THE COMPLICATED INTERSECTION BETWEEN GASTROINTESTINAL HEALTH and EATING DISORDERS Valerie Edwards, MS, RD, LD February 25, 2017 OBJECTIVES
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Indigestion, Antacids, Achlorhydria and H. Pylori. by Michael T
FEATURE ARTICLE Indigestion, antacids, achlorhydria and H. pylori. by Michael T. Murray, N.D. digestive aids include hydrochloric Perhaps the most effective treatment of used to describe a feeling of acid and pancreatic enzyme prepara- chronic reflux esophagitis is to utilize Thegaseousness term "indigestion" or fullness is in often the tions. This article will take a critical look gravity. The standard recommendation abdomen. It can also be used to describe at the use of these agents and contrast is to simply place four-inch blocks "heartburn." Indigestion can be attributed their use with natural digestive aids. The under the bedposts at the head of the to a great many causes, including not topic of H. pylori will also be addressed. bed. This elevation of the head is very only increased secretion of acid but also effective in many cases. decreased secretion of acid and other General considerations Another recommendation to heal digestive factors and enzymes. The A 1983 article in the American the esophagus is using deglycyrrhizinated dominant treatment of indigestion is the Journal of Gastroenterology asked the licorice (DGL). Although DGL is primarily use of over-the-counter preparations. question "Why do apparently healthy used for treating peptic ulcers, I have These preparations include antacids people use antacids?"1 The answer: used it clinically in cases of heartburn which work by binding free acid, and reflux esophagitis, the medical term with success. DGL is further discussed drugs like Tagamet, Zantac, and Pepcid for heartburn. Reflux esophagitis is below. which inhibit the release of antacids by most often caused by the flow of gastric blocking histamine (H2) receptors juices up the esophagus leading to a Common antacid medications including antacids. -
Common Bile-Duct Mucosa in Choledochoduodenostomy Patients--- Histological and Histochemical Study
HPB Surgery 1988, Vol. 1, pp. 15-20 (C) 1988 Harwood Academic Publishers GmbH Reprints available directly from the publisher Printed in Great Britain Photocopying permitted by license only COMMON BILE-DUCT MUCOSA IN CHOLEDOCHODUODENOSTOMY PATIENTS--- HISTOLOGICAL AND HISTOCHEMICAL STUDY E. ELEFTHERIADIS*, V. TZIOUFA 1, K. KOTZAMPASSI and H. ALETRAS Departments of Surgery and Pathology1, University of Thessaloniki, Greece We describe the histological and histochemical changes of the common bile-duct mucosa in specimens obtained by means of peroral cholangioscopy, 1-12 years after choledochoduodenal anastomosis. Our findings- hyperplasia of the superficial epithelium, metaplastic goblet cells containing predominantly acid sialomucins, and pyloric-like gland formation containing neutral mucins- express a morphological and functional differentiation of the common bile-duct mucosa that probably facilitates its survival in a different environment. We consider that these adaptive changes may explain the uneventful long-term postoperative period of choledochoduodenostomized patients. KEY WORDS" Common bile duct, choledochoduodenal anastomosis, adaptation, peroral cholangio- scopy. INTRODUCTION After choledochoduodenal anastomosis (CDA), the common bile-duct mucosa (CBDM) is exposed to a different environment, no longer being protected by the sphincter of Oddi. Although, theoretically, this new environment i.e. gastric acid and food flowing through the anastomosis- should affect it, both clinical practice and experimental data have shown no evidence -
Ost , Is Essential for Intestinal Bile Acid Transport and Homeostasis
The organic solute transporter ␣-, Ost␣-Ost, is essential for intestinal bile acid transport and homeostasis Anuradha Rao*, Jamie Haywood*, Ann L. Craddock*, Martin G. Belinsky†, Gary D. Kruh‡, and Paul A. Dawson*§ *Department of Internal Medicine, Section on Gastroenterology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston–Salem, NC 27157; †Medical Science Division, Fox Chase Cancer Center, Philadelphia, PA 19111; and ‡Department of Medicine, Section of Hematology/Oncology, University of Illinois, Chicago, IL 60612 Communicated by David W. Russell, University of Texas Southwestern Medical Center, Dallas, TX, December 28, 2007 (received for review November 28, 2007) The apical sodium-dependent bile acid transporter (Asbt) is respon- Ost␣-Ost efficiently transports the major species of bile acids sible for transport across the intestinal brush border membrane; when expressed in transfected cells (3, 4); and (iv) expression of however, the carrier(s) responsible for basolateral bile acid export Ost␣ and Ost mRNA is positively regulated via the bile into the portal circulation remains to be determined. Although the acid-activated nuclear receptor farnesoid X receptor (FXR) heteromeric organic solute transporter Ost␣-Ost exhibits many (6–9), thereby providing a mechanism to ensure efficient export properties predicted for a candidate intestinal basolateral bile acid of bile acids and protection against their cytotoxic accumulation. transporter, the in vivo functions of Ost␣-Ost have not been Although these data are consistent with a role in bile acid investigated. To determine the role of Ost␣-Ost in intestinal bile transport, the in vivo functions of Ost␣-Ost have not been acid absorption, the Ost␣ gene was disrupted by homologous investigated. -
Does Your Patient Have Bile Acid Malabsorption?
