Fatty Liver Cholecystitis K80.1 K81.9 Cholangitis K80.3 K83.0 Cholangitic Liver Abscess K80.3 + K75.0 K75.0
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Choledochoduodenal Fistula Complicatingchronic
Gut: first published as 10.1136/gut.10.2.146 on 1 February 1969. Downloaded from Gut, 1969, 10, 146-149 Choledochoduodenal fistula complicating chronic duodenal ulcer in Nigerians E. A. LEWIS AND S. P. BOHRER From the Departments ofMedicine and Radiology, University ofIbadan, Nigeria Peptic ulceration was thought to be rare in Nigerians SOCIAL CLASS All the patients were in the lower until the 1930s when Aitken (1933) and Rose (1935) socio-economic class. This fact may only reflect the reported on this condition. Chronic duodenal ulcers, patients seen at University College Hospital. in particular, are being reported with increasing frequency (Ellis, 1948; Konstam, 1959). The symp- AETIOLOGY Twelve (92.3 %) of the fistulas resulted toms and complications of duodenal ulcers in from chronic duodenal ulcer and in only one case Nigerians are the same as elsewhere, but the relative from gall bladder disease. incidence of these complications differs markedly. Pyloric stenosis is the commonest complication CLINICAL FEATURES There were no special symp- followed by haematemesis and malaena in that order toms or signs for this complication. All patients (Antia and Solanke, 1967; Solanke and Lewis, except the one with gall bladder disease presented 1968). Perforation though present is not very com- with symptoms of chronic duodenal ulcer or with mon. those of pyloric stenosis of which theie were four A remarkable complication found in some of our cases. In the case with gall bladder disease the history patients with duodenal ulcer who present them- was short and characterized by fever, right-sided selves for radiological examination is the formation abdominal pain, jaundice, and dark urine. -
Imaging of Biliary Infections
3 Imaging of Biliary Infections Onofrio Catalano, MD1 Ronald S. Arellano, MD2 1 Division of Abdominal Imaging, Department of Radiology, Address for correspondence Onofrio Catalano, MD, Division of Massachusetts General Hospital, Harvard Medical School, Abdominal Imaging, Department of Radiology, Massachusetts Boston, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, White 270, 2 Division of Interventional Radiology, Department of Radiology, Boston, MA 02114 (e-mail: [email protected]). Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts Dig Dis Interv 2017;1:3–7. Abstract Biliary tract infections cover a wide spectrum of etiologies and clinical presentations. Imaging plays an important role in understanding the etiology and as well as the extent Keywords of disease. Imaging also plays a vital role in assessing treatment response once a ► biliary infections diagnosis is established. This article will review the imaging findings of commonly ► cholangitides encountered biliary tract infectious diseases. ► parasites ► immunocompromised ► echinococcal Infections of the biliary tree can have a myriad of clinical and duodenum can lead toa cascade ofchanges tothehost immune imaging manifestations depending on the infectious etiolo- defense mechanisms of chemotaxis and phagocytosis.7 The gy, underlying immune status of the patient and extent of resultant lackof bile and secretory immunoglobulin A from the involvement.1,2 Bacterial infections account for the vast gastrointestinal tract lead -
Primary Biliary Cholangitis: a Brief Overview Justin S
REVIEW Primary Biliary Cholangitis: A Brief Overview Justin S. Louie,* Sirisha Grandhe,* Karen Matsukuma,† and Christopher L. Bowlus* Primary biliary cholangitis (PBC), previously referred to supported by the higher concordance of PBC in monozy- as primary biliary cirrhosis, is the most common chronic gotic compared with dizygotic twins.4 In addition, certain cholestatic autoimmune disease affecting adults in the human leukocyte antigen haplotypes have been associ- United States.1 It is characterized by a hallmark serologic ated with PBC, as well as variants at loci along the inter- signature, antimitochondrial antibody (AMA), and specific leukin-12 (IL-12) immunoregulatory pathway (IL-12A and bile duct pathology with progressive intrahepatic duct de- IL-12RB2 loci).5 struction leading to cholestasis. PBC is potentially fatal and can have both intrahepatic and extrahepatic complications. PATHOGENESIS