Gastroenterology Flashcards
What is Crohn’s disease?
Definition – chronic inflammatory disease occurring sporadically anywhere in the GI tract characterised by granulomatous transmural inflammation, most commonly affecting the terminal ileum. Typically presents in late adolescence or early adulthood
What causes Crohn’s disease?
Cause – not fully understood but thought to be due to an abnormal reaction of the immune system to abnormal gut flora in those with a genetic susceptibility
How does Crohn’s disease present? (think particularly about how this is different to UC)
Diarrhoea (less likely to be bloody than UC) and abdominal pain (often post-prandial)
Weight loss (more prominent than in UC)
Fatigue, malaise, malabsorption and vitamin deficiency and anorexia
Mouth ulcers
Perianal disease – abscess, fistulae, strictures, and skin tags
Abdominal mass
Bowel obstruction and fistulas
Lesions anywhere from mouth to anus with skip lesions
Clubbing
What associated conditions and presentations might be seen alongside classical Crohn’s features?
Gallstones are more common secondary to reduced bile acid absorption
Oxalate renal stones and liver disease due to the above issue
Arthritis
Increased risk of bowel caner
Osteoporosis
Erythema nodosum and pyoderma gangrenosum
Episcleritis (more common in CD) and uveitis (more common in UC)
How should suspected Crohn’s disease be investigated?
- Endoscopy (colonoscopy) showing deep ulcers, skip lesions and cobble stone appearance
- Biopsy/Histology – inflammation in all layers, increased goblet cells and granulomas
- Abdominal x-ray with small bowel enema showing strictures (Kantor’s string sign), proximal bowel dilation, rose thorn ulcers, skip lesions, fistulae, and thickened bowel wall
- Stool microscopy and culture
- Raised CRP/ESR, faecal calprotectin and WCC
- FBC, B12, folate and haematinics for anaemia
- LFTs and U&Es and vit D levels
What two bits of general advice should be given to all Crohn’s disease patients?
Stop smoking and avoid NSAIDs as they can exacerbate
How should you induce a remission in a Crohn’s patient?
- Glucocorticoids (prednisolone first line or hydrocortisone/methylprednisolone IV if severe) to induce remission with reducing regimen or 5-ASA drugs such as mesalazine are second line to induce remission
- Azathioprine/Methotrexate used as an add-on to induce remission but not alone
- Infliximab used in refractory disease and fistulating Crohn’s alongside azathioprine or methotrexate
- Metronidazole for isolated peri-anal disease
What should you monitor during a hospital stay for someone with a Crohn’s flare?
- Stool chart for frequency and consistency
* Routine bloods as above
How should remission be maintained in Crohn’s?
- Azathioprine or mercaptopurine
- Methotrexate
- 5-ASA drugs such as mesalazine if previous surgery
What surgery is often required in Crohn’s?
Majority of patient will eventually require surgery, usually Ileocaecal resection.
Colonic resection is usually not indicated as recurrence rate is high.
What is ulcerative colitis?
Definition – superficial inflammatory reaction that always starts at the rectum
and never extends past the Ileocaecal valve, continuous disease due to haemorrhagic colonic mucosa +/- pseudopolyps formed by inflammation. Peak incidence 15-25 years and 55-65 years.
What causes ulcerative colitis?
Cause – thought to be inappropriate immune response against abnormal colonic flora in genetically susceptible individuals
What are the clinical features of ulcerative colitis?
Bloody diarrhoea and mucus
Crampy abdominal pain, typically in left lower quadrant
Often painless as mucosa has no nerve endings
Urgency and tenesmus suggesting rectum involved
Weight loss (more prominent in CD), malaise, fever and anorexia
Inflammation does not spread beyond submucosa
Clubbing
How are ulcerative colitis flares categorised?
Mild – <4 stools daily with/without blood, no systemic disturbance, and normal inflammatory markers
Moderate – 4-6 stools a days with minimal systemic disturbance
Severe – >6 stools a day containing blood and systemic disturbance – fever, tachycardia, abdominal pain, distention, reduced bowel sounds, anaemia, and hypoalbuminemia. Be aware of toxic megacolon.
