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Z MD1 GI block > Disease of the small bowel > Flashcards

Disease of the small bowel Flashcards

1
Q

what is coeliac disease

A
  • immunologically mediated disease in genetically susceptible individuals
  • driven by gluten found in wheat, rye and barley
  • results in chronic inflammation of the small bowel mucosa
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2
Q

treatment for coeliac disease

A

gluten free diet

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3
Q

prevalence of coeliac disease

A

1:100

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4
Q

what is the genetic association with coeliac disease

A

HLA-DQ2 and HLA-DQ8

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5
Q

at what age does coeliac disease manifest itself

A

can be any time in life from infancy to late adulthood

- two peaks though - infancy and 30-50

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6
Q

where is most of the proliferation occurring of the cells in the mucosa

A

in the proliferative zone (above the stem cells)

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7
Q

what do paneth cells secrete

A

defensin - important against infection - helps keep microbiota in control

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8
Q

what is the normal ratio to IELs to enterocyte

A

1 per 5 enterocytes

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9
Q

what type of T cell are IELs

A

CD8 (innate)

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10
Q

where are IELs found

A

on the surface of the villi and some in the crupts

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11
Q

where are CD4 cells found in the duodenum

A

in the lamina propria

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12
Q

which parts of the small intestine does coeliac disease affect the most

A

the duodenum and the jejenum (only severe cases affect the ileum)

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13
Q

features of stage/type 1 coeliac disease

A

increased ratio of IELs to enterocytes

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14
Q

features of stage/type 2 coeliac disease

A
  • crypts enlarge to keep up with the increased number of cells being lost (crypt hyperplasia)
  • increased ratio of IELs to enterocytes
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15
Q

features of stage/type 3 coeliac disease

A
  • crypts are large (crypt hyperplasia) and surface is flat due to atrophy and apoptosis (villous atrophy)
  • increased ratio of IELs to enterocytes
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16
Q

which zone of the crypt enlarges during

- increased ratio of IELs to enterocytes

A

the proliferative zone

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17
Q

what are some other causes of IELs, villous atrophy and crypt hyperplasia other than coeliac disease

A
  • tropical sprue
  • small bowel bacterial overgrowth (common in immune deficiencies)
  • common variable ID
  • autoimmune eteropathy
  • drugs
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18
Q

clinical presentation of coeliac disease

A
  • GI upset: diarrhoea, bloating, abdominal cramps, flatulence
  • anaemia
  • vitamin deficiencies
  • malabsorption of nutrients
  • failure to thrive as an infant
  • osteoporosis
  • lethargy, migraines, infertility, mouth ulcers
  • increased prevalence of autoimmune diseases
  • can be completely ASYMPTOMATIC
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19
Q

what is the “look” of the diarrhoea in a person with coeliac disease

A

greasy –> because they are not absorbing nutrients (especially fat)

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20
Q

4 elements in the pathogenesis of coeliac disease

A
  • genetics
  • environment
  • T cells
  • gluten
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21
Q

how does the environment contribute to coeliac disease

A
  • breast feeding is protective
  • timing/amount of gluten introduced to infant diet (too much gluten, too soon –> increases risk)
  • infections such as gastroenteritis
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22
Q

gluten peptide is rich is which amino acids

A

proline and glutamine

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23
Q

what does having a high content of proline in a peptide confer to it

A

makes it hard to digest - some resistance to digestion by intestinal proteases –> certain peptides pass through the intestinal epithelium intact

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24
Q

what happens to the peptides that pass through the epithelial wall intact

A

glutamine is deamidated to glutamate by tissue transglutaminase (tTG)

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25
Q

what is special about glutamate

A

it is highly negatively charged

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26
Q

what does glutamate do

A

binds to HLA-DQ2 in the 4,6 and 7 positions by its negative charges –> presented to CD4 T cells

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27
Q

what happens when glutamate is presented to CD4 T cells

A

activated:

  • produce cytokines (IL-4, TNF-alpha and IFN-gamma) –> damages the enterocytes
  • help plasma cells to produce anti-tTG
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28
Q

what is the significance of anti-tTG produced by plasma cells

A

it is a test for coeliac disease

can be seen in the blood

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29
Q

what is the major cause of damage to enterocytes in CD?

