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DEMS I > GI polyps and carcinoma > Flashcards

GI polyps and carcinoma Flashcards

1
Q

Define polyp

A

morbid excrescence

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2
Q

Sessile vs pedunculated polyp

A

Sessile: mass without a stalk. Pedunculated: mass with a stalk

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3
Q

architecture of polyps

A

tubular ( no villi, tubular structures) and villous (long villi projections)

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4
Q

adenoma

A

precursor to malignancy

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5
Q

adenocarcinoma

A

invasive

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6
Q

What does it mean that non-neoplastic polyps are usually syndromic

A

They are associated with a genetic syndrome that overall predisposes to cancer development

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7
Q

List types of non-neoplastic polyps

A

inflammatory polyps, hamartomatous polyps and hyperplastic polyps

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8
Q

presentation and cause 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 with ulceration/erosion, epithelial hyperplasia

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9
Q

What are hamartomatous polyps

A

Childhood “tumor-like” over-growth / mature tissue / developing where it is normally present (e.g. colonic tissue developing in the colon). Types: juvenile (sporadic and syndromic), Cowden (syndromic), Bannayan-Ruvalcaba-Riley (syndromic), Cronkhite-Canada (syndromic) and Peutz-Jeghers (syndromic)

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10
Q

Where do polyps occur

A

variable locations in lower GI tract

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11
Q

Juvenile polyp histology

A

Cystically dilated crypts, surface erosion. syndromic juvenile polyps often have foci of dysplasia

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12
Q

Peutz-Jeghers polyps histology

A

complex glandular architecture separated by increased smooth muscle bundles

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13
Q

Polyps clinical consequences

A

risk of future GI carcinoma and extra-GI manifestations

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14
Q

Peutz-Jeghers syndrome mean age, genes, GI lesions, extra-GI manifestations (not on test)

A

10-15yrs, LKB1/STK11 genes, causes arborizing hamartomatous polyps (Small intestine > colon > stomach) and colonic adenocarcinoma. Extra GI: mucocutaneous pigmented lesions and increased risk of other cancers

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15
Q

Juvenile polyposis mean age, genes, GI lesions, extra-GI manifestations (not on test)

A

<5 years, SMAD4/BMPR1A genes, juvenile hamartomatous polyps with risk of gastric, small intestinal, colonic, and pancreatic adenocarcinoma. Extra GI: Pulmonary arteriovenous malformations, digital clubbing

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16
Q

Cowden syndrome, Bannayan-Ruvalcaba-Riley syndrome mean age, genes, GI lesions, extra-GI manifestations (not on test)

A

<15 yrs, PTEN gene, Hamartomatous polyps, lipomas, ganglioneuromas, inflammatory polyps, risk of colon cancer. Extra GI: Benign skin tumors, benign and malignant thyroid and breast lesions

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17
Q

Cronkhite-Canada syndrome mean age, genes, GI lesions, extra-GI manifestations (not on test)

A

> 50 yrs, no known genes, Hamartomatous colon polyps, crypt dilatation and edema in nonpolypoid mucosa. Extra GI: Nail atrophy, hair loss, abnormal skin pigmentation, cachexia, and anemia

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18
Q

For hyperplastic polyps: list location, age, size, histology, dysplasa

A

Left colon including rectum, increases with age, small (<0.5cm), Delayed maturation with overgrowth of superficial epithelium (absorptive and goblet cells) resulting in SERRATED architecture and sessile nodule, NO dysplasia

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19
Q

Compare the two common types of serrated polyps

A

Hyperplastic polyps are not pre-malignant, left side of colon, crypts are star shaped. Sessile serrated polyps/adenoma are pre malignant and dysplastic, right side of colon

20
Q

What characteristic is most important in risk of adenoma malignancy

A

size! Larger size means larger risk of malignancy.

