small intestine and colon- NON INFECTIOUS Flashcards
robbins (186 cards)
1
Q
___ is the most common site of GI neoplasia in the western world
A
the colon
2
Q
what part of the GI tract is most often involved in obstruction
A
the small intestine bc of its already narrow lumen
3
Q
what are clinical manifestations of intestinal obstruction
A
abdominal pain and distension, vomiting, constipation
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
5
Q
acquired hernias typically occur ____ly, via the __ and ___ canals, ___, or at sites of ____
A
anteriorly
inguinal, femoral
umbilicus
surgical scars
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
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
8
Q
what etiologies can lead to adhesion between bowel segments, abdominal wall, or operative sites
A
surgical procedure
infection
peritoneal inflammation (endometriosis)
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
10
Q
twisting of a loop bowel about its mesenteric point of attachment, presenting with both obstruction and infarction
A
volvulus
11
Q
in what part of the GI tract is a volvulus most often
A
sigmoid colon
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
13
Q
most common cause of intestinal obstruction in children younger than 2
A
intussusception
14
Q
what etiologies are associated with intusussception
A
idiopathic
viral infection
rotavirus vaccine
reactive hyperplasia of peyer patches
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
16
Q
how does one diagnose intussusception
A
contrast enemas (diagnostic and therapeutic)
air enemas
if a mass is present, surgery
17
Q
(colon) while mucosal or mural infarctions can follow acute or chronic ____, transmural infarction is typically caused by ______
A
hypoperfusion
acute vascular obstruction
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
19
Q
(colon) describe the two phases of intestinal response to ischemia
A
- initial hypoxic injury= at the onset of compromise, epithelial cells lining the intestine are relatively resistant to transient hypoxia
- 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
20
Q
what are the watershed zones in the colon
A
splenic flexture (SMA& IMA)
sigmoid colon (IMA, pudendal, iliac)
21
Q
ischemic ds at a watershed zone in the colon can present as what
A
focal colitis (of splenic flexture or rectosigmoidal colon)
22
Q
(colon) the hairpin turn of intestinal capillaries makes ____ particularly vulnerable to ischemic injury, relative to the ___
A
surface epithelium
crypts
23
Q
(colon) pattern of surface epithelial atrophy/necrosis with normal/hyperproliferative crypts is the morphologic signature of
A
ischemic intestinal ds
24
Q
GI ischemia is most often what pattern
A
segmental and patchy
25
(colon) sharply defined ischemia with intenesly congested and dusky to purple-red bowel--> later is blood tinged mucus or frank blood accumulation
transmural infarction
26
(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
mesenteric venous thrombosis
splanchnic bed
oxygenated
27
in the setting of colonic ischemia, bacterial superinfection and enterotoxin release may induce __ ___, resembling C. Dif
pseudomembrane formation
28
in what population will you find ischemic ds of the colon
women, older than 70, coexisting cardiac or vascular ds
29
what things can precipitate colonic ischemia
therapeutic vasoconstrictors, cocaine, endothelial damage, CMV or E Coli O157:H7, strangulated hernia, or vascular compromise prior to surgery
30
what is the clinical presentation of acute colonic ischemia
sudden onset of cramping, left lower abdominal pain, a desire to defecate, passage of blood or bloody diarrhea
31
when is surgery indicated with acute colonic ischemia
peristaltic sounds diminish/disappear, paralytic ileus, guarding/rebound
32
describe the prognosis with acute colonic ischemia
10% in the first 30 days with appropriate management
| doubled in patients with R sided colonic ds
33
____ might be the initial presentation of more severe ds, including caused by acute occlusion of ______
right sided colonic ischemia
| SMA
34
poor prognostic indicators for acute colonic ischemia
R sided ischemia
COPD
sx persistance for more than 2 weeks
35
clinical presentation of mucosal and mural infarction of the colon
