Lecture 17 Colon Disorders - Pathology

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IBS, IBD, Gallstone Disease, Colon Cancer
Lecture 17
Small Intestine and Colon
 The small intestine begins at the duodenum (just past the stomach) and ends at the
ileocecal valve (at the junction with the large intestine “colon”).
 Duodenum (12 inch =30 cm long) : shortest and widest;
 Jejunum (2.5 m long) : most of digestion & absorption
 Ileum (longest at 3.5 m): water and electrolyte absorption. Ends at ileocecal valve
 Colon (1.5 m long): water and electrolyte absorption
Irritable bowel syndrome
Definition:
 Irritable bowel syndrome (IBS) is a functional GI disorder characterized by
abdominal pain and altered bowel habits (diarrhea and/or constipation) in the
absence of a specific and unique organic pathology.
 Also can be called: spastic colon, irritable colon, and nervous colon.
 In the past, irritable bowel syndrome has been considered a diagnosis of exclusion;
however, it is no longer considered a diagnosis of exclusion, but it does have a broad
differential diagnosis.
 IBS is thought to affect up to one in five people at some point in their life, and it
usually first develops when a person is between 20 and 30 years of age.
 Female: Male 2:1
 The condition is often life-long, although it may improve over several years.

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IBS Causes
1) Altered GI motility
 Altered GI motility includes distinct aberrations in small and large bowel motility.
 Delayed colonic motility may be more common in patients with constipation-
predominant irritable bowel syndrome than in healthy controls. Similarly,
accelerated colonic transit may be more common in patients with diarrhea-
predominant disease than in healthy controls.
2) Enteric infection
 Infection with Giardia lamblia has been shown to lead to an increased prevalence
of irritable bowel syndrome, as well as chronic fatigue syndrome.
 Colonic muscle hyperreactivity and neural and immunologic alterations of the
colon and small bowel may persist after gastroenteritis.
3) Alterations in the intestinal bacteria
 Small bowel bacterial overgrowth provides a unifying mechanism for the
common symptoms of bloating and gaseous distention in patients with irritable
bowel syndrome.
4) Dietary intolerance
 Bloating and distention may also occur from intolerance to dietary fats.
 Reflex-mediated small bowel gas clearance is more impaired by ingestion of
lipids in patients with irritable bowel syndrome than in patients without the
disorder.
IBS Symptoms
 The symptoms vary between individuals and affect some people more severely than
others.
 They tend to come and go in periods lasting a few days to a few months at a time, often
during times of stress or after eating certain foods.
 The most common symptoms of IBS are:
o abdominal (stomach) pain and cramping, which may be relieved by passing stool.
o a change in the bowel habits – such as diarrhea, constipation, or sometimes both
o bloating and swelling of the stomach
o excessive wind (flatulence)
o occasionally experiencing an urgent need to go to the toilet
o a feeling of not fully emptied the bowels after going to the toilet
o passing mucus with stool

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 In addition to the main symptoms described above, some people with IBS experience a
number of other problems. These can include: a lack of energy (lethargy) , feeling sick
backache, bladder problems (such as needing to wake up to urinate at night,
experiencing an urgent need to urinate and difficulty fully emptying the bladder)
IBS Treatment
 There is no cure for IBS, but the symptoms can often be managed by making changes
to diet and lifestyle.
 For example, it may help to:
o identify and avoid foods or drinks that trigger the symptoms
o alter the amount of fiber in the diet
o exercise regularly
o reduce stress levels
 Medication is sometimes prescribed for people with IBS to treat the individual symptoms
they experience.
Inflammatory bowel disease (IBD)
 Is a term mainly used to describe two diseases, ulcerative colitis and Crohn's disease.
 Both Ulcerative colitis and Crohn’s are long term (chronic) diseases that involve
inflammation of the gastrointestinal tract (gut).
 Ulcerative colitis only affects the colon (large intestine), while Crohn’s disease can affect
the entire digestive system, from the mouth to the anus.
 It is sometimes difficult to tell the difference between the two main types of IBD. If this
is the case, it is known as indeterminate colitis.
Anatomy of the Colon

