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Flashcards in Exam 7 L. 4 Deck (19):

Primary hemostasis

The formation of the platelet plug
-sufficient for small vessel injury


Secondary hemostasis

The formation of the fibrin clot through the coagulation cascade
-fibrin clot is needed for medium/large vessels


Tertiary hemostasis

Fibrinolysis to reestablish blood flow through vessels


Normal vessel

Platelet adhesion prevented by:
-negatively charged endothelium (repels platelets)
-nitric oxide


Endothelial damage

1) vasoconstriction: platelets are slowed, giving them time to interact with subendothelium
2) subendothelium exposed: vWF visible
3) platelets tether to vWF ==> activates platelets to bind to fibrinogen
-fibrinogen allows platelets to bind together
4) activated platelets attract and activate more platelets (ADP and Thromboxane A2)
5) activated platelets set the stage for secondary hemostasis (provide docking site for clotting factors need)


What can go wrong with primary hemostasis?

1) platelet: function and number
2) von Willebrand factor: number and function


Primary hemostatic disorders

1) thrombocytopenia
-use, destruction, decreased production
2) acquired
-immune mediated, infectious disease, DIC, drugs
-**thrombocytopenia is the most common acquired disorder of primary hemostasis!!**


Primary hemostatic disorder: von Willebrand's disease

Inherited: Doberman!
-Most common inherited primary hemostatic disorder is von Willebrand's disease!**


Platelet count

1) estimate from a blood smear
-1 per 100x field = 20,000 platelets/ul
-check the feathered edge!!
-A normal dog has between 8 to 10 platelets per high-powered field
2) spontaneous bleeding will not occurring last count is under 30,000 platelets/ul


How do you test platelet function?

1) Buccal mucosal bleeding time
-a test for a defect in primary hemostasis
-makes an incision of standard depth and width in buccal mucosa
2) will be abnormal (>4 minutes) if:
-thrombocytopenic, thrombopathic, vWF deficient/abnormal, abnormal vasculature


Immune-mediated thrombocytopenia (ITP)

1) can be primary or secondary
2) secondary: drugs, infectious agents (especially vectorborne diseases), neoplasia
-for some reason there is antibody versus platelets, and macrophages are gobbling up the platelets


Treatment for ITP

1) Vincristine
- a 1 time shot! (It works or it doesn't)
-prevents microtubule polymerization
-accelerated megakaryocyte fragmentation and platelet release from bone marrow
-no place for vincristine in IMHA treatment


When to transfuse platelets?

1) Severe thrombocytopenia
2) suspect pulmonary or CNS hemorrhage
3) acquired or hereditary thrombopathia


What products contain viable platelets??

1) fresh whole blood
2) platelet rich plasma
-generated from a soft spin of blood
3) platelet concentrate (fresh or cryopreserved)
- PRP that has been spun hard to concentrate platelets


ITP prognosis

1) good!
2) 10-30% mortality rate
3) like IMHA, does require long-term immunosuppressive therapy


Inhibitors of primary hemostasis

1) endothelial cells!*
-Physical barrier: separates platelets and vWF unless there is an injury
2) ADPase, prostacyclin, nitric oxide
-inhibit platelet activation


Pathological inhibitors of primary hemostasis

1) disease:
-metabolites in liver and kidney disease inhibit platelet function


Therapeutic inhibitors of primary hemostasis

1) platelet inhibitors
-aspirin, NSAID's: inhibit TxA2 production ==> platelets don't activate their neighbors!
- Clopidogrel: inhibit platelets by binding to their ADP receptor (platelets cannot be activated by ADP)



1) platelets do a lot!
-1st to site of injury, essential for platelet plug formation, and platelet membranes are needed for secondary hemostasis
2) vWF
-the glue for platelet adhesion to the vessel wall: stops bleeding
3) thrombocytopenia is the most common acquired cause of defective primary hemostasis
4) von Willebrand's disease is the most common cause of inherited defective primary hemostasis