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Histopathology - Path > Upper Gastro-intestinal Disease > Flashcards

Upper Gastro-intestinal Disease Flashcards

1
Q

Describe the layers of the the wall of the upper GI tract that is normal

A
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2
Q

What is the Z line in the normal oesophagus?

A

The Z line is the name for the squamo-columnar junction where squamous epithelium becomes columnar epithelium

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3
Q

Describe the different areas of the normal stomach

A
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4
Q

Describe the picture of normal stomach lining in the body part of the stomach

A
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5
Q

Describe the lining of the antral area of a normal stomach

A
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6
Q
  1. What does this image show?
A
  • Normal duodenum
  • Glandular epithelium with goblet cells - intestinal type epithelium
  • Villous architecture
    • villous:crypt ration of >2:1
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7
Q

Describe reflux oesophagitis/GORD

  1. What is it?
  2. Complications
A
  1. Gastrointestinal reflux disease is when there is reflux of acidic gastric contents and is the most commonest cause of oesophagitis
  2. Can cause ulceration of the oesophagus:
  • necrotic slough
  • inflammatory exudate
  • granulation tissue

Other complications:

  • Haemorrhage
  • Perforation
  • Stricture
  • Barrett’s oesophagus
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8
Q

Describe Barrett’s oesophagus

A
  • Re-epithelisation by metastatic columnar epithelium usually with goblet cells and becomes intestinal type epithelium. Squamous cells metaplasia to columnar epithelium
  • Causing columnar lined oesophagus
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9
Q

Define the following:

  1. Metaplasia
  2. Dysplasia
  3. Adenocarcinoma
A
  1. Metaplasia is where one cell type changes into another e.g. squamous –> columnar
  2. Dysplasia changed showing some of the cytological and histological features of malignancy but no invasion through the basement membrane
  3. Adenocarcinoma - there is then invasion through the basement membrane
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10
Q

Which is the most common type of oesohpahgeal cancer?

A

Adenocarcinoma of the oesophagus

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11
Q

Describe squamous cell carcinoma of the oesophagus

A
  • Associated with alcohol consumption and smoking
  • Affects the mid/lower oesophagus
  • Invasion into the submucosa
  • Prognosis is poor
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12
Q

Describe oesophageal varices

A

Oesophageal varices are extremely dilated sub-mucosal veins in the lower third of the oesophagus. Most commonly due to portal hypertension as a result of liver cirrhosis

Varices can burst and cause severe haemorrhage

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13
Q

Describe gastritis

A
  • Inflammation of the gastric mucosa
  • Acute gastritis - acute insult
  • Chronic gastritis - chronic/peristent insult
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14
Q

What can cause acute gastritis?

A
  • Chemical
    • aspirin/NSAIDs
    • alcohol
    • Corrosives
  • Infection
    • e.g. H.pylori
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15
Q
  1. Describe chronic gastritis and what can cause it
  2. Cells involved
A
  • Chronic gastritis is caused by a constant insult that occurs within the stomach
  • H.pylori commonly associated

other causes:

  • Chemical - NSAIDs, bile reflux
  • Autoimmune (body, auto-antibodies e.g. anti-parietal)
  1. Lymphocytes +/- neutrophils

MALT induction

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16
Q

Describe helicobacter associated gastritis

  1. Cause
  2. Pattern
  3. Outcome
A
  1. Cause = H.Pylori
  2. Pattern = chronic gastritis +/- activity
  3. Outcome = CLO-IM-dysplasia, adenocarcinoma, lymphoma (MALToma)
17
Q

Describe the helicobacter organism as a carcinogen

A
  • Helicobacter infection is associated with an 8x increased risk of gastric cancer
  • Cag-A-positive H.pylori have a needle like appendage that injects toxin into intracellular junctions allowing the bacteria to attach more easily
  • The strain is associated with more chronic inflammation
  • Treatment of the infection with antibiotics drastically reduces the risk of cancer
18
Q

Besides H.pylori infections, what other infections/conditions cause gastritis?

A
  • Infection
    • CMV
    • Strongyloides (immunosuppression)
  • Inflammatory bowel disease
    • Crohn’s disease
19
Q

Why do we worry about gastritis and cancer?

