Bleeding and Thrombotic Disorders Flashcards
Functions of haemostasis
Maintain circulation
Coagulation
Fibrinolysis
Sequence of haemostasis
Vasoconstriction
Primary, secondary and tertiary haemostasis
- recall coagulation cascade (extrinsic, intrinsic and common pathways)
Fibrinolysis process and inhibitors
Laboratory evaluation of bleeding; interpretation of individual results
CBC and blood smear
- why is morphology important
Coagulation
- PT, APTT, TT, D-dimer, fibrinogen assay, mixing test
Platelets
- function test, vWF, bleeding time, function analyser
Clinical features of bleeding disorders
Platelet/vWF vs Coagulopathy
- site of bleeding, petechiae, ecchymosis, haemarthrosis, bleeding after cut/scratches/ surgery
Characteristics of petechiae
Specific investigations of bleeding
Platelet
- CBC then vWF/platelet function test
Coagulopathy
- PT, APTT then mixing test and factor/inhibitor assay
Management options of bleeding disorders - MOA, indication, side effects
Platelet
- platelet transfusion
- DDAVP
Coagulopathy
- plasma(FFP), cryoprecipitate, factor concentrates
- rVIIa
Fibrinolysis
- tranexamic acid
Platelet disorders and causes
Quantitative
- increased destruction
- decreased production
- increased sequestration in spleen
Qualitative
- congenital
- acquired e.g. drugs, uraemia, MDS
ITP
Diagnosis
Pathogenesis: increased destruction and decreased production
Treatment: platelet if <30, corticosteroids, IVIG (Splenectomy/ TPO-RA if unsuccessful)
Drug-induced ITP
Causes e.g. heparin, valproate, antibiotics
Pathogenesis
Onset
Treatment
Coagulopathies
Inherited
Acquired
vWD
Function of vWF
Inheritance
Clinical manifestations
Investigations
Haemophilia
Types
Inheritance
Severity and clinical manifestations
Treatment
Inhibitors of coagulation
Haemophilia (repeated factor concentrates)
Acquired haemophilia e.g. malig, infl, preg
Lupus anticoagulants
DIC
Common causes
Pathogenesis
Lab results
Treatment
Virchow’s triad and examples for each element
Endothelial injury
Circulatory stasis
Hypercoagulability
Congenital diseases causing hypercoagulability
Protein C/S deficiency
- inheritance, normal function, presentation
Factor V Leiden mutation (rare in Chinese)
- MOA
Antithrombin III deficiency
- inheritance, normal function, clinical presentation
Prothrombin mutation
APS
Diagnosis
- recurrent or spontaneous thrombosis
- recurrent miscarriage
- persistent elevation of anti–phospholipid Ab
Causes
- primary and secondary (AI, lymphoproliferative disease, post-viral, phenothiazines)
Treatment
Manifestations of thrombosis
DVT and PE
- presentations and diagnostic methods
Investigations of Thrombophilia
Indication in Hx
Investigations required
Anticoagulant therapy treatment schemes
Standard treatment regime
- UFH/LMWH for 5 days —> bridge to warfarin for at least 3 months
Treatment schemes with NOAC
- dabigatran - bridge from LMWH
- rivaroxaban/apixaban - single drug
Duration of treatment and indications
At least 3 months
- decide on stopping or indefinite extension thereafter — based on bleeding risk, age, compliance, any recurrent events, comorbidities, thrombophilia, D-diner after withdrawal
Indications
- DVT/PE, stroke prevention in AF, prophylaxis in thrombophilia
- high risk of stroke/PVD, ACS
UFH/LMWH
MOA
Compare effects of inhibition on factors, and platelets
Specific uses of each
Administration route, dose
Monitoring
Complications (3) and management (of bleeding)
Vitamin K antagonists
MOA Dosage and monitoring Target INR levels (2.5-3.5 or 2.0-3.0) for different patients Side effects Issues and interactions Management of warfarin overdose
NOAC
Dabigatran vs Xa inhibitors
- target, bioavailability, dosing, renal excretion, protein binding, dialyzable
Efficacy and safety
Advantages vs warfarin
Limitations
Management of bleeding on NOAC (depends on severity)
