GASTRO INTESTINAL TRACT MEDICINE REVISION NOTES

Zollinger Ellison syndrome
TONY SCARIA 2010 KMC

ZES
• non-beta islet cell tumor that produces gastrin  gastric acid
hypersecretion and peptic ulcer disease

Gastrinoma triangle

Gastrinoma triangle
• confluence of the cystic and common bile ducts superiorly,
• junction of the second and third portions of the duodenum inferiorly,
• junction of the neck and body of the pancreas medially

MC site
• Duodenum >> pancreas

Triad of ZES
Peptic ulcer
Diarrhea
Presence of MEN
1

• Most common site for ZES is gastrinoma triangle

• Duodenal tumors are smaller, slower growing, and less likely to
metastasize than pancreatic lesions.
• Less-common extrapancreatic sites include stomach, bones, ovaries,
heart, liver, and lymph nodes.

Diagnosis
• Fasting gastrin level
• usually <150 pg/mL
• gastrinoma > 150-200 pg/mL
• gastrin of ≥200 pg within 15 min of secretin injection has a sensitivity and
specificity of >90% for ZES
• BAO/MAO ratio >0.6 is highly suggestive of ZES, but a ratio <0.6 does
not exclude the diagnosis

• Gastrin provocative tests*
• 1. Secretin injection test
• 2. An increase in gastrin of ≥200 pg within 15 min of secretin
injection has a sensitivity and specificity of >90% for ZES.
• 3. Calcium infusion test study is less sensitive and specific than the
secretin test

Tumour localisation
• Tumor Localization:*
• 1. Endoscopic ultrasound (EUS)
• permits imaging of the pancreas with a high degree of resolution (<5 mm). EUS is
the most sensitive test for primary gastrinoma.
• 2. Somatostatin analogue 111 In-pentreotide (Octreoscan) with
sensitivity and specificity rate of >75%.
• 3. For metastases:
• Abdominal CT scan, MRI, or Octreoscan. Out of these, octreoscan is the most
sensitive for metastasis.
• 4. Selective Arterial Secretin Injection (SASI) is also important imaging
study for ZES

Rx
• 1. PPls are the treatment of choice
• 2. Surgery

Treatment of metastatic lesion
• 1. Streptozocin
• 2. 5-fluorouracil
• 3. Doxorubicin
• 4. IFN-alpha
• 5. Hepatic artery embolization
• 6. pentetreotide

New therapies for ZES
• 1. Radiofrequency ablation
• 2. Cryoablation of liver lesions
• 3. Use of agents that block the VEGF pathway (bevacizumab, sunitinib)
• 4. To block the mammalian target of rapamycin

Pseudomembranous colitis

Pseudomembranous colitis
• Antibiotic associated diarrhea
• may be due to C. diffcile (mainly)as well as Salmonella, C. perfringens
type A, or S. aureus
• Disruption of the normal colonic microbiota by antibiotics allows C.
diffcile overgrowth.
• Toxins released by C. diffcile cause the ribosylation of small GTPases,
such as Rho, and lead to disruption of the epithelial cytoskeleton,
tight junction barrier loss, cytokine release, and apoptos

Diagnosis of pseudomembranous colitis
• Diagnosis is by
• culture or
• detection of toxin A (enterotoxin) and toxin B (cytotoxin) in stool.
• The toxins can be detected by ELISA, LA, tissue culture assay, PCR or probes
• Latex test for detection of glutamate dehydrogenase

IBD
• It includes ulcerative colitis and Crohn’s disease.
Ulcerative colitis
• Limited to mucosa
& submucosa
• Limited to colon &
rectum
Crohns ds
• Transmural
inflammation

NOD2 mutation
• a/w CROHNS ds

Bimodal
• It has two peaks-one between 15-30 years and second between 60-80 years.
• Females are more commonly affected
• High prevalence in urban and high socioeconomic class hygiene hypothesis

Crohns disease

Crohns disease
• regional enteritis (because of frequent ileal involvement) may involve
any area of the GI tract and is typically transmural
• Sparing of rectum

Crohns disease  rectum sparing
Most patients have
involvement of both
small and large intestine
30-40% have
involvement
of small
intestine alone
15-25% have
involvement of
large intestine
alone
Perirectal fistula, abscesses,
fissures and stenosis is
common

Noncaseating granuloma in crohns ds
• Through out gut even in uninvolved segments

