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Kat's Pathology > Upper Gastrointestinal Disease > Flashcards

Upper Gastrointestinal Disease Flashcards

1
Q

Structure of normal GI

A

Epithelium
Submucosa
Muscularis propria

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2
Q

What is present in a normal oesophagus

A

Z line - squamo-columnar junction

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3
Q

Anatomy of the stomach

A 
Oesphagus 
Cardia
Fundus
Body 
Pyloric antrum 
Pylorus 
Dueodenum
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4
Q

Normal stomach (body) histology

A

Lined by gastric mucosa, columnar epithelium (foveolar, mucin secreting)

Specialised glands in the lamina propria

Muscularis mucosa

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5
Q

Normal stomach (antral) histology

A

Lined by gastric mucosa, columnar epithelium (fovelolar, mucin secreting)

Non-specialised glands in the lamina propria (gastric pits)

Muscularis mucosa

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6
Q

Normal duodenum histology

A

Glandular epithelium with goblet cells (intestinal type epithelium)

Villous architecture with a villous:crypt ratio of >2:1

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7
Q

Acute inflammation of the oesophagus

A

Oesophagitis

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8
Q

Chronic inflammation of the oesophagus

A

GORD

Barrett’s oesophagus

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9
Q

GORD

A

Gastro-oesophageal reflux disease
Commonest cause of oesophagitis
Reflux of acidic gastric contents

Causes:
Ulceration: necrotic slough, inflammatory exudate, granulation tissue
Fibrosis

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10
Q

Complications of GORD

A

Haemorrhage
Perforation
Strictures
Barrett’s oesophagus

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11
Q

Barrett’s oesophagus

A

Re-epithelialisation by metaplastic columnar epithelium usually with goblet cells (intestinal type epithelium)
AKA columnar lined oesophagus (CLO)

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12
Q

Metaplasia of the oesophagus

A

Glandular epithelium (intestinal type)

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13
Q

Dysplasia of the oesophagus

A

Changes showing some of the cytological and histological features of malignancy, but no invasion through the basement membrane

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14
Q

Adenocarcinoma of the oesophagus

A

Invasion through the basement membrane

Now the commonest type of oesophageal cancer

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15
Q

Change from GORD-Barrett’s-Cancer

A

Metaplasia - Dysplasia - Cancer

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16
Q

Squamous cell carcinoma of the oesophagus

A

Associated with alcohol and smoking
Mid/lower oesophagus
Invasion into the submucosa

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17
Q

Carconoma of the oesophagus

A

Poor prognosis

Diagnosis of a pre-invasive stage is very important

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18
Q

Cause of oesophageal varicies

A

Cirrhosis of the liver (i.e. increased portal hypertension)

19
Q

Gastritis

A

Inflammation of the gastric mucosa
Acute gastritis: acute insult
Chronic gastritis: chronic/persistent insult

20
Q

Causes of acute gastritis

A

Chemical: aspirin, NSAIDs, alcohol, corrosives
Infection: e.g. helicobacter pylori

21
Q

Causes of chronic gastritis

A

H pylori associated
Chemicals (NSAIDs, bile reflux into the antrum)
Autoimmune (body, auto-antibodies e.g. antiparietal)
Presence of lymphocytes +/- neutrophils
Mucosal associated lymphoid tissue induction (MALT)

22
Q

Helicobacter associated gastritis

A

Caused by H.pylori infection
Pattern: chronic gastritis +/- activity
Outcome: CLO-IM-dysplasia, adenocarcinoma, lymphoma (MALToma)

23
Q

Helicobacter pylori and stomach cancer

A

Helicobacter infection is associated with an 8x increased risk of (non-cardia) gastric cancer
cag-A-positive H.pylori have a needle like appendage that injects toxin into intercellular junctions allowing the bacteria to attach more easily.
This strain is associated with more chronic inflammation.
Treatment of the infection with antibiotics drastically reduces the risk of cancer.

24
Q

Other causes of gastritis

A

Infection: CMV, strongyloides (immunosuppression)
IBD: Crohn’s disease

25
Q

Why is gastritis concerning

A

Chronic gastritis –> ULCER = intestinal metaplasia –> dysplasia –> cancer

26
Q

What should be done to all stomach ulcers

A

All ulcers should be biopsied to exclude malignancy

27
Q

Complications of gastric ulcers

A

Bleeding: anaemia, shock (massive haemorrhage)
Perforation: peritonitis

28
Q

Intestinal metaplasia

A

As in the oesophagus
Intestinal metaplasia in gastric mucosa in response to long term damage
Increased cancer risk

29
Q

Gastric epithelial dysplasia

A

Abnormal epithelial pattern of growth
Some of the cytological and histological features of malignancy are present, but no invasive through the basement membrane

30
Q

Causes of gastric cancer

A

Host factors and genes
Bacterial virulence factors
Environmental factors

31
Q

Environmental factors for gastric cancer

A

Smoking

Poor diet

32
Q

Gastric cancer

A

High incidence in Japan, Chile, Italy, China, Portugal, Russia
More common in men
>95% of all malignant tumors in stomach are adenocarcinomas

33
Q

Classification of stomach adenocarcinomas

A

Intestinal - well differentiated

Diffuse - poorly differentiated (linitis plastica), includes signet ring cell carcinoma

34
Q

Gastric cancer subtypes

A

95% are adenocarcinomas

Rest are: squamous cell carcinoma, lymphoms (MALToma), gastrointestinal stromal tumour (GIST), neuroendocrine tumours

35
Q

Prognosis for gastric cancer

A

Overall survival is 15%

36
Q

Gastric MALToma/ lymphoma

A

Chronic inflammation: Chronic immune stimulation

B cell (marginal zone) lymphocytes

Treatment: If limited to the stomach and H.pylori is present then H.pylori eradication

37
Q

What is present in a normal duodenum

A

Villi

38
Q

Duodenitis, Duodenal Ulcer and H. pylori infection

A

Increased acid production in the stomach which spills over into duodenum
Chronic inflammation and gastric metaplasia with helicobacter infection.

Especially in antral stomach infection = +++++ACID which spills into the duodenum.

39
Q

Duodenal ulcers

A

Duodenitis and duodenal ulcer: good correlation between endoscopy and biopsy pathology

40
Q

Endoscopy findings with duodenal ulcers

A

Endoscopy “itis”: 73.5% progress to ulcer, mainly erosive duodenitis (biopsy – neutrophils)

41
Q

Pathogens causing duodenal ulcers (except H.pylori)

A 
Immunosuppressed
CMV
Cryptosporidiosis 
Giardia lamblia infection 
Whipple's disease - trophryma whippelii
42
Q

Duodenal malabsorption

A

Partial villous atrophy
Histology: villous atrophy, crypt hyperplasia, increased intraepithelial lymphocytes (normal range <20 lymphocytes/100 enterocytes)

43
Q

Coeliac disease

A

Diagnosis requires:
endomysial antibodies and tissue transglutaminase antibodies
Duodenal biopsies:
On gluten rich diet showing villous atrophy
Off gluten showing normal villi
There are other causes of malabsorption with similar histology e.g. tropical sprue

44
Q

Duodenal MALToma/lymphoma

A

Patients with coeliac disease have an increased risk of GIT cancers
MALToma associated with Coeliac is
in the duodenum
T-cell origin: Enteropathy Associated T-cell Lymphoma

Kat's Pathology (105 decks)

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