Small Bowel Diseases Flashcards
Overview of coeliac disease
-Autoimmune condition caused by sensitivity to protein gluten
-1%
-Repeated exposure leads to villous atrophy which in turn causes malabsorption
-Conditions associated with coeliac disease include dermatitis herpetiformis (a vesicular, pruritic skin eruption) and autoimmune disorders (type 1 diabetes mellitus and autoimmune hepatitis). It is strongly associated with HLA-DQ2 (95% of patients) and HLA-DQ8 (80%).
Presentation of coeliac disease
-Malabsorption
-Dermatitis herpetiform
-Autoimmune disorders/ autoimmune thyroid disease, dermatitis herpetiformis, IBS, T1DM, first-degree relatives
-Chronic or intermittent diarrhoea
-Fatigue (prolonged)
-Cramping and distention, recurrent abdo pain
-Persistent or unexplained GI symptoms (nausea, vomiting, acid reflux, diarrhoea, steatorrhoea, pain, reduced appetite, bloating, constipation)
-Weight loss (sudden or unexpected)
-IDA (unexplained)/ other anaemias
-Recurrent mouth ulcers
-Concurrent autoimmune thyroid disease/ type 1 diabetes
-Osteoporosis, osteomalacia, hyposplenism, enteropathy-associated T-cell lymphoma, subfertility, unexplained depression or anxiety, peripheral neuropathy, persistently raised transaminases, dental enamel defect
-Failure to thrive/ faltering growth, delayed puberty in children: before 3 yrs
Investigations of coeliac disease
-Exam: BMI, abdo pain or distention, skin for features of rash
If patients are already taking a gluten-free diet they should be asked, if possible, to reintroduce gluten for at least 6 weeks prior to testing. Serology and endoscopic intestinal biopsy
-Duodenal biopsy (gold standard)= villous atrophy, crypt hyperplasia, intraepithelial lymphocytes, lamina propria infiltration with lymphocytes. All pts with suspected coeliac, can be done jejunal
-Anti tTG IgA (gluten peptides taken up by epithelial cells and deaminated by TTG, autoimmune)(reintroduce gluten for 6 weeks prior to testing): first-choice
-Endomysial antibody IgA): look for selective IgA deficiency giving false negative coeliac result
-Anti-gliadin not recommended
-Anti-casein antibodies also found in some pts
Management of coeliac disease
-Gluten-free diet (TTA antibodies can be checked for compliance)
-Pneumococcal vaccine (5yrs) and influenza A (due to functional hyposplenism)
-Dapsone for rash
-Prednisolone for refractory
-Correct other deficiencies
Complications of coeliac disease
-Anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)
-Hyposplenism
-Osteoporosis, osteomalacia
-Lactose intolerance
-Enteropathy-associated T-cell lymphoma of small intestine
-Subfertility, unfavourable pregnancy outcomes
-Rare: oesophageal cancer, other malignancies
Differential diagnosis of coeliac
-Infective gastroenteritis
-Non-coeliac gluten sensitivity
=IBS-like
-Food allergy (cow’s milk, wheat)
=Hypersensitivity reaction, IgE mediated?
-IBD
-IBS
-Diverticular disease
-Peptic ulcer disease
-Malignancy
-Pancreatic exocrine insufficiency
-SBO
Presentation of ulcerative colitis
-More common on non/ex-smokers, 15-25yrs and 55-65yrs
-Colon ONLY (ileocecal valve limit), starts at rectum (most common site)
-Continuous
-Bloody diarrhoea >6weeks/ rectal bleeding
-Urgency/ incontinence
-Nocturnal defecation
-Tenesmus
-LLQ abdominal pain, pre-defecation pain (relieved by passage of stool)
-Primary sclerosing cholangitis
-Fatigue, malaise, anorexia, fever, weight loss, faltering growth, Hx IBD/coeliac/colorectal cancer
-Exam:
=Pallor, clubbing, or aphthous mouth ulcers.
=Abdominal distension, tenderness or mass, for example, in the left lower quadrant.
=Signs of malnutrition or malabsorption — serial weight loss or, in children, faltering growth or delayed puberty.
=Eye, skin, or joint signs of extra-intestinal manifestations.