EPIDEMIOLOGY The primary disease mechanism in PBC is thought to be T cell lymphocyte–mediated injury against intralobu- PBC affects all races and ethnicities; however, it is best lar biliary epithelial cells. This causes progressive destruc- studied in the Caucasian population. The condition pre- tion and eventual disappearance of the intralobular bile dominantly affects women older than 40 years, with a ducts. Molecular mimicry has been proposed as the ini- female/male ratio of 9:1.2 Although the incidence of PBC tiating event in the loss of tolerance primarily to mito- appears to be stable, the overall prevalence of the disease chondrial pyruvate dehydrogenase complex, E2, during is increasing.3 An individual’s genetic susceptibility, epige- which exogenous antigens evoke an immune response netic factors, and certain environmental triggers seem to that recognizes an endogenous (self) antigen inciting an play important roles. -
6.14 Alcohol Use Disorders and Alcoholic Liver Disease
6. Priority diseases and reasons for inclusion 6.14 Alcohol use disorders and alcoholic liver disease See Background Paper 6.14 (BP6_14Alcohol.pdf) Background The WHO estimates that alcohol is now the third highest risk factor for premature mortality, disability and loss of health worldwide.1 Between 2004 to 2006, alcohol use accounted for about 3.8% of all deaths (2.5 million) and about 4.5% (69.4 million) of Disability Adjusted Life Years (DALYS).2 Europe is the largest consumer of alcohol in the world and alcohol consumption in this region emerges as the third leading risk factor for disease and mortality.3 In European countries in 2004, an estimated one in seven male deaths (95 000) and one in 13 female deaths (over 25 000) in the 15 to 64 age group were due to alcohol-related causes.3 Alcohol is a causal factor in 60 types of diseases and injuries and a contributing factor in 200 others, and accounts for 20% to 50% of the prevalence of cirrhosis of the liver. Alcohol Use Disorders (AUD) account for a major part of neuropsychiatric disorders and contribute substantially to the global burden of disease. Alcohol dependence accounts for 71% of all alcohol-related deaths and for about 60% of social costs attributable to alcohol.4 The acute effects of alcohol consumption on the risk of both unintentional and intentional injuries also have a sizeable impact on the global burden of disease.2 Alcoholic liver disease (ALD) is the commonest cause of cirrhosis in the western world, and is currently one of the ten most common causes of death.5 Liver fibrosis caused by alcohol abuse and its end stage, cirrhosis, present enormous problems for health care worldwide. -
Clinical Biliary Tract and Pancreatic Disease
Clinical Upper Gastrointestinal Disorders in Urgent Care, Part 2: Biliary Tract and Pancreatic Disease Urgent message: Upper abdominal pain is a common presentation in urgent care practice. Narrowing the differential diagnosis is sometimes difficult. Understanding the pathophysiology of each disease is the key to making the correct diagnosis and providing the proper treatment. TRACEY Q. DAVIDOFF, MD art 1 of this series focused on disorders of the stom- Pach—gastritis and peptic ulcer disease—on the left side of the upper abdomen. This article focuses on the right side and center of the upper abdomen: biliary tract dis- ease and pancreatitis (Figure 1). Because these diseases are regularly encountered in the urgent care center, the urgent care provider must have a thorough understand- ing of them. Biliary Tract Disease The gallbladder’s main function is to concentrate bile by the absorption of water and sodium. Fasting retains and concentrates bile, and it is secreted into the duodenum by eating. Impaired gallbladder contraction is seen in pregnancy, obesity, rapid weight loss, diabetes mellitus, and patients receiving total parenteral nutrition (TPN). About 10% to 15% of residents of developed nations will form gallstones in their lifetime.1 In the United States, approximately 6% of men and 9% of women 2 have gallstones. Stones form when there is an imbal- ©Phototake.com ance in the chemical constituents of bile, resulting in precipitation of one or more of the components. It is unclear why this occurs in some patients and not others, Tracey Q. Davidoff, MD, is an urgent care physician at Accelcare Medical Urgent Care in Rochester, New York, is on the Board of Directors of the although risk factors do exist. -
