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Gastrointestinal > Acute & Chronic Gastritis > Flashcards

Acute & Chronic Gastritis Flashcards

1
Q

What receptors are present on parietal cells?

A

acetylcholine receptors, histamine receptors, somatostatin receptors, gastrin receptors

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2
Q

Where does the acetylcholine come from?

A

The vagus nerve

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3
Q

Where does the histamine come from?

A

ECL cells

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4
Q

Where do ECL cells get input from?

A

stimulatory from the vagus nerve and inhibitory from somatostatin from D cells

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5
Q

Where does the somatostatin come from?

A

Via paracrine action from gastric D cells and endocrine action from antrum D cells

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6
Q

Where does the gastrin come from?

A

Via endocrine action from antrum G cells

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7
Q

Where do D cells get input from?

A

stimulatory from gastrin and inhibitory from the vagus nerve

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8
Q

Where do G cells get input from?

A

stimulatory from the vagus nerve and inhibitory from somatostatin from D cells

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9
Q

What prevents the stomach from digesting itself?

A

A thick layer of mucus and bicarbonate

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10
Q

What is on the surface of the layer of mucus?

A

A hydrophobic monolayer

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11
Q

Where does the bicarbonate come from?

A

It is secreted by surface mucus cells

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12
Q

What is the pH in the lumen of the stomach?

A

2

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13
Q

What is the pH of the epithelium of the stomach?

A

7

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14
Q

What damages the mucosal barrier?

A

H. pylori, aspirin, NSAIDs, bile, alcohol

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15
Q

What is the response when acid accesses the mucosa?

A

resident mast cells secrete histamine and initiate inflammation

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16
Q

How do prostaglandins prevent and reverse mucosal injury?

A

inhibit acid secretion, stimulate bicarbonate and mucus secretion, increase mucosal blood flow and modify local inflammation

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17
Q

How often does the mucosa regenerate?

A

Every 2 days

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18
Q

What is acute gastritis?

A

An acute response to injury which heals in a few days

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19
Q

What are the common causes of acute gastritis?

A

chemical injury, alcohol, drugs, stress, shock, burns, head injury, septicaemia, staphylococcal food poisoning

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20
Q

What is the result of inflammatory mediators acting in response to acute gastritis?

A

vasodilation, oedema, haemorrhage, errosions

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21
Q

What is an erosion?

A

A defect in the mucosa above the muscularis mucosae

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22
Q

What happens in an erosion?

A

There is a layer of coagulative necrosis and inflammation is inhibited

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23
Q

What cells are present in chronic superficial gastritis?

A

plasma cells, eosinophils, neutrophils

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24
Q

What is an acute ulcer?

A

Where the damage goes into the muscularis mucosae

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25
Q

What is a chronic ulcer?

A

Where the damage goes into the serosa and fibrosis occurs

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26
Q

What causes stress ulcers?

A

shock, sepsis or severe trauma

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27
Q

What are curling ulcers?

A

Ulcers in proximal duodenum associated with burns/trauma

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28
Q

What are cushing ulcers?

A

gastric and duodenal ulcers in persons with intracranial injury

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29
Q

What causes heamatemesis in ulcers?

A

If the erosion damages an artery

30
Q

What is chronic gastritis?

A

Gastritis for longer than 3 months

31
Q

What are the 3 main types of chronic gastritis?

A

Autoimmune, bacterial (helicobacter associated), chemical

32
Q

Which of these is the rarest form?

A

autoimmune gastritis

33
Q

What is autoimmune gastritis?

A

An immune mediated destruction of parietal cells which leads to atrophy, no acid production and no production of intrinsic factor leading to pernicious anemia (B12 deficiency) - the antrum is spared

34
Q

What is intrinsic factor?

A

A glycoprotein produced by parietal cells required for B12 absorption

35
Q

Which part of the GIT does autoimmune gastritis effect?

A

gastric corpus - antrum is spared

36
Q

What is the result of the loss of acid?

A

Lots of gastrin which leads to ECL cell hyperplasia

37
Q

What does autoimmune gastritis sometimes lead to?

A

the hyperplasia of ECL cells may cause carcinoidosis

38
Q

What autoantibodies are present in autoimmune gastritis?

A

H+/K+ATPase, intrinsic factor, gastrin receptor

39
Q

How does the intrinsic factor antibody cause absorption of B12 in the ileum?

