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GI2 E1 > small intestine and colon- NON INFECTIOUS > Flashcards

small intestine and colon- NON INFECTIOUS Flashcards

robbins

1
Q

___ is the most common site of GI neoplasia in the western world

A

the colon

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2
Q

what part of the GI tract is most often involved in obstruction

A

the small intestine bc of its already narrow lumen

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3
Q

what are clinical manifestations of intestinal obstruction

A

abdominal pain and distension, vomiting, constipation

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4
Q

what is the etiology of hernias

A

weakness or defects in the abdominal wall leading to protrusion of the serosa lined pouch of peritoneum

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5
Q

acquired hernias typically occur ____ly, via the __ and ___ canals, ___, or at sites of ____

A

anteriorly
inguinal, femoral
umbilicus
surgical scars

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6
Q

___ are the most common cause of intestinal obstruction in the US, while ___ are the most frequent cause of intestinal obstruction in the world. They occur because of visceral protrusion and are most frequently associated with _______

A

adhesions, hernias

inguinal hernias

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7
Q

pressure at the neck of the hernial pouch may _____ –> ___—> permanent ____ –> (over time) ___ and ____

A

impair venous drainage of the entrapped viscuss
stasis and edema
incarceration
strangulation

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8
Q

what etiologies can lead to adhesion between bowel segments, abdominal wall, or operative sites

A

surgical procedure
infection
peritoneal inflammation (endometriosis)

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9
Q

what is the etiology of an internal herniation

A

there is an adhesion between small bowel creating a closed loop through which other viscera may slide and become entrapped

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10
Q

twisting of a loop bowel about its mesenteric point of attachment, presenting with both obstruction and infarction

A

volvulus

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11
Q

in what part of the GI tract is a volvulus most often

A

sigmoid colon

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12
Q

segment of the intestine, constricted by a wave of peristalsis, telescopes into the immediately distal segment. when propelled by peristalsis, pulls the mesentery along.

A

intussusception

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13
Q

most common cause of intestinal obstruction in children younger than 2

A

intussusception

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14
Q

what etiologies are associated with intusussception

A

idiopathic
viral infection
rotavirus vaccine
reactive hyperplasia of peyer patches

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15
Q

in the rare event that intussuseption occurs in older kids/adults, its a result of

A

intraluminal mass or tumor that serves as the initiating point of traction

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16
Q

how does one diagnose intussusception

A

contrast enemas (diagnostic and therapeutic)
air enemas
if a mass is present, surgery

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17
Q

(colon) while mucosal or mural infarctions can follow acute or chronic ____, transmural infarction is typically caused by ______

A

hypoperfusion

acute vascular obstruction

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18
Q

(colon) causes of acute arterial obstruction

A

severe atherosclerosis at the origin of the mesenteric vessels, aortic aneurysm, hypercoagulable states, oral contraceptive use, embolization of cardiac vegetations

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19
Q

(colon) describe the two phases of intestinal response to ischemia

A
  1. initial hypoxic injury= at the onset of compromise, epithelial cells lining the intestine are relatively resistant to transient hypoxia
  2. reperfusion injury= initiated by restoration, can trigger multiorgan failure, leakage of gut/lumen bacterial products (i.e lipopolysachs into the systemic circulation, free radical production, Nø infiltrate
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20
Q

what are the watershed zones in the colon

A

splenic flexture (SMA& IMA)

sigmoid colon (IMA, pudendal, iliac)

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21
Q

ischemic ds at a watershed zone in the colon can present as what

A

focal colitis (of splenic flexture or rectosigmoidal colon)

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22
Q

(colon) the hairpin turn of intestinal capillaries makes ____ particularly vulnerable to ischemic injury, relative to the ___

A

surface epithelium

crypts

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23
Q

(colon) pattern of surface epithelial atrophy/necrosis with normal/hyperproliferative crypts is the morphologic signature of

A

ischemic intestinal ds

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24
Q

GI ischemia is most often what pattern

A

segmental and patchy

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25
Q

(colon) sharply defined ischemia with intenesly congested and dusky to purple-red bowel–> later is blood tinged mucus or frank blood accumulation

