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Hugh's MD1 Abdominal > Gastritis, peptic ulcers and celiac's disease > Flashcards

Gastritis, peptic ulcers and celiac's disease Flashcards

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1
Q

How does chemical gastritis appear histologically?

A

Long, turtuous gastric pits

hyperplasia of lamina propria

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1
Q

What are the 5 possible complications of chronic peptic ulcers?

A

Perforation - if there aren’t organ overlying > generalised peritonitis > septicaemia

Penetration - acid into overlying organ (pancreas, liver or colon)

Stenosis - due to scar

Haemorrhage (rapid or slow) - if an artery is eroded

Neoplasm

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1
Q

What are some other causes of intraepithelial lymphocytosis, villi atrophy and crypt hyperplasia?

A

Tropical sprue

Small bowel bacterial overgrowth

Certain Immunodeficiency

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2
Q

What is acute gastritis characterised by?

A

Acute bleeding

Erosion of epithelium

Local inflammation/oedema

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3
Q

How are prostaglandins protective in the stomach?

A

Inhibit gastric acid secretion

Stimulate mucous and bicarbonate secretion

Increase mucosal blood flow

Modifiy local inflammation

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3
Q

What happens if gluten peptide passes through the epithelium?

A

It is deaminated by tissue transglutaminase (tTG) converting glutamine into negatively charged glutamate

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4
Q

Where do H. pylori bacteria sit during infection?

A

Gastric cell surface and intercellular junctions

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5
Q

What pattern of scarring is left post gastric ulceration?

A

Radial

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5
Q

What are the three main types of ulcers?

A

A - Autoimmune

B - Helicobacter pylori

C - Chemicals

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6
Q

How does H. pylori survive in the acid environment of the stomach?

A

Colonises the mucosal barrier

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7
Q

What can damage the mucosal barrier?

A

Helicobacter pylori

Alcohol

NSAIDs

Bile

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7
Q

Which cells are targeted in autoimmune gastritis?

A

Parietal

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7
Q

What can form in the stomach in pan gastritis that usually aren’t present?

A

MALT and subsequent B cell lymphomas

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7
Q

How does damage occur in celiac disease?

A

CD4+ cells releasing TNF-alpha and IL-4

CD8+ cell inducing apoptosis

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8
Q

What on parietal cells do antibodies in autoimmune gastritis target?

A

Na/K ATPase

Intrinsic factor

Gastrin receptor

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8
Q

T/F The lamina propria contains continual mild inflammation?

A

True

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9
Q

Where in the GIT is glucose absorbed?

A

Duodenum

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10
Q

What is the ratio of the villi length to crypt length in the duodenum?

A

4:1

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10
Q

What is the clinical presentation of celiac’s diseaese?

A

GI symptoms: diarrhoea, vomiting, bloating, flatulance

Anaemia vitamin deficiences

Lethargy

Failure to thrive as infant

Other immunopathologies

Osteoporesis

Malabsorption of nutrients

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11
Q

HCl reaching the lamina propria causes what?

A

Activation of mast cell to produce histamine inflammatory mediators

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12
Q

What is the significance of the overhang of folds over the ulcerated tissue in chronic peptide ulcers?

A

Carcinomas don’t have that

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13
Q

Chronic *H. pylori *infection and inflammation can lead to what serious sequelae?

A

Atrophy

Metaplasia > hyperplasia > adenocarcinoma

Lymphoma

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14
Q

What are valves of Kerckring another name for?

A

Circular folds/plica circulares

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16
Q

In which type of gastritis is gastric acid secretion the greatest?

