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Colonic Polyps

Colonic polyps are abnormal tissue growths that protrude from the colonic mucosa into the bowel lumen. They represent a ... MRCP exam preparation.

Updated 9 Jan 2025
Reviewed 17 Jan 2026
42 min read
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MedVellum Editorial Team
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MedVellum Medical Education Platform

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  • FAP (Familial Adenomatous Polyposis) — 100% cancer risk by age 40-50
  • Large villous adenoma (less than 2cm) — high malignant potential
  • High-grade dysplasia on histology — indicates imminent malignant transformation
  • Lynch syndrome (HNPCC) — 50-80% lifetime CRC risk

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Clinical reference article

Colonic Polyps

1. Clinical Overview

Summary

Colonic polyps are abnormal tissue growths that protrude from the colonic mucosa into the bowel lumen. They represent a heterogeneous group of lesions with varying malignant potential, ranging from benign hyperplastic polyps to premalignant adenomas that serve as precursors to the majority of colorectal cancers (CRC).[1,2]

The clinical significance of colonic polyps lies in their role as the primary target for colorectal cancer prevention. The adenoma-carcinoma sequence, first described by Vogelstein and colleagues, demonstrates that approximately 70-90% of sporadic colorectal cancers arise from adenomatous polyps through a stepwise accumulation of genetic mutations over 10-15 years.[3] This long dwell time provides a critical window for intervention through colonoscopic surveillance and polypectomy.

Polyps are extremely common, with autopsy studies demonstrating prevalence rates of 30-50% in individuals over 50 years of age in Western populations.[4] However, only a minority (approximately 5-6%) of adenomas will progress to invasive carcinoma, making risk stratification essential to optimise surveillance resources while ensuring high-risk individuals receive appropriate follow-up.[5]

The introduction of population-based bowel cancer screening programmes has dramatically increased polyp detection rates. In the UK, the NHS Bowel Cancer Screening Programme utilises faecal immunochemical testing (FIT) followed by colonoscopy for positive results, with adenoma detection rates of 12-15% in the screening population.[6] Understanding polyp classification, risk stratification, and evidence-based surveillance intervals is therefore essential for all clinicians involved in gastroenterology and colorectal practice.

Key Facts

ParameterKey Information
Prevalence30-50% of individuals > 50 years have polyps on colonoscopy [4]
Adenoma prevalence20-30% of screened population [6]
Malignant transformation~5-6% of adenomas progress to CRC over 10-15 years [5]
Adenoma-carcinoma timeline10-15 years from adenoma to invasive carcinoma [3]
Adenomatous subtypesTubular (70-80%), Tubulovillous (10-25%), Villous (5-10%) [7]
Villous malignant potential17-40% contain carcinoma if > 2cm [7]
Serrated pathwayAccounts for 15-30% of sporadic CRC [8]
FAP cancer risk100% by age 40-50 without intervention [9]
Lynch syndrome CRC risk50-80% lifetime risk [10]
Polypectomy efficacyReduces CRC incidence by 76-90% [11]

Clinical Pearls

"The Adenoma-Carcinoma Sequence is the Cornerstone" The majority of colorectal cancers (70-90%) arise from adenomatous polyps through sequential genetic mutations. This 10-15 year window for intervention makes colonoscopic surveillance one of the most effective cancer prevention strategies available.[3]

"Villous = Vicious" Villous adenomas carry the highest malignant potential among adenoma subtypes. A villous adenoma > 2cm has a 17-40% chance of harbouring invasive carcinoma. Size, villous histology, and high-grade dysplasia are the key determinants of risk.[7]

"Right-Sided Serrated Lesions Are Dangerous and Easily Missed" Sessile serrated lesions (SSLs) in the proximal colon are often flat, pale, and covered with mucus, making them notoriously difficult to detect. They follow an alternative molecular pathway (BRAF mutation, MLH1 hypermethylation) to MSI-high cancers and may have accelerated carcinogenesis.[8,12]

"Not All Polyps Need Surveillance" Low-risk adenomas (1-2 small tubular adenomas with low-grade dysplasia) do not require surveillance colonoscopy — patients should return to population screening. Surveillance is reserved for intermediate and high-risk findings.[13]

"FAP = Prophylactic Colectomy" Familial adenomatous polyposis (FAP) caused by germline APC mutations leads to 100% colorectal cancer risk by age 40-50. Prophylactic proctocolectomy is indicated, typically by age 25 or when polyp burden becomes unmanageable.[9]

"Lynch Syndrome — Think MSI-High" Hereditary non-polyposis colorectal cancer (Lynch syndrome) results from mismatch repair gene mutations. Cancers are MSI-high, often right-sided, and respond well to immunotherapy. Intensive surveillance from age 25 is essential.[10]

Why This Matters Clinically

Colonic polyps are the most important target for colorectal cancer prevention worldwide. The National Polyp Study demonstrated that colonoscopic polypectomy reduces colorectal cancer incidence by 76-90% and mortality by 53%.[11,14] Accurate histological assessment, appropriate risk stratification, and evidence-based surveillance intervals are essential competencies for gastroenterologists, surgeons, and all clinicians involved in bowel cancer screening.


2. Epidemiology

Incidence & Prevalence

Colonic polyps are among the most common gastrointestinal lesions, with prevalence increasing significantly with age. Geographic variation exists, with higher rates in Western countries correlating with dietary and lifestyle factors.[4]

ParameterValueNotes
Overall prevalence (> 50 years)30-50%Autopsy and colonoscopy studies [4]
Adenoma prevalence (screening)20-30%NHS BCSP data [6]
Adenoma detection rate target≥25%Quality indicator for colonoscopy [15]
Male:Female ratio1.5-2:1Higher adenoma prevalence in males [4]
Age of peak incidence60-70 yearsPrevalence increases with age [4]
Annual adenoma incidence6-8%New adenomas on surveillance [16]
Advanced adenoma prevalence3-6%> 10mm, villous, HGD [6]
CRC lifetime risk (general)4-5%UK population [1]
CRC risk from adenoma~5-6%Over 10-15 years [5]

Risk Factors

Risk FactorRelative RiskEvidence Level
Age > 50 yearsMajor risk factorHigh [4]
Male sexRR 1.5-2.0High [4]
Family history of CRC (FDR)RR 2.0-4.0High [17]
Personal history of adenomaRR 1.5-3.0High [16]
FAP (APC mutation)100% CRC riskHigh [9]
Lynch syndrome (MMR mutations)50-80% CRC riskHigh [10]
Obesity (BMI > 30)RR 1.2-1.5Moderate [18]
Red/processed meat consumptionRR 1.1-1.3Moderate [18]
SmokingRR 1.2-1.5Moderate [18]
Alcohol (> 30g/day)RR 1.2-1.5Moderate [18]
Low fibre dietRR 1.1-1.3Moderate [18]
Inflammatory bowel diseaseIncreased dysplasia riskHigh [19]
AcromegalyRR 2.0-3.0Moderate [20]
Previous pelvic radiotherapyIncreased riskLow

Protective Factors

FactorRelative Risk ReductionMechanism
Aspirin use20-30%COX-2 inhibition, apoptosis [21]
NSAIDs20-40%COX inhibition [21]
High fibre diet10-20%Reduced transit time, SCFA production [18]
Physical activity20-25%Reduced insulin resistance [18]
Calcium supplementation15-20%Bile acid binding [22]
Vitamin D10-20%Cell differentiation [22]
Hormone replacement therapy20-30%In postmenopausal women [18]

3. Pathophysiology

The Adenoma-Carcinoma Sequence (Vogelstein Model)

The adenoma-carcinoma sequence, elucidated by Fearon and Vogelstein in 1990, describes the stepwise genetic progression from normal colonic epithelium to invasive carcinoma through accumulation of specific mutations.[3]

Chromosomal Instability (CIN) Pathway — "Classical" Pathway

This pathway accounts for approximately 70-85% of sporadic colorectal cancers and is characterised by chromosomal instability with widespread loss of heterozygosity (LOH).

