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Gastroenterology > Gut Immunology > Flashcards

Gut Immunology Flashcards

1
Q

surface area of the GI tract

A

200m^2

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2
Q

antigen load of the GI tract

A

massive antigen load
resident microbiota
dietary antigens
exposure to pathogens

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3
Q

GI state ‘restrained activation’

A

tolerance vs active immune response

dual immunological role

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4
Q

GI has tolerance for?

A

food antigens

commensal bacteria

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5
Q

GI has immunoreactivity to?

A

pathogens

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6
Q

is the presence of the bacterial microbiota required?

A

yes

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7
Q

what makes up the gut microbiota?

A

4 major phyla of bacteria: bacteroidetes, firmicutes, actinobacteria, proteobacteria
viruses
fungi

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8
Q

what is dysbiosis?

A

altered microbiota composition

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9
Q

causes of dysbiosis

A 
infection and inflammation
diet
xenobiotics
hygiene
genetics
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10
Q

disease development of dysbiosis - brain

A

stress
autism
MS

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11
Q

disease development of dysbiosis - lung

A

asthma

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12
Q

disease development of dysbiosis - liver

A

NAFLD

NASH

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13
Q

disease development of dysbiosis - adipose tissue

A

obesity

metabolic disease

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14
Q

disease development of dysbiosis - intestine

A

IBD

coeliac disease

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15
Q

disease development of dysbiosis - systemic

A

T1DM
atherosclerosis
rheumatoid arthritis

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16
Q

anatomical physical barriers to pathogens in GI tract

A

epithelial barrier

peristalsis

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17
Q

chemical physical barriers to pathogens in GI tract

A

enzymes

acidic pH

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18
Q

immunological barriers to pathogens in GI tract

A

following invasion
MALT
GALT

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19
Q

epithelial barrier is made up of?

A

mucus layer - goblet cells
epithelial monolayer - tight junctions
Paneth cells - bases of crypts, secrete antimicrobial peptides (defensins) and lysozymes

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20
Q

how do commensal bacteria act as mucosal defense?

A

occupy ecological niche

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21
Q

where is MALT found?

A

Found in the submucosa below the epithelium, as lymphoid mass containing lymphoid follicles

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22
Q

follicles in MALT are surrounded by?

A

HEV postcapillary venules, allowing easy passage of lymphocytes

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23
Q

what cavity is rich in immunological tissue?

A

oral

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24
Q

GALT consists of what?

A

Consists of B & T lymphocytes, macrophages, APC (dendritic cells), and specific epithelial & intra-epithelial lymphocytes

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25
Q

GALT - non-organised

A

intraepithelial lymphocytes e.g. T cells, NK cells

lamina propria lymphocytes

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26
Q

GALT - organised

A

Peyer’s patches (small intestine)
Caecal patches (large intestine)
Isolated lymphoid follicles
Mesenteric lymph nodes (encapsulated)

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27
Q

where are Peyer’s patches found?

A

submucosa small intestine mainly distal ileum

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28
Q

peyer’s patches consist of?

A

Aggregatedlymphoid follicles covered with follicle associated epithelium (FAE)

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29
Q

what is not included in FAE (follicle associated epithelium)?

A

goblet cells
secretory IgA
microvilli

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30
Q

peyer’s patches have an organised collection of what cells?

A

naive T cells

B cells

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31
Q

development of the Peyer’s patches requires what?

A

exposure to bacterial microbiota

32
Q

how does antigen uptake occur in peyer’s patches?

A

via M (microfold) cells within FAE

33
Q

M cells express what receptors?

A

IgA receptors

34
Q

expression of IgA receptors on cells facilitates what?

A

uptake of IgA-bacteria complex in the Peyer’s patches

35
Q

mature naive B cells express which immunoglobulin on its surface in Peyer’s patches?

A

IgM

36
Q

when does the immunoglobulin on the surface of mature naive B cells switch class? to what?

A

on antigen presentation

IgA

37
Q

what cells influence B cell maturation and via what?

A

T cells and epithelial cells

via cytokines

38
Q

B cells can further mature into?

A

IgA secreting plasma cells

39
Q

what cells secrete IgA?

A

90% of gut B cells

40
Q

what does secretory IgA do?

