21. Common Characteristics Of Liver Disease - Lucile Packard Children's Hospital blood. Liver encephalopathy is also called portalsystemic encephalopathy,hepatic encephalopathy, or hepatic coma. Symptoms may http://www.lpch.org/DiseaseHealthInfo/HealthLibrary/digest/livdisea.html

Clinical Nutrition Gastroenterology, Nutrition, and Hepatology Liver Transplantation Gastroenterologists ... Healthy Eating In A Fast Food World: Tips for Parents and Children Digestive and Liver Disorders Common Characteristics of Liver Disease What are some common liver disease symptoms? When diagnosing liver disease, the physician looks at the patient's symptoms and conducts a physical examination. In addition, the physician may request a liver biopsy, liver enzyme tests, an ultrasound, or a CT scan (computed tomography scan). Some common liver disease symptoms include the following, each of which are described briefly below: jaundice cholestasis liver enlargement portal hypertension ascites liver encephalopathy liver failure What is jaundice? Jaundice is a yellow discoloration of the skin and whites of the eyes due to an abnormally high level of bilirubin (bile pigment) in the bloodstream, which is then excreted through the kidneys. High levels of bilirubin may be attributed to inflammation or other abnormalities of the liver cells, or blockage of the bile ducts. Sometimes jaundice is caused by the breakdown of a large number of red blood cells, which can occur in newborns. Jaundice is usually the first sign, and sometimes the only sign, of liver disease. What is cholestasis?

22. Common Characteristics Of Liver Disease - Liver, Hepatic, Biliary Disorders Heal liver. Liver encephalopathy is also called portalsystemic encephalopathy,hepatic encephalopathy, or hepatic coma. Symptoms may http://www.umm.edu/liver/common.htm

Liver, Hepatic, Biliary Disorders Liver Disorders... Characteristics of Liver Disease Liver Function Tests ... Site Index Liver Disease Common Characteristics of Liver Disease What are some common liver disease symptoms? When diagnosing liver disease, the physician looks at the patient's symptoms and conducts a physical examination. In addition, the physician may request a liver biopsy, liver function tests, an ultrasound, or a CT scan (computerized tomography scan). Some common liver disease symptoms include the following, each of which are described briefly below: jaundice cholestasis liver enlargement portal hypertension ascites liver encephalopathy liver failure What is jaundice? Jaundice is a yellow discoloration of the skin and eye whites due to abnormally high levels of bilirubin (bile pigment) in the bloodstream. Urine is usually dark because of the bilirubin excreted through the kidneys. High levels of bilirubin may be attributed to inflammation or other abnormalities of the liver cells or blockage of the bile ducts. Sometimes jaundice is caused by the breakdown of a large number of red blood cells, which can occur in newborns. Jaundice is usually the first sign, and sometimes the only sign, of liver disease. What is cholestasis?

23. SpringerLink: Neuroradiology - Abstract Volume 39 Issue 5 (1997) Pp 326-328 Abstract We report MRI in a patient with portalsystemic encephalopathy, in whichthe high signal in the basal ganglia on T1-weighted images showed marked http://link.springer-ny.com/link/service/journals/00234/bibs/7039005/70390326.ht

Neuroradiology ISSN: 0028-3940 (printed version) ISSN: 1432-1920 (electronic version) Table of Contents Abstract Volume 39 Issue 5 (1997) pp 326-328 Effects of portal-systemic shunt embolization on the basal ganglia: MRI S. Matsumoto (1)(2), H. Mori (1), K. Yoshioka (1), H. Kiyosue (1), E. Komatsu (1) (1) Department of Radiology, Oita Medical University, Hasama-machi, Oita, 879-55, Japan (2) Department of Radiology, McMaster University, 1200 Main Street, West Hamilton, Ontario L8N 3Z5, Canada Received: 21 June 1996 Accepted: 26 July 1996 Abstract We report MRI in a patient with portal-systemic encephalopathy, in which the high signal in the basal ganglia on T1-weighted images showed marked resolution after successful embolization of the intrahepatic portal-systemic venous shunt. Key words Article in PDF-Format Last change: May 16, 1997 helpdesk.link@springer.de