A

By binding to B12 and forming a complex

40
Q

What blood test is used for autoimmune gastritis?

A

A blood test which detects the levels of gastrin - this should be high because there is no acid to stimulate somatostatin release so nothing inhibits gastrin production

41
Q

What type of metaplasia occurs in autoimmune gastritis?

A

intestinal and pyloric gland metaplasia in the gastric body

42
Q

What are some causes of chemical gastritis?

A

reflux of bile and alkaline duodenal juices, long term use of NSAIDs

43
Q

What is the body’s response to chemical gastritis?

A

compensatory foveolar hyperplasia, elongation and tortuosity of gastric pits, vasodilation, oedema, fibromuscular hyperplasia of the lamina propria and mild inflammatory cell infiltration

44
Q

What else may occur in chemical gastritis?

A

erosions/ulceration and intestinal metaplasia

45
Q

How do H. pylori survive the high acid content of the stomach?

A

They colonise the area of the stomach protected by bicarbonate and mucus

46
Q

What is urease (from H. pylori)?

A

an enzyme that breaks urea down into ammonia - ammonia is toxic to cells - does it so that the bacteria can create CO2 which will bind to acid and create a neutral environment

47
Q

What is the response in an acute H. pylori infection?

A

acute inflammatory response, transient hypochlorhydria followed by infiltration with chronic inflammatory cells

48
Q

Where do you see lots of neutrophils?

A

Intraepithelial and in the lamina propria

49
Q

Where do you see lymphocytes?

A

In the lamina propria

50
Q

Can an infection of H. pylori be cleared by the body?

A

generally no

51
Q

Where do H. pylori selectively attach to?

A

intercellular junctions - results in breakdown of junctions which allows acid to get in

52
Q

What is the long term result of a chronic H. pylori infection?

A

mucosal atrophy and intestinal metaplasia

53
Q

What may be the result of the intestinal metaplasia?

A

adenocarcinoma

54
Q

What other cancer may be caused by chronic H. pylori infection?

A

B-cell lymphoma of MALT

55
Q

What is the main long term outcome of antral predominant gastritis?

A

duodenal ulcer due to colonisation of duodenum by H. pylori

56
Q

What is the main long term outcome of multifocal atrophic gastritis?

A

In younger patients gastric ulcer and in older patients gastric cancer

57
Q

What are the two major patterns of H. pylori gastritis?

A

antrum-predominant or pan gastritis

58
Q

What happens to acid output in antrum-predominant or pan gastritis?

A

increased acid secretion in antrum-predominant and decreased acid in pan gastritis

59
Q

What is at risk in antrum predominant?

A

duodenal ulcers

60
Q

What is at risk in pan gastritis?

A

cancer - adenocarcinoma and B cell lymphoma

61
Q

What diseases are associated with H. pylori infections?

A

peptic ulcer disease, gastric adenocarcinoma, gastric B cell lymphoma of MALT, iron defieiceny anemia, atrophic gastritis

62
Q

What deficiency may be caused by atrophic gastritis?

A

B12 deficiency

63
Q

What is the most common cause of peptic ulcers?

A

H. pylori

64
Q

What are the common sites of peptic ulcers?

A

D1 and antrum, oesophagus Z line, gastro-enterostomy stoma (surgical connective between stomach and jejunum), Meckel’s diverticulum

65
Q

What is the difference between acute and chronic peptic ulcers?

A

acute ulcers are superficial and heal well where as chronic is deep and has scarring

66
Q

What does a chronic ulcer look like macroscopically?

A

There are mucosal folds radiating up to the border and sometimes an acute inflammatory exudate

67
Q

What are the 4 layers of the floor of a chronic ulcer?

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 which may damage nerves and vessels
68
Q

What are the complications of peptic ulcer disease?

A

perforation leading to generalised peritonitis, haemorrhage, penetration into an adjacent organ, stenosis

69
Q

What artery is commonly perforated by an ulcer in the duodenum?

A

gastroduodenal

70
Q

What does a gastric carcinoma look like macroscopically?

A

The folds of the mucosa won’t go right up to the carcinoma

71
Q

What are other types of gastric carcinomas not caused by gastritis?

A

diffuse type gastric carcinoma and signet-ring cell carcinoma

Gastrointestinal (40 decks)

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