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MD3002 - GI Disease/Pathology > Gastro-Oesophgeal Inflammation and Peptic Ulceration > Flashcards

Gastro-Oesophgeal Inflammation and Peptic Ulceration Flashcards

1
Q

Who is acute oesophagitis common in?

A

infection in immunocompromised patients

Corrosiveness (suicide attempt)

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2
Q

What pathogens are responsible for acute oesophagitis?

A
  • Herpes simplex viruses
  • Candida
  • Cytomegalovirus (CMV)
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3
Q

Examples of specific chronic oesophagitis?

A
  • Tuberculosis
  • Bullous pemphigoid and Epidermolysis bullosa
  • Crohn’s disease
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4
Q

What is the most common nonspecific chronic oesophagitis?

A

reflux oesophagitis

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5
Q
A

Oesophgeal inflammation

A. Multiple Herpetic Ulcers

B. Multinucleate squamous cells – Herpes virus inclusions

C. Cytomegalovirus Nuclear and cytoplasmic inclusion

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6
Q

What is reflux oesophagitis?

A
  • regurgitation of gastric contents
  • squamous epithelium damaged
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7
Q

What causes regurgitation of gastric contents?

A
  • Gastro-oesophageal reflux disease (GORD)
  • ‘Incompetent’ GO junction
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8
Q

What can cause an ‘incompetent GO’ junction?

A
  • Alcohol and tobacco
  • Obesity
  • Drugs e.g. caffeine!
  • Hiatushernia
  • Motility disorders
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9
Q

What occurs when squamous epithelium is damaged?

A
  • Eosinophils epithelial infiltration
  • Basal cell hyperplasia
  • Chronic inflammation
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10
Q
A
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11
Q
A

A. Scattered intraepithelial eosinophils

B. Eosinophilic esophagitis with basal zone hyperplasia

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12
Q

What can severe reflux lead to?

A

ulceration

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13
Q

What is stricture?

A

abdnormal narrowing of canal or duct in the body

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14
Q

Describe Barrett’s Oesophagus

A
  • Longstanding reflux
  • Lower oesophagus becomes lined by columnar epithelium
    • Intestinal metaplasia
    • gastric/biliary reflux
    • Helicobacter pylori (increases HCl production)
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15
Q

Who is likely to get barrett’s oesophagus?

A

age 40-60

more common in men than women

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16
Q

What does barrett’s oesophagus increase the risk of?

A

Premalignant - risk of adenocarcinoma of distal oesophagus 100x general population

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17
Q
A

Barrett’s Oesophagus

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18
Q

What is acute gastritis caused by?

A
  • Chemical injury
    • drugs (NSAIDs)
    • alcohol (high %)
    • corrosives
  • Helicobacter pylori associated
    • usually transient phase
    • often become chronic
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19
Q

What is H pylori? And how does it spread? How does it cause 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
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20
Q

What is H pylori a causative factor for?

A
  • gastritis and duodenal ulcers
  • risk factor for gastric cancer (adenocarcinoma)
  • Strong link with MALT (mucosa assoicated lymphoid tissue) lymphoma
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21
Q

What are the associated symptoms of H pylori?

A
  • Dyspepsia
  • Atrophic gastritis
  • Iron deficiency anaemia
  • Idiopathic Thrombocytopenic Purpura
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22
Q

What is produced by H pyrloi to raise the gastric pH and allow it to colonise?

A

urease

can produce bad breath

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23
Q

Pethogenesis of H pylori

A
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24
Q

What symptoms are assoicated with H pylori when it causes an acute infection?

A

nausea, dyspepsia, malaise and halitosis

25
Q

How long does acute infection with H pylori tend to last?

A

2 weeks

26
Q

What are the characterisitcs of the gastric mucosa with acute infection with H pylori?

A

Gastric mucosa is inflamed with neutrophils and inflammatory cells with marked persistent lymphocyte penetration

27
Q

What does the outcome of H pyrlori as a chronic infection depend on?

A
  • Pattern of inflammation
  • Host response
  • Bacterial virulence
  • Environmental factors
  • Patient age
28
Q
A
  • A. Helicobacter pylori silver stain
  • B. Intraepithelial and lamina propria neutrophils infiltration
  • C. Lymphoid aggregates, with plasma cells infiltrate in lamina propria
29
Q

What are the 2 distribution patterns of H pyrloi associated with gastritis?

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
30
Q

What is chemical (reflux) gastritis caused by?

