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GI 2 Exam 1 > S.I./Colon Key Concepts > Flashcards

S.I./Colon Key Concepts Flashcards

1
Q

what is the most common site of gastrointestinal ischemia?

A

the colon

  • lesions can be continuous but are most often segmental and patchy
  • mucosa is hemorrhagic and may be ulcerated
  • bowel wall is thickened by edema that may involve the mucosa or extend into the submucosa and muscularis propria
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2
Q

what is the main cause of transmural infarction?

A

acute arterial obstruction

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3
Q

initially the tissue in intensely congested and dusky to purple-red -> later, blood-tingued mucus or frank blood accumulates in the lumen and the wall becomes edematous, thickened and rubbery

  • coagulative necrosis of the muscularis propria within 1-4 days, and perforation may occur
  • serositis, with purulent exudates and fibrin deosition may be prominent
A

transmural infarction

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4
Q

arterial blood continues to flow for a time, resulting in a less abrupt transition from affected to normal bowel

  • propagation may lead to secondary involvement of the splanchnic bed
  • ultimate result is similar to that produced by acute arterial obstruction because impaired venous drainage eventually prevents oxygenated arterial blood from entering the capillaries
A

mesenteric venous thrombosis

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5
Q

crypts may be hypoproliferative
- inflammatory infiltrates are initially absent in acute ischemia, but neutrophils are recruited within hours of reperfusion

A

ischemic intestine

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6
Q

this is accompanied by fibrous scarring of the lamina propria, and uncommonly, stricture formation

A

chronic ischemia

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7
Q

in both acute and chronic ischemia, bacterial superinfection and enterotoxin release produces what?
- resembles C. diff-associated pseudomembranous colitis

A

pseudomembrane formation

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8
Q

biopsy specimens from the second portion of the duodenum or proximal jejunum (which are exposed to highest concentration of dietary gluten) are diagnostic in what?

A

celiac disease

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9
Q

increased numbers of intraepithelial CD8 T lymphocytes (intraepithelial lymphocytosis), crypt hyperplasia, and villous atrophy

  • loss of mucosal brush-border most likely leads to malabsoprtion
  • increased crypt mitotic activity may limit the ability of absorptive enterocytes to fully differentiate and express proteins necessary for terminal digestion and transepithelial transport
  • increased numbers of plasma cells, mast cells, and eosinophils
A

celiac disease

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10
Q

what is a sensitive (NOT specific) serologic marker of celiac disease?

A

increase in the number intraepithelial lymphocytes, particularly in the villus (even in the absence of epithelial damage and villous atrophy)

NOTE: combination of histology and serology is the most specific diagnosis of celiac

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11
Q

may occur through any weakness or defect in the wall of the peritoneal cavity, including inguinal and femoral canals, the umbilicus and sites of surgical scars

A

abdominal hernias

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12
Q

a segment of intestine that telescopes into the immediately distal segment
- most common cause of intestinal obstruction in children younger than 2 years of age

A

intussusception

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13
Q

most common at the splenic flexure, sigmoid colon and rectum (watershed zones where two arterial circulations terminate)

A

ischemic bowel disease

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14
Q

malformation of submucosal and mucosal blood vessels

- common cause of lower intestinal bleeding in those older than 60

A

angiodysplasia

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15
Q

malabsorption associated with what disease, is the result of pancreatic insufficiency
- leading to inadequate pancreatic digestive enzymes, and deficient luminal breakdown of nutrients

A

cystic fibrosis

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16
Q

immune-mediated enterophathy, triggered by the ingestion of gluten-containing grains
- malabsorptive diarrhea is due to loss of brush border surface area, including villous atrophy, and possibly deficient enterocyte maturation as a result of immune-mediated epithelial damage

A

celiac disease

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17
Q

prevalent in areas with poor sanitation

- estimated to affect more than 150 million children worldwide, may contribute to a large number of deaths

A

environmental enterophathy

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18
Q

osmotic diarrhea due to inability to break down or absorb lactose
- AR form is rare and severe, acquired form usually presents in adulthood and is common

A

lactase deficiency

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19
Q

X-linked disorder characterized by severe persistent diarrhea and autoimmune disease that is caused by mutation in FOXP3 resulting in defective function of regulatory T cells

A

autoimmune enteropathy

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20
Q

rare AR disease due to a mutation in microsomal triglyceride transfer protein that is required for enterocytes to process and secrete triglyceride-rich lipoproteins

A

abetalipoproteinemia

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21
Q

comma-shaped, flagellated, gram-neg org

  • dx by stool culture since biopsy findings are nonspecific
  • acute self-limited colitis
  • mucosal and intraepithelial meutrophil infiltrates are prominent, particularly within superficial mucosa
  • cryptitis (neutrophil infiltration of crypts)
  • crypt abscess (accumulation of luminal neutrophils)
  • CRYPT ARCHITECTURE IS PRESERVED
A

Campylobacter

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22
Q

up to 40% of what syndrome are associated with campylobacter infection?

