Upper GI Tract Pathology Flashcards

1
Q

In this lecture we were told about 5 of the commonest upper GI conditions:

A
  • Oesophageal Reflux
  • Oesophageal Cancer
  • Gastritis
  • Peptic Ulceration
  • Gastric Cancer
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2
Q

What is oesophageal reflux?

A

Reflux of gastric acid into the oesophagus

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3
Q

What causes oesophageal reflux?

A

Often caused by a hiatus hernia

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4
Q

What are the consequences of oesophageal reflux?

A
  • Thickening of squamous epithelium
  • Ulceration of the oesophagus
  • Fibrosis -> Stricture formation
  • Barrett’s Oesophagus
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5
Q

Define Barrett’s Oesophagus?

A

A Type of metaplasia where the squamous epithelium transforms into glandular epithelium
It predisposes one to oesophageal cancer (i.e. pre-malignant) - Adenocarcinomas

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6
Q

How common is oesophageal cancer?

A

The 3rd commonest form of alimentary tract cancer

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7
Q

What are the types of oesophageal cancer?

A

Two histological types:

  • Squamous Carcinoma
  • Adenocarcinoma
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8
Q

Which type of oesophageal cancer does Barrett’s oesophagus predispose you to>

A

Adenocarcinoma

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9
Q

What are the risk factors for oesophageal cancer?

A

Squamous:

  • Alcohol
  • Smoking
  • Dietary Carcinogens

Adenocarcinoma:

  • Barrett’s Metaplasia
  • Obesity
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10
Q

What are the local effects of oesophageal cancer?

A

Obstruction
Ulceration
Perforation -> food in thoracic cavity -> infection -> abscess

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11
Q

How does oesophageal cancer spread/

A

Direct to surrounding structures
Through lymphatics to regional lymph nodes
Through blood, most often to the liver

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12
Q

Whats the prognosis on oesophageal cancer?

A

Pretty fucking dire mate

5yr survival is <15%

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13
Q

What is gastritis?

A

Inflammation of the stomach mucosa

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14
Q

What types of gastritis are there?

A

Type A - Autoimmune
Type B - Bacterial
Type C - Chemical Injury

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15
Q

What happens in type A gastritis?

A

Autoantibodies attack parietal cells and intrinsic factor.

Causes atrophy of the specialised gastric epithelium that secrete gastric acid (parietal cells)
–> Decrease Acid Secretion & Loss of intrinsic factor

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16
Q

Which type of gastritis is commonest?

A

Type B (bacterial)

17
Q

What bacteria is involved in type B gastritis?

A

Heliobactor Pylori (A gram -ve bacterium)

18
Q

How does type B gastritis work?

A

Heliobacter pylori releases ammonia –> stomach detects pH rise –> Parietal cells release more acid –> Inflames itself

19
Q

How is type B gastritis treated?

A

Antibiotics

20
Q

What causes Type C gastritis?

A

Drugs e.g. NSAIDS
Alcohol
Bile Reflux from Duodenum

21
Q

What is peptic ulceration?

A

An imbalance of acid secretion and the mucosal barrier
Can be related to too much acid or acid where it shouldn’t be
(Usually associated with H pylori causing an increase in HCl secretion)

22
Q

Where does peptic ulceration take place?

A

Lower oesophagus
Body + antrum of stomach
1st & 2nd sections of duodenum

23
Q

What are hte complications of peptic ulceration?

A

Bleeding:

  • Acute haemorrhage
  • Chronic (more common, due to capillaries breaking) can lead to anaemia

Perforation:

  • Digestive contents enter peritoneal cavity
  • Causes Peritonitis

Fibrosis:
- Can heal to form obstruction of the GI tract

24
Q

How common is gastric cancer?

A

The 2nd commonest alimentary tract cancer

25
How does gastric cancer develop?
Through phases of metaplasia and dysplasia of the stomach epithelium
26
What conditions are heliobactor pylori associated with?
Peptic Ulceration Type B gastritis Past infection is highly associated with gastric cancer
27
Histology of gastric cancer?
Adenocarcinoma, as it effects the stomach lining which is glandular epithelium
28
How does gastric cancer spread?
Direct - to surrounding structures Lymphatics Blood - Mostly often to liver Transcoelomic - Through peritoneal cavity
29
Whats the prognosis for gastric cancer?
Almost as bad as oesophageal Bet you didnt see that coming did ya 5 yr survival <20%