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Clinical Pathology > Pathology of the GI tract > Flashcards

Pathology of the GI tract Flashcards

1
Q

Describe the normal oesophagus

A
  • Lined by squamous epithelium
  • Distal 2cm below diaphragm lined by glandular columnar mucosa
  • Cricopharyngeal sphincter & gastro-oesophageal junction
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2
Q

What layers make up the normal histology of the oesophagus?

A
  • Mucosa (epithelium & lamina propria)
  • Submucosa
  • Muscularis propria
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3
Q

What is Oesophagitis?

A
  • Inflammation of the oesophagus either acute or chronic
  • Infectious=bacterial, viral (HSV1, CMV), fungal (candida)
  • Chemical= reflux, ingestion of corrosive substance
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4
Q

What is reflux oesophagitis?

A
  • Commonest form
  • Caused by reflux of gastric (gastro-oesophageal reflux) acid &/or bile (duodeno-gastric reflux)
  • Leading symptom= heartburn
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5
Q

What are the risk factors for reflux oesophagitis?

A
  • Hiatus hernia
  • Defective lower oesophageal sphincter
  • Inc intra-abdominal pressure
  • Inc gastric fluid vol due to gastric outflow stenosis
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6
Q

What are the types of hiatus hernia?

A
  • Sliding hernina= reflux symptoms

- Paraoesophageal hernia= strangulation

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7
Q

What changes in histology will be seen in reflux oesophagitis?

A
  • Squamous epithelium= basal cell hyperplasia, elongation of papillae, inc cell desquamation
  • Lamina propria= inflammatory cell infiltration (neutrophils, eosinophils, lymphocytes)
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8
Q

What are complications of reflux oesophagitis?

A
  • Ulceration
  • Haemorrhage
  • Perforation
  • Benign stricture (segmental narrowing)
  • Barrett’s oesophagus
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9
Q

Describe Barrett’s oesophagus

A
  • Cause= longstanding reflux
  • RF= male, Caucasian, overweight, same as for reflux
  • Macroscopy= Proximal extension of squamo-columnar junction
  • Histology= Squamous mucosa replaced by columnar mucosa- glandular metaplasia (same as stomach lining)
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10
Q

What types of columnar mucosa are there in Barrett’s oesophagus?

A
  • Gastric cardia type
  • Gastric body type
  • Intestinal type= specialised Barrett’s mucosa
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11
Q

How and why is Barrett’s oesophagus monitored?

A
  • Premalignant condition w/ inc risk of developing adenocarcinoma
  • Regular endoscopic surveillance to detect early neoplasia
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12
Q

How does Barrett’s oesophagus progress into cancer?

A

1) Barrett’s oesophagus
2) Low-grade dysplasia
3) High-grade dysplasia
4) Adenocarcinoma

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13
Q

What are the 2 types of oesophageal carcinoma? Risk factors? Location? Macroscopy?

A
  • Adenocarcinoma= tobacco, obesity, Barrett’s oesophagus, diet (smoked/cured/pickled meat or fish), H.Pylori, hypochlorhydria (allows bacterial growth) male, Caucasian. Lower oesophagus. Plaque-like, nodular, fungating, ulcerating, infiltrating, depressed.
  • Squamous cell carcinoma= tobacco, alcohol, male, black, HPV, thermal injury-hot beverages, nutrition-nitrosamines. Middle & lower 3rd. Preceded by squamous dysplasia
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14
Q

What does the ‘T’ stand for in TNM staging?

A
  • Depth of invasion of the primary tumour
  • T1= tumour invades lamina propria, muscularis mucosae/submucosa
  • T2= tumour invades muscularis propria
  • T3= tumour invades adventitia
  • T4= tumour invades adjacent structures
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15
Q

What does the ‘N’ stand for in TNM staging?

A
  • Regional lymph nodes
  • N0= no node mets
  • N1= 1-2 node mets
  • N2= 3-6 node mets
  • N3= 7+ node mets
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16
Q

What does the ‘M’ stand for in TNM staging?