A

Guillain-Barre syndrome

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23
Q

most prominent in the left colon, but ileum may be involved (due to Peyer patches)

  • mucosa is hemorrhagic and ulcerated
  • pseudomembranes may be present
  • tropism for M cells, so aphthous-appearing ulcers may occur, similar to those seen in Crohn’s disease
A

Sigella infection

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24
Q

this sickness causes infection of Peyer patches in the terminal ileum

  • enlarged, sharply delineated, plateau-like elevations up to 8cm in diameter
  • draining lymph nodes enlarged
  • neutrophils accumulate within the superficial lamina propria
  • macrophages containing bacteria, red cells, and nuclear debris mix with lymphocytes and plasma cells in the lamina propria
  • mucosal damage creates oval ulcers, oriented along the axis of the ileum, that may perforate
A

Typhoid fever

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25
Q

this sickness causes an enlarged, soft spleen with uniformly pale red plump, follicular markings and prominent phagocyte hyperplasia
- liver shows small randomly scattered foci of parenchymal necrosis in which hepatocytes are replaced by macrophage aggregates, called typhoid nodules

A

typhoid fever

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26
Q

infection of this organism preferentially involves the ileum, appendix, and right colon

  • organisms multiply extracellularly in lymphoid tissue, resulting in lymph node and Peyer patch hyperplasia and bowel wall thickening
  • mucosa overlying lymphoid tissue may become hemorrhagic, and aphthous-like erosions and ulcers may develop, along with neutrophil infiltrates and granulomas
A

Yersinia

NOTE: can be confused with Crohn disease

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27
Q

adherent layer of inflammatory cells and debris at sites of colonic mucosal injury

  • surface epithelium is stripped down, and the superficial lamina propria contains a dense infiltrate of neutrophils and occasional fibrin thrombi within capillaries
  • superficially damaged crypts are distended by a mucopurulent exudate that forms an eruption reminiscent of a volcano
A

C. diff-associated colitis with pseudomembranes

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28
Q

dense accumulation of distended, foamy macrophages in the small intestinal lamina propria

  • macrophages contain periodic acid-Schiff (PAS)-positive, diastase-resistant granules that represent lysosomes stuffed with partially digested bacteria
  • intact rod-shaped bacilli can also be identified by electron microscopy
  • villous expansion caused by dense macrophage infiltrate imparts a shaggy gross appearance to the mucosal surface
A

Whipple disease

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29
Q

when would you see macrophages accumulating within mesenteric lymph nodes, synovial membranes of affected joints, cardiac valves, and the brain?

A

Whipple disease

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30
Q

org that secretes a preformed toxin that causes massive chloride secretion
- water follows resulting is osmotic gradient -> secretory diarrhea

A

Vibrio cholerae

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31
Q

most common bacterial enteric pathogen in developed countries, also causes traveler’s diarrhea
- most isolates are noninvaside

A

Campylobacter jejuni

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32
Q

often triggered by antibiotic therapy that allows colonization by this organism

  • releases toxins that disrupt epithelial function
  • associated inflammatory response includes characteristic volcano-like eruptions of neutrophils from colonic crypts that spread to form mucopurulent pseudomembranes
A

C. difficile

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33
Q

very common cause of self-limited diarrhea both in adults and children
- spreads from person to person in sporadic cases and by water in epidemic cases

A

norovirus

34
Q

most common cause of severe childhood diarrhea and diarrheal mortality worldwide
- diarrhea is caused by a loss of mature enterocytes, resulting in malabsorption as well as secretion

A

rotavirus

35
Q

what are the most common sites involved in Crohn disease?

A

terminal ileum, ileocecal valve, and cecum

36
Q

multiple, separate, sharply delineated areas of disease, results in skip lesions

  • strictures are common
  • aphthous ulcer may progress -> elongated, serpentine ulcers oriented along the axis of the bowel
  • edema and loss of normal mucosal texture
  • patchy distribution results in a coarsely textured COBBLESTONE appearance in which diseased tissue is depressed below the level of normal mucosa
  • Fissures develop between mucosal folds and may extend deeply to become fistula tracts
A

Crohn disease

37
Q

what is a hallmark of Crohn disease that is found in 35% of cases and may occur in areas of active disease, OR uninvolved regions in any layer of the intestinal wall

