Tumors of the Intestines. Malignant Lesion. Adenocarcinoma. sessile Serrated Adenomas

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1 Tumors of the Intestines Non-Neoplastic Polyps Neoplastic Epithelial Polyps Other Tumors Hyperplastic, Hamartomatous, Juvenile, Peutz-Jeghers, Inflammatory abd Lymphoid Polyphs Benign Polyphs Malignant Lesion Gastrointestinal Stomal Tumor (GIST) Carcinoid Tumor Lymphoma Adenoma Adenocarcinoma Squamous Cells Carcinoma of the Anus Tubular Adenoma Villous Adenoma Tubulovillous Adenoma sessile Serrated

2 Non-Cancerous Benign Tumor Pre-malignant Lesion Polyps Malignant Tumor Sessile Pedunculated Hyperplastic Polyps Adenoma Villous Tubulovillous Solitary Multiple/ Hyperplastic Polyposis Tubular Tubulovillous Sessile Serrated Familial Polyposis Gardner and Turcot Peutz-Jeghers and Cowden Colorectal Carcinoma Intestinal Malignancy Intestinal Malignancy Extraintestinal Tumors Intestinal Malignancy Extraintestinal Malignancies Osteoma Fibroma Glioma

3 Hyperplastic Polyps Juvenile Polyps (children) Retention Polyps (adult) Non-Neoplastic Polyps Most are sporadic Small Abundant crypts lined by Increase in age Nipple like o Well-differentiated Goblet 90% happens in the Colon Hemispherical cells Half of people over the age Smooth protrusion of o Absorptive cells of 60 are having polyps Mucosa into the lumen Separated by scant Lamina Can be either Propria o Solitary Have no malignant potential o Multiple /Hyperplastic Polyposis Hyperplastic Serratred have malignant potential; may evolve into Colorectal Carcinoma Incidence Rounded Hamartomatous o Juvenile Polyps Smooth proliferation of mainly the Children <5 years old Slightly lobulated Lamina Propria o Retention Polyps Sometimes Pedunculated Enclosing a wide spaced Adults at any age Size and dialted Cystic gland Hamartomatous o Children large Not a premalignant lesion proliferations; no malignant o Adult smaller transformation

4 Familial Polyposis Peutz-Jeghers Premalignant Polyps Autosomal Dominant Disorder o Defect on APC gene on chromosome 5q21 High risk in developing Colorectal Carcinoma Minimum of 100 polyps for diagnosis Gardner and Turcot o Just a variant of FPS o Have occurrence of extraintestinal tumors Osteomas Fibromas Gliomas Autosomal Dominant Disorder o Defect on LKB1 gene encoding for Threonine Kinase Characterized by o Mucocutaneous lesion Hyperpigmented macules on Lips Oral mucosa o Benign hamartomatous lesion on the GIT colonic May affect other part of GIT especially the Duodenum (Duodenal Adenoma) May have signs of Haemorrhage and may pass through the faeces Most polyps are Tubular Adenoma Occasionally may present with Villous Adenoma Cowden Autosomal Dominant Disorder o Defect in PTEN (Phosphatase and Tensin Homologue) Tumor Suppressor gene o Encodes for Phosphatase Characterized by o Hamartomatous polyps of GIT o Increase risk of developing Neoplasms in Thyroid Breast Uterus Skin

5 Tubular Villous Tubulovillous Incidence o Before the age of % o After the age of % Male and female are equally affected Increase the risk of developing Colonic Carcinoma Clinical Manifestations Sized of o Smaller remain asymptomatic o Larger may cause severe bleeding leading to Iron Deficiency Anemia Occult and overt Rectal bleeding Villous Adenoma is often symptomatic o Occult and overt Rectal bleeding o Secrete mucoid material rich in K + and protein leading to Hypoproteinaemia Hypokalaemia All mandatory to be excised May arise anywhere in the colon but commonly at the Rectosigmoid junction Can be either o Small Sessile in nature o Larger Pedunculated with Raspberry like head May happen anywhere in the Colon but commonly in o Rectum o Rectosigmoid junction The polyps tend to be larger in size Generally can be either o Sessile o Cauliflower like o Velvety Can be either o Pedunculated o Sessile o Or both In Pedunculated Adenoma o Stalks are lined by normal Colonic mucosa o Head are composed of Neoplastic Epithelium Branching glands (Tubular) lined by cells that are Tall Having Hyperchromatic nuclei Disorderly arranged o In benign lesion, well separated by Lamina Propria o Dysplasia is common Intramucosal Carcinoma in the mucosa Invasive Carcinoma extend into the Submucosa of the stalk Villous Adenoma is subsequently seen Frondlike viliform extensions of mucosa o Covered by Columnar Epithelium that is Dysplastic Disorderly arranged Sometimes pile-up Broad mix of tubular and villous area Various degree of Dysplasia

