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Mucosal Surfaces > L15: Ibd, Host And Microbiota > Flashcards

L15: Ibd, Host And Microbiota Flashcards

1
Q

Where does crohns affect

A

Any part of the gi tract from oral to rectum

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2
Q

What are skip lesions in crohns

A

Areas of non inflamed then inflamed again

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3
Q

What does transmural inlfammation in crohns mean

A

All layere eg from mucosa to serosa. Forms strictures and fistulae

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4
Q

What are strictures and fistulae

A

Strictures are narrowing of gi tract due to chronic inflammation and scarring process

Fistulae are tunnels connecting 2 tissues/ organs which dont usually. Forming new passages for leakage eg of faeces

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5
Q

What can fistulae form

A

Abscesses

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6
Q

How does uc compare

A

Only in colon, no skip lesions, from caecum all the wag to rectum usually

More superficial inflammation to mucosa

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7
Q

Where does crohns usually occur

A

Terminal ileum

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8
Q

Give some extra intestinal symptoms

A

Inflammation in eye, enteropsthic arthritis

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9
Q

Where does uc husallt start

A

Rectum

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10
Q

Whats the precalence in %

A

0.78 in 2018 but can increase to 1% in 2028

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11
Q

Give some fsctors of prevalence

A

Westernised diet, usually youngner onset (20-40), environment eg stress, smoking ,

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12
Q

What % have a relapse with uc

A

90%

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13
Q

What do early relapses indicate

A

Worse disease course

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14
Q

Who usually gets uc

A

Yojnger males

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15
Q

How many people usually indergo surgery eith crohns agter 10 years

A

50%

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16
Q

What are taken all the time whth these conditions

A

Corticosteroides

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17
Q

What haplens with crohns overtime so needs to be treated fast (target wbc)

A

Fistulae and strictures

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18
Q

How many genes are related to ibd

A

300 genes eg nos in inflammation upreg

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19
Q

What causes the intiial inflammation

A

Impaired barriers, dysbiosis, causing microbe interaction eith inflam cells

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20
Q

Which article discusses cytokines in ibd

A

Neurath 2014

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21
Q

Which types of genes were involved in ibd

A

Amps, chemokines, cyotkines

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22
Q

Which ibd has increased il-1b wg from inflammasome causing inflamation via granulochtes and th17

A

Crohns

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23
Q

Why was increased il18 important in crohns

A

Induces macrophages which secrete inflammatory ifny

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24
Q

How is il6 important in ibd

A

Platelet increase, reduced mucosal T death= inflammation bc induces th2

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25
Q

Which ibd is seen high th17

A

Both uc and crohns

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26
Q

Why is th1 seen crohns

A

Too much ifny and tnf release = inflammation

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27
Q

What would be the resolution to inflammatjon but not presenf eg due to lack of fibre

A

Ra, tgfb ——> increase in dc producing tregs

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28
Q

Does il10 block il1b inflammasome

A

Yes

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29
Q

Why are ifna and b good for ibd

A

Help regenrstion of epi cells, induce t regs

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30
Q

What do microbiota do to do with ifna and b

A

Increase its release from apc by binding tlr9

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31
Q

Which gene is upreg in ibd blockign tgf b and therefore tregs

A

Smad7 signalling protein

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32
Q

What sorts of things do you need to look at when diagnosing ibd

A 
Hereditary factors (3%)
Nsaids can dause acute symptoms 
Smoking history 
Travel 
Gastroenteritis which triggers ibd
Extra intestinal manifeststions
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33
Q

Which eim are present (neurath 2019)

A

Iritis, conjunctivitis, thrombosis, arthritis, liver damage

34
Q

What blood markeds are looked for

A

Crp creaxtive protein inflam marker
Full blood count fbc = anemic
Liver functioning trsts /LFT

35
Q

How is it diagnosed

A

Capsule endoscopy, colonsocopy and biopsy, mri, ct

36
Q

What is lost in mucosa with ibd

A

Mucosa, crytps, too mant inflam cells nesr

37
Q

Why can too high th2 eg from il6 and il4 cause ibd

A

Attracts eosinophils, basophils, mast cells

38
Q

What type of inflammation do th1 allow

A

Monocytic which secrete cytokines like tnf and ifny

39
Q

What 2 approaches to therapt are there

A

Step up (gentle to immunosuppressants eg methotrexate to biologics to surgery)

Step doen (biologica to surgery)

