Gastroenterology: Pathology - Oesophagus and stomach Flashcards

1
Q

What is the most common cause of oesophagitis?

A

Reflux (GERD)

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1
Q

Describe the pathogenesis of reflux oesophagitis

A

Reflux of gastric juices results in mucosal injury
Conditions which decrease oesophageal tone or increase abdominal pressure contribute to GERD, e.g.:
- Alcohol and tobacco use
- Obesity
- CNS depressants
- Pregnancy
- Hiatus hernia
- Delayed gastric emptying
- Increased gastric volume

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2
Q

What is Barrett oesophagus?

A

Metaplastic change in distal oesophagus in response to prolonged injury (e.g. in chronic GERD)
Squamous epithelium is replaced by columnar intestinal epithelium

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3
Q

What are some of the risks associated with Barrett oesophagus?

A
  1. Ulceration
  2. Stricture
  3. Epithelial dysplasia
  4. Oesophageal adenocarcinoma (risk ~30x baseline)
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4
Q

What is the hallmark morphological feature of Barrett oesophagus?

A

Goblet cells present above the gastro-oesophageal junction

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5
Q

In what % of cirrhotic patients do varices occur?

A

90%

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6
Q

What are the two main causes of oesophageal varices?

A

Alcoholic liver disease
Hepatic schistosomiasis

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7
Q

Describe the pathogenesis of oesophageal varices

A

Severe portal HTN causes congestion at sites of shared portal and systemic circulation
Results in congestion of subepithelial and submucosal venous plexus in distal 1/3 oesophagus
Normally distal 1/3 of oesophagus drains via L gastric vein to portal circulation and via azygos vein to systemic circulation

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8
Q

What % of patients die during first variceal bleeding episode, and what is the usual cause of death?

A

Up to half
Death either due to shock, or hepatic coma triggered by hypovolaemia

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9
Q

Of those who survive an initial episode of variceal bleeding, in what % will additional instances of haemorrhage occur within the next 12 months?

A

> 50% will have another bleeding episode within the next 12 months
Mortality similar to first episode (up to half)

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10
Q

What % of deaths of patients with advanced cirrhosis are caused by variceal rupture?

A

> 50%

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11
Q

Which oesophageal cancer is more common: squamous cell or adenocarcinoma?

A

Squamous cell carcinoma (although rates of adenocarcinoma are increasing in developed world)

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12
Q

What causes oesophageal adenocarcinoma?

A

Typically due to Barrett oesophagus and long-standing GERD (especially if documented dysplasia)

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13
Q

Besides Barrett oesophagus, what other factors increase risk of oesophageal adenocarcinoma?

A

Tobacco
Obesity
Prior radiation

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14
Q

Describe the sex predilection of squamous cell carcinoma and adenocarcinoma

A

Both more common in men

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15
Q

What is the typical site of oesophageal adenocarcinoma?

A

Distal 1/3
May invade into gastric cardia

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16
Q

What is the overall 5-year survival of oesophageal adenocarcinoma?

A

<25% because often diagnosed late (if diagnosed when limited to mucosa or submucosa, 5-year survival is 80%)

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17
Q

Six risk factors for oesophageal squamous cell carcinoma

A
  1. Alcohol and tobacco
  2. Poverty
  3. Caustic oesophageal injury
  4. Achalasia
  5. Frequent consumption of very hot beverages
  6. Previous radiation
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18
Q

What is the typical site of oesophageal squamous cell carcinoma?

A

Upper 1/3 20%, middle 1/3 50%, lower 1/3 30%

19
Q

Six normal gastroprotective factors and two normal damaging forces of the gastric mucosa

A

Gastroprotective factors:
1. Mucin secretion by surface foveolar cells
2. Bicarbonate secretion into mucous by surface epithelial cells
3. Mucosal blood flow (delivers O2, HCO3 and nutrients whilst removing H+)
4. Apical surface membrane transport
5. Epithelial regenerative capacity
6. Elaboration of prostaglandins

Normal damaging forces:
1. Gastric acidity
2. Peptic enzymes

20
Q

Describe the pathogenesis of acute gastritis and gastric ulceration

A

Due to imbalance between normal gastroprotective forces and normal damaging forces, combined with superimposed injury from environmental or immunologic agents

21
Q

Describe 4 causes of impaired gastroprotective defences, and 6 causes of gastric mucosal injury

A

Impaired defences due to:
1. Ischaemia
2. Shock
3. Delayed gastric emptying
4. Other host factors

Causes of mucosal injury:
1. H. pylori infection
2. NSAIDs, aspirin
3. Cigarettes
4. Alcohol
5. Gastric hyperacidity
6. Duodenal-gastric reflux

22
Q

What causes stress ulcers?

