IBD Flashcards

1
Q

What conditions make up IBD?

A

Ulcerative colitis and Crohn’s disease

Also - Proctitis = UC that only occurs in the last 6 inches of the rectum; may also refer to any inflammation of the rectum; Proctocolitis = inflammation of the colon and rectum; Pancolitis = inflammation affecting the whole of the colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the epidemiology of UC?

A
  • Most often affects Caucasians in temperate climates; rare in Africa and Asia
  • 2-3x more common than Crohn’s
  • Similar incidence between males and females
  • Most present age 15-30
  • More common in non smokers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What causes UC?

A

Environmental trigger in a genetically susceptible individual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the relationship between smoking and UC?

A

Reduces your risk of UC i.e. if your diagnosed with UC then stop smoking, you increase your risk of relapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the pathophysiology of UC and Crohn’s?

A

Auto-inflammatory response to bacterial endotoxins/dietary antigens - taken up by M cells in Peyer’s patches and MALT - passed to APCs + CD4 T-cells - secretion of proinflammatory cytokines + activation of Th1 cells - uncontrolled inflammatory cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What areas of the bowel are affected in UC?

A

Inflammation ascends from rectum through colon
Continuous inflammation ie no skip lesions
Generally confined to mucosa + sub-mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does UC present?

A

Bloody diarrhoea +/- mucous
Abdominal pain/discomfort
Tenesmus (need to evacuate bowel) - rectal involvement

Systemic inflammatory response - fever, malaise, anorexia

Non-specific extra-GI symptoms:

  • Erythema nodosum
  • Episcleritis
  • Anterior unveitis
  • Acute arthropathy
  • Aphthous ulcers
  • Pyoderma gangrenosum (all of the above are related to the activity of the UC)
  • Sacroiliitis/Ank spond.
  • Primary sclerosing cholangitis (these two are unrelated to the activity of colitis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the two key clinical features that can help differentiate UC from Crohn’s?

A
UC = voluminous bloody diarrhoea more common 
Crohn's = extra-GI features more common
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the time course of UC? How do you classify severity?

A

Relapse/remitting - some patients may have a single flareup and remit for rest of life, others will have chronic unremitting

Mild = <4 stools/day with no systemic disturbance and normal ESR/CRP

Moderate = 4-6 stools/day with minimal systemic disturbance

Severe = >6 stools/day and evidence of systemic disturbance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some complications of UC?

A
Perforation 
Bleeding → iron deficiency anaemia 
Venous thrombosis 
i)	Give prophylaxis to all inpatients 
Colon cancer 
i)	Increase of 15% in patients who have had a pancolitis for 20+yrs 
Toxic megacolon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do you investigate UC?

A

PR - blood on glove

Sigmoidoscopy/colonoscopy + biopsy - abnormal, inflamed and bleeding mucosa; ulceration
i) Non malignant biopsy might show inflammatory infiltrates, goblet cell depletion, ulcers and crypt abscesses

Bloods (during acute attacks):↑ WCC, ↑ platelets, ↑ ESR and CRP, Iron deficiency anaemia, P-ANCA +ve (usually –ve in Crohn’s)

Stool samples - to exclude infective colitis i.e. C.diff, campylobacter and E.coli; Calprotectin – indicates migration of neutrophils into intestinal mucosa – raised in IBD

Scans: AXR – presence of air and colonic dilatation, USS– thickening of wall and presence of free fluid in abdominal cavity, barium enema – show macroscopic extent of disease and presence of any ulcers
i) Not to be done during a severe attack

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How to treat UC?

A

Mild - 5-ASA (sulphasalazine) - maintains remission; or mesalazine

Moderate - steroid to initiate remission then 5-ASA
i) Hydrocortisone, prednisolone, desxamathasone (oral, IV or enema/topical)

Severe - Trial high dose steroid for 5-7 days (not longer or reduce operability)

i) If no remission with steroid, use IV ciclosporin
- If this contraindicated (e.g. HTN, renal impairment) use Infliximab (anti TNF-alpha)
- If remission not achieved with medical management then surgery is indicated

ii) Try to maintain remission with 5-ASA or use immunosuppressant: cyclosporin, methotrexate, azathioprine etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What surgery is required?

A

Whole colon needs removing or disease will return in part of colon not resected:

  • Permanent ileostomy
  • Temporary ileostomy – colon removed → endo of ileum folded over to make pouch = new rectum →(2nd operation) connect pouch to anus

There is a risk of sexual dysfunction on males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some other indications for surgery?

