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IBD Flashcards

1
Q

what type of bug is TB

A

acid fast bacilli

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2
Q

what is crohns disease

A

chronic inflammatory and ulcerating condition of the GI tract that can affect anywhere from the mouth to the anus

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3
Q

where is crohns most common

A

terminal ileum and colon

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4
Q

what is the most common age group for crohns diagnosis

A

early 20s (50% 20-20, 90% 10-40)- commoner in males

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5
Q

other than the bowl where can crohns affect

A

stomach, oesophagus, mouth, rectum/anus

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6
Q

what is the presentation of crohns

A 
abdominal pain (colicky),
small bowl obstruction,
diarrhoea,
bleeding PR,
anaemia,
weight loss, 
tender abdomen
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7
Q

is crohns curable

A

no but patients can go into lasting remission

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8
Q

what investigations should be done for crohns

A

endoscopy and mucosal biopsy

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9
Q

what appearance is seen in endoscopy

A

cobble-stone appearance

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10
Q

what is the endoscopic pattern of crohns disease

A

Patchy, segmental disease with skip areas (lesions) anywhere in GI tract
(skip areas= bits of unharmed tissue surrounded by damaged tissue)

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11
Q

what does the normal colonic mucosa look like

A

crypts packed together like rack of test tubes

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12
Q

describe a biopsy of crohns

A

chronic inflammation in lamina propria (fills with inflammatory cells)

  • cryptisis
  • crypts are irregular shape- look shattered
  • crypt abscess can form
  • granulomas (macrophages in a tight ball like sarcoidosis) non caseating
  • transmural inflammation
  • deep knife like fissuring ulcers
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13
Q

describe a non caseating granuloma

A

abnormal collection of macrophages and derivates such as giant cells that do not show a soft centre

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14
Q

are granulomas always found in crohns

A

no 50% of people dont

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15
Q

how does crohns cause bowl obstruction

A

fibrosis- stricture- obstruction

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16
Q

what happens to the wall of the bowl in crohns

A

is thickened- deep fissuring ulceration destroys mucosa (cobble stoning)

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17
Q

why does anaemia, fatigue, weight loss and diarrhoea happen in crohns

A

as lumen filled with pus- cannot absorb aswell

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18
Q

what types of polyps might be seen in crohns

A

pseudopolyps

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19
Q

how is crohns transmural inflammation

A

affects all 3 layers of the bowel

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20
Q

what are the complications of crohns

A 
malabsorption,
fistulas,
intractable disease,
bowl obstruction,
anal disease,
perforation,
malignancy,
amyloidosis,
rarely toxic megacolon
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21
Q

what is an iatrogenic cause of malabsorption in crohns

A

short bowl syndrome due to repeated resections and recurrences

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22
Q

what can result from malabsorption in crohns

A

Hypoproteinemia, Vitamin deficiency, Anaemia, gallstones

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23
Q

what type of anaemia does iron deficiency lead to

A

microlytic- small red blood cells

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24
Q

what is macrolytic anaemia and what causes it

A

blood with an insufficient concentration of hemoglobin- red blood cells larger than normal

vitamin B12 and folate deficiency

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25
Q

what is blind loop syndrome

A

bacterial overgrowth in the small intestine

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26
Q

what is included in anal disease in crohns

A

sinuses, fissures, skin tags, abscesses, perineum falls apart

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27
Q

what is intractable disease from crohns

A

failure to tolerate or respond to medical therapy, continuous diarrhoea or pain, may require surgery, not curative

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28
Q

what is amyloidosis

A

a rare disease that occurs when a substance called amyloid builds up in your organs

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29
Q

what is amyloid

A

an abnormal protein that in produced in bone marrow

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30
Q

what is toxic megacolon

A

dilated bowel

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31
Q

where does crohns and UC have a high incidence

A

north america and northern europe, high in scotland

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32
Q

what genetic defects are associated with crohns

A

NOD2 (CARD15)on chromosome 16
(encodes a protein in bacterial recognition)

HLA-DR1
HLA-DQw5

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33
Q

what are the environmental triggers to crohns

A

smoking increases risk

infectious agents (viral, mycobacterium) cause similar pathology

vascilutis could explain segmental distribution

sterile environment theory

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34
Q

what autoimmune features could cause crohns

A

persistent T cell and macrophage activation

excess pro inflammatory cytokine production

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35
Q

why do gene defects cause crohns

A

as they prevent a controlled effective immune response to a trigger (more susceptible to environmental agents)

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36
Q

what is ulcerative colitis

A

chronic inflammatory (mucosal and submucosal inflammation) disorder confined to the colon and rectum of unknwon aetiology

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37
Q

bloody diarrhoea with infection excluded= think what?

