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BY PROF . MOHAMED A. EL GHARBAWI e-mail : elgharma2@yahoo.com Web Site: www.dr-elgharbawi.com

TUMOURS OF THE INTESTINE. BY PROF . MOHAMED A. EL GHARBAWI e-mail : elgharma2@yahoo.com Web Site: www.dr-elgharbawi.com. OBJECTIVES. BY END YOU WILL KNOW: Tumors of small intestine ( Nice to know ) Colorectal polyps ( Good to know ) Pathology of COLON CANCER ( Good )

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BY PROF . MOHAMED A. EL GHARBAWI e-mail : elgharma2@yahoo.com Web Site: www.dr-elgharbawi.com

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  1. TUMOURS OF THE INTESTINE BY PROF. MOHAMED A. EL GHARBAWIe-mail:elgharma2@yahoo.comWeb Site: www.dr-elgharbawi.com

  2. OBJECTIVES BY END YOU WILL KNOW: Tumors of small intestine (Nice to know) Colorectal polyps (Good to know) Pathology of COLON CANCER (Good) Diagnosisof COLON CANCER (Must Know) Treatment of COLON CANCER (Nice)

  3. ANATOMY OF GI TRACT

  4. TUMOURS OF THE SMALL INTESTINE COMMONLY BENIGN RARELY MALIGNANT BENIGN SMALL INTESTINAL TUMOURS • Adenomas (most common) • Leiomyoma • Lipoma • Fibroma • Hemangioma • Lymphangioma • Neurofibroma Treatment: Surgical resection or endoscopic removal if possible.

  5. TUMOURS OF THE SMALL INTESTINE MALIGNANT SMALL INTESTINAL TUMOURS • Rare • 2% of all GIT malignancy • Age: 50 – 65 years • Risk Factors: Red meat, Smoked food, Crohn’s disease, HNPCC (Hereditary Nonpolyposis Colorectal Cancer), FAP (Familial Adenomatous Polyposis) and Puetz- Jeghers syndrome.

  6. TUMOURS OF THE SMALL INTESTINE • Clinical Picture: Mostly asymptomatic Partial intestinal obstruction (large tumors) 25% have palpable abdominal mass May present with bleeding Jaundice: Liver metastasis / Biliary obstruction Ascites, Cachexia, Hepatomegaly (Advanced)

  7. TUMOURS OF THE SMALL INTESTINE • TYPES OF MALGNANT SMALL INTESTINE TUMOURS: 1. Adenocarcinoma: - 35 – 50 % - From epithelium - Commonly in Duodenum 2. Carcinoid tumor: - 20 – 40 % - From Chromaffin cell - Commonly in Ileum

  8. TUMOURS OF THE SMALL INTESTINE 3. Lymphoma: - 10 – 15 % - From Lymphocytes - Commonly I Ileum 4. GIST: - 10 – 15 % - From Interstitial cell of Cajal - Any Site

  9. TUMOURS OF THE SMALL INTESTINE ADENOMAS & ADENOCARCINOMA On microscopy, adenomas may be Tubular, Villous or Tubovillous. Villous adenomas are most aggressive. Tubular adenomas are least aggressive. Adenocarcinomas: usually on top of adenomas. Mostly in DUODENUM. Treatment: Wide local surgical resection with the Lymph nodes Chemotherapy has no effect

  10. TUMOURS OF THE SMALL INTESTINE CARCINOID TUMOUR (ARGANTAFFENOMA) ( Good to know) Arise from Chromaffen cells Commonest in Appendix, then ileum & rectum Commonly present with Acute Appendecitis 10% present with Carcinoid Syndrome: only in presence of liver metastases (25-50% of metastatic patients), Serotonin is directly (Active substance) poured into the circulation causing Diarrhoea, Flushing, Abdominal cramps, Tachycardia, Hypotension & Fibrosis of endocardium and Rt heart valves.

  11. TUMOURS OF THE SMALL INTESTINE CARCINOID TUMOUR (CONT.) Symptoms of Carcinoid syndrome is rare in patients with no liver metastases. Serotonin, bradykinin and substance P secreted by the original tumor are metabolised completely and inactivated by the liver when it passes into the liver for 1st time.

