ECC2- Hemostatic Disorders

  1. What are the basic steps of hemostasis?
    • 1. Primary hemostasis- platelet plug
    • 2. Secondary hemostasis- fibrin mesh
    • 3. Fibrinolysis- removal of the clot
    • 4. Neoangiogenesis- formation of a new vessel
  2. Describe how platelet adhesion occurs.
    • vonWillibrand Factor released from endothelial cells and binds to collagen in the subendothelial matrix
    • vWF binds to platelet receptors, causing them to adhere to the vessel wall
  3. For platelet activation to occur, they must undergo _____________; factors involved in this process include... (5)
    conformational changes; Thrombin, ADP, collagen, thromboxane A2, platelet-activation factor
  4. After platelet activation, ___________ occurs to release __________.
    platelet degranulation; internal granules ("sticky glove" analogy)
  5. __________ is the most potent platelet activator.
    Thrombin
  6. Describe the fibrinolysis step of hemostasis.
    • breakdown of mature clot that starts as soon as the clot forms
    • results in the formation of FDPs/ D-Dimers
  7. What drives fibrinolysis?
    plasminogen is activated by tissue plasminogen activator (tPA)--> plasmin
  8. *********At what stage of the coag cascade does Protein C prevent coagulation?
    Protein C blocks Factors VIII and V
  9. ********At what stage of the coag cascade does TFPI prevent coagulation?
    prevents tissue factor (TF) from being activated to move to factor VII
  10. *******(At what stage of the coag cascade does antithrombin + heparin prevent coagulation?
    antagonizes factors X and II
  11. Thrombosis is treated using a(n) ___________.
    fibrinolytic agent ("clot buster")
  12. Hyperfibrinolysis is ______________ and must be address with a(n) _____________.
    too much clot break down; antifibrinolytic agent ("clot stabilizer")
  13. What are clinical signs of primary hemostatic disorders? (7)
    • mucosal bleeding- petechia, ecchymosis, epistaxis, GI hemorrhage, gingival bleeding
    • blood loss/ anemia- pale MMs, signs of anemia (tachycardia, tachypnea)
  14. What are clinical signs of secondary hemostatic disorders?
    • cavitary bleeding- pleural space, pulmonary parenchyma, abdominal cavity, joints (signs depend on site)
    • dyspnea, coughing
    • neurologic signs
    • anemia
    • blood loss and shock
  15. What tests evaluate primary hemostasis? (4)
    • platelet number
    • platelet function- BMBT, vWF, PFA
  16. What tests evaluate secondary hemostasis? (4)
    • (OS)PT
    • aPTT
    • ACT
    • Lee-White CT (glass tube test)
  17. What are normal values for the BMBT?
    • dogs <4 minutes
    • cats <3 minutes
    • [remember: there's no point in measuring BMBT is platelet numbers are decreased!]
  18. What is (OS)PT evaluating?
    [Prothrombin time] measures the extrinsic and common pathways
  19. What is aPTT evaluating?
    [activated Partial Thromboplastin Time] measures the intrinsic and common pathways
  20. What is ACT evaluating?
    [Activated Clotting Time] measures the intrinsic and common pathways, but is less sensitive than aPTT
  21. What are your rule outs for primary hemostatic disorders? (7)
    • [thrombocytopenia] destruction of platelets, consumption of platelets, decreased production of platelets, sequestration of platelets
    • vWF deficiency
    • [thrombocytopathy] renal failure, medications (Hetastarch, Aspirin,Plavix)
  22. What are rule outs for secondary hemostatic disorders? (5)
    • inherited factor deficiencies (Hemophilia A- VIII, Hemophilia B (IX)
    • liver disease (decreased factor production)
    • anticoagulant rodenticide (Vit K antagonism)
    • DIC
    • traumatic coagulopathy (loss of clotting factors, hypothermia)