A

transmural infarction

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26
Q

(colon) in ____ _____ ____. the arterial blood flow makes the transition from normal to affected bowel slower. propagation can lead to secondary involvement of the ____. impaired drainage will eventually prevent ____ blood from entering

A

mesenteric venous thrombosis
splanchnic bed
oxygenated

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27
Q

in the setting of colonic ischemia, bacterial superinfection and enterotoxin release may induce __ ___, resembling C. Dif

A

pseudomembrane formation

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28
Q

in what population will you find ischemic ds of the colon

A

women, older than 70, coexisting cardiac or vascular ds

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29
Q

what things can precipitate colonic ischemia

A

therapeutic vasoconstrictors, cocaine, endothelial damage, CMV or E Coli O157:H7, strangulated hernia, or vascular compromise prior to surgery

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30
Q

what is the clinical presentation of acute colonic ischemia

A

sudden onset of cramping, left lower abdominal pain, a desire to defecate, passage of blood or bloody diarrhea

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31
Q

when is surgery indicated with acute colonic ischemia

A

peristaltic sounds diminish/disappear, paralytic ileus, guarding/rebound

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32
Q

describe the prognosis with acute colonic ischemia

A

10% in the first 30 days with appropriate management

doubled in patients with R sided colonic ds

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33
Q

____ might be the initial presentation of more severe ds, including caused by acute occlusion of ______

A

right sided colonic ischemia

SMA

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34
Q

poor prognostic indicators for acute colonic ischemia

A

R sided ischemia
COPD
sx persistance for more than 2 weeks

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35
Q

clinical presentation of mucosal and mural infarction of the colon

A

nonspecific abdominal sx, intermittent bloody diarrhea and intestinal obstruction

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36
Q

clinical presentation of chronic ischemia of the colon

A

can masquerade as inflammatory bowel ds, with episodes of bloody diarrhea interspersed with periods of healing

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37
Q

clinical presentation of CMV infection

A

ischemic GI disease due to viral tropism for endothelial cells

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38
Q

clinical presentation of radiation enterocolitis

A

acute: anorexia, abdominal cramps, malabsorptive diarrhea
chronic: indolent, inflammatory entero colitis

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39
Q

clinical presentation of necrotizing enterocolitis

A

acute transmural necrosis in neonates born premature or of low birth weight

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40
Q

a lesion characterized by malformed submucosal and mucosal blood vessels

A

angiodysplasia

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41
Q

where in the GI tract will you most likely find angiodysplasia

A

cecum or right colon

due to the greatest wall tension in the cecum

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42
Q

in what population will you likely find angiodysplasia

A

> 60 yo

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43
Q

describe the pathogenesis of angiodysplasia

A

normal distension and contraction may occlude the submucosal veins–> focal dilation and tortuosity

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44
Q

(colon) ectatic nests or tortuous veins, venules, or capillaries

A

angiodysplasia

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45
Q

describe complications associated with angiodysplasia

A

limited injury can lead to significant bleeding because there are only two thin walls protecting it

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46
Q

(colon) malabsorption typically presents as ____, with a clinical presentation of ___, and a hallmark presentation of ___

A

chronic diarrhea

weight loss, anorexia, abd distension, borborygmi (rumbling in tummy), M wasting, diarrhea + dysentery, flatus, abd pain

steatorrhea

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47
Q

the most common malabsorptive disorders in the US

A

pancreatic insufficiency, celiac ds, crohn

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48
Q

what is the etiology of malabsorption

A

disturbance in at least 1 of the 4 phases of nutrient absorption

  • intraluminal digestion (break down)
  • terminal digestion (hydrolysis of carbs and peptides in the brush border)
  • trans-epithelial transport (transported across and processed within the small intestine epithelium)
  • lymphatic transport of absorbed lipids
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49
Q

what complications can result from malabsorption

A

anemia/mucositis (x VitB12, folate, pyridoxine absorption)
bleeding (x vit k absorbed)
osteopenia
tetany

