Growths of colon

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Information about Growths of colon
Health & Medicine

Published on March 9, 2014

Author: prithwiraj2012

Source: slideshare.net

Growths of colon A PRESENTATION FROM DEPARTMENT OF SURGERY, RGKMC EDITED BY PRITHWIRAJ MAITI FINAL YEAR MBBS R.G.KAR MEDICAL COLLEGE

Tumours of colon • Polyp/ tumour/ swelling arises from mucosal surface with a stalk/ pedicle- a mass projecting into the bowel lumen beyond the surface epithelium.

Classification • Inflammatory – Ulcerative colitis – Segmental colitis – Dysenteric colitis – Crohn’s disease – Diverticulitis • Metaplastic - Hyperplastic polyps • Harmartomatous • Peutz–Jeghers polyp • Juvenile polyp • Cronkhite-Canada syndrome • Neoplastic – Adenoma • Tubular • Tubulovillous • Villous – Adenocarcinoma – Carcinoid tumour • Others – Lipoma – Haemangioma – Leiomyoma

• Metaplastic polyp- Not premalignant • Hamartomatous polyp – Peutz-Jegher’s polyp• • • • Autosomal dominant, familial Multiple Premalignant Melanosis of oral mucosa, lips, and digits

– Juvenile polyp• Commonest in infant and children • Cause intussusception, prolapse, bleeding PR • Colonoscopic polypectomy • Not premalignant

Colonic Adenoma • Neoplastic – Adenoma • Tubular-70% • Tubulovillous-25% • Villous-5% – Solitary/ multiple – Sessile/ pedunculated – Premalignant • • • • Size Sessile Villous Dysplasia

Clinical features • • • • • • • Asymptomatic Anaemia Bleeding P/R Prolapse Diarrhoea, spurious diarrhoea Colicky abdominal pain Tenesmus

Investigation and treatment Investigations: • Hb • Serum electrolyte • Colonoscopy– – – – Size Texture Colour ulceration Treatment: • Colonoscopic polypectomy • Per anal polypectomy • Resection anastomosis • Total polypectomy if FAP

Familial adenomatous polyposis (FAP) Extracolonic manifestations of FAP • Endodermal derivatives: Younger age group- 15-20 years. – Adenomas and carcinomas of the 80 % with a positive family duodenum, stomach, small intestine, thyroid and biliary tree. history. The remainder arise as a – Fundic gland polyps. result of new mutations in the – Hepatoblastoma. adenomatous polyposis coli (APC) • Ectodermal derivatives: gene. – Epidermoid cysts. This has been identified on the – Pilomatrixoma. short arm of chromosome 5. – Congenital hypertrophy of the retinal pigment epithelium (CHRPE). Clinical features– Brain tumours. Pain abdomen, • Mesodermal derivatives: Loose stool with blood and – Desmoid tumours. mucous, – Osteomas. Weight loss. – Dental problems. • Autosomal dominant. • • • • • • •

SPECIAL NOTE  FAP + Benign mesodermal tumours (such as desmoid tumours)+ Osteomas+ Epidermoid cysts can also occur= Gardner’s syndrome. • FAP+ Brain tumor= Turcot’s syndrome.

Investigations and treatment Investigations: – Double contrast barium enema – Colonoscopy Treatment: – Proctocolectomy with ileo-anal anastomosis

Screening policy • At-risk family members are offered – Genetic testing in early teens. – Should be examined at the age of 10–12 years, repeated every year. • Who are going to get polyps will have them at 20 years, require operation. • If there are no polyps at 20 years, 5 yearly colonoscopy upto 50 years. • If still no polyps, there is probably no inherited gene. • Carcinomatous change may exceptionally occur before the age of 20 years

Hereditary non-polyposis colorectal cancer (HNPCC: Lynch syndrome) • Increased risk of colorectal cancer and also cancers of the endometrium, ovary, stomach and small intestines. • Autosomal dominant condition. • Cause-a mutation in one of the DNA mismatch repair genes. ( MLH1 and MSH2). • The lifetime risk of developing colorectal cancer 80%. • Mean age of diagnosis is 45 years. • Most cancers develop in the proximal colon. • Females with HNPCC have a 30–50% lifetime risk of developing endometrial cancer.

COLORECTAL CARCINOMA (CRC) • One of the most common cancers in the world. • US: 4th most common cancer (after lung, prostate, and breast cancers). 2nd most common cause of cancer death (after lung cancer). • 2001 130,000 new cases of CRC 56,500 deaths caused by CRC

AETIOLOGY  Older age,  Male gender,  High intake of fat, alcohol, red meat;  Obesity,  Sedentary life style,  Smoking,  Inflammatory bowel disease,  HNPCC,  FAP,  Family history of colorectal cancer.

Development of CRC • Result of interplay between environmental and genetic factors. • Central environmental factors. • Diet and lifestyle. • 35% of all cancers are attributable to diet. • 50%-75% of CRC in the US may be preventable through dietary modifications.

Colon cancers result from a series of pathologic changes that transform normal colonic epithelium into invasive carcinoma. Specific genetic events, shown by vertical arrows, accompany this multistep process. The various chemopreventive agents exert their effects at different steps in this pathway, and this is depicted on the basis of the available epidemiologic evidence.