24. SpringerLink: Neuroradiology - Abstract Volume 39 Issue 3 (1997) Pp 171-174 report three patients who had highsignal lesions in the globus pallidus on T1-weightedimages, a finding seen in patients with portal-systemic encephalopathy. http://link.springer-ny.com/link/service/journals/00234/bibs/7039003/70390171.ht

Neuroradiology ISSN: 0028-3940 (printed version) ISSN: 1432-1920 (electronic version) Table of Contents Abstract Volume 39 Issue 3 (1997) pp 171-174 Atypical MRI features of Wilson's disease: high signal in globus pallidus on T1-weighted images H. Mochizuki (1), K. Kamakura (1), T. Masaki (1), M. Okano (1), N. Nagata (1), A. Inui (2), T. Fujisawa (2), T. Kaji (3) (1) Third Department of Internal Medicine, National Defense Medical College, 3-2, Namiki, Tokorozawa, Saitama, Japan (2) Department of Pediatrics, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, Japan (3) Department of Radiology, National Defense Medical College, 3-2, Namiki, Tokorozawa, Saitama, Japan Received: 26 January 1996 Accepted: 1 April 1996 Abstract Most reports of MRI in Wilson's disease have been of abnormal low-signal lesions on T1-weighted images and high signal intensity on T2-weighted images. In contrast, we report three patients who had high-signal lesions in the globus pallidus on T1-weighted images, a finding seen in patients with portal-systemic encephalopathy. The possible causes include the paramagnetic effect of copper or iron and accumulation of Alzheimer type II glial cells. Key words Article in PDF-Format Last change: April 3, 1997

25. MEDLINE Abstract TI Comparison of lactulose and neomycin in the treatment of chronicportal-systemic encephalopathy. A double blind controlled trial. http://www.uptodate.com/patient_info/topicpages/abstrcts/Abstrx24/733777.htm

TI - Comparison of lactulose and neomycin in the treatment of chronic portal-systemic encephalopathy. A double blind controlled trial. AU - Conn HO; Leevy CM; Vlahcevic ZR; Rodgers JB; Maddrey WC; Seeff L; Levy LL SO - Gastroenterology 1977 Apr;72(4 Pt 1):573-83

26. OHSU Health.com - Liver, Biliary, And Pancreatic Disorders Liver encephalopathy is also called portalsystemic encephalopathy,hepatic encephalopathy, or hepatic coma. Symptoms may include http://www.ohsuhealth.com/liver/common.asp

Allergy and Asthma Arthritis Alternative Medicine Blood Disorders Bone Disorders Breast Health Cancer Cardiovascular Diseases Childbirth and Pregnancy Dermatology Diabetes Digestive Disorders Drug Information Ear, Nose and Throat Endocrinology Environmental Medicine Eyecare Glossary Gynecology: Health/Oncology Home Health Care Household/Common Emergency Infectious Diseases Men's Health Mental Health Nervous System Disorders Oral Health Orthopaedics Pathology Pediatrics Plastic Surgery Pregnancy and Childbirth Prostate Health Radiology Respiratory Disorders Skin Cancer Spine, Shoulder and Pelvis Surgical Care Travel Medicine Urology Women's Health Liver Disorders Index The Liver: Anatomy and Functions The Biliary System: Anatomy and Functions The Pancreas: Anatomy and Functions ... Liver Transplantation Common Characteristics of Liver Disease What are some common liver disease symptoms? When diagnosing liver disease, the physician looks at the patient’s symptoms and conducts a physical examination. In addition, the physician may request a liver biopsy, liver function tests, an ultrasound, or a CT scan (computerized tomography scan). Some common liver disease symptoms include the following, each of which are described briefly below:

27. Santé Environnementale Et Santé Au Travail, Université De Montréal Translate this page in unleaded gasoline. (1999) Role of Manganese in the Pathogenesisof portal-systemic encephalopathy. (1998) Articles sans comité http://www.mdtrav.umontreal.ca/Page_cv.asp?varno=197