A

noncaseating granulomas

38
Q

always involves the rectum and extends proximally in a continuous fashion to involve part or all of the colon

  • NO skip lesions, NO mural thickening, serosal surface is normal, NO strictures, NO granulomas
  • inflammation can damage the muscularis prorpia and disturb neuromuscular function -> TOXIC MEGACOLON
  • colonic mucosa may be slightly red and granular or have extensive broad-based ulcers that are aligned along the long axis of the colon, but do NOT replicate the serpentine ulcers of Crohn’s
  • pseudopolyps seen
  • may lead to mucosal atrophy, with flat and smooth mucosal surface that lacks normal folds
  • inflammatory process is diffuse and generally limited to the mucosa and superficial submucosa
A

UC

39
Q

what is pancolitis?

A

UC that includes the entire colon

40
Q

small, flask-like outpouchings (usually 0.5-1cm in diameter) that occur in a regular distribution alongside the teniae coli

  • thin wall composed of flattened or atrophic mucosa, compressed submucosa and attenuated or absent muscularis propria
  • hypertrophy of the circular layer of muscularis propria is common
  • may cause segmental diverticular disease-associated colitis, fibrotic thickening in and around the colonic wall, or stricture formation (803)
A

colonic diverticula

41
Q

chronic, relapsing abdominal pain, bloating, and changes in bowel habits without obvious gross or histologic pathology
- psychologic stress, diet, gut microbiome, abnormal GI motility, and increased enteric sensory responses to GI stimuli

A

IBS

42
Q

umbrella term for UC and CD
- thought to arise from a combination of alterations in host interactions with intestinal microbiota, intestinal epithelial dysfunction, and aberrant mucosal immune responses

A

IBD

43
Q

limited to the colon, is continuous from the rectum and ranges from only rectal disease to pancolitis
- neither skip lesions nor granulomas present

A

UC

44
Q

most commonly affects the terminal ileum and cecum, but any site with gastrointestinal tract can be involved
- skip lesions and noncaseating granulomas are common

A

CD

45
Q

risk of what increases in IBD patients who have had colonic disease for more than 8-10 years

A

epithelial dysplasia and adenocarcinoma

46
Q

two forms of microscopic colitis, both of which cause chronic watery diarrhea
- intestines are grossly normal, and the diseases are identified by their characteristic histologic features

A

collagenous and lymphocytic colitis

47
Q

common disease of the sigmoid colon, in western populations older than age 60
- causes include low fiber diets, colonic spasm, and unique anatomy of the colon

A

diverticular disease

48
Q

most commonly found in the left colon, typically less than 5mm

  • smooth nodular protrusions of the mucosa, often on the crests of mucosal folds
  • may occur singly but are more frequently multiple, particularly in the sigmoid colon and rectum
  • histo: composed of goblet cells and absorptive cells -> delayed shedding of these cells leads to crowding that creates the serrated surface architecture = hallmark
A

hyperplastic polyps

49
Q

less than 3cm

  • pedunculated, smooth-surfaced, reddish lesions with characteristic cystic spaces apparent after sectioning
  • dilated glands filled with mucin and inflammatory debris
  • remainder of polyp composed of lamina propria expanded by mixed inflammatory infiltrates
A

juvenile polyps

50
Q

most common in the small intestine, but may occur in stomach, colon, bladder or lungs

  • polyps are large and pedunculated with a lobulated contour
  • histo: characteristic arborizing network of connective tissue, smooth muscle, lamina propria, and glands lined by normal-appearing intestinal epithelium
A

Peutz-Jeghers polyps

51
Q

what is helpful in distinguishing polyps of Peutz-Jeghers syndrome from juvenile polyps?

A

the arborization and presence of smooth muscle intermixed with lamina propria (Peutz-Jeghers)

52
Q

vary in size from .3-10cm, can be pedunculated or sessile (no peduncle), with the surface having a texture resembling velvet or a raspberry

  • histo hallmark: nuclear hyperchromasia, elongation, and stratification
  • prominent nucleoli, eosinophilic cytoplasm, and a reduction in the number of goblet cells
  • epithelial cells fail to mature as they migrate from crypt to surface
A

epithelial adenoma

53
Q

histologically similar to hyperplastic polyps, but are more commonly found in the right colon

  • malignant, but lack cytologic features of dysplasia that are present in other adenomas
  • serrated architecture throughout the full length of the glands, including crypt base, crypt dilation, and lateral growth
A

sessile serrated adenomas

54
Q

occurs when dysplastic epithelial cells breach the basement membrane to invade the lamina propria or muscularis mucosae

  • little or no metastatic potential (b/c no lymphatic channels in colonic mucosa)
  • polypectomy is usually curative
  • invasion beyond the muscularis mucosa -> invasive adenocarcinoma and carries risk of metastasis
A

intramural carcinoma

55
Q

what is the “first hit” according to the Knudson hypothesis?

