirm eradication success.
H. pylori is a gram-negative, microaerophilic bacterium that colonizes the stomach and is associated with gastritis, peptic ulcers, and gastric cancer. It is spiral-shaped with multiple sheathed flagella that enable movement. H. pylori infection is transmitted orally and causes inflammation and damage to the gastric mucosa through virulence factors like urease and cytotoxin. Diagnosis involves invasive tests on gastric biopsy or non-invasive breath, stool, and blood tests. Eradication of H. pylori can cure peptic ulcers.
Inflammation of the intestinal mucosa caused by H. pyloriNasreddine Saidi
1. The document discusses the mucosal immune response to pathogens like H. pylori in the intestinal tract.
2. It describes the innate and adaptive immune effectors in the epithelium, lamina propria, and Peyer's patches that respond to these pathogens.
3. The normal response of the mucosal immune system is tolerance to food antigens to avoid inflammation, but it mounts a strong response to pathogens through IgA antibodies, T cells, and other effectors.
H. pylori is a gram-negative bacterium found in the stomach that can cause several diseases if left untreated. It is acquired in childhood and persists indefinitely without treatment. H. pylori infection is associated with peptic ulcer disease, gastric cancer, and gastric MALT lymphoma. Eradicating H. pylori infection cures most cases of peptic ulcer disease and gastric MALT lymphoma and may reduce the risk of gastric cancer progression. However, most infected individuals do not develop clinically significant complications from H. pylori.
H. pylori is a common human pathogen that causes peptic ulcer disease and gastric cancer by infecting the stomach and causing inflammation. It is transmitted through poor sanitation and hygiene. Over time, the inflammation can lead to cell damage in the stomach lining and increase cancer risk. Treating H. pylori infections with antibiotics can eliminate gastric cancer risk by eradicating the bacteria. The risk level depends on how much damage has already occurred, so follow up after treatment may be needed to check cancer risk in areas where it is more common.
This document provides information on Helicobacter pylori, including its scientific classification, history of discovery, morphology, culture characteristics, pathogenesis, clinical manifestations, and methods of laboratory diagnosis. Key points include that H. pylori was identified in 1982 as the cause of chronic gastritis and gastric ulcers, it is a gram-negative, microaerophilic, spiral bacterium that colonizes the stomach, and diagnostic tests include rapid urease test, histology, culture, PCR, serology, and urea breath test.
H. Pylori is commonly transmitted in childhood in crowded, poor living conditions through oral-oral or fecal-oral routes. It persists by mimicking human glycans to avoid immune responses. Around half the world is infected, with higher prevalence in developing regions. It colonizes the stomach using urease and vacuolating cytotoxin A (VacA) and CagA pathogenicity island virulence factors. Acute infection causes diarrhea and slowed growth while chronic infection leads to gastritis in most cases. H. Pylori is associated with diseases like gastric ulcers and cancer.
Helicobacter pylori has coexisted with humans for at least 60,000 years based on human migration patterns and findings in ancient mummies. H. pylori is a gram-negative, microaerophilic, spiral-shaped bacterium that typically resides in the stomach. It can cause peptic ulcers and gastritis, and may lead to gastric cancer or lymphoma. Diagnostic tests include breath, stool, biopsy, and serology tests. Immunohistochemistry provides reliable detection and is especially useful for visualizing coccoid forms, though it is more expensive than histochemical staining methods. A vaccine is in development that aims to prevent H. pylori's ability to inhibit host immune responses.
The document discusses a study design on molecular diagnosis and genotyping of Helicobacter pylori and its pathogenesis. The study aims to develop a multiplex PCR assay for definitive diagnosis of H. pylori directly from clinical samples. It also aims to analyze the prevalence of virulence factors like cagA, vacA among H. pylori strains and their impact on clinical conditions like gastric ulcer and cancer. Furthermore, the study will examine the effects of cagA positive and negative H. pylori strains on gastric epithelial cell lines, analyzing cell proliferation, apoptosis and cytokine production.
Helicobacter pylori is a gram-negative, spiral-shaped bacterium that infects the stomachs of approximately half of the world's population. It is the primary cause of peptic ulcers and is associated with chronic gastritis and gastric cancer. In Pakistan, a study found the prevalence of H. pylori infection to be 74.4%, with risk factors including presence of household animals and larger family size. H. pylori infection is usually treated with a combination of proton pump inhibitors, antibiotics, and bismuth to achieve eradication rates as high as 93%.
This document provides an overview of Helicobacter pylori, including its historical discovery in 1982 by Marshall and Warren which revolutionized ulcer treatment. It describes H. pylori's morphology as a spiral-shaped, flagellated, gram-negative bacterium that lives in the stomach mucus layer. The document discusses H. pylori's worldwide prevalence, routes of transmission, virulence factors, mechanisms of infection, associated diseases like ulcers and stomach cancer, and laboratory tests for diagnosis. In conclusion, H. pylori infection typically causes long-term gastritis in most cases, while clinical complications represent an imbalance in gastric homeostasis.
Helicobacter pylori is a gram-negative bacterium that infects the stomach of half of the human population, causing chronic gastric inflammation. Common symptoms include abdominal pain, nausea, and vomiting. Diagnosis can be made through stool, blood, or breath tests. Treatment typically involves a combination of amoxicillin, clarithromycin, and a proton pump inhibitor in a regimen known as triple therapy. The prescribed medications can be very expensive, so it is important to have health insurance coverage.
Laboratory diagnosis of H. Pylori infection, Ola ElgaddarOla Elgaddar
A short presentation for the different laboratory techniques used in diagnosing Helicobacter Pylori infection. A special focus is given for the diagnostic performance of every test.
Helicobacter pylori associated Peptic ulcer diseaseS M Ali Hasan
Helicobacter pylori is a common cause of peptic ulcer disease. It infects about half of the global population and transmission occurs through person-to-person contact or from infected instruments. Only 10-15% of infected individuals develop ulcers or other diseases. In Bangladesh, H. pylori infection rates are very high, ranging from 67-92% in studies. Treatment involves antibiotic regimens but resistance is a problem, with high rates of resistance to clarithromycin, metronidazole, and levofloxacin seen in Bangladesh. Management of peptic ulcers involves testing and treating H. pylori, endoscopic treatment for bleeding ulcers, and maintenance therapy to prevent
Helicobacter pylori es una bacteria espiral gramnegativa que infecta el estómago humano y causa gastritis y úlceras pépticas. Inicialmente se pensó que era una especie de Campylobacter, pero los estudios genómicos modernos demostraron que pertenece a un género diferente llamado Helicobacter. La infección por H. pylori puede ser asintomática o causar síntomas como dolor abdominal, y se transmite principalmente de persona a persona.
Este documento presenta información sobre Helicobacter pylori, una bacteria que coloniza el estómago y causa inflamación. Describe su historia, morfología, factores de riesgo, transmisión, patogenia, diagnóstico y tratamiento. El documento también analiza los efectos de H. pylori, incluida la gastritis crónica y su posible vínculo con el cáncer gástrico.
Helicobacter pylori es una bacteria gram-negativa que coloniza el estómago humano. Tiene forma de bacilo curvado y es microaerofílica. Coloniza el antro gástrico y las áreas de metaplasia, donde está protegida del ácido gástrico. Posee mecanismos de patogenicidad como la producción de ureasa, toxinas y enzimas que causan inflamación y daño al epitelio gástrico, contribuyendo al desarrollo de úlceras pépticas.
