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Clinical Pathology > GI Tract 1 (Upper GI) > Flashcards

GI Tract 1 (Upper GI) Flashcards

1
Q

What type of epithelium lines most of the oesophagus?

A

Stratified squamous

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2
Q

What are the possible aetiologies of oesophagitis?

A
  • Bacterial, viral (HSV1, CMV), fungal (candida)
  • Ingestion of corrosive substances
  • Reflux of gastric contents
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3
Q

What is the commonest cause of oesophagitis?

A

Reflux oesophagitis - caused by reflux of gastric acid (gastro-oesophageal reflux) and/or bile (duodeno-gastric reflux)

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4
Q

What are the risk factors for reflux oesophagitis?

A
  • Defective lower oesophageal sphincter
  • Hiatus hernia
  • Increased intra-abdominal pressure
  • Increased gastric fluid volume due to gastric outflow stenosis
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5
Q

What is an hiatus hernia?

A
  • Abnormal bulging of a portion of the stomach through the diaphragm
  • Sliding hiatus hernia = reflux symptoms
  • Para-oesophageal hernia = strangulation
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6
Q

What histological changes are seen in reflux oesophagitis?

A
  • Squamous epithelium
    • Basal cell hyperplasia, elongation of papillae, increased cell desquamation
  • Lamina propria
    • Inflammatory cell infiltration (neutrophils, eosinophils, lymphocytes)
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7
Q

What are the possible complications of reflux oesophagitis?

A
  • Ulceration
  • Haemorrhage
  • Perforation
  • Benign stricture (segmental narrowing)
  • Barrett’s oesophagus
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8
Q

What is the cause of Barett’s oesophagus?

A

Longstanding reflux

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9
Q

What are the risk factors for Barrett’s oesophagus?

A

Same as for reflux (male, Caucasian, overweight)

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10
Q

What are the macroscopic findings in Barrett’s oesophagus?

A

Proximal extension of the squamo-columnar junction

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11
Q

What are the histological features of Barrett’s oesophagus?

A

Squamous mucosa replaced by columnar mucosa > “glandular metaplasia”

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12
Q

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

A
  • Gastric cardia type
  • Gastric body type
  • Intestinal type = “specialised Barrett’s mucosa”
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13
Q

What is the relevance of Barrett’s oesophagus?

A

Premalignant condition with an increased risk of developing adenocarcinoma

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14
Q

What is the potential disease progression for Barrett’s oesophagus?

A

Barrett’s -> low-grade dysplasia -> high grade dysplasia -> adenocarcinoma

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15
Q

What are the 2 histological types of oesophageal cancer?

A
  • Squamous cell carcinoma

- Adenocarcinoma

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16
Q

What are the risk factors for adenocarcinoma?

A

Male gender, tobacco, obesity, alcohol, Western populations

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17
Q

What are the macroscopic features of oesophageal adenocarcinoma?

A

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

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18
Q

What are the risk factors for oesophageal squamous cell carcinoma?

A
  • Tobacco and alcohol
  • Nutrition (potential sources of nitrosamines)
  • Thermal injury (hot beverages)
  • HPV
  • Male
  • Ethnicity (black)
  • More common in Eastern population
19
Q

In what part of the the oesophagus are squamous cell carcinomas usually found?

A

Middle and lower third

20
Q

In what part of the the oesophagus are adenomas usually found?

A

Distally

21
Q

What are the features of Helicobacter pylori?

A
  • Gram negative spiral shaped bacterium
  • 2.5-5.0 micrometres long
  • 4 to 6 flagellae
  • Lives on the epithelial surface protected by the overlying mucus barrier
22
Q

What is peptic ulcer disease?

A

Localised defect extending at least into submucosa

23
Q

What are the major sites of peptic ulcer disease?

A
  • First part of duodenum
  • Junction of antral and body mucosa
  • Distal oesophagus (GOJ)
24
Q

What are the main aetiological factors in peptic ulcer disease?

A
  • Hyperacidity
  • H. pylori infection
  • Duodeno-gastric reflux
  • Drugs (NSAIDs)
  • Smoking
25
Q

What is the histology of an acute gastric ulcer?

A
  • Full-thickness coagulative necrosis of mucosa (or deeper layers)
  • Covered with ulcer slough (necrotic debris + fibrin + neutrophils)
  • Granulation tissue at ulcer floor
26
Q

What is the histology of a chronic gastric ulcer?

A
  • Clear-cut edges overhanging the base
  • Extensive granulation and scar tissue at ulcer floor
  • Scarring often throughout the entire gastric wall with breaching of the muscularis propria
  • Bleeding
27
Q

What are the complications of peptic ulcers?