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Crohn’s Disease
 Chronic IBD, of Unknown etiology , Characterised by Focal, Asymmetrical . Transmural
and occasionally granulomatous inflammation
 It may affect any part of the gastrointestinal tract but particularly the terminal ileum and
proximal colon.
 Fistulae and strictures may occur.
 Unlike ulcerative colitis, there may be unaffected bowel between areas of active disease
(skip lesions).
 The clinical course is characterised by exacerbations and remission.
 Possible causes: a) Infectious agents such as Mycobacterium paratuberculosis,
Pseudomonas spp. and Listeria spp. have all been implicated. b) An increase in TNF-
alpha, high-fat diets and genetic mutations.
 Age of onset: 2 peaks 1) 15-30 Y (more common). Peak 2) 60-80 Y
 Female: Male 1.8:1 Children this is reversed!
Anatomical distribution of Crohn’s Disease
 Crohn’s disease may affect any part of the alimentary tract from mouth to anus.
 About 30% are confined to the small bowel (“regional enteritis”), usually involving the
terminal ileum (“ileitis”).
 50% involve both small and large bowel (“ileocolitis”), usually in continuity.
 About 20% of cases are confined to the colon alone.
 Perianal lesions occur in approximately 30% , but are only rarely the presenting or sole
site of Crohn’s disease.
 Oral and gastroduodenal lesions are also commonly found when carefully sought, but are
clinically important in only a minority of cases.

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Crohn’s Disease- Symptoms
 Abdominal pain, cramping or swelling
 Anemia
 Fever
 Gastrointestinal bleeding
 Joint pain
 Malabsorption
 Persistent or recurrent diarrhoea
 Stomach ulcers
 Vomiting
 Weight loss
Crohn’s Disease- Extra Intestinal

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Investigations
 Serum levels of C-reactive protein (CRP) are useful for assessing a patient's risk of
relapse.
 C-reactive protein is produced by the cells in the liver. It is a a marker of inflammation
in the body
 High CRP levels are indicative of active disease or a bacterial complication. CRP levels
can be used to guide therapy and follow-up.
 Also High erythrocyte sedimentation rate (ESR)
 Antibodies to the yeast Saccharomyces cerevisiae (ie anti-S. cerevisiae antibodies
(ASCA) are more common in Crohn's disease than in ulcerative colitis.
 Perinuclear antineutrophil cytoplasmic antibody (p-ANCA), is more common in
ulcerative colitis than in Crohn's disease.
 These two tests are sometimes useful in differentiating the two conditions but they are not
particularly specific and need to be combined with clinical assessment.
 CBC, U&Es (Urea & Electrolytes), LFTs.
 Stool culture and microscopy. Abdomen X-ray
 Ileocolonscopy and biopsy from the terminal ileum as well as the affected sites
 Small bowel follow through X-ray., If upper GI symptoms- Upper GI endoscopy. If
lower GI symptoms- Flexible sigmoidoscopy
Crohn’s Disease: Consequences of Transmural Inflammation
 Inflammatory masses
 Fistuli
 Intestinal obstruction
 Perforation

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Ulcerative Colitis
 Ulcerative colitis is an idiopathic chronic inflammatory bowel disease that affects only
the mucosa of the colon and is clinically characterized by diarrhea, abdominal pain and
hematochezia.
 The extent of disease is variable and may involve :
 Distal disease (left-sided colitis): colitis confined to the rectum (proctitis) or
rectum and sigmoid colon (proctosigmoiditis).
 More extensive disease includes: left-sided colitis (up to the splenic flexure, 40%
of patients), extensive colitis (up to the hepatic flexure) and pancolitis (affecting
the whole colon, 20% of patients).
 Some patients with pancolitis may have involvement of the terminal ileum due to
an incompetent ileocecal valve.
 The severity of the disease may also be quite variable histologically, ranging from
minimal to florid ulceration and dysplasia. Carcinoma may develop.
 The typical histological (microscopic) lesion of ulcerative colitis is the crypt abscess, in
which the epithelium of the crypt breaks down and the lumen fills with
polymorphonuclear cells.
 The lamina propria is infiltrated with leukocytes. As the crypts are destroyed, normal
mucosal architecture is lost and resultant scarring shortens and can narrow the colon.

