DOCSLIB.ORG

The Duodenal Ulcer Is the Chronic Recurrent Disease Which Is Characterized by Ulcer Defect on a Mucosa of the Duodenum

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Duodenal Ulcer Is the Chronic Recurrent Disease Which Is Characterized by Ulcer Defect on a Mucosa of the Duodenum Definition Peptic ulcer of a stomach and duodenum (ICD 10: K25-26)– chronic disease with polycyclic behaviour, which chracterized by secretoric, motoric and trophic modifications this organs and development ulcerous defects of its mucose. Contrary to general belief, more peptic ulcers arise in the duodenum, than in the stomach. About 4% of stomach ulcers are caused by a malignant tumor, so multiple biopsies are needed to make sure, duodenal ulcers are generally benign. Gastric ulcer The gastric ulcer is a chronic disease. The main features of peptic ulcer is the presence of ulcer defect in the mucosa. It forms the basis of pathology of many gastroenterological diseases. Such phenomenon is explained by not only considerable distribution of disease but also the dangerous complications which always accompany gastric ulcers. Etiology and pathogenesis Frequency of morbidity of the peptic ulcer among the adult population is about 4 %. It is more frequently seen patients in age group between 50 - 60 years. Disturbance between the factors of aggression and defense mechanism of mucosa leads to peptic ulcer. Etiology and pathogenesis Aggression factors: hydrochloric acid (HCl), pepsin, reverse diffusion of ions of hydrogen (H+), products of lipid hyperoxidizing. Aggressive factors (hydrochloric acid and pepsin) Parietal cells secrete hydrogen ions in concentration which is three times as high as the concentration of hydrogen ions present in the blood. Each secreted hydrogen ion combines with a chlorine ion. The final step in the secretion of hydrogen ions is performed by means of the proton pump which includes the specific K+, H+-ATPase occuring on the membranes of microvilli. This K+, H+-ATPase exchanges hydrogen for potassium across the microvillus membrane. The parietal cells produce a pure solution of HCl which mixes with the secretion of non-parietal cells. The HCl secretion is regulated by chemical, nervous and humoral factors. The membrane of parietal cells harbours specific receptors (H2- receptors) responding to histamin released from the neigbouring mast cells. Then there are receptors sensitive to muscarine effects of acetylcholine which is released by the vagus nerve’s endings. Parietal cells contain receptors which respond to endogenous circulating gastrin. Etiology and pathogenesis Defense mechanism: mucus and alkaline components of gastric juice, property of epithelium of mucosa to permanent renewal, local blood flow of mucosa and submucosa. Etiology and pathogenesis Numerous scientific developments of the past testify to the important infectious factor in the mechanism of origin of peptic ulcer, mainly, by helicobacter pylori. Etiology Scientific classification Kingdom:Bacteria Phylum:Proteobacteria Class:Epsilon Proteobacteria Order:Campylobacterales Family:Helicobacteraceae Genus:Helicobacter Species:H. pylori Binomial name Helicobacter pylori The bacterium was discovered in 1979 by Australian pathologist Robin Warren, who did further research on it with Barry Marshall beginning in 1981; they isolated the organisms from mucosal specimens from human stomachs and were the first to successfully culture them. In their original paper, Warren and Marshall contended that most stomach ulcers and gastritis were caused by infection by this bacterium and not by stress or spicy food as had been assumed before. Etiology Immunohistochemical staining of H. pylori from a gastric biopsy. H. pylori colonized on the surface of regenerative epithelium (Warthin-Starry's silver) Stomach disease An ulcer is a crater-like lesion on the skin or mucous membrane caused by an inflammatory, infectious, or malignant condition. Jonson’s classification (1965) Type I - ulcers of lesser curvature (3 cm higher than the pylorus) 13% Type II - double localization of ulcers simultaneously in the 71% stomach and duodenum Type III - ulcers of pyloric and of stomach (not farther than 3 cm from 11% the pylorus). Clinical management Pain. The pain symptom in the peptic ulcer disease is very important. There are typical staging for this disease: hunger - pain - food intake - facilitation - again hunger - pain - food intake - facilitation (so during all days). Clinical management Patients with the cardial ulcer pain arises at once