Presentation of Crohn’s disease
-Slight female predominance
-Increasing incidence
-More common in smokers
-Entire GI tract (mouth ulcers, upper GI symptoms, perianal disease), most common terminal ileum and colon
-Palpable mass in RIF
-Gallstones due to reduced bile acid reabsorption
-Pain (prominent in children)
-Diarrhoea (non-bloody)! Bloody? 4-6 weeks, nocturnal diarrhoea
-Weight loss (more prominent), lethargy
-Deep fissuring ulcers, fistulae, all layers to serosa, structures, adhesions, perianal skin tags/ulcers
80% of patients have small bowel involvement, usually in the ileum, with around 30% of patients having ileitis exclusively
50% of patients have ileocolitis
20% of patients have colitis exclusively
30% of patients have perianal disease
-Exam:
=Pallor, clubbing, or aphthous mouth ulcers.
=Abdominal tenderness or mass, for example, in the right lower quadrant.
=Perianal pain or tenderness, anal or perianal skin tag, fissure, fistula, or abscess.
=Signs of malnutrition and malabsorption — serial weight loss or, in children, faltering growth or delayed puberty.
=Extra-intestinal manifestations, including abnormalities of the joints, eyes, liver, and skin.
Presentation of Crohn’s disease complication
A history of recurrent urinary tract infections and passing gas or faeces in the urine — may suggest a fistula allowing faecal leakage into the bladder.
A history of passing gas or faeces through the vagina — may suggest a fistula allowing faecal leakage into the vagina.
Perianal discharge of mucus or pus — may suggest a fistula allowing faecal leakage through the perianal skin.
Partial bowel obstruction (abdominal colicky pain and distention, and diarrhoea due to stasis of bowel contents and bacterial overgrowth) or complete bowel obstruction (severe abdominal pain, vomiting, no flatus, and complete constipation) — may suggest intestinal stricture.
Pathophysiology of ulcerative colitis
-Red, raw mucosa and bleeds easily
-Inflammation limited to mucosa (beyond submucosa if fulminant disease)
-Continuous
-Pseudo polyps (widespread ulceration)
-Inflammatory cell infiltrate in lamina propria
-Crypt abscesses (neutrophils)
-Depletion of goblet cells
-Drainpipe colon
-Granulomas infrequent
-Loss of haustrations on barium enema
Pathophysiology of Crohn’s
-Submucosal or transmural inflammation common
-Granulomas
-Patchy changes/ skip lesions
-Increased goblet cells
-Cobblestone appearance
Diagnosis of IBD
-Colonoscopy and biopsy, if severe avoided as perforation risk so flexible sigmoidoscopy preferred.
-Small bowel enema: Crohn’s= terminal ileum, strictures, rose thorn ulcers, fistulae, proximal bowel dilation
-Bowel enema: UC= loss of haustrations, superficial ulceration/ pseudopolyps, drainpipe colon
-FBC (anaemia iron, folic acid, B12, platelet high for active inflammation), faecal calprotectin, raised inflammatory markers, CRP and ESR, low albumin
-Thyroid function to exclude hyperthyroidism
-Stool microscopy and culture (pseudomembranous colitis?)
-Fulminant UC disease: inflammation beyond submucosa
Differential diagnosis of IBD
-Infective colitis
-Pseudomembranous colitis
-Microscopic colitis (watery chronic diarrhoea in older people, lansoprazole/aspirin/sertraline/ranitidine/simvastatin)
-Intestinal ischaemia sudden onset abdo pain disproportionate, acute abdo, associated with eating)
-Diverticulitis
-Coeliac
-IBS
-Anal fissure
-Malignancy
-Endometriosis
-Laxative misuse
Severity and triggers of UC flares
Flares:
-Stress
-Medications (NSAID, abs)
-Cessation of smoking
-Mild: < 4 stools/day, only a small amount of blood
-Moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
-Severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers, abdo tenderness/distention/reduced bowel sounds)
IBD drugs
-UC: 5-ASA, glucocorticoids, azathioprine, anti-TNF, colectomy, aminosalicylates
-Crohn’s: glucocorticoids, azathioprine, methotrexate