1-HEPATIC+_+BILIARY+DISORDER-2017.pdf - HEPATOBILIARY AND PANCREATIC SYSTEM LECTURE 1 Allister Rechea MD 1 most of the blood supply to the liver is

1-HEPATIC+_+BILIARY+DISORDER-2017.pdf - HEPATOBILIARY AND...

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HEPATOBILIARY AND PANCREATIC SYSTEM LECTURE 1 Allister Rechea, MD 1
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Anatomy 2
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FUNCTIONAL HISTOLOGY OF THE LIVER 4
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Liver Lobules There are 3 ways to describe the liver in terms of a functional unit: the classic lobule, the portal lobule and the liver acinus. The classic lobule The Portal lobule The Acinus The Acinus- is the structural unit that provides the best correlation between blood perfusion, metabolic activity and liver pathology Zone 1 Cells: first to show morphologic changes after bile duct occlusion; last to die if circulation is impaired and first to regenerate Zone 3 cells: first to show ischemic necrosis (centrilobular); first to show fat accumulation; last to respond to toxic substance and bile stasis
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Acute liver failure (ALF) ( fulminant hepatic failure /fulminant hepatitis) is an uncommon condition in which rapid deterioration of liver function results in development of coagulopathy, (prothrombin time >20 sec or prolonged by 4-6 seconds or INR > 1.5) and any degree of mental alteration ( encephalopathy ) in a previously healthy individual patient without preexisting cirrhosis and with an illness of less than 26 weeks ' duration. patients with Wilson disease, hepatitis B virus acquired from mother during childbirth, or autoimmune hepatitis may be considered to have acute liver failure despite cirrhosis if disease recognized for < 26 weeks
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classifications of presentations hyperacute - associated with acute acetaminophen toxicity, acute Hepatitis A or E progression from jaundice to encephalopathy < 1 week severe coagulopathy moderate intracranial hypertension acute - associated with hepatitis B progression from jaundice to encephalopathy 1-4 weeks moderately severe coagulopathy mild to moderate intracranial hypertension subacute - associated with nonacetaminophen drug toxicity progression from jaundice to encephalopathy 4-12 weeks mild coagulopathy severe jaundice absent or mild intracranial hypertension
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Pathophysiology of ALF Mechanisms of acute liver injury Direct hepatocyte damage Innate immune-mediated response Immune cells express receptors that are able to recognize type-specific molecular changes Pathogen-associated molecular patterns (PAMPs) in viral hepatitis Damage-associated molecular patterns (DAMPs) in toxin-mediated liver injury 9
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Pathophysiology of ALF Pattern of cytokines released depends on type-specific signal transduction pathways activated Affects the liver initially but eventually systemically Mechanisms of hepatocyte death in ALF Necrosis (e. g. acetaminophen) Apoptosis Apoptotic hepatic cell death Serum M30 antigen is a marker 10
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Clinical Findings in ALF History Date of onset of jaundice and encephalopathy Alcohol use Medication use (prescription and illicit or recreational) Herbal or traditional medicine use Family history of liver disease (Wilson disease) Exposure to risk factors for viral hepatitis (travel,
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  • Winter '17
  • acute liver failure, liver disease, liver biopsy, Wilson Disease

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