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Platelets and Bleeding Disorders:
Objectives:
1) Understand how platelets contribute to normal coagulation
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3) Understand main causes of abnormal platelets
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Bleeding History:
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Personal Bleeding History:
1) Easy bruising?
2) Nosebleeds – how many, how long + hospital treatment?
3) Menstrual bleeding
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5) Mucous membranes and joint bleeding
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Family History – inherited conditions
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Production of platelets is controlled by thrombopoeitin
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They are 1-2 um in size
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Primary Haemostasis:

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Primary haemostasis is the formation of the primary platelet plug and
involves platelets, blood vessel endothelium and von Willebrand
Factor
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If the endothelium is injured then it becomes pro-coagulant and:
1) Vasoconstriction – locally-induced and transient to slow local blood
flow (enabling adherence of platelets to exposed subendothelial
substances) + activation of coagulation
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3) Platelet Activation – adhesion of the platelets to the vessel wall will
activate them and cause them to change shape
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➢ Thromboxane-A2 and platelet-activating-factor are released
by activated platelets
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4) Platelet Aggregation – thromboxane A2, platelet-activating-factor,
ADP and serotonin are platelet agonists and will recruit additional
platelets
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Abnormalities of Platelets:

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Abnormalities of platelets can be congenital or acquired
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Thrombocytopenia  LOW platelet count
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Usually transfused over 30 minutes
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2) For surgery or childbirth
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Platelet transfusions should not be used if thrombotic thrombocytopenic
pupura, heparin-induced or post-transfusion purpura
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Immune Thrombocytopenia:

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This is a condition in which there is immune destruction of the platelets
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Usually idiopathic although can be due to drugs, SLE, HIV, lymphoma
and Evan’s Syndrome
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TREATMENT:
1) Steroids
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3) Anti-D
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5) Treatment of underlying cause
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It is usually asymptomatic and the platelet count falls 5-14 days after
heparin is first given
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This is an antibody to the heparin-PF4 complex
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The 4T Score for Heparin-Induced Thrombocytopenia is used:
1) Thrombocytopenia  2 points if the fall in platelet counts is more
than 50% of baseline
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3) Thrombosis  2 points if there is a new proven thrombosis or skin
necrosis or systemic reaction
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4) Alternative cause  2 points if no other possible cause
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MUST STOP HEPARIN + START ANOTHER
ANTICOAGULANT (NOT WARFARIN INITIALLY)
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➢ Increased numbers of megakaryoctyes = increased platelets
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➢ Clinical features may be absent! If present, there may be:
❖ Burning in the hands and feet
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❖ Bleeding when platelets are very high
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➢ Treatment may be: none or drugs like hydroxyurea to lower
platelet count and aspirin
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Secondary (reactive) causes are MOST COMMON and include:
1) Infection
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3) Malignancy
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5) Inflammatory Disorders
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Inherited Bleeding Disorders:

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Haemophilia = complete absence of factor VIII (haemophilia A) or
factor IX (haemophilia B)
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Usually haemophilia is recessive sex-linked inheritance and thus
patients are usually MALE
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Haemophilia phenotype can vary:
1) Severe – less than 1% activity of factor VIII and IX
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➢ Spontaneous bleeding into joints and muscles
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➢ Later onset of symptoms
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3) Mild – more than 5% activity of factor VIII and IX
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➢ Very few or no bleeding episodes
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➢ On demand treatment for mild or moderate forms – this involves
treatment of bleeding episodes if they arise
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It is a deficiency (partial) of von Willebrand Factor which is a protein
required for platelet adhesion
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It is inherited in an autosomal dominant fashion and thus a family
history of bleeding tendency is usually present
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e
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2) Nosebleeds
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4) Heavy menstrual periods
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Treated with tranexamic acid, DDAVP and Von Willebrand Factor
concentrate
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This can occur with:
1) Liver disease
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3) Disseminated Intravascular Coagulation and Fibrinolysis
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5) Thrombolytic drugs like plasminogen activators
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Conditions which can lead to
DIC include:
1) Sepsis
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3) Malignancy
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DIC is diagnosed via multiple tests including prothrombin time,
activated thromboplastin time, platelet count and fibrinogen
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Fibrin Degradation Products and D-Dimers  normal D-dimer levels
are less than 55mg/l – in DIC these are elevated due to enhanced

thrombin formation and fibrinolytic activity = increased fibrin
degradation products
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➢ Normal PT = 9-11 seconds
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Fibrinogen  may be normal in DIC (normal levels = 1
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5g/l)
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➢ Mechanical heart valves and haemolytic disorders can also cause
fragmentation of red blood cells
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2) PROLONGED PT
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4) LOW FIBRINOGEN
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➢ Keep platelet count above 50 x10^9/l if patient is bleeding
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➢ Aim for fibrinogen over 1
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➢ IF NOT BLEEDING THEN DO NOT GIVE BLOOD PRODUCTS
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