Colon diseases

Question 1

What is the treatment for mild UC?

Answer 1

Sulfalazine, mesalazine, olsalazine help induction of remission/maintenance treatment.

Steroids help with induction remission e.g. prednisolone or hydrocortisone, if improving within two weeks reduce steroids slowly, if not treat as moderate UC.

Question 2

What is the definition of mild UC?

Answer 2

110

ESR

Question 3

What is the treatment for moderate UC?

Answer 3

Oral prednisolone 40mg for 1 week then 30mg for 1 week then 20mg for 4 more weeks + 5-ASA + steroid enemas twice daily.

If improving reduce steroids gradually, if not treat as severe UC

Question 4

What is the definition of moderate UC?

Answer 4

4-6 motions a day
Moderate rectal beeding
37.1-37.8 pyrexia at 6am
70-90BPM
Hb 105-110

Question 5

What is the treatment of severe UC?

Answer 5

Nil by mouth, IV hydration.

IV hydrocortisone, rectal hydrocortisone.

Monitor obs and stool character.

Daily bloods- consider blood transfusion if Hb 45 or >6stools day on day 3, consider rescue therapy e.g. ciclosporin or infliximab or colectomy.

Question 6

What is the definition of severe UC?

Answer 6

Stools > 6 daily
Large rectal bleeding
Temperature > 37.8
Resting pulse > 90 BPM
Hb  30 or CRP > 45

Question 7

Which areas of the bowel does UC affect?

Answer 7

Just the rectum- proctitis- 50%
Part of the colon as well as rectum- left sided colitis- 30%
Entire colon- 20%

Never extends to involve the rest of the colon.

Question 8

Pathology of UC

Answer 8

Involves only the mucosal layer.

Causes hyperaemic/haemorrhagic granular colonic mucosa +/- pseudopolyps formed by inflammation.

Punctate ulcers may extend deep into the lamina propria, but inflammation is not normally transmural.

Question 9

Appearance of UC on radiology

Answer 9

Steel pipe appearance

Loss of haustra

Question 10

When do you immunomodulate with UC, and what with?

Answer 10

If no remission comes with steroids, or prolonged use is required.

e.g. azathioprine, infliximab, methotrexate, adalimumab or calcineurein inhibitors e.g. tacrolimus and ciclosporin.

Question 11

Which inflammatory bowel disease is smoking protective against?

Answer 11

UC

Question 12

Symptoms of UC?

Answer 12

Episodic or chronic diarrhoea (+/- blood and mucus), crampy abdominal discomfort, bowel frequency relates to severity, urgency/tenesmus = rectal UC, fever, malaise, anorexia, weight loss.

Question 13

Appearance of UC on colonoscopy

Answer 13

Inflammatory infiltrate
Goblet cell depletion
Glandular distortion
Mucosal ulcers
Crypt abscesses

Question 14

What are the complications of UC?

Answer 14

Perforation and bleeding
Toxic megacolon (>6cm)
Venous thrombosis- give prophylaxis to all inpatients
High risk of colon cancer- give routine colonoscopy.
Renal calculi

Question 15

What region of the GI tract does Crohn’s disease affect?

Answer 15

Anywhere from mouth to anus especially the terminal ileum- around 70% will have TI disease- and proximal colon.

Question 16

What is the appearance of the bowel in Crohn’s disease?

Answer 16

Skip lesions (regions of unaffected bowel), colon strictures, cobblestoning, rose thron ulcers.

Question 17

What is the management of Crohn’s disease?

Answer 17

Supportive therapy for affect on individual’s life
Help to quit smoking
Optimise nutrition- enteral is preferred, TPN is a last resort in severe disease
Assess severity by monitoring observations, inflammatory markers, WCC, CRP etc.

Treatment of mild attacks i.e. symptomatic but systemically well- Prednisolone 30mg for 1 week then 20 for 3 weeks and see in clinic every three weeks- if looking better reduce by 5 mg weekly and stop when parameters are fine.

