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
Describe the epidemiology of gastric cancer
* High incidence in Japan, Chile, Italy, China, Portugal and Russia * More common in men * \>95% of all malignant tumours in stomach are adenocarcinomas
26
What are the two morphological types of adenocarcinoma/gastric cancer?
* Intestinal - well differentiated * Diffuse - poorly differentiated (Linitis plastica), includes signet ring cell carcinoma
27
95% of gastric cancer is adenocarcinoma, what makes up teh other 5%? What is the overall survival rate?
* Squamous cell carcinoma * Lymphoma (MALToma) * Gastrointestinal stromal tumours (GIST) * Neuroendocrine tumours 15% overall survival rate
28
Describe Gastric MALToma/lymphoma
* 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
Describe duodenitis
* 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
What other pathogens can cause duodenitis and ulcer development, other than H.pylori?
* Immunosuppression * CMV * Cryptosporidiosis * Giardia lamblia infection * Whipple's disease - Tropheryma whippelii
31
Describe partial villous atrophy * What it can lead to * Histology
1. Malabsorption 2. Histology * Villous atrophy * Crypt hyperplasia * Increased intraepithelial lymphocytes
32
1. What is coeliac disease? 2. What is needed for a diagnosis?
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
What type of cancer are patients with coeliac disease at risk from?
* 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