nonspecific abdominal sx, intermittent bloody diarrhea and intestinal obstruction
36
clinical presentation of chronic ischemia of the colon
can masquerade as inflammatory bowel ds, with episodes of bloody diarrhea interspersed with periods of healing
37
clinical presentation of CMV infection
ischemic GI disease due to viral tropism for endothelial cells
38
clinical presentation of radiation enterocolitis
acute: anorexia, abdominal cramps, malabsorptive diarrhea
chronic: indolent, inflammatory entero colitis
39
clinical presentation of necrotizing enterocolitis
acute transmural necrosis in neonates born premature or of low birth weight
40
a lesion characterized by malformed submucosal and mucosal blood vessels
angiodysplasia
41
where in the GI tract will you most likely find angiodysplasia
cecum or right colon
| due to the greatest wall tension in the cecum
42
in what population will you likely find angiodysplasia
>60 yo
43
describe the pathogenesis of angiodysplasia
normal distension and contraction may occlude the submucosal veins--> focal dilation and tortuosity
44
(colon) ectatic nests or tortuous veins, venules, or capillaries
angiodysplasia
45
describe complications associated with angiodysplasia
limited injury can lead to significant bleeding because there are only two thin walls protecting it
46
(colon) malabsorption typically presents as ____, with a clinical presentation of ___, and a hallmark presentation of ___
chronic diarrhea
weight loss, anorexia, abd distension, borborygmi (rumbling in tummy), M wasting, diarrhea + dysentery, flatus, abd pain
steatorrhea
47
the most common malabsorptive disorders in the US
pancreatic insufficiency, celiac ds, crohn
48
what is the etiology of malabsorption
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
49
what complications can result from malabsorption
anemia/mucositis (x VitB12, folate, pyridoxine absorption)
bleeding (x vit k absorbed)
osteopenia
tetany
50
describe secretory diarrhea
isotonic stools
| persist during fasting
51
describe osmotic diarrhea
occurs with lactase deficiency
more than 50 mOsm more concentrated than plasma
abates with fasting
52
describe malabsorptive diarrhea
associated with steatorrhea
| relieved by fasting
53
describe exudative diarrhea
purulent, bloody stools
| continue during fasting
54
what parts of digestion are altered by celiac ds
terminal digestion and trans-epithelial transport
55
what part of digestion is altered by chronic pancreatitis
intraluminal digestion
56
what part of digestion is altered by cystic fibrosis
intraluminal digestion
57
what part of digestion is altered by primary bile acid malabsorption
intraluminal digestions, trans-epithelial transport
58
what part of digestion is altered by whipple disease
lymphatic transport
59
what part of digestion is altered by abetalipoproteinemia
trans-epithelial transport
60
what part of digestion is altered by gastroenteritis
terminal digestion and trans-epithelial transport
61
what part of digestion is altered by IBD
intraluminal digestion, terminal digestion, transepithelial transport
62
two main sx related to GI pathology are
abd pain
| hemorrhage
63
function of a goblet cell
to produce mucus
64
which part of the GI tract has villi on histology
small intestine
65
what is the most common CA type of the GI tract
adenocarcinoma
66
what is the function of a lacteal
fat absorption
67
air filled space in the bowel is indicative of what
obstruction
68
relate the etiology of cystic fibrosis to the GI tract
absence of CFTR --> defects in Cl- and HCO3 secretion --: defective luminal hydration, intestinal obstruction --> formation of pancreatic intraductal concretions
69
what are some GI complications with cystic fibrosis
eventual exocrine pancreatic insufficiency
70
treatment for cystic fibrosis sx in the gi tract
oral CFTR enzyme supplement
71
describe the etiology of celiac ds
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
72
what compound contains most of the ds-producing components in celiac ds
gliadin
73
what other pathologies are associated with celiac ds
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
74
biopsy of what part of the GI tract will allow for celiac ds diagnosis? what will you see?