StageGenetic EventConsequence
Normal epitheliumGermline stateNormal cellular function
Hyperproliferative epitheliumAPC mutation (5q21)Loss of β-catenin regulation, aberrant Wnt signalling
Early adenomaDNA hypomethylationGene expression dysregulation
Intermediate adenomaKRAS mutation (12p12)Constitutive RAS-MAPK signalling, proliferation
Late adenomaSMAD4/DCC loss (18q21)Loss of TGF-β tumour suppression
CarcinomaTP53 mutation (17p13)Loss of "guardian of the genome", genomic instability
Metastatic carcinomaAdditional mutationsInvasion and metastasis genes

Key Molecular Players:

GeneLocationFunctionConsequence of Mutation
APC5q21Tumour suppressor (Wnt pathway)Adenoma initiation, increased β-catenin
KRAS12p12Proto-oncogene (RAS-MAPK)Adenoma growth and progression
SMAD418q21Tumour suppressor (TGF-β)Loss of growth inhibition
TP5317p13Tumour suppressorLoss of apoptosis, genomic instability
DCC18q21Cell adhesionCell migration and invasion

Timeline: The adenoma-carcinoma transition typically requires 10-15 years, providing the rationale for screening and surveillance intervals.[3,5]

The Serrated Pathway (Alternative Pathway)

The serrated neoplasia pathway represents an alternative route to colorectal carcinogenesis, accounting for 15-30% of sporadic CRC. It is characterised by BRAF mutation, CpG island methylator phenotype (CIMP), and microsatellite instability (MSI).[8,12]

StageGenetic/Epigenetic EventLesion
InitiationBRAF V600E mutationMicrovesicular hyperplastic polyp
ProgressionCIMP-high, MLH1 hypermethylationSessile serrated lesion (SSL)
DysplasiaAdditional mutations, MLH1 silencingSSL with dysplasia
CarcinomaMSI-high phenotypeSerrated adenocarcinoma

Characteristics of Serrated Pathway Cancers:

  • Predominantly right-sided (proximal colon)
  • MSI-high phenotype (15-20% of sporadic CRC)
  • Often poor differentiation with mucinous features
  • Better prognosis stage-for-stage than MSS cancers
  • Responsive to immune checkpoint inhibitors [8,12]

Clinical Implications:

  • SSLs are often flat, pale, and covered with mucus
  • Easily missed at colonoscopy (miss rate up to 20-30%)
  • May have accelerated progression ("interval cancers")
  • High-definition colonoscopy and chromoendoscopy improve detection [12]

Mismatch Repair Deficiency Pathway (Lynch Syndrome)

Lynch syndrome results from germline mutations in DNA mismatch repair (MMR) genes, leading to microsatellite instability and accelerated carcinogenesis.[10]

GeneFrequency in LynchProteinCancer Risk
MLH140-50%MutL homologue 150-80% CRC
MSH235-40%MutS homologue 250-80% CRC
MSH610-15%MutS homologue 610-40% CRC
PMS25-10%Postmeiotic segregation 215-20% CRC
EPCAM1-3%Epithelial cell adhesionVia MSH2 silencing

Characteristics:

  • MSI-high phenotype
  • Right-sided predominance
  • Younger age of onset (mean 44 years)
  • Multiple synchronous/metachronous cancers
  • Better prognosis than sporadic MSS cancers
  • Lynch-associated CRCs respond to immunotherapy [10]

4. Classification of Colonic Polyps

Histological Classification (WHO 2019)

Colonic polyps are classified based on histological features into neoplastic and non-neoplastic categories.[7]

CategoryPolyp TypeMalignant Potential
Conventional NeoplasticTubular adenomaLow-Moderate
Tubulovillous adenomaModerate-High
Villous adenomaHigh
Serrated NeoplasticSessile serrated lesion (SSL)Moderate-High
SSL with dysplasiaHigh
Traditional serrated adenoma (TSA)Moderate-High
Non-NeoplasticHyperplastic polypVery Low (unless proximal/large)
Inflammatory polypNone
Hamartomatous polypVariable (syndrome-dependent)
Juvenile polypLow (unless syndrome)
Peutz-Jeghers polypModerate (syndrome-associated)

Adenomatous Polyps (Conventional Pathway)

TypeDefinitionPrevalenceCancer Risk
Tubular adenomaless than 25% villous component70-80%Low (1-2% if less than 1cm)
Tubulovillous adenoma25-75% villous component10-25%Moderate (8-15%)
Villous adenoma> 75% villous component5-10%High (17-40% if > 2cm)

Risk Factors for Malignant Transformation:

FactorImpact on Risk
Size > 10mm10x increased risk vs less than 10mm
Size > 20mm40-50% contain advanced histology
Villous histology3-4x increased risk vs tubular
High-grade dysplasia25-40% already contain carcinoma
Number ≥3 adenomasIncreased metachronous risk
Proximal locationMay be harder to detect completely

Serrated Lesions (Updated WHO 2019 Terminology)

The WHO 2019 classification updated terminology for serrated lesions:[7,12]

Current Term (WHO 2019)Previous TermLocationKey Features
Hyperplastic polyp (HP)SamePredominantly left colon/rectumSmall (less than 5mm), no dysplasia, minimal risk
Sessile serrated lesion (SSL)Sessile serrated adenoma/polyp (SSA/P)Predominantly right colonArchitectural distortion, inverted crypts
SSL with dysplasiaSSA/P with cytological dysplasiaRight colonPrecursor to serrated adenocarcinoma
Traditional serrated adenoma (TSA)SameLeft colonEosinophilic cytoplasm, ectopic crypts

Histological Features of SSL:

  • Horizontally branching (L-shaped or inverted T-shaped) crypts at base
  • Crypt dilation and irregular serration
  • Crypt base extension along muscularis mucosae
  • Absent or minimal cytological dysplasia (until advanced)
  • BRAF mutation positive (~80%)
  • MLH1 promoter hypermethylation when progressing

Hamartomatous Polyps

TypeSyndromeGeneHistologyCancer Risk
Peutz-Jeghers polypPeutz-Jeghers syndromeSTK11 (LKB1)Smooth muscle arborising into lamina propriaCRC 39%, all cancers 85%
Juvenile polypJuvenile polyposis syndromeSMAD4, BMPR1ACystic dilated glands, oedematous stromaCRC 10-40%
PTEN hamartomaCowden syndromePTENSimilar to juvenileCRC 9-16%

Paris Classification (Endoscopic Morphology)

TypeSubtypeDescriptionClinical Significance
0-I (Polypoid)0-IpPedunculated (on stalk)Easier complete excision
0-IsSessile (broad-based)Higher incomplete excision risk
0-II (Non-polypoid)0-IIaSlightly elevated (less than 2.5mm)Serrated lesions common
0-IIbFlatDifficult to detect
0-IIcSlightly depressedHigher submucosal invasion risk
0-IIa+IIcMixedVariable
0-IIIExcavated/ulceratedUsually malignant

Dysplasia Grading

GradeFeaturesClinical Implications
Low-grade dysplasia (LGD)Mild nuclear changes, pseudostratification limited to lower halfStandard surveillance intervals
High-grade dysplasia (HGD)Marked nuclear changes, loss of polarity, stratification into upper cryptHigh-risk; 1-year surveillance; consider carcinoma-in-situ

5. Clinical Presentation

Symptoms

The majority of colonic polyps are asymptomatic and detected incidentally during screening or investigation for other conditions. Symptomatic presentation is more common with large polyps (> 2cm) or those in the rectum.[1,2]

SymptomFrequencyAssociated Features
Asymptomatic80-90%Detected on screening or incidentally
Rectal bleeding10-20%Usually bright red, intermittent, small volume
Occult blood lossVariableDetected on FIT; may cause IDA
Change in bowel habitRareUsually with large or multiple polyps
Mucous dischargeRareCharacteristic of large villous adenomas
TenesmusRareLow rectal polyps
Abdominal painRareNon-specific; consider other causes
HypokalaemiaVery rareSecretory villous adenoma (McKittrick-Wheelock syndrome)
Prolapse per rectumVery rarePedunculated rectal polyp

