hemostasis in pathology
DESCRIPTION
referred from Robbins, Basic pathology, *8th edition.TRANSCRIPT
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What is normal hemostasis?Normal hemostasis- process by which bleeding
at any site arrested by the formation of a hemostatic plug.
1. Followed by removal of plug so that normal flow of blood through vessels is maintained.
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Components of hemostasisBlood vessels- vasoconstrictionPlateletsCoagulationFibrinolytic systemInhibitor of coagulation
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Blood vesselsEndothelial vessels activate
◦Coagulation cascade◦Fibrinolytic systems◦Protein C systems◦vWF
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Properties of blood vesselsProthrombotic prop.
◦vWF◦Tissue factor –factor 3 +
thromboplastin◦Fibrinolysis inhibitor- PAIs
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Antithrombotic prop.◦Antiplatelet effect- prostacyclins,
nitric oxide◦Anticoagulant effect –
thrombomodulin Thrombomodulin inactivates thrombin to
make it an anticoagulant!
◦Fibrinolysis properties- t-PA Clear fibrin deposits from endothelial
surfaces.
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Role of plateletsPlatelet adhere to exposed subendotheliat
collagenAdhered platelet undergo release reaction
resulting in formation of aggregation.
1. adhesion-vWF- glycoprotein Ib assoc.2. secretion/release- Ca2+ , ADP,
thromboxane A23.aggregation-glycoprotein 2b- 3a
receptors◦Conformational changes of GP2b-3a allows
platelet to bind fibrinogens.
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2 pathways of coagulationIntrinsicExtrinsic
*final common pathway=◦Prothrombin
thrombin
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Assessment of the pathwaysPT(prothrombin time)- extrinsic
pathway◦Factor 7, 10, 2, 5
PTT(partial thromboplastin time-intrinsic pathway◦Factor 12, 11, 9, 8, 10, 5, 2 +
fibrinogen
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Control of coagulationAntithrombin
◦protein C and S
Fibrinolytic cascade◦Plasminogen plasmin FSP
(fibrin split products)◦D-dimer is the most important FSP
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Summary of hemostasisPrimary hemostasis
◦BV constriction◦Platelet plug formation
Secondary hemostasis◦Activation of clotting cascade◦Deposition &stabilisation of fibrin
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Tertiary hemostasis◦Dissolution of fibrin clot◦Removal of fibrin plug
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Bleeding disordersVascular abnormalitiesPlatelet disordersCF (clotting factor) disordersDIC (disseminated intravascular
coagulation)
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Vascular abnormalities Infection
◦ Eg: meningococcemia,rickettsiosses, infective endocarditis
Drug reactionHereditary hemorrhagic telangiectesia
◦ Autosomal dominant inheritance
Cushing syndromeHeroch-scholein purpura
◦ Systemic hypersensitivity disease of unknown cause◦ Polyarthralgia and acute glomerulonephritis◦ Palpable purpuric rash, colicly abdomnal pain
◦ =treated with steroids
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ITP
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ITP (idipathic thrombocutopenic purpura)Autoimmune disorder
accelerated destruction of sensitized platelets by phagocytic cells in the RES.
*very2 important
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Clasification of ITPChildren / adult onsetAcute / chronicPrimary / secondary (idiopathic)
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Acute-children (post-infection)Chronic-adult (> female, 20-40 yrs.
Old)Autoimmune disordersAntiplatelet Ab (IgG)IgG coated platelets removed by
spleen> megakaryocytes in bone marrow
*blood picture !!! Very important.
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Characteristic of ITPSudden onset of bruising /
petechiaeCase history of infectious disease
◦Appear respiratory tract infection in about 3 weeks prior to onset of bleeding
Dangerous-intracerebellar hemorrhage
<20,000 platelet count.
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ITP bone marrow aspirate
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Additional infost-PA most important
plasminogen. plasminogen is activated by streptokinase.
To prevent excessive thrombi destruction, free plasminogen quickly bind to α2-antiplasmin.
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PAIsEndothelial cells regulate
anticoagulation balance by secreting PAIs. (plasminogen activation inhibitor)
PAI-block fibrinolysis, procoagulation efct.◦ increased by certain cytokines.◦ role in I.V thrombosis accompanying
severe inflammation.