Gastro-Oesophageal Inflammation and Peptic Ulceration

Question 1

Achalasia

Answer 1

Increased tone of the lower oesophageal sphincter (LES)
• Impaired smooth muscle relaxation
• Can be cause of oesophageal obstruction

Question 2

Achalasia triad:

Answer 2

1. Incomplete LES relaxation
2. Increased LES tone and
3. Aperistalsis of the oesophagus

Question 3

Primary achalasia

Answer 3

• Neuronal, ganglion cell degeneration (Vagus N) – rare familiar cases

Question 4

• Secondary achalasia

Answer 4

• Chagas disease (Trypanosoma cruzi infection) – destruction of myenteric plexuses
• Diabetic autonomic neuropathy, amyloidosis, sarcoidosis, polio, Down syndrome
• Herpes simplex infection

Question 5

treatment for achalasia

Answer 5

Laparoscopic myotomy, balloon dilatation and Botox injection

Question 6

Oesophagitis - acute

Answer 6

• Infection in immunocompromised patients
• Herpes simplex viruses
• Candida
• Cytomegalovirus (CMV)
• Corrosives

Question 7

Oesophagitis - chronic

Answer 7

• Specific
• Tuberculosis
• Bullous pemphigoid and Epidermolysis bullosa
• Crohn’s disease
• Non-specific: reflux oesophagitis

Question 8

Reflux Oesophagitis

Answer 8

Reflux Oesophagitis
• Regurgitation of gastric contents
• Gastro-oesophageal reflux disease (GORD)
• ‘Incompetent’ GO junction

• Squamous epithelium damaged

Question 9

causes of reflux oesophagi’s

Answer 9

• Alcohol and tobacco
• Obesity
• Drugs e.g. caffeine!
• Hiatus hernia
• Motility disorders

Question 10

what kind of squamous epithelium damage

Answer 10

• Eosinophils epithelial infiltration
• Basal cell hyperplasia
• Chronic inflammation

Question 11

reflux oesophagitis - ulceration

Answer 11

• Severe reflux leads to ulceration
• May lead to healing by fibrosis
• Stricture
• Obstruction

Question 12

Barrett’s Oesophagus

Answer 12

• Longstanding reflux
• Age 40-60 more men than women
• Lower oesophagus becomes lined by columnar epithelium

Question 13

Gastric Inflammation - acute gastritis

Answer 13

• Usually due to chemical injury

* H pylori-associated

Question 14

chronic gastritis

Answer 14

• Active chronic (H pylori-associated)
• Autoimmune
• Chemical (Reflux)

Question 15

Helicobacter pylori-associated acute gastritis

Answer 15

• Usually transient phase

* Often becomes chronic

Question 16

H pylori-associated Gastritis

Answer 16

• Gram negative spiral-shaped or curved bacilli
• Oral-oral, faecal-oral, environmental spread
• Occupies protected niche beneath mucus where pH approx. neutral
• Does not colonise intestinal type epithelium
• Found in 90% of active chronic gastritis

Question 17

Helicobacter pylori

Answer 17

• Causative factor in gastric and duodenal ulcers
• Risk factor for gastric cancer (adenocarcinoma)
• Strong link with MALT (Mucosa Associated Lymphoid Tissue) Lymphoma

Question 18

H pylori – acute infection

Answer 18

• Can cause acute infection with symptoms that include nausea,
dyspepsia, malaise and halitosis
• Acute infection tends to last about two weeks
• Gastric mucosa is inflamed with neutrophils and inflammatory cells with marked persistent lymphocyte penetration

Question 19

H pylori –chronic infection

Answer 19

• Local inflammation and gastritis
• Outcome depends on:
- Pattern of inflammation 
- Host response
- Bacterial virulence
- Environmental factors
- Patient age

Question 20

H pylori-associated Gastritis - two distribution patterns

Answer 20

• 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 ulcer

Question 21

Chemical (Reflux) Gastritis

Answer 21

• Caused by regurgitation of bile and alkaline duodenal secretion
• Loss of epithelial cells with compensatory hyperplasia of gastric foveolae
• Associated with
- Defective pylorus
- Motility disorders

Question 22

Autoimmune Chronic Gastritis

Answer 22

• Autoimmune reaction to gastric parietal cells
• Loss of acid secretion (hypochlorhydria / achlorhydria)
• Loss of intrinsic factor
- vit b12 def
- microcytic anaemia

• Associated with marked gastric atrophy and intestinal metaplasia
• Increased risk of gastric cancer
• Serum antibodies to gastric parietal cells and intrinsic factor

Question 23

peptic ulceration

Answer 23

• Breach in mucosal lining of alimentary tract as a result of acid and pepsin attack
• Major sites
•
- First part of duodenum
- Junction of antral and body mucosa in stomach
- Distal oesophagus
- Gastro-enterostomy stoma

Question 24

otological factors for peptic ulceration

Answer 24

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

Question 25

complications of peptic ulceration

Answer 25

* Haemorrhage * Penetration of adjacent organs e.g. pancreas * Perforation * Anaemia * Obstruction * Malignancy

Question 26

Acute Peptic Ulcers

Answer 26

• 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

Question 27

Chronic Peptic Ulcers

Answer 27

``` • Tend to occur at mucosal junctions - e.g. antrum - body • Pathogenesis - Hyperacidity - not whole story - Mucosal defence defects ```

Question 28

Chronic Gastric Ulcer

Answer 28

``` • Normal pH of gastric juice 1-2 • Mucosal defences - Mucus-bicarbonate barrier - Surface epithelium - less important • Mucus-bicarbonate barrier - Dissolved by biliary reflux • Surface epithelium - Damaged by NSAIDs - Injured by H pylori ```

Question 29

Chronic Duodenal Ulcer

Answer 29

``` • Increased acid production - More important than for gastric ulcer - Can be induced by H pylori • Reduced mucosal resistance - Gastric metaplasia occurs in response to hyperacidity - Then colonised by H pylori ```

Question 30

pathology of chronic duodenal ulcer

Answer 30

* Usually small (<20 mm) * Sharply ‘Punched out’ with defined edges * Defined structure

Question 31

complications of chronic duodenal ulcer

Answer 31

* ‘Bleed, burst or block’ * Penetration of adjacent organs e.g. pancreas * Malignant change: rare in gastric ulcer and ‘never’ in duodenal ulcer