Thrombosis

Thrombosis

• 1.
  THROMBOSIS Presented by Dr. YOGITACHANDRAKAR B.A.M.S., M.D. Assist. Professor Department of Rog Nidan Avum Vikriti Vigyan
• 2.
  DEFINITION  Formation ofsolid mass by the constituents of blood, its known as thrombus and this process is called Thrombosis  Intra Vascular coagulation  Localized 4/22/2020 2 DR.YOGITACHANDRAKAR
• 3.
  HAEMATOMA Extra vascular Coagulation Outerside of capillary Peripheral vascular coagulation 4/22/2020 3 DR.YOGITACHANDRAKAR
• 4.
  HARMFUL EFFECTS Ischemic injury(Blockage of coronary artery) Thromboembolism (Tortoucity and Zig zag like structure of vein in circulation) 4/22/2020 4 DR.YOGITACHANDRAKAR
• 5.
  PATHOPHYSIOLOGY  In normalfunctioning endothelial wall is also act as Antithrombin  Antithrombin process is done by clotting factors  Any changes and Alteration of endothelial wall act as thrombogenesis  Initially homeostasis then followed by formation of mass of thrombas 4/22/2020 5 DR.YOGITACHANDRAKAR
• 6.
  PREDISPOSING FACTOR  Injuryto the Endothelial wall  Alteration in Blood flow – Venous thrombi more  Turbulence of blood flow – Arterial thrombi more  Hypercoagulity of Blood 4/22/2020 6 DR.YOGITACHANDRAKAR
• 7.
  PROCESS OF THROMBOSIS 1.Role of Blood vessels wall 2. Role of platelets 3. Role of clotting factors 4. Role of Hypercoagulity of blood 5. Alteration in the blood flow 4/22/2020 7 DR.YOGITACHANDRAKAR
• 8.
  ROLE OF BLOODVESSELS WALL  Endothelial wall play dual role – Antithrombic function and Thrombogenic factor 1. Antithrombic function – a. Antithrombin – III (Heparin like substance) b. Thrombomoduling c. Inhibitors of platelets aggregation (ADPase, Prostacyclin, Prostaglandin) and d. Tissue Plasminogen (Fibrinolytic activity) 4/22/2020 8 DR.YOGITACHANDRAKAR
• 9.
  2. Thrombogenic factor a.Thromboplastin (Initiator of Thrombin) b. Von willbrand factor (Adherence of platelets on Subendothelial wall) c. Platelets activating factor d. Inhibitor of Plasminogen This above two function are responsible for injury to the endothelial wall, further it performs Haemostasis then Thrombogenesis (Thrombus) 4/22/2020 9 DR.YOGITACHANDRAKAR
• 10.
  ROLE OF PLATELETS Platelet Adhesion  Platelet releasing action  Platelet aggregation Injury – Subendothelial wall ruptured and endothelial wall destroy – Von willbrand factor attract the platelet – Non activated platelets flow in our axial flow then after it sticking with ER – Activation of platelet – canaliculi dilated and formation of pseudopode granules - 4/22/2020 10 DR.YOGITACHANDRAKAR
• 11.
  Two type ofgranules are there – Alpha and dense granules Alpha release fibrinogen, PDGF(platelet derived growth factor), Fibrinoactin, catanoic protein Dense release ADP, Ca++ ion, Histamine, Serotonin, Epinephrine After the releasing action additional platelets adhere to injured area, it is called secondary adherence of platelets. Then after it attracts the other clotting factor, fibrinogen converted into fibrin, and clot formed 4/22/2020 11 DR.YOGITACHANDRAKAR
• 12.
  ROLE OF CLOTTINGFACTORS Coagulation mechanism is the conversion of the plasma fibrinogen into solid mass of fibrin. The coagulation system is involved in both haemostatic process and thrombus formation. a. Protease inhibitors b. Fibrinolytic system Plasmin acts on fibrin to destroy the clot and produces fibrin split products (FSP) 4/22/2020 12 DR.YOGITACHANDRAKAR
• 13.
  ROLE OF HYPERCOAGULITYOF BLOOD Etiology – Genetic cause – Deficiency of protein and clotting factor Acquired cause – Extensive burn Advance stage of cancer Nephritic syndrome Cigarette smoking Oral contraceptive pills Obesity Pupeurium 4/22/2020 13 DR.YOGITACHANDRAKAR
• 14.
   Increases Clottingfactor (I,II,V,VI,VII,X)  Increases platelet count and their adherence  Decreases Antithrombin (III) – coagulation inhibitor  Decreases Fibrin split plug 4/22/2020 14 DR.YOGITACHANDRAKAR
• 15.
  ALTERATION IN THEBLOOD FLOW  Turbulence of blood flow  Stasis / slowing of blood flow Both condition affect and disturb the normal axial blood flow. then after margination of platelets and attached to wall and releasing action starts and clot formed. 4/22/2020 15 DR.YOGITACHANDRAKAR
• 16.
  MORPHOLOGY Grossly  Venous thrombi– Red, Occlusive  Arterial thrombi – White, Mural  Line of Zahn – mixed line thrombi  Red venous thrombi are soft gelatinous  White arterial thrombi are pale and firm 4/22/2020 16 DR.YOGITACHANDRAKAR
• 17.
  Microscopically – 1.Composition ofthrombus depending upon the rate of blood flow Rapidly flow – Arterial flow Slowness of flow – Venous flow 2. Line of Zahn Arterial - Composition of platelets and Ca++ ion Venous - Composition of RBCs and platelets 4/22/2020 17 DR.YOGITACHANDRAKAR
• 18.
  CLINICAL EFFECTS  Cardiacthrombi – sudden death  Arterial thrombi – Hypoxia, ischemia, infarction, Necrosis, gangrene  Venous thrombi – Odema, thromboembolism, Skin ulcer, poor wound healing  Capillary thrombi – DIC (Disseminated intravascular coagulation) 4/22/2020 18 DR.YOGITACHANDRAKAR
• 19.
  FATE OF THROMBOSIS Resolution – tissue plasminogen converted into plasmin and clot formed  Organization – phagocytic activity starts then granulation tissue formation  Propagation – increase the size of thrombi due to Ca++ and blocked the lumen completely  Thromboembolism – infected and friable thrombi may get detached from the vessel wall and goes to circulation and produce ill effects 4/22/2020 19 DR.YOGITACHANDRAKAR