Gastro-oesophageal inflammation and Peptic Ulcers

Question 1

What is Achalasia?

Answer 1

Increased tone of the lower oesophageal sphincter which can be caused by impaired smooth muscle relaxation or oesophageal obstruction.

Question 2

What is the Achalasia triad

Answer 2

• Incomplete lower oesophageal sphincter (LES) relaxation,
• Increased LES tone,
• Aperistalsis of the oesophagus

Question 3

What are the causes of achalasia

Answer 3

Primary - Neuronal or ganglion cell degeneration (familiar causes).

Secondary - Chagas disease (destruction of myenteric plexus), Diabetic autonomic neuropathy, amyloidosis, sarcoidosis, polio, down syndrome and herpes simplex infection.

Question 4

What is the treatment of Achalasia?

Answer 4

Laparoscopic myotomy, balloon dilation and botox injection

Question 5

What are some of the acute and chronic causes of oesophageal inflammation

Answer 5

Acute - Infection in immunosupressed patients (HSV, candida, CMV) and corrosives.

Chronic - TB, Bollus pemphigoid, epidermolysis bullosa, Crohn’s disease

Non-specific - reflux oesophagitis

Question 6

What is reflux oesophagitis (Gastro-oesophageal reflux diseease) and what are some of the causes?

Answer 6

It is regurgitation of gastric contents due to incompetent GO junction. It can be due to alcohol and tobacco, obesity, drugs, hiatus hernia and motility disorders

Question 7

What can GORD cause?

Answer 7

Eosinophils epithelial infiltration, basal cell hyperplasia and chronic inflammation. Severe reflux can lead to ulceration which may lead to healing by fibrosis.

Question 8

What is Barrett’s oesophagus

Answer 8

• Longstanding reflux where the lower oesophagus becomes lined by columnar epithelium due to intestinal metaplasia. This premalignancy increases risk of adenocarcinoma.

Question 9

What are some of the acute and chronic causes of gastric inflammation (gastritis)

Answer 9

Acute - Usually due to chemical injury (NSAIDS/Alcohol) but can also be H pylori associated.

Chronic - Active chronic is H pylori associated, it can be autoimmune or due to chemical (reflux)

Question 10

Describe the pathogenesis of H. Pylori

Answer 10

• H pylori produces Urease which produces ammonia which neutralises the pH of the stomach, allowing it to colonise. It then causes mucosal damage which leads to inflammation and mucosal cell death

Question 11

What are the symptoms of an acute infection due to H pylori?

Answer 11

Nausea, dyspepsia, malaise and halitosis. The gastric mucosa is inflamed with neutrophils and inflammatory cells with marked persistent lymphocyte penetration

Question 12

Describe the two distribution patterns seen with H pylori associated Gastritis

Answer 12

• Diffuse involvment of antrum and body. Therefore there is atrophy, fibrosis and intestinal metaplasia. Associated with gastric ulcers +cancers.
• Antral but with no body involvement. Gastric acid secretion is increased and it is associated with duodenal ulcers

Question 13

What is chemical (reflux) gastritis and what is it associated with?

Answer 13

It is irritation of the stomach caused by regurgitation of bile and alkaline duodenal secretion. There is loss of epithelial cells with compensatory hyperplasia of gastric pits. It is associated with defective pylorus or motility disorders.

Question 14

What is autoimmune chronic gastritis and what is it associated with?

Answer 14

It is an autoimmune reaction to gastric parietal cells resulting in a loss of acid secretion (hypochlorhydria/achlorhydria) and a loss of intrinsic factor which causes Vit B12 deficiency (pernicious anaemia). It is associated with marked gastric atrophy and intestinal metaplasia.

Question 15

What are peptic ulcerations?

Answer 15

• Breach in mucosal lining of alimentary tract as a result of acid and pepsin attack.

Question 16

Where are the major sites of peptic ulceration?

Answer 16

• First part of duodenum,
• Junction of antral and body mucosa in stomach,
• Distal oesophagus,
• Gastro-enterostomy stoma.

Question 17

What are the Aetiological factors for peptic ulceration

Answer 17

• Hyperacidity,
• H pylori gastritis,
• Duodenal reflux,
• NSAIDs,
• Smoking,
• Genetic factors,
• Zollinger-Ellison syndrome

Question 18

What are some of the complications of peptic ulcers?

Answer 18

• Haemorrhage,
• Penetration of adjacent organs,
• Perforation,
• Anaemia,
• Obstruction,
• Malignancy

Question 19

What are some defining features that differentiate between gastric and duodenal ulcers

Answer 19

Duodenal - more common, tends to be in blood group O, the acid levels are high or normal.
Gastric - Blood group A and acid levels are normal to low.

Question 20

What are some causes of acute peptic ulcers?

Answer 20

• Acute gastritis,
• Stress response,
• Extreme acidity

Question 21

What is the pathogensis of chronic peptic ulcers and where do they normally occur?

Answer 21

Patho - Hyperacidity and mucosal defence defects (mucus-bicarbonate barrier and damage to surface epithelium). Most commonly occur at mucosal junctions eg, antrum to body

Question 22

Describe why chronic duodenal ulcers can occur?

Answer 22

• Increased acid production,

- Reduced mucosal resistance (Gastric metaplasia occurs in response to hyperacidity and then colonised by H pylori)

Question 23

What are the complications of ulcers?

Answer 23

• Bleed, block or burst. So can have penetration of adjacent organs and there can be malignant changes although rare in gastric ulcers and ‘never’ in duodenal

Question 24

Describe the defined structure of ulcers

Answer 24

• Granulation tissue at base,
• Underlying inflammation and fibrosis,
• Loss of muscularis propria