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MET3a > IBD > Flashcards

IBD Flashcards

1
Q

What is IBD made up of?

A

Crohn’s disease

Ulcerative Colitis

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2
Q

Define IBD

A

Chronic
Idiopathic
Relapsing and remitting
Inflammatory disorders of the GI tract

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3
Q

Which parts of the body does Crohn’s affect?

A

Anywhere between mouth and anus

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4
Q

Which parts of the body does ulcerative colitis affect?

A

Large intestine only

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5
Q

What should IBD not be confused with?

A

IBS - much less acute and dangerous! much more common!

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6
Q

Where is IBD prevalent in?

A

Increase in Europe and higher latitudes
Argentina
Rise in newly industrialised countries

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7
Q

NOD 2 gene

A

Protein which helps immune cells in body detect invading pathogens

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8
Q

Autophagy

A

Another way to protect against invading pathogens

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9
Q

Purpose of epithelial barrier

A

Separates microbiota in gut from immune system

If not separated = profound inflammatory reaction = destruction of bowel wall, ulcers

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10
Q

Genetic cause of IBD

A

Mutations/changes in 100s of genes which protect body against invading pathogens
e.g. NOD2, autophagy

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11
Q

Environmental factors affecting IBD

A 
Physical activity
Appendectomy - protective in UC
Smoking
Stress
Vitamin D/UV exposure is protective
Hygiene
Diet
Sleep
Medications
Microbiome
Genetic susceptibility
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12
Q

Hygiene Hypothesis

A

Large decline in infectious diseases = TB, hep A, RF etc.

But large increase in immune mediated disorders = RA, asthma, T1D, MS

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13
Q

Smoking link with Crohn’s

A

Accelerates progression of Crohn’s
Less likely to respond to treatment
Cessation Is an effective treatment

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14
Q

Smoking link with UC

A

Onset follow smoking cessation

Nicotine patches as effective as 5ASA (but badly tolerated unless you are a smoker)

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15
Q

Which drugs can initiate a relapse in IBD?

A

NSAIDs
Oral contraceptive pull = Crohns
Opiods (loperamide, codeine) - provoke colonic dilatation in acute severe UC

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16
Q

What diet is good at treating Crohns?

A

Elemental/polymeric liquid diet

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17
Q

Foods badly affecting IBD

A

High animal fat diet
Low fibre intake
Emulsifiers and thickeners
May alter gut microbiome

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18
Q

Link between physical activity and IBD

A

Regular active exercise reduced risk of

  • developing Crohns but not UC
  • relapse of Crohns and possibly UC
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19
Q

What type of people are more likely to get UC?

A 
White people
Men to women equal
20-40 year olds
Second peak >60
Higher rate of monozygotic twins
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20
Q

4 sites of UC

A

Proctitis (rectum)
Proctosigmoiditis
Left sided colitis (all the `way up to splenic flexure)
Pancolitis (all the way around)

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21
Q

In which UC site are different drug administration methods used?

A

Proctitis - suppositories
Left sided colitis - enemas
Whole colon - oral therapy

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22
Q

What anatomy is UC limited to?

A

Colon and rectum only

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23
Q

What is the most common site in UC

A

Almost always rectum with variable proximal extent

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24
Q

Where is there inflammation in UC

A

Lamina propria

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25
Q

How do patients with UC present?

A 
Urgent diarrhoea
Bloody stools
Fatigue (all immune mediated disease)
Weight loss
Cancer (rare)
Extra-intestinal manifestations
26
Q

What is the hallmark of UC?

A

Diarrhoea

27
Q

What extra-manifestations are there in IBD?

A 
Mouth - ulcerations
Eyes - uveitis
Joints - Arthritis/arthropathy/RA
Skin - erythema nodosum shins/feet, pyoderma gangrenosum
Perianal disease
28
Q

What is perianal disease much more common in?

A

Crohns!! rather than UC

29
Q

What are the signs of UC?

A 
tender abdomen - LIF generally mild
Pallor
tachycardia
leukonychia - malnutrition
extra-intestinal manifestations
30
Q

Ix of UC

A 
Bloods
- anaemia microcytic
- low ferritin 
- low albumin
- raised inflammatory markers = CRP, ESR< thrombocytosis, faecal calprotectin
- MC&amp;S
- OC&amp;P (parasites)
- Plain AXR
Endoscopy - gold standard
31
Q

What is faecal calprotectin?

A

Inflammatory marker expressed by immune cells in lining of gut wall particularly neutrophils that you can detect in stool
Good way to differentiate between IBS and IBD

32
Q

What are you looking for on an AXR?

A

Toxic megacolon
Pancolitis severe disease shows this
Dilation of large intestine

33
Q

UC Histology

A

Lumen and epithelial layer only affected
Always continuous so will not see areas of unaffected bowel in between
Crypt architecture distortion/twisted
Crypt abscess (neutrophils in crypt)

34
Q

Crohns histology

A

Affects whole gut wall unlike UC

Not continuous so will see areas of unaffected areas in between 2 sites of affected bowel

35
Q

What is a hallmark of chronic inflammation on histology?