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50
Q

describe secretory diarrhea

A

isotonic stools

persist during fasting

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51
Q

describe osmotic diarrhea

A

occurs with lactase deficiency
more than 50 mOsm more concentrated than plasma
abates with fasting

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52
Q

describe malabsorptive diarrhea

A

associated with steatorrhea

relieved by fasting

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53
Q

describe exudative diarrhea

A

purulent, bloody stools

continue during fasting

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54
Q

what parts of digestion are altered by celiac ds

A

terminal digestion and trans-epithelial transport

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55
Q

what part of digestion is altered by chronic pancreatitis

A

intraluminal digestion

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56
Q

what part of digestion is altered by cystic fibrosis

A

intraluminal digestion

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57
Q

what part of digestion is altered by primary bile acid malabsorption

A

intraluminal digestions, trans-epithelial transport

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58
Q

what part of digestion is altered by whipple disease

A

lymphatic transport

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59
Q

what part of digestion is altered by abetalipoproteinemia

A

trans-epithelial transport

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60
Q

what part of digestion is altered by gastroenteritis

A

terminal digestion and trans-epithelial transport

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61
Q

what part of digestion is altered by IBD

A

intraluminal digestion, terminal digestion, transepithelial transport

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62
Q

two main sx related to GI pathology are

A

abd pain

hemorrhage

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63
Q

function of a goblet cell

A

to produce mucus

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64
Q

which part of the GI tract has villi on histology

A

small intestine

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65
Q

what is the most common CA type of the GI tract

A

adenocarcinoma

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66
Q

what is the function of a lacteal

A

fat absorption

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67
Q

air filled space in the bowel is indicative of what

A

obstruction

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68
Q

relate the etiology of cystic fibrosis to the GI tract

A

absence of CFTR –> defects in Cl- and HCO3 secretion –: defective luminal hydration, intestinal obstruction –> formation of pancreatic intraductal concretions

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69
Q

what are some GI complications with cystic fibrosis

A

eventual exocrine pancreatic insufficiency

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70
Q

treatment for cystic fibrosis sx in the gi tract

A

oral CFTR enzyme supplement

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71
Q

describe the etiology of celiac ds

A

gliadin (a fraction of gluten)–> induce epithelial cells to express IL-15–> activates CD8 intraepithelial lymphocytes–> NKG2D receptor for MIC-A are both activated, with the NKG2D expressing lymphocytes attaching the enterocytes that express MIC-A –> epithelial damage

gliadin also interacts w HLA-DQ2 and HLA-DQ8 to stimulate CD4 T cells to produce cytokines that contribute to tissue damage

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72
Q

what compound contains most of the ds-producing components in celiac ds

A

gliadin

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73
Q

what other pathologies are associated with celiac ds

A

HLA-DQ2, HLA-DQ8
genes involved in immune regulation and epithelial function
T1DM, thyroiditis, sjogren, igA nephropathy
ataxia, autism, depression, epilepsy, down syndrome, turner syndrome

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74
Q

biopsy of what part of the GI tract will allow for celiac ds diagnosis? what will you see?

A

second portion of the duodenum or proximal jejunum,

inreased CD8 cells, crypt hyperplasia, villous atrophy, loss of mucosal/brush border surface area,

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75
Q

in what population do you see celiac ds present in

A

adults 30-60 y.o, though many remained undiagnosed for a long time
women (accentuated effects w menstruation)

between 6 and 24 months,

76
Q

sx with celiac ds in adults

A

chronic diarrhea, bloating, chronic fatigue, anemia

77
Q

sx with celiac ds in children

A

irritability, abd distension, anorexia, chronic diarrhea, failure to thrive, weight loss, M wasting

78
Q

what extraintestinal complaints are associated w celiac ds

A

arthritis/joint pain, aphthous stomatitis, iron deficiency anemia, delayed puberty, short

dermatitis herpetiformis: IgA Abs cross react to cause prura, microabscesses, and subepidermal blisters