• Earliest lesion in crohns ds is aphthous ulcer coalesce to form
serpentine ulcer

Transmural inflammation in crohns ds 
creeping fat appearance

Skip lesions + cobble stone appearance in
crohns ds

• Pseudo polyps can occur in CD. But much less frequent than UC

• Extensive CD in
• Malabsorption & malnutrition
• Loss of albumin
• IDA & vitamin B12 deficiency

Extraintestinal manifestation of Crohns ds

Extraintestinal manifestation
• uveitis,
• migratory polyarthritis,
• sacroiliitis,
• Ankylosing spondylitis,
• erythema nodosum, and
• clubbing of the fngertips,
• Pericholangitis and primary sclerosing cholangitis
• also occur in Crohn disease but are more common in ulcerative colitis.
• INCREASED RISK OF ADENOCARCINOMA

• Laboratory Features:
• 1. Anemia, Leucocytosis.
• 2. Increased ESR, CRP level.
• 3. Hypoalbuminemia
• 4. ASCA antibodies (ANTISACCHAROMYCEAL CERVICEAL Ab)(60-70%)
• 5. p-ANCA (5-10%)
• 6. Anti goblet antibodies (30%)
• 7. Anti colon antibodies (13%)
• 8. Pancreatic auto antibodies (30%)TONY SCARIA 2010 KMC

• Endoscopic features:
• 1. Rectal sparing
• 2. Aphthous ulceration
• 3. Fistula
• 4. Skip lesions
• 5. COBBLE STONE APPEARNACE

• Diagnosis confirmed by endoscopy & biopsy

RADIOLOGICAL SIGNS OF CROHNS DISEASE
• Apthous ulcer
• Central flecks of barium surrounded by halo
• Rose thorn appearance
• String sign of kantor
• creeping fat on CT scan

Rose thorn appearance

String sign of kantor

Prominent vasa recta in active crohns disease
 COMB SIGN

Ulcerative colitis

• UC is a disease of large intestine, rectum is the most common site.
• Backwash ileitis- Inflammation involving 1-2 cm of ileum.
• Mucosa has fine granular surface like sand paper in mild
Inflammation. In more severe inflammation mucosa is hemorrhagic,
edematous and ulcerated.
• The disease process is limited to mucosa and superficial sub mucosa
except in fulminant disease.

• Pseudopolyp- due to epithelial regeneration in long standing disease.
• Toxic mega colon- Bowel wall become very thin and the mucosa is
severely ulcerated.
• Cryptitis is present leading to crypt abscess, and crypt distortion.

Histopathology of ulcerative colitis
• No fissures aphthous ulcers or granulomas
• Mucosal inflammation is limited to mucosa

• Laboratory investigations-
• 1. Anemia
• 2. Raised ESR, CRP levels.
• 3. Increased platelet count
• 4. Low serum albumin
• 5. Leukocytosis.
• Serological markers:
• 1. P-ANCA (60-70%)
• 2. Anti-saccharomyces cerevisiae antibody(10-15%)
• 3. Anti goblet cell antibody (40%)
• 4. Anti colon antibody (36%)
• 5. Pancreatic autoantibody (41%)

Radiological features of UC
• Earliest change is fine mucosal granularity
• Deep ulceration appear as ‘ collar-button’ ulcers.
• Loss of haustration in long standing disease colon become
shortened and narrowed.
• Polyp can be seen which may be due to post inflammatory polyp,
pseudopolyp, adenomatous polyps or carcinoma.
• Loss of haustral folds lead pipe or pipe stem colon

Thumb printing is also seen in UC d/t mucosal
edema

MTX is not used in Rx of UC

• Ulcerative colitis has more malignant potential than crohns ds

Indications for surgery in IBD

Surgical procedures
• Segmental intestinal resection
• Heinecke mickulicz pyloroplasty
• Stricture <12 cm
• Finneys pyloroplasty
• Longer strictures
Primary sclerosing cholangitis does not
resolve with colectomy

• Pseudopolyps are seen in both
• UC & CD
• More common in UC
• Not a premalignant condition