Severe- looks ill- admit for IV steroids, NBM and IV fluids.
Treat perianal disease with PR prednisolone
Monitor obs and stools
Consider need for blood transfusion if Hb

Question 18

Complications in Crohn’s

Answer 18

Toxic megacolon (rarer than in UC), PSC (also rarer than in UC), abscess formation, fistulae e.g. bladder, anal, vaginal or enterocutaneous, perforation, colon cancer, rectal haemorrhage, fatty liver, colangiocarcinoma, malnutrition.

Others: amyloidosis, renal calculi, osteomalacia.

Question 19

Pathological appearance differentiating crohn’s from UC

Answer 19

Skip lesions
Transmural involvement
non-caseating granulomas
Fissuring with the formation of fistulas.

Question 20

Criteria of IBS diagnosis

Answer 20

Pain is relieved by defecation OR associated with altered stool form or bowel frequency (constipation and diarrhoea may alternate) AND there are >2 of urgency, incomplete evacuation, abdominal bloating/distension, mucous PR, worsening of symptoms after food.

Other symptoms: nausea, bladder symptoms, backache- symptoms last >4 months (chronic) and are exacerbated by stress, menstruation or gastroenteritis (post-infectious IBS).

Question 21

Signs of IBS

Answer 21

Examination often normal but there may be general abdominal tenderness

Question 22

What should make you think that the diagnosis is NOT IBS?

Answer 22

Age > 40 esp. male

History

Question 23

Management of IBS

Answer 23

1. Exclude other diagnoses- If symptoms are classic of IBS- just do FBC, CRP, ESR and coeliac serology.

If > 50 or any marker of organic disease e.g. blood, weight loss, pyrexia then do colonoscopy.

Refer if family history of bowel/ovarian cancer

If diarrhoea, do LFTs, stool cultures, B12/folate, anti-endomysial antibodies (coeliac disease), TSH- consider barium follow-through and referral +/- rectal biopsy.

2. Refer if any reasonable doubt it may be something else.
3. Treatment aimed at lifestyle and symptom control-

• Ensure healthy diet
• Avoid things such as caffeine, alcohol etc
• If they have constipation- avoid insoluble fibre e.g. bran as this can make symptoms work e.g. flatulence, but therapeutic agents such as bisacodyl and sodium picosulfate are good. Ispaghula can be used as it is a non-fermentable water-soluble fibre, but lactulose less good as it ferments.

Diarrhoea- avoid sorbitol sweeteners; try a bulking agent +/- loperamide.

Colic/bloating- oral antispasmodics.

Psychological symptoms/visceral hypersensitivity- emphasise the positive that most patients improve within 1 year, consider CBT, hypnosis and tricyclics e.g. amytriptyline.

Question 24

Investigation for Crohn’s

Answer 24

Blood tests- all normal including ESR, CRP, U&Es, LFTs, B12, ferritin, INR, folate etc.

Cultures- to rule out C.diff, E.coli, Campylobacter etc.

Colonoscopy + rectal biopsy even if mucosa looks normal (20% have microscopic granulomas)

Barium swallow rarely used.

MRI can look for pelvic disease, fistulae, activity of disease and presence of strictures.

Question 25

Investigations for UC

Answer 25

Blood- routine, ESR, CRP, LFTs + culture Stool- culture Erect CXR- to look for perforation AXR- loss of haustra, mucosal thickening, check for toxic megacolon (dilated > 6cm) Colonoscopy- with biopsy- looks for disease extent, can help to confirm diagnosis- look for inflammatory infiltrate, goblet cell depletion, glandular distortion, mucosal ulcers and crypt abscesses.

Question 26

Coeliac disease presentation

Answer 26

Suspect in all with diarrhoea and weight loss, especially if iron or B12 deficient. Will have stinking stools/steatorrhoea, diarrhoea, abdominal pain, bloating, nausea + vomiting, aphthous ulcers, angular stomatitis, weight loss, fatigue, weakness, osteomalacia, failure to thrive (children). 1/3 are asymptomatic.

Question 27

Pathophysiology of coeliac disease

Answer 27

A T-cell mediated autoimmune disease in which prolamin (alcohol soluble proteins in rye, oats, barley and wheat) intolerance causes vollous atrophy and malabsorption, including of bile acids.

