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BRS YR2 > Immunology of the Gut > Flashcards

Immunology of the Gut Flashcards

1
Q

What are the implications of the large surface area of the GI tract?

A

exposure to a massive antigen load

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2
Q

What does the massive antigen load consist of?

A
  • resident microbiota
  • dietary antigens
  • pathogen exposure
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3
Q

What is the impact of this large antigen load?

A

GI is in a state of ‘restrained activation’

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4
Q

What is a state of ‘restrained activation’

A
  • tolerance (food and commensal bacteria) vs active immune response
  • dual
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5
Q

What does immune homeostasis and development of a healthy immune system require?

A

the presence of bacterial microbiota

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6
Q

What are the 4 major phyla of bacteria?

A
  • Bacteroidetes
  • Firmicutes
  • Actinobacteria
  • Proteobacteria
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7
Q

What is the benefits of the gut microbiota?

A

provides traits that we can no evolve on our own

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8
Q

What factors stimulate bacterial growth/cell numbers?

A
  • ingested nutrients

- secreted nutrients

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9
Q

What factors inhibit bacterial growth/cell numbers?

A
  • chemical digestive factors
    = bacterial lysis
  • peristalsis, contractions and defecation
    = bacterial elimination
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10
Q

What chemical digestive factors are produced in the stomach?

A
  • HCl
  • Pepsin
  • Gastric lipase
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11
Q

What chemical digestive factors are produced in the liver?

A
  • Bile acids
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12
Q

What chemical digestive factors are produced in the pancreas?

A
  • Trypsin
  • Amylase
  • Carboxypeptidase
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13
Q

What chemical digestive factors are produced in the small intestine?

A
  • brush border enzymes
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14
Q

What chemical digestive factors are produced in the colon?

A

no host digestive factors

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15
Q

What is the general relationship between the toxicity of chemical digestive factors and the bacterial content?

A

the more toxic the digestive factors, the smaller the bacterial content

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16
Q

What is dysbiosis?

A

altered microbiota composition

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17
Q

What is the impact of symbionts on the host?

A

no effect, truly neutral

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18
Q

What is the impact of commensals on the host?

A

no effect, but benefit from being part of the host

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19
Q

What is the impact of pathobionts on the host?

A 
no effect (normally)
can cause dysregulated inflammation and disease
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20
Q

What are the important factors of immunological equilibrium in the gut?

A
  • symbionts
  • commensals
  • pathobionts
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21
Q

What can cause dysbiosis?

A
  • infection
  • inflammation
  • diet
  • drugs/glutens
  • hygiene
  • genetics
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22
Q

What happens during dysbiosis?

A

production of bacterial metabolites and toxins

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23
Q

What are some examples of bacterial metabolites and toxins?

A
  • TMAO
  • SCFAs
  • 4 - EPS
  • bile acids
  • AHR ligands
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24
Q

What is the effect of TMAO?

A

encourages the deposition of cholesterol in vessel walls leading to atherosclerosis

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25
Q

What is the effect of 4-EPS?

A

autism

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26
Q

What is the effect of SCFA’s?

A

decreased: IBD
increased: stress

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27
Q

What is the effect of AHR ligands?

A
  • MS
  • rheumatoid athritis
  • asthms
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28
Q

What are the 2 primary physical types of barriers?

A
  • Anatomical

- Chemical

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29
Q

What are the different types of anatomical barriers?

A
  • epithelial barriers

- peristalsis

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30
Q

What are the different types of chemical barriers?

A
  • enzymes

- acidic pH

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31
Q

What is involved in the epithelial barrier?

A
  • mucus layer (goblet cells)
  • epithelial monolayer, tight junctions
  • paneth cells (in small intestines)
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32
Q

What is the role of Paneth Cells?

A
  • bases of crypts of Lieberkuhn

- secrete antimicrobial peptides (defensins) and lysozyme

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33
Q

How do commensal bacteria act as barrier?

A
  • occupy an ecological niche

- act as an ecological barrier

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34
Q

What is involved in the immunological barriers?

A
  • MALT (Mucosa Associated Lymphoid Tissue)

- GALT (Gut Associated Lymphoid Tissue)

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35
Q

Where is MALT located?

