keepgoing
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A 22-year-old college student comes to the emergency room complaining of right upper quadrant abdominal
pain for several hours. He admits to drinking excessive amounts of alcohol 3 days ago. Over the
course of the last few days he recalls that he ingested the contents of an entire bottle of
acetaminophen. On exam he is afebrile, with normal vital signs and slight tenderness in the right
upper quadrant. Which of the following is the most likely set of liver function enzymes in this
patient?
Aspartate aminotransferase (AST) Alanine aminotransferase (ALT) Alkaline
phosphatase Amylase
A. High High High Normal
B. High High Normal Normal
C. High Low High High
D. Normal Normal High Normal
E. Normal High Normal High
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| dncosta
Licensed, finally
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B would be my guess
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| po
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Transaminases.—The transaminases are enzymes involved in the transfer of amino groups of aspartate and alanine to ketoglutaric acid. The AST enzyme (formerly designated serum glutamic-oxaloacetic transaminase) is present in cardiac, skeletal, kidney, and brain tissue, as well as in the liver. In contrast, alanine aminotransferase (ALT [formerly known as serum glutamate pyruvate transaminase]) is present almost exclusively in the liver and is a better index of liver cell injury. An AST increase in the absence of an ALT increase is reflective of cardiac or muscle disease. A rare cause of increased AST is when AST exists as a macroenzyme (macro-AST). In this condition, the AST is complexed with an immunoglobulin and thus is not cleared from the blood. Macro-AST does not indicate serious liver disease. It is a condition analogous to macroamylasemia, which causes an increased amylase in the absence of acute pancreatitis. The AST can be falsely low after dialysis.
The ratio of AST to ALT is sometimes a useful marker to diagnose specific liver diseases. AST is distributed both in cytosol and in mitochondria, but the normal serum activity of AST is predominantly related to cytosol. ALT is distributed mainly in the cytosol. In alcoholic hepatitis, the damage is primarily to the mitochondria, and thus the AST increase is higher than that of the ALT. Patients with alcoholic liver disease have pyridoxine deficiency, and ALT is more sensitive to pyridoxine deficiency than is AST; therefore, ALT levels tend to be lower. In viral hepatitis, the ALT is higher than the AST. In alcoholic hepatitis, the AST:ALT ratio is greater than 2.0, and the AST increase is not more than 250 U/L. The ratio of AST to ALT is less useful in chronic liver disease because hepatitis B virus-related cirrhosis and other causes of cirrhosis can also increase the AST:ALT ratio to more than 1.0.
The pattern of AST and ALT increases provides some indication of the underlying cause of liver disease. In choledocholithiasis, an AST increase is the earliest abnormality detected and is usually not more than fivefold. In the presence of cholangitis, the increase can be up to 10-fold. Typically, in choledocholithiasis, the AST increase is transient and returns to normal within 72 hours. In viral and drug-induced hepatitis, the transaminase levels steadily increase and peak in the low thousands range within 7 to 14 days. In uncomplicated viral hepatitis, the transaminases return to normal in about 6 weeks. In ischemic hepatitis, which typically occurs in patients with cardiac failure and hypotension, the transaminases abruptly increase within 24 hours and may even be higher than 10,000 IU/L; they rapidly return to normal within a week. Transaminase increases greater than 10,000 IU/L are also noted with an overdose of acetaminophen and in herpes simplex hepatitis. In a patient with increased transaminases, a decrease usually indicates improvement; however, in a patient with acute liver disease, a rapid decrease may mean profound worsening of the patient’s condition.
Many medications cause increases in AST. The most common ones are acetaminophen; nonsteroidal anti-inflammatory drugs; angiotensin-converting enzyme inhibitors; nicotinic acid; antibacterial agents such as isoniazid, sulfonamides, and erythromycin; and antifungal agents such as griseofulvin and fluconazole.
Finally, conditions such as nonalcoholic steatohepatitis (NASH) and both hyperthyroidism and hypothyroidism can cause increased transaminases. NASH is associated with various conditions such as diabetes mellitus and obesity, a jejunoileal bypass, drugs such as amiodarone, and total parenteral nutrition; however, NASH can be present without an obvious association.