second portion of the duodenum or proximal jejunum,
inreased CD8 cells, crypt hyperplasia, villous atrophy, loss of mucosal/brush border surface area,
75
in what population do you see celiac ds present in
adults 30-60 y.o, though many remained undiagnosed for a long time
women (accentuated effects w menstruation)
between 6 and 24 months,
76
sx with celiac ds in adults
chronic diarrhea, bloating, chronic fatigue, anemia
77
sx with celiac ds in children
irritability, abd distension, anorexia, chronic diarrhea, failure to thrive, weight loss, M wasting
78
what extraintestinal complaints are associated w celiac ds
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
what is the trx for celiac ds
gluten free diet
80
what diagnostic tests are performed for celiac ds
serologic test
most sensitive= igA abs against tissue transglutaminase
HLA-DQ2/8 (absence is highly negative predictive value)
81
individuals w celiac ds have a higher than normal rate of ____, with the most associated being _______
malignancy
| enteropathy-associated T cell lymphoma
82
what hx is consistent with environmental enteropathy
poor sanitation, developing countries/impoverished communities
malabsorption/malnutrition
stunted growth
83
describe the etiology environmental enteropathy
defective intestinal mucosal immune function
chronic exposure to fecal pathogens
repeated bouts of diarrhea within the first 2-3 years of life
84
what is the prognosis of environmental enteropathy
can't rally give abx or nutritional supplements
| there is irreversible loss of physical development and cognitive deficits
85
clinical presentation of autoimmune enteropathy
severe, persistent diarrhea
86
in what population does autoimmune enteropathy present
young children
87
what is IPEX
a severe familial form of autoimmune enteropathy
Immune dysfunction
Polyendocrinoapthy
Enteropathy
X linked
88
what gene mutations are associated with autoimmune enteropathy
FOXP3 on CD4 cells
auto-ab to enterocytes and goblet cells
Abs to parietal/islet cells
89
what is the trx for autoimmune enteropathy
immunosuppression (cyclosporine)
| hematopoietic stem cell transplant
90
lactase is located in the ..
apical brush border of villous absorptive epithelial calls
91
what is the clinical presentation of congenital lactase deficiency
explosive diarrhea with watery, frothy stools and abd distension upon milk ingestion
92
what is the clinical presentation of acquired lactase deficiency
=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
what is abetalipoproteinemia, what is the etiology
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
oid red-O stain on histology
for lipids.. abetalipoproteinemia
95
what population presents with abetalipoproteinemia and what is the clinical presentation
infancy
| failure to thrive, diarrhea, and steatorhhea
96
complete absence of all plasma lipoprotiens containing apolipoprotein B, decreased Vit ADEK absorption, acanthocytic red cells (burr cells) in peripheral blood smears
apolipoproteinemia
97
chronic, relapsing abdominal pain, bloating, and changes in bowel habits
IBS
98
the two types of IBS are ___ or ____ predominant
constipation or diarrhea
99
2 etiologies that lead to diarrhea predominant IBS
increased colonic contractions
| excess bile acid synthesis
100
gene mutations associated with IBS
serotonin reputake transporters, cannbinoid receptors, TNF related inflammatory mediators,
5HT3 receptor
101
effective trxs in IBS
5HT3 receptor antagonists
opioids
psychoactive drugs
102
population associated with IBS
20-40 yo females
103
population associated with IBD
teens and early 20s, females, caucasians, ashkenazi jews
104
compare and contrast Crohn and ulcerative colitis
types of lesions
morphology
CD= skip lesions
transmural inflammation, ulcerations, fissures
UC= continuous from colon to rectum
pseudopolyps
ulcers
105
hygiene hypothesis relates to the fact that _____ infections can prevent IBD development
helminths
106
genetic mutations associated with crohn
NOD2--> NF-KB
ATG16L1
IRGM
107
perianal fistrulas in which IBD
only CD
108
fat/vitamin malabsorption in which IBD
CD
109
malignant potential in which IBD
UC, CD if there is colonic involvement