UC CD
Rectal involvement Most common site of involvement
is rectum
Rectal sparing
Ileal involvement Involvement only as backwash
ileitis
Most common site of involvement
is ileum
Inflammation Limited to mucosa & submucosa Transmural inflammation
Antibody P-ANCA ASCA
Toxic megacolon Common than in CD Very rare
Perianal abscess strictures
obstruction
Rare Common
Sclerosing cholangitis Common rare
Pyoderma gangrenosum Common Rare
Uveitis & arthritis Common Common
Surgery Curative Palliative

Toxic megacolon
• Transverse colon > 6cm
• Sigmoid >12 cm

Irritable bowel syndrome

Intestinal TB

Ulcerative form Hypertrophic form Mixed form
• Most frequent
• Transverse ulcers
Causative organism is mycobacterium tuberculosis (M Bovis
is largely eliminated )

Location of intestinal TB
• ileocaecal region (most common)> ascending colon > jejunum >
appendix > duodenum > stomach > sigmoid > rectum > esophagus

Radiological features of ileocaecal
tuberculosis
Sterlin sign rapid emptying of narrowed terminal ileum into shortened rigid obliterated caecum on
barium examination.
Thickened ileocaecal valve
Fleischner’s sign (inverted umbrella defect) wide gaping patulous ileocaecal immediately adjacent
terminal ileum
Deep fissures + large shallow linear/stellate ulcers with characteristic elevated margins.
Symmetric annular 'napkin ring' stenosis(purse string stenosis)
Widened ic angle (normal is 90o) it becomes obtuse

Colon involvement
• Segmental colonic involvement
• Diffuse ulcerating colitis + pseudopolyps
• Amputated/ coned/ contracted caecum

• Gastroduodenal:
• Simultaneous involvement of pylorus + duodenum 'linitus plastic'
appearance.
• Linitus plastic may also be a feature of gastric lymphoma and scirrhous
carcinoma, eosinophilic gastritis

Megaloblastic anemia in ileocaecal TB
• Ileum is the physiological site. For absorption of vitamin B12. Also, TB
is mentioned to be a cause of folic acid deficiency which is therefore
going to result in megaloblastic anemia.

Typhoid ulcers

Typhoid ulcers
Typhoid ulcer is
longitudinal
Tuberculous ulcer is
transverse

Typhoid ulcer
• Most commonly affects ileum & colon
• Terminal ileum  longitudinal ulcers
• Humans are the only reservoir
• Liver shows typhoid nodule

Liver shows typhoid nodule

Erythrophagocytosis
Macrophage will phagocytose RBC

• Peripheral blood
• Leucopenia with neutropenia
• Relative lymphocytosis

• Complication
• Perforation
• Hge

Amebiasis

Most common site for
amebiasis is caecum

Flask shaped ulcer in amebiasis
Ulcers are seen up to mucosa &
submucosa only  never
reaches upto muscularis propria

Celiac disease

celiac disease
• non tropical sprue,
• gluten-sensitive enteropathy
• Delayed type hypersensitivity to gluten containing foods on
genetically susceptible individuals

Genetic susceptibility Environmental factors Immunological factor
• HLA DQ2
• HLA DQ8
• Gliadin, which is a component
of gluten that is present in
barley rye oats & wheat
(BROW)
• Anti tissue transglutaminase
antibodies. (Most sensitive and
most specific)
• Anti endomysial antibody
• Anti alpha gliadin antibody -
Not done now a days
• IgA anti reticulin antibody - Not
done now a days

Pathogenesis
of celiac ds
Gliadin deamination by tTG
Deamidated peptide binds on specific
MHC in susceptible individual(HLADQ2/8)
CD4 t cell activation proliferation of CD8
cells
Cytokine mediated epithelial damage

• The changes seen on biopsy are
• 1. Absence or reduced height of villi
(Flat appearance)
• But thickness of mucosa is unchanged
• 2. Crypt hyperplasia
• 3. Increased intra epithelial
lymphocytes  intra epithelial CD8
cells
• 4. Cuboidal appearance of epithelial
cells.