28. Congenital Porto-Systemic Shunt As The Major Cause Of Galactosemia FULL TEXT; Raskin NH, Price JB, Fishman RA. portalsystemic encephalopathydue to congenital intrahepatic shunts. N Engl J Med. 1964;270225-229. http://www.int-pediatrics.org/newip/volumes/16,2,3,4/16-4/review/sakura/sakura.h

International Pediatrics Volume 16, Number 4 Review Article Congenital Porto-Systemic Shunt as the Major Cause of Galactosemia Nobuo Sakura, MD, PhD; Nobuyuki Mizoguchi, MD; Hiroaki Ono, MD, PhD; Yutaka Nishimura, MD; Kumiko Naito, MD From the Department of Pediatrics (Dr Sakura, Dr Mizoguchi, Dr Ono, Dr Nishimura), and the Department of Radiology (Dr Naito), Hiroshima University School of Medicine, Hiroshima, Japan Address reprint requests to the Department of Pediatrics, Hiroshima University School of Medicine, Kasumi 1-2-3, Minami-ku, Hiroshima, 734-8551, Japan (Dr Sakura). Please give Japanese version time to download. Click on Japanese characters. Abstract Introduction It is well known that inherited deficiencies of galactose-metabolizing enzymes resulted in hereditary galactosemias, but increasing evidence has accumulated that porto-systemic (PS) shunts caused hypergalactosemia. In our screening programs, the most common cause of persistent hypergalactosemia is PS shunts rather than hereditary galactosemias. To date we have identified 15 cases with PS shunts detected by neonatal mass-screening for galactosemia. In this report, we have reviewed the clinical manifestations and outcome of these cases, and insisted that mass-screening for galactosemia by Paigen method is useful for the early diagnosis of PS shunts during the neonatal period.

29. P Subject headings liver cirrhosis; portalsystemic encephalopathy; nutritionalstatus; albumin; somatosensory evoked potentials Yang SS,Wu CH,Chen LL,Mi SC http://www.wjgnet.com/1007-9327/4/380.htm

P.O.Box 2345, Beijing 100023,China World J Gastroenterol Email: wcjd@public.bta.net.cn WJG ISSN 1007-9327 CN 14-1219/ R http:// www.wjgnet.com 1998 by The WJG Press Nutritional status in non-alcoholic sub-clinical porto-systemic encephalopathy Yang SS, Wu CH, Chen LL, Mi SC, Chen DF Subject headings liver cirrhosis; portal-systemic encephalopathy; nutritional status; albumin; somatosensory evoked potentials Yang SS,Wu CH,Chen LL,Mi SC, Chen DF.Nutritional status in non-alcoholic sub -clinical porto-systemic encephalopathy. World J Gastroenterol, 1998;4(5):380-384 Abstract AIM To understand the role of nutritional status in cirrhotic patients without clinical porto-systemic encephalopathy (PSE). METHODS Fifty-one non-alcoholic patients with cirrhosis without PSE were studied prospectively and compared with 20 healthy volunteers. The nutritional evaluation included serum prealbumin, albumin, transferrin, body mass index (BMI), mid-arm muscle circumference (MAMC), and grip power. The occurrence of subclinical PSE (SPSE) was defined when N20-N65 inter-peak latencies of median nerve-stimulated somatosensory evoked potentials were 2.5 standard

30. Bulletin Of Russian Peoples Friendship University PORTAL SYSTEMIC ENCEPHALOPATHY AND DIURETIC THERAPY IN PATIENTS WITH ALCOHOLICLIVER CIRRHOSIS. portalsystemic encephalopathy were in 34,1% of patients. http://www.med.pfu.edu.ru/_new/english/win/library/vestnik/v991e/09.htm

Bulletin of Russian Peoples Friendship University. "Medicine" PORTAL SYSTEMIC ENCEPHALOPATHY AND DIURETIC THERAPY IN PATIENTS WITH ALCOHOLIC LIVER CIRRHOSIS N.D.KISLIY, M.MULLA OSMAN, N.N.OMELCHUK, G.R.ZLATINSKAJA Department of Hospital Therapy RPFU. Moscow. 117198. M-Maklaya st 8. Medical faculty P.N.POPOV, S.A.AZEVICH, S.M.SCHEMILCHANOVA Municipal Hospital N 53. Moscow. 109432. Trofimova st 26. 357 patients (216 men and 141 women) with alcoholic liver cirrhosis were studied. Their mean age was 50,5 0,6 years. Portal-systemic encephalopathy were in 34,1% of patients. Diuretic therapy complicated with portal-systemic encephalopathy in 25,9% of patients with alcoholic liver cirrhosis. Grade of portal-systemic encephalopathy correlate with quantity of hemoglobin, red cells, albumin, urea, creatinine and bilirubin.

