Overview of Gastrointestinal Function

Total Page:16

File Type:pdf, Size:1020Kb

Overview of Gastrointestinal Function Overview of Gastrointestinal Function George N. DeMartino, Ph.D. Department of Physiology University of Texas Southwestern Medical Center Dallas, TX 75390 The gastrointestinal system Functions of the gastrointestinal system • Digestion • Absorption • Secretion • Motility • Immune surveillance and tolerance GI-OP-13 Histology of the GI tract Blood or Lumenal Serosal Side or Mucosal Side Structure of a villus Villus Lamina propria Movement of substances across the epithelial layer Tight junctions X Lumen Blood Apical membrane Basolateral membrane X X transcellular X X paracellular GI-OP-19 Histology of the GI tract Blood or Lumenal Serosal Side or Mucosal Side Motility in the gastrointestinal system Propulsion net movement by peristalsis Mixing for digestion and absorption Separation sphincters Storage decreased pressure GI-OP-42 Intercellular signaling in the gastrointestinal system • Neural • Hormonal • Paracrine GI-OP-10 Neural control of the GI system • Extrinsic nervous system autonomic central nervous system • Intrinsic (enteric) nervous system entirely with the GI system GI-OP-14 The extrinsic nervous system The intrinsic nervous system forms complete functional circuits Sensory neurons Interneurons Motor neurons (excitatory and inhibitory) Parasympathetic nerves regulate functions of the intrinsic nervous system Y Reflex control of gastrointestinal functions Vago-vagal Afferent reflex Salivary Glands Composition of Saliva O Proteins α−amylase lactoferrin lipase RNase lysozyme et al mucus O Electrolyte solution water Na+ , K + - HCO3 Functions of saliva • Oral protection buffering of hot, cold, acid, base • Oral hygiene bacteriostatic • Lubrication swallowing • Digestion carbohydrates and lipids GI-ME-11 Structure of the esophagus Pharynx Upper Esophageal Sphincter Skeletal (UES) muscle Skeletal and smooth muscle Smooth muscle Diaphragm Lower Esophageal Sphincter Stomach GI-010 (LES) Regulation of the UES during a swallow Reflex Reflex relaxation contraction (neural) (neural) Persistalsis Regulation of the UES during a swallow Reflex Reflex relaxation contraction (neural) (myogenic) VIP (NO ?) Anatomical and functional divisions of the stomach LES Fundus Pyloric Oxyntic gland Orad gland area area Gastric juice Oxyntic gland pylorus G cell Caudad Body Gastrin duodenum (Corpus) Antrum GI-S-15 Mechanism of acid secretion by the parietal cell H O 2 Lumen - Cl- H+ K+ H2O Cl- - + ATP Cl K ADP K+ ATP ADP Na+ H 0 H+ + OH - HCO - Na+ 2 3 Carbonic anhydrase CO2 Blood + GI-S-07 Stimulation of acid secretion in parietal cells Receptors Histamine (H2) Gastrin ACh G G G AC PL-C PL-C H+ H+ Lumen GI-S-13 Stimulation of acid secretion in parietal cells Receptors Histamine (H2) Gastrin ACh G G G AC PL-C PL-C cAMP IP3 + DAG Protein kinase A Ca2+ Protein kinase Substrates C Sequestered H+ / K+ pumps Substrates Sequestered H+ / K+ pumps H+ Membrane-exposed H+ / K+ pumps Lumen GI-S-13 Cephalic phase vagal nucleus of acid secretion vagus nerve thought, sight, smell, taste, or chewing of food H+ ACh Parietal cell GRP ECL cell G cell Histamine Gastrin Efferent pathways