A

UC

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38
Q

what age group has peak incidence

A

30s, can occur in any

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39
Q

where does UC affect

A

confined to colon and rectum

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40
Q

where in GI tract does crohns usually spare

A

the rectum

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41
Q

what is the clinical presentation of UC

A

diarrhoea, mucus and blood PR

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42
Q

what are the different onsets of UC

A

chronic course with exacerbation and remission

continuous low grade activity

a single attack

an acute colitis (toxic megacolon)

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43
Q

what investigations should be done for UC- bloody diarrhoea and mucous

A

endoscopy and mucosal biopsy

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44
Q

what is seen on an endoscopy in UC

A

red inflamed rectum- diffusely ulcerated, almost always involving the rectum

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45
Q

what does UC never go higher than

A

the ileoceacal valve

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46
Q

describe a biopsy of UC

A

massive influx of inflammatory cell- colonic mucosa gone, no barrier, infiltrate of inflammatory cells in the submucosa destroying the crypts

crypts are irregularly shaped and branching- acute cryptitis

crypt abscesses

severe ulceration with fibrinopurulent exudate

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47
Q

what are the features of chronic inactive UC

A

low grade chronic inflammation with crypt distortion and low grade diarrhoea

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48
Q

what is a surgery used in severe UC

A

subtotal colectomy- bowl removed

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49
Q

what can cure UC

A

removal of the large bowl

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50
Q

are pseudopolyps seen in UC

A

yes

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51
Q

where in inflammation confined to in UC

A

the mucosa and submucosa (except in toxic megacolon) SUPERFICIAL ULCERATION

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52
Q

are there granulomas in UC

A

no

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53
Q

what are the complications of UC

A 
intractable disease,
toxic megacolon,
colorectal carcinoma,
blood loss,
electrolyte disturbance,
anal fissures,
extra GI manifestations: eyes, liver, joints, skin,
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54
Q

describe intractable disease in UC

A

continuous diarrhoea, flares may be due to intercurrent infection by enteric bacteria or CMV (cytomegalovirus)

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55
Q

describe toxic megacolon

A

acute or acute on chronic (an exacerbation) fulminant colitis- colon swells and will rupture unless removed by emergency colectomy- colon fills with fluid, pus and blood

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56
Q

why does UC lead to colorectal cancer

A

as chronic inflammation leads to epithelial dysplasia and then carcinoma

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57
Q

why is more of the colon predisposed to cancer in UC than in crohns

A

as diffuse not patchy in UC

58
Q

what electrolyte imbalance in common in UC

A

hypokalemia

59
Q

name the extra GI manifestations of UC

A

eyes- uveitis
liver- primary sclerosing cholangitis (autoimmune destruction of bile ducts)
joints- arthritis, ank spondylitis
skin- pyoderma gangrenosum, erythema nodusum

60
Q

what gene is UC associated with

A

HLA-DR2
NOD-2 (familial cases)
(immune system at fault)

61
Q

what is aberrant immune response

A

autoimmune disease

62
Q

describe the autoimmune response in UC

A

persistent activation of T cells and macrophages

autoantibodies (e.g. ANCA)

excess proinflammatory cytokine production

bystander damage due to neutrophillic inflammation

63
Q

what might alter the autoimmune response in both UC and crohns

A

probiotics (as microbiome is abnormal)

64
Q

what are the environmental trigger of UC

A

unknown- smoking actually help

65
Q

in UC or crohns are fistula more common

A

in crohns- UC superficial ulceration

66
Q

what has a higher cancer risk UC or crohns

A

UC

67
Q

in UC or crohns is extra GI symptoms more common

A

UC

68
Q

what is the clinical presentation of crohns

A

abdominal pain and peri-anal disease

69
Q

what is the clinical presentation of UC

A

diarrhoea and bleeding

70
Q

what are the three components of the pathogenesis of IBD

A

genetic disposition
mucosal immune system
environmental triggers

71
Q

what does over reactive effector T cells do

A

inflammation/ disease

72
Q

what does an absence of regulatory T cells cause

A

uncontrolled inflammation/ aggressive disease

73
Q

what immune factor mediates crohns

A

Th1 mediates

74
Q

what immune factor mediates UC

A

mixed Th1/ Th2 mediated disease/ NKTC

75
Q

which does smoking aggravate, UC or crohns

A

crohns

76
Q

what should you avoid in crohns

A

NSAIDS e.g. ibruprofen

77
Q

what are the symptoms of UC

A 
Diarrhoea + bleeding
Increased bowel frequency (HOW OFTEN?)
Urgency
Tenesmus
Incontinence
Night rising- shouldn’t have to poo at night 
Lower abdo pain (esp. LIF)
(proctitis can cause constipation
78
Q

