R "This report aims to give the Moroccan citizen the means to judge for itself the relevance of the proposed high-speed line and the actual figures announced by policymakers. Also, true anatomy and physiology book online to trigger debate and allow citizens and experts to give their views on a project of this magnitude. The few figures announced by the State or by the National Railways can not be credible in the absence of detailed data that the supported. " of Capdema. The The The Bodies R The Elaine N Marieb, doctor of zoology, is currently a professor at Halyoke Community College o For five weeks beginning with the right upper quadrant pain, anorexia, asthenia, pruritus, jaundice and dark urine. No other symptoms. No history of alcohol abuse, snuff or drugs. Do not travel in the last 10 years. No history of other symptoms apparatus, not cardiac disease, joints, endocrine, or digesivas. It does not take drugs. No previous surgeries and transfusions. Physical examination showed moderate obesity, jaundice and right upper quadrant pain. There was palmar erythema and some ruby points in the chest. No signs of ascites or evidence of encephalopathy. No edema, or clubbing. Normal pulmonary and cardiac auscultation. No adenopathies. Hepatomegaly three finger breadths below the costal limit, with tenderness. No splenomegaly. Hemoglobin: 12.6 g / dL, WBC: 6200 / mm3, platelet 170000/mm3, creatinine: 0.8 mg / dl, prothrombin time: 19 sec; thromboplastin parcila time: 55 sec, total bilirubin: 25 mg / dl , direct bilirubin: 14 mg / dl, albumin: 2.5 g / dl, alkaline phosphatase: 130 U / L, AST: 3023 U / L; TGP: 2270 U / L. Abdominal ultrasound was performed which showed hepatomegaly without regular masses. No ascites. No evidence of cholelithiasis or colecistis ascitis.No. The portal venous Doppler study was normal and liver as well. It's a complicated case, my initial idea was that it could be caused by infectious, according to the symptoms presented by the patient, plus it does not comment on the sexual habits of the patient, but no fever and the serology read the hepatitis virus was negative, I thought likely to be in the window period, but rarely develop symptoms at that stage. Discarded drug hepatitis, he denies taking. While finding high total bilirubin at the expense of direct and elevated transaminases also made me think of an obstructive cause, I dismissed it because, alkaline phosphatase is normal and ultrasound cholelithiasis and cholecystitis denied. Palmar erythema and ruby points in the chest made me think that there was a bleeding disorder, because the liver is affected, as well as the times are lengthened. Dismissed cancer or malignancy, because the patient did not present weight loss or ascites, in addition to the ultrasound does not refer masses. By ruling out the possibility that obstructive, infectious, alcoholic, drug and tumor, I thought it important to know whether it might be autoimmune, as there are studies that serve to aid in the diagnosis of autoimmune diseases that do not appear in the case, as the ANCAs. When searching for information on hepatitis auntoinmune, found that patients often have abdominal pain, jaundice, dark urine and fatigue, also is often associated with autoimmune hemolytic anemia and immune thrombocytopenic purpura. I found the most frequently presents at any age and antinuclear and anti smooth muscle. In the laboratory, has variable elevation of SGOT and SGPT, and minimum elevation or normal values of alkaline phosphatase. May be elevated bilirubin, albumin and elongation decreased prothrombin time. Serology for hepatitis viruses are negative. What I call the attention of this case report was the clinical picture of the patient who had right upper quadrant pain, anorexia, asthenia, pruritus, jaundice and dark urine, which can not bear to think that may be a box that cholestasis and Jaundice occurs by the release of bilirubin in the blood, but we discarded it because there is no presence of cholelithiasis, another thing that caught my attention were the laboratory findings was that the direct and total bilirubin were high, alkaline phosphatase was high, low albumin but more important were the tranasaminasas they were very high, the patient had a hipertrasaminasemia which are markers of injury and disease that can cause hipertrasaminasemia hepatitis are so high so I thought that possibly a viral hepatitis but discard it that all the serological tests for hepatitis were negative, but to have those values as high transaminase must be caused by inflammation that causes great damage to the liver so it concludes that this patient has autoimmune hepatitis. I also thought it might be cancer but on ultrasound abdominal masses were not so discard it and could not be any pathology infeccionsa because your account will leukocytes were normal and the clinical pathology with a concuereda not infectious. Autoimmune hepatitis is a disorder caused by an alteration in the larger complex of histompatibilidad and lymphocytes mainly CD4 lymphocytes that cause liver damage from apoptosis causing autoimmune hepatitis. Laboratory findings include variable elevations of transaminase (SGOT / AST and SGPT / ALT) with normal or minimally elevated alkaline phosphatase and gamma glutamyl transpeptidase (GGT). May have elevated bilirubin, decreased albumin and prolonged prothrombin time which these findings are very similar to what is present. Typically the levels of immunoglobulin G (IgG) are elevated. As part of the evaluation, serological markers for viral hepatitis were negative. Most patients have some autoantibody. The clinical case was interesting, because as it is getting more and more information, poses different diagnostic routes. at first I thought it might have been an obstructive process, but