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Ulcerative Colitis extension:
Ulcerative Colitis- Epidemiology
 More common than Crohn’s
 Incidence: 10 per 100,000
 Prevalence 240 per 100,000 in the UK
 Age of onset: 2 peaks 1) 15-25 Y (more common). Peak 2) 55-65 Y
 Male: Female= 1:1
 Idiopathic: ?autoimmune condition triggered by colonic bacteria  inflammation
 Genetic component: sibling of an individual who has IBD 17-35 x more risk of
development
 UC decreased in smokers.

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Smoking in IBD
Ulcerative Colitis
 Smoking can protect against UC
 Ex-smokers & nonsmokers are more likely to develop UC
Crohn’s disease
 Twofold risk in current smokers
 Smokers are less responsive to treatment
 Smokers are more likely to develop recurrence of disease after surgery
Ulcerative Colitis- Symptoms
 Bloody diarrhea
 Abdominal Pain (severe and colicky)
 Tenesmus: a clinical symptom, where there is a feeling of constantly needing to pass
stools, despite an empty colon.
 Systemic symptoms: malaise, fever, weightless

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Ulcerative Colitis- Extra-intestinal
 Approximately 4% of patients will have extra-intestinal disease which may include:
 Aphthous ulcers
 Ocular manifestations 5%
o Episcleritis
o Anterior uveitis
 Acute arthropathy affecting the large joints 26%
o Sacroiliitis
o Ankylosing Spondylitis 3%
 Deramatology 19%
o Pyoderma gangrenosum
o Erythema nodosum
 Primary Sclerosing Cholangitis (inflammation causes scars within the bile ducts. These
scars make the ducts hard and narrow and gradually cause serious liver damage).
 Erythema nodosum is an inflammation of the layer of fat lying underneath the skin. The
inflammation causes red rounded lumps (nodules) to form just below the skin surface,
which are tender. Erythema nodosum most commonly affects both shins (‫.)ﺍﻟﺴﺎﻗﻴﻦ‬ Usually,
the nodules heal within six to eight weeks with no treatment needed.

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Diffuse Erythema nodosum In UC
Patchy Erythema nodosum in CD
Ulcerative Colitis- Investigations
 Blood: CBC : anemia, thrombocytosis→VTE (Venous thromboembolism is a disease that
includes both deep vein thrombosis (DVT) and pulmonary embolism (PE)
 LFTs ( Liver function test), U+Es (Urea & Electrolytes)
 CRP:sensitive to measure disease activity and monitor progress
 Serology- pANCA Vs. ASCA
 Stool cultures and microscopy (to exclude infectious causes; Entameba histolytica).
 Imaging
 Abdomen x-ray- acute setting
 Barium enema- can show mucosal structure
 Flexible Sigmoidoscopy and Biopsy- for diagnosis

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Pseudomembranous Colitis
 An acute colitis characterized by formation of an adherent inflammatory exudate
(pseudomembrane) overlying the site of mucosal injury
 Most commonly due to overgrowth of C.difficile, a gram-positive, anaerobic spore
forming bacilus
 Typically occurs after broad-spectrum antibiotics (especially clindamycin, ampicillin, or
cephalosporins) eradicate normal intestinal flora
 Signs/Symptoms
o Self-limited diarrhea to invasive colitis with megacolon or perforation as possible
complications
 Diagnosis
o Detection of C.diff toxin in stool, proctoscopy or colonoscopy
 Treatment
o Stop offending antibiotic and give flagyl or vancomycin
 Prognosis
o High rate of recurrence (20%) despite high response rate to treatment

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Gallstone Disease
Gallbladder & Bile
 Gallstones are small, pebble-like (‫)ﺣﺼﺎﺓ‬ substances that develop in the gallbladder.
 The gallbladder is a small, pear-shaped sac located below the liver in the right upper
abdomen.
 Gallstones form when bile in the gallbladder hardens into pieces of stone-like material.
 Bile helps the body digest fats. Bile is made in the liver, then stored in the gallbladder
until the body needs it.
 The gallbladder contracts and pushes the bile into the common bile duct (CBD) that
carries it to the small intestine, where it helps with digestion.