Helicobacter pylori (IgAs y test de ureasa)egs-141-00197v
Este documento evalúa los niveles de inmunoglobulina A secretora anti-Helicobacter pylori y la prueba de ureasa en niños en Cumaná, Venezuela. Los resultados mostraron que el 44,4% de las muestras de saliva fueron positivas para inmunoglobulina A, mientras que el 36,1% de las biopsias fueron positivas para la prueba de ureasa. Hubo una asociación significativa entre los resultados positivos de inmunoglobulina A e infección activa de H. pylori. Se recomienda
This document discusses Helicobacter pylori, a bacteria that can cause stomach ulcers and cancer in humans. It is a gram-negative, microaerophilic spiral bacteria that colonizes the stomach lining. It produces urease enzyme and can survive in low acid environments. Diseases caused by H. pylori include ulcers, gastritis, stomach cancer, and MALT lymphoma. Treatment involves antibiotics, proton pump inhibitors, and supplements. The bacteria is transmitted person-to-person through fecal-oral routes or contaminated food/water. Prevention focuses on good hygiene and properly cooking/treating food and water.
This document provides information about Helicobacter pylori (H. pylori), including how it is transmitted, symptoms it causes, specimens used to test for it, and methods for diagnosing and confirming infection. H. pylori is a bacteria that infects the stomach and is associated with gastric ulcers and cancer. It is transmitted orally-orally or orally-fecal. Common symptoms include abdominal pain and weight loss. Diagnosis can be made through serology tests of whole blood, serum, stool or breath samples, or biopsy during endoscopy. Serology tests detect antibodies but cannot confirm active infection. Stool and breath tests can diagnose active infection and confirm cure. Biopsy during endoscopy
This document discusses guidelines for treating H. pylori infection from the 2010 Maastricht IV/Florence consensus report. It recommends first-line treatments including standard triple therapy, sequential therapy, and bismuth quadruple therapy. For second-line treatment for infections that failed first-line treatment, levofloxacin-based triple therapy is recommended. However, resistance to levofloxacin is rising. Optimal treatment regimens depend on the local prevalence of clarithromycin resistance. Culture-guided, high-dose dual PPI, and rifabutin-based therapies are recommended for infections that failed two prior treatments.
Este documento resume información sobre gastritis y Helicobacter pylori. Describe los diferentes tipos de gastritis, incluyendo aguda, crónica y específicas. Explica los factores de virulencia de H. pylori y su papel en la inflamación gástrica y el daño tisular. También discute la asociación entre H. pylori, dispepsia, ERGE, úlceras pépticas, AINES e incremento de riesgo de cáncer gástrico.
El documento describe las características generales, microbiológicas, epidemiológicas y patogénicas de Helicobacter pylori, la bacteria asociada a la gastritis crónica y factor de riesgo para el cáncer gástrico. Se explica su mecanismo de transmisión, genética, habilidad para evadir el sistema inmune, e interacción con las células epiteliales gástricas que causan inflamación y daño. Finalmente, se detallan las recomendaciones para el diagnóstico y tratamiento de la
This document discusses the embryology and anatomy of the stomach. It provides the following key points:
1. During embryonic development, the stomach rotates along its longitudinal and anteroposterior axes, causing its final adult position with the cardiac portion on the left and pylorus on the right.
2. The adult stomach is located in the left upper quadrant and extends across the midline, with the greater curvature forming the anterior wall and lesser curvature the posterior wall.
3. Radiological techniques for examining the stomach include barium studies, CT, MRI, and virtual endoscopy, which allow evaluation of stomach morphology, layers, and relationships to surrounding organs.
El documento describe Helicobacter pylori (H. pylori), una bacteria espiral Gram-negativa que infecta crónicamente el estómago de más del 50% de la población mundial y causa úlceras gástrica e intestinales. Se transmite principalmente a través de la ingestión de alimentos o agua contaminados. Presenta factores de virulencia como adhesinas, ureasa y toxinas que le permiten adherirse a la mucosa gástrica y debilitarla, causando inflamación y daño tisular. Su diagnóstico se real
Este documento describe Helicobacter pylori, la bacteria que causa úlceras pépticas. Se transmite a través de la vía oral-fecal y puede causar infección sintomática o asintomática. El tratamiento tradicional involucra una terapia triple de antibióticos como amoxicilina y claritromicina junto con inhibidores de bomba de protones. Sin embargo, la resistencia a antibióticos está aumentando, lo que requiere terapias alternativas como una terapia cuádruple o el uso de levoflaxac
Este documento resume las principales recomendaciones de las guías Maastricht IV/Florence sobre el manejo de la infección por Helicobacter pylori. Se recomienda investigar y tratar a H. pylori en pacientes con úlcera péptica, dispepsia no investigada en menores de 55 años, dispepsia funcional, antecedentes de úlcera que requieran AINE, linfoma MALT, cáncer gástrico, entre otros. También se brindan recomendaciones sobre diagnóstico, tratamiento erradic
Helicobacter pylori es un bacilo gramnegativo que coloniza la mucosa gástrica y tiene un papel causal importante en la úlcera péptica, el cáncer gástrico y la gastritis. Su presencia induce una gastritis crónica que puede provocar diferentes enfermedades como úlcera duodenal, adenocarcinoma gástrico o linfoma MALT. La erradicación de H. pylori reduce significativamente las recidivas de úlcera y el riesgo de cáncer gástrico.
This document discusses Helicobacter pylori infection. It begins with a summary of the discovery of H. pylori, including Giulio Bizzozero's initial description in 1892 and Robin Warren and Barry Marshall's cultivation of H. pylori in 1982. It then covers the epidemiology of H. pylori infection, indications for treatment, methods for diagnosing infection, treatments for infection, and the role of H. pylori eradication in preventing gastric cancer. Key points include that over 50% of the world's population is infected with H. pylori and treatment aims to cure ulcers and reduce cancer risk. Diagnosis involves non-invasive tests like serology or breath tests
The document discusses hepatitis and acute liver failure. It notes that hepatitis viruses and other infections, toxins, and autoimmune diseases can cause hepatitis, an inflammation of the liver. Hepatitis A virus is commonly the cause in children, while hepatitis B and C viruses can lead to liver cancer or chronic liver disease. Hepatitis A and E do not result in chronic infections. Vaccines exist for hepatitis A and B but not other types. Egypt has the world's highest hepatitis burden, with 10% of the population aged 15-59 infected with hepatitis C.
Common gut parasites that infect humans include helminths (worms) and protozoa. Four main soil-transmitted helminths that can infect the gut are Ascaris lumbricoides, Trichuris trichiura, Ancylostoma duodenale, and Necator americanus. Ascaris is the most widespread human gut nematode found primarily in tropical areas with poor sanitation. It has an indirect life cycle where eggs passed in feces must mature in soil before being infectious. Symptoms are often mild but can include abdominal pain and obstruction. Diagnosis is by finding eggs in stool and treatment involves anthelmintic drugs. Löeffler syndrome is a rare lung condition
Common intestinal helminths and protozoa infect millions worldwide, especially in low and middle income countries with poor sanitation. The four main soil-transmitted intestinal worms are Ascaris lumbricoides, Trichuris trichiura, Ancylostoma duodenale, and Necator americanus. A. lumbricoides is the most prevalent worm globally and causes malnutrition and obstruction. Ancylostoma duodenale and N. americanus are hookworms that infect through skin penetration and commonly cause anemia. Transmission occurs through ingestion of worm eggs from contaminated food, water, or soil. Symptoms often include abdominal pain and diarrhea. Diagnosis is via stool examination and
The document discusses the history and discovery of Helicobacter pylori and its role in peptic ulcer disease. It describes how in the 1980s, Drs. Barry Marshall and Robin Warren discovered that H. pylori infection was a major cause of peptic ulcers, overturning decades of belief. Their discovery was initially met with resistance from the medical community but was later recognized with the 2005 Nobel Prize in Physiology or Medicine. The document also discusses the epidemiology, diagnosis, treatment and antibiotic resistance of H. pylori infection.
