1. The plasma under study is tested in the usual manner
by both the prothrombin time and the partial thromboplastin time.
2. Mix equal volumes of the test plasma and normal
control plasma. About 0.5 mL of the mixture is
3. Mix equal volumes of the test plasma and BaSO4
treated normal plasma. About 0.5 mL of the mixture
4. Determine the prothrombin time and the partial
thromboplastin time each of the mixtures.
significant coagulation disorder is present.
2. If the normal plasma fails to correct an abnormal
prothrombin time or partial thromboplastin time, it is
likely that the patient has a circulating anticoagulant.
3. If normal plasma corrects either the prothrombin time
or the partial thromboplastin time, the presumptive
diagnosis is as indicated in the table.
4. Factor XII deficiency will have a pattern similar to that
of factor VIII deficiency. The correct diagnosis can
be further elucidated by the lack of a real bleeding
tendency in the factor XII deficiency. Definite diagnosis
can be established only by having samples of plasma
known to be specifically deficient in factor VIII and
factor XII. Failure of correction of the patient’s partial
thromboplastin time by plasma known to be deficient
in factor VIII establishes the diagnosis of hemophilia.
Likewise, failure of correction of the patient’s partial
thromboplastin time by plasma known to be deficient
in factor XII establishes the diagnosis of Hageman trait.
5. Factor XI deficiency may have a pattern similar to
that of factor VIII or factor IX deficiency. The correct
diagnosis can be further elucidated by the sex-linked
recessive transmission of factor VIII or factor IX
deficiency. Definitive diagnosis can be established
only by having available sample of plasma known
to be deficient in factors VIII, IX, and XI. Failure of
correction of the patient’s partial thromboplastin
time by plasma known to be deficient in factor XI
establishes the diagnosis of factor XI deficiency.
The two-stage prothrombin method is needed to
distinguish a true deficiency of prothrombin from the
pattern indicated for factor X deficiency.
A severe deficiency of fibrinogen will have a pattern
similar to that of factor V deficiency. A quantitative method
for fibrinogen is required to determine the fibrinogen
For delving further into details of coagulation disorder
diagnosis, Tulip diagnostics provides kits for estimation
of—antiplasmin, antithrombin III, A2, antitrypsin, factor
II reagent, factor V reagent, factor VII reagent, factor VIII
reagent, factor VIII R:AG antiserum, factor IX, factor X
reagent, factor XIII, fibrinogen reagent,—macroglobulin,
PTT reagent, thrombin reagent, thrombin coagulase and
Some properties of the coagulation factors are given below:
1. Fibrinogen group: Factors, I, V, VIII, XIII.
• Thrombin interacts with them all
Prothrombin Partial thromboplastin time Presumptive diagnosis
Test plasma alone Test plasma Test plasma Test plasma Deficiency of
+BaSO4 plasma alone +BaSO4 plasma factor
Normal Normal Long Normal VIII
Clinical Hematology: Bleeding Disorders 305
(Courtesy: Tulip Group of Companies)
• Activity lost in coagulation process (not present in
• Increase during inflammation, in pregnancy and
• Factors V and VII lose activity in stored plasma
• Liver parenchyma synthesis (except factor VIII).
2. Prothrombin group: Factors II, VII, IX and X.
• Activated form contains an active serine center
• Liver parenchymal cell synthesis
• All except prothrombin (II) are not consumed during
coagulation (present in serum)
• Dependent on vitamin K for synthesis
• Stable, well preserved in stored plasma.
3. Contact group: Factors XI, XII.
• Activated forms contain an active serine center
• Not dependent on vitamin K for synthesis
• Stable, well preserved in stored plasma.
Factor VIII is most important as far as coagulation
disorders are concerned. Its structure is as follows:
VIII C = Part has coagulant activity.
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