according to the results of laboratory tests did not indicate that identity, so I dismissed it. Then, I thought of such infectious process either viral or bacterial type, but according to síngnos and symptoms presented by the patient were not consistent with the common presentation in addition to laboratory tests for viral hepatitis were negative, which was also discarded. The presence of transaminasemia, was a fact that a lot of attention, so it was noted that there was indeed a process inflmatorio noninfectious type, so one thought in an immunological process. For confirmacción of this disease entity, shall be required for laboratory testing more complex such as the identification of ANA or ASMA, which are the most common and also the liver biopsy for confirmation of autoimmune hepatitis. I think it was a complicated case, since according to epidemiology was a little confusing the fact whether it was actually the condition but despite these details, I think is a good exercise to extend the range of options We can offer the patient to make a timely Diagnosis of COP improving the quality of life of patients and lead to medical practice increasingly effective. Starting with the location of the main symptoms for which the patient comes to see, right upper quadrant pain and jaundice presence of which makes me think of home problems Liver and Biliary. The possibility of a bile duct problem for elevated total bilirubin at the expense of direct bilirubin, infers a problem by cholestasis of which a common cause is blockage (possibly a litho or inflammation), but the hypothesis is eliminated obstructive by abdominal echogram rule out cholelithiasis and cholecystitis. Even though not yet arrived to discard neoplastic process, the echogram has ruled out the presence of masses. Liver injury is evident by high levels of transaminases, however hypoalbuminemia is a marker of liver damage late with what makes our condition as chronic, also clear that there are vascular problems (coagulation factors) for the thoracic petechiae . Possible chronic liver disease are possible: alcohol (cirrhosis), viral, autoimmune, drug (isoniazid, nitrofurantoin, methyldopa, etc) and metabolic (a1-antitrypsin deficiency). Which thanks to the same clinical case can be eliminated one by one, alcoholic or drug by drug and alcohol abuse negative refer also not using drugs that may cause liver damage. Serologic tests were negative and therefore discarded test eliminates the metabolic alpha1 antitrypsin. Which leads us to believe that the pathology may be of autoimmune origin. To reach this diagnosis is to be reached by exclusion and ask for proof of circulating autoantibodies (ANA, SLM and LKM) if this result is positive we can ask for a liver biopsy finding in it chronic inflammatory infiltrate, which expands the portal areas and extending the lobes, with erosion of limiting plate and the appearance of fibrosis. The treatment is based on glucocorticoids (prednisone / prednisolone), giving symptomatic improvement, clinical, biochemical and histological and prolongs survival. A great case, investigate and learned a lot. In this case report the patient had anorexia, pruritus, jaundice, right upper quadrant pain, hepatomegaly, and dark urine that leads us to a liver or biliary disease. Looking hepatitis can rule out the etiology of both alcoholic and drug due to the absence of these. Rule out viral hepatitis taking into account the negative tests for viruses, the absence of cholelithiasis and malignant obstruction helps us rule out cholestasis. Laboratory tests show elevated transaminase and alkaline phosphatase, albumin is low and elevated direct bilirubin. These tests are consistent with autoimmune hepatitis is characterized by hepatocellular necrosis and inflammation sustained by corresponding elevation of transaminases. The clinical manifestations of this disease can be confused with acute hepatitis. Laboratory data correspond to a severe stage as transaminases are very high with bilirubin, albumin is low and there is also elevated alkaline phosphatase. The tests to be performed include measuring the amount of immunoglobulins in the blood that should be high (more than 2.5g/100ml) and circulating antibodies and antinuclear antibodies (ANA), smooth muscle antibodies (antibodies against smooth fiber) which can also be detected in chronic viral hepatitis antibodies and liver and kidney microsomes (anti-LKM). As they all said. This case seemed unreal, poor Christian was as healthy and even paid his taxes, but as I read the data would formandome trial patient diagnosis, but to continue with the reading of the data were discarded as probable diagnoses . Suspected obstructive process at the beginning, after a disease by drugs, then an infection, HIV, malignancy and so I went to think of some autoimmune phenomenon but not sure until today in class accidentally said the response of the case. Each data directed to one of these diagnoses, but other laboratory tests, examenesde history cabinet and the ruling iban slowly. In the end gets the diagnosis of autoimmune hepatitis, which should seek to corroborate relevant laboratory tests such as antibodies. I consider this type of clinical exercises are good because they help us develop our clinical judgment, to always think diferenes diagnostic options and not close our minds to a single option. In addition to teaching us cases that could arise on any given day and prepares us for when the time comes to face the patient to do it the right way. As you begin to read a case, symptoms, signs and physical examination made me suspect an obstructive defect in the liver that caused the jaundice, pruritus and coliuria, which was consistent with the laboratories in which bilirubin was elevated direct, but alkaline phosphatase did