What are the associated conditions and features of someone with Ulcerative colitis?
Primary sclerosing cholangitis more common
Increased risk of colorectal cancer compared to CD
Erythema nodosum and pyoderma gangrenosum
Arthritis
Episcleritis (more common in CD) and uveitis (more common in UC)
Osteoporosis
How should suspected ulcerative colitis be investigated?
- Endoscopy – widespread ulceration with preservation of adjacent mucosa causing a pseudopolyps appearance
- Biopsy/Histology – no spread beyond submucosa, inflammatory cell infiltrate in lamina propria, neutrophil migration to form crypt abscess, depletion of goblet cells, infrequent granulomas
- Abdominal X-ray with barium enema showing loss of haustra, superficial ulceration (pseudopolyps) and drainpipe colon as disease is long standing and to rule out toxic megacolon – transverse colon > 6cm in combination with systemic upset
- Stool microscopy and culture
- Raised CRP/ESR, faecal calprotectin and WCC
- FBC, B12, folate and haematinics for anaemia
- LFTs and U&Es and vit D levels
How do you induce remission in someone with mild-moderate ulcerative colitis?
Inducing Remission
Mild-moderate disease
Proctitis
• Topical aminosalicylate
• If remission not achieved within 4 weeks, then add oral aminosalicylate
• If remission still not achieved, then add a topical or oral steroid.
Proctosigmoiditis and left sided UC
• Topical aminosalicylate
• If remission not achieved by 4 weeks adding high dose oral aminosalicylate OR switching to high dose aminosalicylate and 4-8 weeks of a topical corticosteroid
• If remission still not achieved stop topicals and add oral aminosalicylate and oral corticosteroid
Extensive disease
• Topical aminosalicylate and high dose oral aminosalicylate
• If remission not achieved within 4 weeks stop topicals and add oral corticosteroid for 4-8 weeks
How do you induce remission in someone with severe ulcerative colitis?
Severe colitis
• Treat in hospital as can be life threatening
• IV steroids (IV hydrocortisone or methylprednisolone) or IV ciclosporin if steroids contraindicated
• If no improvement after 72 hours consider adding IV ciclosporin or surgery
• Infliximab can be used if ciclosporin cannot
• If toxic megacolon, then manage aggressively with medical treatment for 24-72 hours and if no improvement in this time then a colectomy is performed
What should you monitor during a hospital admission for a ulcerative colitis flare?
- Stool chart for frequency and consistency
* Routine bloods as above
How is remission maintained in ulcerative colitis?
Maintaining remission
Mild-moderate flare
• Proctitis and proctosigmoiditis – topical/oral aminosalicylate OR both
• Left sided and extensive UC – low maintenance dose oral aminosalicylate
Severe or >2 exacerbation in past year
• Oral azathioprine or oral mercaptopurine
• Infliximab or adalimumab if intolerant of immunomodulation
Methotrexate NOT RECOMMENDED
What surgery is required in ulcerative colitis?
Needed in about 1/5 if total failure of medical therapy or fulminant colitis with toxic dilatation or perforation. Completion proctectomy (permanent stoma) or ileo-anal pouch (can have stoma reversal but can get infection so give antibiotics for 2 weeks).
What is Coeliac’s disease?
Definition – Example of malabsorption caused by an autoimmune condition with sensitivity to gluten. Repeated exposure to gluten leads to villus atrophy and malabsorption. Affects 1 in 100 people and commonly misdiagnosed as irritable bowel syndrome. More common in women
What are the risk factors for Coeliac’s disease?
Other autoimmune disease such as thyroid disease, T1DM, first degree relative with coeliac Dermatitis herpetiformis (itchy burning blisters on elbows, scalp, shoulders, and ankles) Usually presents prior to 3 years
What are the clinical features of Coeliac’s disease?
