Gastro-oesophageal Inflammation and Peptic Ulcers Flashcards

1
Q

What is Achalasia?

A

decreased tone of lower oesophageal sphincter:

- can be caused by impaired by smooth muscle relaxation or oesophageal obstruction

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2
Q

What is the Achalasia triad?

A
  • incomplete LES relaxation
  • increased LES tone
  • aperistalsis of the oesophagus
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3
Q

What are the causes of Achalasia?

A

Primary:

  • neuronal or ganglion cell degeneration (related to vagus n.)
  • familiar causes

Secondary:

  • Chagas disease (destruction of myenteric plexus)
  • diabetic autonomic neuropathy
  • amyloidosis
  • sarcoidosis
  • polio
  • Downs Syndrome
  • Herpes Simplex infection
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4
Q

What is the treatment for Achalasia?

A
  • laparoscopic myotomy
  • balloon dilation
  • botox injection
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5
Q

What are the acute and chronic causes of oesophageal inflammation?

A

Acute:
- infection in immunosuppressed patients (HSV, candida, CMV and corrosives)

Chronic:

  • TB
  • bullous pemphigoid
  • epidermolysis bullosa
  • Crohn’s Disease

Non-specific:
- reflex oesophagitis

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6
Q

What is reflux oesophagitis and its causes?

A
  • regurgitation of gastric contents due to incompetent gastro-oesophageal junction
  • can be due to alcohol and tobacco, obesity, drugs, hiatus hernia and motility disorders
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7
Q

What can GORD cause?

A
  • eopsinophils epithelial infiltration
  • basal cell hyperplasia
  • chronic inflammation
  • severe reflux can lead to ulceration which can lead to healing by fibrosis
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8
Q

What is Barrett’s oesophagus?

A
  • longstanding reflux where lower oesophagus becomes lined by columnar epithelium due to intestinal metaplasia
  • premalignancy which increases risk of adenocarcinoma
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9
Q

What are the acute and chronic causes of gastric inflammation (gastritis)?

A

Acute:
- chemical injury (NSAIDS/alcohol, can alsp be H pylori associated)

Chronic:

  • active chronic is H. pylori associated
  • can be autoimmune
  • can be due to chemical reflux
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10
Q

Describe the pathogenesis of H. pylori

A
  • H.pylori produces urease which produces ammonia which neutralises pH of stomach allowing colonisation
  • then causes mucosal damage which leads to inflammation and mucosal cell death
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11
Q

What are the symptoms of an acute H. pylori infection?

A
  • nausea
  • dyspepsia
  • malaise
  • halitosis
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12
Q

What happens in an acute H. pylori infection?

A

gastric mucosa is inflamed with neutrophils and inflammatory cells with marked persistent lymphocyte penetration

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13
Q

Describe the 2 distribution patterns seen with H. pylori associated gastritis

A

diffuse involvement of antrum and body:

  • atrophy, fibrosis and intestinal metaplasia
  • associated with gastric ulcers and cancers

antral but no body involvement:

  • gastric acid secretion is increased
  • associated with duodenal ulcers
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14
Q

What is chemical (reflux) gastritis and what is associated with it?

A
  • irritation of the stomach caused by regurgitation of bile and alkaline duodenal secretion
  • loss of epithelial cells with compensatory hyperplasia of gastric pits
  • associated with defective pylorus or motility disorders
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15
Q

What is autoimmune chronic gastritis and what is it associated with?

A
  • autoimmune reaction to gastric parietal cells resulting in loss of acid secretion
  • decreased stomach acid and intrinsic factor
  • causes vitamin B12 deficiency (pernicious anaemia)
  • associated with marked gastric atrophy and intestinal metaplasia
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16
Q

What are peptic ulcerations?

A
  • breach in mucosal lining of alimentary tract as a result of acid and pepsin attack
17
Q

Where are the major sites of peptic ulceration?

A
  • first part of duodenum
  • junction of antrum and body mucosa in stomach
  • distal oesophagus
  • gastro-enerostomy stoma
18
Q

What are the aetiological factors for peptic ulceration?

A
  • hyperacidity
  • H. pylori gastritis
  • duodenal reflux
  • NSAIDs
  • smoking
  • genetic factors
  • Zollinger-Ellison syndrome
19
Q

What are some of the complications of peptic ulcers?

A
  • haemorrhage
  • penetration of adjacent organs
  • perforation
  • anaemia
  • obstruction
  • malignancy
20
Q

What are some defining features that differentiate between gastric and duodenal ulcers?

A

Duodenal:

  • more common
  • commonly blood group O
  • acid levels are high or normal

Gastric:

  • blood group A
  • acid levels are low or normal
21
Q

What are some acute causes of peptic ulcers?

A
  • acute gastritis
  • stress response
  • extreme acidity
22
Q

What is the pathogenesis of chronic peptic ulcers and where do they normally occur?

A
  • patho-hyperacidity and mucosal defence defects

- most commonly occur at mucosal junctions

23
Q

Describe why chronic duodenal ulcers can occur?

A
  • increased acid production

- reduced mucosal resistance

24
Q

What are the complications of ulcers?

A
  • bleed, block or burst
  • can have penetration of adjacent organs
  • can have malignant changes altho rare in gastric ulcers and never in duodenal
25
Q

Describe the defined structure of ulcers

A
  • granulation tissue at base
  • underlying inflammation and fibrosis
  • loss of muscularis propria