31. Hep C Vets, Fibrosis & Cirrhosis, Signs And Symptoms hypertension. The initial presentation may occasionally be that of hepatocellularfailure with ascites or portalsystemic encephalopathy. http://hepcvets.com/cirrhosis/signs.html

What's New? Our Latest Additions Hepatitis C Books On Liver Disease (Recommended) Clinical Trials Depression Drugs Used In Treatment Fibrosis/Cirrhosis Genotypes Hepatitis B HEPC INFO Only List Sign Up HEPC INFO Only Full Text Medical Articles Herbs/Alternative Medicine Insurance Issues Liver Disease Glossary Miscellaneous Vaccine Information Veterans Table Of Contents Viral Loads What The Heck Is....VERY INFORMATIVE 2002 NIH Hepatitis C Consensus Hep C Vets Bulletin Board Hepatitis C Bulletin Board Poetry/Short Stories Symptoms and Signs Of Cirrhosis People with cirrhosis often have few symptoms at first. Symptoms generally present themselves after two major problems occur: the loss of functioning liver cells and the distortion of the liver caused by scarring. Among the findings of cirrhosis are: Fatigue, weakness, and exhaustion. Gallstones . Gallstones often form in persons with cirrhosis. Intense itching . Some people with cirrhosis experience intense itching. Jaundice . In the later stages of cirrhosis, jaundice (yellow skin) may occur. Loss of appetite, nausea, and weight loss.

32. Postgraduate Medicine: Hepatic Encephalopathy Often, the term portalsystemic encephalopathy is used to emphasize thefailure of the liver to detoxify toxins that escape from the intestine. http://www.postgradmed.com/issues/2001/02_01/assi.htm

Hepatic encephalopathy Metabolic consequence of cirrhosis often is reversible Souheil Abou-Assi, MD; Z. Reno Vlahcevic, MD* VOL 109 / NO 2 / FEBRUARY 2001 / POSTGRADUATE MEDICINE CME learning objectives To understand the pathogenesis of hepatic encephalopathy in chronic liver disease To recognize the clinical manifestations and diagnostic tools used to detect hepatic encephalopathy To be aware of the precipitating factors for hepatic encephalopathy and to try to avoid them in patients with cirrhosis The authors disclose no financial interests in this article. Supported by a grant from the National Institutes of Health and a grant from the Department of Veterans Affairs. *Deceased. This is the first of three articles on cirrhosis This page is best viewed with a browser that supports tables. Preview : Hepatic encephalopathy is characterized by neuropsychiatric manifestations ranging from a slightly altered mental status to coma, and neuromuscular symptoms may be present. This complication of chronic or acute liver disease is a result of the failure of the liver to detoxify toxins originating in the intestine. The pathogenesis probably is multifactorial, although the predominant causative agent appears to be ammonia. In this article, Drs Abou-Assi and Vlahcevic discuss the timely recognition and correction of factors contributing to this often reversible condition. Abou-Assi S, Vlahcevic ZR. Hepatic encephalopathy: metabolic consequence of cirrhosis often is reversible. Postgrad Med 2001;109(2):52-70

33. CV: Vemuganti RM and Butterworth RF (1995) Selective alterations of extracellular brain amino acidsin relation to function in portalsystemic encephalopathy Results of an http://www.neurosurg.wisc.edu/cvvem.htm

