GI Polyps and Carcinoma Flashcards
Polyp comes from the Greek for ___________.
morbid excrescence
True or false: adenomas don’t need to be worried about.
False. They can be precursors to adenocarcinomas.
The two main categories of histologic structure that polyps can resemble are ___________.
villous or tubular
There are three kinds of non-neoplastic polyps: _______________.
inflammatory, hamartomatous, and hyperplastic
_____________ polyps form from repeated injuries and healings.
Inflammatory
What are hamartomas?
Non-neoplastic overgrowth of normal, mature tissue where it typically occurs
True or false: hamartomas can present with or without non-GI symptoms and can portend cancer.
True. Syndromic hamartomas (Peutz-Jeghers) increase risk of GI carcinoma.
____________ polyps are flat, nubby little lesions that present with a serrated appearance on histologic exam.
Hyperplastic
In terms of nuclei, how will low-grade dysplasia and high-grade dysplasia differ?
Low-grade: pencil-shaped nuclei still roughly in line, but larger and darker than normal cells
High-grade: wildly different nuclei with no tendency to orient in any way toward the apical side
Most colorectal cancer is sporadic or genetic?
Sporadic
Microsatellite instability results from failure of which system?
The mismatch-repair system
Beta-catenin is the activating signal for the _______ pathway.
Wnt
Describe the Wnt pathway.
Beta-catenin is a transcription factor for growth proteins. APC is a scaffold protein that works to destroy beta-catenin (which it does statically). Wnt is a surface receptor. When it is stimulated, it activates a pathway that inhibits APC and allows beta-catenin to go free.
What percent of colon cancer is due to FAP?
5%
Lynch syndrome tends to appear on the ________ side.
right