after the food intake, with the ulcers of lesser curvature - in 50-60 minutes, in pyloric localization - approximately in two hours. In other patients the pain attack is accompanied by salivation. Clinical management Vomiting, the sign of disturbance of gastric motility, is the second typical symptom of gastric ulcer. More frequent gastrostasis arises as a result of failure of stomach muscul, it's atony which can be due to organ ischemia. Vomiting could arise both on empty stomach and after food intake. Clinical management Heartburn is one of the early symptoms of gastric ulcer, however in prolonged disease it can be hidden or disappear. Often it precedes pain (initial heartburn) or accompanies a pain symptom. Mostly heartburn arises after the food intake, but can appear independently. Diagnosis programme Anamnesis and physical examination. General and biochemical blood analysis. Coagulogram. Examination of gastric secretion by the method of aspiration of gastric contents. Endoscopy. Gastric pH-metry. Multi position biopsy of edges of ulcer and mucosa of stomach. Gastric Dopplerography. Sonography of abdominal cavity organs. X-Ray examination of stomach. FEGDScopy This picture displays the endoscope detecting a gastric ulcer Differential diagnosis Chronic gastritis, like gastric ulcer is characterized by the pain syndrome, that arises after the food intake. In such patients it is possible to observe nausea and vomiting of gastric content, heartburn and belching. However, unlike gastric ulcer, in gastritis typical symptom of "quick satiation by food is seen. Unsteady emptying, diarrhea are also more inherent to gastritis. In gastric ulcer frequently the delay in gastric empting leads to constipation for 4-5 days. Differential diagnosis The cancer of stomach, it is comparative with gastric ulcer, has considerably more short anamnesis. The most typical clinical signs of this pathology are: absence of appetite, weight loss, rapid fatigability, depression, unsociability, apathy. In such patients X-Ray examination expose the "defect of filling", related to exophytic tumor and deformation of walls of organ. A final diagnosis is set after the results of multi position biopsy of shady areas of mucosa of stomach. Tactic and choice of treatment method Conservative treatment of gastric ulcer always must be complex, individually differentiated, according to the etiology. Conservative therapy must include: anticholinergic drugs (atropine, methacin, platyphyllin) and myolitics (papaverine, halidor, nospanum); antiacid drugs - in accordance with the results of pH-metry; Conservative therapy Proton pump inhibitors: These drugs are potent inhibitors of H+,K+-ATPase. This enzyme, located in the apical secretory membrane of the parietal cell, plays a key role in the secretion of H+ (protons). These drugs can completely inhibit acid secretion and have a long duration of action. They promote ulcer healing and are also key components of H. pylori eradication regimens. Proton pump inhibitors have replaced H2-blockers in most clinical situations because of greater rapidity of action and efficacy. Conservative therapy Proton pump inhibitors include esomeprazole (NEXIUM), lansoprazole (PREVACID), and pantoprazole (PROTONIX) , all available orally and IV, and omeprazole (PRILOSEC) and rabeprazole, available only orally in the US. Omeprazole (PRILOSEC) is available without a prescription in the US. Long-term proton pump inhibitor therapy produces elevated gastrin levels, which lead to enterochromaffin- like cell hyperplasia. However, there is no evidence of dysplasia or malignant transformation in patients receiving this treatment. Some may develop vitamin B12 malabsorption. Conservative therapy H2 blockers: These drugs cimetidine (TAGAMET), , ranitidine (ZANTAC), famotidine (PEPCID), , available IV and orally; and nizatidine (AXID) (available orally) are competitive inhibitors of histamine at the H2 receptor, thus suppressing gastrin- stimulated acid secretion and proportionately reducing gastric juice volume. Histamine- mediated pepsin secretion is also decreased. Conservative therapy H2 blockers are well absorbed from the GI tract, with onset of action 30 to 60 min after ingestion and peak effects at 1 to 2 h. IV administration produces a more rapid onset of action. Duration of action is proportional to dose and ranges from 6 to 20 h. Doses should often be reduced in elderly patients. Conservative therapy For duodenal ulcers, once daily oral administration of cimetidine 800 mg, ranitidine 300 mg, famotidine 40 