Question 28

What is the typical demographic of someone with IBS?

Answer 28

Female > male

Question 29

What conditions/genetics are associated with coeliac disease?

Answer 29

HLA-DQ2 (95%), rest are DQ8. Autoimmune disease Dermatitis herpetiformis

Question 30

What is the typical demographic of someone with coeliac disease?

Answer 30

Irish much more common Females same prevalence as males Typical age peaks in infancy and 50-60 years 10% prevalence in first degree relatives and 30% RR in siblings

Question 31

Treatment of coeliac's disease

Answer 31

Gluten-free diet. | Can prescribe some gluten-free foods.

Question 32

How is a diagnosis of coeliac disease made?

Answer 32

Low Hb, B12 and ferritin (causing a high red cell weight distribution due to the mixed anaemias) Antibodies: alpha gliadin, transglutaminase and anti-endomysial (an IgA antibody) levels- high antigliadin and antiendomysial levels are very sensitive, but IgA deficiency may result in a false negative result. Do an endoscopy with a duodenal biopsy- Macroscopically will show smoothing of the villi and elongation of the crypts causing the small bowel to resemble the large bowel and more disease proximally than distally in the bowel Microscopically will show villous atrophy, raised intraepithelial lymphocytes and crypt hyperplasia. Endoscopy can be done again to check for the efficacy of a gluten-free diet.

Question 33

How to check if treatment is working in coeliac disease

Answer 33

Appearance of small bowel has reverted back to normal. Antibody titres back to normal.

Question 34

What are the complications of coeliac disease?

Answer 34

Anaemia, secondary lactose intolerance, GI T-cell lymphoma (rare, suspect if refractory symptoms or weight loss), increased risk of malignancy (gastric, oesophageal, bladder, breast, brain), myopathies, neuropathies, hyposplenism, osteoporosis

Question 35

What is tropical sprue and what is its appearance in the small bowel? What is its cause, what are the symptoms and how is it treated?

Answer 35

A coeliac-like disease that occurs frequently in people living in the tropics. Variable macro/microscopic appearance, but affects the entire small bowel. Diarrhoea etc like in coeliac disease, but also get B12 and folate deficiency which may lead to pernicious anaemia. No causative agent has been found but bacterial overgrowth has been implicated. Treatment- broad spectrum antibiotics.

Question 36

Whipple's disease- causative agent

Answer 36

Gram-positive actinomycete called Tropheryma whippleii.

Question 37

What is Whipple's disease?

Answer 37

A systemic disease which results in GI malabsorption caused by a bacteria.

Question 38

Treatment of whipple's

Answer 38

any antibiotic that crosses the blood brain barrier Ceftriaxone or penicillin plus streptomycin

Question 39

What will you see on a biopsy in Whipple's disease?

Answer 39

Small intestinal mucosa will be distended with macrophages in the lamina propria, which will be infiltrated with rod shaped bacilli on electron microscopy

Question 40

What organs does Whipples affect?

Answer 40

All, but mostly the intestine, CNS and joints

Question 41

What are the differences between crohn's and UC?

Answer 41

Crohn's UC Mouth to anus Colon/anus only Skip lesions Continuous lesions Thickened bowel wall Bowel wall normal thickness Transmural inflammation Mucosal inflammation Granulomas No granulomas Deep fissuring ulcers No fistula formation Cancer rare Cancer common Non-surveillance Surveillance Smoking worsens Smoking protects Fat wrapping No fat wrapping

Question 42

Signs of Ulcerative colitis

Answer 42

Acute severe: fever, tachycardia, distended tender abdomen. Extraintestinal signs: Skin signs- erythema nodosum, pyoderma gangrenosum, aphthous ulcers. Eye signs-episcleritis, iritis, conjunctivits Bone and joint signs- sacroilitis, large joint arthritis, ankylosing spondylitis. Gastrointestinal signs: PSC, fatty liver disease, colangiocarcinoma, nutritional deficits. Other: sarcoidosis.