A

the activation of CD8 cells!! (CD4 activated damage is minor compared to this)

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30
Q

what is the role of the innate immunity for coeliac disease

A

gliadin causes the enterocytes to:

  • start expressing atypical binding molecules (MIC-A and MIC-B)
  • secrete IL-5 –> makes CD8 cells express NKG2D receptor –> binds to the MIC ligands on enterocytes –> secretes IFN-gamma and activates APOPTOSIS
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31
Q

what is the receptor on the CD8 cells called that binds to MIC A and MIC B

A

NKG2D

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32
Q

What are the atypical binding proteins expressed by enterocytes when exposed to gliadin

A

MIC A and MIC B

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33
Q

how does coeliac disease give you a higher chance of getting cancer

A

the CD8 cells, when they are activated indirectly through gliadin, become autoreactive, and proliferate at a higher level (can become malignant) –> cancer (T cell malignancy)

34
Q

2 mechanisms that cause coeliac disease

A

activation of CD8 cells –> apoptosis

activation of CD4 cells –> apoptosis

35
Q

how do you diagnose coeliac disease

A
  • serological testing (tTG, deamidated gliadin peptide)
  • HLA-DQ haplotyping
  • small bowel biopsy (best!)
36
Q

long term risks of untreated coeliac disease

A
  • osteoporosis (due to lack of absorption of vitamin D - fat soluble vitamin)
  • autoimmune disease
  • increased risk of cancer (small bowel lymphoma, small bowel adenocarcinoma, oesophageal cancer)
37
Q

macroscopic look of chronic gastroenteristis

A
  • no rugae in the bastric body of the stomach
  • little haemorrhages on the surface
  • antrum is normal
38
Q

what protects the stomach epithelium from HCl

A

mucus cells produce:
- mucus
- bicarbonate –> into the mucus which neutralizes the HCl
- surface of mucus has phospholipid bilayer (repels water)
Right next to the epithelial layer the pH is neutral - keeping cells alive

39
Q

what is intrinsic factor important for?

A

the absorption of B12

40
Q

what endrocrine cells are located in the antrum of the stomach

A

G cells and D cells

41
Q

what stimulates the secretion of somatostatin?

A

gastrin

42
Q

what does somatostatin do?

A
  • inhibits gastrin secretion by G cells
  • inhibits HCl secretion by parietal cells
  • inhibits histamine secretion by ECL cells
43
Q

Where is gastrin produced and what does gastrin do?

A

made by G cells and activates parietal cells to produce HCL

44
Q

what three factors do parietal cells need to produce HCl

A

Histamine (from ECL cells)
ACh (from enteric neurons)
Gastrin (from G cells)

45
Q

what things can break down the mucus layer on the epithelial cells of the stomach

A
  • bacteria
  • NSAIDs
  • bile (refluxed)
  • alcohol
46
Q

what happens if HCl is able to get through to the epithelial cells of the stomach (mucus has been degraded)

A

HCl goes into the lamina propria –> activates mast cells to produce histamine –> inflammation (oedema and inflammatory infiltrate)

47
Q

normal role of prostaglandins and the mucus barrier of the stomach

A
  • inhibit acid secretion
  • stimulate HCO3 and mucus secretion
  • increase mucosal blood flow
48
Q

most common causes of acute gastritis

A
  • chemical injury (alcohol or drugs - NSAIDS, aspirin, iron tablets and other drugs)
  • stress
  • shock
  • burns
  • head injury
  • septicaemia
  • staph food poisoning
49
Q

what is acute gastritis due to

A
  • breakdown of the gastric barrier directly or

- microcirculatory changes accompanying shock or sepsis (reduced in blood flow –> ischaemia)

50
Q

what is the inflammatory response in acute gastritis

A

inflammatory mediators result in vasodilatation, oedema, haemorrhage and erosions –> acute haemorrhagic or erosive gastritis
(oedema first –> then if continues –> erosion)

51
Q

how long does acute gastritis last for

A

24-48 hours

52
Q

histology of chronic gastritis

A
  • large accumulation of lymphocytes, plasma cells and eosinophils
  • cells atrophy
53
Q

difference between an ulcer, an acute erosion and chronic erosion

A

ulcer - defect above the muscularis mucosae
acute erosion - defect down into the muscularis mucoase
chronic erosion - defect penetrates through the submucosa and into the serosal layer –> base becomes fibrosed

54
Q

what are Curling ulcers

A

ulcers in the proximal duodenum associated with severe burns/trauma

55
Q

what are Cushing ulcers

A

gastric and duodenal ulcers in persons with intracranial injury

56
Q

what are NSAID-induced ulcers due to

A

inhibition of cyclooxygenase and prostaglandin synthesis which normally promotes bicarbonate secretion, mucin synthesis, vascular perfusion and inhibition of HCl secretion

57
Q

3 main causes of chronic gastritis

A

ABC!

