Gastrointestinal physiology johnson pdf

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Get this from a library! Gastrointestinal physiology. [Leonard R Johnson;] -- This volume in the Mosby Physiology Monograph Series explains the fundamentals. Gastrointestinal Physiology Leonard R. Johnson PhD, Leonard R. Johnson This concise, readable text provides You Can Download the PDF. Gastrointestinal Physiology. Leonard R. Johnson, Eighth edition, , p. Elsevier Mosby, Philadelphia, ISBN Gastrointestinal.

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Gastrointestinal Physiology, Johnson - Ebook download as PDF File .pdf), Text File .txt) or read book online. Gastrointestinal Physiology, Johnson. Gastrointestinal Physiology. 8th Edition. Mosby Physiology Monograph Series ( With STUDENT CONSULT Online Access). Authors: Leonard Johnson. Gastrointestinal Physiology. 7th Edition. Mosby Physiology Monograph Series. Authors: Leonard Johnson. eBook ISBN: eBook ISBN.

In Harper and Raper described a hormone released from the small intestine that stimulated pancreatic enzyme secretion and accordingly named it pancreozymin. From Vantrappen G. The most prominent. The physiology of gastric motility and gastric emptyingYamada. Gastrointestinal system -- Physiology. Neural input that activates the sympathetic system.

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Gastrointestinal physiology pdf 1. Gastrointestinal Physiology Leonard R. Blaustein et al: Copyright John F. Kennedy Blvd. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher.

This book and the individual contributions contained in it are protected under copyright by the Publisher other than as may be noted herein. Notices Knowledge and best practice in this field are constantly changing.

As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein.

In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided i on procedures featured or ii by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications.

It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and. Includes bibliographical references and index. ISBN pbk. Mosby physiology monograph series. Digestive System Physiological Phenomena. WI ] QP Marybeth Thiel Content Development Specialist: Maria Holman Publishing Services Manager: Hemamalini Rajendrababu Project Manager: Saravanan Thavamani Design Manager: Steven Stave Illustrations Manager: Karen Giacomucci Marketing Manager: Katie Alexo Printed in China Last digit is the print number: This eighth edition is directed to the same audience.

All chapters contain considerable amounts of new material and have been brought up-to-date with current information, without introducing undue amounts of controversy to confuse students.

Hopefully the learning objectives will provide a guide to the important concepts and be an aid to understanding them. I am grateful to my own students for pointing out ways to improve the book. Numerous colleagues in other medical schools and professional institutions have added their suggestions and criticisms as well. I am thankful for their interest and help, and I hope that anyone having criticisms of this edition or suggestions for improving future editions will transmit them to me.

In all previous editions, the motility chapters were wri en by Dr. Norman W.

Weisbrodt, who has since retired. I am grateful to him for allowing me to use his material as I saw fit. I would like to thank H. Ehrlein and his colleagues over a period of 25 years.

This video project was supported by an educational grant from Janssen Research Foundation. Finally, I thank Ms. Marybeth Thiel of Elsevier for suggestions and for helping with the communications and organizational work that are a necessary part of such a project. Objectives Describe the four major functions of the gastrointestinal GI tract. Understand the differences between and significance of endocrine, paracrine, and neurocrine agents.

Identify the major GI hormones, their functions, sites of release, and stimuli for release. Identify the important neurocrines and their functions in the GI tract. Identify the important paracrines and their functions in the GI tract. Understand the causes and resulting physiology of gastrinoma Zollinger-Ellison syndrome and pancreatic cholera Werner Morrison syndrome.

The functions of the gastrointestinal GI tract are regulated by peptides, derivatives of amino acids, and a variety of mediators released from nerves. All GI hormones are peptides, but it is important to realize that not all peptides found in digestive tract mucosa are hormones. The GI tract peptides can be divided into endocrines, paracrines, and neurocrines, depending on the method by which the peptide is delivered to its target site.

