Liver Disease and Vitamin K Deficiency
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Questions and Answers

What post-translational modification is crucial for converting PIVKA factors into their biologically active forms?

  • Hydroxylation of proline residues
  • Methylation of lysine residues
  • Carboxylation of glutamic acid residues (correct)
  • Glycosylation of serine residues

    • What is the primary function of gamma-carboxylated glutamic acid residues in vitamin K-dependent proteins?

  • Facilitating protein folding through disulfide bond formation
  • Promoting protein degradation via ubiquitinylation
  • Binding calcium ions, leading to a conformational change and phospholipid binding (correct)
  • Enhancing enzymatic activity by binding to substrates

    • How does Warfarin induce a functional vitamin K deficiency?

  • By directly inhibiting the carboxylation of glutamic acid residues
  • By chelating calcium ions, preventing their binding to clotting factors
  • By interfering with the action of vitamin K epoxide reductase (VKORC-1) (correct)
  • By promoting the degradation of vitamin K-dependent clotting factors

    • Which of the following laboratory findings is typically associated with vitamin K deficiency?

    <p>Prolonged prothrombin time (PT) and activated partial thromboplastin time (APTT) (B)</p> Signup and view all the answers

    What is the recommended initial intravenous dose of vitamin K for treating active bleeding or prior to liver biopsy in a patient with vitamin K deficiency?

    <p>10 mg (A)</p> Signup and view all the answers

    Which of the following is a direct consequence of biliary obstruction in liver disease?

    <p>Impaired absorption of vitamin K (A)</p> Signup and view all the answers

    In severe hepatocellular disease, what changes are MOST likely observed in coagulation factors?

    <p>Reduced levels of factor V and fibrinogen, alongside a deficiency of factors II, VII, IX, and X. (A)</p> Signup and view all the answers

    What is dysfibrinogenemia, as it relates to liver disease?

    <p>A functional abnormality of fibrinogen. (C)</p> Signup and view all the answers

    How does decreased thrombopoietin production from the liver contribute to hemostatic abnormalities?

    <p>It results in thrombocytopenia. (C)</p> Signup and view all the answers

    Why does hypersplenism, associated with portal hypertension, frequently result in thrombocytopenia?

    <p>The spleen sequesters and destroys platelets in large quantities. (B)</p> Signup and view all the answers

    What is the MOST likely mechanism by which damaged liver cells can trigger disseminated intravascular coagulation (DIC)?

    <p>Release of thromboplastins from damaged liver cells. (B)</p> Signup and view all the answers

    How does Warfarin induce vitamin K deficiency?

    <p>By acting as a vitamin K antagonist. (D)</p> Signup and view all the answers

    What are the MOST common causes of vitamin K deficiency in adults and children?

    <p>Inadequate diet, malabsorption, or inhibition by drugs like warfarin. (A)</p> Signup and view all the answers

    Flashcards

    PIVKA Factors

    Prothrombin-induced vitamin K absence factors that require carboxylation for activation.

    Gamma-carboxylation

    Modification of glutamic acid residues that allows binding of calcium ions in proteins.

    Vitamin K epoxide

    An oxidized form of vitamin K involved in the carboxylation process.

    Vitamin K deficiency

    A condition often diagnosed by prolonged PT and APTT due to low levels of factors II, VII, IX, and X.

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    Prothrombin complex concentrate

    A treatment for rapid correction of bleeding due to vitamin K deficiency.

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    Liver Disease

    A condition that impairs liver function leading to multiple hemostatic abnormalities.

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    Biliary Obstruction

    Blockage of bile ducts causing impaired vitamin K absorption and decreased clotting factors.

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    Thrombocytopenia

    A deficiency of platelets in the blood, often seen in liver disease due to decreased thrombopoietin and hypersplenism.

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    Dysfibrinogenemia

    Functional abnormalities of fibrinogen found in many patients with liver disease, affecting blood clotting.

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    PIVKA

    Proteins formed in the absence of vitamin K, showing as normal levels but non-functional clotting proteins.

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    Malabsorption

    A condition where the body cannot absorb nutrients properly, leading to vitamin K deficiency among others.

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    Warfarin

    A medication that acts as a vitamin K antagonist, leading to reduced activity of several clotting factors.

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    Study Notes

    Liver Disease and Vitamin K Deficiency

    • Liver disease contributes to multiple haemostatic abnormalities
    • Biliary obstruction impairs vitamin K absorption, decreasing the synthesis of factors II, VII, IX, and X by liver cells.
    • Severe hepatocellular disease additionally reduces levels of factor V and fibrinogen, and increases plasminogen activator.
    • Functional abnormality of fibrinogen (dysfibrinogenaemia) is common in liver disease patients.
    • Decreased thrombopoietin production from the liver leads to thrombocytopenia.
    • Hypersplenism associated with portal hypertension frequently causes thrombocytopenia.
    • Disseminated intravascular coagulation (DIC) might be linked to thromboplastin release from damaged liver cells and reduced antithrombin, protein C, and a2-antiplasmin levels.
    • Impaired removal of activated clotting factors and increased fibrinolytic activity also contribute to the prothrombotic state often seen in liver disease.

    Vitamin K

    • Vitamin K is fat-soluble and obtained from green vegetables and gut bacteria.
    • Newborn vitamin K deficiency may arise due to liver immaturity, lack of gut bacteria synthesis, and low breast milk levels.
    • Children and adults may develop vitamin K deficiency due to poor diet, malabsorption, or drug inhibition (e.g., warfarin).
    • Warfarin decreases the functional activity of factors II, VII, IX, X, and proteins C and S, though immunological tests may show normal levels.
    • Non-functional proteins formed in vitamin K absence are called PIVKA proteins.
    • Vitamin K-dependent protein activation involves carboxylation of glutamic acid residues.
    • Gamma-carboxylated glutamic acid binds calcium ions, changing the shape of vitamin K-dependent proteins.
    • This exposes hydrophobic regions for phospholipid binding.
    • Vitamin K is cycled back to its reduced form via VKORC-1 reductase.
    • Warfarin inhibits vitamin K epoxide reductase, causing dysfunction.

    Vitamin K Deficiency in Children or Adults

    • Vitamin K deficiency, often resulting from obstructive jaundice, pancreatic disease, or small bowel disease, can cause bleeding disorders.
    • Diagnosis is confirmed by prolonged prothrombin time (PT) and activated partial thromboplastin time (APTT).
    • Low plasma levels of factors II, VII, IX, and X are also observed.

    Treatment

    • Prophylaxis: 5 mg of vitamin K orally daily.
    • Active bleeding or pre-liver biopsy: 10 mg vitamin K slowly intravenously.
    • Correction typically occurs within 6 hours.
    • Repeat dose may be needed over the following 2 days.
    • Rapid correction is possible through prothrombin complex concentrate infusion.

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    Liver Disease and Vitamin K Deficiency PDF

    Description

    This quiz covers the relationship between liver disease and vitamin K deficiency, focusing on the impact on hemostasis and various clotting factors. It explores how liver dysfunction can lead to significant hematological abnormalities, such as thrombocytopenia and dysfibrinogenemia, and the roles of vitamin K in this context.

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