GI polyps and carcinoma Flashcards
- State the nomenclature of polyps, including sessile vs. pedunculated, tubular vs. villous, serrated vs. conventional adenomas, and neoplastic vs. non-neoplastic.
sessile is flat to mucosa
pedunculated has a stalk
villous architecture- finger like projections
tubular- looks like glands
- Recognize the names and clinical features of different types of non-neoplastic polyps discussed in the lecture and state which ones are associated with syndromes.
inflammatory
Hamartomas
hyperplastic
- Compare and contrast the differences between hyperplastic polyps and sessile serrated polyps/adenomas.
non malignant vs. premalignant
Left sided vs right sided
star shaped vs. serrated knife
non-dysplastic vs. dysplastic
- State the basic facts about neoplastic polyps, the concept of cytologic dysplasia, and what features confer increased risk for malignancy.
size most important characteristic that correlates with risk in overall patient
high grade dysplasia increases risk of malignancy in that polyp only
- List the four main molecular/pathway aberrations associated with colon cancer.
WNT/APC/B-catenin- classical adenoma-carcinoma pathway
-Wnt ligands are important for development and growth, allows Beta catenin to go to the nucleus. APC helps perform destruction complex to sequester B-catenin and P and Ub it. Beta catenin needs to be shut down as cells mature on the top of the crypt
KRAS/MAP kinase?PI3 kinase signaling pathway- activating muatation for proliferation
Microsatellite instability-
defects in mismatch repair proteins
methylation induced gene silencing
TGF-Beta
- State the important risk factors for colorectal carcinoma.
Strong-
advanced age, country of birth, FAP/HNPCC, long standing UC
Moderate- high red meat, previous cancer or adenoma, pelvic radiation
modest- high fat diet, smoking and etoh, obesity, cholecystectomy
- Explain the basis for the hereditary cancer syndromes of FAP and HNPCC.
FAP- APC mutations, increases risk of colon cancer, only 5% of colon cancer though Chromosome 5 (POLYP)
HNPCC (Lynch syndrome)- develop colon cancer at an earlier age. inherit mut of mismatch repair gene, aquire second allele muattion over time leading to microsatellite instability–> sessile serrate adenoma
- Describe the various ways colorectal carcinoma can present and the tools we use to screen and diagnose cancer.
early- no Sxs, fatigue wt loss, anemia
advancing- constipation, urgency, narrowing of stool, cramping/ pain, blood loss, anemia, wt loss
colonoscopy, barium enema, fecal ocuult blood, DNA/mut detection in stool
- Recognize the basic histologic features of invasive colorectal carcinoma.
scant mucin production, dirty necrosis, neoplastic glands invading into muscularis propria–>desmoplastic response
- Recognize the most important prognostic features for colorectal carcinoma and describe their importance in staging.
depth of invasion
presence of lymph node involvement
distant metastasis
- Describe the importance of KRAS mutational status in the treatment of colon cancer with EGFR inhibitors.
if they are KRAS wildtype then EGFR inhibitors will work. If KRAS is constisitutively on then EGFR inhibitors wont do anything
inflammatory polyps-
often present with bleeding
often due to rectal prolapse
cycles of injury and healing result in polyp
hamartomatous polyps-
occur in childhood tumor like overgrowth of tissue in the correct location variable location in lower GI benign features histologically risk of future GI carcinoma -both Peutz-jeghers and juvenile polyposis=40% cumulative risk for CA Extra-GI manifestations need to consider familial screening
Peutz Jeghers syndrome extraGI manifestations
mucocutaneous pigmented lesions: increased risk of thryroid breast lung gonadal and bladder cancers
Juvenile Polyposis extraGI manifestations
pulmonary AVM, digital clubbing
