Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Recognise colorectal cancer across symptomatic, screening and emergency presentations, investigate without false reassurance, and coordinate stage-specific multidisciplinary treatment and surveillance safely.
Colorectal cancer is usually an adenocarcinoma arising through accumulated molecular change in colonic or rectal epithelium. Sporadic risk rises with age, smoking, excess adiposity and processed meat intake; important high-risk groups include people with longstanding colitis, previous colorectal neoplasia and inherited syndromes such as Lynch syndrome or familial adenomatous polyposis.
The central clinical decision is not simply whether bleeding is present, but whether the pattern needs urgent cancer investigation and whether an emergency complication is developing. Symptoms can be subtle, intermittent or attributed incorrectly to haemorrhoids, anticoagulation or irritable bowel syndrome.
Management depends on anatomical site, TNM stage, tumour biology, physiological fitness and patient priorities. Colon and rectal pathways differ: rectal MRI and decisions about neoadjuvant radiotherapy or systemic therapy are integral to rectal-cancer planning, whereas resectable colon cancer usually proceeds to oncological segmental colectomy.
Most cancers arise through accumulated molecular changes in conventional adenomas or serrated lesions, progressing over time from dysplasia to invasion.
Lynch syndrome, familial adenomatous polyposis and other pathogenic germline variants substantially increase risk and alter surveillance for relatives.
Longstanding colitis, age, smoking, alcohol, obesity, inactivity and dietary patterns modify risk, while many affected people have no obvious single cause.
Driver alterations allow abnormal epithelial cells to escape normal growth control and expand within an adenomatous or serrated precursor.
Further molecular change permits malignant glands to breach the muscularis mucosae, invade bowel wall and access lymphatic or venous channels.
Tumour reaches lymph nodes and commonly the liver through portal venous drainage, with later peritoneal, pulmonary or other metastases.
Occult blood loss causes microcytic iron-deficiency anaemia, lethargy, dyspnoea or syncope; weight loss and a right-sided abdominal mass may appear before obvious bowel change.
Progressive constipation, looser stools around narrowing, colicky pain, visible blood and abdominal distension suggest a distal lesion, especially when symptoms are new and persistent.
Tenesmus, urgency, mucus, bleeding and a sense of incomplete evacuation should prompt inspection and digital rectal examination where appropriate, with urgent referral even if FIT is low when a mass is felt.
Absolute constipation, vomiting, marked distension, peritonism, fever, shock or free air indicate an oncological surgical emergency; closed-loop caecal dilatation can perforate remotely from a distal tumour.
Hepatomegaly, jaundice, ascites, respiratory symptoms, bone pain, cachexia or venous thromboembolism may be the first clue to advanced disease and require prompt staging rather than symptom-only treatment.
Young diagnosis, multiple colorectal tumours, endometrial or related Lynch-spectrum cancers, polyposis, or a strong multigenerational family history warrants genetics-led assessment rather than informal reassurance.
Bright blood with haemorrhoids or fissure may explain symptoms, but persistent bleeding, anaemia or altered bowel habit still requires colorectal assessment.
Pain, diarrhoea, fever and segmental inflammatory imaging suggest IBD or diverticulitis, although cancer can obstruct, perforate or coexist.
A longstanding fluctuating pain-stool pattern without bleeding, weight loss, anaemia or mass supports IBS; new alarm features override prior reassurance.
Circumferential tumour can block the colon, while pressure or local invasion causes perforation, peritonitis and emergency surgery with higher risk.
Chronic occult loss, particularly from proximal tumours, causes iron-deficiency anaemia; brisk bleeding occurs less often but can destabilise.
Hepatic, pulmonary or peritoneal spread causes organ dysfunction, pain, ascites and systemic weight loss that influence treatment tolerance and prognosis.
Quantitative symptomatic FIT estimates bleeding from lower gastrointestinal lesions; it does not prove or exclude cancer and is not a licence to ignore a palpable mass or progressive symptoms.
The symptomatic referral cut-off and the population-screening cut-off answer different questions. England's screening programme changed sensitivity in 2026, while devolved programmes may use other rules.
A low rectal lesion can be directly palpable and may be missed if clinicians request remote tests without examination. Record lesion position and avoid traumatising a painful area.
A stenosing tumour can prevent complete colonoscopy; the unseen proximal colon still requires evaluation before or after urgent treatment because another advanced lesion may coexist.
MMR or MSI status is not an optional academic result: it informs Lynch investigation and can alter systemic treatment, especially in advanced disease.
Bowel frequency, continence, stoma confidence, fertility, intimacy and return to work are meaningful outcomes alongside recurrence and survival and should be discussed early.
Attributing repeated rectal bleeding to haemorrhoids without examining the patient or assessing cancer risk.
Using a screening-programme FIT threshold to interpret a symptomatic patient's result.
Treating iron deficiency while failing to identify its colorectal source.
Ordering CEA as a diagnostic rule-out test for bowel cancer.
Failing to complete proximal-colon assessment after an incomplete examination caused by stenosis.
Planning rectal-cancer surgery before high-quality pelvic MRI and specialist MDT discussion.
Your practice draft is saved in this browser.
A 67-year-old has six weeks of tenesmus and bright rectal bleeding. Quantitative FIT is below the local symptomatic threshold, but digital rectal examination identifies a firm irregular low rectal mass. What is the most appropriate next action?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Take cultures where feasible without delaying therapy, check allergy and organ function, obtain source control urgently, and narrow or stop treatment with microbiology advice.
Dihydropyrimidine dehydrogenase assessment, performance status, renal function, interactions and toxicity plans are essential; mucositis, diarrhoea, cytopenia and cardiotoxicity require prompt oncology contact.
Iron treatment must not postpone source investigation. Oral preparations may worsen gastrointestinal symptoms; intravenous products require monitored administration and selection based on timing and tolerance.