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home - Stomach - Peptic Ulcer Disease - Peptic Ulcer Disease Causes 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

Peptic Ulcer Disease Causes

GENETIC, ENVIRONMENTAL, AND PSYCHOLOGICAL RISK FACTORS Blood groups O and A, the Lewis phenotype Le(a + b-), and non-secretors of ABH in particular, have been associated for increased risk of DU.Alcohol damages the gastric mucosal barrier to hydrogen ions.Alcohol is associated with acute gastric mucosal hemorrhages. EtOH stimulates acid secretion (non-alcohol constituents also stimulate acidproduction).Alcohol is not associated with PUD and may even promote ulcer healing.Diet may influence peptic ulcer pathogenesis.No evidence that foods cause, perpetuate, or reactivate peptic ulcers. Miscellaneous causes of peptic ulcer disease: Stress ulcers in intensive care —These are superficial. Occur within 18 hours.Cirrhosis — This has a 30% prevalence. Incidence anually of 5%. 50% recurrence and complication rate.Organ transplantation — Due to immunosuppression (esp sirolimus), corticosteroids, and CMV infection.Chronic obstructive pulmonary disease — PUD occurs in 30 % of patients with chronic lung disease. Smoking related.Rheumatic disease — Point prevalence of ulcers in patients on long-term NSAID treatment is20 %. but rarely clinically significant.Need prohylaxis if high risk.Paracetamol — Risk increased only if >2g/day and in combo with NSAID.Bisphosphonates — Acute ulceration is seen but rarely clinically significant. Risk is increased with coadministration of NSAIDs.Corticosteroids — Only a problem if with NSAIDs.Clopidogrel — Risk is for GI bleeding especially if NSAIDs/ aspirin.Sirolimus — Associated with big ulcers in transplant patients and small bowel ulceration.Spironolactone — This is dose and age related risk (threefold increase).Selective serotonin reuptake inhibitors — Risk is highest with concurrent use of SSRIs and NSAIDs or aspirin.Gastrinoma.Systemic mastocytosis — This is a mast cell infiltration of many tissues with large histamine release and consequent acid hypersecretion.Carcinoid syndrome — Probably related to ectopic histamine production and can usually be controlled with H2 receptor antagonists.Basophilia in myeloproliferative disorders —Causes increased histmine production.Polycythemia vera-This may be due to reduced mucosal blood flow due to increased viscosity.Antral G cell hyperfunction — This is an exaggerated response to H. pylori-induced hypergastrinemia. PPI suppresses gastrin levels.Idiopathic hypersecretory (H. pylori-negative, NSAID-negative) DU — 10% DU have increased acid output but normal gastrin levels and no precipitant.Herpes simplex virus type I — HSV-I in 30 and 32 % of DU and GU, respectively. Only found in margin of ulcers and its role is unknown.Cytomegalovirus — Cytomegalovirus (CMV) has been associated with PUD in immunocompromised patients.-usually multiple ulcers and gastric.Post-gastric surgery.Antral exclusion- described in patients after gastric resection in whom antral mucosa was retained in the duodenal pouch.Stomal ulcers have been reported after Roux-en-Y gastric bypass in patients who had no known ulcer history before surgery-probably secondary to acid hyperseretion.Duodenal obstruction —Unusual cases of DU have been linked to a variety of duodenal abnormalities, including congenital duodenal webs, hypertrophic pyloric stenosis, annular pancreas.Vascular insufficiency, crack cocaine, and methamphetamine — Vascular insufficiency ulcers often fail PPI therapy, but can respond to revascularization.Crack cocaine may cause mucosal vasoconstriction with subsequent gastroduodenal ulcers- cocaine and amphetamines are also associated with giant ulceration.Radiation —The second portion of the duodenum being especially sensitive to radiation injury. Should respond to PPI.Chemotherapy — Certain forms of chemotherapy have been associated with peptic disease eg 5-FU.Sarcoidosis —The stomach is the most common site of GI sarcoidosis. It always occurs with pulmonary disease.Idiopathic — Some ulcers have no cause. May be related to keloid-like healing which prevent vascularisation and healing. NSAID’sZollinger-Ellison Syndrome TNFalphaIL-1 betaCOX1 TNFalphaIL-1 betaCOX1 Factors protective against peptic ulcer disease:Freshly milled and unmilled rice, unrefined wheat or wheat bran, home pouded maize (as opposed to comme-cial) -these are all protective against DU.Chili peppers- these may protect against damage, possibly by activating mucosal adaptation.Increase in dietary polyunsaturated and essential fatty acids - can be protective against H. pylori.High consumption of fruits and vegetables, dietary fiber, and vitamin A -are associated with a reduced risk of ulcer disease. Detrimental Factors Contributing to PUDCoffee is a strong stimulant of acid secretion but no evidence for increased ulcer disease.A bland diet does not enhance healing.Frequent small meals may sustain acid production.Milk stimulates more acid secretion than it buffers largely because of its calcium and protein content.However, human milk contains potentially protective factors, including growth factors, surface active phospholipids, and prostaglandin E2. Thus, it is possible that milk has antiulcer actions that override the stimulation of acid secretion.Psychologic factors- Poorly tolerated stress or depressive symptoms at baseline increase the risk of ulcer development over the next 9 to 15 years, impair healing and promote relapse of ulcers.PUD complications become much more prevalent during periods of catastrophe. eg WW” bombardment LondonPsychological factors exacerbate both H. pylori and non-H. pylori ulcers to a similar extent. Comorbidities Drugs other than NSAIDs Secretory Conditions: Miscellaneous Antiulcer prophylaxis is routine in most centres Twin studies provide evidence for a clear genetic predisposition to PUD that is independent of any predisposition to H pylori infection. Cytokine PolymorphismsPolymorphisms in TNFalpha ,IL-1- beta but not IL-6 are linked to DU,Polymorphisms in TNF-alpha are linked to GU and gastric cancer, but not DUCyclooxygenase-1 and PG productionT1676C COX-1 polymorphism was associated with GU in non-NSAID users and with both GU and DU in NSAID users. Peptic ulcer Disease Causes Written by Dr Sebastian Zeki

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