Endocrines, or hormones, are released into the general circulation and reach all tissues unless these substances are excluded from the brain by the blood-brain barrier. Members of these la er two groups are classified as candidate hormones. A paracrine. Thus a paracrine may release or inhibit the release of an endocrine substance, thereby ultimately regulating a process remote from its origin.

Histamine, a derivative of the amino acid histidine, is an important regulatory agent that acts as a paracrine. Some GI peptides are located in nerves and may act as neurocrines or neurotransmi ers. Neurocrines conceivably may stimulate or inhibit the release of endocrines or paracrines.

Acetylcholine ACh , although not a peptide, is an important neuroregulator in the GI tract. One of its actions is to stimulate acid secretion from the gastric parietal cells. The word hormone was coined by W.

Hardy and used by Starling in to describe secretin and gastrin and to convey the concept of bloodborne chemical messengers. The GI hormones are released from the mucosa of the stomach and small intestine by nervous activity, distention, and chemical stimulation coincident with the intake of food. Released into the portal circulation, the GI hormones pass through the liver to the heart and back to the digestive system to regulate its movements, secretions, and growth.

These hormones also regulate the growth of the mucosa of the stomach and small and large intestines, as well as the growth of the exocrine pancreas. Many of the demonstrated actions of these peptides are pharmacologic and do not occur under normal circumstances.

This chapter is concerned primarily with the physiologic effects of the GI peptides. The actions of the GI peptides also may vary in both degree and direction among species.

The actions discussed in the remainder of this chapter are those occurring in humans. Discovery Four steps are required to establish the existence of a GI hormone. First, a physiologic event such as a meal must be demonstrated to provide the stimulus to one part of the digestive tract that subsequently alters the activity in another part.

Five GI peptides have achieved full status as hormones. These are pancreatic polypeptide, neurotensin, and substance P. Some of these peptides function physiologically as paracrines or neurocrines. Another GI peptide, Ghrelin, is released from the body of the stomach and functions as a hormone to regulate food intake. This topic is covered in Chapter It was synthesized by Bodanszky and coworkers later the same year. By Gregory and his colleagues had extracted and isolated hog gastrin; Kenner and his group synthesized it the same year.

A er 60 years all of the criteria for establishing the existence of a GI hormone had been satisfied. In Ivy and Oldberg described a humoral mechanism for the stimulation of gallbladder contraction initiated by the presence of fat in the intestine.

The hormone was named cholecystokinin a er its primary action. The only controversy involving CCK was a mild one over nomenclature. In Harper and Raper described a hormone released from the small intestine that stimulated pancreatic enzyme secretion and accordingly named it pancreozymin. Following proof that the release of insulin was a physiologic action of the peptide. GIP also stimulates insulin release.

Its release is under neural control and accounts for the interdigestive migrating myoelectric complex. In either case it is still referred to as GIP. Released from the intestinal mucosa by fat and glucose. For this reason. Enterogastrone literally means a substance from the intestine entero- that inhibits -one the stomach gastr-. GIP became the fourth GI hormone. During fasting it is released cyclically and stimulates upper GI motility.

These alterations in structure protect the molecules from aminopeptidases and carboxypeptidases and allow most of them to pass through the liver without being inactivated. The sixth amino acid from the C-terminus of gastrin is tyrosine. Chemistry The GI hormones and some related peptides can be divided into two structurally homologous families. The amino-terminus N-terminus of gastrin is pyroglutamyl. This tetrapeptide. All the biologic activity of gastrin can be reproduced by the four C-terminal amino acids.

The NH2 group following Phe does not signify that this is the N-terminus. When sulfated. Both forms occur with equal frequency in nature. G-Gly is the substrate for an amidation reaction that results in the formation of the mature.

