What is the causation triad of IBD?
Genetic susceptibility + altered microbiome + environmental trigger.
How does smoking affect IBD?
Worsens Crohn’s disease; protective in ulcerative colitis.
Most sensitive noninvasive marker of intestinal inflammation?
Faecal calprotectin (≥150 µg/g suggests active inflammation).
First infections to exclude in suspected IBD?
Stool M/C/S, C. difficile, ova/cyst/parasite.
Preferred imaging for small-bowel Crohn’s disease?
MR enterography (capsule only if no stricture).
Histologic chronicity marker in UC?
Basal plasmacytosis.
Key histologic feature distinguishing Crohn’s?
Transmural inflammation ± granulomas.
Mnemonic CCAT in IBD histology?
Crypt abscess, Chronic changes, Architectural distortion, Transmural inflammation.
UC endoscopic pattern?
Continuous mucosal inflammation from rectum proximally.
Crohn’s endoscopic pattern?
Skip lesions with cobblestoning and transmural ulcers.
Tool used to grade UC severity?
Truelove–Witts criteria.
Definition of ASUC?
≥6 bloody stools/day plus systemic toxicity (fever, tachycardia, anaemia).
Crohn’s classification system?
Montreal classification (Age, Behaviour, Location).
Crohn’s behaviour codes in Montreal classification?
B1 inflammatory, B2 stricturing, B3 penetrating ± p perianal.
Harvey–Bradshaw Index cut-off for moderate–severe Crohn’s?
> 8 points.
Two poor prognostic factors in Crohn’s?
Deep ulcers and age <40 years.
Short-term target in STRIDE-II?
Symptom control.
Intermediate target in STRIDE-II?
CRP and faecal calprotectin improvement.
Long-term STRIDE-II goal?
Endoscopic ± histologic healing (deep remission).
STRIDENT (Australia) treat-to-target biomarker?
Faecal calprotectin ≤250 µg/g by 24 weeks.
Why treat to biomarker normalisation in IBD?
Deep remission lowers hospitalisation and surgery risk.
First-line therapy for mild–moderate UC?
5-ASA (mesalazine/sulfasalazine).
5-ASA delivery principle?
Use both oral and rectal formulations to reach all colonic segments.
Role of corticosteroids in IBD?
Induction only; not for maintenance.