Definition/General
Introduction:
Colonic adenomas are benign neoplastic polyps with malignant potential
They represent the precursor lesions to most colorectal cancers
Cytological recognition is important for cancer prevention.
Origin:
Arise from colonic epithelial cells
Result from APC gene mutations
Clonal proliferation of dysplastic epithelium
Adenoma-carcinoma sequence.
Classification:
Tubular adenoma (80%)
Villous adenoma (10%)
Tubulovillous adenoma (10%)
Serrated adenoma
Dysplasia grading.
Epidemiology:
Common lesions (30% adults >50)
Male predominance
Increasing with age
Western countries higher prevalence.
Clinical Features
Presentation:
Often asymptomatic
Rectal bleeding
Change in bowel habits
Mucus discharge
Abdominal pain (large lesions).
Symptoms:
Intermittent bleeding
Mucoid stools
Diarrhea (villous adenomas)
Rarely symptomatic.
Risk Factors:
Age >50 years
Male gender
Family history
High-fat diet
Smoking
FAP syndrome.
Screening:
Colonoscopic screening
FOBT positivity
Family history screening
Surveillance intervals.
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Gross Description
Appearance:
Polypoid lesions
Smooth surface (tubular)
Villiform surface (villous)
Lobulated appearance
Firm consistency.
Characteristics:
Reddish color
Friable surface
Mucoid secretion (villous)
Well-defined borders.
Size Location:
Size: Few mm to several cm
Left colon predominance
Rectosigmoid common
Multiple adenomas possible.
Multifocality:
Synchronous adenomas (30%)
Familial clustering
Metachronous development.
Microscopic Description
Histological Features:
Dysplastic glandular epithelium
Crowded nuclei
Loss of goblet cells
Nuclear stratification
Increased mitotic activity.
Cellular Characteristics:
Enlarged hyperchromatic nuclei
Pseudostratification
Prominent nucleoli
Reduced mucin
Elongated cells.
Architectural Patterns:
Tubular glands
Villous projections
Crowded architecture
Back-to-back glands
Surface maturation.
Grading Criteria:
Low-grade dysplasia: Mild atypia, surface maturation
High-grade dysplasia: Severe atypia, loss of polarity.
Immunohistochemistry
Positive Markers:
CK20
CDX2
Villin
Ki-67 (increased)
p53 (high-grade).
Negative Markers:
CK7
Chromogranin
Synaptophysin.
Diagnostic Utility:
Confirms adenomatous nature
Dysplasia grading
Proliferation assessment.
Molecular Subtypes:
Conventional adenoma
Serrated adenoma
Mixed patterns.
Molecular/Genetic
Genetic Mutations:
APC mutations (80%)
KRAS mutations (40%)
TP53 mutations (high-grade)
PIK3CA mutations.
Molecular Markers:
Wnt pathway activation
β-catenin nuclear accumulation
Loss of APC function.
Prognostic Significance:
Size >1 cm
Villous histology
High-grade dysplasia
Multiple adenomas.
Therapeutic Targets:
Endoscopic resection
NSAIDs
Lifestyle modifications
Surveillance.
Differential Diagnosis
Similar Entities:
Hyperplastic polyp
Inflammatory polyp
Adenocarcinoma
Serrated polyp.
Distinguishing Features:
Adenoma: Dysplastic epithelium
Hyperplastic: Serrated architecture
Carcinoma: Invasion present.
Diagnostic Challenges:
Serrated adenoma recognition
High-grade dysplasia vs carcinoma
Sampling adequacy.
Rare Variants:
Serrated adenoma
Mixed hyperplastic-adenomatous polyp
Flat adenoma.
Sample Pathology Report
Template Format
Sample Pathology Report
Complete Report: This is an example of how the final pathology report should be structured for this condition.
Specimen Information
Colonic cytology, polypoid lesion, adequate
Diagnosis
Adenomatous polyp
Dysplastic Features
Dysplastic epithelium with [nuclear stratification] and [atypia]
Architectural Pattern
Architecture: [Tubular/Villous/Tubulovillous]
Dysplasia Grade
Dysplasia: [Low-grade/High-grade]
Size Assessment
Size: [<1 cm/>1 cm] (clinical correlation)
Final Diagnosis
Colonic cytology: Adenomatous polyp with [grade] dysplasia