circulation GI-S-05 Gastric phase vagal nucleus vagus nerve of acid secretion distension sensed by mechanoreceptors distension in the stomach, presence of amino acids and peptides H+ Amino acids and peptides ACh Parietal cell G cell GRP ECL cell ACh Histamine Gastrin Efferent pathways Afferent pathways circulation GI-S-06 Protection of the epithelial lining of the stomach pH 2 Gastric lumen - - Mucus layer HCO3 HCO3 pH 7 Mucus GI-S-19 Motility in the stomach • Reservoir storage without increased pressure • Grinding and mixing mechanical disruption for digestion and absorption • Regulated pumping optimal delivery to duodenum GI-S-32 The gastrointestinal system Small Intestine Digestion Absorption Secretion Motility Pancreatic Secretion Aqueous Component (ductule cells) water Function: acid neutralization bicarbonate Enzymatic Component (acinar cells) proteases Function: digestion lipases saccharidases Intestinal phase vagal nucleus of pancreatic secretion vagus nerve afferent pathways acid and digestion products for vagal in the duodenum reflex protein amino acids I cells peptides fat H+ efferent S cells pathways for circulation vagal reflex HCO - CCK 3 H O 2 Ach pancreas Secretin Enzymes ductule cells acinar cells GI-SILPGB-02 Secretion from the liver and gallbladder Figure15 NaNa++ ClCl -- KK++ CaCa2+2+ Liver BileBile wwaatteerr acidsacids Figure11 PortalPortal - circulationcirculation HCO3 Gallbladder Secretin Na+ -- HCOHCO3 H20 3 ClCl-- NaNa++ HH2200 Figure14 CCK Ach Sphincter of Oddi BileBile BileBile acidsacids Duodenum Ileum Functions of Bile • Emulsification of dietary lipids required for lipid digestion • Solubilization of lipid digestion products required for lipid absorption • Excretion of waste products bilirubin and cholesterol GI-SILPGB-30 Organic components of bile • Bile acids / bile salts 70% • Phospholipids 20% • Cholesterol 5% • Bilirubin 1% • Everything else 4% GI-SILPGB-40 Components of bile Bile acids package products of lipid digestion into mixed micelles for absorption Products of lipid digestion Mixed micelle + - - + - + - -- Free fatty acid Lysolecithin - + - Cholesterol Monoglyceride GI-SILPGB-36 Digestion and absorption in the small intestine Proteins degradation to amino acids and peptides combined action of lumenal and membrane- bounds proteases absorption by multiple transporters Carbohydrates degradation to monosaccharides combined action of lumenal and membrane- bounds proteases absorption by several transporters Lipids Absorption of monosaccharides in the small intestine Na+/ K+ ATPase SGLT1 K+ ATP¤ADP Na+ Na+ Glucose / Glucose / Glut 2 Galactose Galactose Fructose Fructose Glut 5 Lumen Blood (Apical) (Basolateral) GI-SILPGB-16 Fluid balance in the GI tract 9000 ml 8900 ml VolumeVolume VolumeVolume enterenteriinngg absorbedabsorbed intestinesintestines byby intestinesintestines ~ 20% total 100 ml body water ! Volume excreted Important Principle The absorption of water is dependent on and proportional to the absorption of solutes GI-LI-25 Bad things happen when solutes are not absorbed Colon Jejunum Ileum Na+ Lactose glucose + galactose H2O H2O Normal Diarrhea SCFA CO2 Lactose Lactose H2OLactose H2O Lactase deficiency GI-LI-24 H2O.
