Please enable JavaScript.
Coggle requires JavaScript to display documents.
Peptic Ulcer Disease (PUD) (Pathophysiology (Helicobacter pylori (Highly…
Peptic Ulcer Disease (PUD)
Key Facts
Duodenal ulcers are most commonly found in the duodenal cap
Gastric ulcers are most commonly seen on the lesser curve of the stomach but can be found anywhere in the stomach
A peptic ulcer consists of a break in the superficial epithelial cells penetrating down to the muscularis mucosa of either the stomach of the duodenum; there is a fibrous base and an increase in inflammatory cells
Epidemiology
More common in developing countries due to Helicobacter pylori
Ulcers due to NSAIDs is increasing
More common in the elderly
Decline in incidence in men and increasing in women
Duodenal ulcers affect around 10% of the adult population and are 2-3 times MORE COMMON than gastric ulcers
Causes
Increased gastric acid secretion (minor)
Smoking (minor)
Drugs e.g. NSAIDs, steroids & SSRI's
Delayed gastric emptying
Helicobacter pylori infection
Blood group O
Pathophysiology
Helicobacter pylori
Highly adapted to the stomach environment and exclusively colonises gastric epithelium and inhabits the mucous layer or just beneath it
Causes major destruction to the mucin layer that protects the mucosa
Causes the decrease in duodenal HCO3 thereby increasing the acidity of the stomach as there will be less alkali to buffer the acid
Ischaemia of the gastric cells
Causes gastric cells to produce less mucin resulting in less protection from acid meaning acid is able to damage mucosa resulting in ulcer (breach in mucosal surface)
Caused by low blood pressure or atherosclerosis
NSAIDs
Cyclo-oxygenase 1 is needed for prostaglandin synthesis
NSAIDs inhibit COX-1, therefore reduced mucosal defence
Mucous secretion is stimulated by prostaglandins
Too much acid production
Too much acid overwhelms the mucin and results in ulceration
Stress can result in increased acid production
Proton pump inhibitors and H2 blockers used to treat this
Usually the gastric mucosa is protected by a layer of MUCIN that is produced by gastric cells
Alcohol has a direct toxic effect on gastric cells in high concentrations
Ulcers result in gastritis (inflammation of the gastric cells)
Clinical Presentation
Nausea may accompany the pain
Anorexia and weight loss - particularly with gastric ulcers
Recurrent burning epigastric pain
Pain of duodenal ulcers classically occurs at night & is worse when patient is hungry
Pain in both gastric and duodenal ulcers can be relieved by antacids
Epigastrium as the site of pain
Complications
Can result in peritonitis as acid enter peritoneum - will see air under diaphragm on erect X-ray
Can result in acute pancreatitis if the ulcer hits the pancreas
In duodenal ulcers, the ulcer can get deep until it hits an artery (most commonly gastroduodenal) - can result in haemorrhage & present as emergency
Diagnosis
Endoscopy is essential in all ALARM patients and those who are over 55
Non-invasive H.pylori testing
C-Urea breath test
Stool antigen test
Serology
Usually an endoscopy is not necessary, but if found to have a gastric ulcer then rescope 6-8 weeks later to ensure no malignancy
Invasive H.pylori testing
Histology
Biopsy urease test
Endoscopy
Under 55yrs - non invasive testing
Treatment
H.pylori eradication
Triple therapy
2 separate antibiotics
PPI for acid suppression
H2 antagonists to reduce acid release
Stop NSAIDs
Surgery if complications arise such as haemorrhage
Lifestyle adjustments
Avoid irritating foods
Reduce smoking
Reduce stress