Alcoholic Liver Disease and Its Relationship with Metabolic Syndrome
Research and Reviews Alcoholic Liver Disease and Its Relationship with Metabolic Syndrome JMAJ 53(4): 236–242, 2010 Hiromasa ISHII,*1 Yoshinori HORIE,*2 Yoshiyuki YAMAGISHI,*3 Hirotoshi EBINUMA*3 Abstract Alcoholic liver disease (ALD), which occurs from chronic excessive drinking, progresses from initial alcoholic fatty liver to more advanced type such as alcoholic hepatitis, liver fibrosis, or liver cirrhosis when habitual drinking continues. In general, chance of liver cirrhosis increases after 20 years of chronic heavy drinking, but liver cirrhosis can occur in women after a shorter period of habitual drinking at a lower amount of alcohol. Alcoholic liver cirrhosis accounts for approximately 20% of all liver cirrhosis cases. The key treatment is abstinence or substantial cutting down on drinking; the prognosis is poor if the patient continues drinking after being diagnosed with liver cirrhosis. Factors that exert adverse effects on the progression of ALD include gender difference, presence of hepatitis virus, immunologic abnormality, genetic polymorphism of alcohol-metabolizing enzymes, and complication of obesity or overweight. Recently, particular attention has been paid to obesity and overweight as risk factors in the progression of ALD. Conditions such as visceral fat accumulation, obesity, and diabetes mellitus underlie the pathologic factor of metabolic syndrome (MetS). In liver, MetS may accompany fatty liver or steatohepatitis, with possible progression to liver cirrhosis in some cases. Caution is required for patients with MetS who have a high alcohol intake because alcohol consumption further accelerates the progression of liver lesions. Key words Alcoholic liver disease, Metabolic syndrome, Obesity, NAFLD/NASH Introduction following hypertension and smoking, as a global disease burden. -
Non-Alcoholic Fatty Liver Disease
Non-alcoholic fatty liver disease Description Non-alcoholic fatty liver disease (NAFLD) is a buildup of excessive fat in the liver that can lead to liver damage resembling the damage caused by alcohol abuse, but that occurs in people who do not drink heavily. The liver is a part of the digestive system that helps break down food, store energy, and remove waste products, including toxins. The liver normally contains some fat; an individual is considered to have a fatty liver (hepatic steatosis) if the liver contains more than 5 to 10 percent fat. The fat deposits in the liver associated with NAFLD usually cause no symptoms, although they may cause increased levels of liver enzymes that are detected in routine blood tests. Some affected individuals have abdominal pain or fatigue. During a physical examination, the liver may be found to be slightly enlarged. Between 7 and 30 percent of people with NAFLD develop inflammation of the liver (non- alcoholic steatohepatitis, also known as NASH), leading to liver damage. Minor damage to the liver can be repaired by the body. However, severe or long-term damage can lead to the replacement of normal liver tissue with scar tissue (fibrosis), resulting in irreversible liver disease (cirrhosis) that causes the liver to stop working properly. Signs and symptoms of cirrhosis, which get worse as fibrosis affects more of the liver, include fatigue, weakness, loss of appetite, weight loss, nausea, swelling (edema), and yellowing of the skin and whites of the eyes (jaundice). Scarring in the vein that carries blood into the liver from the other digestive organs (the portal vein) can lead to increased pressure in that blood vessel (portal hypertension), resulting in swollen blood vessels (varices) within the digestive system. -
Non-Alcoholic Fatty Liver Disease Information for Patients
