Gastritis, peptic ulcers and celiac's disease Flashcards Preview

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

Flashcards in Gastritis, peptic ulcers and celiac's disease Deck (69):
1

How does chemical gastritis appear histologically?

Long, turtuous gastric pits

hyperplasia of lamina propria

1

What are the 5 possible complications of chronic peptic ulcers?

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

1

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

Tropical sprue 

Small bowel bacterial overgrowth

Certain Immunodeficiency

2

What is acute gastritis characterised by?

Acute bleeding

Erosion of epithelium

Local inflammation/oedema

3

How are prostaglandins protective in the stomach?

Inhibit gastric acid secretion

 

Stimulate mucous and bicarbonate secretion

Increase mucosal blood flow

Modifiy local inflammation

 

3

What happens if gluten peptide passes through the epithelium?

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

4

Where do H. pylori bacteria sit during infection?

Gastric cell surface and intercellular junctions

5

What pattern of scarring is left post gastric ulceration?

Radial

5

What are the three main types of ulcers?

A - Autoimmune

B - Helicobacter pylori

C - Chemicals

6

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

Colonises the mucosal barrier

7

What can damage the mucosal barrier?

Helicobacter pylori

Alcohol

NSAIDs

Bile

 

7

Which cells are targeted in autoimmune gastritis?

Parietal

7

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

MALT and subsequent B cell lymphomas

7

How does damage occur in celiac disease?

CD4+ cells releasing TNF-alpha and IL-4

CD8+ cell inducing apoptosis

 

8

What on parietal cells do antibodies in autoimmune gastritis target?

Na/K ATPase

Intrinsic factor

Gastrin receptor

8

T/F The lamina propria contains continual mild inflammation?

True

9

Where in the GIT is glucose absorbed?

Duodenum

10

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

4:1

10

What is the clinical presentation of celiac's diseaese?

GI symptoms: diarrhoea, vomiting, bloating, flatulance

Anaemia vitamin deficiences

Lethargy

Failure to thrive as infant

Other immunopathologies

Osteoporesis

Malabsorption of nutrients

11

HCl reaching the lamina propria causes what?

Activation of mast cell to produce histamine inflammatory mediators

12

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

Carcinomas don't have that

13

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

Atrophy 

Metaplasia > hyperplasia > adenocarcinoma

Lymphoma

 

14

What are valves of Kerckring another name for?

Circular folds/plica circulares

16

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

Antrum-predominant

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