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CARCINOMA COLON
DR ASHWINI KUMAR
ASSISTANT PROFESSOR
DEPARTMENT OF GENERAL SURGERY
AIIMS-P
TOPICS TO BE COVERED
Epidemiology,
Risk Factors,
Pathogenesis,
Types
&
Preventive Measures
CARCINOMA COLON
• Colorectal carcinoma -most common malignancy of
the gastrointestinal tract.
• Approximately 1/3 of the tumours are in the rectum
and 2/3 in the colon.
• The burden of disease is greater in men than in
women (56% vs 44%).
• Colorectal cancer-more in resource-rich countries.
• More than 90% of cases diagnosed are in people
older than age 50 years
9/
RISK FACTORS
• The prevalence-closely associated with intake of red meat and
particularly processed meat products (haem and N-nitroso
compounds).
(What do you consider as red meat?
Red meat refers to all mammalian muscle meat, including, beef, veal,
pork, lamb, mutton, horse, and goat)-WHO
• Increased risks for colorectal cancer have also been associated with
smoking and alcohol
• Acromegaly, which is associated with increased levels of circulating
human growth hormone and insulin-like growth factor-1, increases
risk.
9/4/20XX
• Patients with ureterosigmoidostomy are also at increased risk
for both adenoma and carcinoma formation
• Pelvic irradiation may increase the risk of developing rectal
carcinoma.; for example patients with prostate cancer and are
treated with radiation, the risk of rectal cancer increases
significantly
• Other factors that increase the risk of developing colorectal
cancer include infammatory bowel disease (IBD) .
• Cholecystectomy may marginally increase the risk of right-
sided colon cancer.
9/4/20XX
PROTECTIVE FACTORS
A protective effect of dietary fibre is also suggested by epidemiological
studies. increased roughage is associated with reduced colonic transit
times that in turn reduce exposure of the mucosa to dietary carcinogens.
• However, there is increasing evidence associating the colonic
microbiota with inflammation, gene methylation and dysplastic
changes.
• The epidemiological evidence supporting prostaglandin inhibitors,
particularly ASPIRIN, in preventing colorectal cancer is substantial
• high magnesium and calcium intake may be protective.
• A protective potential for antioxidants such as vitamin E and selenium
is as yet unproven
9/4/20XX
EPIDEMIOLOGY-IN BRIEF
• Ageing-Age 50 years and above
• Heredity - 80% sporadic ,20% family history present
• Diet-high in animal fat at more risk
• Alcohol
• Obesity and sedentary life style pre
• Smoking
• Inflammatory Bowel Disease-long term colitis
GENETIC ASSOCIATIONS
• Mutations of the APC gene occur in two-thirds of colonic
adenomas and are thought to develop early in the
carcinogenesis pathway.
• K-ras mutations result in activation of cell signalling pathways
and are more common in larger lesions, suggesting that that
they are later events in mutagenesis.
• The p53 gene is frequently mutated in carcinomas but not in
adenomas and therefore thought to be a marker of invasion.
EVIDENCE FOR ADENOMA–CARCINOMA
SEQUENCE
• The distribution of adenomas is similar to that of cancers
(70% left sided)
• Larger adenomas are more likely to be dysplastic than small
adenomas
• The majority of early cancers have adjacent adenomatous
tissue
• Adenomas are found in one-third of specimens resected for
colorectal cancer
• Incidence of colorectal cancer decreases within a screening
programme that involves colonoscopy and polypectomy
9/4/20XX
TYPES
Macroscopically, the tumour may take one of
several forms: annular cancers tend to give rise to
obstructive symptoms whereas ulcerating cancers
tend to present with bleeding.
• Most large bowel cancers arise from the left
colon, notably the rectum (38%), sigmoid (21%)
and descending colon (4%). Cancer of the
caecum (12%) and ascending colon (5%) is less
common but may be gradually increasing in
incidence.
• Cancer of the transverse colon (5.5%), flexures
(2–3%) and appendix (0.5%) are relatively
uncommon.
Microscopically the neoplasm is a columnar cell
adenocarcinoma
METASTASIS
• Spread Colonic cancer can spread locally, via the lymphatics, bloodstream
(haematogenous) or across the peritoneal cavity transcoelomic spread).
