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MD3002 > *Gastro-Oesophageal Inflammation and Peptic Ulceration > Flashcards

*Gastro-Oesophageal Inflammation and Peptic Ulceration Flashcards

1
Q

Identify the main types of oesophagitis.

A

Acute and chronic

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2
Q

Identify the main features of acute oesophagitis, especially how it comes about.

A

ACUTE OESOPHAGITIS

  • Corrosives
  • Infection in immunosuppressed patients (e.g. HIV, immunosuppressive treatment after transplant)
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3
Q

Identify the main organisms responsible for infection of immunosuppressed patients causing acute oesophagitis.

A
  • Candida
  • Herpes Simplex Virus
  • Cytomegalovirus
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4
Q

Identify the main types of chronic oesophagitis.

A

CHRONIC OESOPHAGITIS

  • Specific chronic oesophagitis
  • Non-specific chronic oesophagitis (i.e. reflux oesophagitis, i.e. contents from stomach travelling upwards to oesophagus and causing inflammation)
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5
Q

How does specific chronic oesophagitis come about ?

A
  • Tuberculosis
  • Bullous pemphigoid and Epidermolysis bullosa
  • Crohn’s disease
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6
Q

Describe the histology of acute oesophagitis due to each of CMV and HSV.

A

CMV: Nuclear and cytoplasmic inclusion
HSV: Multinucleate squamous cells with nuclear inclusions only (macroscopically, note ulcers)

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7
Q

What is the main cause of reflux (non specific chronic) oesophagitis ? Identify some predisposing factors to reflux oesophagitis.

A

GORD, usually due to incompetent GO junction.

Predisposing factors to reflux oesophagitis include:

  • Alcohol and tobacco
  • Obesity
  • Motility disorders
  • Hiatus hernia (part of stomach through diaphrahm and into thoracic cavity)
  • Drugs (e.g. caffeine)
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8
Q

What is the type of cell which lines the oesophagus normally ?

A

Stratified squamous epithelium

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9
Q

What are the main pathophysiological traits of reflux oesophagitis ?

A
  • Eosinophil epithelial infiltration
  • Basal cell hyperplasia (because epithelium cannot cope with strong acid being refluxed)
  • Chronic inflammation
  • Severe reflux also leads to ulceration (epithelium shed, exposing lamina propria), which may lead to healing by fibrosis, including strictures and potential obstruction (i.e. dysphagia)
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10
Q

Explain the differences in lining of the oesophagus between health and reflux oesophagus.

A

NORMAL: stratified squamous epithelium

REFLEX OESOPHAGITIS: Basal cell hyperplasia, thickness of epithelium bigger, papilla of lamina propria between sets of epithelia getting deeper

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11
Q

Describe the main histological features of reflux oesophagitis.

A
  • Scattered intra-epithelial eosinophils
  • Basal zone hyperplasia
  • Hyperchromatic cells
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12
Q

What is Barrett’s oesophagus ?

A

Consequence of long standing reflux (long standing GORD)

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13
Q

Describe the epidemiology of Barrett’s oesophagus.

A

Males more affected than females

Ages 40 to 60 especially affected

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14
Q

Describe the histology of Barrett’s oesophagus.

A
  • Stratified squamous epithelium lining the lower oesophagus is replaced by simple columnar epithelium (i.e. intestinal metaplasia)
  • Goblet cells are present (normally in the intestines)
  • Chronic inflammatory cells also present (lymphocytes, plasma cells)
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15
Q

What are the main causes of Barrett’s oesophagus.

A
  • H pylori infections seems to predispose patients to Barrett’s oesophagus
  • Combination of biliary and gastric reflux gives higher risk
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16
Q

What is the special feature of Barrett’s oesophagus ?

A

It is premalignant - risk of adenocarcinoma of the distal oesophagus is 100x that of the general population

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17
Q

What is the examination of choice for investigation ?

A

Gastroscopy

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18
Q

What must Barrett oesophagitis patients undergo regular gastroscopies ?

A

Because Barrett’s oesophagus is pre-malignant

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19
Q

How do we managed Barrett’s oesophagitis ?

A

Minimizing acid content

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20
Q

Identify the main types of stomach inflammation.

A

Acute gastritis

Chronic gastritis

21
Q

What are the main causes of acute gastritis ?

A
  • Usually due to chemical injury (something chemical brought into stomach, such as drugs including NSAIDs or alcohol) to the stomach mucosa
  • Often H pylori associated
22
Q

What are the main types/causes of chronic gastritis ?