110
recurrence post surgery in which IBD
CD
111
toxic megacolon in which IBD
UC
112
in crohn disease, see polymorphism in ___ receptors leading to activation of ____
IL23
| Th17
113
pro-inflammatory cytokines involved in pathogenesis of IBD
```
TNF
IFNgamma
IL13
IL10
TGF B
```
114
____ mutations lead to epithelial dysfunction in crohn
NOD2
115
____ mutations lead to epithelial dysfunction in ulcerative colitis, as well as ___ mutations which are strongly associated with maturity onset DM of the young (MODY)
ECM1,
HNFA
116
Ab against bacterial flagellin are most common in which IBD
CD
117
clinical presentation of crohn onset
non-bloody diarrhea, fever, rectal abscess, small intestinal and colonic ulcers and fistulas beginning at age 20
118
most common site involved with crohn
terminal ileum, ileocecal valve, cecum
119
colon with aphthous ulcer/cobblestone appearance/ fissures/ creeping fat
crypt abscess with distortion of mucosal architecture
paneth metaplasia
noncaseating granulomas
crohn ds
120
intermittant mild bloody diarrhea, fever, abd pain with RLQ pain, fever
reactivation with triggers, onset associated with the initiation of smoking
crohn
| note: opposite of UC, where smoking actually relieves sx
121
complications of crohn (5)
- 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
extra-intestinal manifestations of crohn only
erythema nodosum
clubbing
pericholangitis
123
extraintestinal manifestations of crohn and ulcerative colitis
```
migratory polyarthritis
sacroiliitis
ankylosing spondylitis
uveitis
primary sclerosing cholangitis
```
124
normal small intestine with backwash ileitis
broad based ulcers
pseudopolyps fusing to get mucosal bridges and atrophy, WITHOUT any mural thickening or strictures
ulcerative colitis
125
a very dire complication of IBD if not treated, happens as a result of colonic dilation
toxic megacolon, sign risk of perforatin
126
clinical presentation of ulcerative colitis
relapsing attacks of bloody diarrhea with stringy, mucoid material, lower abd pain, cramps that are TEMPORARILY RELIEVED BY DEFECATION
127
trx for ulcerative colitis
colectomy, though extraintestinal manifestations may persist
| smoking may partially relieve sx (opposite of crohn)
128
what type of IBD is indicated with an P-ANCA, anti-nø Abs
UC more likely than crohn
129
what type of IBD is indicated with Ab-S. cerevisiae
crohn more likely to UC
130
what are the risk factors for colitis associated neoplasia
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
begin survelliance for CA ____ after onset of IBD unless they have ____, at which point you begin surveillance right away due to increased risk
8 years
primary sclerosing cholangitis
132
etiology of diversion colitis
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
what type of colitis is strongly associated with celiac ds and autoimmune ds
microscopic colitis
134
in what population will you see diverticular ds
western adult populations older than 60
135
etiology of diverticular ds
acquired pseudodiverticular outpouchings of the colonic mucosa and submucosa
136
where are diverticula most commonly found in the GI tract
sigmoid colon
137
clinical presentation of diverticular ds
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
most common neoplastic polyp of the GI tract
adenoma
139
are hyperplastic polyps benign or malignant? in what populations will you see them?
=benign
| 60s-70s
140
polyps will present with a "piling up" of ___ and ____
goblet cells
| absorptive cells
141
hyperplastic polyps vs sessile serrated adenomas
benign vs malignant potential (respectively)
142
hyperplastic polyps are most commonly found where
left colon
143
patients with inflammatory polyps present with what clinical triad
rectal bleeding+mucus discharge+ inflammatory lesion of the anterior rectal wall
144
etiology of inflammatory polyp
impaired relaxation of anorectal sphincter--> recurrent abrasion and ulceration--> entrapment of ulcer in fecal stream--> mucosal prolapse
145
etiology of hamartomatous polyps
caused by germline mutations in tumor suppressor genes or proto-oncogenes
146
juvenile polyps
when present
how happen
trx?