University of Wisconsin Department of Neurological Surgery CURRICULUM VITAE Raghavendra Rao L. Vemuganti Assistant Scientist Dept. of Neurological Surgery University of Wisconsin-Madison F4/309 Clinical Science Center 600 Highland Avenue Madison, WI 53792, USA Education 1982 B.Sc., Zoology, Botony and Chemistry, Andhra University, India 1984 M.Sc., Life Sciences (Animal Sciences), University of Hyderabad, India 1986 M.Phil., Life Sciences (Neurochemistry), University of Hyderabad, India 1991 Ph.D. Life Sciences (Neurochemistry), University of Hyderabad, India Fellowships 1984-1985 M.Phil. Fellowship, University of Hyderabad, India 1989-1991 Senior Research Fellowship award, Indian Council of Medical Research, India 1992-1993 Post-doctoral Fellowship Medical Research Council of Canada funded project 1993-1994 Post-doctoral Fellowship award, Jasper Foundation, University of Montreal 1993-1996 Medical Research Council of Canada, Direct Post-doctoral Fellowship Awards 1989 Best poster award, Indian Academy of Neuroscience Annual Meeting, Calcutta, India

34. CCHS Clinical Digital Library portalsystemic encephalopathy Access document; Other Symptoms andSigns of Liver Disease Access document. Chapter 43. Drugs and http://cchs-dl.slis.ua.edu/clinical/gastroenterology/general.htm

Clinical Resources by Topic: Gastroenterology General Gastroenterology Clinical Resources Pediatrics Geriatrics Atlases Radiology ... Miscellaneous Resources See also: Gastrointestinal Clinical Procedure Resources General Gastroenterology Patient/Family Resources Harrison's Principles of Internal Medicine 15th Ed.-2001: Table of contents Health Sciences Library subscription INFO Chapter 282: Approach to the Patient with Gastrointestinal Disease Table of contents Biologic Considerations: Access document Clinical Considerations: Access document Diagnostic Approaches: Access document Feldman: Sleisenger and Fordtran's Gastrointestinal and Liver Disease 7th Ed.-2002 (MD Consult): Table of contents Health Sciences Library subscription INFO Chapter 1 - Gastrointestinal Hormones and Neurotransmitters: Access document Introduction: Access document Cellular Communication: Access document Neural Regulation of the Gastrointestinal Tract: Access document Peptide Hormones of the Gastrointestinal Tract: Access document Other Chemical Messengers of the Gastrointestinal Tract: Access document Signal Transduction: Access document Regulation of Gastrointestinal Growth by Hormones and Transmitters: Access document Regulation of Gastrointestinal Hormones by Intraluminal Releasing Factors: Access document References: Access document Chapter 2 - Mucosal Immunology and Mechanisms of Gastrointestinal Inflammation: Access document Introduction: Access document Mucosal Immune Responses: Access document Inflammatory Responses: Access document References: Access document Chapter 3 - Cellular Growth and Neoplasia:

35. Federico2 Acta Neurologica Scandinavica. 2001;103198200 portal-systemic encephalopathymay be seen with hyperammonemia that complicates chronic liver disease. http://www.brain.org.au/publications/abstracts2001/federico2.html

Reversible parkinsonism, sudden stupor, and hyperammonemia in a patient with portal vein thrombosis. Federico P and Zochodne DW. Acta Neurologica Scandinavica. 2001;103:198-200 Portal-systemic encephalopathy may be seen with hyperammonemia that complicates chronic liver disease. We report an unusual case of reversible parkinsonism associated with hyperammonemia and portal vein thrombosis. An active 90-year-old male developed motor slowing and resting hand tremor over 6 months. Examination showed asterixis, bradykinesia, cogwheel rigidity, rest tremor, and a parkinsonian gait. Serum venous ammonia was elevated at 145 microM. The next day, the patient became comatose and serum ammonia was 178 microM. With lactulose therapy,serum ammonia level normalized and examination showed only minimal parkinsonismafter 1 week. An abdominal CT scan identified portal vein thrombosis withporto-systemic shunting that reversed after 7 months of treatment. Examination 2 years later showed no signs of parkinsonism. Parkinsonism can dominate the clinical picture of patients with hyperammonemia before the onset of encephalopathy.

