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
Treatment of mild to moderate UC
-Proctitis
=Topical (rectal) aminosalicylate: for distal colitis rectal mesalazine has been shown to be superior to rectal steroids and oral aminosalicylates
=If remission is not achieved within 4 weeks, add an oral aminosalicylate
=If remission still not achieved add topical or oral corticosteroid
-Proctosigmoiditis and left-sided ulcerative colitis
=Topical (rectal) aminosalicylate
=If remission is not achieved within 4 weeks, add a high-dose oral aminosalicylate OR switch to a high-dose oral aminosalicylate and a topical corticosteroid
=If remission still not achieved stop topical treatments and offer an oral aminosalicylate and an oral corticosteroid
-Extensive disease
=Topical (rectal) aminosalicylate and a high-dose oral aminosalicylate:
=If remission is not achieved within 4 weeks, stop topical treatments and offer a high-dose oral aminosalicylate and an oral corticosteroid
Treatment of severe UC
-Should be treated in hospital
-IV steroids are usually given first-line
=IV ciclosporin may be used if steroids are contraindicated
-If after 72 hours there has been no improvement, consider adding IV ciclosporin to IV corticosteroids or consider surgery
Maintaining remission in UC
Following a mild-to-moderate ulcerative colitis flare
-Proctitis and proctosigmoiditis
=Topical (rectal) aminosalicylate alone (daily or intermittent) or
=An oral aminosalicylate plus a topical (rectal) aminosalicylate (daily or intermittent) or
=An oral aminosalicylate by itself: this may not be effective as the other two options
-Left-sided and extensive ulcerative colitis
=Low maintenance dose of an oral aminosalicylate
Following a severe relapse or >=2 exacerbations in the past year
-Oral azathioprine or oral mercaptopurine
Inducing Crohn’s remission
-Glucocorticoids (oral, topical or intravenous) are generally used to induce remission. Budesonide is an alternative in a subgroup of patients
-Enteral feeding with an elemental diet may be used in addition to or instead of other measures to induce remission, particularly if there is concern regarding the side-effects of steroids (for example in young children)
-5-ASA drugs (e.g. mesalazine) are used second-line to glucocorticoids but are not as effective
-Azathioprine or mercaptopurine* may be used as an add-on medication to induce remission but is not used as monotherapy. Methotrexate is an alternative to azathioprine
-Infliximab is useful in refractory disease and fistulating Crohn’s. Patients typically continue on azathioprine or methotrexate
-Metronidazole is often used for isolated peri-anal disease
Maintaining Crohn’s remission
-Stopping smoking is a priority (remember: smoking makes Crohn’s worse, but may help ulcerative colitis)
-Azathioprine or mercaptopurine is used first-line to maintain remission
+TPMT activity should be assessed before starting
methotrexate is used second-line
Surgery in Crohn’s disease
-Around 80% of patients with Crohn’s disease will eventually have surgery
-Stricturing terminal ileal disease → ileocaecal resection
-Segmental small bowel resections
-Stricturoplasty
-Perianal fistulae
=An inflammatory tract or connection between the anal canal and the perianal skin
=MRI is the investigation of choice for suspected perianal fistulae - can be used to determine if there (is an abscess and if the fistula is simple (low fistula) or complex (high fistula that passes through or above muscle layers)
=Patients with symptomatic perianal fistulae are usually given oral metronidazole
=Anti-TNF agents such as infliximab may also be effective in closing and maintaining closure of perianal fistulas
=A draining seton is used for complex fistulae
A seton is a piece of surgical thread that’s left in the fistula for several weeks to keep it open. This is useful because persisting fistula tracks after premature skin closure predispose to abscess formation
-Perianal abscess
=Requires incision and drainage combined with antibiotic therapy
=A draining seton may also be placed if a tract is identified
Extra-intestinal features of IBD
-Arthritis: pauciarticular, asymmetric
-Erythema nodosum
-Episcleritis (more common Crohn’s)
-Osteoporosis
-Unrelated to disease activity:
=Arthritis: polyarticular, symmetric
=Uveitis (UC)
=Pyoderma gangrenosum
=Clubbing
=Primary sclerosing cholangitis (more common UC)
Crohns:
=small bowel cancer (standard incidence ratio = 40)
=colorectal cancer (standard incidence ratio = 2, i.e. less than the risk associated with ulcerative colitis)
=osteoporosis
Features of Whipple’s disease
Whipple’s disease is a rare multi-system disorder caused by Tropheryma whippelii infection. It is more common in those who are HLA-B27 positive and in middle-aged men.
-Malabsorption: diarrhoea, weight loss
-Large-joint arthralgia
-Lymphadenopathy
-Skin: hyperpigmentation and photosensitivity
-Pleurisy, pericarditis
-Neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia, myoclonus
-Middle aged men
Investigation of Whipple’s disease
-Jejunal biopsy= macrophage deposition containing PAS granules
Management of Whipple’s disease
-Oral co-trimoxazole for 1 year
-IV penicillin
Malabsorption syndromes
-Whipple’s
-Coeliac
-Zollinger-Ellison (excessive levels of gastrin from tumour= ulcers, diarrhoea)
-SIBO (chronic diarrhoea, bloating, flatulence, abdominal pain. Hydrogen breath test, SB aspiration and culture. Rifaximin)
-Osteomalacia
-Giardiasis
-CF