6 Colorectal Carcinoma 98% are Adenocarcinoma o Anus usually Squamous Cell Carcinoma Peak incidence during o years old o Below 50 years old <20% Affecting male more than female If develop during early life, should suspect o Familial Polyposis o Ulcerative Colitis Multifactorial Disorder o Genetic Adenoma-carcinoma Pathway Familial o APC inactivation Sporadic o Inactivation of multiple genes Microsatellite Instability Pathway Familial o Inactivation of DNA repair gene MLH1 MSH2 Sporadic o Inactivation of DNA repair gene MLH1 MSH2 o Environmental (Dietary) Low content fiber diet High content refined Carbohydrate diet High fat content diet Decreased intake of protective micronutrients Vitamin A, C and E Malignant Tumor of the Intestine Sites o 25% - Caecum and Asc o 25% - Dsc and Prox Sigmoid o 25% - Dist Sigmoid and Rectum o 25% - scattered elsewhere Often lesion appears solitary, frequently destroy the earlier Adenomatous lesion If multiple, deform the colonic structure Morphological patterns o If happen in Proximal Colon Polypoid Exophytic growth Extend along the wall of Caecum and Asc Colon o If happen in Distal Colon Annular (ring shape) Encircling the lesion Napkin-ring constrictions Narrowing of the lumen o Both patterns may infiltrate the whole wall of intestine and leading to firm masses on the Serosa Clinical Manifestations Remain asymptomatic for years Pattern o If happens at the Proximal Colon Iron Deficiency Anemia Fatigue Weakness o If happens at the Distal Colon Occult bleeding Changes in bowel habit Crampy pain on the Left Lower Quadrant All Colorectal Carcinoma will metastasize to distant tissue, in order of preference o Pericolic Lymph Nodes o Lungs o Bones o Serosal membrane of Peritoneum Most of the cases are Adenocarcinoma Ranging from welldifferentiated to poorly differentiated All are Anaplastic Most produce Mucin o Since Mucin is secreted inside the wall of the Intestine rather into the Lumen, the secretion may dissect through the wall and enable invasion Diagnosis Screening o Digital Rectal examination o Fecal testing for occult blood o Barium enema o Sigmoidoscopy and Colonoscopy o Serum markers Carcinoembryogenic antigen Non-specific False positive results in o Various kind of tumor Lungs, ovary, breast o Non-cancerous condition Liver cirrhosis, UC, pancreatitis Diagnostic o Biopsy Metastasize study o CT scan and X ray

7 Neoplasms of the Small Intestine Adenoma Adenocarcinoma Gastrointestinal Stromal Tumors Less common compared to Colon Ca Most of the cases are benign Clinical Manifestations o Anemia o Rarely cause Intussusception Obstruction o If happen near to Ampulla of Vater may cause biliary obstruction leading to Jaundice Adenocarcinoma o Cramping pain o Nausea o Vomiting o Weight loss o At the time of diagnosis, distant metastasize is common Based on Histochemical markers, it is divided into o Tumors that show Smooth Muscle differentiation o Tumors that show Neural differentiation Often called Gastrointestinal Autonomic Nerve Tumors o Tumors with Smoot Muscle/Neural dual differentiation o Tumors that lacking are lacking of differentiation toward the two lineages GIST commonly occurs at the Stomach o But can also be at Small and Large intestine Due to genetic disorder o Somatic mutation in CD117 gene encodes for Tyrosine Kinase Receptor o This enable the receptor to keep on stimulated without binding to the ligand Can grow as Most of the cases are o Napkin-ring encircling Adenocarcinoma pattern Ranging from welldifferentiated o Polypoid fungating to poorly masses like in the Colon differentiated Most originate from the All are Anaplastic Duodenum including the Most produce Mucin Ampulla of Vater o Since Mucin is secreted inside the wall of the Intestine rather into the Lumen, the secretion may dissect through the wall and enable invasion A prominent mass arose from the Muscularis layer Exophytic growth Retained the covering mucosa except at the central ulcerated area Can be either o Spindle shaped cells for Smooth muscle differentiation o Epitheloid as for Neural differentiation Area of haemorrhage and ulcer

8 Carcinoids of GIT No age exempt, peak incidence at the age of 60 Derived from the Neuroendocrine cells of the GIT mucosa May release peptide and non-peptide hormone leading to their clinical manifestations Arise from o Pancreas o Peripancreatic tissue o Lungs o Biliary tree o Liver o GIT Ileum Rectum Stomach Colon Can be further divided depending on o Growth pattern Trabecular Glandular Undifferentiated Mixed o Hormone produced Bradykinin Serotonin Histamine Prostaglandin o Site of origin Foregut Pancreas Stomach Duodenum Midgut Jejunum Ileum Appendix Ascending Colon Hindgut Transverse Colon Descending Colon Rectum Small Tumor cells are Button-like submucosal o Uniform elevation o Monotonous in Intact or ulcerated appearance Mucosa o Scanty cytoplasm Cut surface is solid yellow o Nucleus is tan Round to oval Can be either Fined stippled o Multiple gastric and chromatin ileum o Forming discrete o Solitary appendix Islands Glands Cords or Trabaculae Mitoses is infrequent Cellular atypia is uncommon Presence of membrane bound secretory granules Clinical Manifestations Cutaneous flushes and cyanosis o Due to vasomotor disturbances Diarrhea, abdominal pain, nausea and vomiting o Due to increase in GIT motility Cough, dypsnea and wheezing o Due to Bradykinin liberated to the lung leading to Asthmatic like attack Nodular liver in metastatic cases Zollinger-Ellison syndrome o Hypersecretion of Gastrin Systemic fibrosis o Heart valve stenosis o Peritoneum o Pelvic fibrosis