Ulcerative Colitis vs Crohns vs Coeliac PDF

Preview

Summary

Ulcerative Colitis Crohn’s CoeliacDefinition Autoimmune Currently understood to be post-infectious Autoimmune disorder affecting the small intestineRisk FactorsFamily history Poor diet Recent smoking cessationFamily history SmokingFamily history Other autoimmune diseases IgA Infection e. rotavirus ...

Description

Definition

Risk Factors

DDx

Epidemiology Aetiology

Clinical Features

Ulcerative Colitis Autoimmune

Crohn’s Currently understood to be post-infectious

Family history Poor diet Recent smoking cessation

Family history Smoking

Crohn’s disease Infective colitis Coeliac disease

Colorectal cancer Diverticulitis IBS

Ulcerative colitis Infective colitis Coeliac disease Peptic ulcer GORD

Colorectal cancer Diverticulitis IBS Food allergy Appendicitis

5-7 per 100,000 in UK Affects slightly more women than men

Autoimmune – reaction to gut flora Predominantly a Th2 response –  levels in gut mucosa Involves cytokines IL-5 and IL-13, but key Th2 cytokine IL-4 is not raised in UC Genetic – family history in 35-40% of cases

Genetic Autoimmune response to GI tract – potentially dysregulated response to normal gut flora Mainly Th1 and Th17 mediated

Bloody stool Cramps Abdominal pain is in lower left quadrant Weight loss Anaemia

Fatigue Fever Pain experienced is normally in lower right abdomen

Colonoscopy with biopsies Abdominal imaging to check for megacolon (endoscopy  barium enema) Blood tests and microbiology for C. diff Serology for markers to distinguish from Crohn’s p-ANCA more common in ulcerative colitis (antibody ASCA more common in Crohn’s)

Colonoscopy with biopsies Abdominal imaging to check for megacolon (endoscopy  barium enema) Blood tests and microbiology for C. diff Serology for markers to distinguish from Crohn’s p-ANCA more common in ulcerative colitis (antibody ASCA more common in Crohn’s)

Pathophysiology

10 per 100,000 in UK Affects men and women equally Peak incidence between 15-20

Coeliac Autoimmune disorder affecting the small intestine Family history Other autoimmune diseases IgA Infection e.g. rotavirus or adenovirus causing initial reaction IBS Allergy Colorectal Crohn’s cancer UC Giardiasis Prevalence of about 1% Affects more men than women (like most autoimmune disease) Most common age of diagnosis in US is 40 but can occur at any age Initial peak in infancy on first exposure Another peak in middle age (40-50s) HLA-DQ2 alleles (95% Europeans) HLA-DQ8 (Middle East) N.B. both genes have low penetrance, so having them  coeliac disease. Is caused by reaction to gliadin (a prolamine contained within gluten) Autoimmune response truncates villi leading to flattened appearance  malabsorption Abdominal cramping, “colicky” pain Pale diarrhoea (high volume) Bloating (sometimes with abdominal distension) Mouth ulcers Weight loss Malabsorption*  anaemia, Vit. D and Vit. K  clotting abnormalities Growth stunting in infants 1. Peptides (e.g. gliadin) are absorbed through duodenal wall through leaky tight junctions 2. Once in the lamina propria, tTG deamidates the gliadin from glutamineglutamate which renders them a better fit for MHC2 protein 3. Dendritic cells present to CD4+ Tcells (through MHC2 protein) 4. The peptides are then recognised as foreign bodies and are marked for destruction by TH2 cells, who also release inflammatory cytokines 5. Sensing the cytokines, B-cells begin to make antibodies (IgA and IgG) to destroy the pathogen 6. This leads to destruction of the peptides within the lamina propria and to villous atrophy

Investigations

FBC (to check for anaemia and rule out infectious causes) + iron studies tTG antibodies (IgA-tTg and IgG-tTG B12/B9 deficiencies Thyroid function Occasionally endoscopy and barium enema are performed

Endoscopy

Distribution Site of origin Progression

Lesions

Loss of vascular pattern, with ulcerated mucosa Colon Rectum

Pronounced cobblestone appearance Panintestinal involvement Terminal ileum

Proximally contiguous Friable mucosal pseudopolyps with freely hanging mesentery Ulcers Superficial inflammation: mucosal/ submucosal No granulomata

Scalloping of duodenal intestinal mucosa Duodenum

Patchy/ discontinuous Skip lesions  cobblestone appearance Aphthous ulcers Long strictures Fistulae Creeping fat Transmural, yet focal inflammation Bowel wall thickening (string sign)

Histology C rypt abscesses (blue arrow) No granulomata

Noncaseating granulomata Lymphoid aggregates

Villous atrophy and crypt hyperplasia

Barium XRay

Scalloping and fissures visible on the barium follow through, widely associated with coeliac disease “Lead pipe colon”: Ahaustral (smooth) appearance, looks like thick garden hose

Complicati ons

Mgmt.

Prognosis

Severe stenosis Toxic megacolon  risk of colorectal carcinoma (2x) Topical (cream, pessary or enema) aminosalicylate-1 – induce remission and lengthen remission Oral aminosalicylate-1 if topic is ineffective Oral prednisolone >30% require bowel resection (colectomy) with ileostomy

“String sign”: Thin luminal contrast, usually in terminal ileum  spasm and eventual fibrosis Strictures Fistulas  infection Perianal disease Malabsorption  nutritional disease Many patients will have bowel resections, but this is not curative as Crohn’s can spread to other parts of GI Bowel resection stoma Immunomodulators: corticosteroids e.g. prednisolone 5-aminosalicyic acid Incurable but doesn’t shorten life expectancy

Malabsorption related: Clotting abnormalities (vitamin K) Bone abnormalities (vitamin D) Neurological (pernicious anaemia) Avoid gluten

Patients who adhere to gluten free diet suffer no ill effects...