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GI 2 > Chapter 17 Part 8 > Flashcards

Chapter 17 Part 8 Flashcards

1
Q

Where in the GI tract are polyps most common?

A

colon

rectum

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2
Q

What is the difference between sessile polyps and pedunculated polyps?

A
  • sessile = small elevations of the mucosa

- pedunculated = with a stalk

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3
Q

What are the three types of benign polyps?

A
  • hyperplastic
  • inflammatory
  • hamartomatous
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4
Q

What is the most common type of neoplastic polyp?

A

adenoma

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5
Q

Where and in what age group are hyperplastic polyps most commonly found?

A
  • -descending colon

- -6th-7th decade of life

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6
Q

What is the theory behind how hyperplastic polyps are formed?

A

-result from decreased epithelial cell turnover and delayed shedding of surface epithelial cells, so goblet cells and absorptive cells “pile up”

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7
Q

What can the presence of a hyperplastic polyp be a clue for?

A
  • an adjacent, more clinically important lesion

- -since epithelial hyperplasia can occur as a nonspecific rxn adjacent to (or overlying) a mass or inflammatory lesion

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8
Q

What is the morphology of hyperplastic polyps?

A
  • less than 5 mm
  • smooth, nodular
  • on the crests of mucosal folds
  • multiple
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9
Q

Clinically, it is important to distinguish hyperplastic polyps from what else?

A
  • sessile serrated adenomas

- -histologically similar, but sessile serrated adenomas have malignant potential

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10
Q

Inflammatory polyps can be a part of which syndrome and what is its clinical triad?

A
  • Solitary Rectal Ulcer Syndrome (SRUS)

- rectal bleeding, mucus discharge, lesion on anterior rectal wall

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11
Q

What is the cause of inflammatory polyps in SRUS?

A

-impaired relaxation of anorectal sphincter that creates a sharp ledge at the anterior rectal shelf and leads to recurrent cycles of injury and healing

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12
Q

What is the distinctive histological feature of inflammatory polyps?

A

–mixed inflammatory infiltrates, erosion, and epithelial hyperplasia … all together with prolapse-induced fibromuscular hyperplasia of the lamina propria

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13
Q

True or False: many hamartomatous polyp syndromes are caused by germline mutations in tumore suppressor genes or proto-oncogenes

A

True, so some of these syndromes are associated with increased cancer risk

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14
Q

What are two syndromes associated with hamartomatous polyps?

A
  • -Juvenile Polyposis

- -Peutz-Jeghers Syndrome

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15
Q

The vast majority of juvenile polyps occur in what age group?

A

younger than 5 yrs

-the infantile form is severe

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16
Q

What is the typical location and presentation of juvenile polyps?

A
  • rectum
  • rectal bleeding

-maybe intussusception, intestinal obstruction, or polyp prolapse through the anal sphincter

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17
Q

True or False: sporadic juvenile polyps are often solitary

A

True; referred to as “retention polyps”

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18
Q

What is the inheritance pattern of the genetic form of juvenile polyposis?

A

autosomal dominant
–3-100 hamartomatous polyps that may require colectomy to limit the chronic (and sometimes severe) hemorrhaging associated w/ polyp ulceration

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19
Q

What are extraintestinal manifestations of juvenile polyposis?

A
  • congenital malformations
  • digital clubbing
  • pulmonary arteriovenous malformations
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20
Q

True or False: dysplasia is common in syndromic juvenile polyposis

A

True; early colon cancer (45% by age 45)

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21
Q

What is the morphology of juvenile polyps?

A
  • less than 3 cm
  • pedunculated
  • smooth, red surface
  • cystic spaces characteristic after sectioning
  • dilated glands filled w/ mucin and inflammatory debris
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22
Q

What is the most common gene mutated in juvenile polyposis?

A

SMAD4

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23
Q

What is the inheritance pattern of Peutz-Jeghers Syndrome and the median age of onset?

A
  • autosomal dominant, but it’s rare

- 11 yrs old

24
Q

What is the GI presentation of Peutz-Jeghers Syndrome and the cutaneous presentation?

A
  • multiple GI hamartomatous polyps

- hyperpigmentation of lips, nostrils, buccal mucosa, palms, genitalia, and perianal region (dark blue to brown macules)

25
Q

What are two important severe complications of Peutz-Jeghers Syndrome?

A
  • polyps can initiate intussusception, often fatal
  • marked increase for malignancies: sex cord tumors of the testes, gastric and small intestine cancers, colon, pancreatic, breast, lung, ovarian, and uterine cancers
26
Q

What is the genetic mutation in Peutz-Jeghers Syndrome?

A

loss of fxn mutation in STK11 ( tumor suppressor gene that encodes serine/threonine kinase 11, which regulates cell polarization)

27
Q

Where in the GI tract are polyps of Peutz-Jeghers most common?

