Download Free Medical Tumors of the small and large intestines PowerPoint Presentation

Tumors of the small and large intestines PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on anal cancer, which is titled "Tumors of the small and large intestines", to know about the tumors of the small and large intestines including non-neoplastic polyps, neoplastic ( epithelial) polyps, mesenchymal lesions, and lymphoma.

Tags : anal cancer, Tumors, small, large, intestines, non-neoplastic polyps, neoplastic, epithelial, polyps, mesenchymal lesions, lymphoma

Published on : May 06, 2021 | Views : 2061 | Downloads : 12

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Tumors of the small and large intestines Non-neoplastic polyps Neoplastic ( epithelial) polyps Mesenchymal lesions Lymphoma
Slide 2-

Tumors of the small and large intestine Epithelial tumors are a major cause of morbidity and mortality worldwide The colorectal cancer is the GIT segment most commonly affected by tumors It is the host to more primary tumors than any other tumor of the body. Colonic carcinoma is second to bronchogenic carcinoma as a cause of death in USA. Adenocarcinoma in colorectum represent 70% of all malignancy of GIT Benign tumors, primarily epithelial, are present in 25 to 50% of older adults.
Slide 3-

Terminology of Intestinal Tumors Polyps and Polyposis Syndromes Polyp is a mucosal growth that protrude into the lumen of gut. It could be sessile or pedunculated Polyps may be formed as the result of abnormal mucosal maturation, inflammation, or as epithelial proliferation with dysplasia
Slide 4-

Terminology of Intestinal Tumors Polypoid lesions is the inflammatory masses, hamartomas and tumors arising from the submucosa or muscle coat, but also protruding into the lumen. Polyposis is multiple polyps. Polyposis syndrome is hereditary, characterized by the presence of multiple pedunculated or sessile tumors of the mucosa
Slide 5-

Tumors of the small and large intestineClassification Non-neoplastic polyps Hyperplastic polyps Hamartomatous polyps (Juvenile & Peutz-Jeghers polyps) Inflammatory polyps Lymphoid polyps Neoplastic ( epithelial) polyps Benign polyps (adenoma) Malignant lesions Adenocarcinoma Carcinoid Anal zone carcinoma Mesenchymal lesions GIT stromal tumors (benign & malignant) Others ( lipoma, neuroma, angioma, Kaposi sarcoma) Lymphoma
Slide 6-

Intestinal Polyps Non-Neoplastic Polyps Represent 90% of all epithelial polypi found in large intestine. Found in more than half of all persons age 60 years or older. Types: 1. Hyperplastic polyp. 2. Hamartomatous polyp (Juvenile & Peutz- Jeghers) 3. Inflammatory polyp 4. Lymphoid polyp
Slide 7-

Intestinal Polyps 1] Hyperplastic Polyp Asymtomatic > 50% are located in the rectosigmoid, 20% in the ascending colon. Smooth, moist, round, small (0.5cm) sessile lesions. Multiple polyps are frequent. Composed of well-formed glands and crypts lined by differentiated goblet or absorptive cells. Pure hyperplastic polyps have no malignant potential. Larger hyperplastic polyps; foci of adenomatous change.
Slide 8-

Non-Neoplastic Polyp 2] Hamartomatous polyp Juvenile Polyps (retention polyp) Developmental malformations affecting the glands and lamina propria, having no malignant potential. commonly occur in children under 5 years old in the rectum. In adult called retention polyp. Painless rectal bleeding after defecation. Large, rounded, smooth lesions with a stalk Histology: mucus-filled, cystically dilated tubules lined by normal or inflamed mucosa. Juvenile polyposis syndrome. Occurrence of multiple hamartomatous polyps throughout the GI tract.
Slide 9-

Non-Neoplatic Polyps 2] Hamartomatous Polyps Peutz-Jehgers polyps Uncommon hamartomatous polyps accompanied by mucosal and cutaneous pigmentation around the lips, oral mucosa, face and genitalia. Rare, autosomal dominant. Caused by germ-line mutation in the LKB1 gene, which encodes a serine threonine kinase. Polyps tend to be large and pedunculated. May occur anywhere in the GI tract. Have an increased risk of developing carcinoma of the pancreas, breast, lung, ovary and uterus.
Slide 10-

hamartomatous polyp
Slide 11-

Non-Neoplastic Polyps 3] Inflammatory Polyps Occur in patients with longstanding IBD, especially in chronic ulcerative colitis. Usually multiple. Represent an exuberant reparative response to longstanding mucosal injury called pseudopolyps
Slide 12-