79
Q

what is the trx for celiac ds

A

gluten free diet

80
Q

what diagnostic tests are performed for celiac ds

A

serologic test
most sensitive= igA abs against tissue transglutaminase
HLA-DQ2/8 (absence is highly negative predictive value)

81
Q

individuals w celiac ds have a higher than normal rate of ____, with the most associated being _______

A

malignancy

enteropathy-associated T cell lymphoma

82
Q

what hx is consistent with environmental enteropathy

A

poor sanitation, developing countries/impoverished communities
malabsorption/malnutrition
stunted growth

83
Q

describe the etiology environmental enteropathy

A

defective intestinal mucosal immune function

chronic exposure to fecal pathogens

repeated bouts of diarrhea within the first 2-3 years of life

84
Q

what is the prognosis of environmental enteropathy

A

can’t rally give abx or nutritional supplements

there is irreversible loss of physical development and cognitive deficits

85
Q

clinical presentation of autoimmune enteropathy

A

severe, persistent diarrhea

86
Q

in what population does autoimmune enteropathy present

A

young children

87
Q

what is IPEX

A

a severe familial form of autoimmune enteropathy

Immune dysfunction
Polyendocrinoapthy
Enteropathy
X linked

88
Q

what gene mutations are associated with autoimmune enteropathy

A

FOXP3 on CD4 cells
auto-ab to enterocytes and goblet cells
Abs to parietal/islet cells

89
Q

what is the trx for autoimmune enteropathy

A

immunosuppression (cyclosporine)

hematopoietic stem cell transplant

90
Q

lactase is located in the ..

A

apical brush border of villous absorptive epithelial calls

91
Q

what is the clinical presentation of congenital lactase deficiency

A

explosive diarrhea with watery, frothy stools and abd distension upon milk ingestion

92
Q

what is the clinical presentation of acquired lactase deficiency

A

=just a downregulation after an enteric viral or bacterial infection and may resolve over time

abd fullness, diarrhea, flatulence due to fermentation of the unabsorbed sugars made by bacteria

93
Q

what is abetalipoproteinemia, what is the etiology

A

an inability to secrete TG-rich lipoproteins

mutation in MTP, that catalyzes transfer of lipids to be exported, will lead to intracellular lipid accumulation –> vacuolization of small intestine epithelial cells

94
Q

oid red-O stain on histology

A

for lipids.. abetalipoproteinemia

95
Q

what population presents with abetalipoproteinemia and what is the clinical presentation

A

infancy

failure to thrive, diarrhea, and steatorhhea

96
Q

complete absence of all plasma lipoprotiens containing apolipoprotein B, decreased Vit ADEK absorption, acanthocytic red cells (burr cells) in peripheral blood smears

A

apolipoproteinemia

97
Q

chronic, relapsing abdominal pain, bloating, and changes in bowel habits

A

IBS

98
Q

the two types of IBS are ___ or ____ predominant

A

constipation or diarrhea

99
Q

2 etiologies that lead to diarrhea predominant IBS

A

increased colonic contractions

excess bile acid synthesis

100
Q

gene mutations associated with IBS

A

serotonin reputake transporters, cannbinoid receptors, TNF related inflammatory mediators,

5HT3 receptor

101
Q

effective trxs in IBS

A

5HT3 receptor antagonists
opioids
psychoactive drugs

102
Q

population associated with IBS

A

20-40 yo females

103
Q

population associated with IBD

A

teens and early 20s, females, caucasians, ashkenazi jews

104
Q

compare and contrast Crohn and ulcerative colitis

types of lesions
morphology

A

CD= skip lesions
transmural inflammation, ulcerations, fissures

UC= continuous from colon to rectum
pseudopolyps
ulcers

105
Q

hygiene hypothesis relates to the fact that _____ infections can prevent IBD development