A

Perforation (gas under diaphragm on erect XR)
Toxic megacolon
Dysplasia
i) If there are signs of dysplasia (i.e. has turned flat) at 2 locations in the colon – surgery to avoid possibility of malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the epidemiology of Crohn’s disease?

A
  • Condition of young adults – diagnosis occurring between 20-29, second incidence peak 70+yrs
  • More common in western societies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the aetiology of Crohn’s disease?

A

Similar to UC - Genetic susceptibility + environmental factors (dietary/bacterial Ags) + patient’s immune response

Genetics - two specific mutation have been implicated increased susceptibility
i) CARD 15 and NOD-2 gene s on chromosome 16 are thought to be responsible in some patients

17
Q

What is the relationship between smoking and Crohn’s?

A

Unlike UC it is a risk factor – 2x more likely to develop than non-smokers and those who continue to smoke present with more severe symptoms

18
Q

What areas of the bowel are affected in Crohn’s?

A

Can affect the whole GI tract i.e. mouth to anus (whereas UC is confined to the large bowel)

Skip lesions are present
i) Patches of healthy bowel followed by inflammation and so on – characteristic on endoscopy

Affects all layers of the bowel (transmural)
i) As a result can fistulate (to become hollow) or form strictures - common complications of Crohn’s that do not occur as often with UC

19
Q

How does Crohn’s present?

A

Abdominal pain - esp common in RIF as terminal ileum often affected
Diarrhoea
Vomiting
Perianal abscesses, fistulae, skin tags, anal/rectal strictures
Weight loss, malaise, fever
Malabsorption syndromes depending on what areas of bowel affected
Same extra GI features as UC (but more common)

20
Q

What are some complications of Crohn’s?

A

Increased risk of cancer
i) Adenocarcinoma of distal ileum with a very poor prognosis

Toxic megacolon
i) Where a deeper layer of the bowel becomes affected and colon becomes massive (>6cm diameter dilatation) with an increased risk of perforation

21
Q

How do you investigate Crohn’s?

A

Barium swallow: strictures, mucosal changes, fistulae etc will show; cobblestoning appearance

Colonoscopy: view and biopsy
i) Histological abnormalities i.e. inflammatory infiltrate and granuloma even when bowel looks normal, transmural

CT: can show fistulae, thickening of bowel wall and abscesses

Stool samples/bloods - same as UC

22
Q

What are some behavioural modifications for Crohn’s?

A

Smoking cessation – enough to induce remission in many patients

Low residue and low fat diets can help reduce symptoms, especially in those with strictures
i) Restricts foods that increase bowel activity i.e. milk + products and prune juice and high fibre foods

Avoid: anti-diarrhoeal agents + opioids due to chance of precipitating toxic megacolon

23
Q

What are some pharmacological treatments for Crohn’s?

A

5-ASA not used

Steroids – prenisolone PO

i) If patient symptomatic but systemically well
ii) IV hydrocortisone if severe

Immunosuppressants used in severe disease
i) Azathioprine, methotrexate, cyclosporin

Abx
i) Metronidazole - to reduce intestinal flora and diarrhoea

Infliximab

i) For patients who don’t respond to other treatment
ii) TNFα antibody → reduces inflammation

Supplementation
Many will require iron and B12 supplements; Fat soluble vitamins ADEK

24
Q

What is the surgical treatment for Crohn’s?

A

80% of patients will end up having surgery
i) Bowel resection – potentially several within a lifetime – needs to be a conservative operation to avoid complications; indications: fistulating disease, stricture causing obstruction, disease not responding to above treatment

ii) Strictureplasty: stricture is cut longitudinally and sutured transversely to widen it
iii) Abcesses - drained percutaneously

25
Q

What is toxic megacolon? How does it present and how is it managed?

A

he acute and severe dilatation of the bowel
- Colon unable to remove faeces and gas - builds up - possibly to the point of rupture

May be triggered by:

  • Hypokalaemia
  • Opiates
  • Anticholinergics
  • Barium enemas etc.
  • IBD, bowel infections and ischaemia

Presentation:

  • GI pain, distension, diarrhoea
  • Mental state changes*
  • Fever, tachycardia, hypotension, shock
  • Raised white cell count; anaemia; electrolyte abnormalities*
  • Severely dilated bowel - >6cm, loss of haustra - on AXR or CT

Management:

  • Aggressive fluid resus +/- vasopressors
  • IV Abx, broad spec e.g. Tazocin
  • (manage the acute presentation of IBD)
  • NBM + NG tube for decompression
  • If no response in 24-72hrs then surgery indicated = colectomy