Benign and malignant

lesion of lower GI
Salma Marji
Reem Nassar
Ghayda`a Nemer
Farah Qandeel
Eba`a AbuMahfouz
Zainab almadani
Abrar Assanie
Ala`a Azab
Anatomy

The wall of the colon and rectum comprise five distinct

layers: mucosa, submucosa, inner circular muscle, outer
longitudinal muscle, and serosa.

In the colon, the outer longitudinal muscle is separated into

three teniae coli , which converge proximally at the
appendix and distally at the rectum
Blood supply
 Till the distal transverse colon (midgut), it is supplied by
superior mesenteric artery. Distal to it (hindgut), it is
supplied by inferior mesenteric artery.
 venous and lymphatic drainage
 The SMV drains the small
intestine, cecum, and ascending
and transverse colon , The IMV
drains the descending colon, the
sigmoid colon, and the rectum
The IMV fuses with the splenic
vein, which then joins the SMV to
form the portal vein.

 Lymphatic drainage is in the

inferior mesenteric lymph nodes
 Polyp
 Any projection from the
surface of the intestinal
(colorectal) mucosa into
the lumen regardless of
the histological nature.
 ● Can either be
pedunculated (with a
stalk) or sessile (flat).
 ● Approximately 50%
occur in the
rectosigmoid region,
and 50% are multiple.
 Classification of polyps

Non-neoplastic Neoplastic

Malignant
Hyperplastic Benign Adenomas
Adenocarcinoma

Inflammatory

Juvenile polyposis
PeutzJeghers
Hamartomatous Cronkhite–Canada
Cowden syndrome
Hyperplastic polyps
 The most common non-neoplastic
polyps in the colon
 They are typically located in the
rectosigmoid and are less than 5
mm in size.
 They have low malignant
potential.
 Almost always asymptomatic
 they must be distinguished from
sessile serrated adenoma / polyp
that may demonstrate very
similar histopathologic features
and are considered to have
malignant potential.
 No further treatment is required
 Hamartomatous
 Juvenile polyposis Syndrome  Peutz-Jeghers syndrome

 Cronkhite–Canada syndrome  Cowden Syndrome

 Juvenile polyposis Syndrome
 Autosomal Dominant, mutation in BMPR1A and SMAD4
 Multiple polyps throughout the GI tract around age
10 years.
 50% lifetime risk of colorectal cancer
 Colonoscopic surveillance is recommended 1–2 yearly
from the age of 15–18 years.
 Most frequent presentation: painless hematochezia
Peutz-Jeghers syndrome
 Autosomal Dominant
 STK11 mutations
 It is characterized by:
1. polyposis of the small intestine
and, to a lesser extent, polyposis of
the colon
2. Melanotic pigmentation of face,
lips, oral mucosa, and palms
 Increased risk of both
gastrointestinal and non
gastrointestinal cancers including
breast cancer
 Cronkhite–Canada syndrome:
Rare, nonheritable syndrome
Intestinal polyposis with alopecia, nail atrophy and brown
macular hyperpigmentation

 Cowden Syndrome:
Autosomal Dominant
There is an increased risk of colorectal cancer.
Benign and malignant disease of the breast and thyroid are
the main risks.
 Inflammatory Polyps

 Non-Neoplastic
 ● Occur most commonly in the context of inflammatory bowel disease, but
they may also occur after amebic colitis, ischemic colitis.
 ● Usually smaller than 2 cm
 ● Management do not require excision unless they cause symptoms (eg,
bleeding, obstruction). Because they cannot be distinguished from
adenomatous polyps based on gross appearance, they should be removed.
 Adenoma

 Adenoma is a benign tumor of glandular tissue, such as the mucosa of

stomach, small intestine, and colon, in which tumor cells form glands or gland
like structures
 Colorectal adenomas are extremely common in the Western world and the
prevalence rises with age; 50% of people over 60 years of age have
adenomas, and in half of these the polyps are multiple

 They are more common in the rectum and distal colon and are either
pedunculated or sessile

 Sessile: broad base attached to colon / Pedunculated: attached via stalk

Adenoma
 Histologically, they are classified as
either tubular, villous or tubulovillous,
according to the glandular
architecture. Nearly all forms of
colorectal carcinomas develop from
adenomatous polyps, although not all
polyps carry the same degree of risk.