McKittrick-Wheelock Syndrome: A rare but important clinical entity caused by large secretory villous adenomas (usually rectal), resulting in:

  • Profuse mucous diarrhoea (> 1-3L/day)
  • Severe hypokalaemia
  • Hyponatraemia
  • Dehydration
  • Pre-renal acute kidney injury Management requires urgent resection with aggressive electrolyte replacement.[23]

Signs

SignSignificance
Usually normal examinationMost polyps cause no detectable signs
Palpable rectal polyp (DRE)Low rectal polyps may be palpable
PallorSuggests iron deficiency anaemia from chronic occult blood loss
Abdominal massVery rare; massive polyps or associated malignancy
Mucocutaneous pigmentationPerioral/buccal pigmentation in Peutz-Jeghers syndrome
Extraintestinal featuresOsteomas, epidermoid cysts (Gardner syndrome/FAP)

Red Flags — Urgent Investigation Required

[!CAUTION] Red Flags Requiring Urgent Referral (2WW Pathway):

  • Rectal bleeding with change in bowel habit (> 40 years)
  • Unexplained iron deficiency anaemia
  • Palpable abdominal or rectal mass
  • Family history suggestive of polyposis syndrome
  • FIT positive result

[!CAUTION] High-Risk Polyp Features Requiring Close Follow-up:

  • 100 polyps on colonoscopy (consider FAP)

  • ≥5 adenomas or any adenoma ≥20mm
  • High-grade dysplasia
  • Sessile serrated lesion ≥10mm or with dysplasia
  • Invasive carcinoma in polyp (pT1)

6. Clinical Examination

Physical Examination Approach

Most patients with colonic polyps will have an entirely normal physical examination. However, systematic examination is essential to exclude associated malignancy and identify features of polyposis syndromes.

Structured Approach:

  1. General inspection:

    • Nutritional status, pallor (anaemia), cachexia (malignancy)
    • Mucocutaneous pigmentation (Peutz-Jeghers)
    • Skin lesions (epidermoid cysts — FAP/Gardner)
  2. Abdominal examination:

    • Usually unremarkable
    • Palpable mass (rare — very large polyps or carcinoma)
    • Hepatomegaly (metastatic disease if concurrent malignancy)
  3. Digital rectal examination (DRE):

    • Palpable low rectal polyps
    • Rectal mass
    • Blood or mucus on glove
  4. Extraintestinal manifestations (polyposis syndromes):

    • Head: Osteomas (mandible, skull — FAP/Gardner)
    • Eyes: Congenital hypertrophy of retinal pigment epithelium (CHRPE — FAP)
    • Mouth: Perioral pigmentation (Peutz-Jeghers), dental abnormalities (FAP)
    • Skin: Epidermoid cysts, desmoid tumours (FAP/Gardner)

Polyposis Syndrome Physical Features

SyndromeKey Clinical Features
FAP> 100 colorectal polyps, osteomas, epidermoid cysts, desmoid tumours, CHRPE, dental abnormalities
Attenuated FAP10-100 polyps, right-sided predominance, later onset
Gardner syndromeFAP + prominent extraintestinal manifestations (osteomas, fibromas, desmoids)
Turcot syndromeFAP + CNS tumours (medulloblastoma in APC; glioblastoma in Lynch)
Peutz-JeghersMucocutaneous pigmentation (lips, buccal, fingers), hamartomatous polyps throughout GI tract
Juvenile polyposisJuvenile polyps, digital clubbing, congenital abnormalities
Cowden syndromeMultiple hamartomas, trichilemmomas, papillomatous papules, macrocephaly
Lynch syndromeNo specific physical signs; associated cancers (endometrial, ovarian, urological)

7. Investigations

Colonoscopy — Gold Standard

Colonoscopy is the gold-standard investigation for polyp detection, characterisation, and removal. It allows direct visualisation, tissue sampling, and therapeutic polypectomy.[1,2]

AspectDetails
Sensitivity95-99% for polyps > 10mm [24]
Specificity85-90% [24]
Complete to caecumEssential quality indicator; target > 90% completion
Bowel preparationSplit-dose PEG solutions; Boston Bowel Preparation Scale ≥6
Adenoma detection rate (ADR)Quality indicator; target ≥25% (minimum) [15]
Withdrawal timeMinimum 6 minutes in negative colonoscopy [15]

Enhanced Colonoscopy Techniques

TechniquePurposeEvidence
High-definition colonoscopyImproved mucosal visualisationStandard of care
ChromoendoscopyDye spray (indigo carmine) highlights flat lesionsImproves ADR, especially for serrated lesions [12]
Narrow-band imaging (NBI)Electronic chromoendoscopyUseful for polyp characterisation
Autofluorescence imagingHighlights neoplastic tissueLimited clinical use
AI-assisted detectionComputer-aided detectionEmerging; improves ADR [24]

Polyp Characterisation During Colonoscopy

AssessmentWhat to Document
LocationSegment (caecum, ascending, transverse, descending, sigmoid, rectum)
SizeMeasured against open biopsy forceps (6mm) or snare
MorphologyParis classification (0-Ip, 0-Is, 0-IIa, etc.)
Surface patternPit pattern (Kudo classification), vascular pattern (NICE classification)
NumberTotal polyp count
Completeness of excisionDocumented for each polyp

Histopathology — Essential for Risk Stratification

All removed polyps should be sent for histological assessment. The pathology report should include:[7]

FeatureClinical Significance
Polyp typeAdenoma (tubular/tubulovillous/villous), serrated, hyperplastic, hamartomatous
Size> 10mm indicates higher risk
Dysplasia gradeLow-grade vs high-grade
Completeness of excisionComplete, incomplete, or indeterminate margins
Presence of invasive carcinomaIf present, requires Haggitt/Kikuchi staging and additional reporting

Malignant Polyp Assessment (Carcinoma in Polyp)

If invasive carcinoma is identified within a polyp, additional histological features determine management:[25]

FeatureLow-RiskHigh-Risk
DifferentiationWell or moderately differentiatedPoorly differentiated
Lymphovascular invasion (LVI)AbsentPresent
Margin≥1mm clear marginless than 1mm or involved margin
Depth (sessile)Sm1 (upper 1/3 submucosa)Sm2/Sm3 (middle/deep submucosa)
Depth (pedunculated)Haggitt level 1-3Haggitt level 4
Tumour buddingLow/absentHigh-grade budding

Haggitt Classification (Pedunculated Polyps):

LevelLocation of Invasion
0Carcinoma in situ (intramucosal)
1Invasion into polyp head
2Invasion into polyp neck
3Invasion into polyp stalk
4Invasion into submucosa below stalk (at bowel wall level)

Kikuchi Classification (Sessile Polyps — Submucosal Invasion):

LevelDepth
Sm1Upper third of submucosa
Sm2Middle third of submucosa
Sm3Lower third of submucosa

CT Colonography (Virtual Colonoscopy)

AspectDetails
IndicationIncomplete colonoscopy, patient preference, frailty
Sensitivity (polyps > 10mm)85-95% [24]
Sensitivity (polyps 6-9mm)70-85%
Sensitivity (polyps less than 6mm)45-65%
LimitationCannot perform polypectomy; less accurate for flat/serrated lesions
AdvantageNon-invasive, extracolonic pathology detection

Investigations for Polyposis Syndromes

SyndromeInvestigations
FAP suspectedGenetic testing (APC mutation), upper GI endoscopy (duodenal adenomas), fundoscopy (CHRPE)
Lynch suspectedIHC for MMR proteins, MSI testing, genetic testing (MLH1, MSH2, MSH6, PMS2, EPCAM)
Peutz-JeghersGenetic testing (STK11), upper GI endoscopy, small bowel imaging (MRE/capsule)
Juvenile polyposisGenetic testing (SMAD4, BMPR1A), upper GI endoscopy
Family screeningColonoscopy in at-risk relatives, genetic counselling

