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Alcoholic Liver Diseasea Robert C. Huebert and Vijay H. Shah Print Publication Year: 2014 Published Online: Aug 2014 Publisher: Oxford University Press ISBN: 9780199373338 eISBN: 9780190209728 DOI: 10.1093/med/9780199373338.003.0030 Item type: chapter
Alcoholic liver disease is a major cause of morbidity and mortality in the United States. Alcohol is implicated in more than 50% of liver-related deaths in the United States, and complications of alcoholism contribute to a quarter of a million deaths annually. Also, alcoholic liver disease is a major health care cost expenditure, accounting for nearly $3 billion annually. The clinical spectrum of alcoholic liver disease includes fatty liver, alcoholic hepatitis, and alcoholic cirrhosis. Fatty liver develops in response to short periods (days) of alcohol abuse. It is generally asymptomatic and reversible with abstinence. More advanced liver injury usually requires prolonged alcohol abuse over a period of years. Of note, the majority of people who abuse alcohol for extended periods do not develop more advanced lesions of alcoholic liver disease. However, alcoholic hepatitis or alcoholic cirrhosis (or both) develops in about 20% of these people.
Chronic Pancreatitis Suresh T. Chari Print Publication Year: 2014 Published Online: Aug 2014 Publisher: Oxford University Press ISBN: 9780199373338 eISBN: 9780190209728 DOI: 10.1093/med/9780199373338.003.0043 Item type: chapter
Chronic pancreatitis is an often painful inflammatory condition of the pancreas characterized by progressive fibrosis that leads to irreversible destruction of exocrine and endocrine tissue, resulting eventually in exocrine and endocrine insufficiency. There is considerable heterogeneity in the manifestation and natural history of the condition. Chronic pancreatitis is classified broadly into chronic calcifying pancreatitis, chronic obstructive pancreatitis, and chronic autoimmune pancreatitis.
Alcoholic liver disease Stephen F. Stewart and Chris P. Day Print Publication Year: 2010 Published Online: Dec 2012 ISBN: 9780199204854 eISBN: 9780199570973 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/ med/9780199204854.003.152201_update_001
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The incidence of alcoholic liver disease (ALD) follows the trend of per capita alcohol consumption, with hepatic injury which extends from fatty liver to alcoholic hepatitis and cirrhosis. It is unclear how alcohol causes liver disease, but postulated mechanisms include (1) oxidative stress and acetaldehyde generated by the metabolism of ethanol, and (2) innate and adaptive immune responses. Factors determining the susceptibility to liver disease in heavy drinkers are believed to include a variety of host and environmental factors. Clinical manifestations are extremely variable, and some patients remain while others suffer the effects of severe hepatic failure. Although patients can come to light with a life-threatening complication, most often they develop symptoms which are not immediately related to the liver, such as nonspecific digestive symptoms or psychiatric complaints. The key to the early recognition of alcohol-related disease is having a high index of suspicion, with confirmation by (1) direct questioning for alcohol history and alcohol-related symptoms; (2) clinical examination for signs of chronic liver disease; (3) supportive investigations, including elevation of serum ##-glutamyl transferase (##GT) and aspartate transaminase (AST); and (4) liver biopsy, which is often required for accurate prognostication, revealing alcoholic fatty liver, alcoholic hepatitis, or cirrhosis. Management is governed by the stage and severity of the liver disease, but always includes abstinence and adequate nutritional support. In selected patients with severe acute alcoholic hepatitis, corticosteroids and pentoxifylline can reduce mortality. For alcoholic cirrhosis, transplantation remains the only effective treatment, although mainly as a result of concerns about post-transplant recidivism, this remains controversial.