not show the characteristic elevation of a cholestatic pattern and abdominal ultrasonography showed cholelithiasis, cholecystitis, or mass, so I dismissed the lithos or a tumor as a cause of symptoms. Looking at the hypertransaminasemia, I remembered that hepatitis transaminase rises up to 100 times above the normal level, so my second option was hepatitis. On the epidemiology of type I in viral hepatitis, but all the serological tests for hepatitis were negative and no blood transfusions or intravenous drug use decreases the likelihood that we are talking about Hepatitis C. It was not for alcohol or drug because the patient refused the abuse of both. It could not have jaundice secondary to a genetic disorder such as Gilbert's syndrome, etc.. because these would be presented in infants and children, not a 50 year old previously healthy. After evaluating all the possible causes of jaundice and hypertransaminasemia return to the diagnosis of hepatitis, if it was viral or infectious (because there is no leukocytosis) may be an autoimmune hepatitis. I found a case interesting because it allowed me to review several issues to reach the final diagnosis, it definitely had nothing to do with my first suspicion. What draws my attention to thinking it is a patolgia liver is the anatomical area of pain, hepatomegaly and decreased hepatic proteins. In laboratory tests, Hb level is slightly decreased, which added to the fact that the unconjugated bilirubin is elevated me to believe that there is some haemolysis of the blood. Elevated conjugated bilirubin suggests a possible obstruction but not secondary to a problem of stones or gallbladder. The alpha1-antitrypsin and the normal duration of 5 weeks of an acute padeciemto discarded. The low albumin, the elongate time indicate that there is a problem in the liver that intervioene with the synthesis of proteins, as well as elevated transaminases indicate a very possible hepatitis. White blood cells are normal, there is an infection, platelets near the lower limit in the normal, creatinine rule out a possible kidney disease because it is still normal. Actually I was lost, but after we got the hint that it might be autoimmune hepatitis, I found that sometimes accompanied by antibodies against the blood which causes hemolysis, is a chronic condition more acute, affects women more than in men but is more common in men around age 45, the onset may be sudden, when hepatitis is inflammation, decreased albumin, elongation of clotting times, transaminases rise and in this case were very elevated autoantibodies should be sought to confirm the autoimmune hepatitis. For it was a very interesting case to me what caught my attention was first the transaminasemia TGO: 3023 and TGP: 2270, which speaks of a pattern of hepatocellular damage and are late indicators so it is a chronic process , and elevation of total bilirubin at the expense of direct BT: 25, BD: 13 which we could suggest a cholestatic pattern, that we could orient chronic hepatitis given by the two patterns, but the serology is negative. One type of autoimmune chronic hepatitis is why we could assume that this type of hepatitis diagnostico.Pero occurs more in women and one of the possible causes associated with hepatitis A which came out negative in our patient and made us doubt such diagnosis. And the histology obtained from liver biopsy is a major element in the result can be diagnostico.Y from interface characteristic findings and the presence of inflammation with plasma cells. The first thing that I find my way this case was to cholelithiasis (although the probability is very low as a man and his age) as the clinical directed me to this diagnosis, for several reasons, one was the clinic that the patient, although in an atypical form for cholelithiasis, and the other were the laboratories in which altered LFTs out showing a picture of cholestasis with liver damage from my point of view, but later tells us no gallstones or cholecystitis, so that my first impression was discarded. The next thing I thought of hepatomegaly and epidemiology according to their age was cancer, hepatocellular carcinoma may be an obstruction of bile ducts that is causing the changes in direct bilirubin mainly, but serology tests for hepatitis viruses were negative, which are a risk factor for this cancer, also another impediment was the sex and age as it is not common, but could be an atypical presentation, but also the time of presentation of symptoms is very early for a cancer of this type. I also thought the patient with cirrhosis but not alcoholic, ruling out other diseases. In some drug-induced hepatitis but the patient does not consume drugs. To all this we have left is an autoimmune hepatitis, according to the investigation conducted, the type of autoimmune hepatitis with which studies the patient is a type 1 autoimmune hepatitis is the most common and can be seen at any age. It usually presents with antinuclear antibodies (ANA) or anti-smooth muscle (ASMA), so you should make the patient these tests to confirm the diagnosis, as well as in type 1 autoimmune hepatitis serological markers for viral hepatitis are negative, and if these tests conducted clinical and serological results were negative. Another factor that tells me this diagnosis is that a quarter of patients present as acute icteric hepatitis similar to viral hepatitis and autoimmune hepatitis can occasionally present as an acute fulminant hepatitis with jaundice, decreased prothrombin time and encephalopathy (although this This patient has no sign). 25% of patients present with symptoms of cirrhosis such as jaundice, dark urine, ascites, encephalopathy or variceal bleeding. It should also perform quantification of IgG as characteristically levels of immunoglobulin G (IgG) are elevated.