8. Management

Management Algorithm

                    COLONIC POLYP DETECTED
                              ↓
┌──────────────────────────────────────────────────────────────────┐
│                       POLYPECTOMY                                │
├──────────────────────────────────────────────────────────────────┤
│  PEDUNCULATED (0-Ip):                                            │
│  ➤ Hot snare polypectomy (diathermy)                             │
│  ➤ Clip base of stalk if bleeding risk (> 2cm or thick stalk)    │
│                                                                  │
│  SESSILE less than 10
mm:                                                  │
│  ➤ Cold snare polypectomy (preferred for diminutive polyps)     │
│  ➤ Avoids delayed bleeding and post-polypectomy syndrome        │
│                                                                  │
│  SESSILE 10-20
mm:                                                │
│  ➤ En bloc or piecemeal EMR (endoscopic mucosal resection)      │
│  ➤ Consider cold snare piecemeal for appropriate lesions        │
│                                                                  │
│  SESSILE > 20mm (Laterally Spreading Tumours):                    │
│  ➤ EMR (en bloc if possible, piecemeal if necessary)            │
│  ➤ ESD (endoscopic submucosal dissection) for en bloc excision  │
│  ➤ Refer to specialist centre if not amenable                   │
│  ➤ Surgical resection if endoscopic excision not feasible       │
│                                                                  │
│  SEND ALL POLYPS FOR HISTOLOGY                                   │
└──────────────────────────────────────────────────────────────────┘
                              ↓
┌──────────────────────────────────────────────────────────────────┐
│                    HISTOLOGY RESULT                              │
├──────────────────────────────────────────────────────────────────┤
│  NON-NEOPLASTIC (Hyperplastic):                                  │
│  ➤ No surveillance required (distal/small)                      │
│  ➤ Proximal hyperplastic polyps ≥10
mm: consider as serrated     │
│                                                                  │
│  ▼ ADENOMAS — STRATIFY BY BSG 2020 CRITERIA ▼                   │
│                                                                  │
│  LOW-RISK ADENOMA:                                               │
│  ➤ 1-2 adenomas, all less than 10mm, tubular, low-grade dysplasia        │
│  ➤ NO SURVEILLANCE — return to population screening             │
│                                                                  │
│  INTERMEDIATE-RISK ADENOMA:                                      │
│  ➤ 3-4 small adenomas, OR                                        │
│  ➤ Any adenoma 10-19mm                                           │
│  ➤ Surveillance colonoscopy at 3 YEARS                          │
│                                                                  │
│  HIGH-RISK ADENOMA:                                              │
│  ➤ ≥5 adenomas, OR                                               │
│  ➤ Any adenoma ≥20mm, OR                                         │
│  ➤ High-grade dysplasia                                          │
│  ➤ Surveillance colonoscopy at 1 YEAR                           │
│                                                                  │
│  SERRATED LESIONS (BSG 2020):                                    │
│  ➤ Hyperplastic polyps (distal, less than 10mm): No surveillance         │
│  ➤ SSL less than 10mm without dysplasia: 3-year surveillance             │
│  ➤ SSL ≥10mm OR with dysplasia: 1-year surveillance             │
│  ➤ ≥5 serrated lesions proximal to sigmoid: 1-year surveillance │
│                                                                  │
│  PIECEMEAL EXCISION OF LARGE POLYPS:                             │
│  ➤ Site check at 2-6 months to ensure complete excision         │
│  ➤ Then risk-stratified surveillance                            │
└──────────────────────────────────────────────────────────────────┘
                              ↓
┌──────────────────────────────────────────────────────────────────┐
│              MALIGNANT POLYP (Carcinoma in Polyp)                │
├──────────────────────────────────────────────────────────────────┤
│  ASSESS RISK FEATURES (Haggitt/Kikuchi):                         │
│                                                                  │
│  LOW-RISK — Polypectomy may be curative:                         │
│  ➤ Well or moderately differentiated                            │
│  ➤ No lymphovascular invasion                                   │
│  ➤ Clear margin (≥1mm)                                          │
│  ➤ Sm1 invasion (sessile) or Haggitt 1-3 (pedunculated)        │
│  ➤ Low tumour budding                                           │
│  ➤ Management: Surveillance colonoscopy at 3 months, then 1 year │
│                                                                  │
│  HIGH-RISK — Surgical resection recommended:                     │
│  ➤ Poorly differentiated                                        │
│  ➤ Lymphovascular invasion present                              │
│  ➤ Margin less than 1mm or involved                                      │
│  ➤ Sm2/Sm3 invasion (sessile) or Haggitt level 4 (pedunculated) │
│  ➤ High-grade tumour budding                                    │
│  ➤ Management: MDT discussion → Segmental colectomy             │
│                                                                  │
│  ➤ ALL MALIGNANT POLYPS REQUIRE MDT DISCUSSION                  │
│  ➤ CT staging prior to surgical decision                        │
│  ➤ Consider patient fitness and preference                      │
└──────────────────────────────────────────────────────────────────┘

BSG Post-Polypectomy Surveillance Guidelines (2020)

The British Society of Gastroenterology (BSG) 2020 guidelines provide evidence-based surveillance intervals based on baseline colonoscopy findings.[13]

Risk CategoryBaseline FindingsSurveillance Interval
Low-risk1-2 adenomas, all less than 10mm, tubular, LGDNO surveillance — return to population screening
Intermediate-risk3-4 small adenomas, OR any adenoma 10-19mmColonoscopy at 3 years
High-risk≥5 adenomas, OR any adenoma ≥20mm, OR HGDColonoscopy at 1 year

Serrated Lesion Surveillance (BSG 2020):

FindingSurveillance
Hyperplastic polyps (distal, less than 10mm)None
SSL less than 10mm without dysplasia3 years
SSL ≥10mm1 year
SSL with dysplasia1 year
≥5 serrated lesions proximal to sigmoid1 year
Large (≥10mm) serrated polyp with incomplete excisionSite check at 2-6 months

Key Changes from Previous Guidelines:

  1. Low-risk adenomas no longer require surveillance
  2. Reduced surveillance burden (fewer colonoscopies)
  3. Serrated lesions explicitly addressed
  4. Two surveillance episodes then stop (if clear), unless ongoing high-risk findings

ESGE Polypectomy and Surveillance Guidelines

The European Society of Gastrointestinal Endoscopy (ESGE) provides complementary guidance:[26]

TopicESGE Recommendation
Cold snare polypectomyPreferred for sessile polyps ≤9mm
Hot snare polypectomyFor polyps 10-19mm or pedunculated polyps
EMR/ESDFor polyps ≥20mm; en bloc preferred
Prophylactic clippingConsider for large polyps, anticoagulation, proximal colon
SurveillanceSimilar risk stratification to BSG; 3-year for low-risk, 3-year for intermediate-risk, 1-year for high-risk

Polypectomy Techniques

TechniqueIndicationAdvantagesDisadvantages
Cold biopsy forcepsDiminutive polyps (less than 3mm)SimpleIncomplete excision risk
Cold snare polypectomy (CSP)Sessile polyps ≤9mmLow complication rate, no delayed bleedingNot for thick stalks
Hot snare polypectomy (HSP)Polyps 10-19mm, pedunculatedHaemostasisPost-polypectomy syndrome, perforation
Endoscopic mucosal resection (EMR)Large sessile polyps ≥20mmRemoves larger lesionsPiecemeal = recurrence risk
Endoscopic submucosal dissection (ESD)Large lesions requiring en blocEn bloc excision, accurate stagingLonger procedure, higher skill required
Underwater EMRAlternative techniqueFloating submucosa, easier liftRequires experience

Management of Polyposis Syndromes

Familial Adenomatous Polyposis (FAP)

