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Y2S2 GI > Gastro-Oesophageal Inflammation and Peptic Ulceration > Flashcards

Gastro-Oesophageal Inflammation and Peptic Ulceration Flashcards

1
Q

Achalasia

A

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

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2
Q

Achalasia triad:

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

Primary achalasia

A

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

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4
Q

• Secondary achalasia

A
  • Chagas disease (Trypanosoma cruzi infection) – destruction of myenteric plexuses
  • Diabetic autonomic neuropathy, amyloidosis, sarcoidosis, polio, Down syndrome
  • Herpes simplex infection
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5
Q

treatment for achalasia

A

Laparoscopic myotomy, balloon dilatation and Botox injection

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6
Q

Oesophagitis - acute

A
  • Infection in immunocompromised patients
  • Herpes simplex viruses
  • Candida
  • Cytomegalovirus (CMV)
  • Corrosives
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7
Q

Oesophagitis - chronic

A
  • Specific
  • Tuberculosis
  • Bullous pemphigoid and Epidermolysis bullosa
  • Crohn’s disease
  • Non-specific: reflux oesophagitis
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8
Q

Reflux Oesophagitis

A

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

• Squamous epithelium damaged

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9
Q

causes of reflux oesophagi’s

A
  • Alcohol and tobacco
  • Obesity
  • Drugs e.g. caffeine!
  • Hiatus hernia
  • Motility disorders
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10
Q

what kind of squamous epithelium damage

A
  • Eosinophils epithelial infiltration
  • Basal cell hyperplasia
  • Chronic inflammation
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11
Q

reflux oesophagitis - ulceration

A
  • Severe reflux leads to ulceration
  • May lead to healing by fibrosis
  • Stricture
  • Obstruction
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12
Q

Barrett’s Oesophagus

A
  • Longstanding reflux
  • Age 40-60 more men than women
  • Lower oesophagus becomes lined by columnar epithelium
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13
Q

Gastric Inflammation - acute gastritis

A
  • Usually due to chemical injury

* H pylori-associated

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14
Q

chronic gastritis

A
  • Active chronic (H pylori-associated)
  • Autoimmune
  • Chemical (Reflux)
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15
Q

Helicobacter pylori-associated acute gastritis

A
  • Usually transient phase

* Often becomes chronic

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16
Q

H pylori-associated Gastritis

A
  • 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
17
Q

Helicobacter pylori

A
  • Causative factor in gastric and duodenal ulcers
  • Risk factor for gastric cancer (adenocarcinoma)
  • Strong link with MALT (Mucosa Associated Lymphoid Tissue) Lymphoma
18
Q

H pylori – acute infection

A

• 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

19
Q

H pylori –chronic infection

A 
• Local inflammation and gastritis
• Outcome depends on:
- Pattern of inflammation 
- Host response
- Bacterial virulence
- Environmental factors
- Patient age
20
Q

H pylori-associated Gastritis - two distribution patterns

A

• 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

21
Q

Chemical (Reflux) Gastritis

A

• 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

22
Q

Autoimmune Chronic Gastritis

A

• 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
23
Q

peptic ulceration

A

• 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

24
Q

otological factors for peptic ulceration

A
  • Hyperacidity
  • H pylori gastritis
  • Duodenal reflux
  • NSAIDs
  • Smoking
  • Genetic factors
  • Zollinger-Ellison syndrome
25
Q

complications of peptic ulceration

A
  • Haemorrhage
  • Penetration of adjacent organs e.g. pancreas
  • Perforation
  • Anaemia
  • Obstruction
  • Malignancy
26
Q

Acute Peptic Ulcers

A

• 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

27
Q

Chronic Peptic Ulcers

A 
• Tend to occur at mucosal junctions 
- e.g. antrum - body
• Pathogenesis
- Hyperacidity - not whole story
- Mucosal defence defects
28
Q

Chronic Gastric Ulcer

A 
• 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
29
Q

Chronic Duodenal Ulcer

A 
• 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
30
Q

pathology of chronic duodenal ulcer

A
  • Usually small (<20 mm)
  • Sharply ‘Punched out’ with defined edges
  • Defined structure
31
Q

complications of chronic duodenal ulcer

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

Y2S2 GI (26 decks)

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