coeliac and inflammatory bowel disease Flashcards

1
Q

what is coeliac disease

A

gluten sensitive enteropathy or coeliac spruce
AI mediated disease of SI triggered by gluten in genetically predisposed individuals leads too malabsorption
cessation of symptoms when no gluten in diet

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2
Q

what is gluten

A

compound of wheat, rye and barely left behind after washing off the starch
consists of gliadin and glutenins

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3
Q

what are the genetic abnormalities of coeliac disease

A

ass with HLA-DQ2 and HLA-DQ8 in 95/5%
genes located on Chr 6p21
others being investigated
strong hereditary predisposition affecting 10% first degree relatives

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4
Q

who gets coeliac disease

A

Western Europe and USA, esp Irish and Scandanavian
inc in africa and asia
lots have it undiagnosed
high prevalence in downs syndrome, T1 DM, AI hepatitis, thyroid gland abnormalities
bimodal presentation in childhood and late 30s, 20% over 60

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5
Q

how does gluten cause coeliac disease

A
gluten in wheat and small bowel mucosa 
tissue transglutaminase
dominates glutamine in gliadin 
neg charged protein 
IL-15
Natural killer Tc ells and intraepithelial T lymphocytes
tissue destruction and villous atrophy
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6
Q

what does wheat do to the small bowel mucosa

A

inflammation and flat lining (crypts but loss of villi)

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7
Q

what are the types of coeliac disease

A

malabsorption leads to symptoms
asymptomatic coeliac disease - blood test
classical and atypical CD

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8
Q

symptoms of classic CD with GI symptoms

A
diarrhoea (smelly, bulky, rich in fat)
flatulence in some
borborygmus 
weight loss
in kids - fail to thrive 
weakness and fatigue 
sev abdo pain 
IBS like symptoms
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9
Q

classic presentation of ssteatorhoea

A

bulky pale offensive stool

rich in fat

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10
Q

atypical CD due to extra intestinal symptoms

A

anaemia
osteopenia and osteoporosis
muscle weakness, pins and needles, loss of balance
itchy skin conditions eg dermatitis
lack of periods, delayed periods, infertility in women and infertility and impotence in men
bleeding disorders due to vit K deficiency

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11
Q

atypical presentation of CD

A

emaciation
pot belly due to gaseous distension
muscle wasting
osteoporosis

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12
Q

investigations for CD

A

general - FBC, U and Es, LFTs
serology - TTGA, endomysial IgA (CT covering smooth muscle fibres), deaminated gliadin peptide (IgA and G). gluten free disease
can be neg in 6.4-9%
genetics and +TTGA to avoid biopsy in kids
duodenal biopsy

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13
Q

how do routine coeliac disease tests work

A

assess tissue damage
overreaction of immune system - antibodies to protein involved in damaged eg TTGA (tissue transglutaminase), endomysium and deaminated gliadin peptide

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14
Q

microscopic features of coeliac disease

A

at least 4 biopsies sampled from duodenum at upper GIT endoscopy as can be patchy
there is
villous hypertrophy, crypt hyperplasia, inc lymphocytes in lamina propria/chronic inflammation, intraepithelial lymphocytes, recovery of villous atrophy on gluten free diet

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15
Q

what is villous atrophy

A
chronic inflammation (packed full of blue cells)
crypt hyperplasia to replace villi
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16
Q

complications of coeliac disease

A

enteropathy associated T-cell lymphoma
high risk of adenocarcinoma in SB and other organs (LB, Yes, panc)
ass dermatitis hepetiformis
infertility and miscarriage
refractory coeliac disease despite sticking to diet
may be reduced by diet

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17
Q

what constitutes IBD

A
Crohn's disease
UC
Diverticular disease
ischaemic colitis
drug induced colitis
infective colitis 
CD and UC - idiopathic IBD (important to differentiate - surgery and treatment differs)
overlap in presentation, features and treatment
18
Q

what is Crohn’s disease

A

idiopathic chronic IBD often complicated by fibrosis and obstructive symptoms
can affect any part of GIT mouth to anus

19
Q

what is the epidemiology of CD

A

high prevalence in west, inc by jewish origin
inc in africa, South America and Asia
bimodal pres in teens/20s and 60/70s

20
Q

what causes CD

A

exact unknown
genetic, infectious, immunologic, environmental, dietary, vascular, smoking, NSAIDs and psych
defects in mucosal barrier allowing pathogens and antigens to induce unregulated inflammatory reaction