what diarrhoea can antibiotics cause

A

C diff

79
Q

what is a severe UC episode

A 
>6 bloody stools/24 hour
\+
1 or more of
  Fever
  Tachycardia
  Anaemia
  Elevated ESR
80
Q

what further assessments should you do

A

bloods: CRP, albumin
plain AXR
endoscopy
histology

81
Q

what is absent in an inflammed colon

A

stool

82
Q

what is seen on a AXR in UC

A

stool distribution- Bowl black as full of acid, lack of stool

Mucosal oedema / ‘thumb-printing’- swelling of the mucosal bowel wall, thickens

toxin megacolon

83
Q

what can be seen on an endoscopy in UC

A

Loss of vessel pattern
Granular mucosa
Contact bleeding- inflamed tissue friable to bleed

84
Q

what leads to abscesses in UC

A

distortion of crypts

85
Q

what determines the risk of colorectal cancer

A

severity of inflammation
duration of disease
disease extent

86
Q

what is primary sclerosing cholangitis

A

chronic inflammatory disease of biliary tree- 80% have associated IBD

87
Q

what is peri-anal disease

A

recurrent abscess formation- pain, can lead to fistula with persistent leakage, damaged sphincters

88
Q

what determines the symptoms of crohns

A

the site of the disease

89
Q

what are the symptoms of crohns in the small intestine

A

abdominal cramps, diarrhoea, weight loss

90
Q

what are the symptoms of crohns in the colon

A

abdominal cramps
diarrhoea with blood
weight loss

91
Q

what are the symptoms of crohns in the mouth

A

painful ulcers,
swollen lips,
angular chielitis

92
Q

what are the symptoms of crohns in the anus

A

peri-anal pain,

abscess

93
Q

what blood abnormalities would suggest crohns

A

CRP, albumin, platelets, B12 (terminal ileum B12 deficiency), ferritin

94
Q

loss of haustra markers can lead to what

A

formation of a fistula= crohns

95
Q

what small bowel assessments could be done in crohns

A

Barium follow-through
Small bowel MRI (gold standard with intravenous and swallow contrast)
Technetium-labelled white cell scan

96
Q

what lifestyle changes can help in IBD

A

smoking cessation- crohns

diet- low residue (fibre) diet so bowel doesn’t have to work as hard

97
Q

what does smoking cause recurrence in 70% of cases

A

crohns relapse

98
Q

what is the treatment for UC

A

5ASA (mesalazine)

steroids (acute/ severe flare not long term)

immunosuppressants (steroid sparing agents)

anti-TNF therapy

99
Q

what is the treatment for crohns

A

steroids (acute/ severe
flare not long term)

immunosuppressants (maintenance therapy)

anti TNF therapy

100
Q

what is the mechanisms of action of 5 ASA

A

acts on mucosal surface, has a topical anti inflammatory effect. reduces the risk of colon cancer

101
Q

what are the side effects of 5ASA

A

diarrhoea, idiosyncratic nephritis - monitor renal function before and during

102
Q

what are the two ways 5 ASA can be administered

A

oral (tablets or granules)- delayed, pH dependant release

topical= suppositories, enemas

103
Q

what part of the GI tract do ALL 5-ASA conjugates reach

A

the colon

104
Q

what are the pros/ cons of suppositories and enemas

A

suppositories: only reach 20cm but adhere to mucosa better
enemas: go further but don’t adhere as well

105
Q

what is the mechanisms of action of corticosteroids in IBD

A

systemic anti-inflammatory properties, to induce remission

106
Q

what are the two types of administration of corticosteroids in IBD and examples of each

A

oral; prednisolone (has more systemic effects)

topical: budesonide (less SE as less first pass metabolism)

short course- high dose initially reducing over 6-8 weeks

107
Q

why should steroids be used as a bridge to maintenance therapy + what are the side effects

A

as people become dependant + side effects;

  • musculoskeletal (avascular necrosis, osteoperosis)
  • GI
  • cutaneous (ance, thinning of skin)
  • metabolic (weight gain -increased appeptite- diabetes, hypertension)
  • neuropsychiatric (trouble sleeping, manic, depressed)
  • cataracts
  • growth failure in children
108
Q

give examples of immunosupression therapies in IBD

A

azathioprine/ mercaptopurine

methotrexate

109
Q

what is the active for of azathioprine

A

6-TGN

110
Q

what should you avoid prescribing azathioprine with

A

allopurinol

111
Q

what are the side effects of azathioprine

A

pancreatitis
leucopaenia
hepatitis
small skin of lymphoma, skin cancer

112
Q

what immune response is associated with crohns

A

Th1 cells, production of interleukins and TNF-alpha by DC cells and macrophages

Polarized T cell responses initiate an inflammatory cascade that involves endothelial activation, chemokine production, and white blood cell (WBC) recruitment.