Alkaline Phosphatase.—Alkaline phosphatase refers to a family of enzymes that catalyze hydrolysis of phosphate esters at an alkaline pH. Alkaline phosphatase is present in bone, placenta, intestine, and kidney, as well as in liver tissue; however, more than 80% of circulating alkaline phosphatase is in the liver and bone. During pregnancy, the alkaline phosphatase is concentrated predominantly in the placenta. Liver alkaline phosphatase is synthesized by the bile duct epithelial cells. The response to obstruction of bile ducts is increased synthesis and release of alkaline phosphatase. This outcome can result even if the obstruction is in a few small bile ducts and is insufficient to cause an increase in bilirubin. If, on fractionation, the alkaline phosphatase is found to be of hepatic origin, it indicates cholestasis at some level: diffusely within the liver (intrahepatic cholestasis), extrahepatic (gallstones or tumors), localized within the liver (hepatocellular carcinoma), or patchy involvement within the liver (granulomatous disease). Levels of alkaline phosphatase are also increased in hyperthyroidism, cardiac failure, lymphoma, and hypernephroma. If a laboratory does not have the capability to measure the liver fraction of alkaline phosphatase, measurement of γ-glutamyltransferase (GGT) is recommended. This is the only recommended use of routine GGT testing in evaluation of liver disease. An increased GGT in the presence of an increased alkaline phosphatase level indicates that the alkaline phosphatase is most likely of hepatic origin. When the alkaline phosphatase level is increased disproportionately to the bilirubin level—that is, bilirubin of less than 1.0 mg/dL and alkaline phosphatase greater than 1,000 U/L—suggested diagnoses are granulomatous or infiltrative diseases of the liver, including sarcoidosis, fungal infections, tuberculosis, and lymphoma. In patients with primary biliary cirrhosis (PBC) and primary sclerosing cholangitis, the initial finding is also an increased alkaline phosphatase but normal bilirubin level.
Recognizing the common pitfalls associated with interpretation of alkaline phosphatase levels is important. The test must be performed in fasting patients. Patients with blood group O and B who are secretors can have increased alkaline phosphatase after eating a fatty meal because of the release of the intestinal enzyme. In children, the alkaline phosphatase level is increased up to 3 times the upper limit of normal, and in pregnant patients, it can be increased up to 2 times that of normal. The alkaline phosphatase level may be low in patients with hypothyroidism, in some patients with Wilson’s disease and hemolysis, and in those with congenital hypophosphatasia.
Causes of intrahepatic cholestasis include PBC and drugs such as erythromycin, chlorpromazine, estrogens, and methyltestosterone; drugs are the most common cause. Typical causes of extrahepatic cholestasis are common bile duct gallstones or strictures and pancreatic cancer resulting in biliary obstruction.
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| jole
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B
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| inkspot
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B man its simple!
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Aagae Aagae Dekho hota hai kiya !!!
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| Addicudo
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Yea ... Its B .. !! Thought of A for a second .. but then no history of Bilary sys occlusion .. so B it is then !
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| po
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yah sometimes one shudn't think too much
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| kingusmle
Forum Elite
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B
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| keepgoing
Forum Guru
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Posts: 1,676
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The correct answer is B. This patient is suffering from hepatic injury as a result of
acetaminophen overdose. Acetaminophen, when broken down by the liver, produces a hepatotoxic
metabolite that can cause liver necrosis. When ingested in large quantities, massive destruction
may occur, potentially resulting in liver failure and mandatory liver transplant for survival.
This patient's liver is even more susceptible to hepatotoxicity from acetaminophen after an
alcohol binge, which renders it less able to metabolize the toxic byproducts.
Both aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are contained within
liver cells and are released when liver cells are destroyed, as in this case (often these enzymes
can be elevated to tens of thousands in an acute injury). Alkaline phosphatase is primarily
located within the cells of the bile ducts and biliary tree. Thus, an elevation of this enzyme
usually indicates pathology within the biliary tree (i.e., stones within the bile ducts, cancers
in the biliary tree, or other obstructive processes causing damage in the biliary tree). Amylase
is located within several different types of cells, but is used primarily in the diagnosis of
pancreatitis, in which it becomes elevated. Therefore, in this patient, both the AST and ALT would
likely be very high. It is unlikely that there would be any abnormality in the levels of alkaline
phosphatase or amylase.
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