 Tubular: most common 75%,

rectosigmoid in 20% mostly
pedunculated

 Tubulovillous 15%

 Villous: 10%, rectosigmoid in 80%,

mostly sessile
 Adenoma
 Familial adenomatous polyposis (FAP):
 is an uncommon autosomal dominant disorder.

 All have APC gene mutation

 hundreds to thousands of polyps in colon

 if untreated 100% of patients develop cancer by the fourth or fifth decade of life

 prophylactic colectomy is often recommended to prevent the development of cancer

 In those affected, cancer will develop within 10–15 years of the appearance of
adenomas and 90% of patients will develop colorectal cancer by the age of 50 years.

 Despite surveillance, approximately 1 in 4 patients with FAP have cancer by the time
they undergo colectomy.
 Adenoma
FAP variants:
❖ Gardner’s Syndrome:
Epidermoid cysts (extremities, face, scalp) (50%), Benign
osteomas, especially skull and angle of mandible (50–90%),
Dental abnormalities (15–25%)

❖ Turcot’s syndrome :
FAP with primary CNS tumors (astrocytoma or
medulloblastoma)
 Hereditary Non-Polyposis Colorectal
Cancer/Lynch Syndrome
HNPCC :
 “Autosomal dominant”
 Inherited mutation of DNA mismatch repair enzymes
 About 80% lifetime risk of colon cancer
 could arise from adenomas “ flat adenoma” or without pre-existing
adenoma “de novo”.
 The most common malignancies are colorectal and endometrial
cancers.
 Lynch type I: results in more colonic cancers, often on the right side
 Lynch type 2: results in more extracolonic cancers
 Adenoma- carcinoma

 Some types of polyps can change into cancer over time ( usually many
years ) , but not all polyps become cancer (~ 30% of people >40 years
old have adenomatous polyps , but only 1% of adenomatous polyps
ever become malignant )
  Treatment of adenomatous polyps

involves colonoscopic polypectomy.

● If some cannot be safely removed
colonoscopically, biopsy should be performed
and a segmental resection of the colon done if
the lesion is:
● Villous adenoma
● Large, ulcerated, dysplastic.
● Indurated.
 Epidemiology

 One of the most common cancers in the world.

 The most common GI cancer.
 Third most common cancer (after lung& prostate/after lung & breast)
 Third most common cause of cancer death.
 Nearly equal incidence in both sexes.
 Some statistics show slight male predominance.
 Peak incidence is 60-70 years of age.
Aetiology
 When colorectal cancer is found in a
young person:
 (1) preexisting ulcerative colitis .
 (2) one of the polyposis syndromes
Patient factors: must be suspected.
 (3) individuals with hereditary
nonpolyposis colorectal cancer
syndrome also known as Lynch
syndrome.
  (1) Low contents of unabsorbable
vegetable fiber
 (2) High contents of refined
carbohydrates
 (3) High fat content
 (4) Decreased intake of protective
Environmental factors: micronutrients such as vitamins A, C,
& E.
 (5) Epidemiologic studies suggest that
use of aspirin & other NSAIDs exerts a
protective effect against colon
cancer. In the Nurses' Health Study,
women who used 4 to 6 tablets of
aspirin daily for 10 years or more had
a lower incidence of colon cancer.
 Two well-defined genetic pathway
of colon cancer:
Colorectal Carcinogenesis: 1. Chromosomal instability
pathway
2. Microsatellite instability
 Chromosomal instability

Chromosomal inactivity/Adenoma-carcinoma sequence:

Sequence of genetic events seen in colorectal cancer, lead to cancer over many
years, progression probably take 10-40 yrs.
Clinical Phenotype: FAP
Mutation APC gene
Left sided predominant cancers(descending colon, sigmoid, rectum)
 Microsatellite instability

Less common in colorectal cancer development

Right-sided predominant cancers (proximal tumors)
Can arise de novo without polyp (No precursor lesions)
Mismatch paired, gene mutation lead to accumulation of errors.
 Screening

Stool based test: Direct visualization:

➢ fecal occult blood test (FOBT) ➢ Colonoscopy
➢ Fecal immunochemical test (FIT) ➢ Flexible sigmoidoscopy
➢ FIT-DNA test ➢ CT colonography
 Screening

American cancer society guidelines for CRC:

 Low-risk patients: colonoscopy every 10 yrs., flexible sigmoidoscopy every 5
yrs., FOBT yearly or CT colonprophy every 5 yrs.