A

Antrum-predominant

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17
In what cause of acute gastritis is there particularly low amounts of inflammation?
NSAID caused
18
What is chemical gastritis caused by?
Reflux of bile and alkaline duodenal juices into the antrum of the stomach
18
What environmental factors contribute to the development of celiacs
Exposure to gluten (eg too much too soon) Breast milk is protective Infections
20
Why is healing in response to acute gastritis quick?
Due to rapid turn over of gastric epithelium 24-48 hours
22
What are the two patterns of gastritis?
Antrum-predominant Pan gastritis
23
What are the peak ages of development of celiac disease?
30-50
24
T/F Everyone with HLA-DQ2 and DQ8 have celiac disease and everyone with the disease have them?
False, 20-30% of the population at risk don't have disease despite having the HLA subtypes. The latter is true
25
What makes a peptic ulcer different from mucosal erosion?
Peptic ulcers penetrate through the muscularis mucosae
25
What does IELs stand for?
Intra-epithelial lymphocytes
26
What are three methods of diagnosis for celiac disease?
Serology for anti tTG or Genetic testing for HLAs Biopsy of intestine after gluten ingestion
27
Which organ is most effected in celiac's disease?
Small intestine
29
What is the average rate of *H. pylori* infection the developing world?
\>80%
30
What colonisation factors does *H. pylori* have?
Adhesins Motility Urease Microaerophilism
32
Do acute peptic ulcers leave radial scars on healing?
No, there is restoration of submucosa and mucosa
33
What HLA subtypes are strongly associated with the development of celiac's disease? In which ethic groups are they most prevalence?
HLA-DQ2, -DQ8 European and Middle Eastern
34
Are IELs CD4 or CD8?
CD8
36
In what age group in chronic inflammation causing cancer most prominent?
\>70+ y.o.
38
How does the body of the stomach look histologically in autoimmune gastritis?
Loss of secreting tubules Greater number of goblet and neuroendrocrine cells Chronic inflammation
39
Where in the GIT is vitamin B12 most absorbed?
Ileum
40
What is the problem is not diagnosing celiacs disease?
It increases the risk of: MALT lymphoma (x30) Oesophageal cancer S. intestine adenocarcinoma Overall mortality (x2)
42
What can happen to the duodenum in antrum-predominant gastritis?
It changes to become more like the stomach \> *H. pylori* can infect it
43
What does Marsh type II celiac's disease look like?
Increase IELs Longer, branched crypts Villi still present but fatter with immune cell infiltration
44
What are Cushing ulcers? What are they caused by?
Ulcers in the stomach or duodenum in response to head injury
45
How does autoimmune gastritis cause anaemia?
Low intrinsic factor \> No B12 absorption \> Anaemia
46
What happens to villi and crypts in advanced celiac disease?
Villis disappear Crypts lengthen
47
Does *H. pylori* usually cause acute gastritis?
No, usually chronic, not self limiting
49
What contributes to pain in chronic peptic ulcers?
Hypertrophied nerves
50
How is gluten able to remain intact and get through the epithelium to act as an antigen?
It is high in proline (35%) and glutamine (20%) that are resistant to acids and proteases
51
In terms of percentage of the total, does *H. pylori *cause more duodenal ulcers or gastric ulcers?
Duodenal
52
What happens to microvilli in celiac's disease?
Distort, shorten, completely lost
53
How is celiac histology characterised in Marsh's system?
Three types
54
In chronic peptic ulcers, how far does the damage go?
Through the muscularis externa and up to the serosa
56
Why do crypts lengthen in celiac disease?
Zone of proliferation are lengthing to compensate for cell loss
58
After a head injury, what are drug patients in ICU put on?
Proton pump inhibitors
59
T/F Stem cell zones in crypts are where most cell replication in the small intestines occur?
False, it's in zones of proliferation above the stem cell zones
60
In terms of immune cells what happens in celiac disease?
More IELs, more plasma cells in the lamina propria
61
What is a Curling's ulcer? What is it in response to?
An acute peptic ulcer Burns
62
Acute gastritis is usually caused by what? Examples?
Acute sources of damage eg Alcohol Aspirin Toxins Burns Shock Head injury Septicaemia Staphlyococcal poisoning
63
How does the antrum of the stomach look histologically in autoimmune gastritis?
Normal, it's uneffected
64
What is the ratio of IELs to enterocytes in normal duodenum?
1:5
65
What is the second highest cause of gastric and duodenal ulcers?
NSAIDs
66
At what point to antibodies appear in *H. pylori *infection?
Post 4 weeks
67
What is the term given to acute *H. pylori *infection?
Neutrophilic gastritis
68
What is the problem with negatively charged glutamate?
It bind efficiency to HLA-DQ2 and 8 therefore is presented T cells
69
How does the small intestine respond to greater cell loss?
Increase the size of the zone of proliferation

Hugh's MD1 Abdominal (21 decks)

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