GI Flashcards
What is Crohn’s disease?
A chronic disease that causes bowel inflammation
What environmental factor increases risk of developing inflammatory bowel disease?
Smoking
What drugs exacerbate Crohn’s disease?
NSAIDs
Pathology/histology of Crohn’s disease
o Granulomas
o All Layers and levels
o Skip lesions
o Deep ulcers and fissures -> cobblestone appearance
Symptoms of Crohn’s disease
o Diarrhoea
o Abdominal pain
o Weight loss
o Fatigue
Signs of Crohn’s disease
o Bowel ulceration
o Abdominal tenderness
o Perianal abscess/fistulae/skin tags
o Clubbing, skin, joint and eye problems
Investigations for suspected inflammatory bowel disease
o Bloods – cultures, anaemia, B12, folate, ESR, CPR
o Stool sample
o Colonoscopy and biopsy
o AXR
Pharmacological management of Crohn’s disease
o Mild – prednisolone o Severe – IV hydrocortisone o Additional – AZA, monoclonal antibodies o Surgery
Lifestyle management of Crohn’s
Stop smoking, try different diets
Complications of Crohn’s disease
Bowel obstructions, malabsorption
What is ulcerative colitis?
A chronic disease that causes bowel inflammation
Pathology of ulcerative colitis
o Colon only o No granulomas o Mucosal inflammation only o Continuous involvement o Goblet cell depletion and crypt abscesses
Symptoms of ulcerative colitis
o Episodic or chronic diarrhoea (± blood and mucus)
o Crampy abdominal discomfort
o Urgency
o Fatigue, weight loss
Signs of ulcerative colitis
o Fever, tachycardia
o Tender distended abdomen if acute
o Extraintestinal features – clubbing, oral ulcers, conjunctivitis, arthritis, spondylitis, nutritional defects
Management of ulcerative colitis
o Mild – 5-ASA, steroids o Moderate – prednisolone then 5-ASA o Severe – fluids and electrolytes, IV hydrocortisone, ciclosporin o Maintenance – 5-ASAs o Surgery
Complications of ulcerative colitis
Psychosocial and sexual problems, colorectal cancer risk doubled
What is irritable bowel syndrome?
A mixed group of abdominal symptoms for which no organic cause can be found
Epidemiology of IBS
Usually <40yrs old, twice as common in women
Symptoms of IBS
o Chronic > 6 months: o Urgency o Incomplete evacuation o Constipation o Diarrhoea o Abdominal bloating/distension o Worsening of symptoms after food
What can exacerbate IBS symptoms?
Stress, menstruation, gastroenteritis
Signs of IBS
Abdominal distension
What is the tool used to diagnose IBS?
The Rome diagnostic tool
What is the criteria for diagnosis of IBS?
• Recurrent abdominal pain (or discomfort) associated with at least 2 of: o Relief by defecation o Altered stool form o Altered bowel frequency
When do you think differential diagnosis for IBS?
o >60yrs
o Anorexia/weight loss
o Waking at night with pain diarrhoea
o Mouth ulcers
Investigations for suspected IBS
• Bloods – FBC, ESR, CRP and coeliac serology
• Stool sample
• Low threshold for referring if family history of ovarian
or bowel cancer
Management of IBS
• Constipation – adequate water and fibre intake,
physical activity, laxatives
• Diarrhoea – avoid sorbitol, alcohol, caffeine, ‘trigger
foods’, reduce fibre, try bulking agent and loperamide
after loose stool
• Colic/bloating – oral antispasmodics
• Psychological symptoms – CBT
What is coeliac disease?
A disease in which the small intestine is hypersensitive to gluten, leading to difficulty in digesting food.
What is the pathology of coeliac disease?
T-cell response to gluten in small bowel -> villous atrophy and crypt hyperplasia -> malabsorption
What gene is coeliac disease associated with?
HLA DQ2
What skin condiiton is associated with coeliac disease?
Dermatitis herpetiformis
Symptoms of coeliac disease
o Stinking stools/steatorrhoea o Diarrhoea o Abdominal pain, bloating o Nausea and vomiting o Weight loss o Fatigue and weakness
Investigations for suspected coeliac disease
o Bloods – anaemia
o Antibodies – anti-transglutaminase test
o Duodenal biopsy while on gluten-containing diet
o Genotyping
Management of coeliac disease
Life-long gluten free diet
Complications of coeliac disease
Anaemia, dermatitis herpetiformis, osteopenia/osteoporosis, risk of malignancy
List 4 causes of malabsorption
Coeliacs disease, Crohn’s disease, starvation/poor diet, biliary obstruction
What is GORD?