Marsh classification of celiac ds

Zonulin hypothesis to explain celiac ds

• celiac sprue is associated with.
• 1. Dermatitis herpetiformis
• 2. Type 1 DM.
• 3. IgA globulin deficiency
• 4. Down syndrome
• 5. Turner syndrome
Splenic atrophy can
cause Howell jolly
bodies &
pappenheimer bodiesTONY SCARIA 2010 KMC

• Increased risk of
• Enteropathy associated T cell lymphoma
• Small intestinal carcinoma
• SCC of esophagus

Mild (proximal bowel) Progresses to
Severe (distal small bowel or ileal
involvement)
• Iron deficiency anemia
• Folic acid deficiency
• Decreased B12 absorption

• 1. Symptoms may appear at any age, but more typically they appear with the introduction of
cereals in an infant’s diet.
• 2. Usual clinical features are:
• 1. Diarrhea - Due to
• 1. Steatorrhea resulting from changes in jejunal mucosal function.
• 2. Endogenous fluid secretion resulting from crypt hyperplasia
• 3. Secondary lactose deficiency resulting from change in jejunal brush border enzymatic function.
• 4. Bile acid malabsorption on-Due to involvement of ileum.
• 2.Anemia - Due to
• 1. Iron deficiency (Most common) jejunal mucosa involvement
• 2. Folate deficiency
• 3. Vitamin B_12 deficiency if ileum is involved.
• 3. Edema - Due to protein loss.
• 4. Osteomalacia.

• Treatment-
• 1. Removal of all gluten from the diet (Wheat, barley, Rye).
• 2. Rice, soya bean, potato and corn are given.

RX resistant celiac ds
Non responsive celiac ds Refractory celiac ds
Based on symptom Based on histology
Non responsive to gluten free diet for 6-12 months No histological improvement with gluten free diet

Tropical sprue
• In patients from tropics
• Distal small bowel is severely affected
• Etiology
• 1. Infection- Klebsiella pneumoniae, Enterobacter cloacae, E. coli
• 2. Nutrient deficiency – Folate deficiency.
• 3. Toxins – Produced by bacteria.

• Clinical features-
• 1. Chronic diarrhea- It begin as acute diarrhea associated with fever.
• 2. Anorexia with weight loss.
• 3. Abdominal bloating.
• 4. Prominent bowel sounds.
• 5. Nutritional deficiency – Deficiency of folate, vitamin B_12 .

Tropical sprue
• Treatment–
• 1. Tetracycline for 6 months.
• 2. Folic acid.

Bacterial overgrowth syndrome
• stagnant bowel syndrome
• blind loop syndrome

Short loop syndrome
• It is the proliferation of colon type bacteria within the small
intestine
• Causes
Functional Stasis- Anatomic stasis- Direct Communication
between small and large
intestine e.g. enterocolic
anastomosis
Due to impaired peristalsis
.e.g. scleroderma & DM.
Due to change in intestinal
anatomy e.g. diverticula,
stricture, jejunoileal
bypass, dilatation

CF
• 1. Steatorrhea- Due to impaired micelle formation because of
deconjugation of bile acids by the bacteria.
• 2. Diarrhea- Due to
• 1. Steatorrhea
• 2. Bacterial enterotoxin causing fluid recreation.
• 3. Macrocytic anemia- Due to cobalamin deficiency as it is utilized by
the bacteria.

Whipple disease
• chronic multi system disease
• Gram positive bacillus – Tropheryma whippelii

c/c multisystem disorder

Whipple disease

Jejunal biopsy taken by Crosby capsule

HP of whipple ds
• infiltration of the lamina propria with PAS-positive macrophages that
contain gram positive bacilli

• Treatment-
• 1. Drug of choice is double strength trimethoprim/ sulfamethoxazole for 1
year.
• 2. If trimethoprim/sulfamethoxazole is not tolerated, chloramphenicol is an
appropriate second choice

Protein losing enteropathy
• loss of both albumin and globulin in
stool generalised anasarca.
• Diagnosis:Radioactive alpha1 antitrypsin
clearance in stool.
• Clinical features
• 1. Peripheral edema due to
hypoalbuminemia.
• 2. Steatorrhea due to lymphatic block.

Hirschprung disease

Hirschsprung disease
• 1 in 5000 live births
• Male : female = 4:1
• Age @ diagnosis <2 yrs

Hirschsprung disease
• congenital aganglionic megacolon
Defective migration of neural crest cells into mesodermal
layers of gut
Absence of ganglion cells in the submucosal & myenteric
plexus
Decreased peristalsis & contraction of involved aganglionic
segment & dilatation of proximal normal segment

• Most common site of HD is rectosigmoid
Ultrashort Short Long Total Total intestinal
• Rectum/sig
moid
• Entire
rectosigmoi
d
Total colon Rectum till
duodenum