21
Q

villous vs tubular adenomas risk of malignancy

A

Villous adenomas contain foci of invasion more frequently than tubular adenomas

22
Q

What are adenomatous/dysplastic changes

A

Increased number of cells piling up on each other, Loss of basal-orientation of nucleus and darker nuclei, Reduced mucin production and reduced cytoplasm, Increased mitotic activity

23
Q

What is high grade dysplasia called

A

carcinoma in situ

24
Q

Describe tubular adenoma

A

has stalk and tubular appearance

25
Q

Describe villous adenoma

A

sessile (no stalk), villi with fibrovascular core,

26
Q

Risk factors for colorectal cancer

A

age, long standing ulcerative colitis, FAP/HNPCC, red meat, alcohol, smoking,

27
Q

Are most colorectal cancers spontaneous or familial

A

sporadic

28
Q

What are the main molecular pathways in adenoma-carcinoma sequence

A

classical: WNT/APC/ beta-catenin. Microsatellite instability: defects in mismatch repair. K-Ras/MAP kinase/ P13 kinase signaling

29
Q

Describe WNT pathway

A

in resting cells, Beta catenin binds APC forming destruction complex, and beta catenin is destroyed. When WNT binds its receptor, the destruction complex is deactivated so intracellular beta catenin levels rise. Beta catenin goes to nucleus and binds TCF transcription factor which turns on cell cycle genes and causes proliferation

30
Q

How do APC mutations affect cell proliferation

A

When APC is mutated, destruction of Beta catenin doesn’t occur, so cell proliferation occurs continuously

31
Q

Polyps cell proliferation

A

There is no increase in the rate of cell proliferation in the early stage of polyp formation. Polyps represent An increase in the size of the proliferating crypt compartment

32
Q

Which gene is most commonly mutated in colon cancer

A

APC

33
Q

What is familial adenomatous polyposis

A

autosomal dominant APC mutations - incrased risk of colon cancer and lots of polyps. 100% develop invasive adenocarcinoma before age 30

34
Q

Describe K-Ras/MAPK/P13K signaling

A

EGFR > Ras >Raf > MEK1/2 > MAPK leads to cellular proliferation. P13K activates a signaling molecule that inhibits Raf and leads to cell survival

35
Q

Cetuximab MOA

A

Blocks P13K leading to cell death, and blocks Ras leading to stopped cell proliferation

36
Q

What is Lynch syndrome

A

Hereditary Non-Polyposis Colorectal Cancer - develop cancer at earlier age than sporadic types. Tends to be right sided. Due to inherited mutation of mismatch repair gene allele, then acquire second allele mutation over time leading to microsatellite instability

37
Q

Which colon cancers feature high rates of mismatch repair mutations

A

hereditary non-polyposis colorectal cancer and sporadic cancers

38
Q

symptoms of early vs advanced colon carcinoma

A

early: no symptoms or fatigue, weight loss, anemia. Advanced: constipation, urgency, narrowing of stool, cramping/pain, blood loss, weight loss

39
Q

Colon cancer detection

A

colonscopy, barium enema, blood in stool, DNA/mutations

40
Q

Define carcinoma

A

-Invasion of dysplastic epithelial cells into and beyond the lamina propria

41
Q

Adenocarcinoma histology

A

invading into muscularis propria, desmoplastic (fibrotic) response, dirty necrosis in lumen of some glands

42
Q

Where does colon cancer most commonly metastasize to

A

liver

43
Q

histology and genetics of sporadic colon cancer

A

APC mutation- tubular villous adenoma, typical adenocarcinoma. DNA mismatch repair/ MSH2,MLH1 mutations- sessile, serrated adenoma, mucinous adenocarcinoma

44
Q

Histology and genetics of familial adenomatous polyposis

A

APC mutations- tubular, villous adenoma, typical adenocarcinoma. DNA mismatch repair/MUTYH mutation- sessile, serrated adenoma, mucinous adenocarcinoma

45
Q

histology and genetics of hereditary nonpolyposis colorectal cancer

A

DNA mismatch repair/ MSH2, MLH1 mutations. Sessile serrated adenoma, mucinous adenocarcinoma

DEMS I (28 decks)

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