  12. TUMOURS OF THE SMALL INTESTINE CARCINOID TUMOUR (CONT.) Investigations: US, CT, MRI to discover liver metastases Needle Biopsy for tissue diagnosis 24 hours urinary 5 Hydroxy Indol Acetic Acid (N< 10 mg / day, Diagnostic if > 50 mg/day) Treatment: Appendectomy (if tumor at tip) Rt. Hemicolectomy (if tumor at base) Surgical Excision of Liver metastases if possible

  13. CARCINOID OF APPENDIXSURGICAL SPECIMEN

  14. TUMOURS OF THE SMALL INTESTINE LYMPHOMA Affect small intestine only or as a part of systemic lymphoma Primary disease is mostly in ileum (Highest lymphoid tissue) Commonly present with partial small bowel obstruction 10% present with perforation Treatment: Wide Local resection with the lymph nodes / Chemotherapy

  15. INTESTINAL LYMPHOMA

  16. TUMOURS OF THE SMALL INTESTINE GASTRO INTESTINAL STROMAL TUMOURS (GIST) Arise from GI Stroma cells (Intersticial cells of Cajal) (NB. Ramon y Cajal, Spanish Histologist, 1852-1934) Sites: 60-70% in Stomach 25-35% in Small intestine (no prevalence) More GI bleeding than other small intestine malignancy Treatment: Wide local surgical excision with the lymph nodes

  17. SMALL INTESTINE GIST

  18. TUMOURS OF THE SMALL INTESTINE METASTATIC TUMORS involving small intestine Manifest with intestinal obstruction GI bleeding

  19. COLORECTAL POLYPS Definition: A projection from the surface of intestinal mucosa. Classification: 1. Neoplastic Tubular adenoma Villous Adenoma Tubulovillous Adenoma 2. Hamartomatous Juvenile Polyps Peutz-Jeghers Syndrome

  20. INTESTINAL POLYP

  21. COLORECTAL POLYPS 3.Inflammatory Polyp Pseudopolyps Benign lymphoid polyps 4.Familial Adenomatous Polyposis (FAP)

  22. POLYPS OF THE COLON

  23. COLORECTAL POLYPS JUVENILE POLYPS • Not usually premalignant • In Children but may be found in any age • Pedunculated • Single or few • Commonly affect rectum • Bleeding is common • May be intussusception/ obstruction • Identical to adenomatous polyp • Treated by Polypectomy

  24. COLORECTAL POLYPS PUETZ- JEGHERS SYNDROME • Polyposis in small intestine, may be in colon &rectum • Pigmented spots on lips & buccal mucosa • Are Hamartomas • Not pre malignant • Carcinoma may develop occasionally • Multiple in GI, So Surgery is for complications only (Bleeding/ Obstruction) Or for adenomatous transformation

  25. COLORECTAL POLYPS FAMILIAL ADENOMATOUS POLYPOSIS (FAP) • Rare Autosomal Dominant Disease • Hundreds or thousands of adenomatous polyps in rectum and colon • It starts at puberty by polyps in rectum & sigmoid colon. By age of 20years, entire colon and rectum are studded with a big number of polyps (>100). • Sizes range from 1mm to several cms • Polyps: Sessile or pedunculated • Histology: Tubular, Villous and Tubulo-villous • 100% risk of developing Carcinoma by age of 50years

  26. FAMILIAL ADENOMATOUS POLYPOSIS

  27. COLORECTAL POLYPS CLINICAL PICTURE: • After puberty • Symptoms: Diarrhoea, Tenesmus, Lower abdominal pain, Blood& Mucous in Stool, Anemia, Loss of weight and debility • Polyps are felt by rectal examination INVESTIGATIONS: • Barium Enema: Multiple rounded filling defects in colon & rectum • Colonoscopy and biopsy

  28. BARIUM ENEMA / FAPMULTIPLE SMOOTH ROUND FILLING DEFFECTS

  29. POST EVACUATION/ FAPDOUBLE CONTRAST BARIUM ENEMA

  30. COLONOSCPY of FAP

  31. COLORECTAL POLYPS TREATMENT: Surgical: 1. Total Proctocolectmy + End Ileostomy or Continent Ileostomy (KOCK’S) 2. Restorative Proctocolectomy, Ileal-Anal (Pouch) Anastomosis +/- Temporary Ileostomy 3. Total Abdominal Colectomy with Ileo-Rectal Anastomosis The preserved Rectum is examined periodically and endoscopic removal of the developed polyps

  32. TOTAL COLECTOMY + ILEO-RECTAL ANASTOMOSIS

  33. Carcinoma of the colon OBJECTIVES TO KNOW: 1. Pathology of COLON CANCER (Good) 2. Diagnosis of COLON CANCER (Must Know) 3. Treatment of COLON CANCER (Nice)

  34. Incidence: Most common malignancy of the gastrointestinal tract. Men =Women. Risk Factors: (1) Aging: >90% of cases diagnosed are in people at age 50 years. Incidence is rising steadily after age of 50 ys.