• Direct spread may be longitudinal or radial. Radial spread may be
retroperitoneal into the ureter, duodenum and posterior abdominal wall
muscles or intraperitoneal into adjacent organs or the anterior abdominal
wall. In general, involvement of the lymph nodes by tumour progresses from
those closest to the bowel along the course of lymphatics to central nodes.
• Haematogenous spread is most commonly to the liver via the portal vein.
One-third of patients will have liver metastases at the time of diagnosis and
50% will develop metastases at some point, accounting for the majority of
deaths.
• The lung is the next most common site of metastatic disease whereas spread
to the ovaries, brain, kidney and bone is less common. Colorectal cancer can
spread from the serosa of the bowel or via subperitoneal lymphatics to other
structures within the peritoneal cavity, including peritoneum, ovary and
omentum.
CLINICAL FEATURE
• Clinical features Carcinoma of the colon typically occurs in patients over 50
years of age and is most common in the eighth decade of life.
• Emergency presentation occurs in 20% of cases and is associated with a
considerably worse prognosis, even when matched for disease stage
• A first-degree relative who has developed colorectal cancer before the age
of 50 years may indicate one of the colorectal cancer familial syndromes.
• Tumours of the left side of the colon usually present with a change in bowel
habit or rectal bleeding, while proximal lesions typically present with iron
defIciency anaemia or a mass .
• Patients may present with metastatic disease
PATHOGENESIS
• It is now well accepted that the majority of colorectal
carcinomas evolve from adenomatous polyps; sequence of
events is the adenoma-carcinoma sequence.
• WHAT IS POLYP - Polyp is a nonspecific clinical term that
describes any projection from the surface of the intestinal
mucosa regardless of its histologic nature
POLYP
• Colorectal polyps may be classified as
1. Neoplastic (Tubular Adenoma, Villous Adenoma, Tubulovillous
Adenomas, Serrated Adenomas/ Polyps)-TVS
2. Hyperplastic
3. Hamartomatous (Juvenile, Peutz-jeghers, Cronkite-canada), Or
-JPC
4. Inflammatory (Pseudopolyp, Benign Lymphoid Polyp)
NEOPLASTIC POLYPS
• . Adenomatous polyps are common, occurring in up to 25% of the population older
than 50 years of age in the United States.
• these lesions are dysplastic. The risk of malignant degeneration is related to both the
size and type of polyp.
1) Tubular adenomas -malignancy in only 5% of cases,
2) villous adenomas may harbor cancer in up to 40%. (VILLAIN)
3) Tubulovillous adenomas are at intermediate risk (22%).
• Invasive carcinomas are rare in polyps smaller than 1 cm; the incidence increases with
size.
• The risk of carcinoma in a polyp larger than 2 cm is 35% to 50%.
• Although most neoplastic polyps do not evolve to cancer, most colorectal cancers
originate as a polyp
SERRATED POLYPS
• Serrated polyps are a recently recognized, histologically distinct group
of neoplastic polyps.
• These lesions were long thought to be similar to hyperplastic polyps
with minimal malignant potential.
• However, it has become clear that some of these polyps will develop
into invasive cancers
HYPERPLASTIC POLYPS
• .
9/4/20XX
• Hyperplastic polyps are extremely common in the colon.
• These are usually small (<5 mm) and show histologic characteristics of hyperplasia
without any dysplasia.
• They are not considered premalignant, but cannot be distinguished from
adenomatous polyps colonoscopically and are therefore often removed.
• In contrast, large hyperplastic polyps (>2 cm) may have a slight risk of malignant
degeneration.
• Moreover, large polyps may harbor foci of adenomatous tissue and dysplasia.
Hyperplastic polyposis is a rare disorder in which multiple large hyperplastic
polyps occur in young adults.
• These patients are at slightly increased risk for the development of colorectal
cancer.
HAMARTOMATOUS POLYPS
(JUVENILE POLYPS)
• .
9/4/20XX
• In contrast to adenomatous and serrated polyps, hamartomatous polyps (juvenile
polyps) usually are not premalignant.
• These lesions are the characteristic polyps of childhood but may occur at any age.