Chronic or intermittent diarrhoea (often particularly smelly)
Failure to thrive or faltering growth
Persistent or unexplained GI symptoms
Prolonged fatigue
Recurrent abdominal pain cramping or distention
Unexplained iron deficiency anaemia
How is Coeliac’s disease diagnosed?
Immunoglobulin A-tissue transglutaminase or anti-endomysial (NICE) and anti-gliadin (not recommended by NICE) antibodies
Duodenal or Jejunal biopsy showing subtotal villous atrophy, crypt hyperplasia and infiltration of lymphocytes
Note prior to testing patients need to be eating gluten for 6 weeks
Other investigations
FBC and blood smear
How is Coeliac’s disease managed?
Gluten free diet
Check compliance by testing for antibodies
Pneumococcal vaccine due to Hyposplenism and influenza if patient requests
Calcium and vit D supplementation
What complications can occur as a result of Coeliac’s disease?
Malabsorption and malnutrition
Anaemia from iron, folate (more common than B12) and B12
Hyposplenism
Osteoporosis and Osteomalacia
Lactose intolerance
Enteropathy-associated T-cell lymphoma of small intestine
Subfertility
How is a Coeliac’s crisis managed?
Rehydration and correction of electrolyte balance
Steroids if needed
What is the definition of traveler’s diarrhoea and what are the common causes?
Traveller’s diarrhoea = 3 loose to watery stools in 24 hours with or without one or more of abdominal cramps, nausea vomiting or blood in the stools. Typically causes be E.Coli.
What is the definition of acute food poisoning, and what are the common causes?
Acute food poisoning =sudden onset of nausea, vomiting and diarrhoea after the ingestion of a toxin. Typically causes by staph aureus, bacillus cereus or clostridium perfingens.
What is the typical presentation of E.coli gastroenteritis?
E.Coli – recent travel, nausea, watery stools and abdominal cramps
What is the typical presentation of giardiasis gastroenteritis?
Giardiasis – prolonged non-bloody diarrhoea
What is the typical presentation of cholera gastroenteritis?
Cholera – profuse watery diarrhoea, severe dehydration, and weight loss
What is the typical presentation of shigella gastroenteritis?
Shigella – bloody diarrhoea, vomiting and abdominal pain
What is the typical presentation of staph aureus gastroenteritis?
Staph Aureus – severe vomiting and short incubation period
What is the typical presentation of campylobacter gastroenteritis?
Campylobacter – flu like prodrome, followed by abdominal pain, fever, diarrhoea (may be bloody), can mimic appendicitis and can cause Guillain barre syndrome
What is the typical presentation of bacillus cereus gastroenteritis?
Bacillus cereus – vomiting with 6 hours typically with rice OR diarrhoeal illness occurring after 6 hours.
What is the typical presentation of amoebiasis gastroenteritis?
Amoebiasis – gradual onset blood diarrhoea, abdominal pain and tenderness which may last for several week
What is norovirus?
AKA the winter vomiting bug. Transmitted by faecal oral route usually with virus becoming aerosolized with vomiting or flushing toilet
What are the clinical features of norovirus?
Nausea, vomiting, diarrhoea, headache, fever, and myalgia
Vomiting is sudden onset and symptoms usually for a short duration
How should norovirus be investigated?
Stool culture and PCR
How should you manage a patient with norovirus in a hospital?
Limit transmission by isolation of infected and good hand hygiene
Symptoms usually self-resolve within 72 hours
Rehydration and electrolytes
What are the common differnetials for someone suspected of having norovirus?
Salmonella – often causes bloody diarrhoea and high fever
Rotavirus – predominantly in children
E. Coli – longer incubation period and causes severe abdominal cramping unlike norovirus
What is clostridium difficile
Gram positive rod that produces an exotoxin which causes intestinal damage leading to pseudomembranous colitis. Antibiotic use is a major cause of C.Diff diarrhoea in hospitals, particularly clindamycin and 2nd and 3rd generation cephalosporins. Other risk factors include PPIs.
What are the clinical features of clostridium difficile?
