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1Principles of Biomedicine - MD1 > 116 - Acute gastritis > Flashcards

116 - Acute gastritis Flashcards

1
Q

How quickly does acute gastritis heal?

A

A few days, because of rapid cell turnover in stomach.

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2
Q

What is acute gastritis often a response to?

A

Most commonly an acute response to a chemical injury,
alcohol or drugs (NSAIDs, aspirin, iron tablets and other
drugs), stress, shock, burns, head injury, septicaemia,
staphylococcal food poisoning

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3
Q

How does acute gastritis arise?

A

Due to breakdown of gastric barrier directly or via

microcirculatory changes accompanying shock or sepsis.

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4
Q

Chronic superficial gastritis histology

A

No erosion of stomach wall

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5
Q

More severe outcome of gastritis

A

Release of inflammatory mediators results in
vasodilatation, oedema, haemorrhage and erosions -
acute haemorrhagic or erosive gastritis

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6
Q

How can head injury lead to gastritis?

A

Can stimulate gastric acid secretion by affecting brain

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7
Q

Erosive ulcer

A

Degradation of mucosa

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8
Q

Acute ulcer

A

Degradation of mucosa, muscularis mucosae

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9
Q

Chronic ulcer

A

Degradation until subserosa, with fibrosis.

Scarring prevents regeneration of mucosa.

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10
Q

Cushing ulcers

A

Gastric and duodenal ulcers in persons with intracranial

injury

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11
Q

Curling ulcers

A

Ulcers in proximal duodenum associated with severe

burns/trauma

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12
Q

Three main types of chronic gastritis

A

– Autoimmune
– Helicobacter-associated
– Chemical

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13
Q

Other types of chronic gastritis (less common)

A

– Granulomatous (EG: Crohn’s disease)
– Lymphocytic
– Eosinophilic etc.

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14
Q

Autoimmune gastritis aetiology

A

Immune mediated destruction of acid secreting tubules
followed by atrophy with consequent achlorhydria and
loss of intrinsic factor leading to pernicious anaemia
(B12 deficiency)

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15
Q

Autoimmune gastritis areas affected

A

Confined to the gastric corpus (body) mucosa with total

loss of parietal cells. Antrum spared.

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16
Q

Effect of autoimmune gastritis

A

Loss of acid and parietal cells causes hypergastrinaemia
which leads to linear and nodular ECL hyperplasia and
occasionally to carcinoidosis.

Acid-secreting tubules aren’t regenerated, but enterochromaffin cells and D cells proliferate.

17
Q

Autoantibodies generated in autoimmune gastritis

A 
Circulating autoantibodies to parietal cell membrane –
H+/K+ ATPase (90%) and intrinsic factor (70%) and
gastrin receptor (70%).
18
Q

Absorption issue in autoimmune gastritis

A

IF-Ab is secreted into the gastric lumen and can
complex with vitamin B12 preventing its absorption via
receptors in the terminal ileum

19
Q

What characterises histology of autoimmune gastritis?

A

Normal antrum.
Gastric body acid secreting mucosa atrophy.
Linear and nodular hyperplasia of enterochromaffin-like cells

Total atrophy of acid secreting tubules, replaced by intestinal and pyloric gland metaplasia accompanied by
chronic inflammation

20
Q

How does chemical gastritis come about?

A

Reflux of bile and alkaline duodenal juice due to alteredantro-duodenal motility or gastro-jejunostomy.

Long-term use of Aspirin, NSAIDs have a similar effect

21
Q

Effects of chemical gastritis

A

Direct mucosal injury - disruption of the mucus layer and gastric barrier, epithelial desquamation

22
Q 
Histology of chemical gastritis 
1
2
3
4
5
6
7
A

There is compensatory foveolar hyperplasia
Elongation and tortuosity of gastric pits
Vasodilatation and oedema
Fibromuscular hyperplasia of the lamina propria
Only mild inflammatory cell infiltration.