The document is a poem describing the various microhabitats within the human body that are suitable for commensal microbes to colonize, including pores, arm pits, and scalp. It welcomes microbes to build colonies and supplies them warmth, moisture, and nutrients, on the condition they do not cause issues like acne or athlete's foot. The poem acknowledges microbes as guests in the body on this new year's day.
1. The document discusses common mistakes that can occur during upper gastrointestinal endoscopy and how to avoid them. It describes mistakes like missing Cameron ulcers, Dieulafoy lesions, eosinophilic esophagitis, long segment Barrett's esophagus, and confusion between portal hypertensive gastropathy and gastric antral vascular ectasia.
2. Key recommendations include paying close attention to the cardia region in patients with large hiatal hernias, performing urgent endoscopy in cases of new bleeding, asking patients to cough to induce bleeding from possible Dieulafoy lesions, taking multiple biopsies to diagnose eosinophilic esophagitis, and actively searching for the Z-line in cases
This document discusses esophageal atresia, a birth defect where the esophagus fails to develop properly, resulting in an abnormal connection or closure. It defines the condition, describes its epidemiology and embryology, classifications, associated anomalies, pathophysiology, diagnosis, and treatment. Esophageal atresia occurs in about 1 in 3000-4500 births and is diagnosed prenatally by ultrasound or after birth based on symptoms like choking during feeding. Treatment involves surgical repair of the esophagus.
This document discusses gastritis and Helicobacter pylori (H. pylori) infection. It defines gastritis as inflammation of the stomach lining and notes that it is usually caused by infectious agents like H. pylori, autoimmune issues, or hypersensitivity reactions. H. pylori is described as a common chronic bacterial infection that can lead to gastritis. Strains of H. pylori that produce vacuolating cytotoxin and cytotoxin-associated gene A are associated with more severe inflammation and increased risk of ulcers and precancerous lesions. The document provides classifications of gastritis and risk factors for conditions like stress-related gastric ulcers.
This document provides information on diarrhea among under-5 children. It discusses the global burden of diarrhea, key facts about diarrhea including causes and prevention. Specific diarrheal pathogens like rotavirus, cholera, and giardiasis are explained. Treatment of acute watery diarrhea and dysentery are also summarized. The document emphasizes continued feeding and oral rehydration therapy in treating diarrhea.
Cholera is devastating diarrheal disease caused by V. Cholerae that has been responsible for seven global pandemics.
Epidemic cholera remains a significant public health concern in the developing world today.
This document provides information on diarrhea among under-5 children. It discusses key facts about diarrhea including that it is the second largest killer of under-5s globally, responsible for over 750,000 deaths in 2013. Diarrhea is both preventable and treatable through measures like safe water, sanitation, breastfeeding, and oral rehydration therapy. The document also summarizes the main causes and classifications of diarrhea, including acute watery diarrhea, acute invasive diarrhea/dysentery, and persistent diarrhea. It highlights the importance of continued feeding during diarrhea to prevent malnutrition.
Helicobacter pylori colonizes the stomach of about 50% of the world's population and is the main risk factor for peptic ulcers and gastric cancers. It possesses virulence factors like the cag pathogenicity island that increase its ability to induce inflammation and injury. Colonization results from a complex interplay between bacterial virulence mechanisms and host immune responses that can result in a range of outcomes from asymptomatic carriage to severe disease.
This document discusses diarrhea among under-5 children. It notes that diarrhea is the second largest killer of under-5s globally, responsible for over 15,000 deaths annually in Bangladesh. The main types of diarrhea discussed are acute watery diarrhea, acute invasive diarrhea/dysentery, and persistent diarrhea. Key causes include rotavirus, ETEC, Shigella, and various bacteria and parasites. Prevention through oral rehydration therapy, breastfeeding, handwashing, vaccination and improved nutrition and sanitation is emphasized.
This document contains summaries of three gastrointestinal pathology cases and additional information about achalasia, oesophageal carcinoma, small bowel malrotation, and midgut volvulus. Case 1 describes dilatation and narrowing of the esophagus resembling a rat tail or bird beak. Case 2 describes abnormal positioning of the duodenum and small bowel. Case 3 shows irregular narrowing and lack of peristalsis in the colon. Additional sections provide details on the causes, presentations, investigations and treatments of these conditions.
Cholera is devastating diarrheal disease caused by V. Cholerae that has been responsible for seven global pandemics.
Epidemic cholera remains a significant public health concern in the developing world today.
- The document discusses hepatitis and acute liver failure. It notes that hepatitis viruses like hepatitis A, B, C, D, and E can cause hepatitis and affect millions worldwide, killing 1.4 million people per year. Hepatitis A is commonly the cause in children, while hepatitis B and C can lead to liver cancer and chronic liver disease.
- It provides information on the functions of the liver, defines hepatitis as inflammation of the liver that can be self-limiting or progress to fibrosis, and lists the various causes of infectious and non-infectious hepatitis. Hepatitis B in particular is described in terms of epidemiology, transmission, pathogenesis, and interpretation of hepatitis B markers.
Helicobacter pylori and Peptic Ulcer diseaseDiaa Srahin
Case Study
Clinical Case Summary
History
Helicobacter pylori
Biochemical characteristics
Transmission
Epidemiology
Global incidence of H. pylori infection
risk factors for acquisition of H.pylori
Immune responses
Pathogenesis
Helicobacter pylori Virulence Factors
Clinical Presentation
Complications
Peptic Ulcer
Diagnosis
Treatment
Prevention
Hepatitis is inflammation of the liver that is characterized by the presence of inflammatory cells in liver tissue. There are multiple causes of hepatitis including viral, chemical, autoimmune and metabolic. The main viruses that cause hepatitis are hepatitis A, B, C, D, and E viruses. Hepatitis A virus is transmitted through the fecal-oral route and causes an acute infection. Hepatitis B and C viruses are transmitted through blood and bodily fluids and can cause both acute and chronic infections. Hepatitis D virus only occurs in those already infected with hepatitis B. Prevention strategies include vaccination, harm reduction education, and screening of blood and organ donors.
Cirrhosis and portal hypertension in childrenLm Huq
The document discusses the liver, cirrhosis, and portal hypertension. It begins by describing the anatomy and functional units of the liver, including the portal triads and zones. It then discusses cirrhosis and portal hypertension in more detail. Cirrhosis is defined as scarring of the liver from long-term damage that blocks blood flow and can lead to hepatic failure and portal hypertension. The document lists various etiologies of cirrhosis including infections, liver disorders, bile duct blockages, drugs/toxins, and discusses some specific conditions in more detail. It concludes by describing the clinical features and complications of cirrhosis and portal hypertension.