Diarrhoea
Abdominal pain
Raised WCC
Sever toxic megacolon
How should a potential c.diff infection be investigated?
Faecal culture and detection of clostridium difficile toxin (CDT)
C.Diff antigen positive only shows exposure rather than infection
Describe the severity index for classifying C.diff infection?
- Mild – normal WCC
- Moderate – WCC<15, 3-5 loose stools
- Severe – WCC > 15, acute creatinine rise >50% baseline, Temp > 38.5 or evidence of severe colitis from x-ray or examination
- Life-threatening – hypotension, partial or complete ileus, toxic megacolon or CT evidence of severe disease.
What is the management of C.Diff infections?
Isolation and barrier nursed with good hand hygiene
Oral metronidazole for 10-14 days if first episode
If severe, second episode or not responding, then oral vancomycin
Fidaxomicin – can also be trialed particularly if multiple co-morbidities
If life threatening then combination of oral vancomycin and IV metronidazole
Define diverticulas, diverticular disease and diverticulitis?
Diverticulitis – outpouchings of the bowl (diverticula) that are inflamed and ulcerated
Diverticulosis – presence of diverticula
Diverticula disease – diverticula that are symptomatic
How common are diverticula/diverticulosis?
Very common with 30% of westerners having diverticula by age 60, only 25% will experience symptoms and 75% of these will experience episode of diverticulitis.
What causes diverticula to form?
Occur due to increase intra-colonic pressure and usually occurs along the weaker portions of the wall such as where the penetrating arteries enter.
What are the risk factors for diverticula?
Age Lack of dietary fibre Obesity, especially in younger patients Sedentary lifestyle Smoking NSAID use
How does diverticula disease present?
Diverticula Disease
Almost all diverticula are found in the sigmoid colon
Pain in left iliac region eases after passing wind or faeces
Usually the pain comes on after eating
Feeling bloated
Change in bowel habit – constipation or diarrhoea and mucus
How does diverticulitis present?
Severe pain in left lower quadrant +/- guarding (if perforation)
N&V due to ileus or colonic obstruction
Change in bowel habit – constipation more common but diarrhoea also seen
Urinary frequency – urgency or dysuria due to irritation of the bladder by inflamed bowel
PR bleeding
Pneumaturia or faecaluria suggesting colovesical fistula
Vaginal passage of faeces or flatus suggest colovaginal fistula
Pyrexia, tachycardia
Nausea and vomiting
How should diverticulitis and diverticular disease be investigated?
FBC + CRP, G&S if actively bleeding
Erect CXR for perforation
AXR – dilated bowel loops, obstruction, or abscesses (+ barium enema)
CT – best modality for abscesses
Colonoscopy – avoid initially in infective exacerbation due to risk of perforation
What is the Hinchey severity classification for diverticula disease?
Hinchey Severity Classification for diverticula Disease I – para-colonic abscess II – pelvic abscess III – purulent peritonitis IV – faecal peritonitis
How are acute exacerbations or diverticulitis managed?
Oral antibiotics, NBM and liquid diet and analgesia
If severe or does not settle within 72 hours, then admit for IV antibiotics
How is an acute bleed from diverticula disease managed?
Acute Bleed ABCDE Fluids Transfusion if needed Check clotting Monitor conservatively Usually stops of its own accord if not then may not be diverticula related
What general management is there for diverticular disease?
Increase dietary fibre intake
Drainage of colonic abscess surgically or radiologically
Segmental resection if recurrent episode of diverticulitis
Hinchey IV – resection and stoma, often requiring HDU admission
What is GORD?
Symptoms of oesophagitis secondary to refluxed gastric contents. This can be mild reflux at least twice a week or moderate to severe reflux at least once a week.
If left untreated what can GORD cause?
Oesophagitis Ulcers Anaemia Benign strictures Barrett’s oesophagus Oesophageal cancer
What are the clinical features of GORD?