Recommended publications
  • Calcium-Sensing Receptor Is a Physiologic Multimodal Chemosensor Regulating Gastric G-Cell Growth and Gastrin Secretion
    Calcium-sensing receptor is a physiologic multimodal chemosensor regulating gastric G-cell growth and gastrin secretion Jianying Fenga, Clark D. Petersena, David H. Coyb, Jian-Kang Jiangc, Craig J. Thomasc, Martin R. Pollakd, and Stephen A. Wanka,1 aDigestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-1804; bPeptide Research Laboratories, Department of Medicine, Tulane Health Sciences Center, New Orleans, LA 70112-2699; cNational Institutes of Health Chemical Genomics Center, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892; and dDivision of Nephrology, Beth Israel Deaconess Medical Center, Boston, MA 02215 Edited* by Martha Vaughan, National Heart, Lung, and Blood Institute, Bethesda, MD, and approved September 1, 2010 (received for review June 25, 2010) The calcium-sensing receptor (CaR) is the major sensor and The sensing of extracellular Ca2+ and the regulation of Ca2+ regulator of extracellular Ca2+, whose activity is allosterically reg- homestasis has been largely attributed to the calcium-sensing ulated by amino acids and pH. Recently, CaR has been identified in receptor (CaR), a member of the C family of G protein-coupled the stomach and intestinal tract, where it has been proposed to receptors (GPCR). Consistent with this function, CaR is ex- 2+ function in a non-Ca2+ homeostatic capacity. Luminal nutrients, pressed on extracellular Ca -regulating cells such as para- such as Ca2+ and amino acids, have been recognized for decades thyroid, thyroid parafollicular, renal tubular, and bone cells (6). as potent stimulants for gastrin and acid secretion, although the The CaR has a large NH2 terminal extracellular domain molecular basis for their recognition remains unknown.
    [Show full text]
  • Are You Ready for ICD-10-PCS? Expert Tips, Tools, and Guidance to Make the Transition Simple
    Are You Ready for ICD-10-PCS? Expert Tips, Tools, and Guidance to Make the Transition Simple By Amy Crenshaw Pritchett February 19, 2014 1 Agenda In this webinar: Expand your understanding of ICD-10-PCS with can’t miss ICD-10-PCS coding conventions & guidelines. Understand the basic differences between ICD-9-CM Volume 3 and ICD-10-PCS. Learn code structure, organization, & characters: Step 1 to coding section “0” ICD-10-PCS? Pinpoint the body system. To build your ICD-10-PCS code, you must identify the root operation. Study 7 options when assigning your PCS code’s 5th character. Master how to determine the device value for your PCS code’s character. Raise your awareness of unique ICD-10-PCS challenges pertaining to documentation and specificity: Prepare physicians now for more detailed transfusion notes under ICD- 10-PCS. Discover why writing “Right Carotid Endarterectomy” won’t be enough. Know where to find ICD-10-PCS tools, techniques, and best practices. 2 Understanding ICD-10-PCS ICD-10-PCS is a major departure from ICD-9-CM procedure coding, requiring you to know which root word applies. Effective October 1, 2014, this procedure coding system will be used to collect data, determine payment, and support the electronic health record for all inpatient procedures performed in the US. 3 Gear Up for ICD-10-PCS This procedure coding system is starkly different from ICD-9-CM procedure coding: Every ICD-10-PCS code has seven characters, each character defining one aspect of the procedure performed. For instance, not correctly identifying your physician’s approach – the fifth character – and not being able to distinguish between similar root operations can throw off your claims accuracy! 4 Converting to ICD-10-PCS Have your inpatient coders and clinical documentation specialists begun preparing for ICD-10-PCS yet? That’s why we’re here today … to ease your transition from ICD-9-CM procedure coding to ICD-10-PCS.
    [Show full text]
  • Parietal Cell Hyperplasia Induced by Long-Term Administration of Antacids to Rats
    Gut: first published as 10.1136/gut.19.9.798 on 1 September 1978. Downloaded from Gut, 1978, 19, 798-801 Parietal cell hyperplasia induced by long-term administration of antacids to rats G. MAZZACCA1, F. CASCIONE, G. BUDILLON, L. D'AGOSTINO, L. CIMINO, AND C. FEMIANO From the Division of Gastroenterology, 2nd School ofMedicine, University ofNaples, and the Department ofPathology, Institute for Tumoral Diseases, Naples, Italv SUMMARY Suspension of magnesium and aluminum hydroxide (30-60 mEq/24 h) or a comparable volume of water was orally administered by gastric intubation to two groups of 20 male wistar rats each over 60 days. The antacid treatment led to a significant increase in the height (0-464 + 0-02 mm v. 0-318 ± 0 06) and in the volume (472 ± 32 mm3 v. 328 ± 45) of the fundic mucosa ofthe stomach, in the average count of parietal cells per unit area of the mucosa (32-37 ± 1 8 v. 22-3 + 1 6), and in the total parietal cell population of the stomach (53-6 + 3.5 x 106 v. 43-2 + 3.7 x 106). Furthermore fasting serum gastrin concentration was significantly higher in the antacid treated rats (81.2 + 7.4 pg/ml) than in control animals (56-9 ± 6-9 pg/ml). It is known that a feedback mechanism governs the The animals of group B received each time and by relationship between antral gastrin release and the same procedure a comparable volume of water. intraluminal gastric pH (Walsh et al., 1975). During the night each animal was housed in a Furthermore, gastrin exerts a trophic influence on separate cage and the antacid suspension was the the gastric mucosa with increase in the parietal cell only drinking fluid available to the rats of group A.
