Medicine Hack

 INTRODUCTION  Chronic and excessive use of alcohol is one of the major causes of liver disease. 90% of daily heavy drinkers (>60 g alcohol/day) as well as binge drinkers have fatty liver but a smaller percentage (10-35%) of drinkers progress to alcoholic hepatitis which is a precursor for cirrhosis. The long-term risk is 9 times higher in patients with alcoholic hepatitis compared to those with fatty liver alone. Some population-based surveys have documented that men must drink 40 to 80 g of alcohol daily and women must drink 20 to 40 g daily for 10 to 12 years to achieve a significant risk of liver disease. Liver pathology consists of  3 major lesions  that are progressive and rarely exist in a pure form: 1) fatty liver (usually reverses quickly with abstinence), 2) alcoholic hepatitis and 3) cirrhosis. Prognosis of severe alcoholic liver disease (ALD) is bad. Mortality of patients with alcoholic hepatitis concurrent with cirrhosis id nearly 60% at 4 years. Alt

Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are measured by the serum glutamic-oxaloacetic  transaminase (SGOT) and serum glutamic-pyruvic transaminase (SGPT) respectively. They are important markers of hepatocellular injury. Normal values:   (varies from lab to lab but on average) ALT : 7-41 U/L AST: 12-38 U/L AST can be found in various tissues like cardiac/skeletal muscles, kidney, brain and liver. ALT is limited primarily to the liver and thus ALT is a more specific reflection of hepatocellular disease than AST. The highest elevations of both enzymes are seen in viral, toxin-induced and ischemic hepatitis.  On the other hand, alcoholic hepatitis usually gives a lower raise of around < 300 U/L.  AST/ALT ratio is a useful indicator. a) A ratio of > 2 is highly suggestive of alcohol-induced hepatic injury. b) A ratio of > 1 and cirrhosis is often seen in patients of chronic hepatitis B infections. c) A ratio of < 1 is commonly seen in

Definition: Barrett’s esophagus is characterized by an intestinal metaplastic change in the lining mucosa of the esophagus in response to chronic gastro­esophageal reflux.  The condition is named after Norman Barrett, an Australian surgeon who drew attention to the columnar-lined esophagus in 1950. It is still not well understood why some people develop esophagitis and others develop Barrett’s esophagus often without significant esophagitis.  Pathology: In Barrett’s esophagus the junction between squamous esophageal mucosa and gastric mucosa moves proximally. The columnar epithelium is more acid resistant than the squamous epithelium. So this metaplasia appears to be a protective adaptation. The patient of chronic reflux esophagitis will find his symptoms decrease when he has developed Barrett's esophagus. Incidence: It is mainly seen in white man and the prevalence increases with age.  Several types of gastric-type mucosa may be found in the lower esophagus. When inte