Burning retrosternal pain (heartburn) usually after eating and worse at night
Chest pain
Regurgitation of food or sour liquid
Sensation of lump in the throat
Dysphagia
Night time acid reflux can cause hoarseness, chronic cough, laryngitis, new or worsening asthma or disrupted sleep
How should GORD be investigated?
Upper GI endoscopy
24hr oesophageal pH monitoring (gold standard test for diagnosis
What are the indications for an upper GI endoscopy in GORD?
- Age > 55yrs
- Symptoms > 4 weeks or persistent symptoms despite treatment
- Dysphagia
- Relapsing symptoms
- Weight loss
How is GORD managed?
GORD which has not been investigated with endoscopy should treated as dyspepsia
1. Review medications for possible causes
2. Lifestyle advice
3. Trial of full dose proton pump inhibitor for one-month OR test and treat H-pylori. If symptoms persist after either of these then an alternative approach should be tried.
Testing for H-pylori – carbon-13 urea breath test or stool antigen test. Treat with a proton pump inhibitor + amoxicillin + clarithromycin OR a proton pump inhibitor + metronidazole + clarithromycin.
If GORD is endoscopically proven
• Full dose proton pump inhibitor for 1-2 months
• If response, then low dose treatment as required
• If no response, then double dose PPI for 1 month
Endoscopically negative reflux disease
• Full dose PPI for 1 month
• If response, then low dose treatment as required
• If no response, then H2RA (cimetidine/ranitidine) or prokinetic (metoclopramide) for one month
What is Barrett’s oesophagus?
Metaplasia of lower oesophageal mucosa from squamous cell to columnar epithelium. This causes an increased risk of oesophageal carcinoma of about 50-100-fold. Barrett’s can be subdivided into short (<3cm) and long (>3cm).
What are the risk factors for Barrett’s oeosphagus?
GORD
Male (7:1)
Smoking
Central obesity
How is Barrett’s oesophagus managed?
Endoscopic surveillance with biopsies – every 3-5yrs
High dose proton pump inhibitor
If dysplasia of any grade is identified intervention is offered
Endoscopic mucosal resection or radiofrequency ablation
What are gastric/duodenal ulcers?
Definition – erosion of the stomach or duodenal wall due to excess acid/pepsin/bile salts/Helicobacter Pylori or inadequate levels of mucus/bicarbonate/blood flow/cell turnover.
Which type of ulcers are most common and how many are associated with H-pylori?
Duodenal ulcers are 4x more common than gastric and 95% are associated with H-pylori. Gastric ulcers generally occur in elderly on the lesser curvature of the stomach and only 75% are associated with H-pylori.
What causes gastric/duodenal ulcers?
H-Pylori Smoking Drugs: NSAIDs, steroids, SSRIs, and bisphosphonates Zollinger Ellison syndrome Increased gastric emptying (duodenal) Delayed gastric emptying (gastric) Increase stomach acid secretion
What are the clinical features of peptic ulcers?
Duodenal ulcers – epigastric pain usually worst 2-5 hours after eating and related to hunger, types of food and time of day may be relieved by eating
Gastric ulcers – epigastric pain that is exacerbated by eating
Fullness after meals Heartburn (retrosternal pain) Tender epigastrium Alcohol Nausea
(ALARMS symptoms – Anaemia, Loss of weight, Anorexia, Recent onset, Malaena/haematemasis and swallowing difficult
How are peptic ulcers investigated?
Routine bloods
Test for H-Pylori. Testing for H-pylori – carbon-13 urea breath test or stool antigen test.
Endoscopy
Gastrin secretions (when off PPI) for Zollinger Ellison Syndrome
How are peptic ulcers managed?
H-Pylori – PPI and 2 antibiotics (clarithromycin and amoxicillin/metronidazole)
If H-Pylori test is negative, then PPI until ulcer healed
Reduction in weight
Change of diet and lifestyle (alcohol)
How does a perforated peptic ulcer present?
Sudden onset epigastric pain preceded by a history of upper abdominal pain, pain made worse by any kind of movement, especially coughing, or sneezing. May have clinical evidence of peritonitis. Erect CXR may show free air under the diaphragm.