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The anatomy of the Bile duct

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Bile & Gallbladder Stones
 Bile contains water, cholesterol, fats, bile salts, proteins, and a waste product.
 Bile salts break up fat, and bilirubin gives bile and stool ayellowish brown color. If the
bile contains too much cholesterol, bile salts, or bilirubin, it can harden into gallstones. .
 The two types of gallstones are cholesterol stones and pigment stones.
 Cholesterol stones are usually yellow-green and are made primarily of hardened
cholesterol. They account for about 80 percent of gallstones.
 Pigment stones are small, dark stones made of bilirubin.
 Gallstones can be as small as a grain of sand or as large as a golf ball. The gallbladder
can develop just one large stone, hundreds of tiny stones, or a combination of the two.

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Epidemiology
 Fat, Fair, Female, Fertile, Fourty inaccurate, but reminder of the typical patient
 F:M = 2:1
 10% of British women in their 40s have gallstones
 Genetic predisposition – ask about family history
Pathogenesis
 Composition of bile:
o Bilirubin (by-product of hem degradation)
o Cholesterol (kept soluble by bile salts and lecithin)
o Bile salts/acids (cholic acid/chenodeoxycholic acid): mostly reabsorbed in
terminal ileum (entero-hepatic circulation).
o Lecithin (increases solubility of cholesterol). Lecithin: a class of phospholipids,
important in cell structure and metabolism. They are composed of phosphate,
choline, glycerol (as the ester), and two fatty acids.
o Inorganic salts (sodium bicarbonate to keep bile alkaline to neutralise gastric acid
in duodenum)
o Water (makes up 97% of bile)

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 Cholesterol
o Imbalance between bile salts/lecithin and cholesterol allows cholesterol to
precipitate out of solution and form stones
 Pigment
o Occur due to excess of circulating bile pigment (e.g. Hemolytic anemia)
 Mixed
o Same pathophysiology as cholesterol stones
 Other Factors
o Stasis (e.g. Pregnancy)
o Ileal dysfunction (prevents re-absorption of bile salts)
o Obesity and hypercholesterolemia
Complications of Gallstones
 80% Asymptomatic
 20% develop complications :
 Biliary Colic
 Acute Cholecystitis
o Gallbladder Empyema
o Gallbladder gangrene
o Gallbladder perforation
 Obstructive Jaundice
 Ascending Cholangitis
 Pancreatitis
 Gallstone Ileus (rare)
 Gallbladder Empyema: is an uncommon complication of cholecystitis and refers to a
situation where the gallbladder lumen is filled and distended by purulent material (pus).
Differential Diagnosis of RUQ pain
 Gallstone disease (and its related complications)
 Gastritis/duodenitis.
 Peptic ulcer disease/perforated peptic ulcer. Acute pancreatitis
 Right lower lobe pneumonia
 Myocardial Infarction
 If presenting to A&E (Accident & Emergency) with RUQ pain all patients should get
o Blood tests
o Abdominal X-Ray & CXR (to exclude perforation/pneumonia) & ECG

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Intestinal perforation
Air/gas under the diaphragm - erect chest X-ray. This patient has a large volume of free gas under the
diaphragm. Dark crescents have formed separating the thin diaphragm from the liver on the right, and
bowel on the left. This patient had a perforated duodenal ulcer.
Normal CXR

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Which Gallstone Complication?
 Can differentiate between gallstone complications based on:
o History
o Examination
o Blood tests: CBC, LFT, CRP, Clotting, Amylase.
Investigations for gallstone disease
 Bloods (already discussed)
 Abdomen XR (10% gallstones are radio-opaque)
 CXR (to exclude perforation – MUST!)
 ECG (to exclude MI)
 Ultrasound: first line investigation in gallstone disease
o Confirms presence of gallstones
o Gall bladder wall thickness (if thickened suggests cholecystitis)
o Biliary tree calibre (CBD/extrahepatic/intrahepatic) – if dilated suggests stone in
CBD (normal CBD <8mm).
o Sometimes CBD stone can be seen.
 MRCP: To visualise biliary tree accurately (much more accurate than USS)
o Diagnostic only but non-invasive
o Look for biliary dilatation and any stones in biliary tree
 ERCP: Diagnostic and therepeutic in biliary obstruction
o Diagnostic and therepeutic but invasive
o Look for biliary tree dilatation and stones in biliary tree
o Stones can be extracted to unobstruct the biliary tree and perform sphincterotomy
o Risk of pancreatitis, duodenal perforation
 PTC: To unobstruct biliary tree when ERCP has failed
o Invasive – higher complication rate than ERCP
 CT: Not first line investigation. Mainly used if suspicion of gallbladder empyema,
gangrene, or perforation and in acute pancreatitis (USS not good for looking at pancreas)