• Bleeding is a common symptom, and intussusception and/or obstruction may occur
• In contrast to adenomatous polyposis syndromes, these conditions are often
associated with mutation in PTEN.
• Familial juvenile polyposis is an autosomal dominant disorder in which patients
develop hundreds of polyps in the colon and rectum
• Unlike solitary juvenile polyps, these lesions may degenerate into adenomas and
eventually carcinoma
HAMARTOMATOUS POLYPS-
PEUTZ JEGHERS
• .
9/4/20XX
• Characterized by polyposis of the small intestine and,
to a lesser extent, polyposis of the colon and rectum.
• Characteristic melanin spots are often noted on the
buccal mucosa and lips of these patients.
• The polyps of Peutz-Jeghers syndrome are generally
considered to be hamartomas and are not thought to
be at significant risk for malignant degeneration
HAMARTOMATOUS POLYPS
-CRONKITE CANADA
• .
9/4/20XX
• A disorder in which patients develop gastrointestinal polyposis
in association with alopecia, cutaneous pigmentation, and
atrophy of the fingernails and toenails.
• Diarrhea is a prominent symptom, and vomiting,
malabsorption, and protein-losing enteropathy may occur.
• Most patients die of this disease despite maximal medical
therapy, and surgery is reserved for complications of polyposis
such as obstruction
INFLAMMATORY POLYPS
(PSEUDOPOLYPS).
• .
9/4/20XX
• Inflammatory polyps occur most commonly in the
context of inflammatory bowel disease, but may also
occur after amebic colitis, ischemic colitis, and
schistosomal colitis.
• These lesions are not premalignant, but they cannot
be distinguished from adenomatous polyps based on
gross appearance and therefore should be removed
DIFFERENT METHODS AND SCOPY
• .
9/4/20XX
• Anoscope-8 cms
• Proctoscope-for rectum and terminal sigmoid
-25 cm length
• Sigmoidoscope-60 cms in length-till splenic
flexure
• Colonoscpe-100-160 cms till terminal ileum
CONSTIPATION
• .
9/4/20XX
Two or fewer bowel movements per
week
and/or straining at stool more than 25%
of the time.
Rome criteria for chronic constipation

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Carcinoma Colon (large intestine ).pptx

  • 1. CARCINOMA COLON DR ASHWINI KUMAR ASSISTANT PROFESSOR DEPARTMENT OF GENERAL SURGERY AIIMS-P
  • 2. TOPICS TO BE COVERED Epidemiology, Risk Factors, Pathogenesis, Types & Preventive Measures
  • 3. CARCINOMA COLON • Colorectal carcinoma -most common malignancy of the gastrointestinal tract. • Approximately 1/3 of the tumours are in the rectum and 2/3 in the colon. • The burden of disease is greater in men than in women (56% vs 44%). • Colorectal cancer-more in resource-rich countries. • More than 90% of cases diagnosed are in people older than age 50 years 9/
  • 4. RISK FACTORS • The prevalence-closely associated with intake of red meat and particularly processed meat products (haem and N-nitroso compounds). (What do you consider as red meat? Red meat refers to all mammalian muscle meat, including, beef, veal, pork, lamb, mutton, horse, and goat)-WHO • Increased risks for colorectal cancer have also been associated with smoking and alcohol • Acromegaly, which is associated with increased levels of circulating human growth hormone and insulin-like growth factor-1, increases risk. 9/4/20XX
  • 5. • Patients with ureterosigmoidostomy are also at increased risk for both adenoma and carcinoma formation • Pelvic irradiation may increase the risk of developing rectal carcinoma.; for example patients with prostate cancer and are treated with radiation, the risk of rectal cancer increases significantly • Other factors that increase the risk of developing colorectal cancer include infammatory bowel disease (IBD) . • Cholecystectomy may marginally increase the risk of right- sided colon cancer. 9/4/20XX
  • 6. PROTECTIVE FACTORS A protective effect of dietary fibre is also suggested by epidemiological studies. increased roughage is associated with reduced colonic transit times that in turn reduce exposure of the mucosa to dietary carcinogens. • However, there is increasing evidence associating the colonic microbiota with inflammation, gene methylation and dysplastic changes. • The epidemiological evidence supporting prostaglandin inhibitors, particularly ASPIRIN, in preventing colorectal cancer is substantial • high magnesium and calcium intake may be protective. • A protective potential for antioxidants such as vitamin E and selenium is as yet unproven 9/4/20XX
  • 7. EPIDEMIOLOGY-IN BRIEF • Ageing-Age 50 years and above • Heredity - 80% sporadic ,20% family history present • Diet-high in animal fat at more risk • Alcohol • Obesity and sedentary life style pre • Smoking • Inflammatory Bowel Disease-long term colitis
  • 8. GENETIC ASSOCIATIONS • Mutations of the APC gene occur in two-thirds of colonic adenomas and are thought to develop early in the carcinogenesis pathway. • K-ras mutations result in activation of cell signalling pathways and are more common in larger lesions, suggesting that that they are later events in mutagenesis. • The p53 gene is frequently mutated in carcinomas but not in adenomas and therefore thought to be a marker of invasion.
