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home - Stomach - Peptic Ulcer Disease - Helicobacter Pylori Pathophysiology Written by Dr Sebastian Zeki

Knows the range of organic and non-organic causes of dyspepsia. Be
aware of current BSG and NICE guidelines for selecting patients for
investigation. Know the significance of alarm symptoms
Understands the relevance of Helicobacter pylori infection and how it
can be detected and treated.
Recognise the adverse effect of nonsteroidal anti-inflammatory drugs
Understands the physiology of gastric acid secretion, mucosal
protection and gastroduodenal motility and know how drugs can
modify these
Knows the complications of ulcer disease, the principles of surgery
that may be required and be aware of post-operative sequelae

Makes a thorough clinical assessment, perform appropriate
investigations and be familiar with how medical treatments are used.
Show awareness of how to recognise and manage complications

Can explain the steps taken towards making a diagnosis and
planning treatment clearly and comprehensibly


Knows the causes of upper gastrointestinal bleeding and its
Understands the circulatory disturbance associated with blood loss
and the pathophysiology underlying the clinical manifestations of
hypovolaemic shock
Knows the principles of assessing hypovolaemia and of restoring the
circulation. Be able to identify and correct coagulopathy
Knows the principles of using the various risk stratification tools SCE 1
Knows how endoscopic techniques are used to control bleeding CbD, DOPS, SCE 1
Understands how oesophageal and gastric varices develop and the
endoscopic and pharmacological methods that are used to control
blood loss

Can make an accurate clinical assessment, and stratify the risk. Know
the principles of fluid resuscitation and arrange endoscopy
Is aware of methods to secure haemostasis, recognise signs of rebleeding and liaise with other disciplines (such as interventional
radiology or surgery

Assesses and treats patients who have bleeding with appropriate
degree of urgency.


Understands why part or all of the patient’s stomach is removed and
the altered post-surgical anatomy

Understands the problems of a gastro-enterostomy and a Roux-en-y

Has awareness of dumping syndromes
Knows the various surgical operations performed for obesity (bariatric
surgery) and their complications

Can give nutritional advice and choose the appropriate method by
which an enteral feeding tube is inserted into the small bowel

Can initiate the use of pancreatic enzyme therapy
Has ability to recognise and treat early and late dumping syndrome
Able to help the patient carers friends and family understand how
the patient can be encouraged to gain weight

Works closely with dieticians and surgical colleagues

Helicobacter Pylori Pathophysiology

Helicobacter pylori infection and duodenal ulcer *Gastrin has a trophic action on parietal cells and histamine-secreting enterochromaffin-like (ECL) cells. It stimulates parietal cells largely via the release of histamine. * Mucosal defense factorsH. pylori may inhibit Epidermal growth factor (EGF) and transforming growth factor-alpha (TGF alpha) whichare potent gastric acid inhibitors and stimuli of mucosal growth and protection.H. pylori itself releases proteases that degrade normally protective mucous glycoproteins, which overlie the mucosaMetaplasia may weaken the mucosa, making it more susceptible to acid injury. Immune responseResponse includes increased production of IL-1,6,8 and TNFalpha. Bug straineg Cag A Genetic factors eg H. pylori who develop DU have an intrinsically higher parietal cell mass or sensitivity to gastrin than H. pylori-positive healthy adultsGenetic factors may also determine duodenal cytokine response to infection. Increased gastrin response Resides in antrum only DistributionAntrum and body — 80 % Antrum only — 8 % Body only — 10 %- Usually if been on PPI’s or marked atrophy and intestinal metaplasia Gastrin producing cells are gradually lost, precipitat-ing a fall in acid secretion and the development of atrophy with intestinal metaplasiaThese changes facilitate the proximal migration of the bacteria, leading to corpus gastritis. Gastric ulcers and gastric cancer are typically associated with extensive gastritis, widespread intestinal metaplasia and hypochlorhydria. Duodenal ulcers are typically associated with antral predominant gastritis, little or no atrophy, and normal or increased acid secretion. Development of Gastric Ulcer 1. No Defenses Somatostatin Gastrin 3. Decreased somatostatin so gastrin levels go up in chronic H. P Increased acid output Gastric metaplasisa (= gastric epithelium in the first part of the duodenumand colonization 2. Inflammation Environmental Factors eg NSAIDs and H. pyloriIncreased PUD x6 when together (vs average of x3 for each alone) If history of PUD NSAID users whould be tested for H. pyloriAlso some argument that all NSAID users should have a test for H. pylori. Fastors Involved In Duodenal Ulcer Formation Mucosa Submucosa Lymphocytes Plasma cellsMacrophagesEosinophils. Prominent lymphoid follicles ( uncommon in non-H. pylori-infected gastric mucosa; involved in the genesis of primary gastric lymphoma) and plasma cells. Inflammatory cells present in the upper mucosa- looks like a superficial gastritis Pit abscesses HistologyNeutrophils disappear rapidly; the persistence of even small numbers of neutrophils may be predictive of relapse.Lymphocytes and eosinophils decrease more slowly, and some chronic inflamm-tion can be seen after one year.-Lymphoid follicles are the slowest to disappear, and usually remain present throughout the stomach for more than one year.-Intestinal metaplasia and atrophy usually do not resolve by one year . However, eradication may help prevent the development of further gastric atrophy and intestinal metaplasia.-Fibrosis and architectural distortion, including foveolar hyperplasia, may persist long after H. pylori infection is eliminated and, in our experience, often resembles chemical gastropathy. H. pylori organisms reside primarily in the unstirred layer of gastric mucus, adjacent to epithelial cells at the mucosal surface and in gastric pits as have affinity for gastric mucous cellsGastric glands are usually not involved. Eradication The organisms are uncommonly found in the lamina propria, except possibly in patients with AIDS Best place to biopsy:Lesser and greater curvature of the mid antrum Lesser and greater curvature of the mid body Written by Dr Sebastian Zeki

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