The document discusses enteric fevers such as typhoid and paratyphoid. It notes that typhoid occurs only in humans and causes around 21 million cases and 200k deaths worldwide each year. The causative agents are Salmonella typhi and Salmonella paratyphi. Symptoms of typhoid fever typically last 4 weeks and include rose colored spots, abdominal tenderness, diarrhea, and possible complications like bleeding or perforation. Diagnosis involves blood, stool, or bone marrow cultures. Treatment is with antibiotics like ceftriaxone for 14 days. Relapse can occur in 15% of cases.
This document provides information about immunization and vaccine-preventable diseases. It discusses:
1. Immunization is a process that uses vaccines to stimulate immunity against infectious diseases. It has proven effective at controlling and eliminating diseases like smallpox.
2. Major vaccine-preventable diseases that kill children include measles, polio, pertussis, Hib, and pneumococcal diseases. Immunization is one of the most cost-effective health interventions.
3. The document then provides details on specific diseases like pertussis, its symptoms, complications, and treatment with antibiotics or immunization. It emphasizes the importance of clinical diagnosis and avoiding severe outcomes in infants.
The document discusses diarrhea as a leading cause of death among children under 5, providing statistics on prevalence and causes of different types of diarrhea like acute watery diarrhea, acute invasive diarrhea, and persistent diarrhea. It outlines signs and symptoms, causes, complications, and treatments for different forms of diarrhea. The document emphasizes the importance of oral rehydration therapy and continued feeding to treat diarrhea and prevent more serious outcomes like dehydration and malnutrition.
This document discusses infant feeding principles and the benefits of exclusive breastfeeding for the first 6 months. It provides information on breastmilk composition, the importance of early initiation and exclusive breastfeeding, positioning and attachment for breastfeeding, and challenges and difficulties some mothers may face. The document emphasizes that breastmilk provides ideal nutrition and protection against illness for infants and has numerous health, developmental and economic benefits for both mother and baby.
The document provides information on acute respiratory infections (ARIs) in children under 5 years old. It discusses the definition of ARIs, signs of respiratory distress, normal respiratory defense mechanisms, how ARIs spread rapidly in children, common sites of infection, etiological agents, how ARIs harm children, the relationship between ARIs and malnutrition, methods for assessing and classifying pneumonia severity according to IMCI guidelines, treatment principles including antibiotics and other supportive care, prevention strategies, and acute epiglottitis.
The document summarizes health programs and progress in Bangladesh. It notes that Bangladesh has achieved significant reductions in under-5 and maternal mortality rates through effective interventions. Key interventions include oral rehydration therapy for diarrhea, immunizations, integrated management of childhood illness, and newborn health programs. Bangladesh has also seen major declines in malnutrition and fertility rates. Overall, Bangladesh has made major improvements in health indicators through the efforts of the government and development partners.
The document discusses Dengue fever (DF), a mosquito-borne viral disease. It provides details on the history, transmission, clinical presentation, diagnosis and treatment of DF. DF is common in tropical and sub-tropical regions and is caused by the dengue virus, which has four serotypes. While most cases are mild, infection with a second serotype increases the risk of severe dengue which can be fatal if not properly treated through fluid resuscitation. Prevention relies on controlling the mosquito vectors and avoiding mosquito bites. There is no vaccine available for all four serotypes.
This document provides information about renal diseases. It notes that kidney disease can be a silent killer but childhood nephrotic syndrome is mostly curable and acute post-streptococcal glomerulonephritis (APSGN) mostly recovers and does not recur. It also discusses hematuria in children, age-related kidney diseases, preventing acute renal failure (ARF), and learning objectives about renal diseases.
CXR is a commonly performed imaging test that uses ionizing radiation to visualize the inside of the body. It is useful for diagnosing and treating conditions. A standard CXR involves exposing the chest to a small dose of radiation for less than half a second to produce images. It requires no special preparation and carries minimal risk when used appropriately. The CXR must be evaluated systematically by examining bones, the heart, lungs, mediastinum, diaphragm and soft tissues to identify any abnormalities.
This document discusses various B vitamins, including their sources, functions, deficiency symptoms, diagnosis, and treatment. It provides details on thiamine (B1) and its role in energy production. Deficiencies of B1 can cause beriberi, which presents as acute or chronic peripheral neuropathy. It also covers riboflavin (B2) and its role in redox reactions as part of FAD. Riboflavin deficiency can result in ariboflavinosis with mouth sores and dermatitis. The document provides recommendations to prevent deficiencies through a balanced diet and vitamin supplements when needed.
The document discusses abdominal pain, its causes, characteristics, and approaches to diagnosis. It notes that abdominal pain can arise from abdominal wall or organs and may be difficult to localize. Common causes in children include constipation, gastroenteritis, and appendicitis, though some cases require urgent evaluation. Diagnosis involves considering characteristics of the pain, physical exam, and test results. Referred pain is also discussed.
This document discusses childhood injuries and accidents in children. Some key points:
- Injuries are unintentional or intentional damage to the body from things like thermal, mechanical, electrical or chemical energy.
- 95% of childhood injuries occur in low and middle income countries. Drowning is a major killer, especially in these countries.
- Injuries account for 14% of all childhood deaths globally. Road traffic accidents, drowning, falls and burns are among the leading causes.
- Childhood injuries place a significant burden on families and healthcare systems. Many result in lifelong disabilities or even death. Prevention programs can save over 1,000 child lives per day.
This document provides information about immunization against various infectious diseases. It discusses the importance of immunization in preventing millions of deaths per year from diseases like measles, polio, diphtheria, and pertussis. The document outlines the target diseases for immunization programs in Bangladesh and other vaccines available in the country. It also discusses vaccines still in development and provides details on diseases like pertussis, diphtheria, and poliomyelitis, including causes, symptoms, treatment and complications.
This document discusses infant feeding guidelines and the benefits of breastfeeding. It provides the following key points:
1) Exclusive breastfeeding is recommended for the first 6 months as breastmilk provides ideal nutrition and protects infants from illness. Undernutrition contributes to 45% of under-5 mortality globally.
2) Breastfeeding has significant health benefits for both mother and baby, including reducing the risks of obesity, diabetes, breast and ovarian cancer. It improves cognitive development and results in economic gains.
3) Proper breastfeeding techniques such as positioning, attachment and frequent feeding are important to ensure the baby receives enough milk from the breast. Common challenges can be addressed through counseling and support.
The document discusses acute respiratory infections (ARIs) in children under 5 years old. It defines ARI and describes the signs and symptoms, including fast breathing and chest indrawing. Common causes are viruses like RSV and bacteria like Streptococcus pneumoniae. ARIs often spread rapidly in young children due to anatomical factors. They are a major cause of mortality, responsible for around 900,000 child deaths per year. Proper treatment with low-cost measures can reduce the death toll from ARIs.
This document provides an overview of Bangladesh. It begins with a brief description of Bangladesh's location and geography, noting that it is located in South Asia on the Bay of Bengal and has the world's largest delta formed by the Ganges, Brahmaputra, and Meghna rivers. It then discusses Bangladesh's population, demographics, economy, industries, exports, infrastructure, education system, healthcare successes, challenges, and potentials. The document also profiles Bangladesh's climate, landscape, biodiversity, culture, and history. It concludes by outlining some of Bangladesh's current problems including corruption, poverty, pollution, and natural disasters.
