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Hematologic disorders
Hemostasis
not
Homeostasis
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The end product of the coagulation system, which shows a fibrin clot or
thrombus. White threads are fibrin, the structure with yellow on the surface
is a white blood cell, platelets are green, and the red structures are red
blood cells.
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hemostasis
Vascular phase
Platelets phase
Coagulation cascade
extrinsic
common
intrinsic
Fibrinolytic phase
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Coagulation cascade
This process involves multiple proteins, many of which are
synthesized by the liver
fibrinogen, prothrombin, V, VII, IX, X, XI, XII, and XIII
Some are vitamin K dependent
II, VII, IX, and X
The process of coagulation essentially involves three
separate pathways.
Platelets
Coagulation
factors
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Platelets
Platelet Count: quantitative assessment of circulating platelets.
A normal count is within the range of 150,000 to 450,000/mm3
of blood. Below 100,000/ mm3 is
Thrombocytopenia
If it is 50,000-100,000/mm3 excessive bleeding occurs only with
severe trauma. Below 50,000/mm3 shows skin and mucosal
purpura and bleed excessively with minor trauma.
Below 20,000/mm3 may experience spontaneous bleeding
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Coagulation factors
Prothrombin Time (PT): informs about the extrinsic
coagulation pathway (Factor VII) and the common
pathway (Factors V, X, prothrombin and fibrinogen).
Factors VII, X and prothrombin are Vitamin K-dependent
Normal PT is 11 to 15 seconds, depending on laboratory
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intrinsic
tissue factor
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PL: Phospholipid
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Reversible coagulopathies
anticoagulation Therapy
Warfarin Sodium : It interferes with the livers synthesis
of vitamin K-dependent clotting factors
II, VII, IX, and X.
Its therapeutic target is to prevent new thrombi
INR is now used to monitor patients on warfarin therapy.
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Low-molecular-weight heparin
LMWH
can be used instead of regular heparin and is rapidly
becoming the treatment of choice. It has greater activity
against factor Xa than thrombin and longer half-lives.
Half-life of these preparations is about 2 to 4 hours.
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Warfarin
Wisconsin Alumni Research
Foundation
-arin Coumarin
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irreversible coagulopathies
Inherited Coagulation Disorders
Hemophilia A
(Classic hemophilia) is caused by deficiency in factor VIII.
minimally 30% of factor VIII is required for normal activity.
Mild
Moderate
Severe
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Hemophilia B
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In case of Platelet-Related
disorders
platelet transfusions
Infusion of one unit of platelets increases its number by
10,000 to 12,000/mm3.
Six units of platelets are commonly infused at a time.
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2-Antiplatelet therapy
Aspirin acts as an inhibitor of cyclooxygenase, and this causes
irreversible damage to the platelets. This prevents production
of Thromboxan that is needed in platelets aggregation
The old concept of stopping the antiplatelet therapy for three
days
before
surgery
in
no
more
used,
it
obsolete
recommendation..
DO NOT STOP
the use of daily aspirin before routine dental extractions even
in multiple extractions
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Warfarin
Prevention of recurrent MI
Prosthetic heart valves
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Inherited Coagulation
Disorders
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Hemophilia A
F VIII replacement
one unit of F VIII concentrate per kilogram of body weight
raises the F VIII level by 2%
a 70 kg patient would require infusion of 3,500 units to
raise his factor level from < 1% to 100%.
Aminocaprioc acid or Tranexamic acid as mouth wash for
clot stabilization
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Hemophilia B
F IX replacement
By using F IX complex concentrates (prothrombin
complex concentrate [PCC]) F II, VII, IX, and X.
One unit of PCC given by bolus per kilogram of body
weight raises the F IX level by 1 to 1.5%.
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