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Gallstone in Abdominal Ultrasound
 Curved arrow: Two small stones at GB neck
 Straight arrow: Thickened GB wall
 ◄ : pericholecystic fluid = dark lining outside the wall
Biliary tract disease
 Biliary colic is the term used to describe a type of pain related to the gallbladder that
occurs when a gallstone transiently obstructs the cystic duct and the gallbladder contracts.
 Biliary colic and cholecystitis are in the spectrum of biliary tract disease. This spectrum
ranges from asymptomatic gallstones to biliary colic, cholecystitis, choledocholithiasis,
and cholangitis.
 Gallstones may temporarily obstruct the cystic duct or pass through into the common bile
duct, leading to symptomatic biliary colic, which develops in 1-4% of patients with
gallstones annually.
 Cholecystitis occurs when obstruction at the cystic duct is prolonged (usually several
hours) resulting in inflammation of the gallbladder wall.
 Acute cholecystitis develops in approximately 20% of patients with biliary colic if they
are left untreated. However, the incidence of acute cholecystitis is falling, likely due to
increased acceptance by patients of laparoscopic cholecystectomy as a treatment of
symptomatic gallstones.
 Choledocholithiasis occurs when the stone becomes lodged in the common bile duct,
with the potential sequelae of cholangitis and ascending infections.
 Ascending cholangitis or acute cholangitis is an infection of the bile duct (cholangitis),
usually caused by bacteria ascending from its junction with the duodenum. It tends to
occur if the bile duct is already partially obstructed by gallstones.

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Cholecystectomy
 Cholecystectomy is a surgical procedure to remove the gallbladder
 Asymptomatic gallstones do not require operation
 Indications
o A single complication of gallstones is an indication for cholecystectomy
(this includes biliary colic)
o After a single complication risk of recurrent complications is high (and
some of these can be life threatening e.g. cholangitis, pancreatitis)
 Advantages:
o Less post-op pain
o Shorter hospital stay
o Quicker return to normal activities
 Disadvantages:
o Inexperience at performing open cholecystectomies

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Diverticular disease (Diverticulosis)
 Diverticulosis is a condition in which diverticula are present in the intestine without
signs of inflammation.
 Diverticula are small, bulging pouches (saclike) that can form in the lining of the
digestive system. They are found most often in the lower part of the colon.
 Diverticula are common, especially after age 40, and seldom cause problems.
 Diverticula usually develop when naturally weak places in the colon give way under
pressure. This causes small pouches to protrude through the colon wall.
 True diverticula involve all layers of the intestinal wall, whereas false diverticula
involve only the muscularis.
 Diverticular disease occurs with increased frequency in elderly individuals and may be
associated with age-related changes in the bowel.
 Individuals who consume a low-fiber, low-bulk diet also appear at greater risk for the
formation of diverticula.