Bangladesh has made significant progress in health outcomes for women and children through effective interventions. The under-5 mortality rate fell from 151 per 1000 live births in 1990 to 38 per 1000 in 2017, exceeding Millennium Development Goal 4. This was achieved through programs promoting oral rehydration therapy, immunizations, integrated management of childhood illness, and newborn health interventions. Bangladesh also reduced the maternal mortality ratio by 75% and exceeded Millennium Development Goal 5. Current challenges include further reducing child injuries such as drownings, improving nutrition, and addressing emerging issues like non-communicable diseases and environmental health hazards.
Here are the answers to the MCQs:
1. RSV is the commonest c/of bronchiolitis - True
2. ABT is usually required in B - False
3. Most B are later associated with BA - True
4. In EBF babies B is rare - True
5. Anticholingergic nebulization is beneficial in B - False
6. B is usually a killer D - False
7. SARS/MERS is caused by RSV - False
8. Antiviral Rx is beneficial in all B cases - False
1. The patient presented with fatigue, pallor, and weight loss and was found to have enlarged spleen and low blood counts consistent with visceral leishmaniasis. Biopsies revealed Leishmania donovani infection.
2. Additional findings included an ulcerated lesion on the thumb and crusty ulcers on the ankle.
3. Leishmaniasis is a neglected tropical disease spread by sandfly bites that disproportionately affects the poorest populations. It manifests as visceral, cutaneous, or mucosal disease and can cause severe disfigurement if left untreated.
1. A patient presented with weight loss, fatigue, and pallor and was found to have enlarged spleen and liver with pancytopenia. Biopsies revealed Leishmania donovani infection.
2. Leishmaniasis is transmitted by the bite of infected sandflies and presents as cutaneous, mucocutaneous, or visceral disease. Visceral leishmaniasis, known as kala-azar, is the most serious form.
Rabies is a fatal viral disease that affects mammals. It is transmitted primarily through bites from rabid animals, most commonly dogs. The virus travels from the site of exposure to the central nervous system. Symptoms include anxiety, confusion, and paralysis. Once symptoms appear, rabies is almost always fatal. Prevention involves vaccinating domestic animals and promptly treating exposed wounds. For humans, vaccination either before or after exposure can protect from the disease. Rabies remains a problem in many developing countries where access to vaccines and medical care is limited.
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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
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).
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
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.
8. History of HelicobacterHistory of Helicobacter
First observed in 1983 asFirst observed in 1983 as CampylobacterCampylobacter-like-like
organisms (CLO) in stomachs with gastritisorganisms (CLO) in stomachs with gastritis
HelicobacterHelicobacter was coined in 1989.was coined in 1989. 20 spp. Are known.20 spp. Are known.
Only 3 cause human d.Only 3 cause human d.
1. Hp1. Hp (human;(human; no animal reservoir)no animal reservoir)
2. H. cinaedi2. H. cinaedi (male homosexuals; rodents)(male homosexuals; rodents)
3. H. fenneliae3. H. fenneliae (do)(do)
9. 1983:1983: discovered by Warren and Marshall (Australia)discovered by Warren and Marshall (Australia)
ItIt revolutionisedrevolutionised Rx of DU and GURx of DU and GU
Earned themEarned them NobelNobel in 2005in 2005
HpHp colonises stomach. Molecular studies: transmissioncolonises stomach. Molecular studies: transmission
occurred from animaloccurred from animal
Monkey, cat, dog, cheetahMonkey, cat, dog, cheetah all harbour their own speciesall harbour their own species
History of Hp …History of Hp …
10. HpHp DescriptionDescription
G-ve, motile, flagellate, helical; pleomorphic rod:G-ve, motile, flagellate, helical; pleomorphic rod:
penetrates and colonizespenetrates and colonizes gastricgastric mucosa (corkscrew)mucosa (corkscrew)
Fastidious in growth: strictly micro-aerophilic; require
C02. Becomes coccoid in O2 or upon prolonged cultureBecomes coccoid in O2 or upon prolonged culture
Highly adaptiveHighly adaptive
Has a tuft of unipolar flagellae; specially adapted to
colonise mucosa
Very fragile (important! when referring samples to lab)
11. HpHp is unique!is unique!
50%50% world popn. are inf.world popn. are inf.
Survives acidity even at pH <2Survives acidity even at pH <2
Colonization is chr. and may be lifelongColonization is chr. and may be lifelong
Motility is essential for colonisationMotility is essential for colonisation
Hallmark isHallmark is urease:urease: urea to C02 + NH3(a strong base;urea to C02 + NH3(a strong base;
neutralizes strong acid). It isneutralizes strong acid). It is essential for survivalessential for survival
It is a carcinogenIt is a carcinogen
Vacuolating cytotoxin (VacA): increases bacterial fitnessVacuolating cytotoxin (VacA): increases bacterial fitness
StaysStays remote and protected from immune sys.remote and protected from immune sys.
12. EpidemiologyEpidemiology
Worldwide. Varies greatly among countries and popn.Worldwide. Varies greatly among countries and popn.
20 – 50% among mid-age adults in20 – 50% among mid-age adults in HICsHICs
>80%>80% inin L&MICs;L&MICs; 85% by 2yoa85% by 2yoa
Transmission:Transmission: ingestion; commonest: family contact (esp.ingestion; commonest: family contact (esp.
children).children). HpHp has been cultured from feces, dentalhas been cultured from feces, dental
caries.caries. Transmission increases with ageTransmission increases with age
Site of inf.:Site of inf.: gastric antrum (most favoured), bodygastric antrum (most favoured), body
Present in the mucus secretionPresent in the mucus secretion
13.
14. PATHOPHYSIOLOGYPATHOPHYSIOLOGY
HpHp is the first recognized bacterialis the first recognized bacterial carcinogencarcinogen and is 1 ofand is 1 of
most successful pathogens. Colonization is usually lifelongmost successful pathogens. Colonization is usually lifelong
It causesIt causes chr. gastritischr. gastritis (may be asymptomatic),(may be asymptomatic), PUD, gastricPUD, gastric
Ca, gastric MALT lymphoma, gastric atrophyCa, gastric MALT lymphoma, gastric atrophy
Outcome depends on interplay between host &Outcome depends on interplay between host & Hp.Hp. HostHost
immunity and gastric a. largely determine colonizationimmunity and gastric a. largely determine colonization
HpHp makesmakes ammoniaammonia (toxic to epith),(toxic to epith), proteasesproteases,, vacuolatingvacuolating
cytotoxin A (VacA)cytotoxin A (VacA) [damages epith, disrupts tight junctions[damages epith, disrupts tight junctions
and causes apoptosis),and causes apoptosis), phospholipases.phospholipases. CytotoxinCytotoxin
associated geneassociated gene CagACagA can causes inflam. and is carcinogencan causes inflam. and is carcinogen
15. PUD:PUD: acid & pepsin overcome mucosal defenceacid & pepsin overcome mucosal defence
Site of colonizationSite of colonization affects location of ulceraffects location of ulcer
In large amounts of acid,In large amounts of acid, HpHp colonizes the antrum; avoidcolonizes the antrum; avoid
fundal parietal cellsfundal parietal cells
In normal or reduced acid,In normal or reduced acid, HpHp colonizes rest of stomachcolonizes rest of stomach
Inflam. in antrum inducesInflam. in antrum induces G cellsG cells to secrete gastrin: moreto secrete gastrin: more
acid, also increases parietal cell number. Increased acidacid, also increases parietal cell number. Increased acid
load damages duodenum (DU)load damages duodenum (DU)
When Hp colonizes other areas of stomach, inflam. can result When Hp colonizes other areas of stomach, inflam. can result
in atrophy of the stomach lining and eventually ulcers; Cain atrophy of the stomach lining and eventually ulcers; Ca
16. HpHp infinf directlydirectly associateassociatedd withwith
PUDPUD
- lifetime risk 3% in US, 25% Japan- lifetime risk 3% in US, 25% Japan
- eradication provides long-term cure- eradication provides long-term cure
Gastric CaGastric Ca
- strong evidence of risk 0.1-3%- strong evidence of risk 0.1-3%
-- unclearunclear if eradication reduces the riskif eradication reduces the risk
MALT lymphomaMALT lymphoma
-- 72%→ 98% of MALT lymphoma infected with72%→ 98% of MALT lymphoma infected with HpHp
Mucosa-associated lymphoid tissue: MALT
20. ChildhoodChildhood HpHp gastric Ca isgastric Ca is not reportednot reported. Gastric atrophy and. Gastric atrophy and
intestinal metaplasia are risk factors for Caintestinal metaplasia are risk factors for Ca
HpHp inf typically causes (CMI) gastritis: hypergastrinaemia andinf typically causes (CMI) gastritis: hypergastrinaemia and
hyperacidity. Infected stomach can have normal secretionhyperacidity. Infected stomach can have normal secretion
Antral predominant d.Antral predominant d. commonly has hypergastrinaemia,commonly has hypergastrinaemia,
DU, gastric metaplasia of duodenum.DU, gastric metaplasia of duodenum.Antral predominant d.Antral predominant d.
