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Flashcards in Crohns Deck (12):
1

Definition

Inflammatory GI disease characterised by granulomatous inflammation anywhere from mouth to anus. Common in terminal ileum and proximal colon. Exacerbations and remissions.
Transmural, asymmetrical, sometimes granulomatous.
Skip lesions.
Bimodal age distribution.

2

Aetiology

Unknown
Involves immune system dysfunction. Increase TNFa.
Certain gene mutations increase risk.
Gut organism. Eg mycobacterium, pseudomonas.
Triggers eg AB, smoking, infection, fatty diet.
RFs- family history, smoking, female, URTIs, NSAIDs.

3

Symptoms

Diarrhoea or urgency, bad smell.
Abdo pain severe, usually low right.
Fatigue.
Weight loss.
Fever.
Malaise
Anorexia
Vomiting
Joint pain.

4

Differentials

UC
Parasite, gastroenteritis, fungal infection.
TB
IBS
Amyloidosis
Ischaemic colitis
Lymphoma, Colon CA
Diverticulitis

5

Signs

Skip lesions
Granuloma
Mouth ulcer
Fever
Anaemia.
Abdo tenderness or mass. More frequent and severe abdo pain than UC.
Fistulae
Aphthoid and deep ulcers- cobblestoning.
Granulomas
Smoking worsens
Perianal abcess, fistulae, skin tag.
Anal structures.
Clubbing
Skin, joint, eye problems.

6

Management

Nutrition
Stop smoking
Azathioprine steroid sparing
Sulfasalazine not proven in crohns
CS, steroid analogues
Immunomodulators
Immunosuppressants. Methotrexate anti folate (risk leukopenia, infection, pulmonary fibrosis, teratogenic).
Metronidazole
TNFa inhibitors eg infliximab
MAbs
Surgery not curative but can help strictures and fistulae, or respect parts repeatedly flare up.

7

Pathology

Hyperaemia
Mucosal oedema
Discrete superficial ulcers and deeper ulcers= cobblestone.
Thickening bowel wall
Fistulae
Granuloma.

8

Investigation

Bloods- anaemia. FBC, UE, LFT, CRP.
CT and MRI- thickening, obstruction, extramural issues, string sign of kantor (incomplete lumen filling due to spasm due to ulcer).
Barium enema or follow through- stricture, fistulae.
Iliocolonoscopy and biopsy.
Stool culture

9

Complications

SI obstruction
Abcess
Fistulae eg colovesical, colovaginal, perianal. And strictures.
Perforation
Colon CA, cholangioCA
OP and osteomalacia
Fe, folate, B12 deficiency
Renal disease eg ureter obstruction by iliocecal disease
Abortion, miscarriage, stillbirth.

10

Anti metabolite eg Methotrexate

Not antifolate in crohns MOA. Maybe inhibit purine metabolism and T activation.
Low dose can combine with other DMARDs, NSAIDs, steroids.
AE-pneumonitis, hepatotoxicity, mucositis, teratogenic.
Monitor all bloods
DDI- binding competition with eg NSAID, phenytoin, tetracyclines, penicillin= increase myelosuppression.

11

Anti TNF eg infliximab

Dont escalate dose.
Reduce inflammation, angiogenesis.
AE- risk new malignancy if had one previously. Risk serious infections. TB reactivation.

12

Explanation

-Crohns is a disease that can affect the whole of the digestive system. But it usually is worse in th intestines. It happens when your immune system causes inflammation and damage to the walls of your digestive tract. This affects its function, meaning it cant absorbs things and break down your food as well. This leads to diarrhoea, vomiting and pain.
-it usually comes in phases so you will have a bout of symptoms then they will wear off for a while. In the long term it can cause obstruction because of thickening of the walls, and also it can cause holes to form in the walls. It can also have affects on your joints, skin, and eyes. Also abcesses, CA, renal disease and problems with pregnancy.
-lifestyle diet and stop smoking. Avoid triggers.
-drugs to modulate immune systems damaging affects. Also steroids to prevent inflammation.