 Increased-risk patients: colonoscopy at age 40, colonoscopy in patients with

any 1st degree relatives with either colon cancer or adenomatous polyp. Time
between surveillance colonoscopies depends upon cancer potential of polyps.

 CT scan has high yield for detecting larger polyps and cancers, areas of
adherent stool can be mistaken for small polyps.
  Cancers of the right colon are usually
Signs exophytic lesions associated with occult blood
loss, resulting in iron deficiency anemia
and
symptoms:  At advanced stages of the disease, patients
may have a palpable right lower abdominal
mass.

 Cancers that arise primarily in the left and

. sigmoid colon are more frequently annular and
invasive, resulting in obstruction .and
macroscopic rectal bleeding .

 Cancers of the rectum also cause a symptom

complex of rectal bleeding, obstruction, and,
occasionally, alternating diarrhea and
constipation
 Investigations

 CBC, LFT
 Fecal occult Blood test.
 Barium enema.
 CT colonography (virtual colonography)
 Lower Endoscopy/ colonoscopy/ sigmoidoscopy
 Endorectal US for rectal Ca
 CEA Tumor marker. “Follow up & recurrence ”
 CT, MRI, Chest X-ray, PET scan “ metastasis ”
Lower Endoscopy
(diagnostic and
therapeutic )
 Barium Enema
● filling defects
● apple core appearance
  simple and not expensive

 the sensitivity and specificity of

this test are low; More than one
third of the patient who are
having a positive test the cause of
Fecal occult blood test bleeding is not cancer (Other
diseases produce blood like
hemorrhoids, anal fissures and
peptic ulcers.) .

 More than one third of the patient

with colorectal cancer will have a
negative test
Staging of colon cancer

 TNM classification:
In general, the cancer stage becomes more advanced as the tumor enlarges and
invades the colonic wall:
o TNM stage I: extends into submucosa (T1) or muscularis (T2); no nodal
involvement; no metastases.
o TNM stage II (subclassifications A, 8, C): extends past muscularis into tissues
around the colorectal area (T3) or into visceral peritoneum (T4a) or is directly
invasive (T4b); no nodal involvement; no metastases
o TNM stage Ill (subclassifications A, 8, and C): any combination ofTl-T4b with
nodal involvement and no metastases
o TNM stage IV: any combination ofTl-T4b, any N, with distant metastases
Treatment of CRC

Surgery

Chemotherapy (systemic, chemoembolization), before (neoadjuvant) or after

(adjuvant) surgery

Radiotherapy (external, internal) (before or after surgery)

Combination
 1. Right hemicolectomy

2. Left hemicolectomy

3. Total colectomy
Types of surgeries :
4. sigmoidectomy

5. Anterior resection ( removal of the rectum ) ❑

Abdominoperineal resection (removal of the rectum and the
anal canal )

6. Put colostomy (permanent or temporary ) ❑ Put

ileostomy
  Removal of the lymphatics that drain
the tumor region should be part of the
operation because nodal involvement
is present in more than 30% of
specimens
 new chemotherapeutic agent; FOLFOX
Treatment (5- FU, leucovorin and oxaliplatin) is
the standard treatment regimen
currently
 Neoadjuvant chemoradiotherapy is
advised for rectal cancer especially in
the presence of lymph nodes; This
allows shrinkage of the tumor leading
to a more complete resection and
reduces the complications from
postoperative radiation,, , it also
causes enough tumor shrinkage in a
very low rectal cancer to allow
sphincter preservation.
 Follow up

 A frequently used approach is a visit every 3 months for 2 years, every 6

months for 3 years, and then yearly until 5 or 10 years postresection.
 Visits include physical examination and measurement of carcinoembryonic
(CEA) levels. Colonoscopy is usually performed at 1 and 2 years
postoperatively and then every 2 to 3 years after.
 Most recurrences occur in the first 18 to 24 months
 A potentially important new diagnostic modality used to detect widespread
metastases in colorectal cancer is the positron emission tomography (PET)
scan.
 Thank you!
References:
Davidson's principles and practice of medicine 22nd edition
MedStudy 16th Edition internal medicine