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What are the two important functions of normal haemostasis?
- Maintain blood in fluid, clot free state
- Poised to induce rapid, localised plug at site of vascular injury
Describe normal haemostasis
After vascular injury, local neurochemical factors induce a transient vasoconstriction. Platelets adhere to exposed ECM via Von Willebrands factor and are activated, undergoing shape change and granule release; released ADP and thromboxane A2 cause further platelet aggregation to form the primary haemostatic plug. Local activation of coagulation cascade results in fibrin polymerisation 'cementing' platelets into a definitive secondary haemostatic plug.
Which enzyme converts fibrinogen in fibrin?
Which enzyme breaks down fibrin strands to keep them localised to the area of damage?
Platelets expose ... that are important in the intrinsic coagulation pathway?
Injured or activated endothelial cells expose ... which triggers the extrinsic coagulation pathway?
What are the three coagulation pathways?
Intrinsic, extrinsic, and common pathways
What are fibrin split products called?
How can we measure how the fibrinolytic system is working?
By measuring the amount of D-dimers being produced
What activates plasmin?
Tissue plasminogen activator
What is thrombocytopenia?
Decreased circulating platelets in the peripheral circulation
What are the clinical signs of thrombocytopenia?
Epistaxis (nose bleed), ecchymoses (SC bleeding), petechiae (tiny pinpoint haemorrhages in mucosa), haematuria (blood in urine), haematochezia (fresh blood in faeces), hyphaema (bleeding in the chamber of the eye), melena (black, tarry faeces)
How can we diagnose thrombocytopenia in the lab?
- Smear examination - check for platelet aggregates, morphology and size
- Manual platelet count (if numbers fall below the sensitivity of the machine)
List the 4 possible causes of thrombocytopenia
- Increased destruction e.g. primary or secondary immune mediated destruction
- Decreased production e.g. bone marrow disorder
- Increased consumption e.g. DIC, thrombosis
- Increased sequestration e.g. hypersplenism
What is a platelet function disorder?
This is when platelet numbers are normal but they are not functioning correctly
How can we test for a platelet function disorder?
Buccal mucosal bleeding time
What is the normal buccal mucosal bleeding time for cats and dogs?
What is Von Willebrands disease caused by?
Quantitive and functional deficiencies in vWF
What are the three types of von Willebrands disease?
- Partial quantitative disorder
- Loss of large molecular weight multimers
How do we diagnose von Willebrands disease in the lab?
- Buccal mucosal bleeding time (but this is not specific for VWF)
- Quantitative assay
- Functional assay
What is thrombocytosis?
Blood platelet concentration above the reference interval
List some of the causes of thrombocytosis
- Increased production e.g. inflammation, iron deficiency, blood loss, non-haemic neoplasia
- Redistribution eg exercise
- Haemic neoplasia eg primary essential thrombocythemia, acute megakaryocytic leukaemia
How does bleeding manifest in clotting disorders?
Haematomas, GI tract and urinary tract bleeding, haemarthrosis (bleeding into a joint)
Give an example of an a) acquired b) hereditary cause of clotting disorder
- a) vitamin K deficiency, severe hepatic disease, DIC
- b) X-linked deficiency haemophilia A and B, FVII deficiency in beagles
How can we test for clotting disorders?
In vitro tests can be used where clot formation is timed. This requires specific activators for the clotting cascade and is performed on citrated plasma.
What do the following stand for: PT, aPTT, TCT?
- PT = prothrombin time
- aPTT = activated partial thromboplastin time
- TCT = thrombin clotting time
What part of the coagulation cascade do the following test: PT, aPTT and TCT?
- PT = extrinsic/common pathway
- aPTT = intrinsic/common pathway
- TCT = common pathway
Why can high fibrinogen be a good indication of inflammation?
As fibrinogen is a positive acute phase protein
What are the three components of Virchow's Triad?
Endothelial injury, abnormal blood flow and hyper coagulability
What does DIC stand for?
Disseminated intravascular coagulation
An acquired syndrome characterised by the intravascular activation of coagulation with loss of localisation resulting from different causes. It can originate from and cause damage tot he microvasculature, which if sufficiently severe can produce organ dysfunction.
Is DIC always a primary or secondary phenomenon?
Give examples of primary disease conditions that can cause DIC
Neoplasia, severe systemic inflammation, endotoxaemia, sepsis
Describe the pathophysiology of DIC
DIC is triggered by e.g. massive tissue destruction, sepsis or endothelial injury which release tissue factor. This causes widespread microvascular thrombosis which leads to the activation of plasmin. Plasmin causes fibrinolysis, producing D-dimers which inhibit thrombin, platelet aggregation and fibrin polymerisation so ultimately cause bleeding. The widespread microvascular thrombosis also causes vascular occlusion which causes ischaemic tissue damage and microangiopathic haemolytic anaemia.
How can we diagnose DIC?
- CBC - thrombocytopenia
- aPTT and PT clotting times prolonged
- Elevated D-dimers (dogs)
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