  • autoimmune
  • bacterial - H. pylori
  • chemical
58
Q

what is autoimmune gastritis

A
  • immune mediated destruction of acid secreting tubules followed by atrophy (total loss of parietal cells)
  • consequent achlorhydria (no acid production) and loss of intrinsic factor
  • leads to pernicious anaemia (B12 deficiency)
59
Q

where is autoimmune gastritis seen

A

in the gastric corpus mucosa (antrum spared)

60
Q

what is a rare consequence of autoimmune gastritis

A

loss of acid and parietal cells –> hypergastrinaemia –> linear and nodular ECL hyperplasia –> carcinoidosis

61
Q

what causes autoimmune gastritis

A

circulating autoantibodies to parietal cell membrane and intrinsic factor and gastrin receptor

62
Q

why does pernicious anaemia occur with autoimmune gastritis

A

intrinisc factor antibody secreted into the gastric lumen –> can complex with vitamin B12 –> prevents its absoprtion via receptors in the terminal ileum

63
Q

how does autoimmune gastritis lead to hypergastrinaemia

A

D cells are not stimulated to make simvostatin (required for inhibition of G cells)

64
Q

what causes the proliferation of ECL cells in autoimmune gastritis

A

hypergastrinaemia –> ECL proliferation

65
Q

what causes chemical gastritis

A
  • reflux of bile and alkaline duodenal juice due to altered antro-duodenal motility or gastro-jejunostomy
  • long term use of NSAIDs
66
Q

what happens in chemical gastritis

A

direct mucosal injury –> disruption of the mucus layer and gastric barrier –> epithelial dequamation with compensatory foveolar hyperplasia with elongation and tortuosity of gastric pits, vasodilatation and oedema and fibromuscular hyperplasia of the LP and only mild inflammatory cell infiltration –> erosions/ulceration

67
Q

How does H. pylori survive in the GI system

A

it colonises the area under the mucus barrier (neutral pH)

  • motility by flagella
  • can live in very low oxygen tensions
  • adhesins that make it stick to the epithelium and not be washed away
  • urease - breaks down urea into ammonia –> can neutralise HCl
68
Q

what does H pylori acute gastritis cause

A

neutrophilic gastritis –> infiltration with chronic inflammatory cells

69
Q

what is the sequence from chronic gastritis to cancer

A

normal mucosa –> chronic gastritis –> atrophic gastritis –> intermediate metaplasia –> dysplasia –> adenocarcinoma

70
Q

two major patterns of H. pylori gastritis

A
  • antrum predominant

- pan gastritis

71
Q

gastric and duodenal pathology of antrum predominant H. pylori gastritis

A 
gastric:
- chronic inflammation
- polymorphs
duodenal:
- gastric metaplasia
- active chronic inflammation
72
Q

what happens to the acid output in antrum-predominant H. pylori gastritis

A

increased

73
Q

gastric and duodenal pathology of pan-gastritis - H. pylori gastritis

A 
gastric:
- chronic inflammation
- polymorphs
- atrophy
- intestinal metaplasia
duodenal = normal
74
Q

acid output in pangastritis - H. pylori gastritis

A

reduced

75
Q

which gastritis can lead to B cell lymphoma

A

H. pylori pan gastritis

76
Q

What are some diseases associated with H. pylori infection

A
  • peptic ulcer disease
  • gastric adenocarcinoma
  • gastric B-cell lymphoma of MALT
  • iron deficiency anaemia
  • atrophic gastritis
77
Q

is H. pylori the more common cause of duodenal ulcer or gastric ulcer

A

duodenal ulcer

78
Q

ratio of the prevalence between duodenal and antrum peptic ulcer disease

A

D:A = 4:1

79
Q

4 histological layers of chronic peptic ulcer floor

A
  • exudate of fibrin, neutrophils and necrotic debris
  • narrow zone of fibrinoid necrosis
  • zone of cellular granulation tissue
  • zone of fibrosis including endarteritis and hypertrophied nerves
80
Q

complications of peptic ulcer disease

A
  • perforation
  • haemorrhage
  • penetration into adjacent organ
  • stenosis
81
Q

how does stenosis occur from peptic ulcer disease

A

due to cicatrisation or contraction of fibrous scar –> pyloric canal stenosis

Z MD1 GI block (18 decks)

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