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2. Learning Objectives
At the end of the lecture student should be able to-
• Describe mechanism of haemostasis
• Enlist Clotting disorders
• Describe clinical & laboratory assessment
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3. • Dental procedures resulting in
bleeding can have serious
consequences in a pt. having
bleeding disorder………
severe hemorrhage or even
death.
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8. • 2 theories:::
( MARKOWITZ----1903)
(1964)-the
coagulation mechanism results in a final explosive
change of a liquid to a gel.
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15. CLINICAL LABORATARY TESTS
• Help to
Platelet count
Bleeding time
PFA-100 CT
PT/INR
aPTT
TT
FDPs
Factor assays
Tests of capillary
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16. PLATELET COUNT:
• Normal-150,000 to 450,000/mm3
• If < 50,000/mm3
• In such cases platelet transfusion may be necessary.
Hemorrhagic
stroke
Surgical/traumatic
hemorrhage
etc. may occur.
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17. INR Intro.by WHO(1983):itz
the ratio of PT that adjusts for
the sensitivity of the
thromboplastin reagants,such
that normal coagulation
profile is reported as an INR
of 1.0
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29. • No racial
• AGE 6
• SIGNS H H H GI
B h
s bleeding.
H
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30. Treatment
• As such there is no cure only remedy is protection of
the patient from the traumatic injuries.
• Preoperative transfusion of whole blood &
administration of antihemophilic factor concenterate
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31. Von Willebrand’s Disease/
Pseudohemophilia
• Tendency of bleeding in those patients who have normal
platelet count, clotting time, serum fibrinogen,
prothrombin time.
• Hereditary disorder- autosomal dominant
• Spontaneous bleeding, cutaneous echymoses, GI
bleeding, severe menorrhagia , gingival bleeding
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32. Parahaemophilia
• Deficiency of factor V
• Autosomal recessive
• Spontaneous epistaxsis, bleeding into GI, menorrhagia,
gingival bleeding.
• Clotting & Prothrombin time prolonged
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33. Afibrinogenemia &
Hypofibrinogenemia
• Little or no fibrinogen in the tissue
• Types-Acquired & Congenital
• Long periods of freedom from bleeding, hemarthrosis is
less common.
• Clotting & prothrombin time infinite
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34. Dysfibrinogenemia
• Autosomal dominant
• Fibrinogen present in normal amount, but is defective in
its structure & coagulability so that the aggregation of
fibrin monomers are impeded.
• Also seen in liver diseases
• Prothrombin time prolonged
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36. Macroglobulinemia
• Not specifically a blood ‘factor’ diseases
• Generally classified as plasma cell dyscrasia so that
the excessive proliferation of B-lymphocytes results
in the production of large amounts electrophoretically
homogenous M-type globulins
• Hyperviscosity, cryoglobunemia, coagulation
abnormalities,etc
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37. • Neoplastic infilteration of lymphoplasmacytic cell
infilterate
• Pallor weakness & weight loss , lymphadenopathy &
hepatomegaly
• Haemorrhages from nasal & oral cavity
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