27-01-23 - Gastro-Oesophageal Inflammation and Peptic Ulceration Flashcards
Learning outcomes
- Describe achalasia
- Describe the inflammatory disorders of the oesophagus
- Describe the inflammatory disorders of the stomach
- Describe the causes and mechanisms of peptic ulceration
- Describe the structure and complications of acute and chronic peptic ulcers
What is achalasia?
What does achalasia affect?
What are 3 common symptoms of achalasia (achalasia triad)?
- Achalasia is increased tone of the lower oesophageal sphincter (LES)
- Achalasia Impairs smooth muscle relaxation and can be cause of oesophageal obstruction, making it difficult to swallow food/liquid
- 3 common symptoms of achalasia (achalasia triad):
1) Incomplete LES relaxation
2) Increased LES tone and
3) Aperistalsis of the oesophagus
What causes primary achalasia?
What are 7 secondary causes of achalasia?
What are 3 steps of treatment of achalasia?
- The cause of primary achalasia is neuronal, ganglion cell degeneration (Vagus N) – rare familiar cases
- 7 secondary causes of achalasia:
1) Chagas disease (Trypanosoma cruzi infection) – destruction of myenteric plexuses
2) Diabetic autonomic neuropathy
3) Amyloidosis
4) Sarcoidosis
5) Polio
6) Down syndrome
7) Herpes simplex infection - 3 steps of treatment of achalasia:
1) Laparoscopic myotomy
* The affected muscle of the esophagus (lower esophageal sphincter) is cut to allow a better passage of food and liquids from the esophagus into the stomach
2) Balloon dilatation
3) Botox injection
What 2 things can cause acute oesophagitis?
What are the 2 types of chronic oesophagitis?
What does non-specific mean?
Describe the histology of acute oesophagitis (in picture)
- 2 things can cause acute oesophagitis:
1) Infection in immunocompromised patients
* Herpes simplex viruses
* Candida
* Cytomegalovirus (CMV)
2) Corrosives
- 2 types of chronic oesophagitis:
1) Specific, seen in:
* Tuberculosis
* Bullous pemphigoid and Epidermolysis bullosa - distinct autoimmune blistering disorders
* Crohn’s disease - lifelong condition where parts of the digestive system become inflamed
2) Non-specific
* Reflux oesophagitis
* Non-specific is used for a symptom, sign, test result, radiological finding, etc., that does not point towards a specific diagnosis or aetiology
- Describe the histology of acute oesophagitis (in picture)
What is reflux oesophagitis?
What is another name for reflux oesophagitis?
What causes GORD?
What are 5 causative agents of GORD?
What 4 changes do we see in the lining of the oesophagus?
- Reflux oesophagitis is regurgitation of gastric contents
- Reflux oesophagitis is also called Gastro-oesophageal reflux disease (GORD)
- Most cases of GORD are caused by a problem with the lower oesophageal sphincter (LOS).
- This is the muscle around at the bottom of the oesophagus (food pipe) that helps to keep the contents of the stomach from rising back up the oesophagus.
- The LOS can become weakened and may not close properly.
- This allows acid to leak up into the oesophagus, causing symptoms such as heartburn.
- 5 causative agents of GORD:
1) Alcohol and tobacco
2) Obesity
3) Drugs e.g. caffeine
4) Hiatus hernia
5) Motility disorders e.g achalasia - 4 changes do we see in the lining of the oesophagus:
1) Squamous epithelium damaged
2) Eosinophils epithelial infiltration
3) Basal cell hyperplasia
* The enlargement of an organ or tissue caused by an increase in the reproduction rate of its cells, often as an initial stage in the development of cancer.
4) Chronic inflammation
Describe the histology of Reflux oesophagitis (in picture)
What can severe reflux lead to?
How will this heal?
What can this cause?
- Severe reflux leads to ulceration (will only occur in longstanding oesophagitis)
- This may lead to healing by fibrosis
- This can lead to:
1) Stricture (narrowing)
2) Obstruction
What causes Barrett’s Oesophagus?
How does it alter the structure of the oesophagus?
What ages is Barrett’s Oesophagus most common in?
What are 2 suspected causes of Barrett’s Oesophagus?
What can Barrett’s Oesophagus potentially develop into?
How is Barrett’s Oesophagus identified?
