HomeCoursesMEDSCI 203: Mechanisms of DiseaseLecture 16 Lecture 16 1. How can microbes cause damage? (5) "Exotoxins, degredative enzymes, inflammation, auto immune damage, cancer"How can microbes cause damage? (5)== "Exotoxins, degredative enzymes, inflammation, auto immune damage, cancer" 2. What is peptic ulcer disease? A break in the lining of the stomach or small intestineWhat is peptic ulcer disease?== A break in the lining of the stomach or small intestine 3. What are the symptoms of a peptic ulcer? (4) "Abdominal pain, vomiting, weight loss, bleeding"What are the symptoms of a peptic ulcer? (4)== "Abdominal pain, vomiting, weight loss, bleeding" 4. Which microbes cause peptic ulcers? Heliobactor pyloriWhich microbes cause peptic ulcers?== Heliobactor pylori 5. How is H. pylori transmitted? Fecal-oral routeHow is H. pylori transmitted? ==Fecal-oral route 6. What is the spectrum of H. pylori disease? "Gastritis, peptic ulcer, cancer, lymphoma"What is the spectrum of H. pylori disease? == "Gastritis, peptic ulcer, cancer, lymphoma" 7. How does H. pylori translocate to the stomach lining? (2) "Flagellum, screw into tissue due to helical shape"How does H. pylori translocate to the stomach lining? (2)== "Flagellum, screw into tissue due to helical shape" 8. How do H. pylori resist stomach acids? Secrete urease to neutralise acidHow do H. pylori resist stomach acids?== Secrete urease to neutralise acid 9. Why are H. pylori not recognised by immune system? (2) "The LPS they have is poorly recognised by TLR4s, flagellin are poorly recognised by TLR5s"Why are H. pylori not recognised by immune system? (2)== "The LPS they have is poorly recognised by TLR4s, flagellin are poorly recognised by TLR5s" 10. What does VacA inhibit? (3)= ="Phagosomal maturation, T/B cell proliferation, NOS generation" What does VacA inhibit? (3)= ="Phagosomal maturation, T/B cell proliferation, NOS generation" 11. What is the result of a coating of plasminogen/cholesterol? Appears as selfWhat is the result of a coating of plasminogen/cholesterol?== Appears as self 12. What does chronic inflammation lead to? Loss of cell function in inflamed areaWhat does chronic inflammation lead to?== Loss of cell function in inflamed area 13. What does chronic infection of H. pyolori result in? Chronic inflammationWhat does chronic infection of H. pyolori result in? ==Chronic inflammation 14. What is an ulcer? A lesion in mucous membraneWhat is an ulcer? ==A lesion in mucous membrane 15. What is a gastric ulcer? Lesion in the stomachWhat is a gastric ulcer?== Lesion in the stomach 16. What is a duodenal ulcer? Lesion in the duodenumWhat is a duodenal ulcer?== Lesion in the duodenum 17. What is the process of acid production? Food > G-cells produce gastrin > ECL cells produce histamines > parietal cells produce acidWhat is the process of acid production?== Food > G-cells produce gastrin > ECL cells produce histamines > parietal cells produce acid 18. What is the acid feedback loop? Acid > Somatostatin cells > G cells decrease gastrin > decrease acidWhat is the acid feedback loop?== Acid > Somatostatin cells > G cells decrease gastrin > decrease acid 19. How does H. pylori affect the antrum? "Destruction of S cells > no regulation of acid production > inflammation of duodenum > duodenum ulcers, acid hypersecretion"How does H. pylori affect the antrum?== "Destruction of S cells > no regulation of acid production > inflammation of duodenum > duodenum ulcers, acid hypersecretion" 20. What is the end result of gastritis (gastric ulcer)? Gastric cancerWhat is the end result of gastritis (gastric ulcer)?== Gastric cancer 21. What is the end result of high acid production? ==Peptic ulcers 22. How does H. pylori affect cells? (3) "Gene expression, DNA breaks, DNA methylation"How does H. pylori affect cells? (3)== "Gene expression, DNA breaks, DNA methylation" 23. What is the Car pathogenicity island? Type IV secretion systemWhat is the Car pathogenicity island?== Type IV secretion system 24. Which secretion is associated with gastric cancer? Cag proteinWhich secretion is associated with gastric cancer?== Cag protein 25. What happens to Cag in the cell? (2) "Phosphorylated > stimulation of phosphylation cascades, release of ROS from mitochondria"What happens to Cag in the cell? (2)== "Phosphorylated > stimulation of phosphylation cascades, release of ROS from mitochondria" 26. What phosphorylation cascades does CagA stimulate? (4) "Apoptosis, morphological change (barrier disruption), cytokine production, cell proliferation"What phosphorylation cascades does CagA stimulate? (4)== "Apoptosis, morphological change (barrier disruption), cytokine production, cell proliferation" 27. What factors contribute to gastric cancer? (3) "Reactive oxygen species, Reactive nitrogen species, oncotic pathways by CagA"What factors contribute to gastric cancer? (3)== "Reactive oxygen species, Reactive nitrogen species, oncotic pathways by CagA" 28. What are the virulence factors of H. pylori? (7) "Flagella, VacA, CagA, enzymes, LPS, Urease, Outer proteins"What are the virulence factors of H. pylori? (7)== "Flagella, VacA, CagA, enzymes, LPS, Urease, Outer proteins" 29. What is an obvious symptom of an H. pylori infection? Bad breathWhat is an obvious symptom of an H. pylori infection?== Bad breath 30. What is the treatment for a H. pylori infection? "Proton pump inhibitor, antibiotics (clarithromycin, amoxicillin)"What is the treatment for a H. pylori infection?== "Proton pump inhibitor, antibiotics (clarithromycin, amoxicillin)" Loading...