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Diverticulitis
 Diverticulitis occurs when diverticula tear, resulting in inflammation or infection or both ,
due to trapping of intestinal contents and its accumulation in the diverticula. This may
lead to eventual perforation of the intestinal wall and sepsis.
 Signs and Symptoms of diverticulitis include:
o Pain, which may be constant and persist for several days. Pain is usually felt in
the lower left side of the abdomen, but may occur on the right, especially in
people of Asian descent.
o Nausea , vomiting &Fever.
o Abdominal tenderness.
o Constipation or, less commonly, diarrhea.
Diverticulitis Risk Factors
Several factors may increase the risk of developing diverticulitis:
 Aging: The incidence of diverticulitis increases with age.
 Obesity: Being seriously overweight increases the risk of developing diverticulitis.
 Smoking: People who smoke cigarettes are more likely than nonsmokers to experience
diverticulitis.
 Lack of exercise: Vigorous exercise appears to lower the risk of diverticulitis.
 Diet high in animal fat and low in fiber, although the role of low fiber alone isn't clear.
 Certain medications: Several drugs are associated with an increased risk of
diverticulitis, including steroids, opiates and NSAIDs.
Diverticulitis Complications
Patient presents with complications of diverticular disease, acute - chronic.
1) Acute diverticulitis - Feces obstructs the neck of a diverticulum  inflammation.
 Marked by suprapubic pain, shifting to left iliac fossa.
 Fever, nausea and vomiting.
 ‘left-sided appendicitis’.
 Local signs of peritonitis, colicky abdominal pain, raised WBC.
 Change in bowel habit eg. constipation.
2) Perforated diverticulitis - Sudden onset of pain with generalised peritonitis.
 Shocked
 Free gas on erect chest X-ray.

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3) Diverticular abscess - Perforated diverticulum contained by anatomical structures  local
abscess.
 Abdominal mass on examination.
4) Fistulas – most commonly with bladder.
 Colovesical fistula; cystitis, pneumaturia, recurrent UTIs and faecal debris in the urine.
 Colovaginal fistula; faecal discharge per vagina.
 Fistula with the small intestine leads to diarrhea.
5) Hemorrhage - Diverticula erode into adjacent blood vessels.
 Sudden rush of bright or dark red blood per rectum.
 Usually painless.

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Management
 Diverticulosis managed with dietary advice (increased fibre, increased fluids).
 Uncomplicated symptomatic disease managed similarly, with a well-balanced diet and
smooth-muscle relaxants if necessary.
 Anti-spasmodics sometimes helpful.
 Avoid stimulants.
 Anastamoses for bowel resection must be made with rectum to avoid recurrence
 Acute attacks of diverticulitis treated with cephalosporin and metronidazole.
o Serious cases may require hospital admission for bowel rest, i.v fluids, and
antibiotic therapy.
 Diverticular abscesses initially managed as above.
o Paracolic abscesses can  purulent / feculent peritonitis. Usually drained
surgically / under radiological guidance.
o Sometimes need resection.
Summary

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Colorectal Cancer Overview
 Colorectal cancer includes cancers of both the large intestine (colon), and the rectum; the
last 13 cm of the colon.
 Most colon and rectal cancers begin as small, noncancerous (Benign) clumps of cells
called adenomatous polyps. Over time (approximately 10 years) some of these polyps
(only 2%) will progress to cancer.
 Colorectal Cancer arises in the Epithelial cells outlining the lumen of the Colon and
Rectum (a Simple Glandular Columnar Epithelium).
 The cancer is thus called a Colorectal Adenocarcinoma. This is what we mean when we
talk about Colorectal Cancer!
 Colorectal cancer frequently begins without symptoms
 Cancer of the colon is more common in women; cancer of the rectum is more common in
men.
 Synchronous cancers (2 or more primary tumors identified in the same patient and at the
same time) occur in 5% of patients.
Pathophysiology
 The Primary risk factor for colorectal cancer is age. In most cases colorectal cancer
strikes men and women over age 50.
 Several disorders & preexisting conditions are linked to colorectal cancer, including:
1) Familial Adenomatous Polyposis (FAP):
 such as Gardner’s syndrome & Peutz-Jeghers syndrome.
 FAP comprises less than 0.5% of all colorectal cancers.
 FAP is due to mutation within a single gene; the adenomatous polyposis coli (APC) gene,
found in Chromosome 5 which results in hundreds or thousands of colorectal adenomas
developing during adolescence and adulthood, with an almost certain risk of
adenocarcinoma by middle age.
 Normally the APC gene is classified as a tumor suppressor gene. Tumor suppressor genes
prevent the uncontrolled growth of cells that may result in cancerous tumors.
2) Chronic Ulcerative Colitis. 3) Crohn’s Disease.
4) Hereditary Non-Polyposis Colorectal Carcinoma (HNPCC) accounts for 5-10% of all
colorectal cancers, results from a dominantly inherited alteration within one of four DNA
mismatch repair genes.
5) Other pelvic cancers treated with abdominal radiation.
 In these disorders, the risk of cancer at any time is related to the age of onset and
duration of the underlying disease.