A
  • in submucosa below the epithelium
  • as lymphoid mass containing lymphoid follicles
  • follicles are surrounded by HEV postcapillary venules (easy passage of lymphocytes for a response)
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36
Q

What area is rich in immunological tissue?

A

oral cavity

  • palatine tonsil lingual tonsils
  • pharyngeal tonsils (adenoids)
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37
Q

What is the role of GALT?

A

responsible for both adaptive and innate immune response through generations of lymphoid cells and Abs

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38
Q

What type of response is mounted by GALT?

A

both adaptive and innate immune response

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39
Q

What are the non-organised forms of GALT?

A
  • intra-epithelial lymphocytes (in between entry points) (eg: T cells and NK cells)
  • Lamina propria lymphocytes
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40
Q

What are the organised forms of GALT?

A
  • Peyer’s patches
  • Caecal patches
  • Isolated lymphoid follicles
  • Mesenteric lymph nodes (encapsulated)
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41
Q

Where are Peyer’s patches found?

A

small intestine

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42
Q

Where are Caecal patches found?

A

large intestine

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43
Q

How are non-organised GALT released?

A

migrate to the tip of the microvilli prior to that as well as absorptive epithelial cells

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44
Q

What produces mucus secreting goblet cells?

A
  • stem cells

- crypts

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45
Q

Where do Paneth cells migrate to?

A

the bottom of the crypt

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46
Q

How do you characterise Paneth cells?

A
  • presence of dense granules that anti-microbial peptides

- appropriate lamina

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47
Q

Where are intraepithelial lymphocytes?

A

between entry sites

48
Q

What is found in the mucosa of the microvilli?

A
  • macrophage
  • IgA B cells
  • DC
  • I cell
49
Q

Where are Peyer’s patches?

A
  • submucosa small intestine

- mainly in the distal ileum

50
Q

What are Peyer’s patches?

A

aggregated lymphoid follicles covered with follicle associated epithelium (FAE)

51
Q

What are characteristics of Peyer’s patches?

A
  • no goblet cells
  • no secretory IgA
  • lack microvilli
52
Q

What are the causes of infectious diarrhoea?

A
  • Clostridium difficile
  • Klebsiella oxytoca
  • Clostridium perfringens
  • Salmonella spp
    (can cause bloody diarrhoea)
53
Q

What are the causes of non-infectious diarrhoea?

A
  • antibiotics side effect
  • post-infectious IBS
  • IBD
  • Microscopic colitis
  • Ischaemic colitis
  • Coeliac disease
  • Haemorrhoids
54
Q

How do you manage C. difficile?

A
  • Infection control (side room)
  • Discontinue inciting antibiotic agents
  • Management of fluids, nutrition and diarrhoea
55
Q

What would classify a non-severe infection?

A
  • WCC < 15

- Creatinine < 150

56
Q

What would classify a severe infection?

A
  • WCC > 15

- Creatinine > 150

57
Q

What fulminant colitis?

A
  • hypotension
  • shock
  • ileus
  • toxic megacolon
58
Q

How do you treat non-severe C. difficile infections?

A
  • ABx with oral vancomycin/fidaxomicin/metronidazole

- role of Faecal Microbiota Transplantation (FMT)

59
Q

How do you treat severe/fulminant colitis C. difficile infections?

A
  • ABx
  • supportive care
  • close monitoring
  • early surgical consultation
60
Q

What is the first line treatment of fulminant colitis and toxic megacolon?

A
  • Medical therapy with antibiotics and supportive management

- IV fluid resuscitation and inotropic support

61
Q

What are the indications for surgery?

A
  • Colonic perforation
  • Necrosis/Full-thickness ischaemia
  • Intra-abdominal hypertension
  • Abdominal compartment syndrome
  • Clinical signs of peritonitis
  • Worsening abdominal exams
  • End-organ failure
62
Q

What is pseudomembranous colitis?

A
  • manifestation of severe colonic disease

- characteristic yellow-white plaques that form pseudomembranes on the mucosa

63
Q

What tends to cause pseudomembranous colitis?

A

C. difficile

64
Q

How do you confirm pseudomembranous colitis?

