coagulation and clotting Flashcards
What 3 factors stages in forming a blood clot (vasoconstriction, platelet plug, fibrin)
- Vasoconstriction to limit the blood flow
- Activation and aggregation of platelets by thrombin and fibrinogen to form a platelet plug
- Activation of the coagulation cascades resulting in a fibrin clot
How may the following drugs affect this and what stages do they interfere with
aspirin - INHIBITS platelet aggregation
warfarin - INHIBITS vitamin k dependant clotting factors eg factor IX (9) and factor X (10), VII (7)
heparin - ACCELERATES activity of antithrombin in inhibiting factor X (10)
Aspirin and Clopidogrel are often used in conjunction? Why? And what is their function
Both are anti-platelet drugs - inhibit platelet aggregation
Results are more effective when 2 anti-platelet drugs are used together
What is the pattern of getting Vonwillebrands disease
Autosomal dominant = mild disease = type 1
Autosomal recessive = severe disease = type 3
How does Von Willebrands disease affects haemorrhage
Reduces level of factor VIII (8) and reduces platelet aggregation. This makes blood more prone to haemorrhage. Factor VIII is bound by von Willebrand Factor so deficiency in vWF causes deficiency in factor VIII.
what pathways are initiated in coagulation?
Extrinsic pathway - stimulated in response to a blood vessel breaking and tissue factor cells from outside the blood vessel coming into contact with the blood which triggers a rapid cascade of rxns resulting in production of factor x.
Intrinsic pathway - occurs due to injury inside a blood vessel. Begins with activation of factor XII (Hageman factor) which occurs when blood circulates over injured internal surfaces of vessels.
Production of factor X results in the cleavage of prothrombin (II) to thrombin (IIa). Thrombin in turn catalyses the conversion of fibrinogen into fibrin.
Fibrin creates a mesh that traps platelets, blood cells and plasma.
Factor VIII (8) deficiency results in
Haemophilia A
Factor IX (9) def.
Haemophilia B (Christmas disease)
Factor XI (11) deficiency
Haemophilia C
Haemophilias origin
for both - inheritance - sex-linked recessive - males affected, females carriers
A - severe and moderate - require use of recombinant factor VIII (8)
mild and carriers - majority respond to DDAVP (desmopressin). Very mild cases may only require oral tranexamic acid. – less common than B
B - does not respond to DDAVP. Prophylactic cover requires recombinant factor IX (9)
what is role of anticoagulants
role is to prolong clotting time - ‘blood thinners’
warfarin
warfarin
synthesised in liver= affects factors 2, 7, 9, 10
used in patients with mechanical valves
Response measured using INR (should be checked every 4-8 weeks).
– target INRs = mechanical heart valves (3.0 - 4.0). Recurrent VTE while adequately anticoagulated (3.0 - 4.0). Other cases (2.0 - 3.0)
– drug interactions
Medication to avoid - aspirin - as an analgesic, co-proxamol, ketorolac, azole antifungal drugs
– GG&C suggest an INR below or of 3.5 - blood test 48hrs of treatment
–SDCEP suggest 4.0 - blood test within 72hrs of treatment
increased vitamin K diet will affect INR
direct anticoagulants
factor X (10) inhibitor – direct anticoagulant – works in common pathway
rivaroxaban (once a day) & apixaban (twice a day) (factor Xa inhibitor)
dabigatran (twice a day) (direct thrombin inhibitior)
dental treatment under direct oral anticoagulants
– no routine blood test required, standard dose for each patient, tabs taken either once or twice a day, no reversal agent available
–GG&C - patient can undergo the majority of treatment including simple extractions - no alteration of dose. For complex treatment - omit dose before
do you need to stop clopidorgels for XLA?
no