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #198 NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #198 Carol Rees Parrish, MS, RDN, Series Editor Does Your Patient Have Bile Acid Malabsorption? John K. DiBaise Bile acid malabsorption is a common but underrecognized cause of chronic watery diarrhea, resulting in an incorrect diagnosis in many patients and interfering and delaying proper treatment. In this review, the synthesis, enterohepatic circulation, and function of bile acids are briefly reviewed followed by a discussion of bile acid malabsorption. Diagnostic and treatment options are also provided. INTRODUCTION n 1967, diarrhea caused by bile acids was We will first describe bile acid synthesis and first recognized and described as cholerhetic enterohepatic circulation, followed by a discussion (‘promoting bile secretion by the liver’) of disorders causing bile acid malabsorption I 1 enteropathy. Despite more than 50 years since (BAM) including their diagnosis and treatment. the initial report, bile acid diarrhea remains an underrecognized and underappreciated cause of Bile Acid Synthesis chronic diarrhea. One report found that only 6% Bile acids are produced in the liver as end products of of British gastroenterologists investigate for bile cholesterol metabolism. Bile acid synthesis occurs acid malabsorption (BAM) as part of the first-line by two pathways: the classical (neutral) pathway testing in patients with chronic diarrhea, while 61% via microsomal cholesterol 7α-hydroxylase consider the diagnosis only in selected patients (CYP7A1), or the alternative (acidic) pathway via or not at all.2 As a consequence, many patients mitochondrial sterol 27-hydroxylase (CYP27A1). are diagnosed with other causes of diarrhea or The classical pathway, which is responsible for are considered to have irritable bowel syndrome 90-95% of bile acid synthesis in humans, begins (IBS) or functional diarrhea by exclusion, thereby with 7α-hydroxylation of cholesterol catalyzed interfering with and delaying proper treatment. -
Bile Physiology
BILE PHYSIOLOGY DIPENDRA PARAJULI University of Louisville BILE COMPLEX LIPID-RICH MICELLAR SOLUTION ISO-OSMOTIC WITH PLASMA VOLUME OF HEPATIC BILE = 500 – 600 CC/DAY University of Louisville COMPOSITION University of Louisville FUNCTION OF BILE INDUCE BILE FLOW AND PHOSPHOLIPID AND CHOLESTEROL SECRETION ESSENTIAL FOR INTESTINAL ABSORPTION OF DIETARY CHOLESTEROL , FATS AND VITAMINS BIND CALCIUM AND HELP TO PREVENT Ca GALLSTONES AND OXALATE KIDNEY STONE FORMATION EXCRETION OF LIPID SOLUBLE XENOBIOTICS, DRUGS AND HEAVY UniversityMETALS of Louisville BILE FORMATION AND CIRCULATION University of Louisville University of Louisville BILE ACID SYNTHESIS TWO PATHWAYS 1) CLASSICAL / NEUTRAL - RESULTS IN THE SYNTHESIS OF APPROXIMATELY 1:1 RATIO OF CHOLIC AND CHENODEOXYCHOLIC ACIDS 2)ALTERNATE / ACIDIC - YIELDS PREDOMINANTLY UniversityCHENODEOXYCHOLIC of LouisvilleACID BILE ACID SYNTHESIS CLASSICAL / NEUTRAL PATHWAY - PREDOMINANT PATHWAY IN HEALTH - POSTCHOLECYSTECTOMY PATIENTS WITH BILE FISTULA - INFUSED WITH RADIOLABELLED PRECURSORS * [3H]7αOH CHOLESTEROL University* [3H]27-OH CHOLESTEROL of Louisville [3H]7αOH CHOLESTEROL 70-95% CONVERTED TO BILE ACIDS [3H]27-OH CHOLESTEROL <20% CONVERTED TO BIL ACIDS University of Louisville BILE ACID SYNTHESIS ALTERNATE / ACIDIC PATHWAY - MORE IMPORTANT IN CHRONIC LIVER DISEASE -CIRRHOTICS - LOW RATE OF BILE ACID SYNTHESIS - ALMOST EXCLUSIVELY UniversityCHENODEOXYCHOLIC of Louisville BILE ACID SYNTHESIS FINAL STEP = - CONJUGATION OF CHOLIC AND CHENODEOXYCHOLIC ACIDS WITH GLYCINE AND TAURINE - CONJUGATION -
Gastrointestinal Motility