A

helminths

106
Q

genetic mutations associated with crohn

A

NOD2–> NF-KB
ATG16L1
IRGM

107
Q

perianal fistrulas in which IBD

A

only CD

108
Q

fat/vitamin malabsorption in which IBD

A

CD

109
Q

malignant potential in which IBD

A

UC, CD if there is colonic involvement

110
Q

recurrence post surgery in which IBD

A

CD

111
Q

toxic megacolon in which IBD

A

UC

112
Q

in crohn disease, see polymorphism in ___ receptors leading to activation of ____

A

IL23

Th17

113
Q

pro-inflammatory cytokines involved in pathogenesis of IBD

A 
TNF
IFNgamma
IL13
IL10
TGF B
114
Q

____ mutations lead to epithelial dysfunction in crohn

A

NOD2

115
Q

____ mutations lead to epithelial dysfunction in ulcerative colitis, as well as ___ mutations which are strongly associated with maturity onset DM of the young (MODY)

A

ECM1,

HNFA

116
Q

Ab against bacterial flagellin are most common in which IBD

A

CD

117
Q

clinical presentation of crohn onset

A

non-bloody diarrhea, fever, rectal abscess, small intestinal and colonic ulcers and fistulas beginning at age 20

118
Q

most common site involved with crohn

A

terminal ileum, ileocecal valve, cecum

119
Q

colon with aphthous ulcer/cobblestone appearance/ fissures/ creeping fat

crypt abscess with distortion of mucosal architecture

paneth metaplasia
noncaseating granulomas

A

crohn ds

120
Q

intermittant mild bloody diarrhea, fever, abd pain with RLQ pain, fever

reactivation with triggers, onset associated with the initiation of smoking

A

crohn

note: opposite of UC, where smoking actually relieves sx

121
Q

complications of crohn (5)

A
  • iron deficiency anemia
  • serum protein loss, hypoalbuminemia
  • fibrosing stricutres –> require surgery
  • fistulae–> between loops of bowel, abd, perianal skin, bladder, vagina
  • perforations+peritoneal abscesses
122
Q

extra-intestinal manifestations of crohn only

A

erythema nodosum
clubbing
pericholangitis

123
Q

extraintestinal manifestations of crohn and ulcerative colitis

A 
migratory polyarthritis
sacroiliitis
ankylosing spondylitis
uveitis
primary sclerosing cholangitis
124
Q

normal small intestine with backwash ileitis
broad based ulcers
pseudopolyps fusing to get mucosal bridges and atrophy, WITHOUT any mural thickening or strictures

A

ulcerative colitis

125
Q

a very dire complication of IBD if not treated, happens as a result of colonic dilation

A

toxic megacolon, sign risk of perforatin

126
Q

clinical presentation of ulcerative colitis

A

relapsing attacks of bloody diarrhea with stringy, mucoid material, lower abd pain, cramps that are TEMPORARILY RELIEVED BY DEFECATION

127
Q

trx for ulcerative colitis

A

colectomy, though extraintestinal manifestations may persist

smoking may partially relieve sx (opposite of crohn)

128
Q

what type of IBD is indicated with an P-ANCA, anti-nø Abs

A

UC more likely than crohn

129
Q

what type of IBD is indicated with Ab-S. cerevisiae

A

crohn more likely to UC

130
Q

what are the risk factors for colitis associated neoplasia

A

duration of IBD–> risk increases 8-10 years after onset

extent of the ds–> (directly proportional)

nature of the ds –> increased nø= increased risk

131
Q

begin survelliance for CA ____ after onset of IBD unless they have ____, at which point you begin surveillance right away due to increased risk

A

8 years

primary sclerosing cholangitis

132
Q

etiology of diversion colitis

A

secondary to surgical trx of UC, with creation of temporary or permanent ostomy and blind distal segment of the colon so that normal fecal flow is diverted

133
Q

what type of colitis is strongly associated with celiac ds and autoimmune ds

A

microscopic colitis

134
Q

in what population will you see diverticular ds

A

western adult populations older than 60

135
Q

etiology of diverticular ds

A

acquired pseudodiverticular outpouchings of the colonic mucosa and submucosa

136
Q

where are diverticula most commonly found in the GI tract

A

sigmoid colon

137
Q

clinical presentation of diverticular ds

A

most are ax
intermittent cramping, continuous lower abd discomfort, constipation, distension, or sensation of never being able to completely empty the rectum with alternating constipation and diarrhea

138
Q

most common neoplastic polyp of the GI tract

A

adenoma

139
Q

are hyperplastic polyps benign or malignant? in what populations will you see them?