A

binds luminal antigen > prevents adhesion and consequent invasion

41
Q

formation of secretory IgA

A

plasma cell in submucosa secretes dimeric IgA > binds to polyIg receptor > enters cell in vesicle w/ receptor > enzymatic cleavage > secretory IgA

42
Q

lymphocyte homing and circulation

A

Peyer’s patch (antigen presentation and activation) > mesenteric lymph node (lymphocyte proliferation) > thoracic duct > circulation > lamina propria/skin, tonsils, BALT

43
Q

𝝰4β7 Integrin/MAdCAM-1 Adhesion is a crucial pathway for?

A

B cell migration

44
Q

why is the turnover of enterocytes so rapid?

A

lesions are short lived, effects of agents that interfere w/ cell fx, metabolic rate is diminished, enterocytes maybe directly affected by toxic substances in diet

45
Q

what is cholera?

A

acute bacterial disease caused by Vibrio cholerae serogroups O1 & O139

46
Q

mechanism of cholera

A

Bacteria reaches small intestine > contactwith epithelium & releasescholera enterotoxin

47
Q

transmission of cholera

A

faecal oral route

spreads via contaminated water and food

48
Q

main symptoms of cholera

A 
severe dehydration
watery diarrhoea
vomiting
nausea
abdominal pain
49
Q

diagnosis of cholera

A

bacterial culture from stool sample on selective agar is the gold standard, rapid dipstick tests also available

50
Q

treatment of cholera

A

oral-rehydration is the main management

vaccine (Dukoral, oral, inactivated)

51
Q

viral causes of infectious diarrhoea

A

rotavirus (children)

norovirus (winter vomiting virus)

52
Q

protozoal/parasitic causes of infectious diarrhoea

A

Giardia lamblia

Entamoaeba histolytica

53
Q

bacterial causes of infectious diarrhoea

A 
Campylobacter jejuni
E.coli
Salmonella
Shigella
Clostridium difficile
54
Q

description of rotaviruses

A

RNA virus, replicates in enterocytes.

5 types A – E, type A most common in human infections

55
Q

epidemiology of rotavirus

A

Most common cause of diarrhoea in infants & young children worldwide

56
Q

treatment of rotavirus

A

Oral rehydration therapy

57
Q

vaccine against rotavirus

A

Live attenuated oral vaccine (Rotarix) against type A

58
Q

description of norovirus

A

RNA virus

Incubation period 24-48 hours

59
Q

transmission of norovirus

A

Faecal-oral transmission.
Individuals may shed infectious virus for up to 2 weeks
Outbreaks often occur in closed communities

60
Q

symptoms of norovirus

A

Acute gastroenteritis, recovery 1 – 3 days

61
Q

treatment of norovirus

A

not usually required

62
Q

diagnosis of norovirus

A

sample PCR

63
Q

most common species of campylobacter

A

campylobacter jejuni

campylobacter coli

64
Q

transmission of campylobacter

A 
Undercooked meat (especially poultry), untreated water & unpasteurised milk
Low infective dose, a few bacteria (<500) can cause illness
65
Q

treatment of campylobacter

A

Not usually required

Azithromycin (macrolide) is standard antibiotic

66
Q

what is problematic in the treatment of campylobacter infections?

A

resistance to fluoroquinolones

67
Q

campylobacter infection is the commonest cause of what illness in the UK?

A

food poisoning

68
Q

description of E.coli

A

Diverse group of Gram-negative intestinal bacteria

69
Q

how many pathotypes of E.coli are associated with diarrhoea?

A

6

70
Q

list pathotypes of E.coli are associated with diarrhoea

A 
Enterotoxigenic E. coli (ETEC)
Enterohaemorrhagic or Shiga toxin-producing E. coli (EHEC/STEC)
Enteroinvasive E. coli (EIEC)
Enteropathogenic E. coli (EPEC)
Enteroaggregative E. coli (EAEC)
Diffusely adherent E. coli (DAEC)
71
Q

Enterotoxigenic E. coli (ETEC) causes what? has what type of toxin?

A

Cholera like toxin

Watery diarrhoea

72
Q

Enteroinvasive E. coli (EIEC) causes what?

A

Shigella like illness

Bloody diarrhea

73
Q

5-10% of people with Enterohaemorrhagic or Shiga toxin-producing E. coli (EHEC/STEC) have what negative consequence?

A

haemolytic uraemic syndrome > loss of kidney function

74
Q

management of clostridium difficile

A

isolation, stop current antibiotics, Metronidazole, Vancomycin, faecal microbiota transplantation

75
Q

recurrence rate of clostridium difficile after initial infection

A

15-35%

Gastroenterology (9 decks)

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