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    KC Ignacio
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    This document outlines the pathophysiology of hepatic encephalopathy secondary to alcoholic liver cirrhosis. It describes how liver cirrhosis and portosystemic shunting can increase blood ammonia levels, allowing toxic substances to enter the brain. Ammonia is absorbed by astrocytes in the brain, increasing glutamine and osmotic pressure, leading to brain edema, increased intracranial pressure, and altered brain function manifesting as hepatic encephalopathy. Predisposing factors include age over 40, male sex, alcoholism, and exposure to toxins. Precipitating factors are renal failure, GI bleeding, infection, constipation, and drugs.

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    This document outlines the pathophysiology of hepatic encephalopathy secondary to alcoholic liver cirrhosis. It describes how liver cirrhosis and portosystemic shunting can increase blood ammonia levels, allowing toxic substances to enter the brain. Ammonia is absorbed by astrocytes in the brain, increasing glutamine and osmotic pressure, leading to brain edema, increased intracranial pressure, and altered brain function manifesting as hepatic encephalopathy. Predisposing factors include age over 40, male sex, alcoholism, and exposure to toxins. Precipitating factors are renal failure, GI bleeding, infection, constipation, and drugs.

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    65 views1 page

    Pathophysiology

    Uploaded by

    KC Ignacio
    This document outlines the pathophysiology of hepatic encephalopathy secondary to alcoholic liver cirrhosis. It describes how liver cirrhosis and portosystemic shunting can increase blood ammonia levels, allowing toxic substances to enter the brain. Ammonia is absorbed by astrocytes in the brain, increasing glutamine and osmotic pressure, leading to brain edema, increased intracranial pressure, and altered brain function manifesting as hepatic encephalopathy. Predisposing factors include age over 40, male sex, alcoholism, and exposure to toxins. Precipitating factors are renal failure, GI bleeding, infection, constipation, and drugs.

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    of 1

    PATHOPHYSIOLOGY OF HEPATIC ENCEPHALOPATHY

    SECONDARY TO ALCOHOLIC LIVER CIRRHOSIS


    Predisposing Factors

    Precipitating Factors

    Age (above 40)


    Sex (male)

    Alcoholism
    Exposure to industrial toxins
    Long term used of
    drugs/medication

    Liver Cirrhosis

    Inflammation, bacterial translocation, and vasoactive mediators

    Increase pressure in
    the portal veins
    Splanchnic and
    peripheral vasodilation

    Portosystemic Shunting

    Hepatocyte
    Dysfunction

    Toxic substances enters


    systemic circulation

    Blood NH3
    levels

    permeability of
    BBB

    NH3 crossess BBB, absorbed and metabolized by Astrocytes


    levels of glutamine

    osmotic pressure leading to Brain


    edema & ICP

    activity of inhibitory GABA system


    Energy supply to other Brain cells is
    depleted/decreased

    Precipitating Factors
    Renal Failure, GI
    Bleeding, Infection,
    constipation, drugs,
    Diuretic therapy
    Signs & Symptoms:
    Jaundice
    Edema
    Mental Confusion
    Sleep disturbances
    Drowsiness
    Aggressive

    Altered Brain Function


    HEPATIC ENCEPHALOPATHY

    Management
    Independent

    Complication:
    Sepsis

    Watch for Ammonia


    Level
    Reorient the
    patient regarding
    time and place
    Diet
    Dependent
    Lactulose
    ( Duphalac)
    Metronidazole
    (Euromet)
    Cefepime (Zepim)

    Piperacillin Tazobactam
    (Vigocid)

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