A

Chronic gastritis can lead to intestinal metaplasia and ulceration. metaplastic cell change can lead to dysplasia, which is a pre-cancerous change and lead to cancer/increase the risk of cancer

20
Q

What should happen to all gastric ulcers?

A

All gastric ulcers should be biopsied to exclude malignancy

21
Q

What are the complications of ulcers?

A
  • Bleeding
    • Anaemia
    • Shock (consequence of a massive haemorrhage)
  • Perforation
    • Peritonitis
22
Q

Describe intestinal metaplasia

A

Like in the oesophagus, intestinal metaplasia occurs when intestinal epithelium changes into gastric mucosa in response to long term damage/chronic insult

Causes and increased risk of cancer

23
Q

Describe gastric epithelial dysplasia

A
  • Abnormal epithelial pattern of growth
  • Some of the cytological and histological features of malignancy are present, but no invasion through the basement membrane
24
Q

Describe the risk factors for gastric cancers for the following:

  1. Host genetic factors
  2. Bacterial virulence factors
  3. Environmental factors
  4. Different gastric cancer phenotypes
A
  1. Host genetic factors:
  • IL-1B-511*T
  • IL-1-RN*2*2
  1. Bacterial virulence factors
  • cagA PAI
  • vac A s1/m1
  1. Environmental factors
  • Smoking
  • Poor diet
  1. Gastric cancer phenotype
  • Corpus-predominant gastritis
  • Multi-focal atrophic gastritis
  • High gastrin + hypchlorhydria
  • Low pepsinogen I and pepsinogen I/II ratio
  • Bacterial overgrowth causing inflammation
  • Increased risk of gastric cancer
25
Q

Describe the epidemiology of gastric cancer

A
  • High incidence in Japan, Chile, Italy, China, Portugal and Russia
  • More common in men
  • >95% of all malignant tumours in stomach are adenocarcinomas
26
Q

What are the two morphological types of adenocarcinoma/gastric cancer?

A
  • Intestinal - well differentiated
  • Diffuse - poorly differentiated (Linitis plastica), includes signet ring cell carcinoma
27
Q

95% of gastric cancer is adenocarcinoma, what makes up teh other 5%?

What is the overall survival rate?

A
  • Squamous cell carcinoma
  • Lymphoma (MALToma)
  • Gastrointestinal stromal tumours (GIST)
  • Neuroendocrine tumours

15% overall survival rate

28
Q

Describe Gastric MALToma/lymphoma

A
  • Chronic inflammation - therefore causing chronic immune stimulation
  • B cell (marginal zone) lymphocytes
  • Treatment = if limited to the stomach and H.pylori - important to eradicate H.pylori
29
Q

Describe duodenitis

A
  • Inflammation of the duodenum, caused by increased acid production in the stomach whihc spills over into duodenum
  • Chronic inflammation occurs, as well as gastric metaplasia, commonly with helicobacter infection
  • 73.5% progress to ulcer, mainly erosive duodenitis - biopsy shows neutrophils
30
Q

What other pathogens can cause duodenitis and ulcer development, other than H.pylori?

A
  • Immunosuppression
  • CMV
  • Cryptosporidiosis
  • Giardia lamblia infection
  • Whipple’s disease - Tropheryma whippelii
31
Q

Describe partial villous atrophy

  • What it can lead to
  • Histology
A
  1. Malabsorption
  2. Histology
  • Villous atrophy
  • Crypt hyperplasia
  • Increased intraepithelial lymphocytes
32
Q
  1. What is coeliac disease?
  2. What is needed for a diagnosis?
A
  1. Coeliac disease is a lifelong autoimmune condition that is caused by a reaction to gluten, leading to inflammation and malabsorption
  2. Diagnosis requires:
  • Endomysial antibodies and tissue transglutaminase antibodies
  • Duodenal bisopsies:
    • On gluten rich diet showing villous atrophy
    • Off gluten showing normal villi

There are other causes of malabsorption wih similar histology e.g. tropical sprue. An acquired form of malabsorption, with potential infectious aetiology

33
Q

What type of cancer are patients with coeliac disease at risk from?

A
  • Patients with coeliac disease have an increased risk of Gastrointestinal cancers
    • MALToma associated with coeliac is
      • In the duodenum
      • T cell origin - enteropathy associated T cell lymphoma

Histopathology - Path (14 decks)

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