A

=benign

60s-70s

140
Q

polyps will present with a “piling up” of ___ and ____

A

goblet cells

absorptive cells

141
Q

hyperplastic polyps vs sessile serrated adenomas

A

benign vs malignant potential (respectively)

142
Q

hyperplastic polyps are most commonly found where

A

left colon

143
Q

patients with inflammatory polyps present with what clinical triad

A

rectal bleeding+mucus discharge+ inflammatory lesion of the anterior rectal wall

144
Q

etiology of inflammatory polyp

A

impaired relaxation of anorectal sphincter–> recurrent abrasion and ulceration–> entrapment of ulcer in fecal stream–> mucosal prolapse

145
Q

etiology of hamartomatous polyps

A

caused by germline mutations in tumor suppressor genes or proto-oncogenes

146
Q

juvenile polyps

when present
how happen
trx?
complications

A

children younger than 5
focal malformation of epithelium in rectum, present w rectal bleeding
require colectomy
minority also have polyps in the stomach and small bowel that can undergo malignant transformation

147
Q

peutz-jeghers syndrome

mean age
mutated genes
lesions
extra-GI manifestations

A

10-15 yo

STK11/AMP loss of function (absence does not exclude diagnosis)

S.I > colon >stomach
colonic adenocarcinoma

get pigmented macules, risk of CA in other places like breast, lung, pancreas, thyroid

148
Q

cowden syndrome

mean age
mutated genes
lesions
extra-GI manifestations

A

<15

PTEN
PI3K/AKT pathway

hamartomatous/inflammatory intestinal polyps, lipomas, ganglioneuromas

benign skim tumors, thyroid and breast tumors (B&M)

149
Q

FAP

mean age
mutated genes
lesions
extra-GI manifestations

A

10-15
APC
multiple adenomas
congenital retinal pigment epithelium hypertrophy

150
Q

describe how the risk of CA changes with age in peutz-jeghers syndrome

A

at birth, sex cord tumors of the testis
late childhood= gastric and small intestinal CAs
20s-30s= colon, pancreas, breast, lung, ovarian, uterine CAs

151
Q

range from small, often pedunculated polyps to large, sessile lesions
velvety-raspberry texture

male, western by age 60

A

adenomas

152
Q

villous architecture of an adenoma alone does not increase CA risk when ____ is considered, ___ is the most important characteristic that correlates with risk of malignancy

A

polyp size

size

153
Q

intramucosal carcinoma

histologic definition
prognosis

A

when dysplastic epithelial cells breach the basement membrane

have little or no metastatic potential, and complete polypectomy is generally curative

154
Q

at least ___ polyps are necessary for a diagnosis of classic FAP

A

100

155
Q

colorectal adenocarcinoma develops in ____ of untreated FAP patients, often between the ages of ____

A

100%

30-50

156
Q

while colectomy prevents colorectal CA in FAP patients, they can still get adenomas adjacent to the ____ and in the ____

A

ampulla of vater

stomach

157
Q

extraintestinal associations with FAP

A

congenital hypertrophy of the retinal pigment epithelium

158
Q

describe the etiology of non-FAP polyposis

A

MYH associated polyposis

polyps develop at a later age than FAP (beyond teens)
fave fewer than 100 adenomas
delayed appearance of colon CA (>50)

serrated polyps with KRAS mutations

159
Q

what is HNPCC/Lynch Syndrome

A

familial clustering of CA at colorectum, endometrium, stomach, ovary, ureters, brain, small bowel, hepatobiliary tract, pancreas, and skin