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Incidence & Location
 About 30% of all Colorectal Cancer is located in the Rectum,
 25% in the Sigmoid Colon,
 3% in the Descending Colon,
 3% in the Left Flexure,
 8% in the Transverse Colon,
 5% in the Right Flexure,
 10% in the Ascending Colon, and
 15% in the Cecum.
Polyp & Cancer
Causes of Colorectal Cancer
 The exact causes of colorectal cancer are unknown, but the disease appears to be caused
by both inherited and lifestyle factors.
 Diets high in fat and low in fruits and vegetables – such as those that include red meat,
fried foods and high-fat dairy products – may increase the risk of colorectal cancer by
slowing fecal movement through the bowel. This results in prolonged exposure of the
bowel mucosa to digested materials and may encourage mucosal cells to mutate.
 Lifestyle factors –such as cigarette smoking, a sedentary lifestyle, and obesity – also may
increase the risk of developing the disease.
 Genetic factors may determine a person's susceptibility to the disease; whereas dietary
and other lifestyle factors may determine which at-risk individuals actually go on to
develop the disease.
Non-Dietary Risk Factors In Colorectal Cancer
 Medical conditions
o Colorectal adenomas
o Long-standing extensive ulcerative colitis
o Acromegaly & Pelvic radiotherapy

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 Others
o Obesity and sedentary lifestyle-may be related to dietary factors
o Alcohol and tobacco (weak association)
 Hereditary Risk Factors
o Family members with colon cancer
o Family members with colon adenomas
o Family members with breast, ovarian, or uterine cancer
o Cancer Family syndromes (e.g. FAP, HNPCC, Peutz-Jeghers syndrome)
Warning Signs
 No Symptoms — which is why screening for the disease is so crucial
 Blood in or on the stool (orange or bright red).
 Change in bowel habits.
 Stools that are narrower than usual.
 General stomach discomfort (bloating, fullness, and/or cramps).
 Vomiting.
 Diarrhea, constipation, or feeling that the bowel does not empty completely
 Frequent gas pains.
 Weight loss for no apparent reason.
 Rectal bleeding.
 Constant tiredness.
Screening and diagnosis
 Digital (finger) Rectal Exam (DRE), in which the doctor checks for abnormalities
of organs or other structures in the pelvic and lower abdominal area.
 Fecal occult blood test (FOBT), in which a small sample of stool is checked for
blood.
 Flexible sigmoidoscopy, Colonoscopy, which allows to look inside the lower part
of the large intestine for abnormal growths.
 Double-contrast barium enema, an X-ray of the large intestine
 Biopsy, if any polyps or tumors are found during a sigmoidoscopy or
colonoscopy.
 Complete blood count (CBC).

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 Blood chemistry panel.
 Elevated serum carcinoembryonic antigen (CEA) is not specifically associated
with colorectal cancer, but levels are high in 70% of patients.
 If CEA is high preoperatively and low after removal of a colon tumor, monitoring
CEA may help to detect recurrence.
 CA 19-9 and CA 125 are other tumor markers that may be elevated.
Endoscopy
Treatment of colorectal cancer
 Treatment for colorectal cancer depends upon the stage, location, metastasis, and size
of the cancer, as well as the general health.
 Treatment may include:
 Surgery to remove the cancer (Colectomy). Radiation therapy. Chemotherapy.
 Chemoprevention
 Aspirin and other NSAID’s
 Calcium
 Folate
 Fiber
 Hormone Replacement Therapy
 Vitamins/Antioxidants

500

Percent % of people who have a metastasis
Recommendation
 Early detection saves lives – colorectal cancer is preventable, even curable when
detected early.
 If colorectal cancer is found early enough, the patient has more than a 90 percent chance
of survival.
 Colorectal cancer screenings are safe and effective.
 Several screening methods can be used to detect polyps before they become cancerous,
such as fecal occult blood test, colonoscopy, flexible sigmoidoscopy and barium x-ray.
 These tests also can detect cancer in its early stages.
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Lecture 17 Colon Disorders - Pathology

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Lecture 17 Colon Disorders - Pathology