Hemostasis and Disorders

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Hemostasis and Disorders
2013-01-29 01:56:25

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  1. Coagulation Cascade
  2. Extrinsic Pathway
    • "lucky pathway"
    • -only have to remember one factor

    -factor VII ("lucky number 7")

    -PT Pathway
  3. Intrinsic Pathway
    "unlucky pathway"

    • Need to remember multiple numbers
    • XII, XI, IX, VIII

    -PTT Pathway
  4. Common Pathway
    • "Small Bills:
    • FI (Fibrinogen)
    • FII (Prothrombin)
    • FV (interacts with FX: FII --> FIIa)
    • FX

    Deficiency: increase in PT and PTT
  5. Vitamin K
    -Reduced in the LV by epoxide reductase

    -Needed to activated factors: II, VII, IX, X and Protein C and S

    *** Warfarin inhibits epoxide reductase
  6. Anticoagulation
    -Protein C: inactivates V and VIII

    -Protein S: helps protein C inactivate V and VIII

    • -ATIII (antithrombin III): inhibitis activation of II, VII, IX, X, XI, XII
    • -ATIII is activated by heparin

    -tPA: used to activate plasminogen to plasmin --> cleavage of fibrin mesh
  7. Platelet Plug Formation
    • 1. Injury:
    • -(endothelial damage): vWF binds exposed collagen

    • 2. Adhesion:
    • -platelet GP11b binds vWF
    • -platelets release ADP and Ca (necessary for coagulation cascade)

    • 3. Activation:
    • -ADP induces GPIIb/IIIa

    • 4. Aggregation:
    • -Fibrinogen binds GpIIb/IIIa --> links platelets

    Temporary Platelet plug

    • -TXA2 (platelets)
    • -decreased blood flow

    • -PGI2 and NO (endothelial cells)
    • -increased blood flow
  8. Erythrocyte Sedimentation Rate
    -acute phase reactants in plasma (eg: fibrinogen) cause RBC aggregation --> increased ESR

    Increased ESR: infections, autoimmunity, malignancy, GI disease, pregnancy

    Decreased ESR: polycythemia, SCA, CHF, microcytosis, hypofibrinogenemia
  9. Hemostasis
    • 1. Primary
    • -weak platelet plug
    • -platelets interacting with vessel wall

    • 2. Secondary
    • -stabilized platelet plug
    • -coagulation cascade
  10. Primary Hemostasis
    1. Transient vasoconstriction (neural stim, endothelin release)

    • 2. Platelet adhesion (vWF binds GPIb)
    •      ***wVW from Weibel-Palade bodies of endothelium and aplha granules of plt

    • 3. Platelet degranulation (change in shape and degranulation)
    •      -ADP (promotes GPIIb/IIIa)
    •      -TXA2 (plt aggregation)

    4. Platelet aggregation (fibrinogen links plts by GpIIb/IIIa)
  11. Disorders of Primary Hemostasis
    • 1. Immune Thrombocytopenia Purpura (ITP)
    • 2. Microangiopathic Hemolytic Anemia (TTP, HUS)
    • 3. Bernard-Soulier Syndrome
    • 4. Glanzmann thrombasthenia
    • 5. Aspirin
    • 6. Uremia

    -quantitative and qualitative abnormalities of platelets

    -mucosal and skin bleeding: epistaxis, hemoptysis, GI bleeding, hematuria, menorrhage

    -intracranial hemorrhage with severe thrombocytopenia

    • Labs:
    • -increased bleeding time
    • -possible decreased platelet count

    • Symptoms:
    • -petechiae, ecchymoses, purpura, easy bruising

    ***petechiae not usually seen with qualitative disorders
  12. Immune Thrombocytopenia Purpura (ITP)
    FA: "Idiopathic Thrombocytopenia Purpura

    Anti-GpIIb/IIIa antibodes produced by plasma cells in spleen --> splenic macrophage consumption of platelets

    • Acute: children
    • -after viral infection or vaccination
    • -self limiting

    • Chronic: adults
    • -women of child-bearing age
    • -primary
    • -secondary (ie: SLE)
    • ***IgG can cross the placenta

    • Labs:
    • -decreased platelet count
    • -increased megakaryocytes on BM bx

    • Treatment:
    • -corticosteroids: children respond well, adults relapse
    • -IVIg
    • -Splenetctomy
  13. Microangiopathic Hemolytic Anemia