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Outline of Key Learning Areas related to PBL Case AHMEN 32y.o REFUGEE Presenting Symptoms Epigastric pain, waking him at night (=red flag) Other Significant History Refugee prev. in refugee camp (poor dietary, sanitary + physical & mental abuse). Had pain 3 years ago- relieved by antacids. Pain relieved by food and worse when hasn't eaten for awhile. Examination and Signs Anxious, distressed. Weight/height normal Afebrile (therefore probably doesn't have a systemic acute infection) Abdomen tender in epigastrium Voluntary guarding Endoscopy revealed duodenal ulcer with chronic antral gastritis Biopsy taken from antrum + for CLO urease test (H pylori infection confirmed) Principal Hypothesis Differential Diagnoses H pylori infected duodenal ulcer Gastro-oesophageal reflux disease (GORD) Risk Factors and Aetiology Poor diet, unsanitary, physical and mental abuse experienced in refugee camp. Potential previous ulcer (3 years ago) Key Basic Science Learning Issues 1) Anatomy See anatomy lectures/tutorials on abdominal organs. 2) Pathophysiology 3) Microbiology Sequence of events in ulceration Copyright UTS, 2012 H pylori infection: (see appendix 1) 10/32 H pylori is gram-negative has multiple flagella – motile. It burrows and lives deep beneath the mucus layer closely adherentCopyright to theUTS, 2012 epithelial surface. Uses adhesion molecule to bind to surface antigen on epithelial cells. Here surface pH is close to neutral and any acidity is buffered by the organisms production of the enzyme urease. Produces ammonia from urea to raise the pH around the bacterium and between its 2 cell membrane layers. The bacteria spread by person-to-person contact via gastric reflexate or vomit. H pylori exclusively colonises gastric-type epithelium, in close association in patches of gastric metaplasia. The bacterium stimulates chronic gastritis by provoking local inflammatory response in the underlying epithelium. H pylori often causes antral gastritis associated with depletion of somatostatin (from D cells) and increased gastrin (from G cells). The subsequent hypergastrinaemia stimulates acid production by parietal cells, in the minority of patients this effect is exaggerated and leads to duodenal 14/32 Ability to stay in a hostile acidic environment because it creates urease, an enzyme which converts urea to ammonia, making immediate 5 environment more basic. 4) Pathology 7 ulceration. Believed that H pylori infection acts by reducing gastric mucosal resistance to attack from acid and pepsin. Investigations 1) Bloods Results 1) Bloods 2) Imaging Full blood count (FBC): Ordered if Px seems clinically anaemic or has evidence of gastrointestinal bleeding. Does not aid in diagnoses. Upper gastrointestinal endoscopy ⁃ the most specific and sensitive test. ⁃ Histology and urease testing are performed on stomach biopsies obtained during endoscopy. Both tests can detect H pylori; however, the histology determines if the ulcer is neoplastic (rare) and/or if there is evidence of an NSAID being the likely cause. 2) Imaging 3) Other Stool heme test: Often performed, but usually negative in the presence of peptic ulcer disease. 3) Other Helicobacter pylori breath test or stool antigen test + test confirms H pylori present. Management Plan Problem Goal/desired outcome Method Resources/health professional H pylori infection Eradicate H pylori infection Antibiotics (double Tx) GP Chronic antral gastritis Reduce inflammation, reduce secretion of gastric acid. Increase mucosal resistance. Triple Tx (A, A + PPI) GP Duodenal ulcer Repair/rebuild mucosa, heal ulcer. reduce secretion of gastric acid. Increase mucosal resistance. Triple therapy (A, A + PPI) Improve nutrition, improve sanitation Refugee camps improve conditions, Ahmed more informed re diet/sanitation Social workers, GP, dieticians, Medications Mode of action Side effects Any specific monitoring required? Triple Therapy includes: Proton Pump Inhibitor (PPI) eg. Omeprazole PPI: Bind to the H+/K+ - ATPase (proton pump) Use ofofPPIsparietal concerns cells, suppressing about long-term action safety of H+(carcinoid into gastric tumours?) lumen-> 90% inhibit ion. Poor nutrition and sanitation GP Ahmed was given H2 Receptor antagonist (this is not gold standard Tx anymore) Poor English Antibiotics x2 eg. amioxollin, metronidazole, bismuth, clarithromycine, tetracycline. A: eradication of h pylori - rapid healing and low recurrence rate. Standard triple Tx involves bismuth, metronidazole and tetracycline for 2 weeks (90% eradication rate) Antacids Raise the luminal pH of the stomach (More so treating the symptoms not cause) Histamine2 (H2) receptor antagonist eg. cimetidine, ranitidine Block action