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Acute & Chronic Gastritis Flashcards

(71 cards)

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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
What is a chronic ulcer?
Where the damage goes into the serosa and fibrosis occurs
26
What causes stress ulcers?
shock, sepsis or severe trauma
27
What are curling ulcers?
Ulcers in proximal duodenum associated with burns/trauma
28
What are cushing ulcers?
gastric and duodenal ulcers in persons with intracranial injury
29
What causes heamatemesis in ulcers?
If the erosion damages an artery
30
What is chronic gastritis?
Gastritis for longer than 3 months
31
What are the 3 main types of chronic gastritis?
Autoimmune, bacterial (helicobacter associated), chemical
32
Which of these is the rarest form?
autoimmune gastritis
33
What is autoimmune gastritis?
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
What is intrinsic factor?
A glycoprotein produced by parietal cells required for B12 absorption
35
Which part of the GIT does autoimmune gastritis effect?
gastric corpus - antrum is spared
36
What is the result of the loss of acid?
Lots of gastrin which leads to ECL cell hyperplasia
37
What does autoimmune gastritis sometimes lead to?
the hyperplasia of ECL cells may cause carcinoidosis
38
What autoantibodies are present in autoimmune gastritis?
H+/K+ATPase, intrinsic factor, gastrin receptor
39
How does the intrinsic factor antibody cause absorption of B12 in the ileum?
By binding to B12 and forming a complex
40
What blood test is used for autoimmune gastritis?
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
What type of metaplasia occurs in autoimmune gastritis?
intestinal and pyloric gland metaplasia in the gastric body
42
What are some causes of chemical gastritis?
reflux of bile and alkaline duodenal juices, long term use of NSAIDs
43
What is the body’s response to chemical gastritis?
compensatory foveolar hyperplasia, elongation and tortuosity of gastric pits, vasodilation, oedema, fibromuscular hyperplasia of the lamina propria and mild inflammatory cell infiltration
44
What else may occur in chemical gastritis?
erosions/ulceration and intestinal metaplasia
45
How do H. pylori survive the high acid content of the stomach?
They colonise the area of the stomach protected by bicarbonate and mucus
46
What is urease (from H. pylori)?
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
What is the response in an acute H. pylori infection?
acute inflammatory response, transient hypochlorhydria followed by infiltration with chronic inflammatory cells
48
Where do you see lots of neutrophils?
Intraepithelial and in the lamina propria
49
Where do you see lymphocytes?
In the lamina propria
50
Can an infection of H. pylori be cleared by the body?
generally no
51
Where do H. pylori selectively attach to?
intercellular junctions - results in breakdown of junctions which allows acid to get in
52
What is the long term result of a chronic H. pylori infection?
mucosal atrophy and intestinal metaplasia
53
What may be the result of the intestinal metaplasia?
adenocarcinoma
54
What other cancer may be caused by chronic H. pylori infection?
B-cell lymphoma of MALT
55
What is the main long term outcome of antral predominant gastritis?
duodenal ulcer due to colonisation of duodenum by H. pylori
56
What is the main long term outcome of multifocal atrophic gastritis?
In younger patients gastric ulcer and in older patients gastric cancer
57
What are the two major patterns of H. pylori gastritis?
antrum-predominant or pan gastritis
58
What happens to acid output in antrum-predominant or pan gastritis?
increased acid secretion in antrum-predominant and decreased acid in pan gastritis
59
What is at risk in antrum predominant?
duodenal ulcers
60
What is at risk in pan gastritis?
cancer - adenocarcinoma and B cell lymphoma
61
What diseases are associated with H. pylori infections?
peptic ulcer disease, gastric adenocarcinoma, gastric B cell lymphoma of MALT, iron defieiceny anemia, atrophic gastritis
62
What deficiency may be caused by atrophic gastritis?
B12 deficiency
63
What is the most common cause of peptic ulcers?
H. pylori
64
What are the common sites of peptic ulcers?
D1 and antrum, oesophagus Z line, gastro-enterostomy stoma (surgical connective between stomach and jejunum), Meckel’s diverticulum
65
What is the difference between acute and chronic peptic ulcers?
acute ulcers are superficial and heal well where as chronic is deep and has scarring
66
What does a chronic ulcer look like macroscopically?
There are mucosal folds radiating up to the border and sometimes an acute inflammatory exudate
67
What are the 4 layers of the floor of a chronic ulcer?
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
What are the complications of peptic ulcer disease?
perforation leading to generalised peritonitis, haemorrhage, penetration into an adjacent organ, stenosis
69
What artery is commonly perforated by an ulcer in the duodenum?
gastroduodenal
70
What does a gastric carcinoma look like macroscopically?
The folds of the mucosa won’t go right up to the carcinoma
71
What are other types of gastric carcinomas not caused by gastritis?
diffuse type gastric carcinoma and signet-ring cell carcinoma

Gastrointestinal (40 decks)

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