Haemostasis Flashcards
(31 cards)
What happens before, during and after haemostasis broadly and why?
Before- vasoconstriction to limit blood flow to site of injury
During- primary haemostasis- unstable platelet plug formed to limit blood loss and make surface for coagulation
Secondary haemostasis- stabilises platelet plug to stop blood loss
Fibrinolysis- clot is dissolved and the vessel wall is repaired to restore normal function
Describe the mechanism of primary haemostasis
Following vessel wall damage, platelets bind to the vessel wall using their glycoprotein Gp1a or onto exposed collagen if VWF is present using Gp1b.
This causes thromboxane activation leading to A2 and ADP synthesis, promoting platelet activation
This causes granule release and flip-flopping of platelets- exposing Gp2b and Gp3a which bind to the vessel wall and form the platelet plug
What three structures can be affected in primary haemostasis disorders?
Platelets
VWF and as a result F VIII
Vessel wall
What are the two causes of platelet disorders and what are their causes?
Thrombocytopenia- caused by leukaemia or accelerated clearance (via ITP immune thrombocytopenic purpura, DIC disseminated intravascular coagulation, splenomegaly)
Impaired platelet function- hereditary eg missing glycoproteins or acquired via NSAIDS/Aspiring/Clopidogrel
What is the cause of VWF disorders? And what are the types?
Von willebrand disease
Deficiency T1 & T3
Abnormal function T2
What are the two causes of vessel wall disorders?
What do these disorders typically affect?
Hereditary disorders
Acquired
Collagen on vessel wall
What is ITP?
What Is its pathophysiology?
Immnune thrombocytopenic purpura
Autoantibodies bind to platelets and take them to macrophages- engulfed
How does aspirin work?
How long are its effects?
What haemostasis is it given for?
Inhibits synthesis of thromboxane A2 so the platelet plug cannot be formed
Typically lasts 7 days as platelets are resynthesised after this
Primary
How does clopidogrel work?
What haemostasis is it given for?
Binds to ADP preventing platelet activation = no platelet plug formed
Primary haemostasis
What are the clinical and dermatological features of primary haemostasis disorders?
Immediate extensive bleeding after trauma
Extensive menses
Gum bleeds
Nose bleeds
Easy bruising
Non blanching purpura
Petechiae
What are the tests for primary haemostasis disorders?
Platelet count
Bleeding time
How are primary haemostasis disorders treated?
Treat underlying condition eg
Replace low platelet or missing VWF
Splenectomy
Immunosuppression via prednisolone
What is the role of the coagulation cascade?
Produce thrombin (factor IIa) from prothrombin (factor II) which converts fibrinogen (factor I) to fibrin (factor Ia) to stabilise platelet plug
What are the two pathways of secondary haemostasis?
What does this convert prothrombin into?
Intrinsic: 12-11-9-8-10
Extrinsic: 7-10 (joins intrinsic at this point)
Factor 10a turns prothrombin into thrombin with the help of 5
Prothrombin (factor II) becomes thrombin which then makes fibrinogen into fibrin
What are the three principles of disorders of coagulation?
Deficiency of coagulation factor
Dilution
Increased consumption
What are the two types of disorder of coagulation factors and what are examples of the two?
Hereditary (haemophilia A/B, factor 11/12 deficiency),
Acquired (liver disease, anticoagulants)
What are the two hallmark features of haemophilia?
Haemarthrosis- bleeding into joint
Muscle wasting- later on
What injections should be avoided in haemarthrosis?
Intramuscular injections as muscle bleeding is hard to control
How does dilution occur in coagulation disorders?
A blood transfusion is given following a haemorrhage, however this blood does not contain plasma, and therefore coagulation factors = dilution of coagulation factors
What is Disseminated intravascular coagulation (DIC) and what is this an example of?
What can it end up causing?
Example of increased consumption coagulation disorder
This happens when tissue factor becomes overactive leading to rapid coagulation, which causes drainage of platelets and coagulation factors and deposition of fibrin in the vessels. This leads to organ failure
What is consumed in DIC?
What conditions can It be associated with?
What molecule can you detect in DIC blood tests?
Coagulation factors and platelets
Sepsis, inflammation, major tissue damage
D-dimer- breakdown product of fibrin
How do the clinical features of primary and secondary haemostasis defects differ?
Primary- superficial bleeding (due to no platelet plug) straight after injury
Secondary- deeper bleeding rather that on superficial cuts (as platelet plug can still be formed) and prolonged onset of bleeding after trauma
What do PT and APTT measure specifically and generally?
PT- extrinsic pathway (factor 7)
APTT- intrinsic pathway
Both ultimately measure time to make cross linked fibrin (activation of thrombin to make fibrin)
Describe the causes behind the following test results:
Prolonged APTT but normal PT
Prolonged PT but normal APTT
Prolonged PT and prolonged APTT
Normal PT and APTT
Haemophilia A/B, factor 11/12 deficiency (as these are needed before factor 10)
Factor 7 deficiency
DIC, Dilution, liver failure, anticoagulant drugs
Primary haemostasis disorder, healthy patient