is probably higher in childrenis probably higher in children
But gastric Ca is more common in body predominant d.:But gastric Ca is more common in body predominant d.:
hypochorhydria and atrophy of parietal cells. Whenhypochorhydria and atrophy of parietal cells. When Hp Hp willwill
cause an antral/body predominant d. is unclearcause an antral/body predominant d. is unclear
Host response …Host response …
21. EM:EM: HpHp on the gastricon the gastric
mucosa of a childmucosa of a child
22. Section of a gastric biopsy:Section of a gastric biopsy: HpHp gastritisgastritis
24. McColl K. N Engl J Med 2010;362:1597-1604
Gastric-biopsy:Gastric-biopsy: HpHp adhering to epithelium and underlying inflammationadhering to epithelium and underlying inflammation
25. DISEASE IN CHILDRENDISEASE IN CHILDREN
Ac. & chr. GastritisAc. & chr. Gastritis
PUD:PUD: typically DU. Classic CF are not reliable in youngtypically DU. Classic CF are not reliable in young
children; only Dx by endoscopychildren; only Dx by endoscopy
AP without PUDAP without PUD (adult: non-ulcer dyspepsia)(adult: non-ulcer dyspepsia)
HpHp eradication doesn’t help (9%). Resolution of nodulareradication doesn’t help (9%). Resolution of nodular
lymphoid hyperplasia may take 6mo to resolve andlymphoid hyperplasia may take 6mo to resolve and
inflam. infiltrate 4y. It isn’t sure ifinflam. infiltrate 4y. It isn’t sure if HpHp has a major rolehas a major role
GERD:GERD: there may actually be an rise in reflux inthere may actually be an rise in reflux in Hp Hp eradication Rx.eradication Rx.
SS of above d. can be v. similar. Upper GI endoscopy is the only reliableSS of above d. can be v. similar. Upper GI endoscopy is the only reliable
method of Dx, and hencemethod of Dx, and hence Hp RxHp Rx. In UK 5% of 5–16y are colonized. In UK 5% of 5–16y are colonized
withwith Hp. Hp. Most have no SSMost have no SS
26. Recurrent APRecurrent AP
Chr. gastritis without PU could be a c/of RAP in children, andChr. gastritis without PU could be a c/of RAP in children, and
screening is often done; but no consistent evidence. Mostscreening is often done; but no consistent evidence. Most
likely it is a co-existence of 2 common but unrelated d. Hplikely it is a co-existence of 2 common but unrelated d. Hp
eradication doesn’t helperadication doesn’t help
IDAIDA
HpHp can be a/with IDA in asymptomatic children at puberty.can be a/with IDA in asymptomatic children at puberty.
Whether this is c/by iron loss or less absorption is unclear.Whether this is c/by iron loss or less absorption is unclear.
IfIf HpHp is identified in a case of IDA, it should be eradicatedis identified in a case of IDA, it should be eradicated
Growth falteringGrowth faltering
HpHp inf. may lead to it. Confounding variables may contributeinf. may lead to it. Confounding variables may contribute
to both Mn & earlyto both Mn & early Hp Hp colonization. Ifcolonization. If HpHp were found to bewere found to be
a significant c/of it then global impact would be enormous.a significant c/of it then global impact would be enormous.
27. DIAGNOSTIC TESTSDIAGNOSTIC TESTS
Indications:Indications: SS of PUD (RAP, wt loss, NV, anemia)SS of PUD (RAP, wt loss, NV, anemia),,
indigestion, fullness/bloating, belchingindigestion, fullness/bloating, belching
1.1.UBT:UBT: sensitivity/sp. 90%. Psensitivity/sp. 90%. Presence ofresence of HpHp. C UBT are non-. C UBT are non-
radioactive; widely available.radioactive; widely available. False-ve:False-ve: active/recentactive/recent
bleeding, AB/antisecretory Rxbleeding, AB/antisecretory Rx
2.2.Serology:Serology: 82.4% sensitive and 85% sp. It82.4% sensitive and 85% sp. It is widelyis widely
available. High conc. in blood/ saliva are found in activeavailable. High conc. in blood/ saliva are found in active
inf; after Rx, these gradually fall; so, not suitable forinf; after Rx, these gradually fall; so, not suitable for
establishing short/medium term successestablishing short/medium term success
3.3. Fecal Ag tests.Fecal Ag tests. 89-98% sensitivity & >90% sp. G89-98% sensitivity & >90% sp. Goodood
guide to successful eradication. It is simple; should beguide to successful eradication. It is simple; should be
test of choice for assessing eradicationtest of choice for assessing eradication
28. 4. Endoscopy & biopsy are indicated:4. Endoscopy & biopsy are indicated:
remains theremains the gold standardgold standard for Dx. Antral biopsiesfor Dx. Antral biopsies
have the highest yield (unless pt is on PPI)have the highest yield (unless pt is on PPI)
• Indications:Indications: Severe SS, anemia, wt loss, age >50ySevere SS, anemia, wt loss, age >50y
• RUT:RUT: rapid detection (S 79–100%, sp. 92–100%). It hasrapid detection (S 79–100%, sp. 92–100%). It has aa
poor positive predictive value in childhood and need to bepoor positive predictive value in childhood and need to be
confirmed by histologyconfirmed by histology
• Histology:Histology: if urease test negative (>90% sens.if urease test negative (>90% sens.
&sp.)&sp.)
5. Stool immunoassay & PCR5. Stool immunoassay & PCR (under(under
investigation)investigation)
29.
30.