A
  • Active chronic (H. pylori associated)
  • Autoimmune (antibodies, often against parietal cells, leading to increased production of HCl)
  • Chemical (reflux), contents of the duodenum (including bile, which is basic pH) damage mucosa
23
Q

True or False: Acute chronic gastritis also exists.

A

True

24
Q

Describe the timeline of acute gastritis associated to H pylori.

A

Usually just a triansient phase, as it often becomes chronic.

25
Q

H Pylori.

  • Structure/kind of pathogen
  • Transmission
  • Habitat
A

H Pylori

  • Structure/Kind: gram negative, spiral shaped or curved bacilli
  • Transmission: oral-oral, faecal-oral, environmental spread
  • Habitat: niche beneath mucus and above epithelium, at above neutral pH (does NOT colonise intestinal type epithelium)
26
Q

What percentage of active chronic gastritis is H Pylori found in ?

A

H pylori is found in 90% of active chronic gastritis

27
Q

What conditions/symptoms is H Pylori associated with ?

A

Conditions:

  • Causative factor in gastric and duodenal ulcers
  • Risk factor for gastric cancer (adenocarcinoma)
  • Strong link with MALT (Mucosa associated Lymphoid Tissue) Lymphoma

Symptoms:

  • Dysphagia
  • Atrophic gastritis (thinning wall of stomach)
  • Iron deficiency anaemia (e.g. if eroded some blood vessels)
  • Idiopathic thrombocytopenic (low number of platelets) purpura (a small hemorrhage in the skin)
28
Q

Explain the pathogenesis of H pylori infection of the stomach.

A
  • H pylori survive gastric strong acid
  • With flagella, will dive into niche with neutral pH, between mucosa and epithelium
  • Produce urease to cause higher production of HCl by parietal cells in stomach
  • Higher HCl allows colonisation by H pylori
  • Mucosal surface, which protects epithelium is damaged by HCl so epithelium is exposed to HCl, which then destroys surface epithelium of stomach
  • Damaged epithelium means inflammatory cells, both acute and chronic accumulate, cells die, ulcer can occur
29
Q

Distinguish between acute and chronic H pylori gastritis.

A

SYMPTOMS:
Acute- nausea, dyspepsia, malaise, halitosis
Chronic- local inflammation and gastritis (so symptoms of those)

TIMELINE:
Acute- tends to last about two weeks (after that, becomes chronic)
Chronic- months

CELLS INVOLVED:
Acute: Intraepithelial and lamina propria neutrophils infiltration (gastric mucosa also inflamed by neutrophils). Also persistant lymphocyte penetration (as starts going towards chronic phase)
Chronic: Lymphoid aggregates, with plasma cells infiltrate in lamina propria

30
Q

What does the outcome of chronic H pylori infection depend on ?

A
  • Pattern of inflammation
  • Bacterial virulence
  • Host response
  • Environmental factors
  • Patient age
31
Q

Identify the main distribution patterns of H pylori infection. Describe the main features of each.

A

1) Diffuse involvement of antrum and body
- Atrophy (of surface mucosa), fibrosis, intestinal metaplasia
- Associated with gastric ulcer and gastric cancer

2) Antral but not body involvement
- Gastric secretions increased
- Associated with duodenal ulcer (due to increased HCl, getting into duodenum)

32
Q

CHEMICAL (CHRONIC) GASTRITIS

  • Cause/mechanism
  • Histology
  • Clinical
A

CHEMICAL (CHRONIC) GASTRITIS
Cause: Due to regurgitation of bile and alkaline duodenal secretions into stomach, causing direct injury and disruption of mucus layer. This can be due to defective pylorus (e.g. relaxed pyloric sphincter) and motility disorders (e.g. stomach not contracting properly to push bolus into duodenum)

Histology: Loss of epithelial cells with compensatory hyperplasia of gastric foveolae + few inflammatory cells

Clinical: Gastric erosions + gastric ulcers

33
Q

AUTOIMMUNE (CHRONIC) GASTRITIS

  • Define it
  • Histology
  • Clinical
  • Special features
A

AUTOIMMUNE (CHRONIC) GASTRITIS
Definition: Serum antibodies to gastric parietal cells and intrinsic factor leading to loss of acid secretion (hypochlorhydria / achlorhydria) and loss of intrinsic factor (→ vitamin B12 deficiency → macrocytic pernicious anemia)

Histology: Marked glandular atrophy in gastric body and intestinal metaplasia (simple columnar epithelium, including Goblet cells) + lymphocytes infiltration

Clinical: Pernicious anaemia

Special features: Increased risk of gastric cancer (adenocarcinoma)

34
Q

Why is autoimmune gastritis easy to diagnose ?