A
  • Distant metastasis

- M0= no metastasis M1= distant metastasis

17
Q

What are the 4 anatomical regions of the stomach? And the 3 histological regions with different functions?

A

Anatomic regions: Cardia, body, fundus, antrum

Histological regions: Cardia, body, antrum

18
Q

What are the normal stomach defences?

A
  • Balance of aggressive (acid) & defensive forces
  • Surface mucosa
  • Bicarbonate secretion
  • Mucosal blood flow
  • Prostaglandins
  • Regenerative capacity
19
Q

What things can lead to increased aggression (acid) in the stomach?

A
  • Excessive alcohol
  • Drugs
  • Heavy smoking
  • Corrosive/radiation/ chemotherapy
  • Infection
20
Q

What things can lead to impaired defences in the stomach?

A
  • Ischaemia
  • Shock
  • Delayed emptying
  • Duodenal reflux
  • Impaired regulation of pepsin secretion
21
Q

What can H. Pylori lead to?

A
  • Damages epithelium leading to chronic inflammation of mucosa
  • Results in glandular atrophy, replacement fibrosis & intestinal metaplasia
  • More common in antrum than body
22
Q

What are complications of H.Pylori?

A
  • Corpus predominant: MALT lymphoma, Hypochlorhydira atrophy/intestinal metaplasia Gastric ulcer/cancer
  • Antral predominant: Hypergastrinaemia Hyperchlorhydriapre-pyloric gastric ulcer or gastric metaplasiaduodenal ulcer
23
Q

What is peptic ulcer disease? Where are the major sites and causes?

A
  • Localised defect extending at least into submucosa
  • 1st part of duodenum, GOJ, junction of antral & body mucosa
  • Hyperacidity, H.Pylori infection, drugs(NSAIDs), smoking, duodeno-gastric reflux
24
Q

Describe what an acute gastric ulcer would look like histologically

A
  • Full thickness coagulative necrosis of mucosa
  • Covered w/ulcer slough (necrotic debris, fibrin, neutrophils)
  • Granulation tissue at ulcer floor
25
Q

Describe what a chronic gastric ulcer would look like histologically

A
  • Clear-cut edges overhanging at base
  • Extensive granulation & scar tissue at ulcer floor
  • Scarring often throughout entire gastric wall breaching muscularis propria
  • Bleeding
26
Q

What are complications of peptic ulcers?

A
  • Haemorrhage (acute or chronicanaemia)
  • Perforationperitonitis
  • Penetration into adjacent organ (liver, pancreas)
  • Stricturing (hour glass deformity)
27
Q

What are differences between gastric and duodenal ulcers?

A

D: inc up to 35yrs, acid levels are elevated/normal, 95% H.pylori, located at bulbus, mainly blood group O
G: inc with age, acid levels normal/low, 70% H.Pylori, located at lesser curve, antrum-corpus junction, prepyloric, mainly blood group A

28
Q

What are the most/less frequent gastric cancers?

A 
Most= adenocarcinoma
Less= MALT lymphomas, stromal tumours (GIST), endocrine tumours
29
Q

What does a carcinoma of the GOJ or body/antrum show?

A

GOJ: white males, association w/GO reflux NOT H.Pylori/diet

B/A: Associated w/ H.Pylori, diet/salt NOT GO reflux

30
Q

Describe Coeliac disease

A
  • Coeliac sprue or gluten sensitive enteropathy

- Immune mediated enteropathy

31
Q

Describe the pathogenesis of Coeliac disease

A
  • Gliadin= Alcohol soluble component of gluten, contains most of disease-producing component, induces epithelial cells to express IL-15
  • CD8+ Intraepithelial lymphocytes= IL-15–> activation/ proliferation of CD8+ IELs, cytotoxic & kill enterocytes, CD8+ IELs don’t recognise gladden directly.
32
Q

What other diseases can Coeliac disease be associated with?

A
  • Dermatitis herpetiformis
  • Lymphocytic gastritis & colitis
  • Enteropathy-associated T-cell lymphoma
  • Small intestinal adenocarcinoma

Clinical Pathology (56 decks)

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