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GI lectures > Pathology of IBD > Flashcards

Pathology of IBD Flashcards

1
Q

what is crohns disease?

A

chronic inflammatory and ulcerating condition of the GI tract thatcan affect anywhere from the mouth to anus
(most common in terminal ileum and colon)

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2
Q

who usually presents with crohns disease?

A

90% are 10-40 years old
50% 20-30 years old
can occur in children
more common in males

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3
Q

what are the most common sites of crohns disease?

A

2/3rds have small bowel involvement only
1/6 have colonic/anal disease only
1/6 have both

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4
Q

how does crohns disease present?

A 
abdominal pain
small bowel obstruction
diarrhoea
bleeding PR
anaemia
weight loss
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5
Q

what is the clinical course of crohns disease?

A

chronic
exacerbations and remissions
unpredictable response to therapy
small number go into lasting remission within 3 years of diagnosis

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6
Q

describe the typical crohns patient?

A

22 year old male
abdominal pain
bloody diarrhoea for 3 months
tender abdomen

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7
Q

how is crohns investigated?

A

endoscopy and mucosal biopsy

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8
Q

describe the pattern of lesions in crohns disease?

A

patchy, segmental disease with skip areas anywhere in GI tract

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9
Q

what does crohns look like histologically?

A

chronic active colitis - inflammatory cells in lamina propria
non-caseating granulomas (in 50%)
crypt branching

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10
Q

what are the consequences if a crohns patient doesn’t respond to medical therapy (steroids etc)?

A

bowel obstruction

will need surgery

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11
Q

what might be seen in the GI tract with crohns disease?

A 
stricture
thickened wall
fat wrapping
ulceration (can cause fissures)
skip lesions
deep knife like fissures - produces cobblestoning of mucosa
pseudopolyps (rare)
transmural inflammation
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12
Q

name 2 forms of chronic mucosal inflammation associated with crohns

A

cryptitis

crypt abscesses

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13
Q

what are the possible complications of crohns disease?

A 
malabsorption
fistulas
anal disease
intractable disease
bowel obstruction
perforation
malignancy
amyloidosis
rarely toxic megacolon
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14
Q

what might cause malabsorption in crohns disease?

A

short bowel syndrome due to repeated resections and recurrences
hypoproteinaemia, vitamin deficiency, anaemia
gallstones

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15
Q

what fistulas might form in crohns disease?

A 
VesicoColic
EnteroColic
GastroColic
RectoVaginal
TuboOvarian abscess
Blind loop syndrome
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16
Q

what anal diseases might occur in crohns disease?

A 
sinuses
fissures
skin tags
abscesses
perineum falls apart
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17
Q

what is intractable disease?

A

failure to tolerate or respond to medical therapy
continuous diarrhoea or pain
may require surgery - total colectomy

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18
Q

where is crohns disease incidence high/low?

A

high in north America, Europe and Scotland

low in Africa, Asia and south America

19
Q

does ethnicity affect the incidence of crohns disease?

A

more common in jewish people than arab people in isreal

less common in Ashkenazi jews living in isreal vs the USA

20
Q

is there a genetic link in crohns disease?

A

possibly
44% concordance in monozygous twins
possibly NOD2 gene on chromosome 16
association with HLA-DR1 and HLA-DQw5

21
Q

what environmental triggers can worsen IBD?

A 
smoking
infectious agents
vasculitis
sterile environment theory
NSAIDs
22
Q

describe the aberrant immune response in crohns disease

A

persistent activation of T cells and macrophages (failure to switch off)
excess pro-inflammatory cytokine production
maybe alterable by changing intestinal microflora

23
Q

what is the likely pathogenesis of crohns disease?

A

genetic susceptibility to environmental agent(s) which prevents a controlled and effective response to a trigger

24
Q

what 4 things can cause crohns?

A

luminal microbial antigens and adjuvants
genetic susceptibility
environmental triggers
immune response

25
Q

what is ulcerative colitis?

A

chronic inflammatory disease confined to the colon and rectum
mucosal and submucosal inflammation

26
Q

UC is the most common cause of diarrhoea with pus and mucus in temperate climates, true or false?

A

true

27
Q

who is UC most likely to present in?

A

young people (peaks in 30s)
more in males
can present in children/elderly

28
Q

what sites does UC affect?

A

colon and rectum
almost always the rectum
continuous, extending proximally

29
Q

what is the clinical presentation of UC?

A

diarrhoea

mucous and blood PR

30
Q

what is the clinical course of UC?

A

chronic with exacerbation and remission
continuous low grade activity
a single attack
acute fulminant colitis (toxic megacolon)

31
Q

describe the typical UC patient

A

32 yr old male
bloody diarrhoea and mucus
goes to toilet 25 times a day

32
Q

how is UC investigated?

A

endoscopy and mucosal biopsy

33
Q

what would be seen histologically in UC?

A

massive influx of inflammatory cells
basal lymphoplasmacytic infiltrate with irregular shaped branching crypts
crypt abscesses
severe ulceration with fibrinopurulent exudate

34
Q

what would be the consequences if medical therapy were to fail in UC?

A

subtotal colectomy

35
Q

are pseudopolyps seen in UC?

A

yes

not always but often

36
Q

UC gives transmural inflammation, true or false?

A

false

inflammation confined to mucosa/submucosa

37
Q

does UC give granulomas?

A

no

38
Q

does UC give chronic active colitis?

A

yes

  • cryptitis
  • crypt abscesses
39
Q

what are the complications of UC?

A 
intractable disease
 - due to intercurrent enteric bacteria infection
toxic megacolon
colorectal carcinoma
blood loss
electrolyte disturbance (hypokalaemia)
anal fissures (not common)
40
Q

what is toxic megacolon?

A

acute or acute on chronic fulminant colitis
colon swells up to huge size
will rupture unless removed = emergency colectomy

41
Q

what extra GI manifestations can UC cause?

A

eyes - uveitis
liver - primary sclerosing cholangitis
joints - arthritis, ank spondylitis
skin - pyoderma gangrenosum, erythema nodusum

42
Q

where is UC incidence high/low?

A

high in north America,Europe, Scotland

low in Africa, South America, Asia

43
Q

is there a genetic link in UC?

A

possibly
high concordance in monozygotic twins
association with HLA-DR2
familial cases assoc with NOD-2 gene

44
Q

describe the aberrant immune response in UC

A

persistent activation of T cells and macrophages
autoantibodies present (eg ANCA)
excess pro-inflammatory cytokine production
maybe alterable by changing gut microflora

GI lectures (75 decks)

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