31. WHO SHOULD BE TESTED?WHO SHOULD BE TESTED?
Test in all situations that may influence Mx: test only if youTest in all situations that may influence Mx: test only if you
want to treat.want to treat. For adults:For adults: all cases ofall cases of HpHp should be treated,should be treated,
regardless of lesionregardless of lesion
Strategy of Rx dyspepsia without rapid wt loss, GI bleed, orStrategy of Rx dyspepsia without rapid wt loss, GI bleed, or
anemia: PPI x1moanemia: PPI x1mo
Do endoscopy only in persistent SS. There is a low thresholdDo endoscopy only in persistent SS. There is a low threshold
in testingin testing HpHp colonisation in adults, and even though non-colonisation in adults, and even though non-
ulcer dyspepsia is unlikely to resolve swiftly afterulcer dyspepsia is unlikely to resolve swiftly after
eradication, the balance of risk to the individual pt iseradication, the balance of risk to the individual pt is
thought to favor empirical Rxthought to favor empirical Rx
32.
33.
34. First line therapyFirst line therapy
PPI b.d. + clarithromycin 500mg b.d.PPI b.d. + clarithromycin 500mg b.d.
++
amoxicillin 1000mg b.d/metro- 400mg BD minimum of 7damoxicillin 1000mg b.d/metro- 400mg BD minimum of 7d
In case of failureIn case of failure
Second line therapySecond line therapy
PPI b.d. + bismuth subsalicylate/subcitrate 120mg QDS + metro- 500mgPPI b.d. + bismuth subsalicylate/subcitrate 120mg QDS + metro- 500mg
t.d.s. + tetracycline 500mg q.d.s. min. 7dt.d.s. + tetracycline 500mg q.d.s. min. 7d
If bismuth is NA, PPI based triple therapies should be usedIf bismuth is NA, PPI based triple therapies should be used
Subsequent failures should be handled on a case-case basis. PatientsSubsequent failures should be handled on a case-case basis. Patients
failing second-line therapy in primary care should be referredfailing second-line therapy in primary care should be referred
TreatmentTreatment
35. TREATMENTTREATMENT
Principles are similar to any inf, but more bactericidal effect isPrinciples are similar to any inf, but more bactericidal effect is
essential. Even v. small residual Hp will re-coloniseessential. Even v. small residual Hp will re-colonise
Re-colonization means risk ofRe-colonization means risk of ABR.ABR. So, ensure complianceSo, ensure compliance
Treat only those who will benefit. Check eradication with aTreat only those who will benefit. Check eradication with a
UBT/fecal Ag 8w later. If failed, consider 2nd line.UBT/fecal Ag 8w later. If failed, consider 2nd line.
Repeated failures need repeat endoscopy & CSRepeated failures need repeat endoscopy & CS
Non-invasive testing of family, & Rx may be usefulNon-invasive testing of family, & Rx may be useful
PUDPUD further requires antacid and a 3mo PPIfurther requires antacid and a 3mo PPI
Lymphomata require oncological consult, but are veryLymphomata require oncological consult, but are very
uncommon in childrenuncommon in children
36. RecommendationsRecommendations
• Noninvasive test-&-treat strategy forNoninvasive test-&-treat strategy for HpHp is reasonable foris reasonable for
children with upper GI SS but not alarm symptomschildren with upper GI SS but not alarm symptoms
• Ig test is the least accurateIg test is the least accurate
• Recurrence/persistence of SS after eradication Rx forRecurrence/persistence of SS after eradication Rx for
uninvestigated dyspepsia is much less likely to be Rxuninvestigated dyspepsia is much less likely to be Rx
failure; rather SS are unrelated tofailure; rather SS are unrelated to HpHp
• In areas where Hp and its complications are common, Drs. testIn areas where Hp and its complications are common, Drs. test
healthy people for it. Whether there is a benefit to treatinghealthy people for it. Whether there is a benefit to treating
Hp when you have no SS is controversialHp when you have no SS is controversial
37. Key pointsKey points
>> HpHp is a flagellated spiral micro-aerobeis a flagellated spiral micro-aerobe
>> Inf. is a risk factor for gastric CaInf. is a risk factor for gastric Ca
>> Causes PUD and gastritisCauses PUD and gastritis
>> Produces a cell-damaging toxinProduces a cell-damaging toxin
>> Transmission route is unclearTransmission route is unclear
>> Rates are falling in HICsRates are falling in HICs
>> Rx is by eradication using combination therapyRx is by eradication using combination therapy
38. Common Questions/FAQCommon Questions/FAQ
Does everyone withDoes everyone with HpHp get PU?get PU?
No, many have inf. but no PU. The reason is not yet clearNo, many have inf. but no PU. The reason is not yet clear
Should everyone be tested forShould everyone be tested for HpHp??
No, only recommended for those who have SSNo, only recommended for those who have SS
How did I get infected withHow did I get infected with HpHp??
Foodborne, contaminated with human feces, vomit, saliva.Foodborne, contaminated with human feces, vomit, saliva.
Exposure from family members seems to be commonestExposure from family members seems to be commonest
Does everyone treated forDoes everyone treated for HpHp get better?get better?
The majority get rid of it. ABR may occurThe majority get rid of it. ABR may occur
39. Can I get anotherCan I get another H. pyloriH. pylori infection?infection?
Rx does not make a person immune, so there is always theRx does not make a person immune, so there is always the
potential for becoming infected againpotential for becoming infected again
Why is Ig test forWhy is Ig test for HpHp not recommended?not recommended?
We do not recommend it for routine use for Dx or Rx, as itWe do not recommend it for routine use for Dx or Rx, as it
cannot DD between a present and past inf. But, many stillcannot DD between a present and past inf. But, many still
use ituse it
If it is negative, then it is unlikely ofIf it is negative, then it is unlikely of HpHp. But if it is positive,. But if it is positive,
then a currentthen a current Hp Hp inf. should be confirmed with a stoolinf. should be confirmed with a stool
Ag/UBT/endoscopyAg/UBT/endoscopy
40. PreventionPrevention
No vaccineNo vaccine
Improved sanitation decreased HP; will ultimatelyImproved sanitation decreased HP; will ultimately
eliminate it in US. But, without intervention it mayeliminate it in US. But, without intervention it may
remain endemic for another centuryremain endemic for another century
Spontaneous elimination in children is probably aided bySpontaneous elimination in children is probably aided by
ABT for other reasonsABT for other reasons
43. MCQMCQ
Hp is a carcinogenHp is a carcinogen
It can grow anywhere in GITIt can grow anywhere in GIT
Monotherapy is recommendedMonotherapy is recommended
It can cause atrophic gastritisIt can cause atrophic gastritis
Best test is SerologicalBest test is Serological
It causes more DU than GUIt causes more DU than GU
Editor's Notes
Later reclassified as HP
Fastidious: (Microbiology) having complex nutritional requirements
Hp can grow on different solid media containing blood/blood products. Most studies have used Brucella agar or Columbia agar as the agar base. An amount of 7-10% blood improves growth
VacA induces multiple effects on epith and lymphatic cells: vacuolation with alterations of endo-lysosomal function, anion-selective channel formation, mitochondrial damage, and inhibition CD4+ cell proliferation. VacA binds to two types of receptor-like protein tyrosine phosphatases (RPTP), RPTPα and RPTPβ, on the surface of target cell
GASTRIC ANTRUM
Niche. A recess in a wall, as for holding a statue or urn. A cranny, hollow, or crevice, as in rock
Apoptosis: A form of cell death in which a programmed sequence of events leads to the elimination of cells without releasing harmful substances into the surrounding area. Apoptosis plays a crucial role in developing and maintaining the health by eliminating old cells, unnecessary cells, and unhealthy cells. The human body replaces perhaps one million cells/sec. Too little or too much apoptosis can play a role in many d. When apoptosis does not work correctly, cells that should be eliminated may persist and become immortal, Eg, in Ca. When apoptosis works overly well, it kills too many cells and inflicts grave damage. This is the case in strokes and neurodegenerative d like Alzheimer&apos;s, Huntington&apos;s, and Parkinson‘s. Aka programmed cell death and cell suicide
Eradication of Hp dramatically reduces rec. of HP associated PUD. Strong evidence links it to gastric Ca. It is classed as a type I (definite carcinogen). 2.9% of HP inf. dev gastric Ca. No Ca was detected in pts who received eradication early. Eradication prevents recurrence of endoscopically resected early gastric Ca. 72 – 98% MALT lymphoma are inf with H. pylori. However, endpoint may miss the other benefits of H. pylori eradication.