  • Erosions/ulceration may result.
  • Intestinal metaplasia can occur
23
Q 
Colonisation factors of H pylori
1
2
3
4
A

Motility
Microaerophilic
Adhesins
Urease

24
Q

Epidemiology of H pylori in Australia

A

More prevalent in later life (increase in prevalence after ~40 years)

25
Q

Type of gastritis from H pylori
1
2
3

A

1) Neutrophilic gastritis (soluble antigens and chemoattractants, IL-8)
2) Infiltration with chronic inflammatory cells
3) IgM, IgG, IgA appear at about 4 weeks, but don’t offer protection

26
Q

Histology of H pylori
1
2

A

1) Tend to cluster around epithelial tight juncitons
2) Acute foveolitis with clusters of intraepithelial neutrophils, pit abscess and mixed neutrophilic and lymphoplasmacytic infiltration of the lamina propria

27
Q 
Timeline of H pylori infection (serious) 
1
2
3
4
5
6
A

1) Normal mucosa
2) Chronic gastritis
3) Atrophic gastritis
4) Intestinal metaplasia
5) Dysplasia
6) Adenocarcinoma

28
Q

Cancer that can arise from H pylori infection

A

Marginal zone lymphoma (B cell)

29
Q

Two main patters of H pylori gastritis

A

1) Antrum-dominant

2) Pan-gastritis

30
Q 
Antrum dominant gastritis
1
2
3
4
5
A

1) Chronic inflammation and polymorphs
2) Increased acid output
3) Gastric metaplasia in duodenum
4) Active chronic inflammation in duodenum
5) Duodenal ulcer can arise

31
Q 
Pan-gastritis 
1
2
3
4
5
6
A

1) Chronic inflammation, polymorphs
2) Atrophy
3) Intestinal metaplasia
4) Reduced acid output
5) Normal duodenum
6) Gastric ulcer can arise

32
Q

Antrum-dominant gastritis

A

1) Increased acid load
2) Leads to low duodenal pH
3) Leads to Gastric foveolar cell metaplasia of D1 mucosa
4) Colonisation of duodenum by H pylori
5) Active chronic duodenitis +/- erosion
6) Duodenal ulcer

33
Q 
Diseases associated with H pylori
1
2
3
4
5 a, b
A

• Peptic ulcer disease (lifetime risk 1 in 6)
• Gastric adenocarcinoma – lifetime risk related to prevalence
of HP associated atrophic gastritis (1.5%-UK to 19%-China)
• Gastric B-Cell Lymphoma of MALT
• Iron Deficiency Anaemia
• Atrophic gastritis
– Susceptibility to bacterial
gastroenteritis
– B12 deficiency

34
Q

Where are peptic ulcers most common?

A

D1, antrum

35
Q

Other sites of peptic ulcers
1
2
3

A

– Oesophagus at squamocolumnar junction
with gastric cardia or Barrett’s mucosa
– Gastro-enterostomy stoma -
anastomotic/stomal ulcer
– Meckel’s diverticulum – 25% have heterotopic
gastric mucosa and peptic ulceration occurs if
colonised by H. pylori

36
Q

Four zones of chronic peptic ulcer floor

A
  1. Exudate of fibrin, neutrophils and necrotic debris.
  2. Narrow zone of fibrinoid necrosis
  3. Zone of cellular granulation tissue
  4. Zone of fibrosis including endarteritis and hypertrophied nerves
37
Q 
Complications of peptic ulcers
1
2
3
4
A

1) Perforate
2) Haemorrhage
3) Penetrate (erosion into an adjacent organ)
4) Stenosis (contraction of scar can stenose pyloric canal)

38
Q

Where can peptic ulcers penetrate to?

A

Often into pancreas.

39
Q

Potential cause of haemetemesis, melaena

A

Haemorrhaging peptic ulcer

1Principles of Biomedicine - MD1 (157 decks)

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