Gastrointestinal Motility H. J. Ehrlein and M.Schemann 1. Motility of the stomach Anatomic regions of the stomach are the fundus, corpus (body), antrum and pylorus. The functional regions of the stomach do not correspond to the anatomic regions. Functionally, the stomach can be divided into the gastric reservoir and the gastric pump (Fig. 1). The gastric reservoir consists of the fundus and corpus. The gastric pump is represented by the area at which peristaltic waves occur: it includes the distal part of the corpus and the antrum. Due to different properties of the smooth muscle cells the gastric reservoir is characterised by tonic activity and the gastric pump by phasic activity. AB Gastric reservoir Fundus tonic contractions Pylorus Corpus Antrum Gastric pump phasic contractions Figure 1 . The stomach can be divided into three anatomic (A) and two functional regions (B) 1.1 Function of the gastric reservoir At the beginning of the 20 th century it was already observed that with increasing volume of the stomach the internal pressure of the stomach increases only slightly. In dogs, for instance, the increase in pressure is only 1.2 cm of water/100 ml volume. The small increase in gastric pressure indicates that the stomach does not behave like an elastic balloon but that it relaxes as it fills. Three kinds of gastric relaxation can be differentiated: a receptive, an adaptive and a feedback-relaxation of the gastric reservoir. The receptive relaxation consists of a brief relaxation during chewing and swallowing. The stimulation of mechano-receptors in the mouth and pharynx induces vago-vagal reflexes which cause a relaxation of the gastric reservoir (Fig. -
Infectious Diarrhea
Michael Yin Infectious Diarrhea A. Introduction Acute gastrointestinal illnesses rank second only to acute respiratory illnesses as the most common disease worldwide. In children less than 5 years old, attack rates range from 2-3 illnesses per child per year in developed countries to 10-18 illnesses per child per year in developing countries. In Asia, Africa, and Latin America, acute diarrheal illnesses are a leading cause of morbidity (1 billion cases per year), and mortality (4-6 million deaths per year, or 12,600 deaths per day) in children. Most cases of acute infectious gastroenteritis are caused by viruses (Rotavirus, Calicivirus, Adenovirus). Only 1-6% of stool cultures in patients with acute diarrhea are positive for bacterial pathogens; however, higher rates of detection have been described in certain settings, such as foodborne outbreaks (17%) and in patients with severe or bloody diarrhea (87%). This syllabus will focus on bacterial organisms, since viral and parasitic (Giardia, Entamoeba, Cryptosporidium, Isospora, Microspora, Cyclospora) causes of gastroenteritis are covered elsewhere. Clostridium difficile colitis will be covered in the lecture and syllabus on Anaerobes. Diarrhea is an alteration in bowel movements characterized by an increase in the water content, volume, or frequency of stools. A decrease in consistency and an increase in frequency in bowel movements to > 3 stools per day have often been used as a definition for epidemiological investigations. “Infectious diarrhea” is diarrhea due to an infectious etiology. “Acute diarrhea” is an episode of diarrhea of < 14 days in duration. “Persistent diarrhea” is an episode of diarrhea > 14 days in duration, and “chronic diarrhea” is diarrhea that last for >30 days duration. -
Achlorhydria and Anæmia
Jan., 1942] ACHLORHYDRIA AND ANAEMIA: BHENDE 13 Table I ACHLORHYDRIA AND ANJEMIA 84 cases An analysis of 79 cases Diagnosis Number of By Y. M. BHENDE, m.d. (Bom.) cases (From the Department of Pathology, P. G. Singhanee Anaemia 79 Hindu Hospital, Bombay) Chronic gastritis 2 Chronic 1 ' appendicitis inormal gastric juice contains hydrochloric Dyspepsia' 2 acid, pepsin, rennin and the intrinsic factor of Castle. The secreting function of the stomach It is seen at once that the, bulk of the cases may be investigated by means of a fractional is formed by the anaemia group; in fact, it was test meal. As ordinarily performed, the the anaemic state of these patients that neces- examination gives information only as to the sitated their admission to the hospital for hydrochloric-acid formation; the presence of investigation. A detailed analysis of these pepsin and rennin can be recognized by in vitro 79 cases of anaemia, with special reference to test, but for the detection of the intrinsic the state of their gastric secretion, forms the factor in vivo tests are necessary. basis of this communication. each case a detailed Davis (1931) by using the histamine test Procedure.?In clinical was taken. The blood was meal was able to demonstrate that the failure history scrutinized of all the absolute a the stomach function was probably progres- minutely, recording indices, van den and the red cell sive; his investigations (confirmed by many Bergh reaction, fragi- Wassermann or Kahn tests were done others) established the fact that, as a general lity test; rule, the ferment factors of the stomach fail as a routine and, wherever indicated, other A marrow after the hydrochloric acid; and whenever there bio-chemical studies. -
