GI Polyps & Neoplasms Flashcards
1
Q
Sessile vs. Pedunculated Polyp
A
- sessile = no stalk
- pedunculated = stalk
2
Q
Tubular vs. Villous polyp
A
- tubular = smooth-ish borders
- villous = borders look like villi
- villous = “villanous” (worse prognosis)
3
Q
Types of non-neoplastic polyps + key association
A
- non-neoplastic type polyps are frequently “syndromic”, i.e. associated with a genetic syndrome that overall predisposes to cancer development
- inflammatory polyps
- hamartomatous
- juvenile
- peutz-jeghers
- hyperplastic
4
Q
Characteristics of inflammatory polyps
A
- Often present with bleeding
- Often due to mucosal prolapse (very common in the rectum)
- Cycles of injury and healing result in “polyp” formation
- inflamed colonic mucosa ==> ulceration/erosion ==> epithelial hyperplasia
5
Q
Characteristics of hamartomatous polyps
A
- most occur during childhood
- Hamartoma: “tumor-like” over-growth / mature tissue / developing where it is normally present (e.g. colonic tissue developing in the colon)
- Associations: Juvenile (sporadic and syndromic) and Peutz-Jeghers (syndromic)
- benign features on histo, but often have foci of dysplasia
- ==> increase risk for future GI carcinoma
6
Q
Characteristics of hyperplastic polyps
A
Smooth, nodular lesion with flat base (sessile)
- (1) The lesion abuts muscularis mucosa (arrow) and does not have a stalk.
- (2) It is composed of crowded, mixed absorptive and goblet cells
- (3) A serrated architecture results
- (4) This is a benign, usually non-neoplastic lesion to be distinguished from SSPs
7
Q
hyperplastic vs. sessile serrated polyps/adenomas
A
- hyperplastic
- NOT pre-malignant
- common @ L side of colon
- not dysplastic epithelium
- Sessile serrated/adenoma
- pre-malignant
- CAN progress to adenocarcinoma
- common @ R side of colon
- +/- dysplastic epithelium
- pre-malignant
8
Q
Characteristics (general) of adenomas
A
- Size is variable – range from a few mm to several cm (10 cm or more)
- Present in nearly 50% of Western adults by age 50
- Present throughout the colon
- origin: epithelial cells
- gland-forming masses
9
Q
Risk factors (related to adenomas) for malignancy
A
- Have epithelial cytologic dysplasia ranging from low grade to high grade (carcinoma in situ)
- Villous adenomas contain foci of invasion more frequently than tubular adenomas
- SIZE MATTERS
- most important characteristic that correlates with risk of malignancy overall in the patient
- Presence of high grade dysplasia increases risk of malignant transformation in that polyp but not in the rest of the colon
10
Q
Histologic features of adenomas
A
- Cells
- Piling up on each other (no respect!)
- Nuclei
- Darker (hyperchromasia)
- Progressive loss of basal-orientation
- Cytoplasm
- Reduced compared to nucleus (increased N:C ratio)
- Reduced mucin production
- Mitotic Figures
- Increased mitotic activity
11
Q
Risk factors for colorectal cancer
A
- Increase Risk
- Body fatness
- Abdominal fatness
- Red/processed meat
- Alcoholic drinks
- Smoking
- Genetic predisposition
- Decrease Risk
- Physical Activity
- Foods with High Fiber
12
Q
Major genetic syndromes that increase colorectal cancer risk
A
- Sporadic (65-85%)
- Familial Adenomatous Polyposis (FAP) (<1%)
- Hereditary Nonpolyposis Colorectal Cancer (HNPCC) (2-3%)
13
Q
Main molecular pathways to colorectal cancer
A
- WNT/APC/beta-catenin – classical adenoma-carcinoma sequence
- K-Ras/MAP kinase/PI3 kinase signaling pathways—activating mutations
- Microsatellite Instability – defects in mismatch repair proteins
14
Q
Characteristics of WNT/APC pathway to colorectal cancer
A
- Wnt protein ligands are critical for development
- drive proliferation of their target tissues/organs
- Wnt pathway regulates the levels of cytoplasmic b-catenin
- WNT binds to receptor ==> disruption of APC/beta-catenin complex (normally, this complex leads to destruction of beta-catenin/low levels of b-c) ==> elevated beta-catenin levels @ cytosol
- b-catenin translocates to nucleus ==> cell cycle initiation w/TCF (transcription factor)
- mutated/absent APC ==> cells behave as if under constant stimulation by WNT
15
Q
Characteristics Familial Adenomatous Polyposis
A
-
APC mutations can run in families, producing Familial Adenomatous Polyposis (FAP)
- AD mutation @ APC gene ==> increased risk of colon cancer,
- Most people who acquire colon cancer without FAP acquire spontaneous somatic mutations in APC
20
Q
Histologic features of invasive adenocarcinoma
A
- gland formation
- variable - scant mucin production
- invade muscularis propria ==> desmoplastic (fibrotic) response
- “dirty necrosis” w/in some glands
21
Q
Important prognostic factors in colorectal cancer
A
- depth of invasion
- presence/absence of lymph node metastasis
- distant metastasis
