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Chapter: Medicine Study Notes : Haematology and Immunology


Necessary factors for haemostasis (stopping bleeding): o Vasoconstriction o Platelets o Coagulation (= fibrin production)



·        Necessary factors for haemostasis (stopping bleeding):

o  Vasoconstriction

o  Platelets

o  Coagulation (= fibrin production)




·        Key reaction: fibrinogen ® fibrin

·        Intrinsic pathway: 

o   XII ® II via IX and VIII

o   Triggered by damage to endothelium

o   Measured by Partial thromboplastin Time (PTT) = Activated PTT (APTT). Also called PTTK

o   Reduced by heparin treatment

·        Extrinsic Pathway: 

o   VII ® II

o   Triggered by chemicals extrinsic to blood stream 

o   Measured by Prothrombin time or INR (International Normalised Ratio): ratio of Patient PT to Control. Normal < 1.3. INR mainly measures top end of the extrinsic pathway – so INR may not be affected by heparin even though it affects the common pathway. APPT more sensitive to ¯common pathway 

o   Reduced by warfarin treatment


Hypo-Coagulation Diseases


·        Congenital:

o   Haemophilia A

o   Haemophilia B

o   Von Willebrand‟s Disease

o   Rare factor deficiencies

·        Acquired: 

o   Liver diseases ® ¯coagulation factors

o   DIC

o   Vitamin K deficiency: needed for factors 2, 7, 9 and 10 

o   Uraemia: renal failure ® ¯platelets and coagulation function

o   Massive blood transfusions ® dilution of clotting factors

o   Factor inhibitors


Von Willebrand’s Disease


·        ­Bleeding time, ­APTT due to ¯ VIII (VW factor is a binding protein for VIII)

·        Symptoms: Superficial bleeds – mouth, nose, gut, bruising, heavy menstrual bleeding

·        Autosomal dominant

·        Comes in mild, moderate and severe forms




·        Ratio of 4:1 of A (¯factor VIII) to B (¯factor IX)

·        Prevalence of 13 – 18 per 100,000 males in Wellington (high)


·        Symptoms: bleeding into soft tissues, joints, dental extraction. Deep bleeds ® major orthopaedic implications. NOT superficial or gut


·        Classification:

o   Severe: < 1% - joint bleeds, e.g. once a fortnight or month

o   Moderate: 1 – 4 % - some joint bleeds, main problem with trauma, not spontaneous bleeds

o   Mild: 5 – 25% - main problem trauma

·        Lab diagnosis:

o   INR: normal

o   APTT: prolonged

o   Fibrinogen: normal

o   Platelets: normal 

o  Bleeding time: normal

o  Factor assay reduced (do VIII first then IX)

·        Symptoms of a joint bleed:

o  Strange sensation: not really a pain – treat at this point, they will know despite no signs yet

o  Swelling

·        Treatment:

o  Factor replacement: either prophylactic or on demand

o  Choice of factor product: blood derived or recombinant

o  Management of inhibitors


Disseminated Intravascular Coagulation (DIC)


·        = Laying down fibrin inappropriately within vasculature

·        Causes:


o  Activation of extrinsic system by thromboplastin (triggers VII). Thromboplastin is a lipoprotein substance from cell membranes. Due to: massive injury (­­release of thromboplastin), septicaemia (damage to endothelium), tumour cells breaking down


o  Activation of intrinsic system: anoxia, acidosis, sepsis, burns


o  Direct activation of II & X: amniotic fluid embolism, pancreatitis (® release of toxic enzymes into blood)


·        Outcomes:


·        Lab screen: 

o  ­PT (Prothrombin time)

o  ­APTT

o  ¯Fibrinogen

o  ¯Platelets

o  ­Fibrin degradation products

·        Treatment:

o  Correct cause

o  Platelet transfusion

o  Fresh Frozen plasma

o  Cryoprecipitate


Hypercoagulable States     


·        Primary Causes:

o  Factor V Leiden:

§  Most common primary cause 

§  Point mutation on factor V prevents breakdown ® ­levels of Va ® hypercoagulable

§  Heterozygous have lifetime risk of 30 – 40% of thrombotic event, Homozygous then 50 – 60%

§  In thrombotic patients, 20 – 40% have factor V Leiden, mainly in Caucasians

o  Prothrombin gene mutation

o  Antithrombin 3 deficiency: 

§  ® Reduced breakdown of thrombin

§  Heparin co-factor, a2 globulin 

§  Autosomal dominant, 1:2-5000 in Caucasian

§  Found in 2 – 3 % of DVTs 

§  Can also cause mesenteric or brachial thrombosis.  These are rare so ® ­index of suspicion

o   Protein C or S deficiency

o   Homocysteinaemia

·        Secondary Causes:

o   Malignancy 

o   Pregnancy and for 6 weeks afterwards: hypercoagulable, stasis, venous compression. If concurrent primary disorder then prophylaxis with sc heparin (warfarin contra-indicated)

o   Stasis: immobilisation, surgery, local pressure

o   Age

o   Myeloproliferative disorders

o   Antiphospholipid Syndrome (acquired, aggressive)

o   Infection

o   Trauma


Data Interpretation


·        Serum = plasma that‟s clotted: i.e. no clotting factors

·        Citrated plasma: citrate chelates calcium – so can‟t act as a co-factor in clotting.  Add Ca to reverse 

·        Aspirin for Coronary Heart Disease mimics VWD. (i.e. ­bleeding time, everything else normal). T½ of platelets = 3 – 4 days. Need to stop aspirin 10 days before surgery. ½ an aspirin enough to increase bleeding time. 45 minutes to have an effect after oral dose 

·        Heparin ® ­APPT

·        Fractionated Heparin ® ­TT (APPT may be normal)

·        Warfarin ® ­INR

·        Try to determine deficiency (e.g. FVIII or Warfarin ® ¯2,7,9,10) or Inhibition (e.g. aspirin, heparin)


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