- Barrett’s Oesophagus is caused by longstanding reflux
- This results in the lining of the lower oesophagus changing from stratified squamous epithelium to simple columnar epithelium, which lines the intestines
- This is therefore known as intestinal metaplasia
- Barrett’s Oesophagus is most common in ages 40-60 and is more common in males than females
- 2 suspected causes of Barrett’s Oesophagus:
1) Gastric/biliary reflux
2) Helicobacter pylori - Barrett’s Oesophagus is premalignant - risk of adenocarcinoma of distal oesophagus 100x general population
- Barrett’s Oesophagus is identified through gastroscopy
Describe the histology of Barrett’s oesophagus (in picture)
What are 2 causes of acute gastritis?
What are 3 types of chronic gastritis?
- 2 causes of acute gastritis:
1) Usually due to chemical injury
* Drugs e.g. NSAIDs
* Alcohol
2) H pylori-associated (gram negative bacteria)
* Usually transient phase
* Often becomes chronic
- 3 types of chronic gastritis:
1) Active chronic (H pylori-associated)
2) Autoimmune – antibodies against cells in the stomach
3) Chemical (Reflux) – bile can come from duodenum into stomach, error of pyloric sphincter
H pylori-associated Gastritis.
What type of bacteria is H pylori (helicobacter pylori)?
What 3 ways can H pylori spread?
Where does it occupy in the stomach?
What does it not colonise?
What % of active chronic gastritis cases does H pylori make up?
Describe the pathogenesis of H pylori (in picture)
- H pylori-associated Gastritis
- H pylori (helicobacter pylori) is a gram-negative spiral-shaped or curved bacilli
- 3 ways H pylori can spread:
1) Oral-oral
2) Faecal-oral
3) Environmental - H pylori occupies protected niche beneath mucus where pH is approximately neutral
- H pylori does not colonise intestinal type epithelium
- It is found in 90% of active chronic gastritis
- Describe the pathogenesis of H pylori (in picture)
Describe the histology of H pylori gastritis (in picture)
What 7 additional conditions is H pylori associated with?
- 7 additional conditions H pylori is associated with:
1) Causative factor in gastric and duodenal ulcers
2) Risk factor for gastric cancer (adenocarcinoma)
3) Strong link with MALT (Mucosa Associated Lymphoid Tissue) Lymphoma
4) Dyspepsia (indigestion)
* Indigestion is the name for symptoms like heartburn and bloating that can happen after eating.
* Symptoms of indigestion include heartburn, bloating and feeling sick.
5) Atrophic gastritis
* Chronic inflammation of the gastric mucosa with loss of the gastric glandular cells and replacement by intestinal-type epithelium, pyloric-type glands, and fibrous tissue
6) Iron deficiency anaemia
7) Idiopathic Thrombocytopenic Purpura
* Blood disorder characterized by an abnormal decrease in the number of platelets in the blood.
* A decrease in platelets can result in easy bruising, bleeding gums, and internal bleeding.
What are 4 symptoms of H pylori acute infection?
How long does acute infection last for?
How does acute H pylori infection affect the gastric mucosa?
- 4 symptoms of H pylori acute infection:
1) Nausea
2) Dyspepsia
3) Malaise
4) Halitosis (gum inflammation) - Acute infection tends to last about two weeks
- Due to H pylori acute infections, Gastric mucosa is inflamed with neutrophils and inflammatory cells with marked persistent lymphocyte penetration
What does H pylori chronic infection cause?
What 5 factors does the outcome depend on?
Describe the histology of H pylori gastritis (in picture)
- H pylori chronic infection causes Local inflammation and gastritis
- 5 factors the outcome depends on:
1) Pattern of inflammation
2) Host response
3) Bacterial virulence
4) Environmental factors
5) Patient age - Describe the histology of H pylori gastritis (in picture)
What are 2 distribution patterns of H pylori-associated Gastritis.
How do they each present?
What conditions are they each associated with?
- 2 distribution patterns of H pylori-associated Gastritis:
1) Diffuse involvement of antrum and body
* Presents with atrophy, fibrosis and intestinal metaplasia (stomach epithelium replace by intestinal epithelium)
* Associated with gastric ulcer and gastric cancer
2) Antral but not body involvement
* Gastric acid secretion increased and passed into duodenum
* Associated with duodenal ulcer
What is chemical (reflux) gastritis caused by?
How does it affect epithelial cells?