How are perforated peptic ulcers managed?
Management is via laparotomy or laparoscopy to give wash out, primary repair or resection
What is achalasia?
Definition – failure of the oesophageal peristalsis and of the lower oesophageal sphincter muscle fibres to relax due to degenerative loss of ganglia from Auerbach’s plexus. This results in the LOS contracted and oesophagus above dilated.
Who does achalasia most commonly affect?
Usually affecting middle-aged adults equally between men and women.
What are the clinical features of achalasia?
Dysphagia of both liquids and solids
Regurgitation leading to cough and aspiration pneumonia
Epigastric and sternal pain (heartburn)
Weight loss
Very small number of patients show a malignant change
How is achalasia investigated?
Oesophageal manometry – excessive LOS tone which does not relax on swallowing
Barium swallow – grossly expanded oesophagus, fluid level, bird’s beak appearance
CXR – wide mediastinum and fluid level
Endoscopy
How is achalasia managed?
Lifestyle changes – eat slowly and small portions, chewing well with plenty of water
Sleep with extra pillows
Intra-sphincteric injection of botulinum toxin
Pneumatic (balloon) dilation – forceful dilation of the sphincter
Heller Myotomy – dissecting away the outer tough muscle layer
Drug therapy
Sublingual nifedipine
Isosorbide mononitrate
What is Primary Sclerosing cholangitis
Definition – inflammation of the intra and extra hepatic bile ducts (inside and outside the liver) that eventually causes scaring and restructuring resulting in cholestasis and biliary fibrosis, cirrhosis and liver failure. Cause is unclear but potentially autoimmune
Who does primary sclerosing cholangitis occur in?
It is very common that people with PSC also have some form of Inflammatory bowel disease. 4% of UC patients have PSC and 80% of PSC have UC, Crohn’s much less common. HIV also associated with PSC. Otherwise very rare but most common in those aged 40 and twice more common in men.
What are the clinical features of primary sclerosing cholangitis
Most commonly no signs Cholestasis resulting in jaundice and pruritis Right upper quadrant abdominal pain Fatigue Hepatomegaly and Splenomegaly
What investigations should be done if you are considering primary sclerosing cholangitis?
LFTs – ALP and bilirubin raised
Magnetic resonance cholangiopancreatography (MRCP) is first line. Can also consider Endoscopic retrograde Cholangiopancreatography (ERCP). They will both show a beaded appearance
p-ANCA may be positive
Liver biopsy showing signs consistent with PSC can be used to diagnose
How is primary sclerosing cholangitis managed?
No treatment only management of symptoms
Cholestyramine to stop skin itching.
Liver transplant if eligible but in 1/5 of cases it will reoccur.
Eat healthy diet with NO alcohol
What complications can occur as a result of primary sclerosing cholangitis?
Liver cirrhosis and failure Vitamin Deficiency Infection of the bile ducts Cholangiocarcinoma in 10% Increased risk of colorectal cancer
What is primary biliary cholangitis?
Definition – autoimmune disease that causes destruction of the small bile ducts of the liver resulting in bile and other toxins accumulating in the liver and so fibrosis.
Often occurs in people with other autoimmune disease. Affects 1 in 4000 people and much more common in women (9:1), usually middle aged.
What causes primary biliary cholangitis?
Autoimmune cause (the large majority contain anti-mitochondrial antibodies against pyruvate dehydrogenase complex).
What other conditions is primary biliary cholangitis associated with?
Associated with Sjogren’s syndrome (80% of patients)
Rheumatoid arthritis
Systemic sclerosis
Thyroid disease
What are the clinical features of primary biliary cholangitis?
Classic presentation is itching in a middle-aged woman
Fatigue
Pain in URQ (only seen in 10%)
Xanthelasmas and xanthomas
Clubbing
Hepatosplenomegaly
Cholestatic Jaundice
Hyperpigmentation, especially around pressure points
Sjogren’s features such as dry eyes and dry mouth
