logging in or signing up 3 PLATLETS BY DR QAZI aSGuest136595 Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 61 Category: Entertainment License: All Rights Reserved Like it (0) Dislike it (0) Added: June 03, 2012 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript PowerPoint Presentation: Platelets ( Thrombocytes ) Throm = clot BY DR QAZI IMTIAZ RASOOLOBJECTIVES: OBJECTIVES 1.Describe the structure and functions 2.Describe the thrombopoiesis 3. Discuss the role of platelet in coagulation PLATELETS=small plates: PLATELETS=small plates cytoplasmic fragments ,colorless, smallest of formed elements staining shows an blue- outer region and purple granular center Circular/oval, biconcave discs ,Non-nucleated, extensive invagination of cell membrane 2-5 m in diameter. Vol. 5.8 μ mm 3 2. in clusters , 250.000/ mm 3 life span is 7-10 days. 3.60-75% circulate , 30% and graveyard( spleen). 4. (~ 4,000 Platelets / Megakaryocyte ) Produce 200,000,000,000/dayThe cytoplasm: The cytoplasm contains ;- Contractile proteins : actin and myosin ( thromboasthenia ) which contract if activated skeleton of microtubules , peripheral microvesicles Glycogen granules utilized for energy production Lysosomes containing lysosomal granules hydrolytic enzymes. ER ,Golgi apparatus which store large quantities of Ca ++ ions. Mitochondria are capable of forming ATP and ADP.PowerPoint Presentation: 7. Enzyme system that synthesizes PG local, TxA2 , leukotrienes hormones those cause vascular and local tissue reactions. 8. 2 types of granules 1.Dense granules which contain ATP, ADP, serotonin and Ca ++ ,5 -HT,PL,TG,cholesterol 2.Specific ( α ) granules : contain fibrinogen, heparin antagonist, (PF 3+4) platelet derived growth factor (PDGF), 9.Lot of receptors Surface contains membrane bound receptors (GP Ib / IIb / IIIa ) mediate surface adhesion reactions, aggregation reactions interact with coagulation proteinsGenesis : Stem cell Developmental pathway Hemocytoblast Megakaryoblast Promegakaryocyte Megakaryocyte Platelets Genesis HEMOCYTOBLASTS (stem cells)is regulated by hormone thrombopoietin , -TPO synthesis is static and binds to the surface of megakaryocytes and platelets -Produced by liver -Negatively feedbck to regulates free TPO Megakaryocytes : gaint cell 35-160 μ m in the bone marrow Larger fragments shrinkand become platelets pseudopods provide amoeboid movement & phagocytosis PHSC+CSC+ STAG E 1 STAG E 2 STAG E 3Role of Platelets: Role of PlateletsRole of Platelets: Role of Platelets Damage to endothelium allows platelets to bind to exposed collagen von Willebrand factor increases bond by binding to both collagen & platelets Platelets stick to collagen & release ADP , serotonin , & thromboxane A 2 platelet release reactionPowerPoint Presentation: VON WILLEBRAND DISESEPowerPoint Presentation: Platelet Aggregation 1.. During activation, a receptor for fibrinogen becomes exposed on the platelet membrane. 2. Activated platelets release: Fibrinogen ADP/ATP vWF Seratonin Factor V Ca 2 + Factor VIII Platelet derived growth factor (PDGF) ~ promotes healing Platelet factor IV – prevents formation of active thrombin inhibitor from heparin and anti-thrombin III. a -granules dense core granulesPowerPoint Presentation: Activated platelets induces large - morphological changes -are essential because several of the cascade reactions take place on the surface of these platelet( membrane lipids rearrange) phosphatidyl serine which is usually on the inner membrane of the platelet , flips out to outer membrane where binding prothrombin . Activated platelets unactivated fully activated phosphatidyl serinePowerPoint Presentation: Platelet Plug Formation Note;-Platelets not involved in clotting are kept inactive by NO and Prostacyclin scereted by endothelial cells Functions: Functions Coagulation Anticoagulation Thrombolysis