A
  • endoscopy

- biopsy

65
Q

What does chronic inflammation with no granulomas on a colonoscopy indicate?

A

Ulcerative colitis

66
Q

What do Peyer’s patches consist of?

A
  • dome area filled with dendritic cells
  • B cell follicles
  • interfollicular T cells
67
Q

What does the development of the naive T and B cells require?

A

exposure to bacterial microbiota

68
Q

How does antigen uptake to Peyer’s patches occur?

A 
via M (microfold) cells in FAE
- express IgA receptors facilitating the transfer of IgA-bacteria complexes into the Peyer's patches.
69
Q

What can trans-epithelial dendritic cells do?

A
  • open up tight junction proteins and send the dendrites outside into the lumen of the intestinal tract to directly sample bacteria
  • mesenteric lymph nodes
70
Q

What happens in the B cell adaptive response?

A
  • mature naive B cells express IgM in Peyer’s patches
  • on antigen presentation switch to IgA
  • T cells and epithelial cells influence B cell maturation via cytokine production
  • B cells mature to become IgA secreting plasma cells
  • in lamina propria
71
Q

How is secretory IgA produced?

A
  • plasma cell produces IgA
  • taken into enterocyte vesicle
  • enzymatic cleavage
  • leading to secretory IgA in the lumen
72
Q

What does secretory IgA do?

A
  • bind luminal antigen
  • prevents adhesion and invasion
    (secreted by 90% of gut B cells)
73
Q

What happens in lymphocyte homing and circulation?

A
  • lymphocytes from Peyer’s patch move into the mesenteric lymphnode
  • in the lymphnode they proliferate
  • return to circulation via the thoracic duct into the systemic venous system
  • can either enter the peripheral immune system or return to the intestinal mucosa via vessels in the lamine propria
74
Q

What is part of the peripheral immune system?

A
  • skin
  • tonsils
  • BALT (Bronchus Associated Lymphoid Tissue)
75
Q

Why do enterocytes and goblet cells have a rapid turnover?

A
  • first line of defense and may be directly affected by toxicity
  • may have impacts on function, metabolic rate …
  • shorten the effect of lesions
76
Q

What happens if enterocyte and goblet cell turnover is interrupted?

A

severe intestinal dysfunction

77
Q

What is the mechanism behind cholera infections?

A
  • Vibrio cholerae serogroups 01 and 0139
  • bacteria reaches small intestine, contact with epithelium triggers the release of cholera enterotoxin
  • internalised via retrograde endocytosis
  • increased adenylate cyclase acitvity
  • increased cAMP
  • secretion of salts and water follows by CFTR
78
Q

How is cholera transmitted?

A
  • faecal-oral route (contaminated water and food)
79
Q

What are the main symptoms of cholera?

A
  • severe dehydration
  • water diarrhoea
  • vomiting
  • nausea
  • abdominal pain
80
Q

What does CFTR stand for

A

Cystic fibrosis transmembrane conductance regulator

81
Q

How do you diagnose cholera?

A
  • bacterial culture from stool sample on selective agar (GS)

- rapid dipstick tests

82
Q

How do you treat cholera?

A
  • oral rehydration
83
Q

How do you vaccinate against cholera?

A
  • Dukoral
  • oral
  • inactivated
84
Q

What are the possible viral causes of infectious diarrhoea/gastroenteritis?

A
  • Rotavirus (children)

- Norovirus

85
Q

What are the possible bacterial causes of infectious diarrhoea/gastroenteritis?

A
  • Campylobacter jejuni
  • E. coli
  • Salmonella
  • Shigella
  • C. difficile
  • Cholera
86
Q

What are the possible protozoal parasitic causes of infectious diarrhoea/gastroenteritis?

A
  • Giardia lamblia

- Entamoeba histolytica

87
Q

What are rotaviruses?

A
  • RNA virus
  • replicates in enterocytes
  • 5 types (A-E)
88
Q

How common are rotaviruses?

A

most common cause of diarrhoea in children and infants

89
Q

How do you treat rotaviruses?

A
  • oral rehydration therapy

- vaccination (live, attenuated against type A)

90
Q

What is Norovirus?