36. Abstract 1PO-92 TREATMENT OF portal-systemic encephalopathy WITH OCTREOTID AND L-ORNITHINE-L-ASPARTATE.TE Kodua 4 , NN Kipshidze 1 , VI Bakhutashvili 2 , FI Todua 3. http://www.knt-ec.com/event/icim/abstract/1-PO-14.html

ABSTRACTS 1-PO: Gastroenterology: liver disease 3 May 29 (Wed.), 2002 1-PO-81: PROGNOSTIC EFFECT ON GRAFT-VERSUS HOST DISEASE(GVHD) FROM ALLOGENEIC BONE MARROW TRANSPLANTATION BY URSODEOXYCHOLIC ACID N. Iwata , Y. Seto , T. Yamamoto , Y. Amuro , H. Hada , E. Kakishita Dept. of Internal Medicine, Hyogo College of Medicine, Hyogo, Japan The usefulness of ursodeoxycholic acid (UDCA) for treatment of hepatic lesions such as PBC has been reported. Since histological findings of hepatic GVHD is similar to that of PBC, we have reported that UDCA has a prophylactic effect on acute hepatic GVHD. UDCA has an immunomodulating effect, so it may induce some severe infections such as interstitial pneumonia (IP) by cytomegalovirus. Here, we studied the usefulness and side effects of UDCA for the treatment of complications in bone marrow transplantation(BMT). METHODS: Seventy-one patients who had received BMT were used in this study. Thirty-six patients, randomly chosen, were given UDCA 600mg/day orally 4 weeks before BMT (group U). Another 35 patients were started on UDCA just after the onset of acute hepatic GVHD, along with the usual combination of immunosuppressive agents( group C). The rate of acute hepatic GVHD of more than stage 2, based on the classification scale of Thomas et al., was compared between groups U and C. The survival rate and cause of death were compared for one year after BMT. RESULTS:The rate of acute hepatic GVHD of more than stage 2 occurring was 0% in group U vs 20.0% in group C(P

37. ILM - Klinisk Farmakologi Bergqvist, PBF, Hjort, S., Apelqvist, G. Bengtsson, F. Potassiumevoked neuronalrelease of serotonin in experimental chronic portal-systemic encephalopathy. http://www.klinfarm.lu.se/publikationer.html

ILM Hemsida Hematologi Klinisk farmakologi Klinisk Genetik Klinisk Kemi Medicinsk Neurokemi MIG Transfusionsmedicin AVD Personal Forskning Kontakt Avd. chef: Stf.: Karl-Erik Andersson Sekreterare: Gunilla Sernelin Postadress Publikationer Publikationer 1998 Publikationer 1997 Publikationer 1996 Publikationer 1995 Apelqvist G., Wikell C., Hindfelt B., Bergqvist P.B.F., Andersson G., and Bengtsson F. (1999) Altered open-field behavior in experimental chronic hepatic encephalopathy after single venlafaxine and citalopram challenges. Psychopharmacology 143(4), 408-416. Bergqvist P.B.F., Bouchard C., and Blier P. (1999) Effect of long-term administration of antidepressant treatments on serotonin release in brain regions involved in obsessive-compulsive disorder. Biol. Psychiatry, 45(2), 164-174. Bergqvist P.B.F., Dong J., and Blier P. (1999) Effect of atypical antipsychotic drugs on 5-HT2 receptors in the rat orbito-frontal cortex: an in vivo electrophysiological study. Psychopharmacology 143(1), 89-96. Bergqvist P.B.F., Carpenedo R., Apelqvist G., Moroni F., and Bengtsson F. (1999) Plasma and brain levels of oxindole in experimental chronic hepatic encephalopathy: effects of systemic ammonium acetate and L-tryptophan. Pharmacol. Toxicol. 84 .