mg, or nizatidine 300 mg given at bedtime or after dinner for 6 to 8 wk is effective. Gastric ulcers may respond to the same regimen continued for 8 to 12 wk, but because nocturnal acid secretion is less important, morning administration may be equally or more effective. Children ≥ 40 kg may receive adult doses. Below that weight, the oral dosage is ranitidine 2 mg/kg q 12 h and cimetidine 10 mg/kg q 12 h. For GERD, H2 blockers are now mostly used for pain management. Gastritis heals with famotidine or ranitidine given bid for 8 to 12 wk. Conservative therapy Cimetidine and, to a lesser extent, other H2- blockers interact with the P-450 microsomal enzyme system and may delay metabolism
Load more

Recommended publications
  • Gastroscopy and Gastric Photography with the Olympus GTF-A
    Gut, 1970, 11, 176-181 Gut: first published as 10.1136/gut.11.2.176 on 1 February 1970. Downloaded from Gastroscopy and gastric photography with the Olympus GTF-A R. COCKEL AND C. F. HAWKINS From Queen Elizabeth Hospital, Birmingham SUMMARY One hundred patients were examined with the Olympus GTF-A fibregastroscope and gastrocamera. The entire stomach was seen in most cases; the technique permitting this is described in detail. The examination was most rewarding in patients with gastric haemor- rhage and when radiology was equivocal. Advantages and disadvantages of the instrument are discussed. http://gut.bmj.com/ Gastroscopy, once referred to as a 'narrow Description of Instrument peeping speciality' (Rogers, 1937), has been transformed by the development of new in- The Olympus GTF-A is 10.2 mm in diameter in struments (Morrissey, Tanaka, and Thorsen, the flexible part and 12.7 mm in diameter at the 1967). Now, instead of requiring long experience rigid tip of 6.5 cm where the camera is enclosed on September 27, 2021 by guest. Protected copyright. and persistent practice, gastroscopy can be (Figure 2). It is better than the Hirschowitz fibre- performed with little difficulty. A major advance scope because of the clearer view due to the was the application of fibreoptics to gastroscopy quality of fibre bundles, increased magnification, by Hirschowitz and his colleagues (Hirschowitz, and a wider angle of viewing which makes orien- Curtiss, Peters, and Pollard, 1958; Hirschowitz, tation easier. The intragastric camera has a photo- 1961; Hirschowitz, Balint, and Fulton, 1962), for graphing angle of 800, including the whole of the the flexible fibrescope reduces the patient's dis- area seen through the fibre bundle, so avoiding comfort and lessens the risk of oesophageal parallax.
    [Show full text]
  • Dietary, Non-Microbial Intervention to Prevent Helicobacter Pylori- Associated Gastric Diseases
    Review Article Page 1 of 8 Dietary, non-microbial intervention to prevent Helicobacter pylori- associated gastric diseases Young-Min Han1*, Jong-Min Park1*, Migyeong Jeong1, Jun-Hwan Yoo2, Won-Hee Kim2, Seok-Pyo Shin2, Weon-Jin Ko2, Ki-Baik Hahm1,2 1CHA University Cancer Prevention Research Center, CHA Bio Complex, Seongnam 463-400, Korea; 2Department of Gastroenterology, CHA University Bundang Medical Center, Seongnam 463-712, Korea *These authors contributed equally to this work. Correspondence to: Ki-Baik Hahm, MD, PhD. CHA University Bundang Medical Center, 59 Yatap-ro, Bundang-gu, Seongnam 463-712 and CHA Bio Complex Cancer Prevention Research Center, 335 Pangyo-ro, Gundang-gu, Seongnam 463-400, Korea. Email: [email protected]. Abstract: Since the discovery of Helicobacter pylori (H. pylori) infection as the major cause of gastroduodenal disorders including acute and chronic gastritis, gastroduodenal ulcer, chronic atrophic gastritis, and gastric cancer almost three decades ago, the possibility of preventing these clinical diseases through eradicating H. pylori has been the focus of active research, but soon debate in the scientific community, though eradication opens the feasibility of cancer prevention and the removal of bacteria significantly prevents development or recurrence of peptic ulcer diseases and some clinical diseases, was proposed due to uncertainty in either achievement of complete eradication or inefficacy in cancer prevention with eradication alone. Still its linkage to gastric cancer is incontestable. Since the multiple combination of bacterial factors, environmental insults, and the host immune response that drives the initiation and progression of mucosal atrophy, metaplasia, and dysplasia toward gastric cancer is intervened, simple eradication deemed the feasibility of cancer prevention.
