Pathology of Polyps and Colon Cancer Flashcards

1
Q

What are the 3 categories of NON-neoplastic polyps?

A
  1. inflammatory polyps
  2. hamartomatous polyps
  3. hyperplastic polyps
    * polyp= raised protrusion of colonic mucosa
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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.
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3
Q

What causes inflammatory polyps (non-neoplastic polyps)?

A
  • repeated cycles of injury and healing.
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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.
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5
Q

What causes hamartomatous polyps (non-neoplastic polyps)?

A
  • occur sporadically and in some genetic and acquired syndromes.
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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
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7
Q

*** What syndromes are associated with hamartomatous polyps?

A
  • Peutz-Jeghers syndrome
  • Cowden syndrome
  • Bannayan-Ruvalcaba-Riley syndrome
  • Cronkhite-Canada syndrome
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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).
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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.
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10
Q

For what does juvenile polyposis increase your risk?

A
  • colonic adenocarcinoma
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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).
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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.
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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.
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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.
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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.
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16
Q

What is the most common type of colonic polyp?

A
  • hyperplastic polyps
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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).
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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.
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19
Q

*** What will impede the progression of adenoma to carcinoma?

A
  • aspirin because it inhibits COX (which is required for progression to carcinoma).
20
Q

How do we screen for polyps?

A
  • colonoscopy and testing for fecal occult blood.

* polyps are usually clinically silent, but can bleed.

21
Q

What is the goal when screening for polyps?

A

remove adenomatous polyps before progression to carcinoma.

22
Q

What do adenomatous and hyperplastic polyps look like on colonoscopy?

A

identical!

*thus, all polyps are removed to be examined microscopically.

23
Q

What is the risk of an adenomatous polyp progressing to carcinoma?

A
  • size greater than 2 cm
  • sessile growth= flat (rather than pedunculated= has a stalk) and can resemble hyperplastic polyps.
  • villous histology (think villous is the villain). These may secrete protein and potassium causing hypoproteinemia and hypokalemia.
24
Q

Do the majority of adenomas progress to adenocarcinoma?

A

NO

25
Q

What is familial adenomatous polyposis (FAP)?

A
  • autosomal dominant disorder characterized by 100s to 1000s of adenomatous colonic polyps.
  • due to inherited APC mutation (chromosome 5).
26
Q

What is done prophylactically for pts with FAP?

A
  • colon and rectum are removed bc otherwise, almost all pts will develop carcinoma by age 40.
27
Q

What is Gardner syndrome?

A
  • FAP with FIBROMATOSIS (non-neoplastic proliferation of fibroblasts arising in retroperitoneum; desmoid and destructive) and OSTEOMAS (benign tumors of bone that usually arise in the skull).
  • often THYROID cancer is associated
28
Q

What is Turcot syndrome?

A
  • FAP with CNS tumors (medulloblastoma and glioblastoma). Almost inverably fatal
29
Q

What is intramucosal carcinoma?

A
  • occurs when dysplastic epithelial cells penetrate the basement membrane to invade the lamina propria or muscularis mucosa. Once in breeches the muscularis mucosa it can metastasize.
30
Q

What is colorectal carcinoma?

A
  • adenocarcinoma arising from colonic or rectal mucosa; 3rd most common cause of cancer-related death.
  • most commonly arises from adenoma-carcinoma sequence.
31
Q

Aside from the adenoma-carcinoma sequence, what is a second molecular pathway by which colorectal carcinoma can arise?

A
  • microsatellite instability (MSI). Microsatellites are repeating sequences of noncoding DNA; integrity of sequence (stability) is maintained during cell division. However, instability indicates defective DNA copy mechanisms (DNA mismatch repair enzymes).
  • specifically TGF-B and PRO-APOPTOTIC BAX (remember BAL AND BAX; inhibiting this causes uncontrolled cell growth).
32
Q

What is Hereditary nonpolyposis colorectal carcinoma (HNPCC) or “Lynch Syndrome”?

A
  • inherited mutations in DNA mismatch repair enzymes (micosatellite instability).
  • nonpolyposis= carcinoma arises de novo (not from adenomatous polyps) at a relatively early age; usually right sided.
33
Q

*** What is often associated with HNPCC or “Lynch Syndrome”?

A
  • ovarian and endometrial carcinoma
34
Q

Are patients with ulcerative colitis at an increased risk for colorectal carcinoma?

A

YES

35
Q

At what age does screening for colorectal carcinoma begin?

A

age 50

36
Q

Can colorectal carcinoma develop anywhere along the length of the colon?

A

YES

37
Q

How does a left-sided (distal) carcinoma usually grow?

A
  • as a “napkin-ring” lesion that decreased the lumen diameter, presenting with DECREASED STOOL CALIBER, LLQ pain, and blood-streaked stool.
38
Q

How does a right-sided (proximal) carcinoma usually grow?

A
  • as a raised lesion presenting with iron-deficiency anemia (occult bleeding) and vague pain.
  • An older adult with iron-deficiency anemia has colorectal carcinoma until proven otherwise.
39
Q

What pathway of colorectal carcinoma is most common for the right-colon?

A

microsatellite instability pathway

40
Q

*** If a patient presents with Steptococcus bovi endocarditis, what test should you always do next?

A
  • colonoscopy bc it is HIGHLY associated with colonic carcinoma
41
Q

How do we stage colorectal carcinoma?

A
  • T= depth of tumor invasion (tumors limited to the mucosa generally do not spread due to lack of lymphatics in the mucosa).
  • N= spread to regional lymph nodes.
  • M= distant spread; most commonly involves LIVER.
42
Q

What is an important serum tumor marker for assessing treatment response or detecting recurrence of colorectal carcinoma?

A

CEA

43
Q

Is CEA useful for screening for colorectal carcinoma?

A

NO just for assessing treatment response or detecting recurrence.

44
Q

Does mucin production by adenocarcinomas have a better or worse prognosis?

A

worse

45
Q

With what are pure squamous cell cancers of the anal canal often associated?

A

HPV

46
Q

Can tumors of the anal canal have a basaloid pattern?

A

YES (mixed glandular, squamous, or mucinous patterns)