Colon Flashcards

1
Q

What percent of the lamina propria is inflammatory cells in normal colonic mucosa?

A

50%

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2
Q

T/F- water must cross the surface epithelium and collagen table to enter the capillaries of the superficial lamina propria

A

true

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3
Q

Hirschsprung disease is associated with what genetic abnormality?

A

Down syndrome

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4
Q

T/F- Although males get hirschsprung disease more frequently than females, females are more severely affected

A

true

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5
Q

A neonate presents with failure to pass meconium in the immediate postnatal period. What is most likely diagnosis?

A

Hirschsprung disease

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6
Q

Name 5 common causes of acute colitis

A
Bacterial
viral (norovirus, rotavirus, adenovirus)
Protozoal and parasitic
Toxin
Ischemic
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7
Q

Name 4 causes of chronic colitis

A

Ulcerative colitis, Crohn’s disease

Lyphocytic colitis, collagenous colitis

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8
Q

T/F- crypt architecture is not preserved in acute bacterial colitis

A

False, it is preserved

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9
Q

Name 2 examples of toxin damage causing colitis

A
  1. C. dificile (pseudomembranous colitis), most commonly after 3rd gen cephalosporin
  2. Enterohemorrhagic E. Coli (fecal contamination, raw hamburger, sprouts, apples picked in pasture)
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10
Q

What is the pseudomembrane composed of?

A

fibrin, mucin, neutrophils

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11
Q

ichemic colitis most often occurs in older patients with vascular disease and presents with abdominal pain, nausea, vomiting, bloody stools. Where are the watershed zones where this most often occurs?

A

splenic flexure, sigmoid colon, rectum

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12
Q

T/F- Irritable bowel syndrome will show gross and microscopic abnormalities

A

False, it will be normal

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13
Q

In chronic colitis, is crypt architecture and branching preserved or distorted?

A

distorted and irregular crypts are signs of chronicity

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14
Q

Compare ulcerative colitis and Crohns disease

A
  • UC: diffuse, superficial (only mucosal layer affected), colon only
  • Crohns: focal (lymphoid aggregates or granulomas), transmural (mucosa through to serosa), anywhere in the GI tract (especially ileum and colon)
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15
Q

If you see a terminal ileum with a thick wall, stricture, and linear ulcer what is it most likely?

A

Crohn’s disease

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16
Q

Does Crohn’s or ulcerative colitis carry a greater risk for cancer?

A

Ulcerative colitis

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17
Q

The term microscopic colitis encompasses what two diseases?

A
  • Lymphocytic and collagenous colitis

- these will appear normal endoscopically

18
Q

T/F- in collagenous colitis you will see microscopically normal crypt architecture, increased superficial chronic inflammation of the lamina propria, increased numbers of intraepithelial lymphocytes

A

False, that is lymphocytic colitis

19
Q

What will you see histologically in collagenous colitis?

A

A thickened, irregular subepithelial collagen layer entrapping capillaries and cells

20
Q

Is diverticulosis related to the western diet?

A

yes

21
Q

Although only 20% of patients are symptomatic for diverticulosis, what will they present with?

A

cramping, lower abdominal discomfort, constipation/diarrhea, distention

22
Q

Where is the weakest spot in the muscle that allows for diverticuli to form?

A

where
nerves and vessels
penetrate

23
Q

Can diverticulitis perforate?

A

yes

24
Q

T/F- Inflammatory polyps are often associated with IBD, but also seen with ischemic colitis, infectious colitis, necrotizing enterocolitis

A

true

25
Q

Juvenile polyps often present with rectal bleeding or prolapse of polyp through the rectum. Does polyposis syndrome increase risk of malignancy?

A

risk of upper and lower GI malignancies

26
Q

For Peutz-Jeghers syndrome, what is the mode of inheritance? Symptoms? Complications?

A
  • Autosomal dominant
  • Mucocutaneous pigmentation
  • polyps of the upper and lower GI tract with increased risk of carcinoma, pancreatic, breast, and ovarian carcinomas
27
Q

Hyperplastic polyps are commonly found where? Are they malignant or benign?

A
  • Left colon and rectum

- Benign

28
Q

Do sessile, serrated adenomas/polyps have malignant potential? Where are they commonly found?

A

yes, most often on right side of colon

29
Q

How do you distinguish a sessile serrated adenoma from a hyper plastic polyp?

A

Sessile serrated adenoma has normal base, hyper plastic polyp has abnormal base

30
Q

Name three different types of adenomas

A
  1. tubular
  2. tubulovillous
  3. villous
31
Q

Are adenomas a precursor to colon cancer?

A

yes “These are the MAJOR precursor to colon cancer”

32
Q

Once an adenoma passes ______ layer it becomes invasive

A

muscularis mucosae

33
Q

T/F- adenocarcinoma is rare in western populations

A

False, VERY common in western populations and account for 3% of cancer deaths

34
Q

Are adenocarcinomas related to dietary factors?

A

yes, low intake of vegetable fiber and high intake of refined carbohydrates and fat

35
Q

Is the preclinical phase of colorectal cancer long or short?

A

long (10 years)

36
Q

What lesion do the vast majority of colorectal cancers begin with?

A

tubular adenoma

37
Q

T/F- The majority of colorectal adenocarcinomas are associated with familial syndromes such as FAP, HNPCC, juvenile polyposis coli

A
False, 90% are sporadic! 
FAP: 1%
HNPCC: 5%
Juvenile Polyposis coli: 1%
IBD: 1%
38
Q

Familial adenomatous polyposis is an autosomal dominant mutation in what gene?

A

APC (adenomatous polyposis coli) gene

39
Q

How many adenomas would you find in a colon of a person with FAP?

A

at least 100, often more than 1000

40
Q

T/F- colorectal adenocarcinoma will develop in 100% of untreated FAP patients

A

true

41
Q

HNPCC includes lynch syndrome I and II, what is the difference?

A

-Lynch Syndrome I – confined to colorectum

-Lynch syndrome II – colorectal carcinoma associated with extra-colonic cancers
(Endometrium, stomach, small bowel, hepatobiliary tract, pancreas, ovary, urinary tract, brain (GBM), sebaceous neoplasms of the skin (Muir-Torre syndrome))

42
Q

Is HNPCC autosomal dominant or recessive? What type of gene does this affect?

A

dominant

DNA mismatch repair gene (risk of colorectal cancer is 70% by age 70)