Evidence indicates that secretin exists as a helix. Pancreatic glucagon has 29 amino acids. Secretin has 27 amino acids. CCK can activate gastrin receptors e. A glycine-extended G-Gly form of gastrin is then formed by endoproteolytic processing within the G cells. Obviously the tetrapeptide itself and all fragments less than seven amino acids long possess gastrin-like activity.

The second group of peptides is homologous to secretin and includes vasoactive intestinal peptide VIP. The minimally active fragment for the CCK pa ern of activity is therefore the C-terminal heptapeptide.

Peptides with a sulfated tyrosyl residue in position 7 act on CCK-1 receptors. CCK is always sulfated in nature. Each hormone.

Johnson pdf physiology gastrointestinal

Glucagon-like immunoreactivity has been isolated from the small intestine. Glucagon has no active fragment. In summary. On isolation.

Each has many of the same actions as those of secretin and glucagon. During the interdigestive basal state. Current evidence indicates that most G 17 is produced from pro G 17 and most G 34 is derived from pro G G 17 and G 34 are equipotent. Yalow and Berson demonstrated heterogeneity by showing that the major component of gastrin immunoactivity in the serum was a larger molecule that they called big gastrin. An additional gastrin molecule G 14 has been isolated from tissue and contains the C-terminal tetradecapeptide of gastrin.

Thus G 34 is not a necessary intermediate in the production of G Gastrin was originally isolated from hog antral mucosa as a heptadecapeptide see Fig.

This group of peptides is discussed in greater detail later in the chapter. Smaller amounts of G 34 are released from both the antral and the duodenal mucosa. This is primarily G 34 and is released in small amounts during the basal state. Unlike those of other species. G 34 is not simply a dimer of G Most peptide hormones are heterogeneous and occur in two or more molecular forms.

A er a meal. The distributions of the individual GI hormones are shown in Figure The cells containing individual hormones are not clumped together but are dispersed among the epithelial cells. Distribution and Release The GI hormones are located in endocrine cells sca ered throughout the GI mucosa from the stomach through the colon. These cells all are derived from neuroendocrine-programmed cells originating in the embryonic ectoblast. Fa y acids containing eight or more carbon atoms or their monoglycerides are the most potent stimuli for CCK release.

The granules discharge. Fat must be broken down into an absorbable form before release of CCK. Protein in the form of peptides and single amino acids releases both gastrin and CCK. Gastrin is most abundant in the antral and duodenal mucosa. GI endocrine cells have hormone-containing granules concentrated at their bases. Most of its release under physiologic conditions is from the antrum.

These endocrine cells have microvilli on their apical borders that presumably contain receptors for sampling the luminal contents. The endocrine cells of the gut are members of a widely distributed system termed amine precursor uptake decarboxylation APUD cells. Shaded areas indicate where the most release occurs under normal conditions.

Table lists the stimuli that are physiologically important releasers of the GI hormones. Gastrin and motilin are the only hormones shown to be released directly by neural stimulation. GIP also is released by fat and protein. Thus this mechanism acts as a negative feedback control on pancreatic enzyme secretion. Evidence indicates that intestinal releasing factors secreted into the intestine of certain species.

CCK can also be released by acid. Pure alcohol in the same concentration as that of wine does not release gastrin but does stimulate acid secretion. Secretin also is released by fa y acids. Acid and fat in the duodenum. Pancreatic enzymes inactivate these releasing factors. Secretin is released when the pH in the duodenum falls below 4.

The magnitude of the response is not as great as originally believed. In addition to releasing secretin. Motilin is released cyclically approximately every 90 minutes during fasting. The purely physical stimulus of distention activates antral receptors and causes gastrin release. During a meal the pressure of ingested food initiates this response. Gastrin also can be released by calcium. This release is prevented by atropine and ingestion of a mixed meal.

The ingestion and presence of a meal in the intestine result in temporary binding of trypsin and other proteases and allow the releasing factors to remain active and stimulate CCK secretion. It is doubtful whether any of these mechanisms.