    [Show full text]
  • The Consensus of Integrative Diagnosis and Treatment of Acute Pancreatitis-2017
    Received: 27 October 2018 DOI: 10.1111/jebm.12342 GUIDELINE The consensus of integrative diagnosis and treatment of acute pancreatitis-2017 Junxiang Li Jing Chen Wenfu Tang Digestive Disease Committee, Chinese Association of Integrative Medicine Abstract Correspondence Acute pancreatitis (AP) is one of the most common acute abdominal diseases. The digestive Wenfu Tang,Digestive Disease Committee, disease committee, Chinese Association of Integrative Medicine, released Integrated traditional Chinese Association of Integrative Medicine. Chinese and Western medicine for diagnosis and treatment of acute pancreatitis in 2010.1 Since then, Department of Integrative Medicine, West China Hospital, Sichuan University, Chengdu 610041, further studies and great progress have been made by domestic and foreign counterparts from China. the perspective of both Chinese and Western medicine in AP, including the classification, fluid Email: [email protected] resuscitation, organ function maintenance, surgery intervention, enteral nutrition (EN), and The translators note: The consensus of Inte- syndrome differentiation and treatment. It is necessary to update the consensus on diagnosis and grative diagnosis and treatment of Acute treatment of integrated Chinese and Western medicine to meet clinical needs. Therefore, the Pancreatitis-2017 (Chinese version) has been published on Chinese Journal of Integrated Tra- 2012 Revision of the Atlanta Classification Standard (RAC) by the International AP Consensus,2 ditional and Western Medicine on Digestion, the 2013
    [Show full text]
  • Patient Medical History Page One
    Patient Medical History Page One Date: ______/______/______ Patient Name: ________________________________________________________ DOB: ______/______/______ Age: ____________Height: ________ inches Weight: _______ lbs Race:__________________ Gender: M F Marital Status: Single Married Divorced Widowed Occupation: ________________________ Primary Care Physician: ________________________________Referring Physician: ___________________________________ Sleep Complaint: _________________________________________________________________________________________ _______________________________________________________________________________________________________ Past Medical History Please answer all questions to the best of your ability. Do you now or have you ever had : Tuberculosis (TB) Yes No Lung Disease Yes No Cancer Yes No Thyroid Disease Yes No High Blood Pressure Yes No Stomach Disease Yes No Diabetes (Blood sugar high or low) Yes No Intestinal Disease Yes No Heart Attack Yes No Peptic Ulcer Yes No Other Heart Disease Yes No Liver Disease Yes No Kidney Disease Yes No Seizures Yes No Please explain all “Yes” answers: ________________________________________________________________________________________________________ ________________________________________________________________________________________________________ Habits Do you now or have you ever used: 1. Tobacco ( smoke cigarettes, chew tobacco, etc.) Yes No If yes, indicate amount per day: ___________________ If yes, how long ? _______ years Have you quit? Yes No If yes, when?
    [Show full text]
  • Syphilis of the Stomach and Intestines
    kohn: sythilis of the stomach and intestines 685 The aridity immediately after a meal is nil, but steadily increases dunng digestion, and is less in the very young than in the older. Un a barley water diet free hydrochloric acid appears in the stomach in a few minutes, but on a milk diet it does not show itself for an hour or more, due to the fact that the casein absorbs it or combines with it in some way, and the free acid does not appear until the casein has taken up all required for its complete digestion The free acid appears later in disease than in health, due to the in¬ creased amount of food in the stomach and to the slower secretion of the aad; in cases of pylorospasm the acidity is increased. Opinions differ as to the occurrence of lactic and volatile fatty acids, but these probably do not occur in healthy breast-fed infants, while in those ill or on cows’ milk they are fairly common. Part of the acidity is probably due to a fat-splitting enzyme in the infant’s stomach. Pepsin is present at all ages and in all kinds of health, and acts in the infant stomach though to a less degree than in the adult. I he peptic digestion goes on to the stage of peptones, but not beyond that, ihe fact that the stomach contents will not digest fibrin in the thermostat is due to the fact that all the hydrochloric acid is combined with the casein, and while the protein with which it is combined, will be acted upon by the pepsin, a foreign protein with¬ out the addition of more acid mil resist the enzyme Rennin occurs in the stomach after the first few weeks of life- whether during the first week is a moot question.
