Upper GI Pathology Flashcards

1
Q

Which disease is indicated in this histological slide?

A
  • Oesophageal inflammation (oesophagitis).
  • White arrow points to lymphocytes (sometimes neutrophils) between and within the squamous epithelium of the oesophagus.
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2
Q

What are the 2 factors which prevent reflux?

A
  • Sphincter pressure
  • Submucosal glands
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3
Q

What are the risk factors for developing acid reflux?

A
  • Postural and other - obesity, pregnancy.
  • Relaxation of sphincters - tobacco, alcohol, chocolate, fatty foods, opiates.
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4
Q

What are the most common causes of heartburn?

A
  • Reflux
  • Hiatus hernia
  • Barrett’s oesophagus
  • Immunosuppression
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5
Q

Describe a hiatus hernia.

A
  • Protrusion of the stomach through an enlarged diaphragmatic opening. Usually sliding.
    • The stomach slide in and out of the thorax. As this happens there is some compression of the stomach and some acid coming through the sphincter and therefore heartburn.
    • Mostly lifestyle management – lose weight, avoid fatty foods, be careful about posture.
  • Can be paraoesophageal.
    • It is not the whole stomach which comes out but a little side diverticulum of the stomach protruding.
    • Often requires surgical correction of the diaphragmatic hole if symptomatic treatment does not work.
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6
Q

Describe Barrett’s oesophagus.

A
  • This is common. Often presents with recurrent heartburn.
  • Metaplasia is a change from one mature cell-type to another. Metaplasia is typically an adaptive response.
  • Metaplasia may be gastric in type or intestinal.
  • Of itself metaplasia is not premalignant. It is not indicative of cancer risk. However, the metaplasia in the oesophagus may be gastric or intestinal. Intestinal type is getting far from what you would expect to find in the oesophagus so in addition to the metaplasia there is a risk of dysplasia.
    • Risk of developing adenocarcinoma (gland forming) whereas usual oesophageal carcinoma is squamous cell in type.
  • Barrett’s oesophagus is a warning light – progression to carcinoma is rare but it is a risk.
  • Barrett’s oesophagus is an indication for prolonged follow-up with repeat endoscopy and biopsy.
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7
Q

What are the risk factors for Barrett’s oesophagus?

A
  • Age
  • Tobacco
  • Obesity
  • Being white
  • Barrett’s is an indication for follow-up endoscopy. It is not a trivial diagnosis - follow-up to prevent cancerous changes.
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8
Q

Describe how immunosuppression can cause Barrett’s oesophagitis.

A
  • Immunosuppression can predispose an individual to infections which in turn cause oesophagitis.
  • There are 2 organisns in particular:
    • Candida - causes erosive oesophagitis
    • CMV
  • Individual may be immunosuppressed because of:
    • Known immunosuppressive drugs (e.g. steroids)
    • Repeated ABx use
    • Cancer-associated immunosuppression
    • Transplant
    • Lymphoma
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9
Q

What are the different types of acute gastritis?

What causes these?

A
  • Neutrophil predominated, acute inflammation and ulceration
    • NSAIDs
    • Alcohol
    • Tobacco
  • Lymphocytic
    • Infection - Helicobacter Pylori
  • Acute gastritis may progress to ulceration - shown in picture.
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10
Q

Describe acute gastritis.

A
  • Autoimmune
  • Destruction of parietal cells (present in fundus and body of the stomach)
  • Lack of acid and intrinsic factor
  • Vitamin B12 malabsorption
  • Pernicious anaemia (macrocytic)
  • Typically treated with B12 and folate.
  • Presents as a more chronic, ill-defined indigestion associated with anaemia.
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11
Q

How does Helicobacter Pylori cause symptoms?

A
  • Little comma- or rod- shaped bacteria.
  • They are not invasive. They do not get into the cells, they do not penetrate the mucosa, but they do elicit an inflammatory response.
  • Typically, that response is lymphocytic. Immune response in situ reacting against chronic H. pylori infection.
  • Causes increased acidity in the stomach (decreased pH).
  • It is the major cause of duodenal ulceration.
  • Chronic H. pylori is the major risk factor for gastric cancer.
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12
Q

What are the risk factors for peptic ulceration - stomach or duodenum?

A
  • H. pylori
  • Age 35-65
  • Male > female for duodenal ulceration
  • Hyperacidity
  • Smoking
  • Chronic liver or kidney disease
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13
Q

Describe the mechanism of gluten intolerance.

A
  • Gluten is the underlying trigger for disease of the enterocytes. Particularly, one component of gluten – a protein called gliadin.
  • Protein and immune response to protein – lymphoid cells, infiltrate into the epithelium and cause them damage. This happens for 2 reasons: genetic predisposition and infective trigger.
  • It is thought that there is an infective trigger – an adenovirus.
    • Infection of cells and the immune response to this cross react with components of gluten because of the way antigens are presented.
    • It is a misfire of the immune system mistaking gluten which is present in the diet for proteins derived from an adenovirus which caused an infection.
  • Immune response which damages cells which are responsible for producing villi causes villus atrophy. Anti-gliadin antibody can be helpful.
  • The big risk if gluten is not restricted is development of lymphoma in the GI tract.
  • Lymphoma cells are derived from B lymphocytes which are being hyperstimulated by constant exposure to gliadin.
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14
Q

What skin manifestation might make you suspect that the patient has gluten enteropathy?

A
  • Dermatitis herpetiformis
    • Can be an indicator of the presence of anti-gliadin antibodies.
    • Itchy rash - does not necessarily present with any GI symptoms.
  • Can cause pain and dicomfort, weight loss and can increase the risk of lymphoma.
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15
Q

Describe the mechanism of lactose intolerance.

A
  • Lactose intolerance – problem with the disaccharidases on the surface of the villi on the enterocytes.
  • So, lactose accumulation drawing water in – colicky pain, cramp, malabsorption etc.
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