A

Because can do blood test to detect serum antibodies to parietal cells/intrinsic factor

35
Q

H PYLORI CHRONIC GASTRITIS

  • Mechanism
  • Histology
  • Clinical
A

H PYLORI CHRONIC GASTRITIS

Mechanism: Cytotoxins + immune response (refer to pathogenesis of H pylori stomach infection flashcards)

Histology: Active chronic inflammation + atrophy + intestinal metaplasia

Clinical: Peptic ulceration, possibly gastric cancer

36
Q

Define peptic ulceration.

A

Breach in mucosal lining of the alimentary tract as a result of acid and pepsin attack.

37
Q

Identify the main sites of peptic ulceration.

A
  • Distal part of esophagus
  • Junction of antral and body mucosa of stomach
  • First part of duodenum
  • Gastro-enterostomy stoma
38
Q

Identify risk factors for peptic ulcers.

A
  • Hyperacidity
  • H pylori gastritis
  • Duodenal reflux
  • NSAIDs
  • Smoking
  • Genetics
  • Zollinger-Ellison syndrome (pancreas tumor that can cause stomach to produce high levels of HCl)
39
Q

Identify possible complications of peptic ulcers.

A
  • Haemorrhage (may hit blood supply of gastric artery or gastroepiploic artery)
  • Penetration of adjacent organs (e.g. pancreas)
  • Perforation
  • Anaemia (e.g. if haemorrhage)
  • Obstruction (particularly when close to pylorus, then obstruction of pyloric sphincter)
  • Malignancy (gastric adenocarcinoma) (rare in gastric ulcers, ‘never’ in duodenal ulcers)
40
Q

Distinguish between gastric and duodenal ulcers, in terms of:

  • incidence
  • age
  • blood group
  • Acid level
  • H Pylori gastritis
A
  • incidence: 3 to 1 for duodenal ulcers
  • age: Increases with age (G), Increases up to 35 (D)
  • blood group: A (G), O (D)
  • Acid levels: Normal or low (G), high or normal (D)
  • H Pylori gastritis: about 70% (G), 95-100% (D)
41
Q

What is the most common presenting complaint for patients with peptic ulcers ?

A

Heartburn and high epigastric pain

42
Q

What are possible causes of acute peptic ulcers ? Identify the characteristic feature of each.

A

1) related to acute gastritis (full thickness loss of epithelium, rather than just erosion)
2) related to a stress response (e.g. Curling’s ulcer following severe burns)
3) related to extreme hyperacidity (e.g. gastrin-secreting tumours)

43
Q

What are possible causes of chronic peptic ulcers ?

A
  • Mainly: hyperacidity, or mucosal defense defects (mucus-bicarbonate barrier dissolved by biliary reflux) or combination of both
  • Minor role: surface epithelium can be damaged by NSAIDs or injured by H pylori.
44
Q

Where do chronic peptic ulcers tend to occur ?

A

Chronic peptic ulcers tend to happen in mucosal junctions (e.g. antrum-body junction)

45
Q

What is the normal pH of gastric juice ?

A

1-2

46
Q

Describe the histology of peptic ulcers.

A

Sharply punched out with defined edges and structure:
-Loss of epithelium at surface, and of mucosa, and of muscularis propria
From superficial to deep:
-Layer of necrotic debris
-Layer of acute inflammatory cells (eat away dead cells from surface)
-Layer of granulation tissue trying to protect exposed area of ulcer by creating new blood vessels, new capillaries, new fibroblasts
-Layer of fibrosis

47
Q

You identified causes of chronic peptic ulcers. What are possible causes of duodenal chronic ulcers specifically ?

A

-STILL hyperacidity (more important than for gastric ulcers, can be induced by H pylori) and mucosal defense defects (gastric metaplasia occurs due to hyperacidity, then colonised by H pylori)

48
Q

Describe the histology of peptic ulcers.

A

Sharply punched out with well defined edges and structure:

  • Granulation tissue at base
  • Underlying inflammation and fibrosis
  • Loss of muscularis propria
49
Q

How big are peptic ulcers usually ?

A

Usually, peptic ulcers are small (<20 mm)

MD3002 (95 decks)

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