Viral hepatitis—clinical aspects H.J.F. Hodgson Print Publication Year: 2010 Published Online: 2014 ISBN: 9780199204854 eISBN: 9780199570973 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/ med/9780199204854.003.152101_update_002
There are five major hepatitis viruses—A, B, C, D, and E—with the clinical picture depending on the severity of the inflammation induced in the liver, and on whether the virus is cleared from the liver or persists long-term. Acute icteric hepatitis, characterized by jaundice and right upper quadrant abdominal tenderness, is the commonest clinically recognized consequence of infection. This is generally a self-limited condition with low mortality and complete recovery: only hepatitis B and C have the propensity to cause chronic viral hepatitis. Typically, hepatocellular enzyme levels in blood are prominently raised at the time of the onset of symptoms, whilst the serum alkaline phosphatase level is only slightly increased. Specific diagnosis is made by serological testing for particular viruses. Uncomplicated cases recover spontaneously; there is no proven therapy to enhance recovery, but alcohol and potentially hepatotoxic drugs should be withdrawn. Fulminant hepatic failure caused by viral hepatitis has 80% mortality and should be treated (if possible) by orthotopic liver transplantation. Protection against hepatitis A and B is available, both passive (gammaglobulin preparations) and active (vaccinations). Vaccines are not yet available for hepatitis C, but are in clinical trial for E. Vaccination against hepatitis B also protects against hepatitis D. Features of particular hepatitis viruses Page 2 of 5 PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2015. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy). date: 23 January 2017
Hepatitis A virus (HAV)—faecal–oral transmission; incubation 2–6 weeks; acute selflimited hepatitis; no specific treatment. Hepatitis B virus (HBV)—parenteral transmission; incubation 4–24 weeks; may present with acute hepatitis, with prodrome sometimes including prominent arthritis, fever, and urticarial rash, but anicteric attacks are common; most (>90%) patients clear HBV after acute infection, but failure to clear HBsAg (hepatitis B surface antigen) within 6 months defines ‘chronic carriage’, which is associated with a spectrum of histological damage and clinical manifestations ranging from being clinically silent to producing cirrhosis and hepatocellular cancer. Some patients with chronic infection will benefit from treatment with ##-interferons and/or inhibitors of viral replication (nucleotide and nucleoside analogues). Hepatitis C virus (HCV)—parenteral transmission; incubation 2 to 26 weeks; acute episode most often subclinical; 70% of patients fail to clear the virus and become chronic carriers, which often leads to cirrhosis after 15 to 25 years and then predisposes to hepatocellular cancer; treatment is with the combination of IFN-##2a or IFN-##2b plus ribavirin, and more recently direct anti-viral drugs. Hepatitis D virus (HDV)—an RNA virus ‘parasitic’ on HBV, with dual infection tending to produce more severe liver disease; treatment is as for hepatitis B. Hepatitis E virus (HEV)—faecal–oral transmission; incubation about 6 weeks; high risk of fulminant hepatitis if acquired during mid-trimester pregnancy; no specific treatment.
Drugs used in gastroenterology and hepatology Stuart Bloom, George Webster, and Daniel Marks Print Publication Year: 2011 Published Online: May 2012 Publisher: Oxford University Press ISBN: 9780199584079 eISBN: 9780191730672 DOI: 10.1093/med/9780199584079.003.0309 Item type: chapter
Aciclovir - Adefovir dipivoxil - 5-Aminosalicylates (5-ASA) - Antacids and alginates Antibiotics - Anticholinergics - Anti-diarrhoeal agents - Anti-emetics/anti-nausea drugs Antifungals - Antihistamines - Antispasmodics - Azathioprine - Bismuth - Botulinum toxin - Bowel cleansing solutions: see ‘Bowel preparation’ () - Cannabinoids - Cephalosporins Ciclosporin - Ciprofloxacin - Colestyramine - Corticosteroids - Cromoglicate - Dopamine (D) receptor antagonists - Ganciclovir - Gentamicin - Glycopeptides (teicoplanin, vancomycin) - H2 receptor antagonists (H2RA) - Infliximab - Interferon alfa - Lamivudine - Laxatives - Methotrexate - Metronizadole - Misoprostol - -acetylcysteine (NAc) - Nitrates - Octreotide - Opiates - Orlistat - Pancreatic enzyme supplements - Penicillins - Prokinetics - Propranolol - Proton pump inhibitors (PPIs) - Ribavirin - Serotonin (5-HT) receptor antagonists - Sucralfate - Tacrolimus - Terlipressin - Ursodeoxycholic acid (UDCA)
Chronic pancreatitis Richard A. Schatz and Phillip P. Toskes Print Publication Year: 2010 Published Online: 2015 ISBN: 9780199204854 eISBN: 9780199570973 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/ med/9780199204854.003.152402_update_003
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Chronic pancreatitis is most commonly due to chronic alcoholism in adults and cystic fibrosis in children, but there are many other causes/associations. Typical presentation is with (1) abdominal pain—but this is not always a feature and when present can vary from being mild to extremely severe; and/or (2) maldigestion—diarrhoea/steatorrhoea and weight loss. Accurate diagnosis requires a combination of a hormone stimulation test (e.g. secretin– cholecystokinin stimulation of bicarbonate and enzyme secretion) and a structural test, e.g. endoscopic ultrasonography or endoscopic retrograde cholangiopancreatography ERCP). In routine clinical practice common strategy is to evaluate patients suspected of having chronic pancreatitis with a noninvasive test, e.g. faecal elastase (reduced), and initiate treatment if the result is abnormal, reserving invasive tests for cases where diagnostic doubt remains or clinical progress is unsatisfactory. Management requires use of (1) potent enzyme formulations—protease for pain, lipase for steatorrhoea; given before meals and (if pain is a symptom) before bedtime, (2) acid suppressive therapy—H2 antagonist or proton pump inhibitor; (3) abstinence from alcohol; (4) diet that is moderate in fat (30%), high in protein (24%), and low in carbohydrate (40%); (5) pain control—if required, (a) non-narcotic analgesics are the pain-relieving medications of choice, and (b) lateral pancreaticojejunostomy (Peustow procedure) should be considered if there is dilatation of the main pancreatic duct.