Types of colon CA • Synchrous- Multiple primary ca in different parts of colon at the same time. • Metachronus- Growth in different parts of colon in different time. • Gross type– Annular (left side) – Tubular (left side) – Ulcerative (right side) – Cauliflower type (right side).

Histology (WHO) • • • • • • Adencarcinoma- 90% Mucinous adenocarcinoma- 5-10% Signet ring cell carcinoma Small cell carcinoma Squamous cell carcinoma Undifferentiated carcinoma

Spread Via blood Via lymphatics Liver (40% via portal vein; Hard umbilicated) Lung Brain Bones Direct Lymph nodes (Pericolic, Epicolic Intermediate Principal) Abdominal wall Nerves Vessels Ureter, Bladder

Staging of CRC Dukes staging system A B C1 C2 D Mucosa invade Into (B1)/ through (B2) Muscularis propria B1 + LN Involvement B2 + LN Involvement Distant metastatic spread

Staging of CRC TNM system Primary tumor (T) Regional lymph nodes (N) Distant metastasis (M)

TNM classification for colonic cancer T-Tumour stage T1: Into submucosa T2: Into muscularis propria T3: Into pericolic fat or sub-serosa but not breaching serosa T4: Breaches serosa or directly involving another organ N- Nodal stage N0: No nodes involved N1: 1–3 nodes involved N2: ≥4 nodes involved M- Metastases M0: No metastases M1: Metastases

Typical sites and incidence of colon cancer

Clinical feature • • • • • • • • • After 50 years M:F- 3:2 Weight loss Loss of appetite Night sweats, Fever Abdominal pain & mass Acute intestinal obstruction- 20% Rt sided growth- anaemia, palpable mass in RIF. LT sided growth- colicky pain, rectal bleeding, change in bowel habits, sub acute obstruction.

Typical sites and incidence of colon cancer

Investigation • • • • • • • • BARIUM ENEMA COLONOSCOPY AND BIOPSY VIRTUAL COLONOSCOPY USG W/A CEA Hb, PCV, ESR, FOBT CT LFT

• The barium enema of colon• In this case, the classic "apple core” lesion is present, representing an encircling adenocarcinoma that constricts the lumen.

Therapy Surgical resection the only curative treatment. Likelihood of cure is greater when disease is detected at early stage. Early detection and screening is of pivotal Importance.

SURGERY • Rt sided early growth• Rt radical hemicolectomy– Terminal 6 cm of ileum – Caecum – Appendix – Ascending colon – 1/3rd of transverse colon – Lymph node

• Transverse colon growth • Extended Rt hemicolectomy- Rt. hemicolectomy+ transverse colon • Lt sided growth- Left hemicolectomy • Sigmoid growth- Sigmoidectomy

• • • • Elective setting-prepared colon Emergency setting Type of anastomosis colostomy

Adjuvant therapy • Adjuvant chemotherapy • Indication • Node+ • Venous spread • Poorly differentiated CA • Change in CEA – Regime • 5FU + Folinic acid- 6 month. • Preoperative neoadjuvant therapy. • No role of radiotherapy as colonic tumour is radioresistant.

Follow up • For 3 years regular interval once in 3-6 month • By – Regular CEA – USG – Barium enema – Colonoscopy – Serum Alkaline phosphatase (ALP)

Prognosis • • • • • • • • Site Type Size Lymph node status Liver secondaries Age Stage Complication

Screening What is screening? A public health service in which members of a defined population are examined to identify those individuals who would benefit from treatment to reduce the risk of a disease or its complications.

Types of Screening Fecal occult blood test (FOBT) Chemical test for blood in a stool sample. Annual screening by FOBT reduces colorectal cancer deaths by 33%. Flexible sigmoidoscopy can detect about 65%–75% of polyps and 40%–65% of colorectal cancers. Rectum and sigmoid colon are visually inspected.

Current Screening Guidelines Regular screening for all adults aged 50 years or older is recommended FOBT every year Flexible sigmoidoscopy every 5 years Total colon examination by colonoscopy every 10 years or by barium enema every 5–10 years

OGILVIE’S SYNDROME • Colonic pseudoobstruction. • Clinical features: – Distention, – Tympanic, – Nontender. • Cause: – Scleroderma, – Myotonic dystrophy, – Hypothyroidism, DM, – CRF, – Poisoning, – Retroperitoneal irritation by blood fluid, – Idiopathic. • Investigation: – X Ray –Dilated colon – Barium- Normal – CT • Treatment: – Conservative. – Neostigmine, – Tube cecostomy.

Colostomy • A colostomy is a surgical procedure in which a stoma is formed by drawing the healthy end of the large intestine or colon through an incision in the anterior abdominal wall and suturing it into place. This opening, in conjunction with the attached stoma appliance, provides an alternative channel for feces to leave the body.

Types • Loop • End • Double barrel

Temporary Loop colostomy, Devine’s double barrel  For diversion to facilitate distal healing Permanent End  APR

• Diversion • Decompression – Blow hole – Tube caecostomy – Loop transverse colostomy • Irrigation

Complication • • • • • • • • • Prolapse Retraction Necrosis Stenosis Herniation Bleeding Diarrhoea Enteritis Skin excoriation

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