Most chronic diarrhoea in primary care is functional, but organic causes are common enough that identifying them is the main task. Colorectal cancer presenting with diarrhoea alone (without bleeding) is frequently right-sided and presents late — IDA may be the only clue. Nocturnal diarrhoea makes organic disease more likely and should not be attributed to IBS without assessment. C. difficile is significantly under-recognised in primary care — rates of community-acquired C. diff have increased since 2010. In immunocompromised patients, persistent diarrhoea requires urgent specialist assessment due to the broad range of opportunistic pathogens.

Many patients referred with "chronic diarrhoea" do not meet the definition — they have urgency, frequency of normal stools, or faecal incontinence, which require different management pathways. Drug-induced diarrhoea is underdiagnosed — metformin commonly causes diarrhoea and is often overlooked because it was started years before the symptom developed. Post-cholecystectomy bile acid diarrhoea is frequently misdiagnosed as IBS — test via SeHCAT or the local gastroenterology pathway where available. Stool characteristics (fatty vs watery vs bloody) point to completely different pathophysiological mechanisms and diagnostic pathways.

Mechanistic classification directs investigation efficiently. Osmotic diarrhoea that stops with fasting does not need colonoscopy — dietary exclusion and coeliac screen are the first steps. Secretory diarrhoea that persists with fasting requires endoscopic investigation (microscopic colitis is invisible to the naked eye — biopsies are mandatory). Malabsorptive diarrhoea needs coeliac serology and faecal elastase (for pancreatic exocrine insufficiency) before colonoscopy. IBS-D is a positive clinical diagnosis made on a typical pattern, absent red flags and limited baseline tests — with a lower threshold for investigation in new symptoms over 50.

Dermatitis herpetiformis is pathognomonic for coeliac disease — if you see this on skin, the diagnosis is made. Perianal involvement is common in Crohn's disease (fistulae, abscesses, fissures, skin tags) — finding this on PR exam should dramatically raise suspicion for Crohn's and expedite referral. PSC (primary sclerosing cholangitis) is associated with UC and can present before bowel symptoms — abnormal LFTs with IBD should always trigger PSC investigation (ALP elevated, MRCP). Hypoalbuminaemia (<30 g/L) with diarrhoea indicates severe malabsorption or protein-losing enteropathy and requires urgent secondary care assessment.

Faecal calprotectin is endorsed by NICE (HTG320, formerly DG11) for distinguishing IBD from IBS in adults with diarrhoea. A low result makes active colonic inflammation less likely and can avoid colonoscopy in many, but thresholds are assay- and pathway-dependent. Coeliac disease affects 1% of the UK population — anti-tTG IgA can be falsely negative in IgA deficiency (always check total IgA). The patient must be eating gluten in more than one meal every day for at least 6 weeks before testing (NICE NG20). Microscopic colitis is the most underdiagnosed cause of chronic watery diarrhoea in women over 50 — the mucosa often looks normal, so colonoscopy with biopsies is needed; calprotectin may be only mildly elevated.

Toxic megacolon is a surgical emergency and must be referred within hours. Severe UC (Truelove & Witts: ≥6 bloody stools/day + systemic upset) needs hospital IV steroids, not oral treatment at home. Carcinoid tumours and VIPomas are rare but important: diarrhoea + flushing + tachycardia → check 5-HIAA in urine (carcinoid) or VIP levels (VIPoma) — both require oncology input. Positive coeliac serology should always be referred for biopsy before starting gluten-free diet — biopsy is the gold standard and becomes negative (falsely normal) on a gluten-free diet.

Colesevelam is often better tolerated than colestyramine (tablet vs powder, fewer drug-binding interactions); the choice follows the local formulary and specialist advice. PERT dosing and any acid suppression follow specialist advice. Budesonide is the usual induction treatment for microscopic colitis, started via gastroenterology. Critically, loperamide is contraindicated in severe IBD flares (Truelove & Witts severe) and C. difficile — it can precipitate toxic megacolon by reducing gut motility and allowing toxin accumulation.

Low-FODMAP has good dietary evidence for IBS-D when first-line advice fails. It requires dietitian supervision because unsupervised restriction leads to nutritional deficiencies and an overly restrictive diet long-term. IBS-specific psychological therapy helps persistent symptoms. A metformin modified-release switch often reduces GI side effects and can be done in primary care. Probiotics for IBS: BSG 2021 guidelines recommend a trial of a multi-strain probiotic for at least 4 weeks as they are safe and have moderate evidence of benefit.

Coeliac disease needs annual review — untreated or poorly adherent coeliac disease increases risk of enteropathy-associated T-cell lymphoma (EATL, rare but serious), osteoporosis, and nutritional deficiencies. Anti-tTG IgA should normalise within 12 months of strict GFD — failure to normalise usually reflects ongoing gluten exposure (intentional or inadvertent), interpreted with adherence, baseline antibody level, deficiencies and symptom response. C. difficile recurrence is common and each recurrence raises the risk of more. NICE NG199 (2021) recommends fidaxomicin for a further episode within 12 weeks of symptom resolution. FMT is a specialist option for multiply-recurrent C. diff. In patients over 50 with previously "diagnosed" IBS, any change in symptom pattern should trigger re-investigation — new colorectal cancer developing in patients with IBS is a documented pattern of delayed diagnosis.