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home - Stomach - Peptic Ulcer Disease - Zollinger Ellison Clinical Presentation 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

Zollinger Ellison Clinical Presentation

G-cell ECL cell Parietal Acid Gastrin Histamine - 20% Hepatobiliary Source: Enteroendo-crine cells Gas-trinoma cells 70% Duodenum Clinical manifestations and diagnosis of Zollinger-Ellison syndrome (gastrinoma) EpidemiologyPrevalence is 0.1 to1% of PUD.The peak age prevalence is 20- 50.Males are twice as likely as females to be diagnosed with Z-E.Gastrinomas can be either sporadic or associated with multiple endocrine neoplasia type 1.Approximately 80% of patients have the sporadic form although somatic (acquired) mutations in the MEN1 gene are observed-commonly in sporadic gastrinomas. Source: Enter-oendocrine cells Gastrinoma cells The gastrinoma triangle is formed by a line joining the confluence of the cystic and common bile ducts (A) superiorly, the junction of the second and third portion of the duodenum inferiorly (B), and the junction of the neck and body of the pancreas medially (C). 10% pancreas Duodenal gastrinomas tend to be quite small and are often multiple. They have less malignant potential than the solitary, sporadic pancreatic gastrinomas. Gastrin Gastrin has trophic action on parietal cells and histamine-secreting enterochromaffin-like (ECL) cells. Gastrin stimulates parietal cells largely via the release of histamine. 75% 14 % 11 % 90 % Z-E develop peptic ulcers-solitary ulcers <1 cm in diameter. Mets to liver and bone in 1/3rd at presentation. Clinical Presentation:The ulcers recur much more often than in patients with sporadic ulcer disease.Diarrhoea is caused by the high volume of gastric acid that isnt reabsorbed.Diarrhoea is also caused by excess acid which neutralizes pancreatic enzymes and damages small bowel.-Gastrin inhibits absorption of intestinal sodium and water by the small intestine, thereby exacerbating the diarrhoea. Gastrinoma Triangle Written by Dr Sebastian Zeki

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