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)

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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
Q

How does gastric cancer develop?

A

Through phases of metaplasia and dysplasia of the stomach epithelium

26
Q

What conditions are heliobactor pylori associated with?

A

Peptic Ulceration
Type B gastritis
Past infection is highly associated with gastric cancer

27
Q

What type of cancer is gastric cancer?

A

Adenocarcinoma, as it effects the stomach lining which is glandular epithelium

28
Q

How does gastric cancer spread?

A

Direct - to surrounding structures
Lymphatics
Blood - Mostly often to liver
Transcoelomic - Through peritoneal cavity

29
Q

Whats the prognosis for gastric cancer?

A

Almost as bad as oesophageal
Bet you didnt see that coming did ya
5 yr survival <20%