40
Q

Whixh med is used for uc inly

A

5 ASA

41
Q

What types of biologics are there

A

Anti a4:b7, anti tnf, anti il12, anti 23

42
Q

Which article discusses microbiota and ibd involvemnet

A

Ni et al 2017

43
Q

Which tpyes of bacteria are reduced in ibd eg due to wrsternised diet

A

Firmicutes

44
Q

Why do proteobacteria like ecoli increase

A

Inflammation is oxidstive and they are aerotolerant

45
Q

What else does inflammation do to allow outgrowth of commensala

A

Aea eg via nos = nitrate resp by ehec

46
Q

What is reduced due ti lacj of commensala in ibd

A

Farnesoid x activation by bile acids (which is anti tnf)

47
Q

Which yeast are seen to grow in crohns brcause of lack of commenslas and what happens because of it

A

Candida

Further acticates apc and eg th1 pathway, tnf etc

48
Q

Why is ifny release so bad for dysbiosis

A

Allows release of NO and ROS

No for nitrate resp and ros for tetrathionate

49
Q

What is one god thing anout inflammasome till it gets too much

A

Epithelial regeneration

50
Q

Why is it impaired jn ibd

A

Mutation in gene for jnflammasome

51
Q

Which cytokine from microbiota allows diff of th17 and ilc3 = chronic inflammation

A

Il23

52
Q

Where are tlr and nod

A

Innate, paneth and epi cells

53
Q

Which antibody blocks colitogenic pathogens

A

Iga

54
Q

Which types of th17 mutstions sre in ibd

A

Il23 r

55
Q

Which other types of genes are mutated which increase activity or decrewase

A

Hla,
Barrier genes defecting it wg ecm1
Autophagy

56
Q

What is autophagy for

A

Recycle cellular organeles and degradation of ic pathogens

57
Q

Which polymorphisms commin with autophagy in ibd

A

Atg16L1, irgm, LRRK2

58
Q

What does autophaggy usually alow release of from paneth cells

A

Amps

59
Q

What does polymorphism do to cytokines eg in atg16L1, lrrk2 and irgm

A

Alter them so less amp but il1b and il 18 released instead from paneth

60
Q

What types of pathogens are killed by autophagy

A

Salmonella, ehec, mycobacterium tb

61
Q

Whcih receptors regulate autophagy

A

Prr

62
Q

Which article discusses autophagy snd ibd

A

Levine 2011

63
Q

What did atg16L1 reduce

A

Amp

64
Q

How does irgm cause franumolas in crohns if defective

A

Usuallt allows clearing of mycobac tb which if not cleared causes granulomas

65
Q

How many nod2 polymorphisms seen in crohns

A

3

66
Q

Where is nod2 and what does it sense

A

Mac, epi, dc, paneth, neutrophils

Finds bscterial peptidoglycan

67
Q

What type of nfkb cytokines released by nod2 which see loss in crohns and granuloma formation

A

Il1b and il8 and il10

68
Q

Hoe many firmicute otu seen in people without crohns vs with

A

43 vs 13

69
Q

Why is asca a marker of crohns

A

Increased sach cer and candida

70
Q

Which firmicute seen in lower numbers which activates release of il10

A

Faecailbacterium prausnitzii

71
Q

Which ibd has a risk of smokingand what does smokint do

A

Crohns

Reduces diversity

Refuces actinobacteria like collinsella and firmicutes

Worse outcome and recurrence

72
Q

What is an anal fistula and how is it resolved

A

A tunnel from bowek to the skin nesr anus whoch gives farces another route forming abscesses

Need surgery to close tunnel

73
Q

Stoma surgery is an alt. Whag is it

A

Opening of abdomen to dicert faeces and urine away from rectum and collected in stomal bag

74
Q

What are ileoanal pouch surgeries

A

Anal canal is attached to the ileum (anastomoses formed) and rectum/ colon removed

75
Q

What is it callrd when pocuhes get inflammed and what antibiotics used

A

Pouchitis

Ciprofloxacin and metronidazole

76
Q

What is pouchitis due to microbiota

A

Low roseburia and blautia vs increased b vulgatus

77
Q

Why is fmt not a good treatment

A

Overrime you go bsck tk the baseline microbiota

78
Q

Shich diet product increased colitis

A

Casein from milk

79
Q

Which fibre reduced colitis

A

Psyllium from seeds

80
Q

Why does akkermwnsia reduce ivd even if it erodes mucus

A

It produces alotnof scra in return

81
Q

Does fmt composition affect outcome eg for anti pd1 therapy

A

Yes

82
Q

Which microbiota worked for anti pd1 vs which didnt for antitumour effects

A

Bifido and akkermansia were good eg produced cd8 but bacteroidales were weak t reg responses

Mucosal Surfaces (33 decks)

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