AspectManagement
Diagnosis> 100 adenomas OR APC mutation confirmed
ColorectalProphylactic surgery by age 25 or when polyp burden unmanageable
Surgery optionsTotal proctocolectomy + IPAA (gold standard) OR colectomy + IRA (if rectum relatively spared, less than 20 rectal adenomas, patient preference)
Upper GIUpper GI endoscopy every 1-3 years (duodenal adenomas — Spigelman staging)
Desmoid tumoursNSAIDs, tamoxifen, sulindac; surgery for symptomatic or life-threatening
Family screeningGenetic testing and colonoscopy for at-risk relatives from age 10-12

Attenuated FAP

AspectManagement
Definition10-100 adenomas; later onset; right-sided predominance
SurveillanceAnnual colonoscopy from age 18-20
SurgeryWhen adenoma burden unmanageable; colectomy + IRA often feasible

Lynch Syndrome (HNPCC)

AspectManagement
Colorectal surveillanceColonoscopy every 2 years from age 25 (or 5 years before youngest family case)
GynaecologicalAnnual endometrial sampling and transvaginal USS from age 30-35; consider prophylactic hysterectomy + BSO after family complete
Other cancersUrological, gastric, small bowel surveillance per local protocol
Aspirin chemopreventionEvidence from CAPP2 trial; 600mg daily for 2 years reduces CRC risk [27]
Surgery for CRCConsider subtotal colectomy due to metachronous cancer risk

Peutz-Jeghers Syndrome

AspectManagement
GI surveillanceUpper GI endoscopy, colonoscopy, and small bowel imaging (MRE/capsule) every 2-3 years from age 8
PolypectomyEndoscopic removal of symptomatic polyps; surgery for obstruction/intussusception
Cancer screeningBreast (MRI), pancreas, gynaecological surveillance
Family screeningGenetic testing (STK11 mutation)

Juvenile Polyposis Syndrome

AspectManagement
Diagnosis≥5 juvenile polyps in colon, OR juvenile polyps throughout GI tract, OR any juvenile polyps + family history
SurveillanceColonoscopy and upper GI endoscopy every 1-3 years from diagnosis
SurgeryColectomy for polyp burden, significant symptoms, or dysplasia

9. Complications

Complications of Colonic Polyps

ComplicationFrequencyNotes
Malignant transformation5-6% (of adenomas)Main concern; adenoma-carcinoma sequence
Occult bleedingCommonMay cause iron deficiency anaemia
Overt bleedingUncommonMore common with large polyps
ObstructionRareVery large polyps only
IntussusceptionRarePedunculated polyps, Peutz-Jeghers
McKittrick-Wheelock syndromeVery rareSecretory villous adenoma

Complications of Polypectomy

ComplicationIncidenceRisk FactorsManagement
Immediate bleeding1-2%Large polyps, pedunculated, anticoagulationEndoscopic haemostasis (clips, adrenaline injection, coagulation)
Delayed bleeding0.5-2%Hot snare, large polyps, right colon, anticoagulationUsually self-limiting; repeat colonoscopy if persistent
Perforation0.1-0.5%EMR/ESD, large polyps, right colon, diverticular diseaseSmall: Endoscopic clips + conservative management. Large: Surgery
Post-polypectomy syndrome0.5-1%Hot snare, large polyps, thin-walled colonTransmural burn without perforation; IV antibiotics + bowel rest
Incomplete excision5-20% (piecemeal EMR)Piecemeal resection, large sizeSite check at 2-6 months; repeat endoscopy or surgery

10. Prognosis & Outcomes

Polyp Progression Risk

FactorImpact on Malignant Transformation
Size > 10mm10x increased risk vs less than 10mm
Size > 20mm40-50% contain advanced histology
Villous histology3-4x increased risk vs tubular
High-grade dysplasia25-40% harbour invasive carcinoma
Multiple adenomas (≥3)Increased metachronous adenoma and CRC risk
Serrated (SSL with dysplasia)Accelerated progression via serrated pathway

Outcomes After Polypectomy

Outcome MeasureValueEvidence
CRC incidence reduction76-90%National Polyp Study [11]
CRC mortality reduction53%National Polyp Study [14]
Adenoma recurrence rate30-40% at 3 yearsSurveillance studies [16]
Advanced adenoma recurrence5-10% at 3 yearsHigh-risk baseline findings [16]
Interval cancer rate2-8% of all CRCMissed or rapidly growing lesions [24]

Colonoscopy Quality and Outcomes

Quality IndicatorTargetImpact
Adenoma detection rate (ADR)≥25%Each 1% increase in ADR = 3% decrease in interval CRC [15]
Caecal intubation rate≥90%Ensures complete examination
Withdrawal time≥6 minutesImproved polyp detection
Bowel preparation qualityBoston score ≥6Enables adequate visualisation

11. Polyposis Syndromes — Detailed Overview

Familial Adenomatous Polyposis (FAP)

FeatureDetails
InheritanceAutosomal dominant
GeneAPC (5q21) — tumour suppressor
Mutation> 1,000 different mutations described
Colorectal polyps100-1000s of adenomatous polyps
Age of polyp onset10-15 years
Age of CRC (untreated)100% by age 40-50
Extracolonic manifestationsDuodenal adenomas (90%), gastric fundic gland polyps, osteomas, epidermoid cysts, desmoid tumours, CHRPE, dental abnormalities
Duodenal/ampullary cancer risk5-10% lifetime
Desmoid tumour risk10-15%; major cause of morbidity

Genotype-Phenotype Correlations:

Mutation LocationPhenotype
Codons 1250-1464Profuse polyposis (> 5000 polyps)
Codons 1403-1578Higher desmoid tumour risk
5' end (codons 78-167)Attenuated FAP
3' endAttenuated FAP

Lynch Syndrome (HNPCC)

FeatureDetails
InheritanceAutosomal dominant
GenesMLH1, MSH2, MSH6, PMS2, EPCAM
MechanismMismatch repair deficiency → MSI-high
CRC risk50-80% lifetime
Endometrial cancer risk40-60% (females)
Other cancersOvarian, gastric, urinary tract, small bowel, pancreas, brain
CRC characteristicsRight-sided, younger onset (mean 44 years), mucinous/poorly differentiated, MSI-high
Polyp burdenLow (few adenomas, not hundreds)
Immunotherapy responseMSI-high tumours responsive to checkpoint inhibitors

Amsterdam II Criteria (Clinical Diagnosis):

  • ≥3 relatives with Lynch-associated cancer (CRC, endometrial, small bowel, ureter, renal pelvis)
  • One is first-degree relative of the other two
  • ≥2 successive generations affected
  • ≥1 diagnosed before age 50
  • FAP excluded

Revised Bethesda Guidelines (For MSI Testing):

  • CRC diagnosed less than 50 years
  • Synchronous or metachronous Lynch-associated cancers
  • CRC with MSI-high histology less than 60 years
  • CRC with ≥1 first-degree relative with Lynch-associated cancer less than 50 years
  • CRC with ≥2 first/second-degree relatives with Lynch-associated cancer at any age

Peutz-Jeghers Syndrome (PJS)

FeatureDetails
InheritanceAutosomal dominant
GeneSTK11 (LKB1) — serine/threonine kinase
GI manifestationsHamartomatous polyps throughout GI tract (small bowel > colon > stomach)
Mucocutaneous pigmentationPerioral, buccal, digits (fades after puberty)
GI complicationsIntussusception, obstruction, bleeding
Lifetime cancer risk85% (all sites)
CRC risk39%
Breast cancer risk45-50%
Pancreatic cancer risk11-36%
Gynaecological cancersOvarian, cervical (adenoma malignum), uterine
Testicular tumoursSex cord tumours with annular tubules

Juvenile Polyposis Syndrome (JPS)