21
Q

what are the genetics of CD

A

strong evidence for it
first degree relatives 13-18%, 50% in MZ twins
polygenic
NOD2, also CARD15 on Chr16 encodes proteins ass to uncontrolled inflammation to luminal contents and microbes

22
Q

is there an infectious cause of CD

A

60-65% mycobacterium para-TB was investigated, not proven

other infectious organisms implicated inc measles, psuedomas and listeria

23
Q

environmental factors implicated in Crohn’s disease

A

improved hygiene hypothesis - reduces enteric infection in those susceptible, less reg processes so immune response not limited on infection leading to mucosal damage
migration from low risk pop to high risk
cigarette smoking doubles

24
Q

clinical features of CD

A

chronic indolent course punctuated by periods of remission and relapses
abdo pain, received by opening bowels
prolonged diarrhoea (not bloody, blood if colon involved)
loss of weight
low grade fever

25
Q

distribution of CD

A

SB alone - 40%
LB alone - 30%
both - 30%

26
Q

what are the morphologic features of CD

A

fat wrapping serosa (can aid to demarcate the extent of disease)
affects bowel segmentally to give rise to skip lesions
ulceration of mucosa giving rise to cobblestone pattern
strictures

27
Q

microscopic appearance of CD

A

transmural or full thickness inflammation of bowel wall
mixed acute and chronic inflammation eg polymorphs and lymphocytes
preserved crypts
mucosal ulceration
fissuring ulcers
granulomas
fibrosis of wall

28
Q

complications of CD

A

intra-abdo abscess
deep ulcers - fistula
sinus tract - blind ended tract ends in cul de sac
obstruction due to adhesions, strictures (fibrosis)
perianal fistula and sinuses
risk of adenocarcinoma, not as high as UC

29
Q

what is UC

A

chronic IBD
only affects large bowel from rectum to caecum
inflammatory process confined to mucosa and submucosa except in severe cases

30
Q

epidemiology of UC

A

more common in west, higher prevalence in jewish
less freq in africa, south America and Asia
arise at any age but rare before 10, peaks at 20-25 with smaller peals at 55-65

31
Q

what causes UC

A

unknown
similar to CD multiple factors implicated
genetic predisposition not as well defined (high incidence in first degree relative and twins)
HLA-B27 in most pts but not a cause
no specific infective agent
env factors - smoking protective, NSAIDs exacerbate, vits A and E found in low levels in UC

32
Q

clinical features of UC

A
intermittent attacks of bloody diarrhoea 
mucoid diarrhoea 
abdo pain 
low grade fever
weight loss
33
Q

macroscopic features of UC

A

LB, rectum to caecum
rectum only (proctitis), LHS bowel (splenic flexure to rectum) or whole (total colitis)
no ulcers in early disease
diffuse mucosal involvement (haemorrhagic)
chronicity - mucosa flat with shortening of bowel

34
Q

microscopic features of UC

A

inflammation confined to mucosa
diffuse mixed acute and chronic inflammation
crypt architecture distorted
quiescent UC mucosa may be atrophic with little/few inflammatory cells in lamina propria

35
Q

complications of UC

A
lead to surgery 
refractory medical treatment 
toxic megacolon (dilated, ill, bloody diarrhoea, abdo distension, electrolyte imbalance with hypoproteinanaemia)
refractory bleedoing
dysplasia or adenocarcinoma 
unremitting UC
after 8/10 years - annual colonoscopy
36
Q

what are the extra intestinal manifestations of UC and CD

A

ocular - uveitis, irisitis, episcleritis
cutaneous - erythema nodosum, pyoderma gangrenosum
arthropathies - ankylosing spondylitis
hepatic - screlosing cholangitis

37
Q

investigations into UC and CD

A
FBC, U and Es, LFTAs
inflammatory markers like CRP
faecal calprotectin 
endoscopy and biopsies 
radiological imaging 
barium studies, MRI, USS, CT
38
Q

why is it important to differentiate between UC and CD

A

pouch after surgery in UC but not CD due to risk of recurrence
pouch from SB as stool reservoir after removing large bowel

39
Q

what is fissuring

A

deep crevices

same as transmural

40
Q

what are granulomas

A

collections of lymphoid cells
known as granulomatous inflammation
ass to CD

41
Q

layers of SB

A
submucosa 
mucosa
muscularis mucosa 
circular muscularis propria
longitudinal muscularis propria
villi attached to crypts, attached to mucosa