A

small intestine

28
Q

What is the gross appearance of Peutz-Jeghers polyps?

A
  • large
  • pedunculated
  • lobulated
29
Q

What is the histologic appearance of Peutz-Jeghers polyps that differentiates them from juvenile polyps?

A

-arborizing network of connective tissue, smooth muscle, lamina propria, and glands … lined by normal intestinal epithelium

30
Q

What is the most common patient population for adenomatous polyps?

A
  • slight male predominance

- present in 30% of people by age 60 yrs

31
Q

Adenomatous polyps are a precursor to what type of cancer?

A

colorectal adenocarcinoma

32
Q

At what age should people start getting screened for colon cancer?

A

45-50

–unless you’re in a high-risk group, then screenings should begin 10 yrs prior to the youngest age at which a relative was diagnosed

33
Q

True or False: colorectal adenomas are characterized by the presence of epithelial dysplasia

A

True

-hallmarks of epithelial dysplasia are: nuclear hyperchromasia, elongation, and stratification

34
Q

True or False: regular surveillance colonoscopy and polyp removal reduce the incidence of colorectal adenocarcinoma

A

True

35
Q

What is the most important characteristic of an adenoma that correlates it with the risk of malignancy?

A
  • size

- 40% of polyps larger than 4 cm had a foci of cancer, but it’s only specific to that polyp, not others

36
Q

What is the inheritance pattern of Familial Adenomatous Polyposis?

A

autosomal dominant (75% are inherited, 25% are de novo mutations)

-somatic mutation in APC gene, which is a negative regulator in the Wnt pathway (chromosomal instability)

37
Q

What extraintestinal manifestation of FAP can be detected at birth?

A

-hypertrophy of the retinal pigment epithelium

38
Q

What is the minimum required number of polyps to be diagnosed as FAP?

A

100, but thousands may be present by teen years

-morphologically indistinguishable from sporadic adenomas

39
Q

What is the cancer risk in FAP?

A

-100% of patients develop colorectal adenocarcinoma (often before age 30), but almost always by age 50

40
Q

What are common extracolonic sites of adenomas in FAP patients?

A
  • hepatopancreatic ampulla

- stomach

41
Q

What is the prophylactic treatment for individuals with the APC mutation?

A

standard therapy is a colectomy

42
Q

What is the most common malignancy of the GI tract?

A

colonic adenocarcinoma

43
Q

What is the pathogenesis pathway for FAP-induced colonic adenocarcinoma?

A
  • -adenoma-carcinoma sequence
  • -chromosomal instability
  • -(APC/Wnt)
  • -KRAS, SMAD2, SMAD4
  • -p53
44
Q

What is the peak age and dietary risk factors for colonic adenocarcinoma?

A
  • -60-70 yrs

- -low fiber, high fat, high refined carbs

45
Q

What drug can be used for pharmacologic chemoprevention of colonic adenocarcinoma?

A

ASA/NSAID’s because they inhibit COX2 which is necessary to produce prostaglandin E2

(prostaglandin E2 promotes epithelial proliferation)

46
Q

What is the pathogenesis pathway for HNPCC (Lynch Syndrome)?

A
  • Microsatellite Instability Pathway

- DNA mismatch repair

47
Q

Where in the colon is cancer in patients with HNPCC (Lynch Syndrome)

A

-ascending colon

48
Q

Where in the body are additional cancer risks for individuals with Lynch syndrome?

A
  • endometrium
  • ovaries
  • stomach
  • brain/CNS
  • urinary tract
49
Q

What is the most common syndromic form of colon cancer?

A

HNPCC

50
Q

The majority of patients with HNPCC (Lynch Syndrome) have mutations in which genes?

A

MLH1

MSH2

51
Q

The chromosomal instability pathway (APC) is associated with what form of adenoma?

A
  • tubular

- villous

52
Q

The microsatellite instability pathway (MLH1, MSH2) is associated with what form of adenoma?

A

-sessile serrated

53
Q

True or False: colonic carcinomas in the distal colon tend to be annular

A

True; “napkin ring” constrictions that narrow the lumen

-proximal colonic carcinomas extend along one wall and rarely cause obstruction

54
Q

How are right-sided colon cancers most often called to attention?

A

-fatigue and weakness due to IDA

“IDA in an older man or a post-menopausal woman is GI cancer until proven otherwise”

55
Q

What is the clinical presentation of left-sided colon cancers?

A
  • occult bleeding
  • change in bowel habits
  • cramping
  • LLQ discomfort
56
Q

What are the two most important factors for prognosis of colonic adenocarcinoma?

A
  • depth of invasion
  • lymph node metastasis

-also poor differentiation and mucinous histology

57
Q

`What is the most common site of metastatic lesions of colonic adenocarcinoma?

A

-liver (due to portal drainage)

GI 2 (6 decks)

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