38. Toxic, Metabolic And Nutritional Disorders Of The Nervous System - Internet Hand 2001; Stages of Hepatic Encephalopathy The Medical Algorithms Project;portal-systemic encephalopathy - eMedicine/Medicine; Comprehensive http://www.neuropat.dote.hu/toxic.htm

Internet Handbook of Neurology Compiled by K atalin H Department of Neurology University of Debrecen, Hungary Toxic/Metabolic/ Nutritional Disorders Chapters: A Collection of High Quality Online Resources for Health Professionals Toxicology Toxicology Tutorials - National Library of Medicine Toxnet:Toxicology Database Network - National Institutes of Health Laboratoires SERB antidotes et intoxications - S.E.R.B. Laboratories, Paris, FR Withdrawal Syndromes - eMedicine/Emergency Toxicology: Treatment Guides - IPCS INTOX Emergency Treatment of Poisoning - University of Cape Town, ZA Oral Poisonings: Guidelines for Initial Evaluation and Treatment - American Family Physician, January 1998 Poisonings , Pediatric Emergency Manual, University of Iowa Poisoning - Columbia University Carbon Monoxide Toxicity, Carbon Monoxide - eMedicine/Emergency Toxicity, Carbon Monoxide - eMedicine/Pediatrics Carbon Monoxide Poisoning Carbon monoxide poisoning - Postgraduate Medicine, January 1999 A Noninvasive Method For Rapid Diagnosis Of Carbon Monoxide Poisoning Identifying and managing adverse environmental health effects: 6. Carbon monoxide poisoning

39. Hepatic Encephalopathy to West Nile virus.) Chronic hepatitis C patients with advanced liver disease maydevelop hepatic encephalopathy, also called portalsystemic encephalopathy. http://www.hcvadvocate.org/hepatic_encephalopathy.htm

Hepatic Encephalopathy By Liz Highleyman Print this page Causes of Hepatic Encephalopathy The liver carries out many important bodily functions including filtering toxic metabolic byproducts from the blood. Normally blood coming from the intestines flows through the liver, where it undergoes detoxification. In people with decompensated cirrhosis—when the damaged liver is unable to carry out its normal metabolic processes or when blood bypasses the liver—these toxins can build up in the bloodstream. Blood may bypass or be shunted around the liver when blood flow through the liver is blocked by scar tissue (causing portal hypertension) or when an artificial shunt is surgically inserted (a procedure sometimes done to control bleeding varices or ascites). High levels of toxins can affect the central nervous system (the brain and spinal cord), although how they do so is not well understood. Increased levels of ammonia are believed to be most responsible for hepatic encephalopathy. Ammonia is a byproduct of the digestion of proteins by bacteria in the intestines; normally ammonia is metabolized into urea by the liver and excreted by the kidneys as urine. High levels of ammonia appear to alter the balance of neurotransmitters (chemicals that carry messages between neurons) in the brain . This theory is supported by the fact that reducing ammonia usually improves encephalopathy symptoms; however, some people with hepatic encephalopathy do not have elevated blood ammonia levels.

40. 12-98 Encephalopathy PMID 9252134, UI 97394416 Potassiumevoked neuronal release of serotoninin experimental chronic portal-systemic encephalopathy. http://organtx.org/dc/enceph1298.htm

12-98 Encephalopathy Cerebral Blood Flow and Metabolism in Patients With Chronic Liver Disease Undergoing Orthotopic Liver Transplantation Journal of Am. Asso. for the Study of Liver Disease, Vol. 27 No. 2 (Feb.'98) BARBARA J. PHILIPS, IAN R. ARMSTRONG, ANTHONY POLLOCK, AND ALISTAIR LEE Changes in cerebral hemodynamics and metabolism associated with anesthesia and liver transplantation may present particular hazards for patients with cirrhosis. Fifteen patients undergoing liver transplantation were studied, 7 of whom had encephalopathy. Cerebral blood flow (CBF) was measured at the start of surgery, during veno-venous bypass and post reperfusion, using a method based on the Kety-Schmidt method. Cerebral metabolism was assessed by measuring the cerebral metabolic rate for oxygen (CMRO2) and the lactate oxygen index (LOI). The cerebral vascular reactivity to carbon dioxide (CO2) was studied during the preanhepatic and post reperfusion phases. During the preanhepatic period, the median CBF was 44 mL/100 g/min at an arterial carbon dioxide tension (PaCO2) of 3.8 kPa. After reperfusion the CBF increased (P  < .02) to 102 mL/100 g/min, the arterial hydrogen ion concentration increased from 39 nmol/L to 53 nmol/L (P

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