A

Crypt architecture distortion/twisted

36
Q

Treatment options for UC

A 
Steroids
5-Amino salicylic acid
Probiotics
Azathioprine
Methotrexate
Anti-TNF
Anti-integrins
JAK inhibitors
Surgery
37
Q

Examples of 5-ASA

A

Sulphasalazine - bone marrow suppression side effect

Mesalazine

38
Q

Which anti TNFs are used for Tx of UC?

A

Infliximab - infusion
Adalimumab - SC
Golimumab

39
Q

Example of anti-integrin

A

Vedolizumab - blocks alpha4beta7 which binds to MADCAM (adhesion molecule in the blood vessels of gut allowing white cells in to gut

40
Q

Example of Jak inhibitor

A

Tofacitinib

41
Q

Order/protocol of IBD Tx

A

Vast majority on Mesalazine - oral & topical->
Immunomodulators (azathioprine & 6-mercaptopurine) ->
Anti-TNFs, anti-integrins, Jak inhibitors

42
Q

What drugs can get you better quickly in UC?

A

Corticosteroids - IV hydrocortisone, prednisolone, Cortiment MMX

43
Q

Who is more likely to get Crohn’s?

A

Higher in Caucasian
1;1 male to female
15-30 yrs

44
Q

Symptoms of Crohns

A

DEPENDS WHERE DISEASE IS

  • crohns colitis = similar UC symptoms (diarrhoea and urgency)
  • terminal ileum = pain colicky post prandially
  • altered bowel habits = diarrhoea, obstruction
  • PR blood loss
  • weight loss more likely than UC as hurts every time you eat
  • fistulae and abscesses as affecting whole wall
  • oral symptoms
  • extra intestinal manifestations
  • fatigue
45
Q

Where is the most common site of Crohns

A

terminal ileum

46
Q

Signs of Crohns

A
  • mass
  • scars
  • stoma
  • fistula
  • abscess
  • malnutrition
  • oral ulceration
47
Q

Natural cycle of Crohns

A
  • starts of inflammatory
  • then can get scarring -> structuring/fibrosis/permanent narrowing of bowel
  • OR can get penetration
48
Q

Ix in Crohns

A 
Bloods 
- anaemic microcytic
- low ferritin, folate, B12
- raised inflammatory markers
- low albumin
Faeces
- MC&amp;S
- OC&amp;P
- faecal calprotectin
Plain AXR
- loops of small bowel
- megacolon
Barium Follow Through now rare
- strictures
- rose thorn ulcers
CT be wary of radiation as young patients
- terminal ileum thickening
- abscess
MRI
- small bowel
- pelvic/perianal sepsis
Endoscopy
49
Q

Crohns Histology

A

Non caseating granuloma
Regions of unaffected bowel then affected
Giant cells
granulomas

50
Q

Treatment options for Crohns

A

Diet
Steroids = prednisolone, budesonide (topical)
5 ASA not used now as uneffective (Pentosa)
Probiotics not that helpful
ABs (cipro, metro allow healing)
Immunosuppressants
Biologicals - Anti-TNF, anti-integrin, anti-IL 12/23
Surgery

51
Q

Which immunosuppressants are used in Crohns

A

Azathiopurine

MTX

52
Q

Example of anti-IL 12/23

A

Ustkeiumab

53
Q

Complications of extra-intestinal features

A 
LIVER - primary sclerosing cholangitis 
Anaemia
thrombosis
Urinary stones
gallstones
Osteoporosis
Skin, eyes, joints
54
Q

How are joints affected?

A

Saroiliitis
Ankylosing spondylitis
Large joint arthropathy
Small joint arthropathy

55
Q

How is the liver affected?

A

Primary sclerosing cholangitis

  • increasing risk of cancer in bile duct and colon
  • itching and jaundice

Fatty Liver
Autoimmune hepatitis

56
Q

Colorectal Cancer

A

Increased risk in IBD >10 years
>8 years screening offered
- increased risk if extensive colitis, chronic inflammation and sclerosing cholangitis
- screening looks for macro and microscopic dysplasia

57
Q

What causes IBS?

A 
Diet
Psychological
Dysbiosis
Motility
Chronic Pain
58
Q

How do you diagnose IBS?

A

Faecal calprotectin to prove they don’t have IBD

59
Q

Who is more likely to have IBS?

A

Young - teens to 20s

female 2:1

60
Q

Presentation of IBS

A 
Relief after defecation
With or without bloating
No nocturnal symptoms
Normal FBC/CRP/coeliac screen/haemetinics/TFTs
Normal faecal calprotectin
61
Q

Differentials for IBS

A

Coeliac Disease- everyone should have coeliac screening
Bile Salt Malabsorption
Parasitic Infection
Small Intestinal Bacterial Overgrowth
Neuroendocrine tumours - fasting gut hormones
Hyperthyroidism
Carcinoid syndrome

62
Q

IBS Tx

A 
reassurance
FODMAP
Sparing use of anti-spasmodics
CBT if need
ABs in some
Probiotics
Anti-depressants

MET3a (38 decks)

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