Gastro-oesophageal Inflammation and Peptic Ulceration Flashcards
What can acute cause oesophagitis?
- Immunocompromised
- Herpes simplex viruses
- Candida
- Cytomegalovirus (CMV)
What can cause chronic oesophagitis?
- Tuberculosis
- Bullous pemphigoid and epidermolysis bullosa
- Crohn’s disease
- Reflux oesophagitis (non-specific)
What can cause an ‘incompetent’ GO junction and therefore GORD?
- alcohol and tobacco
- Obesity
- Drugs e.g caffeine
- Hiatus hernia
- Motility disorders
What happens to the epithelium in GORD?
- Squamus epithelium damaged
- Eosinophils epithelial infiltration
- Basal cell hyperplasia
- Chronic inflammation
What can severe reflux lead to?
- Ulceration
- May lead to healing by fibrosis:
Stricture
Obstruction
Who is usually affected by Barrett’s Oesophagus?
- Men aged 40-60
How much more likely is adenocarcinoma of distal oesophagus with Barrett’s Oesophagus?
100x
What is the main feature of Barrett’s Oesophagus?
Intestinal METAPLASIA
What is acute gastritis?
- Usually due to chemical injury (drugs/NSAIDs, alcohol)
- H pylori-associated
Usually transient phase
Often becomes chronic
What is chronic gastritis?
- Active chronic (H pylori-associated)
- Autoimmune
- Chemical (reflux)
What is the appearence of H pylori?
- Gram negative
- Spiral shaped or curved bacilli
How is H pylori spread?
- Oral-oral
- Faecal-oral
- Enviromental spread
What space does H pylori occupy?
- Protected niche beneath mucus where pH approx. neutral
- Does not colonise intestinal type epithelium
What percentage of active chronic gastritis is caused by H pylori?
90%
What does helicobacter pylori cause?
- Gastric and duodenal ulcers
- Risk factor for gastric cancer
- Strong link with MALT (Mucosa Associated lymphoid Tissue) Lymphoma
What is an ulcer?
The breaking of epithelium
Describe the pathology of Helicobacter Pylori
- Swims through gastric fluid and into mucus layer
- Once in mucosal layer they produce urease which neutralises acid
- The H pylori divide and produce more urease, this triggers the stomach to produce more HCl
- Huge amounts of acid build up damaging the protected mucu layer and then destroy surface epithelium of stomach leading to the creating of an ulcer
What are the symptoms of a H pylori infection?
Acute infection with symptoms of: - Nausea - Dyspepsia - Malaise - Halitosis Usually lasts about 2 wks
What are the signs in the gastric mucosa of an H pylori infection?
Mucosa is inflamed with neutrophils and inflammatory cells with marked persistent lymphocyte penetration
What does a urease test include?
- TEsting the breath for urease
- Patient blows into special tube if urease is significant -> H pylori infection
What does the outcome of a chronic H pylori infection depend on?
- Pattern of inflammation
- Host response
- Bacterial virulence
- Enviromental factors
- Patient age
HISTOLOGY
LEARN
What are the 2 distribution patterns of H pylori-associated gastritis?
- Diffuse involvement of antrum and body
Atrophy, fibrosis, intestinal metaplasia
Associated with gastric ulcer and gastric cancer - Antral but not body involvement
Gastric acid secretion increased
Associated with duodenal cancer
What is chemical (reflux) gastritis caused by?
- Regurgitation of bile and alkaline duodenal secretion
- Loss of epithelial cells with compensatory hyperplasia of gastric foveolae
What is chemical (reflux) gastritis associated with?
- Defective pylorus
- Motility disorders
Desribe autoimmune chronic gastritis?
- Autoimmune reaction to gastric parietal cells
- Loss of acid secretion (hypochlorhydria / achlorhydria)
- Loss of intrinsic factor
Vitamin B12 deficiency
Macrocytic anaemia (pernicious anaemia) - Associated with marked gastric atrophy and intestinal metaplasia
- Serum antibodies to gastric parietal cells and intrinsic factor
What disease is autoimmune chronic gastritis at an increased risk of causing?
Gastric cancer
How can autoimmune chronic gastritis be diagnosed?
- Serum antibodies
- FBC
What is the definition of peptic ulceration?
Breach in mucosal lining of alimentary tract as a result of acid and pepsin attack
Wht are the major sites of peptic ulceration?
- 1st part of duodenum
- Junction of antral and body mucosa in stomach
- Distal oesophagus
- Gastro-enterostomy stoma
What are the aetiological factors of peptic ulceration?
- Hyperacidity
- H pylori gastritis
- Duodenal reflux
- NSAIDs
- Smoking
- Genetic factors
- Zollinger-Ellison syndrome
What are the complications of peptic ulceration?
- Haemorrghage
- Penetration of adjavent organs e.g. pancreas
- Perforation
- Anaemia
- Obstruction
- Malignancy
How much more common is a duodenal ulcer in comparison to a gastric ulcer?
3 times
What blood groups are gastric and duodenal ulcers meant to affect?
- Gastric
A - Duodenal
O
What are the acid levels usually like in a gastric ulcer?
Normal or low
What are the acid levels usually like in a duodenal ulcer?
High or normal
What percentage of gastric ulcers are caused by H pylori?
About 70%
What percentage of duodenal ulcers are caused by H pylori?
95 - 100%
What is the difference in age groups affected by gastric and duodenal ulcers?
- Gastric
Increases with age - Duodenal
Increases up to 35 years
Which type of ulcer is most likely to occur in people in the lowest socioeconomic status?
GAstric ulcers
What are acute peptic ulcers related to?
- Acute gastritis
Full thickness loss of epithelium, rather than just erosion - Related to a stress response
e.g Curling’s ulcer following severe burns - A result of extreme hyperacidity
e.g Gastrin-secreting tumours
where do chronic peptic ulcers tend to occur?
Mucosal junctions
What are the 2 factors that generally lead to chronic peptic ulceration?
- Hyperacidity - not whole story
- Mucosal defence defects
(mucus-bicrbonate barrier can be dissolved by biliary reflux)
What are chronic duodenal ulcers caused by?
- Increased acid production More important than for gastric ulcer Can be induced by H pylori - Reduced mucosal resistnace Gastric metaplasia occurs in response to hyperacidity Then colonised by H pylori
Desribe the structure of peptic ulcers?
- usually small (>20 mm)
- Sharply ‘punched out’ with defined edges
- Defined structure
Granulation tissue at base
Underlying inflammation and fibrosis
Loss of musscularis mucosa
Complications: bleed, burst or block, penetration of adjacent organs e.g pancreas, malignant change: rare in gastric ulcer and ‘neber’ in duodenal ulcer