Associations
• Downs syndrome
• MEN II

CF
• Full term new born
• Delayed passage of meconeum
• Empty rectum
• Absent fecal soiling

Diagnosis
• Invertogram
• Barium enema
• Rectosigmoid index
• Rectal biopsy  gold standard
• Full thickness biopsy
• 4 cm above dentate line
• Thickened nerves
• Aganglionic segment

Invertogram used in diagnosis of HD

Rx of HD
• Swenson pull through
• Duhamel
• Soave procedure

GIST
• most common mesenchymal tumor of the abdomen
• Most commonly occur in stomach
• arises from benign pacemaker cells, also known as the interstitial
cells of Cajal

Mutations in GIST
• Oncogenic mutation in c-KIT  75 to 80 % of all GIST
• Platelet derived growth factor (PDGFR) 8 %

Spindle cells
Epitheliod cells

• Best & most specific marker for GIST  designed only for GIST (DOG-
1)

GIST may arise a/w carneys triad

• GIST is also a/w NF1

• Rx
• Surgical resection for localised tumours
• Imatinib (tyrosine kinase inhibitors ) if not resectable

Classification of polyp based onn histology
Neoplastic
•Adenoma
•Villous adenoma
•Tubular adenoma
•Tubulovillous
adenoma
Non neoplastic
•Inflammatory
•Hamartomatous
•Hyperplastic polyp

Inflammatory polyp
• in solitary rectal ulcer syndrome
• Recurrent abrasion –>inflammatory polyp

Juvenile polyposis syndrome
• <5 years
• Mutation in SMAD4, BMPR1A involved in TGF β signalling
• Pulmonary arteriovenous malformations, digital clubbing
• Juvenile polyps
• 100 hamartomatous polyp
• increased risk of gastric, small intestinal, colonic, and pancreatic
adenocarcinoma

Peutz jeghers syndrome
• Autosomal dominant
• Heterozygous loss of function mutationo of LKB1/STK11 gene
• Onset is 11 yrs
• Multiple gastro intestinal hamartomatous polyps
• Mucocutaneous hyperpigmentation  lentigines
• around the nose and mouth, on the hands and feet, and within the oral cavity.
• Increased risk of several cancers including colon pancreas breast lung
gonads & uterus

PTEN mutation
Cowden syndrome Bannayan ruvalcaba riley syndrome
• AD
• GI polyps
• Macrocephaly
• Benign skin tumours
• AD
• GI polyps
• Macrocephaly
• Benign skin tumours
• Mental retardation+ developmental retardation
• Decreased risk of malignancy
Benign skin tumors, benign and
malignant thyroid and breast
lesions

Cronkhite Canada syndrome
Non hereditary
Older than 50 years

Cronkhite Canada syndrome
• Nail atrophy,
• hair loss,
• Abnormal skin pigmentation,
• cachexia,
• anemia

Adenomatous polyp Hamartomatous polyp Inflammatory polyp Hyperplastic polyp
Associated with various
syndrome
Recuurent cycle of injury
& healing
• Decresed epithelial
turnover
• Smaller than 5mm
Premalignant
• Majority donot
preogress to
malignancy
• Clinically silent
Not premalignant Not premalignant Not premalignant

Adenomatous polyp  premalignant
Tubular adenoma Tubulovillous adenoma Villous adenoma
Tubular adenomas-mostly tubular
glands, recapitulating mucosal
topology
Tubulovillous adenomas have a
mixture of tubular and villous
elements
Villous adenomas-villous projection
Colorectal adenomas are characterized by the presence
of epithelial dysplasia

• There are 3 types
• 1. Tubular - 5% chance for malignancy
• 2. Tubulovillous - 22% chance for malignancy
• 3. Villous - 40% chance for malignancy

• The malignant risk with an adenomatous polyp is correlated with
three interdependent features-
• polyp size
• maximum diameter is the chief determinant of the risk of an adenoma's harboring
carcinoma
• histologic architecture, and
• Tubular tubulovillous villous
• architecture does not provide substantive independent information
• severity of epithelial dysplasia

FAP
• defined by the presence of more than 100 colorectal adenomas.
• large bowel, but it can also involve stomach duodenum and SI
• AD
• chromosome 5p21(APC GENE)
• Colorectal carcinoma } 10 to 20 years after the onset of polyp.
• Duodenal carcinoma, ampullary carcinoma.