Glucose-Dependent Insulinotropic Polypeptide (GIP): from Prohormone to Actions in Endocrine Pancreas and Adipose Tissue
PHD THESIS DANISH MEDICAL BULLETIN Glucose-dependent Insulinotropic Polypeptide (GIP): From prohormone to actions in endocrine pancreas and adipose tissue Randi Ugleholdt The two incretins, glucagon-like peptide 1 (GLP-1) and glu- This review has been accepted as a thesis with two original papers by University of cose dependent insulinotropic polypeptide (gastric inhibitory Copenhagen 14th of December 2009 and defended on 28th of January 2010 peptide, GIP) have long been recognized as important gut hor- mones, essential for normal glucose homeostasis. Plasma levels Tutor: Jens Juul Holst of GLP-1 and GIP rise within minutes of food intake and stimulate Official opponents: Jens Frederik Rehfeld, Baptist Gallwitz & Thure Krarup pancreatic β-cells to release insulin in a glucose-dependent man- ner. This entero-insular interaction is called the incretin effect and Correspondence: Department of Biomedical Sciences, Cellular and Metabolic Re- search Section, University of Copenhagen, Faculty of Health Sciences, Blegdamsvej accounts for up to 70% of the meal induced insulin release in man 3B build. 12.2, 2200 Copenhagen N, Denmark and via this incretin effect, the gut hormones facilitate the uptake of glucose in muscle, liver and adipose tissue (2). Although the E-mail: [email protected] pancreatic effects of these two gut hormones have been the target of extensive investigation both hormones also have nu- merous extrapancreatic effects. Thus, GLP-1 decreases gastric Dan Med Bull 2011;58:(12)B4368 emptying and acid secretion and affects appetite by increasing fullness and satiety thereby decreasing food intake and, if main- THE TWO ORIGINAL PAPERS ARE tained at supraphysiologic levels, eventually body weight (3). -
Symptomatic Approach to Gas, Belching and Bloating 21
20 Osteopathic Family Physician (2019) 20 - 25 Osteopathic Family Physician | Volume 11, No. 2 | March/April, 2019 Gennaro, Larsen Symptomatic Approach to Gas, Belching and Bloating 21 Review ARTICLE to escape. This mechanism prevents the stomach from becoming IRRITABLE BOWEL SYNDROME (IBS) Symptomatic Approach to Gas, Belching and Bloating damaged by excessive dilation.2 IBS is abdominal pain or discomfort associated with altered with OMT Treatment Options Many patients with GERD report increased belching. Transient bowel habits. It is the most commonly diagnosed GI disorder lower esophageal sphincter (LES) relaxation is the major and accounts for about 30% of all GI referrals.7 Criteria for IBS is recurrent abdominal pain at least one day per week in the Carly Gennaro, DO1; Helaine Larsen, DO1 mechanism for both belching and GERD. Recent studies have shown that the number of belches is related to the number of last three months associated with at least two of the following: times someone swallows air. These studies have concluded that 1) association with defecation, 2) change in stool frequency, 1 Good Samaritan Hospital Medical Center, West Islip, NY patients with GERD swallow more air in response to heartburn and 3) change in stool form. Diagnosis should be made using these therefore belch more frequently.3 There is no specific treatment clinical criteria and limited testing. Common symptoms are for belching in GERD patients, so for now, physicians continue to abdominal pain, bloating, alternating diarrhea and constipation, treat GERD with proton pump inhibitors (PPIs) and histamine-2 and pain relief after defecation. Pain can be present anywhere receptor antagonists with the goal of suppressing heartburn and in the abdomen, but the lower abdomen is the most common KEYWORDS: ABSTRACT: Intestinal gas production is a normal physiologic progress. -
