3. Gastro-Oesophageal Inflammation and Peptic Ulceration Flashcards

1
Q

Inflammatory disorders of the oesophagus?

A
Acute:
Infection in immunocompromised patients. E.g. 
• Herpes simplex viruses
• Candida
• Cytomegalovirus(CMV)
– Corrosives 
Chronic:
Specific. E.g.
• Tuberculosis
• Bullous pemphigoid and Epidermolysis bullosa 
• Crohn’sdisease
Non-specific E.g.
• Reflux oesophagitis
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2
Q

What is GORD?

A

Gastro-oesophageal reflux disease

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3
Q

Causes for reflux oesophagitis (6)

Consequence? Leading to 3 pathologies?

A
• Regurgitation of gastric contents
– Gastro-oesophageal reflux disease (GORD)
– ‘Incompetent’ GO junction
• Alcohol and tobacco
• Obesity
• Drugs e.g. caffeine!
• Hiatus hernia
• Motility disorders

Squamous epithelium damaged –>
– Eosinophils epithelial infiltration
– Basal cell hyperplasia
– Chronic inflammation

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4
Q

Consequences of reflux oesophagitis

A

Severe reflux leads to ulceration. Leading to fibrosis = stricture + obstruction.

Oesophagus narrower and more rigid

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5
Q

What is Barrett’s oesophagus?
Risk?
Diagnosis?

A

Longstanding reflex
Aged 40-60
Lower oesophagus becomes lined by columnar epithelium due to intestinal metaplasia

Risk? 100 times more likely to get adenocarcinoma of distal oesophagus

Diagnosis: Gastroscopy reveals red appearance of oesophagus

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6
Q

Two classifications of gastric inflammation?

A

Acute gastritis:

  • Usually due to chemical injury (e.g. drugs / alcohol)
  • H pylori- associated

Chronic gastritis:

  • Active chronic (H pylori associated)
  • Auto immume
  • Chemical (reflux)
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7
Q

H pylori-associate gastritis:

  • Bacteria shape?
  • Transmission?
  • Occupies?
  • Condition associated with?
  • Treatment?
  • Two distribution patterns?
  • Detections?
A

Bacteria shape?
-Gram negative spiral-shaped or curved bacilli

Transmission;
-Oral-oral, faecal-oral, environmental spread.

Occupies?

  • Occupies protected niche beneath mucus where pH approx 7
  • Does not colonise intestinal type eptithelium

Condition associated with?
-90% active chronic gastritis

Treatment?
-Resolves with therapy (double antibiotics + proton pump inhibitors)

Two distribution patterns:
1. Diffuse involvement of antrum and body
• Atrophy, fibrosis, intestinal metaplasia
• Associated with gastric ulcer and gastric cancer
2. Antral but not body involvement • Gastric acid secretion increased
• Associated with duodenal ulcer

Detection:
-Faecal bacterial, urea breath test, gastric biopsy rapid urease test

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8
Q

Chemical (reflux) gastritis:
Caused by?
Results in…
Associated with?

A

Caused by: Regurgitation of bile and alkaline duodenal secretion

Results in loss of epithelial cells with compensatory hyperplasia of gastric foveae

Associated with:

  • Defective pylorus
  • Motility disorders
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9
Q

Autoimmune chronic gastritis:
What is it? What happens?
Association?
Risk?

A

What is it? What happens?
Autoimmune reaction to gastric parietal cells. Serum antibodies to gastric patietal cells and intrinsic factor.
Loss of acid secretion (hypochlorhydria/achlorhydria)
Loss of intrinsic factor
–> Vit B12 deficiency
–>Macrocytic anaemia (pernicious anaemia)

Association?
With gastric atrophy and intestinal metaplasia

Risk?
Gastric cancer

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10
Q

What are the 3 causes for chronic gastritis?

A
  1. Autoimmune
  2. Bacterial infection (H pylori)
  3. Chemical injury
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11
Q

Peptic ulceration:
What is it? Caused by?
Major sites of ulceration?

A

What is it? Caused by?
Breach in mucosal lining of alimentary tract as a result of acid and pepsin attack

Major sites:
– First part of duodenum
– Junction of antral and body mucosa in stomach 
– Distal oesophagus
– Gastro-enterostomy stoma
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12
Q

Causes for peptic ulcers?

A
– Hyperacidity
– H pylori gastritis 
– Duodenal reflux 
– NSAIDs
– Smoking
– Genetic factors
– Zollinger-Ellison syndrome
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13
Q

Complications of peptic ulceration?

A
– Haemorrhage
– Penetration of adjacent organs e.g. pancreas
– Perforation
– Anaemia
– Obstruction
– Malignancy
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14
Q

Causes for acute peptic ulcers

A

Acute gastritis
Stress response
Extremem hyperacidity

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15
Q

Where to chronic peptic ulcers tend to occur?

A

At mucosal junctions e.g. Antrum- body

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16
Q

CHARACTERIC FEAUTRES OF ALL PEPTIC ULCERS

A
  1. Necrotic debris
  2. Nonspecific acute inflammation
  3. Granulation tissue
  4. Fibrosis
17
Q

Causes of chronic duodenal ulcers?

A
  1. Increased acid production (can be induced by H pylori)
  2. Reduced mucosal resistance.
    - Gastric metaplasia occur in response to hyperacidity
    - Then colonised by H pylori
18
Q

Risk of malignancy in ulcers?

A

Gastric: Rare
Duodenal: “Never”

19
Q

Patholoigy of chronic duodenal ulcer

A

• Usually small (<20 mm)
• Sharply ‘Punched out’ with defined edges
• Defined structure:
-Granulation tissue at base
-Underlying inflammation and fibrosis
-Loss of muscular propria
-Complication such as “Bleed, burst or block”, Penetration of adjacent orange, malignancy

20
Q

What is intrinsic factor?

A

Intrinsic factor (IF), also known as gastric intrinsic factor (GIF), is a glycoprotein produced by the parietal cells of the stomach. It is necessary for the absorption of vitamin B12 (cobalamin) later on in the small intestine.

21
Q

For chronic gastric caused by autoimmune, what is the mechanism + histology + clinical?

A

Mechanism:
Anti-parietal cell and intrinsic factor antibodies

Histology:

  • Glandular atrophy in gastric body
  • Intestinal metaplasia

Clinical:
Pernicious anaemia

22
Q

For chronic gastric caused by bacterial infection of H pylori, what is the mechanism + histology + clinical?

A

Mechanism:
cytotoxins
immune response

Histology:

  • Active chronic inflammation
  • Atrophy
  • Intestinal metaplasia

Clinical:

  • Peptic ulceration
  • ?Gastric cancer
23
Q

For chronic gastric caused by chemical injury, what is the mechanism + histology + clinical?

A

Mechanism:

  • Direct injury
  • Disruption of mucus layer

Histology:

  • Foveolar hyperplasia
  • Few inflammatory cells

Clinical:

  • Gastric erosions
  • Gastric ulcer