  • 9.
  • 10. EVIDENCE FOR ADENOMA–CARCINOMA SEQUENCE • The distribution of adenomas is similar to that of cancers (70% left sided) • Larger adenomas are more likely to be dysplastic than small adenomas • The majority of early cancers have adjacent adenomatous tissue • Adenomas are found in one-third of specimens resected for colorectal cancer • Incidence of colorectal cancer decreases within a screening programme that involves colonoscopy and polypectomy 9/4/20XX
  • 11. TYPES Macroscopically, the tumour may take one of several forms: annular cancers tend to give rise to obstructive symptoms whereas ulcerating cancers tend to present with bleeding. • Most large bowel cancers arise from the left colon, notably the rectum (38%), sigmoid (21%) and descending colon (4%). Cancer of the caecum (12%) and ascending colon (5%) is less common but may be gradually increasing in incidence. • Cancer of the transverse colon (5.5%), flexures (2–3%) and appendix (0.5%) are relatively uncommon. Microscopically the neoplasm is a columnar cell adenocarcinoma
  • 12. METASTASIS • Spread Colonic cancer can spread locally, via the lymphatics, bloodstream (haematogenous) or across the peritoneal cavity transcoelomic spread). • Direct spread may be longitudinal or radial. Radial spread may be retroperitoneal into the ureter, duodenum and posterior abdominal wall muscles or intraperitoneal into adjacent organs or the anterior abdominal wall. In general, involvement of the lymph nodes by tumour progresses from those closest to the bowel along the course of lymphatics to central nodes. • Haematogenous spread is most commonly to the liver via the portal vein. One-third of patients will have liver metastases at the time of diagnosis and 50% will develop metastases at some point, accounting for the majority of deaths. • The lung is the next most common site of metastatic disease whereas spread to the ovaries, brain, kidney and bone is less common. Colorectal cancer can spread from the serosa of the bowel or via subperitoneal lymphatics to other structures within the peritoneal cavity, including peritoneum, ovary and omentum.
  • 13. CLINICAL FEATURE • Clinical features Carcinoma of the colon typically occurs in patients over 50 years of age and is most common in the eighth decade of life. • Emergency presentation occurs in 20% of cases and is associated with a considerably worse prognosis, even when matched for disease stage • A first-degree relative who has developed colorectal cancer before the age of 50 years may indicate one of the colorectal cancer familial syndromes. • Tumours of the left side of the colon usually present with a change in bowel habit or rectal bleeding, while proximal lesions typically present with iron defIciency anaemia or a mass . • Patients may present with metastatic disease
  • 14. PATHOGENESIS • It is now well accepted that the majority of colorectal carcinomas evolve from adenomatous polyps; sequence of events is the adenoma-carcinoma sequence. • WHAT IS POLYP - Polyp is a nonspecific clinical term that describes any projection from the surface of the intestinal mucosa regardless of its histologic nature
  • 15. POLYP • Colorectal polyps may be classified as 1. Neoplastic (Tubular Adenoma, Villous Adenoma, Tubulovillous Adenomas, Serrated Adenomas/ Polyps)-TVS 2. Hyperplastic 3. Hamartomatous (Juvenile, Peutz-jeghers, Cronkite-canada), Or -JPC 4. Inflammatory (Pseudopolyp, Benign Lymphoid Polyp)
  • 16. NEOPLASTIC POLYPS • . Adenomatous polyps are common, occurring in up to 25% of the population older than 50 years of age in the United States. • these lesions are dysplastic. The risk of malignant degeneration is related to both the size and type of polyp. 1) Tubular adenomas -malignancy in only 5% of cases, 2) villous adenomas may harbor cancer in up to 40%. (VILLAIN) 3) Tubulovillous adenomas are at intermediate risk (22%). • Invasive carcinomas are rare in polyps smaller than 1 cm; the incidence increases with size. • The risk of carcinoma in a polyp larger than 2 cm is 35% to 50%. • Although most neoplastic polyps do not evolve to cancer, most colorectal cancers originate as a polyp
