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
How is ulcerative colitis managed?
- aim to induce remission
- common 5-ASAs = sulfasalazine, mesalazine or olsalazine
- mild/moderate: glucocorticoid (e.g. oral prednisolone), oral 5-ASA and rectal 5-ASA
- severe: glucocorticoid e.g. oral prednisolone
- severe with systemic features: hydrocortisone, ciclosporin, infliximab
- maintain remission: 5-ASA, azathioprine
Surgery:
- for severe UC that doesn’t respond to treatment
- colectomy with ileoanal anastomosis (whole colon removed and rectum fused to ileum)
- pan-proctocolectomy with ileostomy (whole colon and rectum remove and ileum brought out on to abdo wall as a stoma)
What is the aetiology of gastro-oesophageal reflux disease (GORD)?
Frequent transient lower oesophageal sphincter relaxation, causing reflux of gastric contents into the oesophagus
What is the pathophysiology of gastro-oesophageal reflux disease (GORD)?
- increased transient relaxation of the lower oesophageal sphincter due to reduced muscle tone, allowing gastric acid to flow back into the oesophagus
- mucosal damage occurs when in contact with gastric contents
What are the risk factors of gastro-oesophageal reflux disease (GORD)?
- FHx of heartburn or GORD
- older age
- hiatus hernia
- asthma
- psychological stress
- NSAID use
- smoking and alcohol
What is the clinical presentation of gastro-oesophageal reflux disease (GORD)?
Oesophageal:
- heartburn aggravated by bending, stooping and lying down and worse with hot drinks or alcohol
- belching
- food/acid brash (food, acid or bile regurgitation)
- water brash (increased salivation)
- odynophagia (painful swallowing)
Extra-oesophageal:
- nocturnal asthma
- chronic cough
- laryngitis
- sinusitis
What are the differential diagnoses of gastro-oesophageal reflux disease (GORD)?
- coronary artery disease
- biliary colic
- peptic ulcer disease
- malignancy
How is gastro-oesophageal reflux disease (GORD) diagnosed?
- often made without further investigations are long as there are no red flag symptoms (dysphagia, weight loss, haematemesis)
- if red flags, then endoscopy and barium swallow
How is gastro-oesophageal reflux disease (GORD) diagnosed managed?
- lifestyle changes (weight loss, smoking cessation, small regular meals, avoid hot drinks, alcohol, citrus fruits)
Pharmacology:
- antacids e.g. magnesium trisilicate mixture
- alginate e.g. gaviscon
- PPIs e.g. lansoprazole
- H2 receptor antagonists e.g, cimetidine
Surgery:
- Nissen fundoplication (restores function of lower oesophageal sphincter by wrapping the stomach around the oesophagus)
- only if not responding to therapy
What is the pathophysiology of oesophageal cancer?
Arises in the mucosa of the oesophagus and progresses locally to invade the submucosa and muscular layer
What are the risk factors of oesophageal cancer?
- male sex
- tobacco and alcohol use
- GORD
- hiatus hernia
- FHx of squamous cell carcinomas
- high temp food and drink
- consumption of smoking and salted foods without refrigeration
What are the symptoms of oesophageal cancer?
- dysphagia
- odynophagia
- weight loss
- voice hoarseness
- hiccups
- cough after eating
What are the differential diagnoses of oesophageal cancer?
- benign stricture
- achalasia
- Barrett’s oesophagus
How is oesophageal cancer diagnosed?
- oesophagoscopy with biopsy
- barium swallow to see strictures
- CT abdomen and thorax
- MRI abdomen and thorax
How is oesophageal cancer managed?
- surgical resection
- systemic chemotherapy if metastatic or incurable
- treat dysphagia
- palliative care
What are the risk factors of stomach cancer?
- pernicious anaemia
- Helicobacter pylori
- low fruit and veg consumption
- high salt diet
- smoking
- family history
What is the clinical presentation of stomach cancer?
- abdominal pain
- weight loss
- lymphadenopathy
- nausea
- dysphagia
- lower GI bleeding
What are the differential diagnoses of stomach cancer?
- peptic ulcer disease
- benign oesophageal stricture
- achalasia
How is stomach cancer diagnosed?
- upper GI endoscopy with biopsy
- endoscopy USS
- abdo/pelvis CT
- chest CT
- CXR
How is stomach cancer managed?
- surgery (gastrectomy)
- peri/postoperative chemotherapy
What are the risk factors for small bowel cancer?
Coeliac and Crohn’s disease
What is the clinical presentation of small bowel cancer?
- pain
- diarrhoea
- anorexia
- weight loss
- anaemia
- may be a palpable mass
How is small bowel cancer diagnosed?
- USS
- endoscopy biopsy to confirm diagnosis
- CT scan may show bowel wall thickening and lymph node involvement
How is small bowel cancer managed?
- surgical resection
- radiotherapy
What is the aetiology of peptic ulcers?
- infection by H.pylori (G-ve gastric pathogen)
- NSAID use
What is the pathophysiology of peptic ulcers?
- imbalance between factors that can damage the gasproduodenal mucosal lining and defence mechanisms
- hyper-secretion of gastric acid as a result of H/pylori infection
What are the risk factors of peptic ulcers?
- H. pylori infection
- NSAID use
- smoking
- increasing age
- FHx
What is the clinical presentation of peptic ulcers?
- abdominal pain
- pointing sign
- epigastric tenderness
- nausea/ vomiting
- early satiety
- weight loss/ anorexia
- diarrhoea
- anaemia symptoms
- GI bleeding
What are the differential diagnoses of peptic ulcers?
- oesophageal cancer
- stomach cancer
- GORD
- biliary colic
- gastroparesis
- acute pancreatitis
- coeliac disease
- IBS
How are peptic ulcers diagnosed?
- H. Pylori urea breath test or stool antigen test
- upper GI endoscopy
- FBC
- fasting serum gastric level
How are peptic ulcers managed?
- if caused by H.pylori ± NSAID use: antibiotic course and PPIs
- PPI only if caused by NSAIDs
- antacids for short-term symptomatic relief
What is the aetiology of acute appendicitis?
Obstruction of lumen of appendix (usually by a hard mass of faecal matter)
What is the pathophysiology of acute appendicitis?
- lumen distal to obstruction starts to fill with mucous and acts as a closed loop obstruction
- this leads to distension and increased intraluminal and intramural pressure
What are the risk factors of acute appendicitis?
- <6m of breastfeeding
- low fibre in diet
- smoking
What is the clinical presentation of acute appendicitis?
- pain in umbilical region that migrates to right iliac fossa (specifically McBurney’s point) after a few hours
- anorexia
- RLQ tenderness
- nausea
- fever
- diminished bowel sounds
- tachycardia
- constipation
What are the differential diagnoses of acute appendicitis?
- acute terminal ileitis due to Crohn’s
- ectopic pregnancy
- UTI
- diverticulitis
- perforated ulcer
- food poisoning
How is acute appendicitis diagnosed?
- FBC (raised CRP, ESR and WCC with neutrophil lecucytosis)
- abdo USS can detect inflamed appendix
- abdo and pelvic CT scan (Gold standard)
- urinary pregnancy test (to exclude)
- urinalysis to exclude UTI
How is acute appendicitis managed?
- appendectomy with supportive care
- IV antibiotics
- IV fluids and antibiotics if appendix mass present