What are gastric foveola?
What 2 conditions is chemical (reflux) gastritis associated with?
- Chemical (reflux) gastritis is caused by regurgitation of bile and alkaline duodenal secretion
- Chemical gastritis results inloss of epithelial cells with compensatory hyperplasia of gastric foveola
- Foveola or gastric pits communicate with the lumen of the stomach and transport gastric cell secretions
- 2 conditions chemical (reflux) gastritis associated with:
1) Defective pylorus
2) Motility disorders
What is Autoimmune Chronic Gastritis?
What 2 factors does Autoimmune Chronic Gastritis lead to a loss of?
What 3 conditions is Autoimmune Chronic Gastritis associated with?
How is Autoimmune Chronic Gastritis diagnosed?
Describe the histology of Autoimmune Chronic Gastritis (in picture)
- Autoimmune Chronic Gastritis is an Autoimmune reaction to gastric parietal cells
- 2 factors Autoimmune Chronic Gastritis lead to a loss of:
1) Loss of acid secretion (hypochlorhydria / achlorhydria)
2) Loss of intrinsic factor
* Vitamin B12 deficiency
* Macrocytic anaemia (Pernicious anaemia – ‘beef tongue’)
- 3 conditions Autoimmune Chronic Gastritis is associated with:
1) Marked gastric atrophy and
2) Intestinal metaplasia
3) Increased risk of gastric cancer - Autoimmune Chronic Gastritis is diagnosed through detection of serum antibodies to gastric parietal cells and intrinsic factor
- Describe the histology of Autoimmune Chronic Gastritis
Describe the following factors of chronic oesophagitis (in picture):
* Aetiology (causes -3)
* Mechanism
* Histology
* Clinical presentation
What is peptic ulceration?
What are 4 common sites for peptic ulceration?
- Peptic ulceration is a breach in mucosal lining of alimentary tract as a result of acid and pepsin attack
- 4 common sites for peptic ulceration (most to least common):
1) First part of duodenum
2) Junction of antral and body mucosa in stomach
3) Distal oesophagus
4) Gastro-enterostomy stoma
Gastric vs duodenal ulcers (in picture):
* Relative incidence
* Age
* Social class
* Blood group
* Acid levels
* Helicobacter gastritis
What 2 factors are acute peptic ulcers related to?
What are acute peptic ulcers a result of?
- 2 factors acute peptic ulcers are related to:
1) Acute gastritis
* Full thickness loss of epithelium, rather than just erosion
2) Stress response
* e.g. Curling’s ulcer following severe burns
- Acute peptic ulcers are a result of extreme hyperacidity e.g. Gastrin-secreting tumours
Where do chronic peptic ulcers occur?
What are 2 parts of the pathogenesis of chronic peptic ulcers?
- Chronic peptic ulcers tend to occur at mucosal junctions e.g. antrum – body
- 2 parts of the pathogenesis of chronic peptic ulcers:
1) Hyperacidity - not whole story
2) Mucosal defence defects
What is the normal pH of gastric juice?
What are the 2 mucosal defences?
What are 3 factors that can lead to chronic peptic ulcers?
What are the 4 layers of peptic ulcers?
- The Normal pH of gastric juice 1-2
- 2 mucosal defences:
1) Mucus-bicarbonate barrier
2) Surface epithelium - less important - 3 factors that can lead to chronic peptic ulcers:
1) Mucus-bicarbonate barrier dissolved by biliary reflux (duodenal-gastric reflux)
2) Surface epithelium damaged by NSAIDs
3) Surface epithelium injured by H pylori
- 4 layers of peptic ulcers:
1) Necrotic debris
2) Non-specific acute inflammation
3) Granulation tissue
4) Fibrosis
Describe the mechanism of gastric injury and protection (in picture)
Describe 6 factors in the pathology of ulcers.
What are 3 complications of ulcers?
- 6 factors in the pathology of ulcers:
1) Usually small (<20mm)
2) Sharply ‘Punched out’ with defined edges
3) Defined structure
4) Granulation tissue at base
5) Underlying inflammation and fibrosis
6) Loss of muscularis propria
- 3 complications of ulcers:
1) ‘Bleed, burst or block’
2) Penetration of adjacent organs e.g. pancreas
3) Malignant change: rare in gastric ulcer and ‘never’ in duodenal ulcer