April 2021 | www.hepatitis.va.gov Non-Alcoholic Fatty Liver Disease Information for Patients What is Non-Alcoholic Fatty Liver Disease? Losing more than 10% of your body weight can improve liver inflammation and scarring. Make a weight loss plan Non-alcoholic fatty liver disease or NAFLD is when fat is with your provider— and exercise to keep weight off. increased in the liver and there is not a clear cause such as excessive alcohol use. The fat deposits can cause liver damage. Exercise NAFLD is divided into two types: simple fatty liver and non- Start small, with a 5-10 minute brisk walk for example, alcoholic steatohepatitis (NASH). Most people with NAFLD and gradually build up. Aim for 30 minutes of moderate have simple fatty liver, however 25-30% have NASH. With intensity exercise on most days of the week (150 minutes/ NASH, there is inflammation and scarring of the liver. A small week). The MOVE! Program is a free VA program to help number of people will develop significant scarring in their lose weight and keep it off. liver, called cirrhosis. Avoid Alcohol People with NAFLD often have one or more features of Minimize alcohol as much as possible. If you do drink, do metabolic syndrome: obesity, high blood pressure, low HDL not drink more than 1-2 drinks a day. Patients with cirrhosis cholesterol, insulin resistance or diabetes. of the liver should not drink alcohol at all. NAFLD increases the risk for diabetes, cardiovascular disease, Treat high blood sugar and high cholesterol and kidney disease. Ask your provider if you have high blood sugar or high Most people feel fine and have no symptoms. -
Diet and Fatty Liver Disease
10/15/2020 Diet and Fatty Liver Disease KRISTEN COLEMAN RD CNSC CRMC LIVER EXPO 2020 1 Fatty Liver Disease Importance of liver health and liver functions of digestion Fatty Liver Disease and Pediatrics Nutrition tips for a healthy liver Foods that cause Fatty Liver What foods to eat to with Fatty Liver Disease 2 1 10/15/2020 Liver Function Removes toxicants from the body Metabolizes / Digests protein, carbohydrates, and fat Glycogen Storage Controls / Regulates neuro-hormonal mechanisms 3 Fatty Liver and Children Fatty liver disease is the most common cause of chronic liver disease in children ◦ Simple Fatty Liver Disease – fat accumulated on live but no cell damage or inflammation ◦ Non-Alcoholic Steatohepatitis (NASH) – fat accumulation with inflammation and cell damage which can lead to cirrhosis or liver cancer Effects 1 in 10 kids ◦ Fatty liver disease in children has doubled in the last 20 years ◦ Why? ◦ Increase in pediatric obesity ◦ Poor nutrition ◦ Limited activity 4 2 10/15/2020 Fatty Liver and Children Children and Diet ◦ Fruit Juice, sports drinks, soda ◦ High carbohydrate snacks – crackers, chips ◦ High fructose corn syrup intake - fruit snacks, sugary yogurts, canned fruits, granola bars ◦ High intake of processed foods – chicken nuggets,- French fries ◦ Limited intake of fiber and water intake ◦ Grazing / frequent snacking Diet treatment for fatty liver in kids is the same as adults 5 How does diet effect/cause Fatty Liver? All carbohydrates are broken down into glucose Glucose travels though the blood stream and delivers energy to our cells If the cells do not need energy the glucose molecule is sent back to the liver for storage. -
Diagnosis and Management of Autoimmune Hemolytic Anemia in Patients with Liver and Bowel Disorders
Journal of Clinical Medicine Review Diagnosis and Management of Autoimmune Hemolytic Anemia in Patients with Liver and Bowel Disorders Cristiana Bianco 1 , Elena Coluccio 1, Daniele Prati 1 and Luca Valenti 1,2,* 1 Department of Transfusion Medicine and Hematology, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy; [email protected] (C.B.); [email protected] (E.C.); [email protected] (D.P.) 2 Department of Pathophysiology and Transplantation, Università degli Studi di Milano, 20122 Milan, Italy * Correspondence: [email protected]; Tel.: +39-02-50320278; Fax: +39-02-50320296 Abstract: Anemia is a common feature of liver and bowel diseases. Although the main causes of anemia in these conditions are represented by gastrointestinal bleeding and iron deficiency, autoimmune hemolytic anemia should be considered in the differential diagnosis. Due to the epidemiological association, autoimmune hemolytic anemia should particularly be suspected in patients affected by inflammatory and autoimmune diseases, such as autoimmune or acute viral hepatitis, primary biliary cholangitis, and inflammatory bowel disease. In the presence of biochemical indices of hemolysis, the direct antiglobulin test can detect the presence of warm or cold reacting antibodies, allowing for a prompt treatment. Drug-induced, immune-mediated hemolytic anemia should be ruled out. On the other hand, the choice of treatment should consider possible adverse events related to the underlying conditions. Given the adverse impact of anemia on clinical outcomes, maintaining a high clinical suspicion to reach a prompt diagnosis is the key to establishing an adequate treatment. Keywords: autoimmune hemolytic anemia; chronic liver disease; inflammatory bowel disease; Citation: Bianco, C.; Coluccio, E.; autoimmune disease; autoimmune hepatitis; primary biliary cholangitis; treatment; diagnosis Prati, D.; Valenti, L. -