  • 17. SERRATED POLYPS • Serrated polyps are a recently recognized, histologically distinct group of neoplastic polyps. • These lesions were long thought to be similar to hyperplastic polyps with minimal malignant potential. • However, it has become clear that some of these polyps will develop into invasive cancers
  • 18. HYPERPLASTIC POLYPS • . 9/4/20XX • Hyperplastic polyps are extremely common in the colon. • These are usually small (<5 mm) and show histologic characteristics of hyperplasia without any dysplasia. • They are not considered premalignant, but cannot be distinguished from adenomatous polyps colonoscopically and are therefore often removed. • In contrast, large hyperplastic polyps (>2 cm) may have a slight risk of malignant degeneration. • Moreover, large polyps may harbor foci of adenomatous tissue and dysplasia. Hyperplastic polyposis is a rare disorder in which multiple large hyperplastic polyps occur in young adults. • These patients are at slightly increased risk for the development of colorectal cancer.
  • 19. HAMARTOMATOUS POLYPS (JUVENILE POLYPS) • . 9/4/20XX • In contrast to adenomatous and serrated polyps, hamartomatous polyps (juvenile polyps) usually are not premalignant. • These lesions are the characteristic polyps of childhood but may occur at any age. • Bleeding is a common symptom, and intussusception and/or obstruction may occur • In contrast to adenomatous polyposis syndromes, these conditions are often associated with mutation in PTEN. • Familial juvenile polyposis is an autosomal dominant disorder in which patients develop hundreds of polyps in the colon and rectum • Unlike solitary juvenile polyps, these lesions may degenerate into adenomas and eventually carcinoma
  • 20. HAMARTOMATOUS POLYPS- PEUTZ JEGHERS • . 9/4/20XX • Characterized by polyposis of the small intestine and, to a lesser extent, polyposis of the colon and rectum. • Characteristic melanin spots are often noted on the buccal mucosa and lips of these patients. • The polyps of Peutz-Jeghers syndrome are generally considered to be hamartomas and are not thought to be at significant risk for malignant degeneration
  • 21. HAMARTOMATOUS POLYPS -CRONKITE CANADA • . 9/4/20XX • A disorder in which patients develop gastrointestinal polyposis in association with alopecia, cutaneous pigmentation, and atrophy of the fingernails and toenails. • Diarrhea is a prominent symptom, and vomiting, malabsorption, and protein-losing enteropathy may occur. • Most patients die of this disease despite maximal medical therapy, and surgery is reserved for complications of polyposis such as obstruction
  • 22. INFLAMMATORY POLYPS (PSEUDOPOLYPS). • . 9/4/20XX • Inflammatory polyps occur most commonly in the context of inflammatory bowel disease, but may also occur after amebic colitis, ischemic colitis, and schistosomal colitis. • These lesions are not premalignant, but they cannot be distinguished from adenomatous polyps based on gross appearance and therefore should be removed
  • 23. DIFFERENT METHODS AND SCOPY • . 9/4/20XX • Anoscope-8 cms • Proctoscope-for rectum and terminal sigmoid -25 cm length • Sigmoidoscope-60 cms in length-till splenic flexure • Colonoscpe-100-160 cms till terminal ileum
  • 24. CONSTIPATION • . 9/4/20XX Two or fewer bowel movements per week and/or straining at stool more than 25% of the time. Rome criteria for chronic constipation

Editor's Notes

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  2. SLOPE. STOMACH LIVER OESOPHAGUS PANCREAS