Gastro-Oesophageal Inflammation And Peptic Ulceration

Question 1

Achalasia

Answer 1

Increased tone of the lower oesophagel sphincter due to impaired smooth muscle relaxation. Can cause oesophageal obstruction.

Question 2

Achalasia triad

Answer 2

• Incomplete lower oesophageal sphincter relaxation.
• Incomplete lower oesophageal sphincter tone
• Aperistalsis of the oesophagus.

Question 3

Causes of Achalasia: Primary? Secondary?

Answer 3

• Primary - ganglion cell degeneration affecting the vagus nerve.
• Secondary - Chagas disease (Trypanosoma cruzi infection) which destroys myenteric plexus. Diabetic autonomic neuropathy. Amyloidosis. Sarcoidosis. Polio. Down syndrome. Herpes simplex infection.

Question 4

Treatment of Achalasia

Answer 4

Laparoscopic myotomy, balloon dilatation and botox injection.

Question 5

Acute Oesophagitis Causes

Answer 5

• Corrosives

- Infection in immunocompromised patients - herpes simplex viruses, candida and cytomegalovirus (CMV).

Question 6

Chronic Oesophagitis Causes

Answer 6

• Tuberculosis
• Bullous pemphigoid and Epidermolysis bullosa (skin disorders which alos affect the oesophagus).
• Crohn’s disease
• Reflux

Question 7

Reflux Oesophagitis

Answer 7

• Regurgitation of gastric content. Caused by gastro-oesophageal reflux disease (GORD) or an incompetent gastro-oesophageal junction (due to alcohol, tobacco, drugs e.g. caffeine, hiatus hernia, and motility disorders).
• Squamous epithelium damaged - eosinophils epithelial infiltration, basal cell hyperplasia (increased cell desquamation), chronic inflammation.
• Severe reflux leads to ulceration
• May lead to healing by fibrosis - stricture or obstruction.

Question 8

Barrett’s Oesophagus

Answer 8

• Longstanding reflux causes metaplasia of the oesophagus epithelium; stratified squamous > columnar epithelium.
• Not sure of exact mechanism - roles of reflux or H.Pylori
• Premalignant - risk of adenocarcinoma of distal oesophagus 100x more likely.

Question 9

Acute Gastritis Causes

Answer 9

Chemical injury ( alcohol or drugs e.g. NSAIDs) or Helicobacter pylori associated (often becomes chronic, usually transient phase).

Question 10

Chronic Gastritis Causes

Answer 10

• active chronic (Helicobacter pylori associated)
• autoimmune
• chemical

Question 11

Helicobacter Pylori-associated Gastritis

Answer 11

• gram negative spiral-shaped or curved bacilli
• oral-oral, faecal-oral, environmental spread
• occupies protected niche beneath mucus where pHapproximately neutral
• does not colonise intestinal type epithelium
• found in 90% of active chronic gastritis

Question 12

Helicobacter Pylori

Answer 12

• causative factor of gastric and duodenal ulcers
• risk factor for gastric cancer (adenocarcinoma)
• strong link to mucosa-associated lymphoid tissue (MALT) lymphoma.
• associated with dyspepsia, atrophic gastritis, iron deficiency anaemia, and idiopathic thrombocytopenic purpura

Question 13

Pathogenesis of H.Pylori

Answer 13

• Enters mucosal layer and attaches
• Secretes urease which neutralises gastric acid, allowing it to colonise
• Mucosal damage by bacterial mucinase, creating an unprotected area of gastric epithelium. Which is now inflamed due to contact with gastric acid, proteases snd effector molecules.
• Mucosal cell death by cytotoxins and ammonia

Question 14

Chemical Gastritis

Answer 14

• Caused by regurgitation of bile and alkaline duodenal secretion.
• Results in loss of wpithelial cells with compensatory hyperplasia of gastric foveolae (cells which produce mucus in stomach).
• Associated with a defective pylorus and motility disorders.

Question 15

Autoimmune Chronic Gastritis

Answer 15

• Autoimmune reaction to gastric parietal cells which causes loss of acid secretion (hypochlorhydria (decreased HCl production)/ achlorhydria (no HCl production)) and loss of intrinsic factor (causes vitamin B12 deficiency and macrocytic pernicious anaemia).
• Associated with marked gastric atrophy and intestinal metaplasia.
• Increased risk of gastric cancer
• Serum antibodies to gastric parietal cells and intrinsic factor.

Question 16

Peptic ulceration

Answer 16

Breach in mucosal lining of ailimentary canal as a result of acid and pepsin attack.

Question 17

Major sites of peptic ulceration

Answer 17

First part of duodenum > junction of antral and body mucosa in stomach > distal oesophagus > gastro-enterostomy stoma

Question 18

Aetiological factors of peptic ulceration

Answer 18

• Hyperacidity
• H. pylori gastritis
• Duodenal reflux
• NSAIDs
• Smoking
• Genetic factors
• Zollinger-Ellison syndrome(condition where the body produces excess gastrin which means too much acid is produced).

Question 19

Complications of peptic ulceration

Answer 19

• Haemorrhage - presents as haematoemesis - HCl erodes blood vessels
• Penetration of adjacent organs e.g. pancreas
• Perforation
• Anaemia - loss of blood via ulcer bleed
• Obstruction - especially if close to pyloric sphincter
• Malignancy

Question 20

Acute Peptic ulcers

Answer 20

-Related to: acute gastritis (full thickness loss of epithelium, rather than just erosion), stress response (e.g. Curling’s ulcer following severe burns), or Extreme Hyperacidity (gastrin-secreting tumours).

Question 21

Chronic Peptic Ulcers

Answer 21

Tend to occur at mucosal junctions. Hyperacidity + mucosal defence defects (mucus-bicarbonate barrier dissolved by biliary reflux. Surface epithelium damaged by NSAIDs or H.Pylori).

Question 22

Chronic Duodenal Ulcer

Answer 22

• Caused by increased acid production (could be induced by H.Pylori), and reduced mucosal resistance (gastric metaplasia occurs in response to hyperacidity, which is then colonised by H.Pylori).
• usually small (<20mm), defined structure; defined edges, granulation at base, underlying inflammation and fibrosis, loss of muscularis propria.
• complications - bleed, burst, block, penetrate adjacent organs, malignant (gastric only)