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
what is ulcerative colitis?
chronic inflammatory disease confined to the colon and rectum mucosal and submucosal inflammation
26
UC is the most common cause of diarrhoea with pus and mucus in temperate climates, true or false?
true
27
who is UC most likely to present in?
young people (peaks in 30s) more in males can present in children/elderly
28
what sites does UC affect?
colon and rectum almost always the rectum continuous, extending proximally
29
what is the clinical presentation of UC?
diarrhoea | mucous and blood PR
30
what is the clinical course of UC?
chronic with exacerbation and remission continuous low grade activity a single attack acute fulminant colitis (toxic megacolon)
31
describe the typical UC patient
32 yr old male bloody diarrhoea and mucus goes to toilet 25 times a day
32
how is UC investigated?
endoscopy and mucosal biopsy
33
what would be seen histologically in UC?
massive influx of inflammatory cells basal lymphoplasmacytic infiltrate with irregular shaped branching crypts crypt abscesses severe ulceration with fibrinopurulent exudate
34
what would be the consequences if medical therapy were to fail in UC?
subtotal colectomy
35
are pseudopolyps seen in UC?
yes | not always but often
36
UC gives transmural inflammation, true or false?
false | inflammation confined to mucosa/submucosa
37
does UC give granulomas?
no
38
does UC give chronic active colitis?
yes - cryptitis - crypt abscesses
39
what are the complications of UC?
``` intractable disease - due to intercurrent enteric bacteria infection toxic megacolon colorectal carcinoma blood loss electrolyte disturbance (hypokalaemia) anal fissures (not common) ```
40
what is toxic megacolon?
acute or acute on chronic fulminant colitis colon swells up to huge size will rupture unless removed = emergency colectomy
41
what extra GI manifestations can UC cause?
eyes - uveitis liver - primary sclerosing cholangitis joints - arthritis, ank spondylitis skin - pyoderma gangrenosum, erythema nodusum
42
where is UC incidence high/low?
high in north America,Europe, Scotland | low in Africa, South America, Asia
43
is there a genetic link in UC?
possibly high concordance in monozygotic twins association with HLA-DR2 familial cases assoc with NOD-2 gene
44
describe the aberrant immune response in UC
persistent activation of T cells and macrophages autoantibodies present (eg ANCA) excess pro-inflammatory cytokine production maybe alterable by changing gut microflora