Both secretin and glucagon. CCK has been shown to stimulate glucagon release. Hormones alter the release of GI peptides in several instances. Patients with atrophic gastritis. Elevated serum calcium stimulates both gastrin and CCK release. Some mechanisms. The myriad activities possessed by these peptides are summarized in Table Each peptide has some action on almost every target tested.

The important physiologic actions of the GI hormones are depicted in Table Numerous guidelines have been proposed for determining whether an action is physiologic. The hormone should be administered as a continuous intravenous infusion rather than as a single bolus because the a bolus produces transient.

In other words. The action should occur in response to endogenous hormone released by normal stimuli i. If most endogenous gastrin is removed by antrectomy. There is considerable debate on the role of gastrin in regulating the tone of the lower esophageal sphincter.

One of the most important and more recently discovered actions of GI hormones is their trophic activity. It does this by causing the release of histamine a potent acid secretagogue from the enterochromaffinlike ECL cells of the stomach and by direct action on the parietal cells. Patients with. The primary action of gastrin is the stimulation of gastric acid secretion.

Gastrin stimulates synthesis of ribonucleic acid RNA. Gastrin is the most important regulator of gastric acid secretion. Exogenous gastrin prevents this atrophy. Thus CCK greatly increases the pancreatic bicarbonate response to low circulating levels of secretin.

Gastrin also stimulates the growth of ECL cells. In addition to its physiologic actions on pancreatic and biliary secretion. As mentioned previously. Additional evidence suggests that the growth-related receptors for G-Gly work in concert with gastrin to regulate the functional development of the gut. This action is shared by CCK. The ability of secretin to inhibit acid secretion may be important in some human diseases.

Because only small amounts of secretin are released under normal circumstances. In addition. G-Gly is stored in gut tissues. Both CCK and secretin also stimulate the growth of the exocrine pancreas. Continued hypersecretion of gastrin results in ECL cell hyperplasia.

In dogs. CCK is the most potent regulator of gallbladder contraction. CCK regulates gallbladder contraction and gastric emptying. Secretin is second only to ACh in promoting pepsinogen secretion from the chief cells of the stomach.

These data support the conclusions that CCK physiologically. Gastrin also inhibits gastric emptying. This action is probably not physiologically important in humans. Of the GI peptides. G-Gly is far less potent by at least four orders of magnitude than gastrin in stimulating gastric acid secretion.

GIP was originally discovered because of its ability to inhibit gastric acid secretion. CCK also functions to regulate food intake.

Several peptides. Its cyclic release into the blood is inhibited by the ingestion of a meal. Motilin stimulates the so-called migrating motility or myoelectric complex that moves through the stomach and small bowel every 90 minutes in the fasted GI tract.

Gastrointestinal Physiology, Johnson

This is the only known function of this peptide. Candidate Hormones Earlier in this chapter. Enteroglucagon belongs to the secretin family. Most constituents of a meal release pancreatic polypeptide.

Physiology pdf gastrointestinal johnson

Before it can be concluded that pancreatic polypeptide is responsible for the physiologic inhibition of pancreatic secretion. Because the peak rate of pancreatic secretion during a meal is less than the maximal rate that can be achieved with exogenous stimuli. Peptide YY was discovered in porcine small intestine and was named for its N-terminal.

Pancreatic polypeptide and peptide YY tyrosine-tyrosine belong to a separate family and are unrelated to either gastrin or secretin. These o en are referred to as candidate. Many have been proposed. It was then isolated and found to be a linear peptide with 36 amino acid residues. The fact that the peptide is located in the pancreas and cannot be removed without also removing its target organ makes this evidence difficult to obtain.

The intestinal L cell makes three forms of glucagon. Peptide YY also inhibits intestinal motility. The enteroglucagons are products of the same gene processed in the pancreatic alpha cell to form glucagon.