    [Show full text]
  • Protein Signature Characterizing Helicobacter Pylori Strains Of
    De Re et al. Infectious Agents and Cancer (2017) 12:22 DOI 10.1186/s13027-017-0133-x RESEARCH ARTICLE Open Access Protein signature characterizing Helicobacter pylori strains of patients with autoimmune atrophic gastritis, duodenal ulcer and gastric cancer Valli De Re1*† , Ombretta Repetto1†, Stefania Zanussi2, Mariateresa Casarotto2, Laura Caggiari1, Vincenzo Canzonieri3 and Renato Cannizzaro1,2,3,4 Abstract Background: Helicobacter pylori (H. pylori) represents a key factor in the etiology of autoimmune atrophic gastritis (AAG), duodenal ulcer (DU) and gastric cancer (GC). The aim of this study was to characterize the differential protein expression of H. pylori isolated from gastric biopsies of patients affected by either AAG, DU or GC. Methods: The H. pylori strains were isolated from endoscopic biopsies from the stomach of patients with gastric disease. Protein profiles of H. pylori were compared by two-dimensional difference in gel electrophoresis (2D-DIGE) coupled with mass spectrometry (MS) for the identification of significantly different spots (Student t-test, p < 0.05). Results: A total of 47 differentially expressed spots were found between H. pylori isolated from patients with either DU or AAG diseases and those isolated from patients with GC (Anova < 0.05, log fold change >1.5). These spots corresponded to 35 unique proteins. The identity of 7 protein spots was validated after one-dimensional electrophoresis and MS/MS analyses of excised gel portions. In H. pylori isolated from DU-patients a significant increase in proteins with antioxidant activity emerged (AroQ, AspA, FldA, Icd, OorA and ScoB), together with a higher content of proteins counteracting the high acid environment (KatA and NapA).
    [Show full text]
  • Orthopaedic Elbow Patient Questionnaire
    ORTHOPAEDIC ELBOW PATIENT QUESTIONNAIRE ORTHOPAEDIC ELBOW PATIENT QUESTIONNAIRE Age: Gender: male female Your Height: ____' _____" Weight: _______ lbs Referring Doctor Information Primary Doctor Information Name: Name: Specialty: Specialty: City: State: City: State: History of Your Current Orthopaedic Problem Hand Dominance: Right Left Both The problem primarily involves: Shoulder R / L Elbow R / L (Check all that apply and circle side) Other ______________________________________________ How long has this been present? Since: ____/ ____/ ____ or For: _______ Days Months Years (dd / mm/ yy) What caused the problem to start? Unknown reason Accident ( Motor vehicle Fall) Did the problem start at work? No Yes Will (has) a worker's compensation claim be filed? No Yes How do you describe your pain? Aching Burning Sharp/ Stabbing Numbness/ Tingling No pain Other ______________________________________________ How severe is the problem? Mild Moderate Severe Is it getting better or worse? Better Same Worse Previous non-surgical treatments for this No previous treatment Physical Therapy Injections problem have included: Cast Brace Manipulation﹤ Other ______________________________________________ Describe any previous surgery for this problem below Doctor Dr.'s Specialty City, State Medications taken for this problem Name of Medication (s) Dose For how long Anti-inflammatories Narcotic pain relievers Other MR 1130 Rev 6/15 Page 1 of 4 ORTHOPAEDIC ELBOW PATIENT QUESTIONNAIRE MR 1130 Rev. 10/16 page 1 of 4 ORTHOPAEDIC ELBOW PATIENT QUESTIONNAIRE MUST HAVE AN OOS LABEL ON THE FRONT SIDE OF THIS FORM ORTHOPAEDIC ELBOW PATIENT QUESTIONNAIRE (2-SIDED FORMS MUST HAVE AN OOS LABEL ON BOTH SIDES) X-rays and tests for this problem Results Date Where Plain X-rays MRI CT Scan Bone Scan Other ____________________ Past Medical History Please check "yes" or "no" in each row.
