Acquired bleeding disorders Flashcards
Name the main acquired bleeding disorders
- Vitamin K deficiency
- Liver disease
- Iatrogenic
- Disseminated intravascular coagulation
- Acquired inhibitors
- Massive transfusion syndrome
What does factor II become?
II–> thrombin–> fibrinogen–> fibrin–> fibrin degradation products
How is an inhibitor or a bleeding deficiency problem diagnosed?
- Mix patient & normal plasma
- Correction= deficiency
- No correction= inhibitor
Describe vitamin K deficiency
- Deficient factors 2, 7, 9, 10
- Functional deficiency
- Causes: obstetrics, jaundice, broad spectrum antibiotics, neonates, prolonged nutrient deficiency
What are types of impaired haemostasis in liver disease?
- Excessive plasmin activity
- Thrombocytopenia
- Platelet dysfunction
- Reduced plasma conc of all coagulation factors except 8
- Delayed fibrin monomer polymerisation due to altered fibrinogen glycosylation
- Treated with fresh frozen plasma/platelet transfusion
What are the causes of haemostatic abnormalities in massive transfusion?
- Dilutional depletion of platelets & coagulation factors
- Underlying disease-liver/renal drug treatment
- DIC-trauma, head injury, prolonged hypotension
Describe the dilutional effects of haemostasis
- Thrombocytopenia
- Citrate toxicity
- Coagulation factor depletion (5,8 & fibrinogen)
- Hypocalcaemia
What is the pathophysiology of DIC? How is it treated?
- Consumption of platelets & clotting factors
- Activation of fibrinolysis
- Microangiopathic haemolysis
- Microvascular thrombosis: tissue ischaemia & organ damage
- Disruption in balance of procoagulant & anticoagulant mechansims
- Treat underlying condition-antibiotics,obs, folic acid, it K, maintain tissue perfusion
What are acute causes of DIC?
- ABO incompatible transfusion
- Fulminant liver disease
- Sepsis
- Trauma/tissue necrosis
- Obstetrics complications
What are chronic causes of DIC?
- Malignancy
- End stage liver disease
- Severe localised intravascular coagulation
- Obstetrics: retained dead foetus
What drugs can interact with oral anticoagulants?
- Corticosteroids
- Sulphonylureas
- NSAIDs
- Ampicillin
- Erythromycin
- Cephalosporins
Which drugs antagonise the effects of warfarin?
- Spironolactone
- Vitamin K
- Rifampicin
- Cholestyramine
What are the causes of haemostatic abnormalities in renal disease?
- Changed interaction of different components of the coagulation system
- coagulation cascade, platelets and vessel wall
What are recommendations for reversal of oral anticoag treatment?
- Life threatening= Vit K IV, four factor concentrate/PCC, octaplex
- Non major= withhold warfarin, Vit K IV
- INR>8 no haemorrhage= withhold warfarin, vit K orally
How are the following monitored: warfarin heparin fondaparinux aspirin fibrinolytic agents
- W=INR
- H= APTT test sensitive anti-thrombin not routinely required
- F=Haematocrit, PT, platelet count, serum creatinine
- A=CBC, platelets, PT, BUN, serum creatinine
- FA=
How is bleeding/overanticoagulation managed?
- Stop infusion
- Consider protamine (neutralises heparin)
What are the complications of the following: warfarin heparin fondaparinux aspirin fibrinolytic agents
- W= excess bleeding, bruising
- H= VTE
- F=rash, itching, mild bleeding
- A= same as warfarin
- FA=same as warfarin
What is the mode of action of aspirin?
- Impede clotting by blocking prostaglandin synthetase action
- prevents formation of the platelet-aggregating substance thromboxane A2
What is the mode of action for warfarin?
Inhibiting the synthesis of vitamin K-dependent clotting factors and the anticoagulant proteins C and S.
What is the mode of action for heparin?
- Inactivating thrombin & activated factor X through an antithrombin-dependent mechanism.
- Binds through a high-affinity pentasaccharide