    [Show full text]
  • Sporadic (Nonhereditary) Colorectal Cancer: Introduction
    Sporadic (Nonhereditary) Colorectal Cancer: Introduction Colorectal cancer affects about 5% of the population, with up to 150,000 new cases per year in the United States alone. Cancer of the large intestine accounts for 21% of all cancers in the US, ranking second only to lung cancer in mortality in both males and females. It is, however, one of the most potentially curable of gastrointestinal cancers. Colorectal cancer is detected through screening procedures or when the patient presents with symptoms. Screening is vital to prevention and should be a part of routine care for adults over the age of 50 who are at average risk. High-risk individuals (those with previous colon cancer , family history of colon cancer , inflammatory bowel disease, or history of colorectal polyps) require careful follow-up. There is great variability in the worldwide incidence and mortality rates. Industrialized nations appear to have the greatest risk while most developing nations have lower rates. Unfortunately, this incidence is on the increase. North America, Western Europe, Australia and New Zealand have high rates for colorectal neoplasms (Figure 2). Figure 1. Location of the colon in the body. Figure 2. Geographic distribution of sporadic colon cancer . Symptoms Colorectal cancer does not usually produce symptoms early in the disease process. Symptoms are dependent upon the site of the primary tumor. Cancers of the proximal colon tend to grow larger than those of the left colon and rectum before they produce symptoms. Abnormal vasculature and trauma from the fecal stream may result in bleeding as the tumor expands in the intestinal lumen.
    [Show full text]
  • GLOSSARY of MEDICAL and ANATOMICAL TERMS
    GLOSSARY of MEDICAL and ANATOMICAL TERMS Abbreviations: • A. Arabic • abb. = abbreviation • c. circa = about • F. French • adj. adjective • G. Greek • Ge. German • cf. compare • L. Latin • dim. = diminutive • OF. Old French • ( ) plural form in brackets A-band abb. of anisotropic band G. anisos = unequal + tropos = turning; meaning having not equal properties in every direction; transverse bands in living skeletal muscle which rotate the plane of polarised light, cf. I-band. Abbé, Ernst. 1840-1905. German physicist; mathematical analysis of optics as a basis for constructing better microscopes; devised oil immersion lens; Abbé condenser. absorption L. absorbere = to suck up. acervulus L. = sand, gritty; brain sand (cf. psammoma body). acetylcholine an ester of choline found in many tissue, synapses & neuromuscular junctions, where it is a neural transmitter. acetylcholinesterase enzyme at motor end-plate responsible for rapid destruction of acetylcholine, a neurotransmitter. acidophilic adj. L. acidus = sour + G. philein = to love; affinity for an acidic dye, such as eosin staining cytoplasmic proteins. acinus (-i) L. = a juicy berry, a grape; applied to small, rounded terminal secretory units of compound exocrine glands that have a small lumen (adj. acinar). acrosome G. akron = extremity + soma = body; head of spermatozoon. actin polymer protein filament found in the intracellular cytoskeleton, particularly in the thin (I-) bands of striated muscle. adenohypophysis G. ade = an acorn + hypophyses = an undergrowth; anterior lobe of hypophysis (cf. pituitary). adenoid G. " + -oeides = in form of; in the form of a gland, glandular; the pharyngeal tonsil. adipocyte L. adeps = fat (of an animal) + G. kytos = a container; cells responsible for storage and metabolism of lipids, found in white fat and brown fat.