4] Lymphoid polyps
Slide 13-

Neoplastic Polyps (Adenomas) Adenomatous Polyp Occur mainly in large bowel. Prevalence: 20% to 30% before age 40, 50% after age 60. Males and females are equally affected Spordic and familial Vary from small pedunculated to large sessile Epithelium proliferation and dysplastia with loss of basal orientation of nuclei (pseudostratified). Divided into: Tubular adenoma has less than 25% villous architecture Villous adenoma villous architecture over 50% Tubulovillous adenoma villous architecture between 25 and 50%.
Slide 14-

All adenomatous lesions arise as the result of epithelial proliferation and dysplasia, which may range from mild to so severe as to represent transformation to carcinoma.
Slide 15-

Neoplastic Polyps 1] Tubular adenoma Represents 75% of all neoplastic polyps. Occurs sporadicaly and in well defined hereditary syndromes. Average age is 60 years 75 % occur in the distal colon and rectum. More than 50% occur singly. Size: few millimeters (sessile) to many centimeters (have stalk). Stalk has a central core of fibrovascular tissue, covered with dysplastic colonic mucosa. Severe dysplasia and invasive carcinoma may supervene.
Slide 16-

Tubular adenoma
Slide 17-

Neoplastic Polyps 2] Villous Adenoma The least common, largest and most ominous of epithelial polyps. Age: 60 to 65 years, M:F ratio roughly equal. Present with rectal bleeding or anemia, large ones may secrete copious amounts of mucoid material rich in protein. 75% located in rectosigmoid area.
Slide 18-

Neoplastic Polyps 2] Villous Adenoma Morphology Size: 1 to 10 cm in diameter. Most are broad, sessile, velvety lesions projecting 1 to 3 cm. Frondlike papillary projections of adenomatous epithelium with a delicate fibrovascular core. All degree of dysplasia with frank invasive carcinoma in up to 40%.
Slide 19-

Neoplastic Polyps 3] Tubulovillous adenoma Intermmediate in size, frequency of having a stalk, degree of dysplasia and malignant potential between tubular and villous adenomas.
Slide 20-

Neoplastic Polyps Clinical features The smaller adenomas are usually asymptomatic, occult bleeding. Villous adenomas are much more frequently symptomatic because of overt or occult rectal bleeding or mucoid material rich in protein and potassium to produce hypoproteinemia or hypokalemia. Adenomas in the immediate vicinity of the ampulla of Vater may produce biliary obstruction.
Slide 21-

Relationship of Neoplastic Polyps to Carcinoma Adenoma to carcinoma sequence is documented by several observations and genetic alterations. The probability of carcinoma occuring in a neoplastic polyp is related to: 1. The size of the polyp. 2. The relative proportion of its villous features. 3. The presence of significant cytologic atypia (dysplasia) in the neoplastic cells.
Slide 22-

Familial Polyposis Syndrome Patients have genetic tendencies to develop neoplastic polyps, most often autosomal dominant. Familial polyposis coli (FPC) Genetic defect ch5 q21. Innumerable neoplastic polyps in the colon (500 to 2500) Polyps are also found elsewhere in alimentary tract Most polyps are tubular adenomas The risk of colorectal cancer is 100% by midlife. Gardener’s syndrome Polyposis coli, multiple osteomas, epidermal cysts, and fibromatosis. Turcot syndrome Polyposis coli, glioma and fibromatosis
Slide 23-

ppt slide no 23 content not found
Slide 24-

Malignant Tumors of Large IntestineAdenocarcinoma Constitutes 98% of all cancers in the large intestine. Worldwide distribution, highest incidence in west. Causes 15% of all cancer-related death in the USA. The mortality rate and incidence is higher in blacks. Peak incidence in the sixth to seventh decade.
Slide 25-

Malignant Tumors of Large IntestineAdenocarcinoma Predisposing factors: IBD, polyposis syndrome. Male:female ratio is 2:1 in rectal cancer, roughly equal in colon cancer, generally males are affected about 20% more than females. Diet appears to play an important role in the risk for colon cancer: - Low content of unabsorpable vegetable fibre. - High content of refined carbohydrates. - High fat content. - ? Increased intake of nitrites, nitrates (nitrosamines). - Reduced intake of vit A, C & E. The use of aspirin and NSAID (cyclooxygenase-2 inhibitors) exerts a protective effect against colon cancer
Slide 26-

