coeliac and inflammatory bowel disease Flashcards by Rebecca Webster

what is coeliac disease

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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what is gluten

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

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what are the genetic abnormalities of coeliac disease

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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who gets coeliac disease

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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how does gluten cause coeliac disease

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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what does wheat do to the small bowel mucosa

inflammation and flat lining (crypts but loss of villi)

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what are the types of coeliac disease

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

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symptoms of classic CD with GI symptoms

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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classic presentation of ssteatorhoea

bulky pale offensive stool

rich in fat

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atypical CD due to extra intestinal symptoms

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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atypical presentation of CD

emaciation
pot belly due to gaseous distension
muscle wasting
osteoporosis

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investigations for CD

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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how do routine coeliac disease tests work

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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microscopic features of coeliac disease

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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what is villous atrophy

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

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complications of coeliac disease

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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what constitutes IBD

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

what is Crohn’s disease

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

what is the epidemiology of CD

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

what causes CD

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

what are the genetics of CD

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

is there an infectious cause of CD

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

other infectious organisms implicated inc measles, psuedomas and listeria

environmental factors implicated in Crohn’s disease

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

clinical features of CD

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

distribution of CD

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

what are the morphologic features of CD

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

microscopic appearance of CD

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

complications of CD

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

what is UC

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

epidemiology of UC

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

what causes UC

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

clinical features of UC

``` intermittent attacks of bloody diarrhoea mucoid diarrhoea abdo pain low grade fever weight loss ```

macroscopic features of UC

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

microscopic features of UC

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

complications of UC

``` 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 ```

what are the extra intestinal manifestations of UC and CD

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

investigations into UC and CD

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

why is it important to differentiate between UC and CD

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

what is fissuring

deep crevices | same as transmural

what are granulomas

collections of lymphoid cells known as granulomatous inflammation ass to CD

layers of SB

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