    [Show full text]
  • Lumen Retiree and Inactive Health Care Plan* Standard Consumer
    Lumen Retiree and Inactive Health Care Plan * Standard Consumer Driven Health Plan (CDHP) (Administered by UnitedHealthcare) Summary Plan Description (SPD) For Retired and Inactive Former Employees CenturyLink, Embarq, Qwest Post-1990 Management, Qwest Post-1990 Occupational Retirees (including Inactive and COBRA Participants) Effective January 1, 2021 This SPD must be read in conjunction with the Retiree General Information SPD , which explains many details of your coverage and provides a listing of the other Benet options under the Plan. * The Lumen brand was launched on September 14, 2020. As a result, Lumen, Inc. is referred to as Lumen Technologies, or simply Lumen. The legal name Lumen, Inc. is expected to be formally changed to Lumen Technologies, Inc. upon the completion of all applicable requirements. Issued Jan. 1, 2021 Table of Contents INTRODUCTION 1 The Patient Protection and Affordable Care Act Known as the “Affordable Care Act” ....................................... 1 The Required Forum for Legal Disputes .......................................................................................................... 2 How to Use This Document ............................................................................................................................... 2 Exempt Retiree Medical Plan Status Notice ...................................................................................................... 2 Lumen’s right to use your Social Security number for administration of benets .............................................
    [Show full text]
  • Human Anatomy and Physiology
    LECTURE NOTES For Nursing Students Human Anatomy and Physiology Nega Assefa Alemaya University Yosief Tsige Jimma University In collaboration with the Ethiopia Public Health Training Initiative, The Carter Center, the Ethiopia Ministry of Health, and the Ethiopia Ministry of Education 2003 Funded under USAID Cooperative Agreement No. 663-A-00-00-0358-00. Produced in collaboration with the Ethiopia Public Health Training Initiative, The Carter Center, the Ethiopia Ministry of Health, and the Ethiopia Ministry of Education. Important Guidelines for Printing and Photocopying Limited permission is granted free of charge to print or photocopy all pages of this publication for educational, not-for-profit use by health care workers, students or faculty. All copies must retain all author credits and copyright notices included in the original document. Under no circumstances is it permissible to sell or distribute on a commercial basis, or to claim authorship of, copies of material reproduced from this publication. ©2003 by Nega Assefa and Yosief Tsige All rights reserved. Except as expressly provided above, no part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without written permission of the author or authors. This material is intended for educational use only by practicing health care workers or students and faculty in a health care field. Human Anatomy and Physiology Preface There is a shortage in Ethiopia of teaching / learning material in the area of anatomy and physicalogy for nurses. The Carter Center EPHTI appreciating the problem and promoted the development of this lecture note that could help both the teachers and students.
    [Show full text]
  • Cellular Localization of Gastric Inhibitory Polypeptide in the Duodenum and Jejunum
    Gut: first published as 10.1136/gut.14.4.284 on 1 April 1973. Downloaded from Gut, 1973, 14, 284-288 Cellular localization of gastric inhibitory polypeptide in the duodenum and jejunum JULIA M. POLAK, S. R. BLOOM', MARION KUZIO, J. C. BROWN, AND A. G. E. PEARSE From the Department ofHistochemistry, Royal Postgraduate Medical School, Hammersmith Hospital, London, and the Department ofPhysiology, University ofBritish Columbia, Vancouver, Canada SUMMARY Indirect immunofluorescence studies using an antiserum to purified porcine gastric inhibitory polypeptide indicate, in the gastrointestinal tract of dog and man, that this polypeptide is present in cells situated predominantly in the mid-zone of the glands in the duodenum and, to a lesser extent, in the jejunum. Absolute correlation of the gastric inhibitory polypeptide cell with one or other of the known endocrine-like cells identified by electron microscopy awaits confirmation by electron immunocytochemistry. It is here identified as an endocrine polypeptide cell of the APUD series and, provisionally, as the D, cell. While the hormonal status of a given polypeptide depends ultimately on physiological experiments the present results strengthen the view that gastric inhibitory polypeptide is indeed a hormone. In 1969 Brown, Pederson, Jorpes, and Mutt described We report here the results of immunofluorescence an enterogastrone, extractable from porcine intestine, studies on the localization of GIP in human and http://gut.bmj.com/ which strongly inhibited gastric acid secretion. The canine intestine. purification of an apparently similar enterogastrone was reported in the same year by Lucien, Itoh, Sun, Material and Methods Meyer, Carlton, and Schally. The first of these poly- peptides, named gastric inhibitory polypeptide Operative samples of duodenal and jejunal mucosa (GIP) by Brown, Mutt, and Pederson (1970), was from seven human subjects were studied.