A

Most commonly occur in setting of shock, sepsis, severe trauma

23
Q

What are Curling ulcers and where do they typically arise?

A

Ulcers occurring in the proximal duodenum in association with severe burns or trauma

24
Q

What are Cushing ulcers? What is the major risk associated with these ulcers?

A

Ulcers arising in persons with intracranial disease
High risk of perforation

25
Q

What is an ulcer?

A

Breach in the mucosa of the alimentary tract that extends through muscularis mucosa into submucosa or deeper

26
Q

Compare and contrast the appearance of acute ulcers vs peptic (chronic) ulcers

A

Acute:
- Rounded, <1cm in diameter
- More often occur in multiples throughout stomach and duodenum
- Arise anywhere within the stomach
- Sharply demarcated with normal adjacent mucosa
- Base often stained brown/black by acid digestion of extravasated blood

Peptic:
- Usually solitary
- More common to duodenum (rate of 4:1 duodenum:stomach) where they usually occur within few cm of pyloric valve and involve the anterior duodenal wall
- Gastric peptic ulcers typically found on lesser curvature where body meets antrum
- Sharply punched out defect with fibrosis and scarring
- Presence of chronic gastritis in other areas of mucosa

27
Q

How common is malignant transformation of peptic ulcers?

A

Very rare

28
Q

What are the three major complications of ulcers and with what relative frequency does each occur? What is responsible for the most ulcer-related deaths?

A
  1. Bleeding (15-20%; causes 25% of ulcer-related deaths)
  2. Perforation (5%; causes 66% of ulcer-related deaths)
  3. Obstruction (2%; usually caused by chronic ulcers)
29
Q

What kind of microbe is H. pylori?

A

Spiral-shaped Gram negative bacillus

30
Q

What are the four features of H. pylori which make it well-suited as a pathogen in the stomach?

A
  1. Flagella: allows motility in viscous mucus
  2. Urease: generates ammonia from endogenous urea to increase local gastric pH
  3. Adhesins: enhance bacterial adherence to surface foveolar cells
  4. Toxins: e.g. cytotoxin-associated gene A
31
Q

With which four conditions is H. pylori associated?

A

Chronic gastritis
Peptic ulcer disease
Gastric carcinoma
Gastric MALToma

32
Q

In what % of patients with duodenal vs gastric ulcers is H. pylori present?

A

85-100% of duodenal ulcers
70% of gastric ulcers

33
Q

Compare and contrast the features of H. pylori-associated vs autoimmune gastritis in terms of:
- Location
- Inflammatory infiltrate
- Acid production
- Gastrin
- Other lesions
- Serology
- Sequelae
- Epidemiological associations

A
34
Q

What is Zollinger-Ellison syndrome?

A

Syndrome of duodenal ulceration and diarrhoea caused by gastrin-secreting tumours of small intestine and pancreas

35
Q

What morphological feature is characteristic of Zollinger-Ellison syndrome?

A

Increased mucosal thickening in stomach due to parietal cell hyperplasia

36
Q

What are the three types of gastric polyps? Which is most common?

A
  1. Inflammatory or hyperplastic (most common; 75%)
  2. Gastric adenomas (10%)
  3. Fundic gland polyps
37
Q

What causes inflammatory or hyperplastic gastric polyps?

A

Usually arise in setting of chronic gastritis

38
Q

Risk of dysplasia in gastric polyps is linked to what?

A

Size of polyp

39
Q

What two conditions can cause fundic polyps?

A
  1. PPI use (decreased gastric acidity stimulates gastrin secretion, resulting in glandular hyperplasia
  2. FAP
40
Q

In what % of gastric adenomas is carcinoma present?

A

Up to 30%

41
Q

What is the main gastric malignancy?

A

Gastric adenocarcinoma (>90%)

42
Q

Two environmental and three host risk factors for gastric adenocarcinoma

A

Environmental:
1. Diet (lack of fresh fruit and vegetables)
2. Cigarette smoking

Host factors:
1. H. pylori-associated chronic gastritis
2. Autoimmune gastritis
3. Previous partial gastrectomy due to increased gastroduodenal reflux

43
Q

What is the most common location for a gastric adenocarcinoma? Which location is seeing the greatest increase in incidence and why?

A

Pylorus/antrum (50-60%)
However incidence of gastric adenocarcinoma in the cardia is increasing (currently 25%), likely due to increased rates of Barrett oesophagus

Body/fundus 15-25%

44
Q

What are the five types of gastric tumours seen?

A
  1. Polyps
  2. Gastric adenocarcinoma
  3. Gastric MALToma
  4. Carcinoid tumour
  5. Gastrointestinal stromal tumour (GIST)
45
Q

What is the most common mesenchymal tumour of the abdomen?

A

GIST