Gastroenterology Murray Longmore, Ian B. Wilkinson, Andrew Baldwin, and Elizabeth Wallin Print Publication Year: 2014 Published Online: Jan 2014 ISBN: 9780199609628 eISBN: 9780191742798 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/med/9780199609628.003.0006
Gastroenterology: Contents Healthy, enjoyable eating - The mouth - Some presenting symptoms: - Dysphagia Nausea and vomiting - Dyspepsia/peptic ulcer - Gastro-oesophageal reflux - Hiatus hernia - Diarrhoea - Constipation - Jaundice - Upper bleeding - Bleeding varices Procedures: - Endoscopy and biopsy - Diseases and conditions: - Liver failure - Cirrhosis Haemochromatosis - #-antitrypsin deficiency - Primary biliary cirrhosis - Primary sclerosing cholangitis () - Autoimmune hepatitis - Non-aloholic fatty liver disease - Wilson's disease - Liver tumours - Inflammatory bowel disease: Ulcerative colitis () - Crohn's disease - Irritable bowel syndrome - Carcinoma of the pancreas - Nutritional disorders Carcinoid tumours - Gastrointestinal malabsorption Coeliac disease - Chronic pancreatitis Alcoholism
Indications for Liver Transplantation Jana G. Hashash and Kapil B. Chopra Print Publication Year: 2013 Published Online: Aug 2013 Publisher: Oxford University Press ISBN: 9780199768899 eISBN: 9780199352913 DOI: 10.1093/med/9780199768899.003.0012 Item type: chapter
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Liver transplantation remains to be the only hope for cure and survival in patients with decompensated end-stage liver disease (ESLD), acute/fulminant liver failure, and those with primary hepatic malignancies. Transplanting a new organ not only requires a fit patient and a matching donor but also mandates the presence of a social support system and an experienced multidisciplinary team, consisting of transplant coordinators, hepatologists, liver transplant surgeons, psychiatrists, social workers, as well as critical care physicians. The health-care providers together with the patients and their support system function as a group throughout the pre-transplantation period and as importantly in the post-operative period as well. Currently, liver disease and the need for precious organs are on the rise, surpassing the number of available livers for donation. In this chapter we will present an overview of the criteria for accepting patients to the transplantation list, the indications for liver transplantation, as well as the absolute and relative contraindications for liver transplantation.
Gastrointestinal and liver disorders Ira Madan and Simon Hellier Print Publication Year: 2013 Published Online: Apr 2013 ISBN: 9780199643240 eISBN: 9780191755668 Item type: chapter
Publisher: Oxford University Press DOI: 10.1093/med/9780199643240.003.0014
Few disorders of the gastrointestinal systems, bar infections, are caused or exacerbated by the work environment. More commonly, gastrointestinal disorders and associated symptoms limit the capacity of individuals to undertake the duties required for their job. The symptoms and treatment of some disorders such as inflammatory bowel disease may lead to the employee requiring periods of long-term sickness absence, to recover from surgery for instance. Advances in investigation, medical treatment, and surgery should improve symptom control and prognosis in many individuals, enabling them to remain in employment. Conditions likely to cause employment problems or risks to individuals and the public include: Inflammatory bowel disease Ileostomy and ileo-anal pouch Irritable bowel disease Gastroenteritis and gastrointestinal infections Viral hepatitis Chronic liver disease Obesity. The Equality Act 20101 is likely to apply to disorders affecting the ability to control defecation. Therefore conditions that lead to regular minor faecal incontinence or to even infrequent loss of bowel control are likely to be defined as a disability under the Act. This will include many cases of ulcerative colitis and Crohn’s disease. The occupational health practitioner has a key role in supporting employees with this disability who understandably may wish the details of their symptoms to remain medically confidential. Liaison with the employer about the nature of any support or adjustments required will be a key aspect of assessment of fitness to work.
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