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    Platelets

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    nirilib
    Platelets are non-nucleated cell fragments that form clots to stop bleeding. They are produced from megakaryocytes in the bone marrow and released into the bloodstream. Platelets aggregate at sites of injury through activation by collagen, thrombin, ADP and other factors. When activated, they secrete contents of granules that promote coagulation and release vasoactive substances that support hemostasis. Testing of platelet count, bleeding time and aggregation assess platelet function disorders.

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    Platelets

    Uploaded by

    nirilib
    918 views23 pages
    Platelets are non-nucleated cell fragments that form clots to stop bleeding. They are produced from megakaryocytes in the bone marrow and released into the bloodstream. Platelets aggregate at sites of injury through activation by collagen, thrombin, ADP and other factors. When activated, they secrete contents of granules that promote coagulation and release vasoactive substances that support hemostasis. Testing of platelet count, bleeding time and aggregation assess platelet function disorders.

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    Platelets are non-nucleated cell fragments that form clots to stop bleeding. They are produced from megakaryocytes in the bone marrow and released into the bloodstream. Platelets aggregate at sites of injury through activation by collagen, thrombin, ADP and other factors. When activated, they secrete contents of granules that promote coagulation and release vasoactive substances that support hemostasis. Testing of platelet count, bleeding time and aggregation assess platelet function disorders.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    918 views23 pages

    Platelets

    Uploaded by

    nirilib
    Platelets are non-nucleated cell fragments that form clots to stop bleeding. They are produced from megakaryocytes in the bone marrow and released into the bloodstream. Platelets aggregate at sites of injury through activation by collagen, thrombin, ADP and other factors. When activated, they secrete contents of granules that promote coagulation and release vasoactive substances that support hemostasis. Testing of platelet count, bleeding time and aggregation assess platelet function disorders.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    of 23

    Platelets

    Dr. Niranjan Murthy H L Asst Prof of Physiology ESIC-MC & PGIMSR, Bangalore

    Small, granulated bodies that aggregate at the site of injury Non-nucleated Half-life of 8-12 days Count- 1.5 to 4 lakhs/mm of blood Synthesis- from megakaryoblasts in marrow

    Thrombopoiesis
    Pluripotent stem cell Committed stem cell
    GM-CSF Thrombopoietin

    Megakaryoblast

    Megakaryocyte
    platelets

    Megakaryocytes
    Giant cells- 35-160m in diameter Multinucleated Forms 1000 platelets Platelets formed by pinching off of cytoplasm Fragmentation is thought to occur in pulmonary capillaries

    Thrombopoietin
    Produced in kidney and liver
    Cause megakaryocyte maturation Bound to platelets

    Platelet morphology
    Non-nucleated, Colorless disc, 2-4 m in diameter Cell membrane: 20 nm in thickness Microtubules with invaginated cell membrane form an intricate canalicular system Phospholipids important in initiation of coagulation Receptors for ADP, vWF, collagen, fibrinogen, thrombin

    Glycocalyx: -net negative charges due to sialic acid -Minimizes adhesion - rich in agonist receptors Surface connected canalicular system: -Internal reservoir of membrane -Storage reservoir of membrane glycoproteins -Route of granule release on activation Cytoskeleton: -Includes membrane skeleton, actin & intermediate filaments and microtubules -Change of shape -Extrusion of granules

    Structure of platelet

    Cytoplasm: contains actin, myosin, glycogen, lysosomes, golgi apparatus, endoplasmic reticulum, few mitochondria and granules Dense granules- contain non-proteins like ATP, ADP, Serotonin, Ca2+ Alpha granules- contain proteins like PDGF, vWF, factor V, fibrinogen, PF4 ADP- plays a role in platelet aggregation vWF- platelet adhesion & regulate factor VIII levels

    Functions of platelets
    1. 2. 3. 4. 5. Hemostasis Coagulation of blood Clot retraction Phagocytosis Storage and transport- serotonin & histamine

    Platelet adhesivenessto exposed collagen Adhesive ligands: vWF, collagen, Fibrinogen

    gpIb/V/IX interact with subendothelial vWF

    Deceleration of platelets

    Collagen and 2 interact

    Platelet activation- by binding of vWF & collagen and thrombin releases granules. Platelet secretion- occurs in association with activation; ADP, vWF, Fibrinogen & Ca2+ Platelet aggregation- by ADP, Ca2+, thrombin, fibrinogen & vWF

    Platelet activators
    1. vWF: multimeric glycoprotein; act via gp Ib 2. Collagen: activation via gp IV interaction and adhesion via 2 3. Thrombin: act via PAR (protease activated receptors) 4. ADP: act via purinergic receptors; present in dense granules; Clopidogrel inhibits ADP associated aggregation

    5. Epinephrine: acts via 2 receptors and TXA2 ; stimulates secretion and aggregation 6. Thromboxane A2: Arachidonic acid derivative via cyclo-oxygenase pathway; vasoconstrictor; Aspirin

    Inhibitors of Platelet activation


    1. Generation of negative regulating molecules a. platelets- cAMP b. Endothelium- PGI2, NO, Heparin 2. Endothelial barrier 3. Generation of ecto-ADPase by endothelial cells which neutralize ADP 4. Tendency of blood flow to wash away thrombin 5. Brief half-life of TXA2 (30sec)

    Thrombocytopenia: Bone marrow depression Hypersplenism Viral infections Idiopathic Thrombocytosis: Splenectomy Epinephrine administration

    Purpura
    Def: Small punctate bleeding below skin and mucosa caused due to capillary defects &/or platelet defects Types: i) Non-thrombocytopenic purpura ii) Idiopathic thrombocytopenic purpura iii) Thrombasthenia

    Petechiae

    Tests for bleeding disorders


    1. Platelet count 2. Bleeding time i) Duke method 1-5mins ii) Ivy method 5-11mins 3. Capillary fragility test <10 petechiae 4. Platelet aggregation test 5. Platelet adhesiveness test 6. Clot retraction time- begins within 30secs,50% in 1hr, 100% within 18-24hrs

    Hemostasis
    Injury to vessel Constriction of injured vessel- vasospasm Platelet adhesion Platelet activation and aggregation Temporary platelet plug formation Activation of clotting factors Fibrin network True clot

    Clot retraction: Due to activation of acto-myosin complex Reduces to 40% of size in 5-30 mins Minimizes size of clot Brings the cut ends of vessel nearer

    Cycloxygenase inhibitors- Aspirin Purine receptor inhibitors- Clopidogrel Role in prevention of coronary thrombosis

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