Download - Approach to bleeding Disorders
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BY
MOHANNAD IBN HOMAID
Approach to bleeding Disorders
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A few points
Content Structure
1st half 2nd half
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Overview
Why is it important ? Why is it so confusing ?
Basic Science Clinical manifestations Laboratory tests
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Basic Science Review
Blood is goldThe 2 arms of Heamostasis
Platelets Clotting Factors
Small Vessel Response To Injury
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Normal Response
Always Goes Through the following: Vascular Phase Platelet Phase Coagulation Phase Fibronlytic Phase
Pointless ? Or useful ?
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Vascular Phase
Not Very important for understandingVasoconstrictionTXA2 and Aspirin
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Platelet Phase
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Platelet Phase
Unfortunately Very important The following occurs:
Platelet Adhesion (vWF later) Platelet Release Reaction
ADP TXA2
Temporary Plug < < BLEEDING STOPS HERE Bleeding time
The Tile
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Coagulation Phase
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Coagulation Phase
VERY IMPORTANT and VERY CONFUSINGWhy is it Confusing ?
Not Tangible Coagulation Phase and 12 factors Cofactors Ca and PF3 Extrinsic vs intrinsic Vitamin K factors Anti-Thrombin 3 And last but not least….
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THE ROMAN NUMBERS
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Coagulation Cascade
What do you need to know ? Simple Steps : extrinsic vs intrinsic Content of both How to test them Where they are made ( liver ) Vitamin K AT-3
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CONFUSING
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THIS SLIDE HAS BEEN INTENTIONALLY LEFT BLANK
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Extrinsic System: 7Intrinsic System: 12-11-9-8Final Common Pathway :10-5-2-1Vitamin K : 2-7-9-10AT-3 : 12 -11-10-9PTT vs PT
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Coagulation Studies
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Fibrinolytic Phase
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Fibrinolytic Phase
Kinnnd of important but very easyTissue plasminogen ActivatorPlasminTest
Fibrin Degradation Products D-Dimer Assay
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Back to the clinical world
Presentation of platelet Defects Blood leaks out of vessels Skin and mucosal surfaces Prolonged bleeding ( temporary plug plug )
Presentation Deep Tissue Bleeding Late Rebleeding ( permanent plug Defect )
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Laboratory Test
Platlets Count Bleeding Time Aggregation Test
Clotting Factors PT and PTT Factor Assay
Fibrinolysis FDP D-Dimer
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Platelet Disorders
Quantitative vs QualitativeThrombocytopeniaImmune Thrombocytopenic PrupuraBernard Soulier SyndromeGlanzmanns ThrombastheniaThrombotic thrombocytopenic Purpura
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Thrombocytopenia
Pathology :Increase Destruction or decrease Productions > >
Clinical Features : depend on degreeLabs:Treatment:
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ITP
Pathology : Auto antibodies Agains PlatletsClinical Features:Labs:Treatment:
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Bernard Soulier Syndrome
Pathology :GP1B receptor Defiency Clinical Features:Labs:
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Glanzmann Thromboasthenia
Pathology :GPIIb-IIIa DefiencyClinical Features:Labs:Treatment:
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TTP
Pathology :UnkownClinical Features: Pentad : HUS + Fever
NeurologicalLabs:Treatment :Plasmapharesis
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Diorders of Coagulations
HemophiliaVon Willebrand Disease
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Hemophilia
Pathology :Factor 8 or 9Clinical Features:
Acute Hemoarthrosis Intracranial Bleeding Hematomas
Labs:Treatment:
Factor Replacement DDAVP
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Von willebrand Disease
Function of vWF Made in platelets and endothelium Adhesion of platelets to exposed Collagen Protection of Circulating Factor 8
Pathology Deficiency of vWF Secondary decrease in Factor 8
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Von Willebrand Disease
Pathology : MentionedClinical Features:Labs:Treatment:
1. DDAVP And factor concentrates
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DIC
Pathology :Inappropriate Activation of platelets and clotting Factors due to : Sepsis ( 50%) Obstetric Complications Malignancy Trauma
Clinical Features:Labs:Treatment: ICU and supportive = Treatment
of underlying Cause
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Questions