Inflammation Wound Healing secrete clotting factors, growth factors for endothelial repair, and vasoconstrictors in broken vessels 2. Form temporary platelet plugs 3. Dissolve old blood clots 4. Phagocytize bacteria,viruses , carbon particles 5. Attract WBCs to sites of inflammationPowerPoint Presentation: Thrombocytosis : It is the increase in the number of platelets, this occurs physiologically in pregnancy and after hemorrhage. Thrombocytopenia : It is the decrease in the number of platelets, this occurs after aplastic anemia, pernicious anemia, and during menstruation. Thromboathenia : It is the decrease in the functions of platelets. How low is too low? 150,000 - 50,000: no symptoms 50,000 - 20,000: first symptoms 20,000-10,000: potentially life-threatening <10,000: risk for spontaneous intracranial hemorrhagePowerPoint Presentation: Physical Signs Bleeding Easy bruising Petechiae Bruising with mild trauma Bruising without trauma Petechiae - a Ecchymoses - b Hematoma - c Epistaxis - nosebleed History of recurrence Gingival bleeding Hematuria , hemoptysis , hematemesis Relatively uncommon presenting features MenorrhagiaLAB TESTS IN DISORDERS OF PRIMARY HEMOSTASIS: LAB TESTS IN DISORDERS OF PRIMARY HEMOSTASIS Platlet count PT PTT Bleeding time Vascular disorder Normal Normal Normal Normal or abnormal Thrombocytopenia Decreased Normal Normal Abnormal Platlet Dysfunction Usually Normal Normal Normal Normal or AbnormalPLATELET DISORDERS: PLATELET DISORDERS Quantitative Thrombocytopenia Thrombocytosis Qualitative Morphologic abnormalities Macrothrombocytes Microthrombocytes Hypogranular or agranular plateletsTHROMBOCYTOPENIA: THROMBOCYTOPENIA result from Abnormal platelet distribution Deficient platelet production Increased platelet destruction Platelet dysfunction Platelet satellitism: Platelet satellitism - Platelet ribbon platelets to white cells Bernard Soulier ( Giant Platelets)Thrombocytosis Too many platelets: Thrombocytosis Too many platelets Primary - i.e. myeloproliferative syndromes Diseases include Essential Thrombocythemia , Polycythemia Vera These platelets are both hyper- and hypo-functional May lead to thrombosis and/or bleeding Secondary - i.e. reactive Causes include inflammation, infection, bleeding, iron deficiency Treat the underlying cause. Usually does not lead to thrombosisDifferential Diagonosis: Differential Diagonosis 1. Pseudothrombocytopenia 2 . ↓ Production- suggested by: other cytopenias normal sized/small platelets suggest a reduced bone marrow response to need 3. ↑ Destruction- suggested by: microangiopathic blood picture (fragmented RBCs, high LDH) Large platelets on smear Associated autoimmune diseaseAspirin inhibits the cyclooxygenase (COX) in the eicosanoid pathways that generate PG and TXA2 : Aspirin inhibits the cyclooxygenase ( COX) in the eicosanoid pathways that generate PG and TXA2 1. TXA2 , produced by the platelets,for aggregation, aspirin reduces both aggregation and coagulation. 2. Importantly, low doses of aspirin cause a steady-state ↓ in platelet COX but not endothelial-cell COX, 3. so the formation of prostacyclin —the PG that opposes aggregation—is not impaired. FIBRINOGEN BLOCKERS: FIBRINOGEN BLOCKERS contrast to aspirin,, the oral anticoagulants, and heparin, which prevent clotting,5 TH drug— plasminogen activators— dissolves a clot after it is formed. 2. Use of such drugs is termed thrombolytic therapy 3 . I.V. of recombinant t-PA or a proteolytic drug called streptokinase within 3-6 hours after M.I . significantly reduces myocardial damage and mortality. 4. Recombinant t-PA has also been effective in reducing brain damage following a stroke caused by blood-vessel occlusion“NO ALCOHOLIC WORTH HIS SALT HAS NORMAL PLATELETS” : “NO ALCOHOLIC WORTH HIS SALT HAS NORMAL PLATELETS” You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.