(CCK); B. When Small Intestine Fills with Fatty Chyme
5. Regulation of bile release: a. Hormone = CHOLECYSTOKININ (CCK); b. When small intestine fills with fatty chyme, -cholecystokinin is released; -sphincter in common bile duct opens; -bile is released into duodenum to emulsify fat. Digestive dissection of F. domesticus Esophagus: -Macroscopically -measure length -measure diameter -external structures -internal structures - Microscopically -external serosa -internal mucosa -cross section of all 4 layers Stomach -Macroscopically -measure length -measure diameter -external structures -internal structures - Microscopically -external serosa -internal mucosa -cross section of all 4 layers Small intestine -Macroscopically -measure length -measure diameter -external structures -internal structures - Microscopically -external serosa -internal mucosa -cross section of all 4 layers Large Intestine -Macroscopically -measure length -measure diameter -external structures -internal structures - Microscopically -external serosa -internal mucosa -cross section of all 4 layers III. Digestive Organs (continued) G. Small Intestine 1. Parts of Small Intestine: a. duodenum - nearest stomach, b. jejunum - mid-region, c. ileum - near large intestine. The distal end of the ilium narrows to form the ileocecal valve (sphincter muscle between small & large intestine). 2. Mucosal Structure a. intestinal villi project into lu men (increasing SA); b. each villus is composed of simple columnar epithelium (with microvilli) and connective tissue with many blood & lymph vessel s (lacteals ); c. absorbed nutrients are carried away by blood & lacteals; d. intestinal glands are located between villi. 3. Secretions of Small Intestine a. mucus, b. digestive enzymes: peptidases * peptides-----> amino acids; sucrase, maltase, lactase * disaccharides-->monosaccharides; lipases * TG-----> 2 fatty acids + monoglyceride. G. Small Intestine 4. Absorption in Small Intestine (90% of total) a. Intestinal villi (and microvilli) increas e absorptive surface area; b. -
Secretin Stimulates the Secretion of Bile from the Liver. It Also Increases Watery Bicarbonate Solution from Pancreatic Duct Epithelium
Name Secretin acetate Cat # PP-1670 Size 1 g, 10 g, 100, g and bulk custom packages CAS# 17034-35-4 Mol. Mass 3055.47 Formula C130H220N44O41 Sequence H-His-Ser-Asp-Gly-Thr-Phe-Thr-Ser-Glu-Leu-Ser-Arg-Leu-Arg-Asp-Ser- Ala-Arg-Leu-Gln-Arg-Leu-Leu-Gln-Gly-Leu-Val-NH2 Purity >95% Secretin is a peptide hormone produced in the S cells of the duodenum in the crypts of Lieberkühn. Its primary effect is to regulate the pH of the duodenal contents via the control of gastric acid secretion and buffering with bicarbonate. Secretin stimulates the secretion of bile from the liver. It also increases watery bicarbonate solution from pancreatic duct epithelium. Pancreatic acinar cells have secretin receptors in their plasma membrane. As secretin binds to these receptors, it stimulates adenylate cyclase activity and converts ATP to cyclic AMP.[12] Cyclic AMP acts as second messenger in intracellular signal transduction and leads to increase in release of watery carbonate.It is known to promote the normal growth and maintenance of the pancreas. Secretin increases water and bicarbonate secretion from duodenal Brunner's glands in order to buffer the incoming protons of the acidic chyme.[13] It also enhances the effects of cholecystokinin to induce the secretion of digestive enzymes and bile from pancreas and gallbladder, respectively. It counteracts blood glucose concentration spikes by triggering increased insulin release from pancreas, following oral glucose intake.<[14] It also reduces acid secretion from the stomach by inhibiting gastrin release from G cells.[citation needed] This helps neutralize the pH of the digestive products entering the duodenum from the stomach, as digestive enzymes from the pancreas (eg, pancreatic amylase and pancreatic lipase) function optimally at neutral pH.[citation needed] In addition, secretin simulates pepsin secretion which can help break down proteins in food digestion.