160
Q

age and location of colon CA in HNPCC/Lynch Syndrome

A

occur at younger ages

located in the right colon

161
Q

etiology of HNPCC/Lynch

A

inherited mutations in genes for proteins responsible for detection, excision, and repair errors that occur during DNA replication

majority in MSH2 + MLH1–> x mismatch repair–> increased size of microsatellite : microsatellites are the most frequent sites of mutations in HNPCC

162
Q

most common malignancy of the GI tract

A

adenocarcinoma

163
Q

in contrast to the colon, the small intestine is an uncommon site for ______, despite being 75% of the length of the GI tract

A

benign and malignant tumors

164
Q

(colon) tubular, villous polyps –> typical adenocarcinoma

APC/WNT mutation

A

FAP + 70-80% of sporadic colon CA

165
Q

(colon) sessile, serrated adenoma –> mucinous adenocarcinoma

MSH2/MLH1 mutation

A

HNPCC + some sporadic colon CA

166
Q

(colon) sessile, serrated adenoma –> mucinous adenocarcinoma

MYH mutation

A

MYH-associated polyps

167
Q

in what populations are adenocarcinomas seen

A

north America, not asia or south america

168
Q

dietary factors associated with colorectal adenocarcinoma

A

low intake of unabsorbable vegetable fiber, high intake of refined carbs and fats

169
Q

protective factors against colorectal adenocarcinoma

A

NSAIDS
can protect and cause polyp regression in FAP
(COX-2 is highly expressed in 90% of colorectal CA)

170
Q

pathogensis of adenocarcinoma

A

APC/B catenin pathway is activated,

microsatellite instability –> stepwise accumulation

171
Q

80% of sporadic colon tumors have a mutation of_____ in the neoplastic process. ___ copies must be inactivated, as ___ is a key negative regulator of ____, a component of the Wnt signalling pathway

A

APC

both, APC, B catenin

172
Q

KRAS mutations happen ____ in carcinoma development, and mutations prevent ___ and promote ___

A

late

apoptosis, growth

173
Q

what are SMAD2+SMAD4 genes associated with

A

code for TGF-B signalling, mutations associated with adenocarcinoma

174
Q

_______ is a hallmark of the APC/B catenin pathway

A

chromosomal instability

175
Q

mutations of ______ can contribute the uncontrolled cell growth

A

type II TGF-B receptor

176
Q

the signature triad of mutations of CIMP (CpG islant hypermethylation phenotype)

A

microsatellite instability
BRAF mutation
MLH1 methylation

177
Q

outline the genetic makeup on every step from normal colon to carcinoma

A

SEQUENTIAL

normal colon: has an APC mutation

mucosa at risk: has xAPC+ x B-catenin

adenomas:
w KRAS mutation= proto-oncogene mutations
x TP53, LOH, SMAD = overexpression of COX2

carcinoma= gross chromosomal changes, many genes

178
Q

genetic mutation sequence that gets you from normal colon to carinoma

A

normal –MLH1, MSH2, LOH, methylation–> sessile serrated adenoma w instability —TGFB, BAX, BRAF, TCF, IGF2R–> carcinoma

179
Q

differentiate the histology of adenocarcinomas in the proximal and distal colon

A

proximal colon= grow as polypoid, exophytic masses

distal colon= annular lesions that produce “napkin ring” constrictions

both forms grow into the bowel wall over time–> columnar cells that resemble dysplastic epithelium

180
Q

adenocarcinomas that produce _________ within the intestine wall an

A

mucin

181
Q

most carcinomas arise within ___, and most colorectal CAs develop ______

A

adenomas, insidiously

182
Q

how do right sided colon CAs usually present

A

fatigue, weakness due to iron deficiency anemia

older man or postmenopasual woman

183
Q

how do left sided colorectal adenocarcinomas present

A

occult bleeding, changes in bowelhabits, or cramping and LLQ

184
Q

two most important prognostic factors

A

depth of invasion

presence of LN metastasis

185
Q

most common site of metastasis of the colon adenocarcinoma, unless they are where in the colon

A

liver

unless the rectum bc its not drained by portal circulation

186
Q

prognosis of adenocarcinoma

A

5 year survival is 65%

GI2 E1 (19 decks)

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