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Pathology MD3002 > Gastro-eosophageal and peptic ulceration > Flashcards

Gastro-eosophageal and peptic ulceration Flashcards

1
Q

Types of acute oesophagitis

A 
-	Infection in immunocompromised patients
o	HSV
o	Candida
o	Cytomegalovirus (CMV)
-	Corrosives
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2
Q

Chronic oesophagitis

A 
-	Specific
o	Tuberculosis
o	Bullous pemphigoid and epidermolysis bullosa
o	Crohn’s disease
-	Non-specific: reflux oesophagitis
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3
Q

Reflux oesophagitis involves

A

regurgitation of gastric contents and damage to the squamous epithelium

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4
Q

regurgitation of gastric contents due to

A
  • Gastro-oesophageal reflux disease (GORD)
  • “incompetente” GO junction
    o Alcohol and tobacco
    o Obesity
    o Durgs (caffeine!)
    o Hiatus hernia
    o Motility disorders
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5
Q

damage to squamous epithelium due to

A
  • Eosinophils epithelial infiltration
  • Basal cell hyperplasia
  • Chronic inflammation
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6
Q

Severe reflux leads to

A

ulceration, may lead to healing by fibrosis: stricture and obstruction.

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7
Q

Barrett’s oesophagus

A
  • Longstanding reflux
  • Age 40-60
  • Men>women
  • Lower oesophagus becomes lined by columnar epithelium
    o Intestinal metaplasia
    o ? role of gastric/biliary reflux
    o ? role of helicobacter pylori
  • Premalignant: risk of adenocarcinoma of distal oesophagus 100x general population
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8
Q

Inflammatory disorders of the stomach

A

Acute/chronic gastritic

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9
Q

Acute gastritis causes

A 
Chemical inhjury (NSAIDs, alcohol)
H pylori
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10
Q

Chronic

A

H pyolori
Chemical injury (reflux)
Autoimmune disease

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11
Q

Helicobacter pylori-associated acute gastritis: usually transient phase, often becomes chronic

A
  • Gram -ive spiral shaped or curved bacilli
  • Oral-oral, faecal-oral, environmental spread
  • Occupied protected niche beneath mucus where pH appox. Neural
  • Does not colonise intestinal type epuithelium
  • Found in 90 of active chronic gastritis
  • Resolves with therapy (double antibiotic and proton pump inhibitors)
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12
Q

H pylori ANTRUM AND BODY

A

o Atrophy, fibrosis, intestinal metaplasia

o Associated with gastric ulcer and gastric cancer

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13
Q

h pylori ANTRUM ONLY

A

o Gastric acid secretion increased

o Associated with duodenal ulcer

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14
Q

Detection of H pylori

A

faecal bacteria, urea breath test, gastric biopsy rapid urease test

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15
Q

Chemical (reflux) gastritis

A
  • Caused by regurgitation of bile and alkaline duodenal secretion
  • Loss of epithelial cells with compensatory hyperplasia of gastric foveolae (one of the pits in the embryonic gastric mucosa from which the gastric glands develop)
  • Associated with defective pylorus or motility disorders
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16
Q

Autoimmune chronic gastritis

A
  • Autoimmune reaction to gastric parietal cells
    o Loss of acid secretion (hypochlorhydia/achlorhydia)
    o Loss of intrinsic factor (Vitamin B12 deficiency, macrocytic anaemia – pernicious)
  • Associated with marked gastric atrophy and intestinal metaplasia
  • Increased risk of gastric cancer
  • Serum antibodies to gastric parietal cells and intrinsic factor
17
Q

What is peptic uleration

A

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

18
Q

Major sites for peptic ulceration:

A
  • First part of duodenum
  • Junction of antral and body mucosa in stomach
  • Distal oesophagus
  • Gastro-enterostomy stoma
19
Q

Aetiological factors for peptic ulceration

A
  • Hyperacidity
  • H pylori gastritis
  • Duodenal reflux
  • NSAIDs
  • Smoking
  • Genetic factors
  • Zollinger-Ellison syndrome
20
Q

Complications of peptic ulceration

A
  • Haemorrhage
  • Penetration of adjacent organs (eg pancreas)
  • Perforation
  • Anaemia
  • Obstruction
  • Malignancy
21
Q

Acute peptic ulcers

A
  • Related to acute gastritis, ful thickness loss of epithelium rather than just erosion
  • Related to a stress response (Curling’s ulcer following severe burns)
  • A result of extreme hyperacidity (Gastrin-secreting tumours)
22
Q

Chronic peptic ulcers

A
  • Tend to occur at mucosal junctions (eg antrum-body)

- Pathogenesis: hyperacidity (not whole story) mucosal defence defects

23
Q

Chronic gastric

A
  • Normal pH of gastric juice 1-2
  • Mucosal defences:
    o mucus-bicarbonate barrier, dissolved by biliary reflux
    o surface epithelium (though less important), damaged by NSAIDs and injured by H Pylori
24
Q

Chronic duodenal

A
  • increased acid production: more important than for gastric ulcer, can be induced by H pylori
  • reduced mucolas resistance: gastric metaplasia occurs in response to hyperacidity, then colonised by H pylori
25
Q

four layers of ulceration

A
  • necrotic debris
  • non-specific inflammation
  • granulation tissue
  • fibrosis
26
Q

Pathology of ulcers

A
  • usually small (<20mm)
  • Sharply “punched out” with defined edges
  • Defined structure
    o Granulation tissue at base
    o Underlying inflammation and fibrosis
    o Loss of muscularis propria
27
Q

Complications of ulcers

A

 Bleed, burst or block
 Penetration of adjacent organs
 Malignant change: rare in gastric ulcer and ‘never’ in duodenal ulcer

Pathology MD3002 (3 decks)

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