Prolonged or recurrent reflux of gastric contents (acid +/- bile) into oesophagus
Epidemiology of GORD
- 25% of adults experience it (heartburn)
* 2-3x more common in men
Causes of GORD
o Lower oesophageal sphincter hypotension o Hiatus hernia o Oesophageal dysmotility o Gastric acid hypersecretion o Delayed gastric emptying
Risk factors for GORD
o Obesity
o Pregnancy
o Smoking
o Alcohol
What is a hiatus hernia?
Part of the stomach protrudes through the oesophageal opening in the diaphragm
What is the pathology of GORD?
Tone of the LOS is reduced, as well as frequent transient relaxations of the LOS -> stomach acid enters oesophagus -> increased mucosal sensitivity to gastric acids
Symptoms of GORD
o Heartburn – burning retrosternal discomfort after
meals, lying or straining, relieved by antacids
o Belching
o Acid brash (acid or bile regurgitation)
o Increased salivation
o Painful swallowing
o Nocturnal asthma, cough
Investigations for suspected GORD
• Endoscopy
• 24 hr oesophageal pH monitoring if endoscopy
normal
Management of GORD
o Lifestyle: - Weight loss - Smoking cessation - Reduce hot drinks, alcohol, citrus fruits, fizzy drinks, spicy food - Raise bed head o Drugs: - Antacids – Gaviscon - PPI – lansoprazole o Surgery if severe - laparoscopic Nissen fundoplication
What is Barrett’s oesophagus?
Metaplasia of oesopahgeal cells = squamous -> columnar -> can progress to cancer, IRREVERSIBLE
Why does Barrett’s oesophagus increase risk of oesophageal cancer?
The new glandular epithelial cells are predisposed to becoming malignant, since they are not genetically stable in the oesophagus
Signs and symptoms of oesopahgeal cancer?
o Dysphagia
o Weight loss
o Retrosternal chest pain
o Hoarseness, cough
What is gold standard investigation for diagnosing oesophageal cancer?
Oesophagoscopy with biopsy
Management of oesophageal cancer
o Lifestyle changes
o Oesophagectomy with perioperative chemo
o Combine with chemo/radiotherapy if necessary
Causes of gastric cancer (adenocarcinoma)
o Helicobacter pylori
o Genetic predisposition
o Unknown
Symptoms of gastric cancer
o Dyspepsia
o Weight loss
o Vomiting
o Dysphagia
Signs of gastric cancer
o Anaemia o Troisier’s sign – enlarged supraclavicular node (Virchow’s node) o Epigastric mass o Hepatomegaly o Jaundice o Ascites
What investigations are used to stage cancer?
CT/MRI - to indentify metastases
Investigations for suspected gastric cancer
o Gastroscopy and multiple ulcer edge biopsies
o Endoscopic ultrasound (EUS) – evaluate depth of
invasion
Management of gastric cancer
o Endoscopic resection in early stages
o Partial gastrectomy if distal, total if proximal
o Combination chemotherapy
o Targeted therapy – monoclonal antibodies
What factors predispose an individual to colorectal cancer?
Neoplastic polyps, IBD, genetic predisposition (FAP and HNPCC), alcohol, smoking
What genes predispose an individual to colorectal cancer?
FAP and HNPCC
What drug can prevent colorectal cancer?
Aspirin
Signs and symptoms of a left-sided colorectal cancer
Bleeding/mucus PR, altered bowel habits or obstruction, tenesmus, mass PR, fistula
Signs and symptoms of right-sided colorectal cancer
Weight loss, anaemia, abdominal pain, obstruction
What is the UK colorectal screening programme?
Faecal occult blood from stool sample, 60-69yrs old
Investigations for suspected colorectal cancer
o FBC – microcytic anaemia
o Sigmoidoscopy or colonoscopy or virtually by CT
o Rectal examination
Management of colorectal cancer
o Surgery – laparoscopic resection, colostomy bag
o Radiotherapy
o Chemotherapy – FOLFOX
o Targeted – monoclonal antibodies
What are the main causes of peptic ulcers?
o H. pylori
o Drugs - NSAIDs, steroids
o Stress – H. pylori and stress
o Lack of blood supply (mucosal ischaemia)– low BP, stomach cells stop making mucin, decreased defence against stomach acid
By what mechanism does H. pylori cause peptic ulcers?
Lives in gastric mucosa – secretes urease -> splits urea into CO2 and ammonia -> damages gastric mucosa -> peptic ulcer
How do NSAIDs cause peptic ulcers?
NSAIDs inhibit prostaglandins -> decreased mucous secretion -> decreased defence against stomach acid