  35. (2) Hereditary Risk Factors: 80% of colorectal cancers occur sporadically. 20% arise in patients with a known family history of colorectal cancer. (3) Environmental and Dietary Factors: Diet high in animal fat, red meat and low in fiber predispose to Colorectal cancer. (4) Bowel disease : Increasing risk for colorectal cancer Long-standing ulcerative colitis. Crohn's pancolitis have similar risk. Familial Adenomatous Polyposis.

  36. (5) Other Risk Factors: • Cigarette smoking . • Patients with ureterosigmoidostomy. • Also in women, gallstones (and the consequent cholecystectomy) are associated with colorectal cancer, especially in the right colon.

  37. Pathology Site: Sigmoid colon: (Commonest)50% May be due to its solid, stagnant and irritant contents, and it is often the seat of precancerous lesions (i.e. FAP and UC) (2) Caecum and ascending colon: 25% (3) Transverse colon: 20%. (4) Descending colon: 5%.

  38. SITES OF CANCER COLON

  39. (5) Multiple synchronous colonic cancers (i.e., two or more carcinomas occurring simultaneously) are found in 5% of patients. Metachronouscancer is a new primary lesion in a patient who has had a previous resection for cancer.

  40. Gross Appearance: Cauliflower growth: Inright colon. (2) Scirrhous growth (annular and tubular): In the left colon. (3) Malignant ulcer: Commonly in caecum.

  41. MACROSCOPY OF CANCER COLON ANULAR/ STRICTURE TYPE CAULIFLOWER TYPE

  42. Microscopic picture • Histologically the tumour is an adenocarcinoma that arises from the columnar epithelium.(well, moderately, or poorly differentiated). • Some tumours have a colloid structure, (In younger patients, with a poor prognosis).

  43. ADENOCARCINOMA OF COLON/ MICROSCPY

  44. SPREAD OF CANCER COLON (1) Direct spread: • Carcinoma grows circumferentially and may encircle the bowel leading to malignant intestinal obstruction; More in the left colon ( A smaller caliber than the right). It takes about 1 year for a tumor to encircle 3/4 of the bowel circumference. Spread

  45. Longitudinal submucosal extension occurs with invasion of the intramural lymphatic network, but it rarely goes beyond 2 cm from the edge of the tumorunless there is concomitant spread to lymph nodes.

  46. Direct spread to the outer layers of the bowel wall, and it may invade adjacent structures: liver, greater curvature of the stomach, duodenum, small bowel, pancreas, spleen, urinary bladder, vagina, kidneys, ureters and abdominal wall. Subacute perforation with inflammatory attachment of bowel to an adjacent viscous can’t be differentiated from actual invasion on gross examination.

  47. (2) Lymphatic spread: • Cancer spreads from the colon to the following lymph node groups, in sequence: 1. Epicolic nodes on the bowel wall. 2. Paracolic nodes between the marginal artery and the bowel. 3. Intermediate nodes on the main vessels. 4. Principal nodes alongside the superior and inferior mesenteric vessels. • From the Principal nodes further spread occurs to the parpa-aortic lymph nodes, then to cysterna chyli and thoracic duct. The left supraclavicular lymph nodes may be involved by retrograde flow from the thoracic duct (Virchow’s glands) giving positive Troisier’s sign.

  48. (3) Blood spread: Venous invasion leads to carry malignant cells via the portal venous system to the liver. Tumor embolizationoccurs through lumbar and vertebral veins to lungs and elsewhere. Metastases to ovaries are mostly hematogenous; and found in 1—10% of women with colorectal cancer. Minimalmanipulation of the tumor prior to ligation of the blood supply helps to avoid hematogenous spread during operation.

  49. (4) Transperitoneal spread: "Seeding" may occur when the tumor has extended through serosa and tumor cells enter the peritoneal cavity, producing local implants or generalized abdominal carcinomatosis. Large metastatic deposits in the pelvic cul-de- sac are palpable as a hard shelf (Blumer's shelf).

  50. (5) Intraluminal spread: Malignant cells shed from the surface of the tumor sweep with the fecal current. Implantation distally on intact mucosa is rare, but viable exfoliated cells can be trapped, commonly in an anastomotic suture or staple line during operation.

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