1. Hemorrhagic Diathesis Causes: Increased fragility of vessels Platelet deficiency or dysfunction Derangement of coagulation

2. 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. 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

4. R/T THROMBOCYTOPENIA Decrease production Aplastic anemia Leukemias Megalobalstic anemia Decrease platelet survival Immune – mediated Non-immune – mechanical

5. Sequestration – seen in marked splenomegaly Dilutional – blood stored > 24hours has less viable platelets R/T THROMBOCYTOPENIA

6. 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

7. 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 )

9. Deposition of Ig fragments in Amyloidosis

13. 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

14. 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

15. 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

16. Plasmin Act. Proteolysis of clotting facotrs