  23. What factors require Vit K for normal function? (4)
    II, VII, IX, X
  24. What is the treatment plan for primary hemostatic disorders? (3)
    • address underlying cause if possible
    • blood products- whole blood, platelet rich plasma
    • enhance platelet function- cryoprecipitate, DDAVP
  25. How does cryoprecipitate work?
    it's a concentration of vWF and factor VIII
  26. What is DDAVP/ how does it work?
    stimulates release of vWF and factor VIII into circulation; it helps with any type of thrmbocytopathy
  27. How are vWF and factor VIII related to one another?
    vWF is bound to factor VIII in circulation; when vWF is activated by thrombin, factor VIII is released and rapidly degrades
  28. What is the treatment plan for secondary hemostatic disorders? (2)
    • treat primary cause: find/ treat primary cause of DIC, Vit K supplementation, liver disease, etc
    • transfusion therapy [if prolonged clotting times AND evidence of ongoing bleeding]
  29. What are the doses for fresh whole blood transfusions?
    • K9/EQ/BV: 20-30mL/ kg
    • FE: 10-15mL/ kg
  30. What are the doses for fresh frozen plasma and frozen plasma?
    • K9/EQ/BV: 10-15mL/ kg
    • FE: 5-7.5mL/kg
  31. What are the consequences of thrombosis?
    • Microthrombosis--> DIC
    • Macrothrombosis--> saddle thrombus, DIC, CATE, AIT, PTE, etc
  32. Thrombosis is secondary to...
    • disruption of virchow's triad
    • venous stasis, vessel injury, hypercoaguable state
  33. How does SIRS lead to DIC?
    • hypercoagulation, blood stasis from vasodilation, endothelial damage (direct or indirect)
    • inflammation and coagulation are linked!!! 
    • DIC is MODS for the hemostatic organ
  34. Describe the diagnosis of DIC. (5)
    • presence of disease-causing DIC= SIRS/ sepsis: heat stroke, IMHA, pancreatitis, neoplasia
    • depletion of endogenous anticoagulant: low antithrombin
    • depletion of clotting factors and/or platelets: low platelet count, low fibrinogen, prolonged PT/aPTT
    • evidence of fibrinolysis: increased D-dimers, FDPs
    • CBC/ biochem panel: schistocytes, evidence of organ failure
  35. Clotting times may be normal with DIC if you catch it during...
    the hypercoaguable phase [Pt/aPTT will be prolonged during the hypocoaguable phase]
  36. What lab abnormalities will you see during the hypercoaguable phase of DIC? (4)
    increased D-dimers, decreased platelet count, schistocytes, evidence of thrombosis or organ dysfunction
  37. What lab abnormalities will you see during the hypocaguable phase of DIC? (3)
    prolonged PT/aPTT, decreased platelets, clinical bleeding
  38. What is the treatment plan for DIC?
    • treat underlying cause
    • plasma products ONLY if bleeding (hypocoaguable phase)
    • anticoagulant ONLY if hypercoaguable phase
  39. Describe the coagulation cascade.
    Image Upload 1
  40. What are indications for using anticoagulants? (3)
    • excessive clot formation
    • hypercoaguable DIC
    • thromboembolic disease
  41. What drugs are platelet inhibitors? (2)
    • aspirin
    • plavix (Clopidogrel)
  42. What drugs are coagulation factor inhibitors? (2)
    • heparin (unfractionated vs low molecular weight)
    • warfarin
  43. Heparin requires sufficient __________ in order to be effective; indications for use of heparin include.. (2)
    • antithrombin levels
    • prevention of DIC in high risk patients
    • clot already present, ex. FATE
  44. Contrast unfractionated heparins versus low molecular weight heparins.
    • Unfractionated: varying sized molecules, inactivate multiple factors, unpredictable pharmacology, monitor using aPTT, dose 75-300units/kg
    • Low molecular weight: more uniform size, only inactivates factor Xa, more predictable effect, does not affect PT/aPTT (difficult to monitor), Dose 1mg/kg
  45. DIC is ALWAYS...
    secondary to another disease!!!
Author
Mawad
ID
325142
Card Set
ECC2- Hemostatic Disorders
Description
vetmed ECC2
Updated