    [Show full text]
  • Expression of Cell Membrane Complement Regulatory Glycoproteins Along the Normal and Diseased Human Gastrointestinal Tract
    522 Gut 1998;42:522–529 Expression of cell membrane complement regulatory glycoproteins along the normal and diseased human gastrointestinal tract Gut: first published as 10.1136/gut.42.4.522 on 1 April 1998. Downloaded from A E Berstad, P Brandtzaeg Abstract tract. Indeed, activated complement has been Background/Aims—Uncontrolled comple- detected in lesions of inflammatory bowel ment activation may be of immunopatho- disease,2–4 coeliac disease,5 and recently also in logical importance in inflammatory Helicobacter pylori gastritis.6 diseases of the gastrointestinal tract. Ex- Certain complement activation products, pression of membrane bound factors that notably the C3b fragment and the C5b-7 com- regulate complement activation was there- plex, can on their own—that is, without associ- fore studied in situ. ated antibody—bind to any nearby cell Methods—Frozen tissue specimens were membrane.7 Therefore it is crucial that com- obtained from patients with Helicobacter plement activity is tightly regulated. Mam- pylori gastritis, coeliac disease, Crohn’s malian cells are protected from complement disease, or ulcerative colitis, and from induced damage by a family of cell membrane histologically normal controls. Sections complement regulatory glycoproteins that were examined by immunofluorescence downregulate activation of homologous com- with monoclonal antibodies to protectin plement on their cell surface.8 Protectin (CD59), decay accelerating factor (DAF), (CD59) is broadly distributed on cells of and membrane cofactor protein (MCP). haemopoietic and non-haemopoietic origin79; Results—Protectin and MCP were widely it inhibits the formation of terminal comple- expressed in normal and diseased mu- ment complex by preventing the binding of C9 cosae.
    [Show full text]
  • Stomach, Duodenum, and Jejunum
    Gut, 1970, 11, 649-658 The endocrine polypeptide cells of the human Gut: first published as 10.1136/gut.11.8.649 on 1 August 1970. Downloaded from stomach, duodenum, and jejunum A. G. E. PEARSE, I. COULLING, B. WEAVERS, AND S. FRIESEN' From the Department of Histochemistry, Royal Postgraduate Medical School, London SUMMARY Thirty specimens of stomach, duodenum, and jejunum, removed at operation, were examined by optical microscopical, cytochemical, and electron microscopical techniques. The overall distribution of four types of endocrine polypeptide cell in the stomach, and three in the intestine, was determined. The seven cell types are described by names and letters belonging to a scheme for nomenclature agreed upon at the 1969 Wiesbaden conference o* gastrointestinal hormones. The gastrin-secreting G cell was the only cell for which firm identification with a known hormone was possible. Although there was wide variation in the distribution of the various cells, from one case to another, striking differences were never- theless observable, with respect to the G cell, between antra from carcinoma and from ulcer cases. http://gut.bmj.com/ This study was undertaken with a view to estab- tive shorthand terminology. Correlation with the lishing the overall topographical distribution of terminology used by Solcia, Vassallo, and Capella the various types of endocrine polypeptide cells (1969b) and by Vassallo, Solcia, and Capella in the human stomach and upper intestine. (1969) had to be equated, if possible, with the Adequate sampling was regarded as a pre- scheme used by Forssmann, Orci, Pictet, Renold, on September 28, 2021 by guest. Protected copyright.