GORD: Hp has been shown to have a protective role against GORD. However. Long term use of PPIs may aggravate HP mediated corpus gastritis increasing the risk of Ca.
Porins. are beta barrel proteins that cross a cellular membrane and act as a pore, through which molecules can diffuse. Unlike other membrane transport proteins, porins are large enough to allow passive diffusion (channels) that are specific to different types of molecules. They are present in outer membrane of G-ve bacteria and some G+ve of group Mycolata (mycolic acid-containing actinomycetes), the mitochondria, and the chloroplast. [poros, passageway].
Th2 cells stimulate B cells in response to extracellular pathogens. As H. pylori is non-invasive and induces a strong humoral response a Th2 response would be expected.
Studies in gene targetted mice have shown that Th2 cytokines are protective against gastric inflammation.
T-cell receptor (TCR) 1 of 2 polypeptide chains (a or ß) on surface of T lymphocytes that recognize and
bind foreign Ag. TCRs are Ag specific; their activity depends on Ag processing by macrophages or other Ag-presenting cells and presence of MHC proteins to which peptides from the Ag are bound
Hp usually is acquired in childhood. Ac. inf causes transient hypochlorhydria and is rarely Dx. Chr. gastritis will dev. in virtually all persistently colonised cases, but 80 – 90% will never have SS. Pts with high acid output are likely to have antal predominant gastritis, predisposing them to DU. Pts with lower acid output are more likely to have corpus gastritis, prediposing GU and Ca.
T helper cells (Th cells) assist other wbc in immunologic processes: maturation of B cells into plasma cells and memory B cells, and activation of cytotoxic T cells and macrophages. Aka CD4+ T cells because they express the CD4 glycoprotein on their surfaces. Th cells become activated when they are presented with peptide Ag by MHCII molecules, which are expressed on the surface of Ag-presenting cells (APCs). Once activated, they divide rapidly and secrete small proteins called cytokines that regulate or assist in the active immune response. These cells can differentiate into one of several subtypes: TH1, 2, 3, 17, 9, or TFH, which secrete different cytokines to facilitate different types of immune responses. Signalling from the APC directs T cells into particular subtypes
Major histocompatibility complex (MHC) is a set of cell surface proteins essential for acquired immune sys to recognize foreign Ag. Its main function is to bind to Ag and display them on the cell surface for recognition by T-cells. MHC molecules mediate interactions of WBCs (immune cells), with other leukocytes or with body cells. MHC determines compatibility of donors for organ transplant, as well as one&apos;s risk to an AID via crossreacting. MHC is aka human leukocyte Ag (HLA). In a cell, protein molecules of the host&apos;s own
phenotype or of other biologic entities are continually synthesized and degraded. Each MHC molecule on the cell surface displays a molecular fraction of a protein, called an epitope. The presented Ag can be either self or non-self, thus preventing an organism&apos;s immune sys targeting its own cells. In its entirety, the MHC population is like a meter indicating the balance of proteins within the cell. The MHC gene family is divided into 3 subgroups: class I, II, III. Class I MHC molecules have β2 subunits so can only be recognized by CD8 co-receptors. Class II MHC molecules have no β2 subunits so can be recognized by CD4. In this way MHC molecules chaperone which type of lymphocytes may bind to the given Ag with high affinity, since different lymphocytes express different TCR co-receptors.
Diversity of Ag presentation, mediated by MHC classes I and II, is attained in at least 3 ways: (1) an organism&apos;s MHC repertoire is polygenic (via multiple, interacting genes); (2) MHC expression is codominant (from both sets of inherited alleles); (3) MHC gene variants are highly polymorphic (diversely varying from organism to organism within a species). MHC and sexual selection has been observed in male mice making mate choices of females with different MHCs and thus demonstrating sexual selection. Also, at least for MHC I presentation, there has been evidence of antigenic peptide splicing which can combine peptides from different proteins, vastly increasing Ag diversity
Nodular lymphoid hyperplasia (NLH) of GIT is presence of multiple small nodules, 2-10mm
In UK 20% of all GP workload are on long term acid suppression attributable to Hp
Aka: Hp; H-pylori; H. pylori Ab test; H. pylori stool Ag test; H. pylori breath test; Urea breath test; CLO test; Rapid urease test (RUT) for H. pylori
Test Preparation: You may need to avoid certain medications; follow any given instructions
Stool Ag test and UBT are recommended & are most frequently done as they are fast and noninvasive. Endoscopy-related tests may also be done
Rapid urease test, aka CLO test (Campylobacter-like organism), is a rapid Dx test for Hp. Urease converts urea to ammonia and CO2. It is done at gastroscopy. An antral biopsy is placed into a medium containing urea and phenol red. The urease hydrolyzes urea to ammonia, raises the pH, changes color yellow (NEGATIVE) to red (POSITIVE).
For FU of eradication, UBT is indicated at an interval of &gt;4w to avoid false negative results.
Sensitivity & specificity of Ig testing is similar to that of UBT. Because Hp. strains differ among areas, knowledge of local strains would optimise accuracy. Is of limited used in determining the success of Rx.
Stool Agtesting can be used for follow up of eradication, an interval of 8 weeks should be allowed. One prospective, multicenter study showed a positive result perform 7 days after completion of theraoy identified patients in whom eradication has been unsuccessful.
Stool Agtesting may be of particular use in children under 6 years
What does test result mean? Positive stool Ag, UBT, or biopsy indicates AP is likely c/by PUD due to HP
Positive Hp Ig may indicate a current/past inf. UBT may still be needed to confirm the inf. is a current one. A negative result: Hp unlikely. But, if SS persist, get a biopsy
What else to know?
UBT is not typically recommended for young children. The preferred test would be stool Ag test. AP has many reasons; an ulcer c/by Hp is only 1 of them. Use of antacids within 1w prior to testing, UBT may be falsely negative. ABT, PPI, bismuth may interfere with all but Ig test
Triple therapy regimens have a cure rate of 80%, without major SE, minimal ABR
Combination of two or more AB increases cure and reduces ABR. Many factors may result in Rx failure: microbial factors, compliance, geographical differences
Rx Strongly recommended
DU/GU; MALT lymphoma; Atrophic gastritis; Recent resection of gastric Ca
Treatment advised
Functional dyspepsia
Gastro-oesophageal reflux disease (patients requiring long-term acid suppressive therapy)
Use of NSAIDs
Culture : no more sensitive than skilled histology; used for ABR
Hp seen on GS: appear enlarged with abnormal morphology. Thickening of the CW of Hp occurs in previously given triple therapy. These abnormal bacteria were also present in patients who had follow up negative UBT