    [Show full text]
  • Ulcer Disease
    understanding PEPTIC ULCER DISEASE A patient’s guide from your doctor and Peptic Ulcer Basics — Peptic ulcer disease occurs when painful sores develop in the lining of the stomach or intestines. — Helicobacter pylori infection is the most common cause of ulcers. — Frequent or long-term use of common pain medications called non-steroidal anti-inflammatory drugs (NSAIDs) may also lead to stomach ulcers. — Ulcers are often successfully treated with antibiotics and acid-blocking medicines. Your Digestive System A B C G D F E H I A. Esophagus F. Large Intestine B. Liver G. Pancreas C. Stomach H. Rectum D. Gallbladder I. Anus E. Small Intestine To help you understand and manage your condition, the AGA Institute provides you with the following information, designed to give you some basic facts, to help you better understand your condition and to serve as a starting point for discussions with your doctor. Your Digestive Tract Your stomach lining is a remarkably resilient membrane. A layer of mucus protects the stomach from its own acids, which begin the process of digestion. Similar mechanisms protect the duodenum (the first part of the small intestine). Some of the gastric juices involved in the digestive process are as toxic as car battery acid, so a healthy stomach and intestinal lining play a key role in your overall health. The most common stomach disease — peptic ulcer disease — occurs when the stomach acid successfully penetrates the stomach or intestinal lining and causes ulcers, an often painful sore in the lining. An estimated 4 million Americans have peptic ulcer disease, and one in 10 patients will experience the disease during his or her lifetime Peptic Ulcer Disease When a type of bacteria called Helicobacter pylori (H.
    [Show full text]
  • Modern Surgery, 4Th Edition, by John Chalmers Da Costa Rare Medical Books
    Thomas Jefferson University Jefferson Digital Commons Modern Surgery, 4th edition, by John Chalmers Da Costa Rare Medical Books 1903 Modern Surgery - Chapter 27. Diseases and Injuries of the Abdomen - Stomach and Intestines John Chalmers Da Costa Jefferson Medical College Follow this and additional works at: https://jdc.jefferson.edu/dacosta_modernsurgery Part of the History of Science, Technology, and Medicine Commons Let us know how access to this document benefits ouy Recommended Citation Da Costa, John Chalmers, "Modern Surgery - Chapter 27. Diseases and Injuries of the Abdomen - Stomach and Intestines" (1903). Modern Surgery, 4th edition, by John Chalmers Da Costa. Paper 25. https://jdc.jefferson.edu/dacosta_modernsurgery/25 This Article is brought to you for free and open access by the Jefferson Digital Commons. The Jefferson Digital Commons is a service of Thomas Jefferson University's Center for Teaching and Learning (CTL). The Commons is a showcase for Jefferson books and journals, peer-reviewed scholarly publications, unique historical collections from the University archives, and teaching tools. The Jefferson Digital Commons allows researchers and interested readers anywhere in the world to learn about and keep up to date with Jefferson scholarship. This article has been accepted for inclusion in Modern Surgery, 4th edition, by John Chalmers Da Costa by an authorized administrator of the Jefferson Digital Commons. For more information, please contact: [email protected]. Contusion of the Abdominal Wall without Injury of Viscera 695 XXVII. DISEASES AND INJURIES OF THE ABDOMEN. Diagnosis of Intra-abdominal Emergencies.—The exact diag- nosis is always difficult and is not unusually impossible. What a surgeon must try to determine, and what he usually can determine, is whether he is dealing with a trivial and temporary derangement for the relief of which an operation is entirely unnecessary, or whether he is confronted with a grave calamity which imperatively demands immediate surgical aid.
    [Show full text]
  • A Systematic Review of Gastrointestinal Manifestations in Diabetic Nephropathy
    Review Article A Systematic Review of Gastrointestinal Manifestations in Diabetic Nephropathy Shimin Zheng1,2 and Juan Ma1,2* 1Department of Gastroenterology, Guangdong Provincial People’s Hospital/Guangdong Academy of Medical Sciences/Guangdong Provincial Geriatrics Institute, Guangzhou, Guangdong, China; 2Medical College of Shantou University, Shantou, Guangdong Province, China Abstract Diabetic nephropathy is the most common microvascular complication of diabetes mellitus. With the increas- ing prevalence of diabetes mellitus, diabetic neuropathy has become the primary cause of chronic nephropathy cases. Diabetes mellitus and chronic nephropathy exert certain effects on the digestive system. diabetic neuropa- thy patients also have digestive system symptoms and gastrointestinal diseases, with most presenting such prob- lems as decreased gastrointestinal tract tension, insufficient gastric motility, decreased contractility, and delayed gastric emptying; these problems are often accompanied by symptoms of digestive system dysfunction, such as constipation, dry stool, tenesmus. This article will summarize and discuss the effects and mechanism of diabetic neuropathy involving the digestive system. Introduction gastroparesis, constipation, diarrhea, and fecal incontinence. These symptoms are often associated with diabetic complications, such Diabetes mellitus (DM) is a global epidemic, characterized by hy- as autonomic neuropathy, peripheral neuropathy, and DN. perglycemia. It is divided into type 1 diabetes mellitus (T1DM) To gain a better understanding of the digestive symptoms caused and type 2 diabetes mellitus (T2DM), which account for 5–10% by diabetic neuropathy in diabetes mellitus, we searched the Pub- and 90–95% of DM cases resepectively.1 Diabetic nephropathy Med database for publications related to “diabetic nephropathy” (DN) is one of the most common microvascular complications as- and “digestive system”.
