20 - Pathology of the GI Tract - 1 Flashcards

1
Q

Oesophagitis classification

A

Acute or chronic

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2
Q

Oesophagitis aetiology

A

Infectious - bacterial, viral, fungal

Chemical - ingestion of corrosive substance, refleux

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3
Q

Risk factors for reflux oesophagitis

A

Defective lower oesophageal sphincter
Hiatus hernia
Increased intra-ab pressure
Increased gastric fluid volume due to gastric outflow stenosis

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4
Q

Types of hernia

A

Sliding hiatus

Para-oesophageal

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5
Q

Sliding hiatus hernia will give what symptoms?

A

Reflux

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6
Q

Para-oesophageal hernia has one big risk what is it

A

Strangulation - necrosis of tissue due to pinching

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7
Q

Histology of reflux oesophagitis

A

Basal cell hyperplasia with elongated papillae and desquamation - lost overlying epithelial layer in severe cases (increased bleeding risk)

Also, inflammatory cell infiltration

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8
Q

Complications of reflux oesophagitis

A
Ulceration 
Haemorrhage
Perforation
Benign stricture
Barrett's oesophagus
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9
Q

Cause of barrett’s oesophagus - what risk factors?

A

Longstanding reflux

Same risk factors

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10
Q

Macroscopy of barrett’s oesphagus

A

Proximal extension of the sqaumo-columnar junction.

Squamous mucosa replaced by columnar mucosa

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11
Q

Barrett’s oesophagus types of columnar mucosa

A

Gastric cardia type or gastric body type

Intestinal type = specialised barrett’s mucosa

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12
Q

Barrett’s oesophagus is a premalignant condition -what do we do?

A

Increased risk of adenocarcinoma

Regular endoscopic surveillance is recommended for early detection of neoplasia

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13
Q

Two histological types of oesophageal carcinoma

A

Squamous cell carcinoma

Adenocarcinoma

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14
Q

Adenocarcinoma localisation, macroscopy, spread and staging

A

Lower oesphagus

Plaque-like, nodular, fungating, ulcerated, depressed, infiltrating

Same as squamous cell carcinoma

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15
Q

Aetiology of chronic gastritis

A
Autoimmune
Bacterial (h.pylori)
Chemical injury
NSAIDs
Bile reflux
Alcohol
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16
Q

What does H.pylori do?

A

Lives on epithelial surface protected by the overlying mucus barrier
Damage leads to chronic inflammation
More common in antrum

17
Q

H.pylori complications

A

Corpus - hypochlorhydria -> atrophy/metaplasia -> gastric ulcer/cancer

No atrophy -> MALT lymphoma

Antral -> hypergastrinaemia -> hyperchlorhydria -> pre-pyloric gastric ulcer -> gastric metaplasia -> duodenal ulcer

18
Q

Acute gastric ulcer histology

A

Full-thickness coagulative necrosis of mucosa
Covered with ulcer slough
Granulation tissue at ulcer floor

19
Q

Chronic gastric ulcer histology

A

Clear-cut edges overhanging base
Extensive granulation + scar tissue
Scarring often throughout entire gastric wall
Bleeding

20
Q

Complications of peptic ulcer

A

Haemorrhage
Perforation -> peritonitis
Penetration into an adjacent organ (liver, pancreas)
Stricturing -> hour-glass deformity

21
Q

SLIDE 39

A

Copy table!

22
Q

Gastric cancer frequency comparison

A

Most: adenocarcinoma
Less: endocrine, MALT lymphoma, stromal tumours

23
Q

Carcinoma of GOJ

A

White males
Association with GO reflux
No association with H.pylori/diet
Increased incidence in recent years (obesity)

24
Q

Carcinoma of gastric body/antrum

A

H.pylori association
Association with diet (salt, low fruit/veg
No association with reflux
Less incidence in recent years

25
Q

Macroscopic subtypes

A
Superficial exophytic
Flat or depressed
Superficial excavated
Exophytic
Linitis plastica
Excavated
26
Q

Histological subtypes

A

Scattered growth
Non-scattered growth
Diffuse type
Intestinal type

27
Q

What does HDGC stand for?

A

Hereditary diffuse type gastric cancer

Germline CDH1/E-cadherin mutation

28
Q

Coeliac disease features

A

Immune mediated enteropathy
Ingestion of gluten containing cereals - wheat, rye, barley
Genetic
0.5% to 1%

29
Q

Pathogenesis of coeliac disease

A
  1. Gliadin is alcohol soluble component of gluten induces epithelial cells to make IL-5
  2. IL-15 produced by epithelium
  3. Activates CD8+
  4. They are cytotoxic and kill enterocytes

Note: CD8 does not recognise gliadin directly hence pathway = gliadin-induced IL-15 secretion pathway

30
Q

Coeliac disease diagnosis is hard - why?

A

Silent disease
Latent disease (30-60yo)
Symptomatic patients - anaemia, chronic diarrhoea, bloating, chronic fatigue

31
Q

Coeliac disease - clinical features

A

No gender pref
Other disease associations - Dermatitis herpetiformis (10%); lymphocytic gastritis and lymphocytic colitis

Coeliac disease associated with enteropathy-associated T-cell lymphoma + small intestinal adenocarcinoma

32
Q

Diagnosis of coeliac disease

A

Non-invasive serologic test: IgA Ab to tissue transglutaminase; IgA or IgG to deamidated gliadin

Tissue biopsy is diagnostic

33
Q

Treatment of coeliac

A

Gluten-free diet