FeatureDetails
InheritanceAutosomal dominant
GenesSMAD4 (20%), BMPR1A (20%), unknown (60%)
Polyp typeJuvenile (hamartomatous) polyps
Diagnostic criteria≥5 juvenile polyps in colon, OR polyps throughout GI tract, OR any juvenile polyp + family history
CRC risk10-40% lifetime
Gastric cancer risk15-21% (with SMAD4 mutations)
Associated featuresDigital clubbing, cardiac/CNS abnormalities (some cases)
Hereditary haemorrhagic telangiectasiaAssociated with SMAD4 mutations

MUTYH-Associated Polyposis (MAP)

FeatureDetails
InheritanceAutosomal recessive (biallelic mutations required)
GeneMUTYH — base excision repair
Polyp burden10-100 adenomas (similar to attenuated FAP)
CRC risk50-100% lifetime (biallelic carriers)
HeterozygotesModestly increased CRC risk
ExtracolonicDuodenal adenomas, osteomas (less than FAP)
ManagementSimilar to attenuated FAP; screening and colectomy when indicated

12. Evidence & Guidelines

Key Guidelines

GuidelineOrganisationYearKey Recommendations
Post-Polypectomy SurveillanceBSG/ACPGBI/PHE2020Risk stratification; low-risk = no surveillance; 3-year and 1-year intervals [13]
Colorectal PolypectomyESGE2017Cold snare for ≤9mm; EMR/ESD for ≥20mm; clipping strategies [26]
Quality in ColonoscopyBSG2016ADR ≥25%, CIR ≥90%, withdrawal ≥6 min [15]
FAP ManagementACMG/NSGC2015Genetic testing, surgery, surveillance protocols [9]
Lynch SyndromeNICE, ACMG2017, 2014Testing criteria, surveillance intervals, aspirin chemoprevention [10,27]

Landmark Studies

StudyDesignKey FindingCitation
National Polyp StudyProspective cohortColonoscopic polypectomy reduces CRC incidence by 76-90%Winawer 1993 [11]
NPS MortalityLong-term follow-up53% reduction in CRC mortality with polypectomyZauber 2012 [14]
CAPP2 TrialRCTAspirin 600mg daily for 2 years reduces Lynch CRC riskBurn 2011 [27]
Vogelstein ModelMolecular analysisAdenoma-carcinoma sequence; APC-KRAS-p53Fearon & Vogelstein 1990 [3]
Serrated PathwayMolecular studiesBRAF-CIMP-MSI pathway for 15-30% CRCJass 2007 [8]
UK FS TrialRCTSingle flexible sigmoidoscopy reduces CRC incidence 23% and mortality 31%Atkin 2010 [28]

13. Patient/Layperson Explanation

What Are Colonic Polyps?

Polyps are small growths on the inner lining of your large bowel (colon and rectum). They are very common — about 1 in 4 people over 50 have them. Most polyps are harmless and cause no symptoms at all.

However, some types of polyps (called adenomas) can slowly change and become bowel cancer over many years if left untreated. Removing these polyps during a colonoscopy prevents this from happening.

How Are Polyps Found?

Most polyps are found in one of three ways:

  1. Bowel cancer screening — The NHS offers a stool test (FIT) to everyone aged 60-74 (soon 50-74). If positive, you'll have a colonoscopy.
  2. Colonoscopy — A camera test to look inside your bowel. Polyps can be seen and removed during this test.
  3. Investigation for symptoms — If you have bleeding, change in bowel habit, or anaemia.

What Happens When a Polyp Is Found?

During colonoscopy, the doctor will remove most polyps immediately using a wire loop (called a snare). This is painless. The polyp is sent to the laboratory to determine what type it is.

Do I Need Follow-up After Polyps Are Removed?

It depends on what type, how many, and how large your polyps were:

What Was FoundWhat Happens Next
1-2 small polyps (less than 1cm), simple typeNo extra follow-up needed. Return to normal screening.
3-4 small polyps, or a medium-sized polypFollow-up colonoscopy in 3 years
5 or more polyps, a large polyp (≥2cm), or high-risk typeFollow-up colonoscopy in 1 year

What If I Have Many Polyps or a Strong Family History?

If you have many polyps (especially > 10) or a strong family history of bowel cancer, you may need:

  • Genetic testing to check for inherited conditions
  • More frequent colonoscopies
  • Family members may also need screening

Your doctor will refer you to a specialist genetics clinic if needed.

Can Polyps Be Prevented?

You can reduce your risk by:

  • Not smoking
  • Limiting alcohol
  • Eating plenty of fibre, fruit, and vegetables
  • Limiting red and processed meat
  • Maintaining a healthy weight
  • Staying physically active
  • Taking part in bowel cancer screening

14. Examination Focus

High-Yield Exam Topics

TopicKey Points
Adenoma-carcinoma sequenceAPC (initiation) → KRAS (progression) → SMAD4/DCC → TP53 (carcinoma); 10-15 years [3]
Serrated pathwayBRAF → CIMP → MLH1 methylation → MSI-high CRC; 15-30% of sporadic CRC [8]
Adenoma typesTubular (70-80%, low risk), Tubulovillous (10-25%), Villous (5-10%, high risk) [7]
High-risk featuresSize ≥20mm, villous, HGD, ≥5 adenomas
BSG 2020 surveillanceLow = no surveillance; Intermediate = 3 years; High = 1 year [13]
Serrated lesion surveillanceSSL ≥10mm or with dysplasia = 1 year; SSL less than 10mm = 3 years [13]
Malignant polyp featuresSm depth, differentiation, LVI, margins, budding [25]
FAPAPC mutation; > 100 polyps; 100% CRC risk; prophylactic colectomy [9]
Lynch syndromeMMR mutations; MSI-high; 50-80% CRC risk; Amsterdam/Bethesda criteria [10]
Peutz-JeghersSTK11; mucocutaneous pigmentation; 85% lifetime cancer risk [9]
Colonoscopy qualityADR ≥25%; each 1% increase = 3% reduction in interval CRC [15]
Polypectomy efficacy76-90% CRC incidence reduction; 53% mortality reduction [11,14]

Sample Viva Questions with Model Answers

Q1: A 55-year-old man has a colonoscopy showing 3 adenomatous polyps, all less than 10mm, tubular, low-grade dysplasia. What is your surveillance plan?

Model Answer: "According to BSG 2020 guidelines, this patient has intermediate-risk findings with 3-4 small adenomas. He should have a surveillance colonoscopy at 3 years. If this is clear, he can have one further colonoscopy at 3 years, then return to population screening.

Key points I would emphasise:

  • Low-risk is 1-2 small tubular adenomas with LGD — these patients do NOT need surveillance
  • Intermediate-risk includes 3-4 small adenomas OR any adenoma 10-19mm
  • High-risk requires ≥5 adenomas, any ≥20mm, or high-grade dysplasia — surveillance at 1 year"

Q2: Describe the adenoma-carcinoma sequence.

Model Answer: "The adenoma-carcinoma sequence describes the stepwise genetic progression from normal colonic epithelium to invasive carcinoma, first characterised by Fearon and Vogelstein in 1990.

The classical pathway involves sequential mutations:

  1. APC mutation (5q21) — initiates adenoma formation by dysregulating the Wnt/β-catenin pathway
  2. KRAS mutation (12p12) — promotes adenoma growth through constitutive RAS-MAPK signalling
  3. SMAD4/DCC loss (18q21) — loss of TGF-β signalling and cell adhesion
  4. TP53 mutation (17p13) — loss of the 'guardian of the genome' allows progression to carcinoma

This process typically takes 10-15 years, providing the rationale for screening intervals.

Importantly, an alternative pathway exists — the serrated pathway, accounting for 15-30% of sporadic CRC, characterised by BRAF mutation, CpG island methylator phenotype, MLH1 hypermethylation, and MSI-high phenotype."


Q3: A colonoscopy shows > 100 adenomatous polyps in a 22-year-old. What is the diagnosis and management?