FAP in APC gene MAP gene

FAP variants
Gardeners syndrome
• FAP + desmoid tumour +
craniofacial osteoma +
epidermoid tumour+ fibroma+
lipoma + impacted molars+
congenital hypertrophy of
retinal pigment epithelium
Turcots syndrome
• FAP + cerebellar
medulloblastoma

CFs of FAP
• Asymptomatic
• Symptomatic
• Loose stools
• Lower abdominal pain
• Weight loss
• Diarrhea
• Blood and mucus with stools

Investigations for FAP
• Sigmoidoscopy
• Double contrast barium enema
• Colonoscopy and biopsy.
• *More than 100 adenomas must be there to make a diagnosis of FAP.

Screening for FAP
• 1. The screening is by colonoscopy
• 2. Pigmented spots in retina (Congenital hypertrophy of retinal
pigment epithelium > 4 in number on each eye).
• 3. DNA test for FAP

Preventing colorectal ca
prophylactic resection
of the colon–total
proctocolectomy and
ileo anal pouch
anastomosis
Medica treatment
• Sulindac
• celecoxib

HNPCC (Hereditary nonpolyposis colorectal
cancer)
• autosomal dominant 2P (short arm of 2) } Lynch syndrome
• early age.
• the endometrium, ovary, stomach and small intestine.
• Lynch 1 syndrome
• MLH1 gene
• Multiple colonic cancers in the proximal colon at an early age
• Lynch 11 syndrome
• MSH2 gene
• colon cancer +extracolonic adenocarcinomas (Breast, ovary, endometrium,
pancreas, stomach, bile duct, ureter and renal pelvis
• (Cancer family syndrome)

HNPCC Arises d/t mismatch repair genes in
MSH2 & MLH1

Amsterdam criteria
Amsterdam criteria 1 (Lynch 1)
• at least 3 relatives must have
histologically verified colorectal
cancer.
• 1. One must be a 1st degree
relative of the other two
• 2. At least 2 successive
generations must be affected
• 3. At least one of the relatives
with colorectal cancer must have
received the diagnosis < age of 50
years
Amsterdam criteria 2 (Lynch 2
• at least 3 relatives must have a cancer
associated with hereditary nonpolyposis
colonic cancer namely colorectal,
endometrial, ovarian, stomach,
pancreas, hepatobiliary, etc.
• 1. One must be a 1st degree relative of
the other two
• 2. At least two successive generations
must be affected
• 3. At least one of the relatives with
HNPCC associated cancer must have
received the diagnosis before the age of
50 years.
Red same

• Muir Torre syndrome
• Variant of LYNCH Syndrome
• Characterised by multiple sebaceous cyst + keratoacanthoma
• Colonic + extracolonic malignancies

Colorectal carcinoma

Carcinoma colon
• 98 % of carcinoma  adenocarcinoma
• MC site of metastasis : liver > lung

Risk factors for colon cancer
Preventive factors Risk factors
High fibre diet Red meat
Ingestion of ca2+ vitamin A C E Diet rich in animal fats red meat
Alcohol /cigarette smoking
Ureterosigmoidostomy
Aspirin & other NSAIDS  regress size of polyp Hereditary factors
 FAP
 HNPCC
Inflammatory bowel ds
 UC >>CD

Site of carcinoma colon
• MC site for carcinoma colon is
rectosigmoid

Ca colon
Right sided
• More diameter
• ulcerated/cauliflower like
• bleeding pallor
• Ill defined pain
• Bowel symptom - Melena
Left sided
• Less diameter
• Stenosing growth
• intestinal obstn
• Colicky pain
• Alternating constipation and
diarrhea

Adenoma carcinoma sequence

diagnosis
Ba enema
Apple core
appearance
CECT 
investigation of
choice for staging
Colonoscopy
Gold standard
for diagnosis
of colon ca
Permits biopsy

TNM staging
Stage 0 Stage 1 Stage 2 Stage 3 Stage 4
TisN0M0 T1N0M0
T2N0M0
T3N0M0
T4NOM0
Any T
N1 – N2
M0
Any T
Any N
M1
Endoscopic
polypectomy for
polyps containing ca
insitu
Surgical resection Surgical resection Surgical resection +
adjuvant CTx
(FOLFOX)
Surgical resection of
isolated resectable
metastasis +
adjuvant
CTx+palliation for un
resectable ds

Ba enema  apple core appearance

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