A

inactivation of APC at 5q21 in colonic epithelium

56
Q

what does the “second hit” cause in colonic epithelium?

A

loss of the intact second copy of APC

57
Q

what does mutation of KRAS at 12p12 lead to?

A

protooncogene mutations

58
Q

mutations of:

  • TP53 at 17p13
  • LOH at 18q21
  • SMAD 2 and 4
A

homozygous loss of additional cancer suppressor genes and over expression of COX-2
= EMERGENCE OF CARCINOMA

59
Q

what is more critical to mutations than occurrence in a specific order?

A

accumulation of different mutations

60
Q

what do mutations of telomerase and “many other” genes lead to?

A

additional mutations, gross chromosomal alterations

= full on carcinoma

61
Q

distributed approximately equally over the entire length of the colon

  • proximal colon: often grow as polypoid, exophytic masses that extend along the wall of the caliber cecum and ascending colon
  • distal colon: tend to be annular lesions that produce “napkin ring” construction and luminal narrowing
A

adenocarcinoma

  • some are poorly differentiated and form few glands
  • others may produce abundant mucin that accumulates within the intestinal wall => poor prognosis
  • some may also be composed of signet-ring cells that are similar to those in gastric cancer, or may display features of neuroendocrine differentiation
62
Q

what is responsible for the characteristic firm consistency of colonic adenocarcinoma?

A

the invasive component of the tumor elicits a strong stromal desmoplastic response

63
Q

mutations in what genes leads to sessile serrated adenoma?

A

MLH1, MSH2 (MSH6, PMS1, PMS2)

64
Q

mutations in what genes leads to carcinoma (from adenoma)?

A

TGF-b, BAX, BRAF, TCF4, IGFR

65
Q

benign epithelial proliferations most commonly found in the left colon and rectum
- no malignant potential, must be distinguished from sessile serrated adenomas

A

hyperplastic polyps

66
Q

these form as a result of chronic cycles of injury and healing

A

inflammatory polyps

67
Q

these occur sporadically or as part of a genetic disease (juvenile polyposis, Peutz-Jeghers Syndrome) -> associated with incrased risk of malignancy

A

hamartomatous polyps

68
Q

benign epithelial neoplastic polyps of the intestines

- hallmark: cytologic dysplasia (precursors of colonic adenocarcinoma)

A

adenoma

69
Q

in contrast to adenomas, these lack cytologic dysplasia and share morphologic features with hyperplastic polyps

A

sessile serrated adenomas

70
Q

what are the two most common forms of familial colon cancer?

A

familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC)

71
Q

caused by APC mutations

- patients typically have more than 100 adenomas and develop colon cancer before the age of 30

A

FAP

72
Q

caused by mutations in DNA mismatch repair enzymes
- patients have far fewer polyps and develop cancer at older ages than FAP, but still younger than those with sporadic colon cancer

A

HNPCC

73
Q

nearly all colonic cancers are what? what are the two most important prognostic factors?

A

adenocarcinomas

- depth of invasion and the presence/absence of lymph node metastases

74
Q

sub-serosal vessels are congested and there is a modest perivascular neutrophilic infiltrate within all laters of the wall
- inflammatory reaction transforms the normal glistening serosa into a dull, granular, erythematous surface

A

acute appendicitis

75
Q

what does the diagnosis of acute appendicitis require?

A

neutrophilic infiltration of the muscularis propria

76
Q

as the process continues, focal abscesses may form within the wall

A

acute suppurative appendicitis

77
Q

further compromise leads to areas of hemorrhagic ulceration and gangrenous necrosis that extends to the serosa, which can be followed by rupture and suppurative peritonitis

A

acute gangrenous appendicitis

78
Q

collateral vessels that develop secondary to persistently elevated venous pressure within the hemorrhoidal plexus
- also occur in portal HTN

A

hemorrhoids

79
Q

most common in children and adolescents

- thought to be initiated by increased intraluminal pressure and compromised venous outflow

A

acute appendicitis

80
Q

what is the most common tumor of the appendix?

A

benign carcinoid

81
Q

what can cause pseudomyxoma peritonei?

A

peritoneal dissemination of mucinous tumors

82
Q

what is the cellular inflammatory response primarily composed of?

A

dense collection of neutrophils and fibrinopurulent debris that coat the viscera and abdominal wall
- serous or slightly turbid fluid begins to accumulate and become suppurative as infection progresses

GI 2 Exam 1 (22 decks)

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