Model Answer: "This is familial adenomatous polyposis (FAP) until proven otherwise, caused by germline mutation in the APC gene on chromosome 5q21. It follows autosomal dominant inheritance.

Diagnosis:

  • Confirm with genetic testing for APC mutation
  • Family history and pedigree analysis
  • Screen first-degree relatives

Management:

  1. Colorectal: Prophylactic surgery is required, typically by age 25 or when polyp burden becomes unmanageable. Options include:

    • Total proctocolectomy with ileal pouch-anal anastomosis (IPAA) — gold standard
    • Colectomy with ileorectal anastomosis (IRA) — if rectum relatively spared (less than 20 rectal polyps)
  2. Upper GI surveillance: Upper GI endoscopy every 1-3 years as 90% develop duodenal adenomas; duodenal cancer risk 5-10%

  3. Other surveillance: Thyroid (annual), desmoid screening

  4. Family screening: Genetic testing and colonoscopy for at-risk relatives from age 10-12

Without intervention, there is 100% risk of colorectal cancer by age 40-50."


Q4: How do you risk-stratify a malignant polyp?

Model Answer: "A malignant polyp contains invasive adenocarcinoma (pT1). Risk stratification determines whether polypectomy alone is curative or surgical resection is needed.

Low-risk features (polypectomy may be curative):

  • Well or moderately differentiated
  • No lymphovascular invasion
  • Clear resection margin ≥1mm
  • Sm1 invasion (upper 1/3 submucosa) for sessile polyps
  • Haggitt level 1-3 for pedunculated polyps
  • Low tumour budding

High-risk features (surgical resection recommended):

  • Poorly differentiated
  • Lymphovascular invasion present
  • Margin involved or less than 1mm
  • Sm2/Sm3 invasion (sessile)
  • Haggitt level 4 (pedunculated)
  • High-grade tumour budding

All malignant polyps require MDT discussion. CT staging is performed before surgical decision. The patient's fitness and preferences are considered.

For low-risk lesions, surveillance includes colonoscopy at 3 months to check the polypectomy site, then at 1 year."


Q5: What are the features of Lynch syndrome and how would you investigate?

Model Answer: "Lynch syndrome, previously called hereditary non-polyposis colorectal cancer (HNPCC), is caused by germline mutations in mismatch repair genes — MLH1, MSH2, MSH6, PMS2, or EPCAM.

Clinical features:

  • Autosomal dominant inheritance
  • Early-onset colorectal cancer (mean 44 years)
  • Right-sided predominance
  • MSI-high tumours (poorly differentiated, mucinous, tumour-infiltrating lymphocytes)
  • Multiple synchronous/metachronous colorectal cancers
  • Extracolonic cancers: endometrial (40-60% risk), ovarian, gastric, urinary tract, small bowel

Investigation:

  1. Clinical criteria: Amsterdam II criteria (≥3 relatives, 2 generations, 1 less than 50 years, FAP excluded)
  2. Tumour testing:
    • Immunohistochemistry for MMR proteins (loss of expression)
    • Microsatellite instability (MSI) testing
  3. Genetic testing: Germline testing for MLH1, MSH2, MSH6, PMS2, EPCAM

Management:

  • Colonoscopy every 2 years from age 25 (or 5 years before youngest case)
  • Gynaecological surveillance from age 30-35
  • Consider prophylactic hysterectomy and BSO after family complete
  • Aspirin chemoprevention (CAPP2 trial — 600mg daily for 2 years)
  • Immunotherapy for metastatic MSI-high CRC"

Common Exam Errors

ErrorCorrect Approach
Recommending surveillance for low-risk adenomasBSG 2020: 1-2 small tubular adenomas with LGD = NO surveillance
Forgetting serrated lesion surveillanceSSLs ≥10mm or with dysplasia need 1-year surveillance
Not knowing Haggitt/Kikuchi stagingCritical for malignant polyp management
Confusing FAP with LynchFAP = APC, hundreds of polyps. Lynch = MMR, few polyps
Quoting outdated surveillance intervalsKnow BSG 2020: Low = none, Intermediate = 3 years, High = 1 year
Missing the serrated pathway15-30% of CRC; BRAF → MSI-high pathway
Not knowing ADR target≥25%; each 1% increase = 3% decrease in interval CRC

15. References

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  2. Dekker E, Tanis PJ, Vleugels JLA, Kasi PM, Wallace MB. Colorectal cancer. Lancet. 2019;394(10207):1467-1480. doi:10.1016/S0140-6736(19)32319-0

  3. Fearon ER, Vogelstein B. A genetic model for colorectal tumorigenesis. Cell. 1990;61(5):759-767. doi:10.1016/0092-8674(90)90186-I

  4. Williams AR, Balasooriya BA, Day DW. Polyps and cancer of the large bowel: a necropsy study in Liverpool. Gut. 1982;23(10):835-842. doi:10.1136/gut.23.10.835

  5. Stryker SJ, Wolff BG, Culp CE, Libbe SD, Ilstrup DM, MacCarty RL. Natural history of untreated colonic polyps. Gastroenterology. 1987;93(5):1009-1013. doi:10.1016/0016-5085(87)90563-4

  6. Logan RF, Patnick J, Nickerson C, et al. Outcomes of the Bowel Cancer Screening Programme (BCSP) in England after the first 1 million tests. Gut. 2012;61(10):1439-1446. doi:10.1136/gutjnl-2011-300843

  7. WHO Classification of Tumours Editorial Board. WHO Classification of Tumours: Digestive System Tumours. 5th ed. Lyon: IARC Press; 2019.

  8. Jass JR. Classification of colorectal cancer based on correlation of clinical, morphological and molecular features. Histopathology. 2007;50(1):113-130. doi:10.1111/j.1365-2559.2006.02549.x

  9. Syngal S, Brand RE, Church JM, et al. ACG clinical guideline: Genetic testing and management of hereditary gastrointestinal cancer syndromes. Am J Gastroenterol. 2015;110(2):223-262. doi:10.1038/ajg.2014.435

  10. Vasen HF, Blanco I, Aktan-Collan K, et al. Revised guidelines for the clinical management of Lynch syndrome (HNPCC): recommendations by a group of European experts. Gut. 2013;62(6):812-823. doi:10.1136/gutjnl-2012-304356

  11. Winawer SJ, Zauber AG, Ho MN, et al. Prevention of colorectal cancer by colonoscopic polypectomy. N Engl J Med. 1993;329(27):1977-1981. doi:10.1056/NEJM199312303292701

  12. Rex DK, Ahnen DJ, Baron JA, et al. Serrated lesions of the colorectum: review and recommendations from an expert panel. Am J Gastroenterol. 2012;107(9):1315-1329. doi:10.1038/ajg.2012.161

  13. Rutter MD, East J, Rees CJ, et al. British Society of Gastroenterology/Association of Coloproctology of Great Britain and Ireland/Public Health England post-polypectomy and post-colorectal cancer resection surveillance guidelines. Gut. 2020;69(2):201-223. doi:10.1136/gutjnl-2019-319858

  14. Zauber AG, Winawer SJ, O'Brien MJ, et al. Colonoscopic polypectomy and long-term prevention of colorectal-cancer deaths. N Engl J Med. 2012;366(8):687-696. doi:10.1056/NEJMoa1100370

  15. Kaminski MF, Thomas-Gibson S, Bugajski M, et al. Performance measures for lower gastrointestinal endoscopy: a European Society of Gastrointestinal Endoscopy (ESGE) Quality Improvement Initiative. Endoscopy. 2017;49(4):378-397. doi:10.1055/s-0043-103411

  16. Martinez ME, Baron JA, Lieberman DA, et al. A pooled analysis of advanced colorectal neoplasia diagnoses after colonoscopic polypectomy. Gastroenterology. 2009;136(3):832-841. doi:10.1053/j.gastro.2008.12.007

  17. Johns LE, Houlston RS. A systematic review and meta-analysis of familial colorectal cancer risk. Am J Gastroenterol. 2001;96(10):2992-3003. doi:10.1111/j.1572-0241.2001.04677.x

  18. World Cancer Research Fund/American Institute for Cancer Research. Diet, Nutrition, Physical Activity and Colorectal Cancer. Continuous Update Project Expert Report. 2018.