When colorectal cancer is found in a young person, preexisting ulcerative colitis or one of the polyposis syndromes must be suspected. Individuals with hereditary nonpolyposis colorectal cancer syndrome (HNPCC, also known as Lynch syndrome), caused by germ-line mutations of DNA mismatch repair genes, are at a high risk of developing colorectal cancers. (HNPCC patients are also at risk of developing other tumors, such as cholangiocarcinomas.)
Slide 27-

Malignant Tumors of Large IntestineAdenocarcinoma Colorectal carcinogenesis Two pathogenetically distinct pathways for the development of colon cancer, both seem to result from accumulation of multiple mutations The APC/B-catenin pathway chromosomal instability that results in stepwise accumulation of mutations in a series of oncogenes and tumor suppressor genes. Localized colon epithelial proliferation followed by the formation of small adenomas, become more dysplastic, and ultimately develop into invasive cancers.
Slide 28-

This adenoma-carcinoma sequence accounts for aboout 80% of sporadic colorectal cancers. Malignant Tumors of Large IntestineAdenocarcinoma Colorectal carcinogenesis
Slide 29-

Malignant Tumors of Large IntestineAdenocarcinoma The DNA mismatch repair genes pathway: 10% to 15% of sporadic cases. There is accumulation of mutations (as in the APC/B-catenin schema) but the involved genes are different. Unlike in the adenoma-carcinoma sequence, there are no clearly identifiable morphologic correlates
Slide 30-

Malignant Tumors of Large IntestineAdenocarcinoma In DNA mismatch repair genes pathway defective DNA repair caused by inactivation of DNA mismatch repair genes is the fundamental and the most likely initiating event in colorectal cancers Inherited mutations in one of five DNA mismatch repair genes (MSH2, MSH6, MLH1, PMS1, AND PMS2) give rise to the hereditary non polyposis colon carcinoma (HNPCC) MLH1 gene is the one most commonly involved in sporadic colon carcinomas
Slide 31-

Malignant Tumors of Large IntestineAdenocarcinoma Microsatellite instability (MSI) is the molecular signature of defective DNA mismatch repair Most microsatellite sequences are in noncoding regions of the genes so mutations in these genes are probably harmless. However, some micorsatellite sequences are located in the coding or promoter region of genes involved in regulation of cell growth.
Slide 32-

HNPCC
Slide 33-

Colorectal Carcinoma Morphology Sixty to 70% of colorectal carcinomas are in the rectum, rectosigmoid and sigmoid colon. Left-sided carcinomas tend to be annular, encircling lesions with early symptoms of obstruction. Neoplasms start superficially, slowly invading the deeper layers with ulceration and eventually metastasis.
Slide 34-

ppt slide no 34 content not found
Slide 35-

Colorectal Carcinoma Morphology Right-sided carcinomas tend to grow as polypoid, fungating masses, obstruction is uncommon. Invasion of the wall and extend to the mesentery, regional lymph nodes and more distal sites. Mucinous adenocarcinoma secret abundant mucin that may dissect through cleavage planes in the wall. Small cell undifferentiated carcinomas are rare (arising from neuroendocrine cells) In UC, poorly differentiated infiltrative adenocarcinoma without an exophytic growth.
Slide 36-

ppt slide no 36 content not found
Slide 37-

ppt slide no 37 content not found
Slide 38-

Colorectal Carcinoma Clinical features The condition tends to be present for a considerable time before producing symptoms. Left-sided lesions tend to present earlier but also have a more infiltrative growth pattern and a poorer prognosis. Right-sided lesions tend to present with weakness, malaise, weight loss, unexplained anemia (secondary to early bleeding).
Slide 39-

Colorectal Carcinoma Spread: - direct extension. - metastasis through: - lymphatic - blood vessels - favored sites are regional lymph node, liver, lungs, bones. Serum levels of carcinoembryonic antigen (CEA) are related to tumor size and extent of spread. They are helpful in monitoring for recurrence of tumor after resection. Overall 5-year survival is 35 to 49% in the United States.
Slide 40-

ppt slide no 40 content not found
Slide 41-

ppt slide no 41 content not found
Slide 42-

ppt slide no 42 content not found
Slide 43-

Colorectal Neoplasm Other Tumors Malignant spindle cell (mesenchymal) tumors and lymphomas. Grossly and microscopically resemble those arising elsewhere in the GI tract. Carcinoid tumors may arise anywhere in the colon, especially the rectum. Squamous cell carcinomas are largely limited to the rectal canal. Initially present as plaque-like lesions, later becoming ulcerated or fungating. Malignant melanoma at the anal verge.
Slide 44-