Hepatitis C and Alcohol
Hepatitis C and Alcohol Eugene R. Schiff, M.D., and Nuri Ozden, M.D. Patients infected with the hepatitis C virus (HCV) who drink heavily are likely to suffer more severe liver injury, promoting disease progression to cirrhosis and increasing their risk for liver cancer. Some research, although not conclusive, suggests that even moderate drinking may spur liver damage in HCV-infected patients. Research areas that have the greatest potential for developing more effective treatment options include HCV virology, immunology, animal models, and the mechanisms of liver injury. KEY WORDS: hepatitis C virus; alcoholic beverage; chronic AODE (alcohol and other drug effects); amount of AOD use; epidemiology; risk factors; disease course; alcoholic liver cirrhosis; gender differences; biochemical mechanism; RNA; mutation; apoptosis; inflammation; hepatocellular carcinoma; regulatory proteins; immune response; alcoholic fatty liver; treatment issues; treatment outcome; interferon epatitis C is an infectious liver the time of infection, male gender, are considerably more likely to test disease caused by the hepatitis obesity, abnormal accumulation of fat positive for HCV infection than those HC virus (HCV). The virus, in the liver (a condition known as fatty with less severe liver disease (Takase et which causes inflammation in the liver liver, or steatosis), and excessive alco al. 1993). and can lead to more serious illness, hol consumption (Poynard et al. 2001). primarily is spread by intravenous This article discusses the mechanisms contact with the blood of an infected by which alcohol may exacerbate Levels of Alcohol person. About 4 million people in the HCV-infected patients’ risk of disease Consumption in HCV United States have been infected, progression, reviews issues in the Patients and the Risk of making it the Nation’s most common treatment of alcoholic patients with Further Liver Disease blood-borne disease, resulting in the HCV infection, and addresses impor deaths of between 10,000 and 12,000 tant areas of future research. -
Or Ascending Cholangitis) Is a Clinical Syndrome That Is Classically Characterized by the Triad Of
ACUTE ASCENDING CHOLANGITIS Introduction Acute cholangitis (or ascending cholangitis) is a clinical syndrome that is classically characterized by the triad of: ● Fever ● Abdominal pain ● Jaundice The condition occurs as a result of obstruction/ stasis and subsequent infection within the biliary tract. In the absence of appropriate treatment the condition has significant potential for mortality and morbidity. It is a medical emergency that requires prompt antibiotic treatment and urgent relief of biliary obstruction (usually by endoscopic retrograde cholangiopancreatography ERCP). History Jean M. Charcot was the first to describe this illness in 1877. He described a triad of fever, jaundice, and right upper quadrant pain. Epidemiology Acute cholangitis is predominantly seen in adults, most commonly around 40-70 years of age. Physiology Normal barrier mechanisms to cholangitis infection include ● The sphincter of Oddi, which normally forms an effective mechanical barrier to duodenal reflux and ascending bacterial infection. ● Continuous flushing action of bile plus the bacteriostatic activity of bile salts which help maintain bile sterility. ● Secretory IgA and biliary mucous probably also function as anti-adherence factors, preventing bacterial colonization Pathology Organisms: Ascending cholangitis is usually associated with Gram-negative or anaerobic sepsis. ● Aerobic organisms include Escherichia coli and Klebsiella and Enterococcus species. ● The most common anaerobic organism is Bacteroides fragilis. Clostridia may also cause serious infection. Causes: Ascending cholangitis essentially occurs as consequence of obstruction of the biliary tract. Stasis leads to secondary bacterial infection; the organisms typically ascending from the duodenum. Biliary obstruction raises intrabiliary pressure and leads to increased permeability of bile ductules, permitting translocation of bacteria and toxins from the portal circulation into the biliary tract.