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MD3002 Pathology > Gastro-oesophageal Inflammation and Peptic Ulceration > Flashcards

Gastro-oesophageal Inflammation and Peptic Ulceration Flashcards

1
Q

What can acute cause oesophagitis?

A
  • Immunocompromised
  • Herpes simplex viruses
  • Candida
  • Cytomegalovirus (CMV)
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2
Q

What can cause chronic oesophagitis?

A
  • Tuberculosis
  • Bullous pemphigoid and epidermolysis bullosa
  • Crohn’s disease
  • Reflux oesophagitis (non-specific)
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3
Q

What can cause an ‘incompetent’ GO junction and therefore GORD?

A
  • alcohol and tobacco
  • Obesity
  • Drugs e.g caffeine
  • Hiatus hernia
  • Motility disorders
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4
Q

What happens to the epithelium in GORD?

A
  • Squamus epithelium damaged
  • Eosinophils epithelial infiltration
  • Basal cell hyperplasia
  • Chronic inflammation
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5
Q

What can severe reflux lead to?

A
  • Ulceration
  • May lead to healing by fibrosis:
    Stricture
    Obstruction
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6
Q

Who is usually affected by Barrett’s Oesophagus?

A
  • Men aged 40-60
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7
Q

How much more likely is adenocarcinoma of distal oesophagus with Barrett’s Oesophagus?

A

100x

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8
Q

What is the main feature of Barrett’s Oesophagus?

A

Intestinal METAPLASIA

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9
Q

What is acute gastritis?

A
  • Usually due to chemical injury (drugs/NSAIDs, alcohol)
  • H pylori-associated
    Usually transient phase
    Often becomes chronic
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10
Q

What is chronic gastritis?

A
  • Active chronic (H pylori-associated)
  • Autoimmune
  • Chemical (reflux)
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11
Q

What is the appearence of H pylori?

A
  • Gram negative

- Spiral shaped or curved bacilli

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12
Q

How is H pylori spread?

A
  • Oral-oral
  • Faecal-oral
  • Enviromental spread
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13
Q

What space does H pylori occupy?

A
  • Protected niche beneath mucus where pH approx. neutral

- Does not colonise intestinal type epithelium

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14
Q

What percentage of active chronic gastritis is caused by H pylori?

A

90%

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15
Q

What does helicobacter pylori cause?

A
  • Gastric and duodenal ulcers
  • Risk factor for gastric cancer
  • Strong link with MALT (Mucosa Associated lymphoid Tissue) Lymphoma
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16
Q

What is an ulcer?

A

The breaking of epithelium

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17
Q

Describe the pathology of Helicobacter Pylori

A
  • Swims through gastric fluid and into mucus layer
  • Once in mucosal layer they produce urease which neutralises acid
  • The H pylori divide and produce more urease, this triggers the stomach to produce more HCl
  • Huge amounts of acid build up damaging the protected mucu layer and then destroy surface epithelium of stomach leading to the creating of an ulcer
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18
Q

What are the symptoms of a H pylori infection?

A 
Acute infection with symptoms of:
- Nausea 
- Dyspepsia 
- Malaise 
- Halitosis 
Usually lasts about 2 wks
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19
Q

What are the signs in the gastric mucosa of an H pylori infection?

A

Mucosa is inflamed with neutrophils and inflammatory cells with marked persistent lymphocyte penetration

20
Q

What does a urease test include?

A
  • TEsting the breath for urease

- Patient blows into special tube if urease is significant -> H pylori infection

21
Q

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

A
  • Pattern of inflammation
  • Host response
  • Bacterial virulence
  • Enviromental factors
  • Patient age
22
Q

HISTOLOGY

A

LEARN

23
Q

What are the 2 distribution patterns of H pylori-associated 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 cancer
24
Q

What is chemical (reflux) gastritis caused by?

A
  • Regurgitation of bile and alkaline duodenal secretion

- Loss of epithelial cells with compensatory hyperplasia of gastric foveolae

25
Q

What is chemical (reflux) gastritis associated with?

A
  • Defective pylorus

- Motility disorders

26
Q

Desribe 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)
  • Associated with marked gastric atrophy and intestinal metaplasia
  • Serum antibodies to gastric parietal cells and intrinsic factor
27
Q

What disease is autoimmune chronic gastritis at an increased risk of causing?

A

Gastric cancer

28
Q

How can autoimmune chronic gastritis be diagnosed?

A
  • Serum antibodies

- FBC

29
Q

What is the definition of peptic ulceration?

A

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

30
Q

Wht are the major sites of peptic ulceration?

A
  • 1st part of duodenum
  • Junction of antral and body mucosa in stomach
  • Distal oesophagus
  • Gastro-enterostomy stoma
31
Q

What are the aetiological factors of peptic ulceration?

A
  • Hyperacidity
  • H pylori gastritis
  • Duodenal reflux
  • NSAIDs
  • Smoking
  • Genetic factors
  • Zollinger-Ellison syndrome
32
Q

What are the complications of peptic ulceration?

A
  • Haemorrghage
  • Penetration of adjavent organs e.g. pancreas
  • Perforation
  • Anaemia
  • Obstruction
  • Malignancy
33
Q

How much more common is a duodenal ulcer in comparison to a gastric ulcer?

A

3 times

34
Q

What blood groups are gastric and duodenal ulcers meant to affect?

A
  • Gastric
    A
  • Duodenal
    O
35
Q

What are the acid levels usually like in a gastric ulcer?

A

Normal or low

36
Q

What are the acid levels usually like in a duodenal ulcer?

A

High or normal

37
Q

What percentage of gastric ulcers are caused by H pylori?

A

About 70%

38
Q

What percentage of duodenal ulcers are caused by H pylori?

A

95 - 100%

39
Q

What is the difference in age groups affected by gastric and duodenal ulcers?

A
  • Gastric
    Increases with age
  • Duodenal
    Increases up to 35 years
40
Q

Which type of ulcer is most likely to occur in people in the lowest socioeconomic status?

A

GAstric ulcers

41
Q

What are acute peptic ulcers related to?

A
  • 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
42
Q

where do chronic peptic ulcers tend to occur?

A

Mucosal junctions

43
Q

What are the 2 factors that generally lead to chronic peptic ulceration?

A
  • Hyperacidity - not whole story
  • Mucosal defence defects
    (mucus-bicrbonate barrier can be dissolved by biliary reflux)
44
Q

What are chronic duodenal ulcers caused by?

A 
- Increased acid production 
More important than for gastric ulcer 
Can be induced by H pylori 
- Reduced mucosal resistnace
Gastric metaplasia occurs in response to hyperacidity 
Then colonised by H pylori
45
Q

Desribe the structure of peptic ulcers?

A
  • usually small (>20 mm)
  • Sharply ‘punched out’ with defined edges
  • Defined structure
    Granulation tissue at base
    Underlying inflammation and fibrosis
    Loss of musscularis mucosa
    Complications: bleed, burst or block, penetration of adjacent organs e.g pancreas, malignant change: rare in gastric ulcer and ‘neber’ in duodenal ulcer

MD3002 Pathology (19 decks)

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