Peptide YY is released by meals. Of its 36 amino acid residues. This 30—amino acid peptide is a potent insulin releaser. It does inhibit neurally stimulated secretion. It stimulates pancreatic secretion. Originally investigators thought that VIP was found in gut endocrine cells.

With the advent of sophisticated immunocytochemical techniques for tissue localization of peptides. These include motilin. It physiologically mediates the relaxation of GI smooth muscle. VIP relaxes smooth muscle. Neurotensin increases blood glucose by stimulating glycogenolysis and glucagon release and inhibiting insulin release. The only other peptide isolated from both the brain and gut and known to have an identical structure in both sites is neurotensin.

Numerous biologically active peptides have been isolated from amphibian skin and later found to have mammalian counterparts. VIP has many of the actions of its relatives. VIP stimulates the synthesis of this potent smooth muscle relaxant. Neurocrines All GI peptides were once believed to originate from endocrine cells and therefore to be either hormones or candidate hormones.

Numerous peptides have been found in both the brain and the digestive tract mucosa. Three peptides have important physiologic functions in the gut as neurocrines listed in Table Luminal protein digestion products may also stimulate gastrin release through a GRP-mediated mechanism. GRP is released by vagal stimulation and mediates the vagal release of gastrin.

One of these. The mammalian counterpart of bombesin is gastrin-releasing peptide GRP. These peptides also inhibit intestinal secretion. The combination of these actions probably accounts for the effectiveness of opiates in treating diarrhea.

If somatostatin is blocked. Opiate receptors on circular smooth muscle cells mediate contraction. The enkephalins function physiologically at these sites and also may be an intricate part of the peristaltic mechanism. They are identical except that the C-terminal amino acid is methionine in one and leucine in the other.

These compounds are present in nerves within both the smooth muscle and the mucosa of the GI tract. Two pentapeptides isolated from pig and calf brains activate opiate receptors and are called enkephalins.

These are important physiologic actions of this peptide. Because the area of release of both paracrines and neurocrines is restricted. It has since been shown to exist throughout the gastric and duodenal mucosa and the pancreas in high concentrations and to inhibit the release of all gut hormones.

In vitro perfused organs are also useful in examining paracrine mediators. In large amounts. Produced in ECL cells by the decarboxylation of histidine.

Gastrin is released from these tumors at a high spontaneous rate that is not altered by feeding. The continual presence of acid in the duodenum overwhelms the neutralizing ability of the pancreas. Histamine is a second important paracrine agent.

Paracrines Paracrines are like hormones in that they are released from endocrine cells. One GI peptide.

Gastrointestinal physiology (eBook, ) [homeranking.info]

These systems allow an investigator to collect and assay small volumes of venous perfusate for the agent in question. The hypergastrinemia results in hypersecretion of gastric acid through two mechanisms. The complications of this disease—fulminant peptic ulceration. This disease is known as gastrinoma or Zollinger-Ellison syndrome. Histamine also potentiates the action of gastrin and ACh on acid secretion. Although parietal cells respond directly to gastrin.

Somatostatin also directly inhibits acid secretion from the parietal cells and the release of histamine from ECL cells.

Gastrointestinal Physiology

They are similar to neurocrines because they interact with receptors close to the point of their release. This is why the histamine H2 receptor—blocking drugs. The reason may be the low pH of gastric contents that is caused by ongoing acid secretion stimulated by preexisting high serum gastrin levels. Steatorrhea is produced by inactivation of pancreatic lipase and precipitation of bile salts at a low luminal pH.

Patients with Zollinger-Ellison syndrome may not release gastrin in detectable amounts in response to food. Acid in the antrum inhibits gastrin release. Patients with gastrinoma may have an exaggerated acid secretory response to calcium infusions that is caused by the release of gastrin from tumor tissue. Normal serum gastrin values must be set by each laboratory for its particular assay. The degree of overlap between patients with gastrinoma and those with ordinary duodenal ulcer disease means that specific tests are required to diagnose the gastrinoma.

