Pathology of Polyps and Colon Cancer Flashcards
1
Q
What are the 3 categories of NON-neoplastic polyps?
A
- inflammatory polyps
- hamartomatous polyps
- hyperplastic polyps
* polyp= raised protrusion of colonic mucosa
2
Q
What is solitary rectal ulcer syndrome?
A
- associated with INFLAMMATORY polyps that causes rectal bleeding, mucus discharge, and an inflammatory lesion on the anterior rectal wall due to impaired relaxation of the anorectal sphincter. This causes a sharp angle at the rectal shelf leading to recurrent abrasion and ulceration of the mucosa.
3
Q
What causes inflammatory polyps (non-neoplastic polyps)?
A
- repeated cycles of injury and healing.
4
Q
What can happen to inflammatory polyps and what will you see histologically?
A
- the polyp may become entrapped, leading to mucosal prolapse.
- may see fibromuscular hyperplasia, mixed inflammatory infiltrates, erosion, and epithelial hyperplasia.
5
Q
What causes hamartomatous polyps (non-neoplastic polyps)?
A
- occur sporadically and in some genetic and acquired syndromes.
6
Q
What will you see histologically with hamartomatous polyps?
A
- tumor-like growths composed of mature tissues that are normally present in the organ.
- juvenile polyps
7
Q
*** What syndromes are associated with hamartomatous polyps?
A
- Peutz-Jeghers syndrome
- Cowden syndrome
- Bannayan-Ruvalcaba-Riley syndrome
- Cronkhite-Canada syndrome
8
Q
Where do juvenile polyps (type of hamartomatous polyp; non-neoplastic) occur most often?
A
- RECTUM and present as rectal bleeding and may protrude through the anal sphincter.
- sporadic juvenile polyps are usually solitary (pedunculated dilated gland with smooth surface).
9
Q
*** What is juvenile polyposis?
A
- autosomal dominant disease (SMAD4, BMPR1A) that presents with 3-100 polyps, which may require colectomy due to the potential for sever hemorrhage.
- PULMONARY ARTERIOVENOUS MALFORMATIONS are extraintestinal manifestations marked by PROTEIN LOSS.
10
Q
For what does juvenile polyposis increase your risk?
A
- colonic adenocarcinoma
11
Q
*** What is Peutz-Jeghers syndrome?
A
- rare, autosomal dominant (LKB1/STK11) disease with multiple hamartomatous polyps (most common in SMALL INTESTINE) and mucocutaneous hyperpigmentation (PEDUNCULATED AND LOBULAR).
- maculoses form around mouth, palms, genitalia, and perianal areas.
- can initate INTUSSUSCEPTION (telescoping of bowel).
- associated with increased risk of malignancies (BREAST, COLON, LUNG, OVARIES, UTERUS OR TESTICLES) and sex cord tumor with annular tubules (SCAT).
12
Q
What is Cowden syndrome?
A
- autosomal dominant hamartomatous polyp syndrome due to PTEN mutation, which encodes a lipid phosphatase that inhibits signaling through the P13K/AKT pathway.
- macrocephaly, benign skin lesions, trichilemmomas, papillomatous papules and acral keratoses.
- increased risk for GI malignancy, breast ca, follicular cancer, thyroid cancer, or endometrial cancer.
- REMEMBER: cows have big heads, cows have hair, cows have big necks so think follicular or thyroid cancer, and females cows have big uterus.
13
Q
What is Bannayan-Ruvalcaba-Riley syndrome?
A
- similar to Cowden but has mental and developmental delays.
- Lower incidence of neoplasia than seen in Cowden.
14
Q
What is Cronkite-Canda syndrome?
A
- nonhereditary disorder occuring in 50s where hamartomatous polyps occur in the stomach, small intestine, colon, and rectum.
- polyps resemble juvenile polyps histologically.
- nail splitting, hair loss, and cutaneous hyper or hypopigmentation can occur.
15
Q
What are hyperplastic polyps (non-neoplastic)?
A
- common epithelial proliferations (most common in left colon) seen in 60s or 70s. No risk of malignancy! :)
- composed of goblet cells with a SERRATED surface.
- may be associated with a reaction adjacent to a more ominous lesion or inflammatory disorder.
16
Q
What is the most common type of colonic polyp?
A
- hyperplastic polyps
17
Q
What are Adenomatous polyps?
A
- neoplastic proliferation of glands; MOST COMMON type of NEOPLASTIC polyp and 2nd most common type of general colonic polyp.
- benign, but PREMALIGNANT; may progress to adenocarcinoma via the adenoma-carcinoma sequence.
- large nucleoli and eosinophilic cytoplasm with reduction in goblet cells (compared to hyperplastic polyps which have lots of goblet cells).
18
Q
What is the adenoma-carcinoma sequence?
A
- the molecular progression from normal colonic mucosa to adenomatous polyp to carcinoma.
1. APC/beta-catenin (adenomatous polyposis coli gene) mutations increase risk for formation of polyp. Both copies of the APC gene must be inactivated. APC is a negative regulator of beta-catenin (component of WNT signaling).
2. K-ras mutation leads to formation of polyp.
3. p53 mutation and increased exression of COX allow for progression to carcinoma.