A
  • Haemorrhage (acute and/or chronic  anaemia)
  • Perforation -> peritonitis
  • Penetration into an adjacent organ (liver, pancreas)
  • Stricturing -> hour-glass deformity
28
Q

What is the most common type of gastric cancer?

A

Adenocarcinoma

29
Q

What are the less common types of gastric cancer?

A
  • Endocrine tumours
  • MALT lymphomas
  • Stromal tumours (GIST)
30
Q

What is the incidence of gastric adenocarcinoma?

A
  • 5th most common cancer in the World (951,594 new cases/year)
  • Wide geographical variation (high rates in Eastern Asia, - Andean regions of South America, Eastern Europe)
  • Steady decline over the past decades
31
Q

What is the aetiology of gastric adenocarcinoma?

A
  • Diet (smoked/cured meat or fish, pickled vegetables)
  • Helicobacter pylori infection
  • Bile reflux (e.g. post Billroth II operation)
  • Hypochlorhydria (allows bacterial growth)
  • ~1% hereditary
32
Q

What are the features of for carcinomas of GOJ?

A
  • White males
  • Association with GO reflux
  • No association with H. pylori / diet
  • Increased incidence in recent years
33
Q

What are the features of carcinomas of the gastric body/antrum?

A
  • Association with H. pylori
  • Association with diet (salt, low fruit
    & vegetables)
  • No association with GO reflux
  • Decreased incidence in recent years
34
Q

A mutation in which protein can predispose a person to gastric cancer?

A

Cadherin

35
Q

What is coeliac disease?

A

Immune mediated enteropathy

36
Q

What is the aetiology of coeliac disease?

A
  • Ingestion of gluten containing cereals
    • Wheat, rye, or barley
  • Genetically predisposed individuals
37
Q

What is gliadin?

A
  • Alcohol soluble component of gluten
  • Contains most of the disease-producing components
  • Induces epithelial cells to express IL-15
38
Q

What is the role of CD8+ intraepithlial lymphocytes cells in coeliac disease?

A
  • IL15 produced by the epithelial activation/proliferation of CD8+ IELs
  • These are cytotoxic and kill enterocytes
  • CD8+ IELs do not recognise gliadin directly
  • Gliadin-induced IL15 secretion by epithelium is the mechanism
39
Q

What are the clinical features of Coeliac disease?

A

Anaemia, chronic diarrhoea, bloating, or chronic fatigue

40
Q

What are the disease associations of Coeliac disease?

A
  • Dermatitis herpetiformis - 10% of patients

- Lymphocytic gastritisandlymphocytic colitis

41
Q

Which cancers are associated with Coeliac disease?

A
  • Enteropathy-associated T-cell lymphoma

- Small intestinal adenocarcinoma

42
Q

What is the diagnostic procedure for Coeliac disease?

A
  • Non-invasive serologic tests usually performed before biopsy
  • The most sensitive tests
  • IgA antibodies to tissue transglutaminase (TTG)
  • IgA or IgG antibodies to deamidated gliadin
  • Anti-endomysial antibodies - highly specific but less sensitive
  • Tissue biopsy is diagnostic (2nd biopsy after GFD)
43
Q

What is the treatment for Coeliac disease?

A
  • Gluten-free diet = symptomatic improvement for most patients
  • Reduces risk of long-term complications including anaemia, female infertility, osteoporosis, and cancer
44
Q

How does the TNM staging system work?

A

Primary tumor (T)

  • TX Primary tumor cannot be assessed
  • T0 No evidence of primary tumor
  • Tis High-grade dysplasia
  • T1 Tumor invades lamina propria, muscularis mucosae, or submucosa
  • T1a Tumor invades lamina propria or muscularis mucosae
  • T1b Tumor invades submucosa
  • T2 Tumor invades muscularis propria
  • T3 Tumor invades adventitia
  • T4 Tumor invades adjacent structures
  • T4a Resectable tumor invading pleura, pericardium, or diaphragm
  • T4b Unresectable tumor invading other adjacent structures, such as the aorta, vertebral body, and trachea

Regional lymph nodes (N)

  • NX Regional lymph node(s) cannot be assessed
  • N0 No regional lymph node metastasis
  • N1 Metastasis in 1-2 regional lymph nodes
  • N2 Metastasis in 3-6 regional lymph nodes
  • N3 Metastasis in 7 or more regional lymph nodes

Distant metastasis (M)

  • M0 No distant metastasis
  • M1 Distant metastasis

Clinical Pathology (65 decks)

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