Bleeding
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Bleeding

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Bleeding Bleeding Presentation Transcript

  • Hemorrhagic Diathesis
    Causes:
    Increased fragility of vessels
    Platelet deficiency or dysfunction
    Derangement of coagulation
  • Vessel Wall Abnormalities
    Common but bleeding is LESS Serious
    Normal Coagulation test
    1. Microbial damage to Microvasculature or DIC
    2. Scurvy – Impaired formation of collagen needed for vessel wall support
  • 3. Drugs – immune complex deposits in vessel wall
    4. Hemoch-Scheonleinpurpura – unknown systemic hypersensitivity disease involve vessels throughout the body & glomerularmesangium
    5. Amyloid Infiltration of blood vessels – weakens the wall
    Vessel Wall Abnormalities
  • R/T THROMBOCYTOPENIA
    Decrease production
    Aplastic anemia
    Leukemias
    Megalobalstic anemia
    Decrease platelet survival
    Immune – mediated
    Non-immune – mechanical
  • Sequestration – seen in marked splenomegaly
    Dilutional – blood stored > 24hours has less viable platelets
    R/T THROMBOCYTOPENIA
  • Idiopathic Immune Thrombocytopenic Purpura ( Autoimmune )
    1. Acute
    Self-limited Hgicdisease
    Resolve w/in 6mos.
    Children after Viral infxn 2 week later  Sudden petechiae, purpura
    Risk for cerebral bleed
    Severe cases Tx w/ corticosteroids
  • 2. Chronic
    Adults women < 40y/o
    Associated with
    Collagen Vascular Disease
    CLL
    HIV
    Repeated episodes of Bleeding
    Tx Steroids. IgG, Splenectomy in severe cases
    Idiopathic Immune Thrombocytopenic Purpura ( Autoimmune )
  • Deposition of Ig fragments in Amyloidosis
  • Thrombotic Microangipathies
    I. Thrombotic Thrombocytopenic Purpura
    1. Fever
    2. Thrombocytopenia
    3. Microangioapthic hemolytic anemia
    4. Transient Neurological damage
    5. Renal Failure
    Deficiency of ADAMTS 13 enzyme
    Results to accumulation of VHMW vWF promote widesopread platelet Microaggregation
  • II. Hemolytic –Uremic Syndrome
    1. MicroangiopathicHemolytic anemia
    2. Thrombocytopenia
    3. Prominence of renal failure
    4. No Neurological damage
    Hx of Enteric infection E. coli
    Release of Shiga –like toxin  Absorbed in GIT  Binds and Damage endothelial cells in Glomerulus & other sites  Platelet Activation & Aggregation
    Thrombotic Microangipathies
  • Widespread formation of hyaline thrombi in microcircualtion
    Platelet consumption & Intravascular thrombi
    Microangiopathic hemolytic anemia
    Multiple Organ failure
    Activation of coagualtion cascades is NOT OF PRIMARY IMPORTANCE
    PT/PTT – usually Normal
    Thrombotic Microangipathies
  • Plasmin Act.
    Proteolysis of clotting facotrs