A
  • RNA virus

- incubation: 24-48hours

91
Q

How are Noroviruses transmitted?

A
  • faecal-oral transmission
  • may shed for up to 2 weeks
  • outbreaks in closed communities common
92
Q

What are the symptoms of Norovirus?

A
  • acute gastroenteritis

- recovery in 1-3 days

93
Q

How do you diagnose Norovirus?

A

Sample PCR

94
Q

What are the causes of food poisoning?

A

Campylobacter

  • Campylobacter jejuni
  • Campylobacter coli
95
Q

How is Campylobacter transmitted?

A
  • undercooked meat
  • untreated water
  • un-pasturised milk
  • low infective dose
96
Q

How do you treat for Campylobacter?

A
  • not usually required
  • Azithromycin is standard ABx
  • Resistance to fluoroquinolones is problematic
97
Q

What are the pathotypes of E. coli?

A

gram negative bacteria

  • Enterotoxic E. coli
  • Enterohaemorrhagic/Shiga toxin-producing E. coli
  • Enteroinvasive E. coli
  • Enteropathogenic E. coli
  • Enteroaggregative E. coli
  • Diffusely adherent E. coli
98
Q

What symptoms is Enterotoxic E. coli associated with?

A
  • cholera like toxin

- water diarrhoea

99
Q

What symptoms is Enterohaemorrhagic/Shiga toxin-producing E. coli associated with?

A

5-10% loss kidney function

haemolytic uraemic syndrome

100
Q

What symptoms is Enteroinvasive E. coli associated with?

A
  • shigella like illness

- bloody diarrhoea

101
Q

How does Clostridium difficile infect the body?

A
  • always present in the gut
  • dysbiosis - intermediate dysbiotic state
  • pathogen induced disturbance and toxin induction
102
Q

How do you manage Clostridium difficile?

A
  • isolation
  • stop ABx
  • Metronidazole (can also trigger infection)
  • Vancomycin
  • reccurence rate 15-35%, increasingly more difficult to treat
  • faecal microbiota transplant
103
Q

What symptoms would indicate a C. difficile infection?

A
  • raised WCC and CRP
  • new onset diarrhoea
  • generalised tenderness
  • signs of dehydration (AKI and dry mucous membranes)
104
Q

How do you diagnose a C. difficile infection?

A
  • stool sample for C. difficile toxin
  • stool cultures
  • Imaging (AXR)
105
Q

What would cause dilation of the large intestine (transverse) secondary to a C. difficile infection?

A

toxic megacolon

106
Q

What clinical features suggest toxic megacolon?

A
  • dilation of bowel

- septic features of the patient

107
Q

What investigations would you do for suspected IBD?

A
  • Stool culture for C. diff infections
  • Stool culture (calprotectin)
  • Endoscopy
108
Q

What are the management options for UC?

A
  • steroids
  • 5 ASA
  • immune suppressants (azathioprine and methotreaxate)
  • biologic therapy
  • diet
  • FMT
  • ABx,PBx
109
Q

What would classify UC as mild?

A
  • 4 BM/day
  • no systemic toxicity
  • normal ESR/CRP
  • mild symptoms
110
Q

What would classify UC as moderate?

A
  • more than 4BM/day
  • mild anaemia
  • mild symptoms
  • minimal systemic toxicity
  • nutrition maintained
  • no weight loss
111
Q

What would classify UC as severe?

A
  • more than 6 BM/day
  • severe symptoms
  • systemic toxicity
  • significant anaemia
  • increased ESR/CRP
  • weight loss
112
Q

What can azathioprine cause?

A

reactivation of diseases like:

  • Hep B/C
  • HIV
  • TB
113
Q

What must be tested when prescribing azathioprine to prevent toxicity?

A

thiopurine methotransferase (TPMT)

114
Q

What is the last line medical treatment for presistant UC?

A

Infliximab with Azathioprine

115
Q

What are the side effects of Infliximab?

A
  • demyelinating disease
  • autoimmunity
  • congestive heart failure
  • hepatoxicity
  • malignancy
  • infection/bone marrow suppression
  • infusion reactions

BRS YR2 (70 decks)

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