Small Intestinal Neoplasms 3-6% of GIT neoplasm, slight preponderance to benign tumors. BENIGN Discovered incidentally, leiomyoma, adenoma and lipoma Large lesions may cause obstruction, bleeding, intussusception, volvulus. ADENOMAS Single or multiple polyps, most often in the duodenum and ileum. There is a risk of malignancy with larger adenomatous polyps. MALIGNANT In descending order of frequency: carcinoid, adenocarcinomas, lymphomas and leiomyosarcomas. Leiomyosarcomas have tyrosine kinase receptors, can be treated by STI-571
Slide 45-

Small Intestinal Neoplasms Adenocarcinoma of small intestine Tumors grow as polypoid fungating ulcerating mass or encircling pattern Site: duodenum ( ampulla of Vater) Presentation: abdominal cramping pain, vomiting and weight loss Patients present late 5 years survival is 70% after en bloc resection
Slide 46-

Small Intestinal Neoplasms Carcinoid Tumors Neoplasms arising from endocrine cells Kulchitsky or enterochromaffin cells found along the length of GIT mucosa. Cells have an affinity for silver salts. 60 to 80% appendix and terminal ileum: 10 to 20% rectum, the remainder in the stomach, duodenum or esophagus. Other Location: Lungs, pancreas, biliary tract, ovaries and liver. Peak age: 6th decade, comprise 2% of colorectal carcinoma and 50% of small intestinal carcinoma. Tumors in the appendix and rectum, although spreading locally, seldom metastasize. Ileal, gastric, and colonic carcinoids are frequently malignant.
Slide 47-

Carcinoid Tumors Morphology Round submucosal elevations that are bright yellow or yellow-gray, may be deeply infiltrative and penetrate muscle to the serosa. Gastric and ileal carcinoids are frequently multiple. Tumor cells arranged in trabecular, insular, glandular or undifferentiated patterns are monotonously similar to each other with regular round nuclei Ultrastructral features: neurosecretory electron dense bodies in the cytoplasm
Slide 48-

Small Intestinal Neoplasms Carcinoid Tumor Clinical features Asymptomatic May cause obstruction, intussusception or bleeding. May elaborate hormones: Zollinger-Ellison, Cushing’s carcinoid or other syndromes. 5 years survival rate is 90%, small bowel Carcinoid with liver metastasis the 5 years survival rate is better than 50%
Slide 49-

Small Intestinal Neoplasms Carcinoid tumor Carcinoid syndrome Syndrome occur in 1% of all pt. with carcinoid & in 20% of those of widespread metastasis Paroxymal flushing, episodes of asthma-like wheezing, right-sided heart failure, attacks of watery diarrhea, abdominal pain, edema and pellagra-like lesions of the skin and oral mucosa. The principal chemical mediator is serotonin (5-hydroxy-tryptamine-5HT). 5-HT is decarboxylated in the liver and lungs to 5-hydroxy-indoleacetic acid (5HIAA) The syndrome is classically associated with ileal carcinoids with hepatic metastases.
Slide 50-

Small Intestinal Neoplasms Lymphoma Up to 40% of lymphomas arise in sites other than lymph nodes, gut is the most. 1% to 4% of all gastrointestinal malignancies are lymphomas. Primary GIT lymphomas exhibit no evidence of liver, spleen, or bone marrow involvement at the time of diagnosis.
Slide 51-

Small Intestinal Neoplasms Lymphoma Sporadic lymphoma arise from the B cells of mucosa-associated lymphoid tissue (MALT). This usually affects adults, lacks a sex predilection, and may arise anywhere in the gut: stomach - 55% to 60% - small intestine - 25% to 30% - proximal colon - 10% to 15% - distal colon - up to 10% -
Slide 52-

Small Intestinal Neoplasms Lymphoma Gastric MALT lymphomas arise in the setting of mucosal lymphoid activation, as a result of Helicobacter associated chronic gastritis. Celiac disease is associated with a higher than normal risk of T-cell lymphomas.
Slide 53-

Small Intestinal Neoplasms Lymphoma Primary GIT lymphomas have a better prognosis than do those arising in other sites. Treatment: combined surgery, chemotherapy, and radiation therapy.
Slide 54-

Thank you