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

Gastritis, peptic ulcers and celiac's disease Flashcards

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
Q

In what cause of acute gastritis is there particularly low amounts of inflammation?

A

NSAID caused

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18
Q

What is chemical gastritis caused by?

A

Reflux of bile and alkaline duodenal juices into the antrum of the stomach

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18
Q

What environmental factors contribute to the development of celiacs

A

Exposure to gluten (eg too much too soon)

Breast milk is protective

Infections

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20
Q

Why is healing in response to acute gastritis quick?

A

Due to rapid turn over of gastric epithelium 24-48 hours

22
Q

What are the two patterns of gastritis?

A

Antrum-predominant

Pan gastritis

23
Q

What are the peak ages of development of celiac disease?

A

30-50

24
Q

T/F Everyone with HLA-DQ2 and DQ8 have celiac disease and everyone with the disease have them?

A

False, 20-30% of the population at risk don’t have disease despite having the HLA subtypes.

The latter is true

25
Q

What makes a peptic ulcer different from mucosal erosion?

A

Peptic ulcers penetrate through the muscularis mucosae

25
Q

What does IELs stand for?

A

Intra-epithelial lymphocytes

26
Q

What are three methods of diagnosis for celiac disease?

A

Serology for anti tTG or

Genetic testing for HLAs

Biopsy of intestine after gluten ingestion

27
Q

Which organ is most effected in celiac’s disease?

A

Small intestine

29
Q

What is the average rate of H. pylori infection the developing world?

A

>80%

30
Q

What colonisation factors does H. pylori have?

A

Adhesins

Motility

Urease

Microaerophilism

32
Q

Do acute peptic ulcers leave radial scars on healing?

A

No, there is restoration of submucosa and mucosa

33
Q

What HLA subtypes are strongly associated with the development of celiac’s disease? In which ethic groups are they most prevalence?

A

HLA-DQ2, -DQ8

European and Middle Eastern

34
Q

Are IELs CD4 or CD8?

A

CD8

36
Q

In what age group in chronic inflammation causing cancer most prominent?

A

>70+ y.o.

38
Q

How does the body of the stomach look histologically in autoimmune gastritis?

A

Loss of secreting tubules

Greater number of goblet and neuroendrocrine cells

Chronic inflammation

39
Q

Where in the GIT is vitamin B12 most absorbed?

A

Ileum

40
Q

What is the problem is not diagnosing celiacs disease?

A

It increases the risk of:

MALT lymphoma (x30)

Oesophageal cancer

S. intestine adenocarcinoma

Overall mortality (x2)

42
Q

What can happen to the duodenum in antrum-predominant gastritis?

A

It changes to become more like the stomach > H. pylori can infect it

43
Q

What does Marsh type II celiac’s disease look like?

A

Increase IELs

Longer, branched crypts

Villi still present but fatter with immune cell infiltration

44
Q

What are Cushing ulcers? What are they caused by?

A

Ulcers in the stomach or duodenum in response to head injury

45
Q

How does autoimmune gastritis cause anaemia?

A

Low intrinsic factor > No B12 absorption > Anaemia

46
Q

What happens to villi and crypts in advanced celiac disease?

A

Villis disappear

Crypts lengthen

47
Q

Does H. pylori usually cause acute gastritis?

A

No, usually chronic, not self limiting

49
Q

What contributes to pain in chronic peptic ulcers?

A

Hypertrophied nerves

50
Q

How is gluten able to remain intact and get through the epithelium to act as an antigen?

A

It is high in proline (35%) and glutamine (20%) that are resistant to acids and proteases

51
Q

In terms of percentage of the total, does *H. pylori *cause more duodenal ulcers or gastric ulcers?

A

Duodenal

52
Q

What happens to microvilli in celiac’s disease?

A

Distort, shorten, completely lost

53
Q

How is celiac histology characterised in Marsh’s system?

A

Three types

54
Q

In chronic peptic ulcers, how far does the damage go?

A

Through the muscularis externa and up to the serosa

56
Q

Why do crypts lengthen in celiac disease?

A

Zone of proliferation are lengthing to compensate for cell loss

58
Q

After a head injury, what are drug patients in ICU put on?

A

Proton pump inhibitors

59
Q

T/F Stem cell zones in crypts are where most cell replication in the small intestines occur?

A

False, it’s in zones of proliferation above the stem cell zones

60
Q

In terms of immune cells what happens in celiac disease?

A

More IELs, more plasma cells in the lamina propria

61
Q

What is a Curling’s ulcer? What is it in response to?

A

An acute peptic ulcer

Burns

62
Q

Acute gastritis is usually caused by what? Examples?

A

Acute sources of damage

eg Alcohol

Aspirin

Toxins

Burns

Shock

Head injury

Septicaemia

Staphlyococcal poisoning

63
Q

How does the antrum of the stomach look histologically in autoimmune gastritis?

A

Normal, it’s uneffected

64
Q

What is the ratio of IELs to enterocytes in normal duodenum?

A

1:5

65
Q

What is the second highest cause of gastric and duodenal ulcers?

A

NSAIDs

66
Q

At what point to antibodies appear in *H. pylori *infection?

A

Post 4 weeks

67
Q

What is the term given to acute *H. pylori *infection?

A

Neutrophilic gastritis

68
Q

What is the problem with negatively charged glutamate?

A

It bind efficiency to HLA-DQ2 and 8 therefore is presented T cells

69
Q

How does the small intestine respond to greater cell loss?

A

Increase the size of the zone of proliferation

Hugh's MD1 Abdominal (21 decks)

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