of histamine (H2 receptor) on the parietal cells and thus reduce acid secretion. A: common side effects include: diarrhoea (30-50% Px), flushing and vomiting when taken w alcohol, nausea, vomiting, abdominal cramps, headache, rash. PPI: A: Ensure Px takes full course (7-14 days). Tx with only single antimcrobial drug is less effective (20-40% eradication rate). High use may be assoc w systemic alkalosis, diarrhoea, constipation. Usually minor: headache, dizziness, diarrhea, muscle pain, confusion. Full course is 6 weeks. Recurrence is common after Tx is stopped (60-100%). Other Psychosocial/ethical/legal considerations Refugee camps- poor dietary and sanitary conditions. Cultural issues- patient beliefs, importance of family involvement in healthcare (language facilitators, information interpreters) Communication barriers can result in confused, feeling powerless in their treatment. PPH/PPD implications Language difficulties: Valid consent (effectively communicated?) Cultural issues- patient beliefs, importance of family involvement in healthcare (language facilitators, information interpreters), communication barriers can result in confused, feeling powerless in their treatment. Resources Davidsons Principles and Practices of Medicine, Lecture notes Resource Page: Peptic Ulcer - refers to an ulcer in the lower oesophagus, stomach or duodenum Ulcers develop when there is an imbalance between mucosal defensive factors & aggressive factors (see figure 1) Maj. defensive factors are mucus, bicarbonate, prostaglandin, NO, and growth factors; Major aggressive: H. pylori, NSAID, gastric acid & pepsin Release of hydrochloric acid (HCL) from the parietal cells of the stomach influenced by histamine, gastrin & acetylcholine Figure 1: Relationship of mucosal defenses and aggressive factors 90% of duodenal ulcer patients and 70% of gastric ulcer patients are infected with H. pylori, the remaining 30% of gastric ulcers are due to NSAIDs. Prevalence of H. pylori infection in the general population is 50% -90% Relationship ofDuodenal mucosal andthan aggressive factors ulcersdefenses 10X more frequent gastric, esophageal. Duodenal ulcers usually occur just distal to the pyloric sphincter. Copyright UTS, 2012 7/32 Risk factors for gastric ulcer include: Long term use of NSAIDs (aspirin, ibuprofen) H pylori infection of the gastric &/or duodenal mucosa Alcohol Smoking Chronic diseases (emphysema, rheumatoid arthritis, cirrhosis, diabetes) Appendix 1: l ze or 5 13/32 CELLS OF THE STOMACH: G CELLS- GASTRIN Parietal Cells- H+ for hydrochloric acid Chief cells- pepsinogen to convert pepsin (protein breakdown) Enterendocrine cells- histamine. Secretion of Hydrocholirc acid by the gastric parietal cells: secretion of hydrochloric acid by the gastric parietal cell Copyright UTS, 2012 9/32 HORMONES OF GIT: Gastrin- gastrin causes an increase in secretion of HCL from parietal cells and increase pepsinogen from chief cells in the stomach. Released from G-cells in stomach in response to distension of the antrum and presence of digestive products. Gastrin is inhibited by somatostatin. Histamine- increases acid secretion. Released from enterochromaffin cells. CCK (Cholecystokinin)- has most effect on gallbladder, decreases gastric emptying and increases release of pancreatic juice which is alkaline and neutralises and chyme. Seretin- produced in SI, mostly affects pancreas, increases pancreatic fluids and bicarbonate secretion. Secretin will also diminish acid secretion in the stomach and reduce stomach emptying. Gastric inhibitory peptide- GIP decreases both gastric acid release and motility. Increases insulin secretion. Acetylcholine- increases acid secretion, increases blood flow, increases mucus secretion and increases bicarbonate secretion. If have excess acidity, somatostatin, CCK, GIP are decreased. How do NSAIDs contribute to increased risk of gastric ulcer? NSAIDs reduce prostaglandin synthesis. However, PGs stimulate bicarbonate and gastric mucus secretion and increase mucosal blood flow. Bicarbonate ions are secreted into the unstirred mucus layer, neutralizing hydrogen ions as they back- diffuse towards the epithelium. Rapid cell turnover and a rich mucosal blood supply are important protective elements. However, high NSAIDs use alters the gastric mucosal barrier: ↓ prostaglandin synthesis ↓ mucus and bicarbonate secretion ↓ submucosal blood flow ↓ mucosal ATP ↓ cell turnover ↓ platelet function (irreversible) Gs and mucosal protection mulate bicarbonate and mucus secretion and increase blood flow. Bicarbonate ions are secreted into the mucus layer, neutralising hydrogen ions as they backowards the epithelium. Rapid cell turnover and a rich blood supply are important protective elements. 15/32