    [Show full text]
  • Location of Major Duodenal Papilla in Human Duodenum Sharmina Sayeed1, Shamim Ara2, Mesbahul Hoque3, Zannatul Ferdous4, Kanetarin Kashem5
    Bangladesh Journal of Anatomy January 2014, Vol. 12, No. 1 pp. 22-24 Location of Major Duodenal Papilla in Human Duodenum Sharmina Sayeed1, Shamim Ara2, Mesbahul Hoque3, Zannatul Ferdous4, Kanetarin Kashem5 Abstract Context: The major duodenal papilla is one of the most fascinating papilla present at the duodenum attracting many gastroenterologists as they do endoscopic retrograde cholangiopancreatiography (ERCP) for diagnosis and treatment purpose of many diseases. Most of the textbooks of Anatomy describe that the summit of major duodenal papilla is situated posteromedially in the descending part of duodenum. Henceforth the present study was undertaken in 70 human duodenums to observe the location of major duodenal papilla. Materials & Methods: A cross-sectional observational study was conducted in the department of Anatomy, Dhaka Medical College, Dhaka from July 2010 to June 2011. Seventy postmortem human duodenums were collected from unclaimed dead bodies that were under examination in the morgue of department of Forensic Medicine and the department of Anatomy of Dhaka Medical College, Dhaka. Location of major duodenal papilla was observed and recorded. Results: The location of major duodenal papilla was observed in the medial wall of second part of duodenum in 78.6% specimens, in the posteromedial wall of second part in 15.7% cases and in the posteromedial wall of the junction between second and third part in 4.3% and absent in 1.4% duodenum. Conclusion: The location of major duodenal papilla varies in position. Key words: Major duodenal papilla. Introduction Location of major duodenal papilla provides The major duodenal papilla (papilla of Vater) is the information to gastroenterologist regarding opening point where the dilated junction of the pancreatic of common bile duct and pancreatic duct in the duct and the bile duct (ampulla of Vater) enters the duodenum during ERCP.
    [Show full text]
  • Colon and Rectum
    AJC12 7/14/06 1:24 PM Page 107 12 Colon and Rectum (Sarcomas, lymphomas, and carcinoid tumors of the large intestine or appendix are not included.) C18.0 Cecum C18.5 Splenic flexure of C18.9 Colon, NOS C18.1 Appendix colon C19.9 Rectosigmoid C18.2 Ascending colon C18.6 Descending colon junction C18.3 Hepatic flexure of C18.7 Sigmoid colon C20.9 Rectum, NOS colon C18.8 Overlapping lesion of C18.4 Transverse colon colon SUMMARY OF CHANGES •A revised description of the anatomy of the colon and rectum better delineates the data concerning the boundaries between colon, rectum, and anal canal. Ade- nocarcinomas of the vermiform appendix are classified according to the TNM staging system but should be recorded separately, whereas cancers that occur in the anal canal are staged according to the classification used for the anus. •Smooth extramural nodules of any size in the pericolic or perirectal fat are con- sidered lymph node metastases and will be counted in the N staging. In contrast, irregularly contoured nodules in the peritumoral fat are considered vascular invasion and will be coded as transmural extension in the T category and further denoted as either a V1 (microscopic vascular invasion) if only microscopically visible or a V2 (macroscopic vascular invasion) if grossly visible. • Stage Group II is subdivided into IIA and IIB on the basis of whether the primary tumor is T3 or T4 respectively. • Stage Group III is subdivided into IIIA (T1-2N1M0), IIIB (T3-4N1M0), or IIIC (any TN2M0). INTRODUCTION The TNM classification for carcinomas of the colon and rectum provides more detail than other staging systems.
    [Show full text]