A

regurgitation of bile and alkaline duodenal secretion

31
Q

What occurs in chemical (reflux) gastritis?

A

Loss of epithelial cells with compensatory hyperplasia of gastric foveolae

32
Q

What is chemical (reflux) gastritis associated with?

A
  • Defective pylorus
  • Motility disorders
33
Q

What occurs in autoimmune chronic gastritis?

A
  • Autoimmune reaction to gastric parietal cells
    • Loss of acid secretion (hypochlorhydria / achlorhydria)
    • Loss of intrinsic factor
      • Vitamin B12 deficiency
      • Macrocytic anaemia (Pernicious anaemia)
34
Q

What is autoimmune chronic gastritis assoicated with?

A

marked gastric atrophy and intestinal metaplasia

35
Q

What does autoimmune chronic gastritis increase the risk of?

A

gastric cancer

36
Q

What is the mechanism, histology and clinical implications of autoimmune chronic gastritis?

A
  • Anti-parietal cell and intrinsic factor antibodies
  • Glandular atrophy in gastric body, Intestinal metaplasia
  • Pernicious anaemia
37
Q

What is the mechanism, histology and clinical implications of bacterial infection chronic gastritis?

A
  • Cytotoxins
  • Immune response
  • Active chronic inflammation
  • Atrophy
  • Intestinal metaplasia
  • Peptic ulceration
  • Gastric cancer
38
Q

What is the mechanism, histology and clinical implications of chemical injury chronic gastritis?

A
  • Direct injury
  • disruption of mucus layer
  • Foveolar hyperplasia
  • few inflammatory cells
  • gastri erosion
  • gastric ulcer
39
Q

What is peptic ulceration?

A

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

40
Q

What are the major sites of peptic ulceration (most to least common)

A
  1. First part of duodenum
  2. Junction of antral and body mucosa in stomach
  3. Distal oesophagus
  4. Gastro-enterostomy stoma (rare)
41
Q

What are the aetiological factors of peptic ulceration

A
  • Hyperacidity
  • H pylori gastritis
  • Duodenal reflux
  • NSAIDs
  • Smoking
  • Genetic factors
  • Zollinger-Ellison syndrome
42
Q

What are the complications associated with peptic ulceration?

A
  • Haemorrhage
  • Penetration of adjacent organs e.g. pancreas
  • Perforation
  • Anaemia
  • Obstruction
  • Malignancy
43
Q

Gastric Vs Duodenal Ulcer

  • relative incidence
A

Gastric = 1

Duodenal = 3 (more common)

44
Q

Gastric Vs Duodenal Ulcer

  • Risk associated with age
A

Gastric = increases with age

Duodenal = increased up to 35 years

45
Q

Gastric Vs Duodenal Ulcer

  • Social Class
A

Gastric = higher in class V

Duodenal = evenly distributed

46
Q

Gastric Vs Duodenal Ulcer

  • Blood group
A

Gastric = A is more likely

Duodenal = O is more likely

47
Q

Gastric Vs Duodenal Ulcer

  • Acid levels
A

gastric = normal or low

duodenal = high or normal

48
Q

Gastric Vs Duodenal Ulcer

  • Helicobacter gastritis
A

Gastric = about 70%

Duodenal = 95-100%

49
Q

What is an acute peptic ulcer related to?

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
50
Q

Where do chronic peptic ulcers tend to occur?

A

at mucosal junctions e.g. antrum-body

51
Q

What is the pathogenesis of a chronic peptic ulcer?

A
  • Hyperacidity - not whole story
  • Mucosal defence defects
52
Q

What is the normal pH of gastric juice?

A

1-2

53
Q

What are the normal mucosal defences?

A
  • Mucus-bicarbonate barrier
  • Surface epithelium - less important
54
Q

What can be dissolved by biliary reflux?

A

mucus-bicarbonate barrier

55
Q

What can damage the surgace epithelium in chronic gastric ulcers?

A
  • Damaged by NSAIDs
  • Injured by H pylori
56
Q

Mechanism of gastric injury and protection

A
57
Q

What is chronic duodenal ulcer caused by?

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
58
Q

What is the pathology of a chronic duodenal ulcer?

A
  • Usually small (<20 mm)
  • Sharply ‘Punched out’ with defined edges
  • Defined structure
    • Granulation tissue at base
    • Underlying inflammation and fibrosis
    • Loss of muscularis propria
59
Q

What are the complications assoicated with 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

MD3002 - GI Disease/Pathology (11 decks)

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