Gastrointestinal Flashcards
What is the pathophysiology of IBS?
Dysfunction in the brain/gut axis results in disorder of intestinal motility and/or enhanced visceral perception (visceral hypersensitivity)
What are the risk factors of IBS?
- female
- previous severe and long diarrhoea
- high hypochondriac anxiety and neurotic score at time of illness
What is the clinical presentation of IBS?
Any of: abdominal pain/ discomfort, bloating, change in bowel habit
Abdo pain relieved by defecation or is associated with altered stool form or bowel frequency (constipation and diarrhoea may alternate)
2+ of: urgency, incomplete evacuation, abdo bloating/distension, mucus in stool, worsening symptoms after food)
Non-intestinal symptoms: painful period, urinary frequency, urgency, nocturia, incomplete emptying, back pain, joint hypermobility, fatigue
Other symptoms: nausea, bladder symptoms and backache
- symptoms are chronic and exacerbated by stress, menstruation or gastroenteritis
What are the differential diagnoses of IBS?
- Crohn’s disease
- ulcerative colitis
- coeliac disease
- colon cancer
- bile acid malabsorption
- lactose intolerance
How is IBS diagnosed?
investigations and the Rome III diagnostic criteria
- FBC to look for anaemia
- ESR and CRP
- stool studies
- anti-endomysial antibodies
- faecal calprotectin (raised in IBD)
- colonoscopy to rule out IBD or colorectal cancer
Rome III diagnostic criteria:
- recurrent abdominal pain or discomfort at least 3 days a month in the past 3 months, associated with two or more of the following:
→ improvement with defecation
→ onset associated with a change in frequency of stool
→ onset associated with a change in form (appearance) of stool
How is IBS managed?
Mild IBS: - education - reassurance - dietary modification Moderate IBS: - pharmacology - psychological treatment Severe IBS: - referral to pain treatment centre
Dietary/ lifestyle modification:
- regular or small frequent meals
- plenty of fluids
- reduce/avoid caffeinated drinks, alcohol and fizzy drinks
- if symptoms persist, then try low FODMAP diet
Pharmacology:
- for pain/bloating: mebeverine or buscopan
- for constipation: laxative (e.g. mavicol), linaclotide
- for diarrhoea: anti-motility agents e.g. loperamide
- try tricyclic antidepressants if no improvement
What is the aetiology of coeliac disease?
Systemic autoimmune disorder triggered by gluten peptides from grains including wheat, rye and barley
What is the pathophysiology of coeliac disease?
- loss of immune tolerance to peptide antigens from proclaiming in grains
- peptides then persist intact in the small intestine and trigger innate and adaptive immune responses
What are the risk factors of coeliac disease?
- family history
- T1DM
- immunoglobulin A deficiency
- autoimme thyroid disease
- Down’s syndrome
- IBD
What is the clinical presentation of coeliac disease?
- 1/3 are asymptomatic
- diarrhoea
- bloating
- abdominal pain/ discomfort
- anaemia
- fatigue
- weight loss
- osteoporosis
- sinking/ fatty stools
What are the differential diagnoses of coeliac disease?
- peptic duodenitis
- Crohn’s disease
- giardiasis
- small-intestinal bacterial overgrowth
How is coeliac disease diagnosed?
- should maintain gluten in diet for 6w before testing to get true results
- FBC (low Hb, B12 and ferritin)
- duodenal biopsy
- serum antibody testing
How is coeliac disease managed?
- lifelong gluten-free diet
- calcium and vitamin D supplement ± iron
- rehydration and corticosteroids if in coeliac crisis
What is the pathophysiology of Crohn’s disease?
- initial lesion starts as an inflammatory infiltrate around intestinal crypts
- transmural granulomatous inflammation (goes deep) affecting any part of the gut from mouth to anus
- terminal ileum and proximal colon are particularly affected
Macroscopic:
- not continuous (i.e. there are skip lesions/ patchy areas where there is a gap between affected and unaffected mucosa)
- involved bowel is usually thickening and narrowed)
- cobblestone appearance due to ulcers and fissures in mucosa
Microscopic:
- inflammation extends through all layers of the bowel
- increase in chronic inflammatory cells and lymphoid hyperplasia
- goblets cells are present
What are the risk factors of Crohn’s disease?
- family history
- strong genetic association
- chronic stress and depression triggers flares
- good hygiene
- NSAID use may exacerbate disease
What is the clinical presentation of Crohn’s disease?
- diarrhoea with urgency, bleeding and pain
- abdominal pain (can present similar to appendicitis)
- weight loss
- malaise
- lethargy
- anorexia
- abdominal tenderness/ mass
- perianal abscess
- anal strictures
What are the differential diagnoses of Crohn’s disease?
- ulcerative colitis
- other causes of diarrhoea e.g. Salmonella app, Giardia or rotavirus
- chronic diarrhoea
How is Crohn’s disease diagnosed?
investigations, examination, bloods - pANCA result
- endoscope (exclude oesophageal and gastroduodenal disease)
- colonoscopy (biopsy to confirm)
- comprehensive metabolic panel
- stool testing to exclude C. diff and Campylobacter
Examination:
- right iliac fossa tenderness
- anal examination
Bloods:
- anaemia is common from malabsorption therefore iron and folate deficiency
- raised ESR, CRP, WCC and platelets
- hypoalbuminaemia in severe disease
- liver biochemistry may be abnormal
- negative pANCA
How is Crohn’s disease managed?
lifestyle, mild attacks, moderate attacks, severe attacks, maintaining remission surgery
- smoking cessation
- treat anaemia
- mild attacks: controlled-release corticosteroids e.g. budesonide
- moderate to severe attacks: glucocorticoids e.g. oral prednisolone
Severe attacks:
- IV hydrocortisone
- treat rectal disease
- transfer to oral prednisolone if improvement shown
- if no improvement, when switch to anti-TNF antibodies e.g. infliximab
Maintaining remission:
- azathioprine
- methotrexate is intolerant to azathioprine
Surgery:
- 80% require surgery at some point
- avoided and only minimal resection
- temporary ileostomy to allow time for affected areas to rest
What is the pathophysiology of ulcerative colitis?
- restricted mucosal disease
Macroscopic:
- affects only from colon to ileocaecal valve
- begins in the rectum and extends
- circumferential and continuous inflammation (no skin lesions)
- mucosa looks reddened and inflamed, bleeding easily
- ulcers and pseudo-polyps in severe disease
Microscopic:
- mucosal inflammation (inflammation doesn’t go any deeper)
- no granulomata
- depleted goblet cells
- increased crypt abscesses
What are the risk factors of ulcerative colitis?
- family history
- NSAID use
- chronic stress and depression trigger flares
What is the clinical presentation of ulcerative colitis?
- runs a course of remissions and exacerbations
- restricted pain usually in lower left quadrant
- episodic or chronic diarrhoea with blood and mucus
- cramps
- bowel frequency linked to severity
- acute UC may have fever, tachycardia and tender distended abdomen
- may have bloody diarrhoea, night diarrhoea with urgency and incontinence in acute attacks
What are the differential diagnoses of ulcerative colitis?
Alternative causes of diarrhoea
How is ulcerative colitis diagnosed?
- colonoscopy with mucosal biopsy = gold standard
- abdominal XR to exclude colonic dilatation
Blood tests - raised WCC and platelets in moderate/severe attacks
- iron deficiency anaemia
- raised ESR and CRP
- pANCA may be positive
- hypoalbuminaemia in severe disease
- may have abnormal liver biochemistry