This test is run by infusing 5 milligrams mg of ionizable. Increased intestinal transit probably also contributes to the diarrhea. Although gastrin levels remain elevated. Pancreatic cholera. This disease also may be treated nonsurgically with some of the powerful new drugs that inhibit acid secretion see Chapter 8.

The tests most widely used in the evaluation of hypergastrinemia include stimulation with protein meals. Secretin inhibits antral gastrin release. In most patients with gastrinoma. Peak gastrin responses are usually obtained 3 hours a er calcium infusion is begun.

Patients with ordinary ulcer disease may show moderate increases in serum gastrin with calcium infusion. Summary 1.

Somatostatin and histamine have important functions as paracrine agents. The GI hormones are located in endocrine cells scattered throughout the mucosa and released by chemicals in food. Two chemically related families of peptides are responsible for much of the regulation of GI function. The GI peptides have many pharmacologic actions. The functions of the GI tract are regulated by mediators acting as hormones endocrines.

San Diego: Physiology of the Gastrointestinal Tract.. Suggested Readings Chao. Acid Related Diseases. Physiology of the Gastrointestinal Tract. Handbook of Physiology. Section 6: The Gastrointestinal System. Annu Rev Physiol. Endocrine cells of the digestive system N Engl J Med. Neural and Endocrine Biology. In Johnson L. New York: Raven Press.. Gastrointestinal hormones. The Zollinger-Ellison syndrome. American Physiological Society.

Raven Press. Gastrointestinal peptides: Makhlouf G. Schnetztor Verlag Gmbh D-Konstanz. Regulation of gastrointestinal mucosal growth. Postpyloric gastrointestinal peptidesJohnson. Fed Proc.. Embryology of the diffuse neuroendocrine system and its relationship to the common peptides.

The basic properties and intrinsic activities of the smooth muscle cells are discussed in this chapter. In this chapter. Regulation Nerves and Smooth Muscle Objectives Understand the anatomy and functions of the enteric nervous system and its relationship with the parasympathetic and sympathetic systems. This integration is mediated by regulatory systems that monitor events within the body primarily the GI tract and in the external environment.

Explain the role of calcium ion in the contraction and relaxation of smooth muscle cells. Describe the anatomy and types of contractions of smooth muscle cells. Thus function arises out of the interaction of regulatory systems and local intrinsic properties.

Understand the roles of the interstitial cells of Cajal and slow waves in the contraction of smooth muscle cells. This volume in the Mosby Physiology Monograph Series explains the fundamentals of gastrointestinal physiology in a clear and concise manner. It provides you with a basic understanding of how the gastrointestinal system functions in health and disease.

Attractively illustrated with clear 2-color diagrams, this volume also facilitates study with learning objectives, overview boxes, chapter summaries, and clinical cases with questions and explained answers.

Stay current with clear, accurate, and up-to-the-minute coverage of the physiology of the gastrointestinal system focusing on the needs of the student. Bridge the gap between normal function and disease with pathophysiology content throughout the book. Master the material more easily with learning objectives, overview boxes, key words and concepts, chapter summaries, and clinical cases with questions and explained answers. Understand complex concepts by examining abundant clear, 2-color diagrams.

Apply what you've learned to real-life clinical situations using featured clinical commentaries. Read more Show all links. Allow this favorite library to be seen by others Keep this favorite library private. Find a copy in the library Finding libraries that hold this item Electronic books Additional Physical Format: Print version: Gastrointestinal physiology.

Document, Internet resource Document Type: Leonard R Johnson Find more information about: Leonard R Johnson. Offers the fundamentals of body systems physiology in a clear and concise manner. This title offers: Reviews User-contributed reviews Add a review and share your thoughts with other readers. Be the first. Add a review and share your thoughts with other readers. Similar Items Related Subjects: Digestive System Physiological Phenomena.

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Nerves and Smooth Muscle -- 3.