complications
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
peutz-jeghers syndrome
mean age
mutated genes
lesions
extra-GI manifestations
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
cowden syndrome
mean age
mutated genes
lesions
extra-GI manifestations
<15
PTEN
PI3K/AKT pathway
hamartomatous/inflammatory intestinal polyps, lipomas, ganglioneuromas
benign skim tumors, thyroid and breast tumors (B&M)
149
FAP
mean age
mutated genes
lesions
extra-GI manifestations
10-15
APC
multiple adenomas
congenital retinal pigment epithelium hypertrophy
150
describe how the risk of CA changes with age in peutz-jeghers syndrome
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
range from small, often pedunculated polyps to large, sessile lesions
velvety-raspberry texture
male, western by age 60
adenomas
152
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
polyp size
size
153
intramucosal carcinoma
histologic definition
prognosis
when dysplastic epithelial cells breach the basement membrane
have little or no metastatic potential, and complete polypectomy is generally curative
154
at least ___ polyps are necessary for a diagnosis of classic FAP
100
155
colorectal adenocarcinoma develops in ____ of untreated FAP patients, often between the ages of ____
100%
| 30-50
156
while colectomy prevents colorectal CA in FAP patients, they can still get adenomas adjacent to the ____ and in the ____
ampulla of vater
| stomach
157
extraintestinal associations with FAP
congenital hypertrophy of the retinal pigment epithelium
158
describe the etiology of non-FAP polyposis
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
what is HNPCC/Lynch Syndrome
familial clustering of CA at colorectum, endometrium, stomach, ovary, ureters, brain, small bowel, hepatobiliary tract, pancreas, and skin
160
age and location of colon CA in HNPCC/Lynch Syndrome
occur at younger ages
located in the right colon
161
etiology of HNPCC/Lynch
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
most common malignancy of the GI tract
adenocarcinoma
163
in contrast to the colon, the small intestine is an uncommon site for ______, despite being 75% of the length of the GI tract
benign and malignant tumors
164
(colon) tubular, villous polyps --> typical adenocarcinoma
APC/WNT mutation
FAP + 70-80% of sporadic colon CA
165
(colon) sessile, serrated adenoma --> mucinous adenocarcinoma
MSH2/MLH1 mutation
HNPCC + some sporadic colon CA
166
(colon) sessile, serrated adenoma --> mucinous adenocarcinoma
MYH mutation
MYH-associated polyps
167
in what populations are adenocarcinomas seen
north America, not asia or south america
168
dietary factors associated with colorectal adenocarcinoma
low intake of unabsorbable vegetable fiber, high intake of refined carbs and fats
169
protective factors against colorectal adenocarcinoma
NSAIDS
can protect and cause polyp regression in FAP
(COX-2 is highly expressed in 90% of colorectal CA)
170
pathogensis of adenocarcinoma
APC/B catenin pathway is activated,
| microsatellite instability --> stepwise accumulation
171
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
APC
| both, APC, B catenin
172
KRAS mutations happen ____ in carcinoma development, and mutations prevent ___ and promote ___
late
| apoptosis, growth
173
what are SMAD2+SMAD4 genes associated with
code for TGF-B signalling, mutations associated with adenocarcinoma
174
_______ is a hallmark of the APC/B catenin pathway
chromosomal instability
175
mutations of ______ can contribute the uncontrolled cell growth
type II TGF-B receptor
176
the signature triad of mutations of CIMP (CpG islant hypermethylation phenotype)
microsatellite instability
BRAF mutation
MLH1 methylation
177
outline the genetic makeup on every step from normal colon to carcinoma
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
genetic mutation sequence that gets you from normal colon to carinoma
normal --MLH1, MSH2, LOH, methylation--> sessile serrated adenoma w instability ---TGFB, BAX, BRAF, TCF, IGF2R--> carcinoma
179
differentiate the histology of adenocarcinomas in the proximal and distal colon
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
adenocarcinomas that produce _________ within the intestine wall an
mucin
181
most carcinomas arise within ___, and most colorectal CAs develop ______
adenomas, insidiously
182
how do right sided colon CAs usually present
fatigue, weakness due to iron deficiency anemia
older man or postmenopasual woman
183
how do left sided colorectal adenocarcinomas present
occult bleeding, changes in bowelhabits, or cramping and LLQ
184
two most important prognostic factors
depth of invasion
| presence of LN metastasis
185
most common site of metastasis of the colon adenocarcinoma, unless they are where in the colon
liver
| unless the rectum bc its not drained by portal circulation
186
prognosis of adenocarcinoma
5 year survival is 65%