  19. Farraye FA, Odze RD, Eaden J, et al. AGA medical position statement on the diagnosis and management of colorectal neoplasia in inflammatory bowel disease. Gastroenterology. 2010;138(2):738-745. doi:10.1053/j.gastro.2009.12.037

  20. Delhougne B, Deneux C, Abs R, et al. The prevalence of colonic polyps in acromegaly: a colonoscopic and pathological study in 103 patients. J Clin Endocrinol Metab. 1995;80(11):3223-3226. doi:10.1210/jcem.80.11.7593429

  21. Rothwell PM, Wilson M, Elwin CE, et al. Long-term effect of aspirin on colorectal cancer incidence and mortality: 20-year follow-up of five randomised trials. Lancet. 2010;376(9754):1741-1750. doi:10.1016/S0140-6736(10)61543-7

  22. Baron JA, Beach M, Mandel JS, et al. Calcium supplements for the prevention of colorectal adenomas. N Engl J Med. 1999;340(2):101-107. doi:10.1056/NEJM199901143400204

  23. McKittrick LS, Wheelock FC. Carcinoma of the colon. Springfield, IL: Charles C Thomas; 1954.

  24. Hassan C, Spadaccini M, Iber M, et al. Artificial intelligence allows leaving-in-situ colorectal polyps. Clin Gastroenterol Hepatol. 2022;20(11):2505-2513. doi:10.1016/j.cgh.2022.01.019

  25. Williams JG, Pullan RD, Hill J, et al. Management of the malignant colorectal polyp: ACPGBI position statement. Colorectal Dis. 2013;15(Suppl 2):1-38. doi:10.1111/codi.12262

  26. Ferlitsch M, Moss A, Hassan C, et al. Colorectal polypectomy and endoscopic mucosal resection (EMR): European Society of Gastrointestinal Endoscopy (ESGE) Clinical Guideline. Endoscopy. 2017;49(3):270-297. doi:10.1055/s-0043-102569

  27. Burn J, Gerdes AM, Macrae F, et al. Long-term effect of aspirin on cancer risk in carriers of hereditary colorectal cancer: an analysis from the CAPP2 randomised controlled trial. Lancet. 2011;378(9809):2081-2087. doi:10.1016/S0140-6736(11)61049-0

  28. Atkin WS, Edwards R, Kralj-Hans I, et al. Once-only flexible sigmoidoscopy screening in prevention of colorectal cancer: a multicentre randomised controlled trial. Lancet. 2010;375(9726):1624-1633. doi:10.1016/S0140-6736(10)60551-X



17. Additional Clinical Scenarios

Scenario 1: The Screening Colonoscopy

Case: A 62-year-old male has a positive FIT as part of the NHS Bowel Cancer Screening Programme. Colonoscopy reveals a 12mm sessile polyp in the ascending colon and a 6mm pedunculated polyp in the sigmoid. Both are removed.

Histology:

  • Ascending colon: Sessile serrated lesion without dysplasia
  • Sigmoid: Tubular adenoma with low-grade dysplasia

Questions:

  1. How do you risk-stratify this patient?
  2. What is the surveillance interval?

Answers:

  1. The patient has an SSL less than 10mm without dysplasia (3-year surveillance) AND an adenoma less than 10mm with LGD (no surveillance if only finding). However, when both present, follow the higher-risk lesion.
  2. The 12mm SSL (which is ≥10mm) actually requires 1-year surveillance per BSG 2020 guidelines. This takes precedence.

Scenario 2: The Malignant Polyp Dilemma

Case: A 58-year-old female has a 25mm sessile polyp removed by piecemeal EMR from the sigmoid colon. Histology shows moderately differentiated adenocarcinoma invading into Sm2, with no lymphovascular invasion and margins clear by 0.5mm.

Questions:

  1. Is this a low-risk or high-risk malignant polyp?
  2. What is your management recommendation?

Answers:

  1. HIGH-RISK — despite no LVI and moderate differentiation:
    • Sm2 invasion (not Sm1) indicates higher lymph node metastasis risk
    • Margin less than 1mm is concerning
    • Piecemeal resection means margin assessment may be incomplete
  2. Management: MDT discussion → recommend surgical resection (sigmoid colectomy) with lymph node clearance. CT staging to exclude distant metastases first.

Scenario 3: The Young Patient with Multiple Polyps

Case: A 28-year-old male presents for colonoscopy due to family history (father died of CRC aged 42). Colonoscopy reveals 8 adenomatous polyps throughout the colon, largest 18mm in the caecum.

Questions:

  1. What diagnoses should you consider?
  2. What further investigations are needed?

Answers:

  1. Consider:
    • Attenuated FAP (10-100 polyps, later onset than classical FAP)
    • MUTYH-associated polyposis (autosomal recessive, 10-100 adenomas)
    • Lynch syndrome (usually few polyps, but strong family history)
  2. Further investigations:
    • Genetic testing: APC mutation (FAP), MUTYH (MAP), MMR genes (Lynch)
    • IHC on adenoma tissue if available
    • Upper GI endoscopy (duodenal adenomas in FAP)
    • Family pedigree and genetic counselling
    • Screen siblings and offspring

Scenario 4: The Serrated Lesion Challenge

Case: A 55-year-old female has a colonoscopy for iron deficiency anaemia. In the proximal transverse colon, a 20mm flat lesion is identified, pale with indistinct margins, covered in adherent mucus. It is removed by piecemeal EMR.

Histology: Sessile serrated lesion with low-grade dysplasia.

Questions:

  1. Why are these lesions clinically important?
  2. What is the surveillance plan?

Answers:

  1. SSLs with dysplasia are important because:
    • They follow the serrated pathway to CRC (BRAF → MLH1 methylation → MSI-high)
    • May have accelerated progression to cancer
    • Often flat and pale — easily missed (high miss rate)
    • Account for many "interval cancers"
  2. Surveillance plan:
    • Site check at 2-6 months (piecemeal resection of large lesion)
    • If clear, 1-year surveillance (SSL with dysplasia = high-risk)
    • High-quality colonoscopy with chromoendoscopy recommended

18. Quick Reference Summary Cards

BSG 2020 Surveillance Quick Reference

FindingSurveillance
1-2 adenomas less than 10mm, tubular, LGDNone — population screening
3-4 small adenomas3 years
Any adenoma 10-19mm3 years
≥5 adenomas1 year
Any adenoma ≥20mm1 year
High-grade dysplasia1 year
SSL less than 10mm without dysplasia3 years
SSL ≥10mm1 year
SSL with dysplasia1 year
Piecemeal EMR of large polypSite check 2-6 months

Polyposis Syndromes Quick Reference

SyndromeGenePolypsCRC RiskKey Feature
FAPAPC> 100 adenomas100%Osteomas, CHRPE, desmoids
Attenuated FAPAPC10-100 adenomas70%Later onset, right-sided
LynchMMRFew adenomas50-80%MSI-high, endometrial cancer
MAPMUTYH10-100 adenomas50-100%Autosomal recessive
Peutz-JeghersSTK11Hamartomas39%Perioral pigmentation
Juvenile polyposisSMAD4/BMPR1AJuvenile polyps10-40%GI bleeding, intussusception

Malignant Polyp Risk Stratification Quick Reference

FeatureLow-RiskHigh-Risk
DifferentiationWell/ModeratePoor
LVIAbsentPresent
Margin≥1mm clearless than 1mm or involved
Depth (sessile)Sm1Sm2/Sm3
Depth (pedunculated)Haggitt 1-3Haggitt 4
Tumour buddingLowHigh
ManagementSurveillanceSurgical resection

Last Reviewed: 2025-01-09 | MedVellum Editorial Team


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