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GI -S > Pathology of the Upper Gastro-Intestinal Tract > Flashcards

Pathology of the Upper Gastro-Intestinal Tract Flashcards

1
Q

What are we referring to when we mention the upper GI tract?

A

Oesophagus
Stomach
Duodenum

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2
Q

What makes these diseases hard to diagnose from symptoms alone?

A

They have relatively non specific clinical presentations.

Upper abdominal or retrosternal discomfort or pain or “indigestion”

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3
Q

What is oesophageal reflux?

A

The reflux of gastric acid into the oesophagus.

This can be a common event and only prolonged contact with gastric contents causes problems.

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4
Q

What is indigestion?

A

Indigestion isn’t very well defined. Its more of a group of symptoms which can present in any selection.

Epigastric pain or burning
Nausea
Heartburn
Fullness
Belching
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5
Q

What can be a common cause of oesophageal reflux?

A

Hiatus hernia of the stomach

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6
Q

Explain the pathophysiology of Oesophageal Reflux

A

The lower oesophageal sphincter is impaired.
Continual reflux of stomach contents into oesophagus occurs as a result.
The oesophagus is not built to deal with gastric acid contents.
Thickening of squamous epithelium
If severe ulceration of the oesophagus can occur.

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7
Q

What is the clinical name for oesophageal reflux?

A

Gastric Oesophageal Reflux Disease (GORD)

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8
Q

What are the complications of GORD?

A

Healing by fibrosis

  • Stricture formation
  • Impaired oesophageal motility.
  • Oesophageal obstruction

Barrett’s oesophagus

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9
Q

What is Barrett’s Oesophagus?

A

Increasingly common

Type of metaplasia
-Transformation of squamous epithelium to adenomatous (glandular) epithelium

Response in some patients to oesophageal reflux

It is a pre-malignant condition.

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10
Q

How common is oesophageal cancer compared to other alimentary tract cancers?

A

It is the third commonest cancer of the alimentary tract

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11
Q

Why does oesophageal cancer have such a marked variation in geographical incidence?

A

While all incidence is rising there is marked variation in geographical incidence because of the strong influence of environmental factors on the disease.

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12
Q

What are the two histological types of oesophageal cancer?

A

Squamous (usually the middle 1/3rd)

Adenocarcinoma (develops from barrettes oesophagus so more associated with lower 1/3rd)

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13
Q

What are the risk factors for the two types of oesophageal cancer?

A

Squamous: Smoking, alcohol and dietary carcinogens

Adenocarcinoma: Barrett’s metaplasia, obesity, smoking

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14
Q

Why does obesity increase risk of adenocarcinoma of the oesophagus?

A

Obesity increases the risk of oesophageal reflux.

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15
Q

What are the local effects of oesophageal cancer and how are they linked?

A

Obstruction: Tumour causes obstruction of food. If severe will effect liquids too. (dysphagia)

Ulceration: Growing tumour outstrips the blood supply of surrounding tissues leading to ulceration.

Perforation: Ulceration can burrow into wall and cause perforation. Food enters surrounding tissue risking infection

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16
Q

Describe the spread of oesophageal cancer

A

Direct = to surrounding structures

Lymphatic spread = To regional lymph nodes

Blood spread = liver

CHECK FOR SPREAD

17
Q

What is the prognosis of oesophageal cancer?

A

Very poor.
5 year survival rate less than 15%

This is due to patients often presenting late and the poor success rate of treatment

18
Q

What is gastritis?

A

Inflammatory process of the stomach

19
Q

What is the aetiology of gastritis?

A

Autoimmune (Type A)
Bacterial (Type B)
Chemical Injury (Type C)

ABC of gastritis

20
Q

Describe autoimmune gastritis

A

This is an organ specific autoimmune disease.

Autoantibodies attack parietal cells and intrinsic factor.

It is associated with other autoimmune disease

21
Q

What are parietal cells?

A

Secrete hydrochloric acid and intrinsic factor.

Found in the gastric glands lining the fundus

22
Q

Describe the pathology of autoimmune gastritis

A

Atrophy of specialised acid secreting gastric epithelium (parietal cells)

Loss of specialised gastric epithelial cells

  • Decreased acid secretion
  • Loss of intrinsic factor leading to Vitamin B12 deficiency
23
Q

Describe bacterial gastritis

A

Commonest type of Gastritis

Helicobacter Pylori associated

24
Q

Describe helicobacter pylori

A

Gram negative bacterium.
Found in the gastric mucous on the surface of the gastric epithelium.
Produces acute and chronic inflammatory response.
Causes increased acid production

25
Q

How does helicobacter pylori survive in the stomach?

A

Brakes down urea using urease. This produces ammonia which acts as an alkali halo around the bacterium. Parietal cells think that the pH of the stomach has dropped and so produce more acid.
pH of the stomach rises

26
Q

What are the causes of chemical gastritis?

A

Drugs: NSAIDs (most common)
Alcohol
Bile reflux

27
Q

What is peptic ulceration?

A

Imbalance between acid secretion and mucosal barrier.

Almost always H. Pylori associated.

28
Q

What parts of the GI tract does peptic ulceration affect?

A

Lower oesophagus
Body and antrum of stomach
First and second parts of the duodenum

29
Q

What are the complications of peptic ulceration?

A

Gastric contents come into contact with the epithelium
Ulcer forms which burrows into stomach layers.

Bleeding

  • Small blood vessel damage can cause a slow bleed (anaemia)
  • Large blood vessel damage can cause Haemorrhage.

Perforation
-Peritonitis as stomach contents leak into peritoneum

Healing by fibrosis
-If fibrosis occurs in narrow part there may be obstruction

30
Q

How common is Gastric cancer compared to other GI tract cancers?

A

Second most common cancer

31
Q

What is the histology of gastric cancer?

A

Adenocarcinoma in the antrum region

32
Q

What is the main cause of gastric cancer?

A

Previous (not current) H. Pylori infections are strongly associated.

Other risk factors also

33
Q

What is the pathology of gastric cancer?

A

Previous H. Pylori infections

Phases of intestinal metaplasia and dysplasia

34
Q

Describe the spread of gastric cancer

A

Direct = spread to surrounding structures

Lymphatic = spread to regional lymph nodes

Blood spread = Liver

Transcoelomic spread = Cancer proliferates through all walls of the stomach and enters peritoneum. Spreads through the peritoneal cavity

35
Q

What is the prognosis of stomach cancer?

A

Very poor
5 Year survival rate less than 20%

There is a poor response to treatment.

GI -S (29 decks)

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