113
Q

what secretes IL2, 17, IFN-y and TNF-alpha

A

Th1 polarised cells

114
Q

what immune response is associated with UC

A

Th2 and NK cells

Polarized T cell responses initiate an inflammatory cascade that involves endothelial activation, chemokine production, and white blood cell (WBC) recruitment.

115
Q

what cells are targeted in the immunosupression therapies for IBD

A

tnf- alpha, MadCAM-1, T cells

116
Q

what is tumour necrosis factor alpha

A

a proinflammatory cytokine

117
Q

what are the antibodies fto TNF

A

infliximab; IV infusion

adalimumab; S/C injection

118
Q

how does anti TNF therapy work

A

promotes apoptosis of activates T-lymphocytes, rapid onset of action

119
Q

why might anti-TNFa treatments be unsafe

A

patient may already have antibodies that block the action of the drug

infections could develop

TB and tumours may reactivate

120
Q

when should Anti-TNFa therapy be used

A

as part of long term strategy, including immune suppression, surgery (Crohns), supportive therapy

refractory / fistulising disease

121
Q

name three anti- TNFa therapies

A

infliximab, remicade, inflectra, remsima

122
Q

when is emergency therapy done in IBD

A

where there is failure to respond to medical therapy, small bowel obstruction, abscess, fistulae

123
Q

when is elective surgery done in IBD

A

when there is failure to respond to therapy, dysplasia of colon mucosa

124
Q

for which IBD can surgery be curable

A

UC- permanent ileostomy/ restorative proctocoloectomy and pouch

125
Q

what is a proctocolectomy

A

surgical removal of the rectum and all/part of the colon

126
Q

what is a proctocolectomy with end ileostomy

A

where the anus is sewed shut and a stoma inserted into the skin of the lower abdomen

127
Q

what are the indications for elective surgery in UC

A

medically unresponsive disease,
intolerability,
dysplasia/ malignancy,
growth retardation in children

128
Q

what are the different end of an elective proctocolectomy

A

ileostomy, a pouch, ileorectal anastomosis

129
Q

what are the pros and cons of a pouch

A

patient can go to the toilet but average 6 bowel movement a day

can have incontinence, nocturnal incontinence/leakage/spotting or the pouch can fail

130
Q

what are the local immediate, early and late complications of a pouch

A

immediate- haemorrhage, enterotomy

early- urinary dysfunction, wound infection, pelvic abscess, anastomotic leak

late- impotence, infertility, pouchitis

131
Q

what are the systemic immediate, early and late complications of a pouch

A

immediate- anaphylaxis

early- atelectasis, ileus (lack of movement in intestines), portal vein thrombosis

late- DVT/PE, small bowel obstruction

132
Q

how do you assess the severity of an acute UC attack

A

truelove and witt criteria:

ESR (inflammation marker in blood)
Haemoglobin
Bloody Stools
Temperature>37.8
Heart rate>90
133
Q

what is a subtotal colectomy

A

resection of part of the colon

134
Q

what are nervi erigenti

A

pelvic splanchnic

135
Q

what are the indications for surgery in crohns

A 
Stenosis causing obstruction
Enterocutaneous fistulas
Intra-abdominal fistulas
Abscesses
Bleeding (acute or chronic)
Free perforation
136
Q

when is a gastrojejunostomy done

A

for duodenal or pyloric stenosis

137
Q

what can be used instead of resection to treate strictures in crohns

A

stricturoplasty- balloon dilatation

138
Q

what is an enterocutaneuos fistula

A

an abnormal connection between the intestines/ stomach and the skin of the abdominal wall

139
Q

what are the different types of lesions in perianal disease

A

primary- fissure, ulcer

secondary- abscess, tags, fistula

incidental- piles hidradenitits

140
Q

what type of IBD can be cured by surgery

A

UC

141
Q

what are the common deficiencies in IBD

A

anaemia, oestoperosis, B12, folate

142
Q

what is modulen

A

nutritional powder

GI (64 decks)

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