    [Show full text]
  • Peptic Ulcer: Rise and Fall
    Wellcome Witnesses to Twentieth Century Medicine PEPTIC ULCER: RISE AND FALL The transcript of a Witness Seminar held at the Wellcome Institute for the History of Medicine, London, on 12 May 2000 Volume 14 – November 2002 ©The Trustee of the Wellcome Trust, London, 2002 First published by the Wellcome Trust Centre for the History of Medicine at UCL, 2002 The Wellcome Trust Centre for the History of Medicine at UCL is funded by the Wellcome Trust, which is a registered charity, no. 210183. ISBN 978 085484 084 7 All volumes are freely available online at www.history.qmul.ac.uk/research/modbiomed/wellcome_witnesses/ Please cite as : Christie D A, Tansey E M. (eds) (2002) Peptic Ulcer: Rise and Fall. Wellcome Witnesses to Twentieth Century Medicine, vol. 14. London: Wellcome Trust Centre for the History of Medicine at UCL. Key Front cover photographs, L to R from the top: Sir Patrick Forrest Professor Stewart Goodwin Professor Roger Jones Professor Sir Richard Doll (1912–2005) Dr George Misiewicz, Dr Gerard Crean (1927–2005) Professor Michael Hobsley Dr Gerard Crean (1927–2005), Professor Colm Ó’Moráin Back cover photographs, L to R from the top: Dr Joan Faulkner (Lady Doll, 1914–2001) Dr John Wood, Professor Graham Dockray Dr Booth Danesh Professor Kenneth McColl Sir James Black (1924–2009), Dr Gerard Crean (1927–2005) Dr Nelson Coghill (1912–2002), Mr Frank Tovey Professor Roy Pounder (chair), Professor Hugh Baron Dr John Paulley, Sir Richard Doll (1912–2005) CONTENTS Introduction Sir Christopher Booth i Witness Seminars: Meetings and publications;Acknowledgements E M Tansey and D A Christie iii Transcript Edited by D A Christie and E M Tansey 1 Biographical notes 113 Glossary 123 Appendix A Surgical Procedures 127 Appendix B Chemical Structures 128 Index 133 List of plates Figure 1 Age-specific duodenal ulcer perforation rates in England and Wales.
    [Show full text]
  • The Bacterium Helicobacter Pylori.Pdf
    The Nobel Prize in Physiology or Medicine for 2005 jointly to Barry J. Marshall and J. Robin Warren for their discovery of "the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease" Introduction This year's Nobel Laureates in Physiology or Medicine made the remarkable and unexpected discovery that inflammation in the stomach (gastritis) as well as ulceration of the stomach or duodenum (peptic ulcer disease) is the result of an infection of the stomach caused by the bacterium Helicobacter pylori. Robin Warren (born 1937), a pathologist from Perth, Australia, observed small curved bacteria colonizing the lower part of the stomach (antrum) in about 50% of patients from which biopsies had been taken. He made the crucial observation that signs of inflammation were always present in the gastric mucosa close to where the bacteria were seen. Barry Marshall (born 1951), a young clinical fellow, became interested in Warren's findings and together they initiated a study of biopsies from 100 patients. After several attempts, Marshall succeeded in cultivating a hitherto unknown bacterial species (later denoted Helicobacter pylori) from several of these biopsies. Together they found that the organism was present in almost all patients with gastric inflammation, duodenal ulcer or gastric ulcer. Based on these results, they proposed that Helicobacter pylori is involved in the aetiology of these diseases. Even though peptic ulcers could be healed by inhibiting gastric acid production, they frequently relapsed, since bacteria and chronic inflammation of the stomach remained. In treatment studies, Marshall and Warren as well as others showed that patients could be cured from their peptic ulcer disease only when the bacteria were eradicated from the stomach.
    [Show full text]