Prothombin Time (PT )
- The blood sample is taken with ESR (sodium citrate) solution.
- The blood sample is 1.8 ml and the ESR solution is 0.2 ml.
- Alcohol intake can increase the PT time.
- A high-fat diet may decrease the PT time.
- There are drugs that decrease the PT like anabolic steroids, digitalis, Benadryl, griseofulvin, oral contraceptives, vitamin K, and chloral hydrate.
- There are some drugs which can increase PT like aminosalicylic acid, barbiturates, beta-lactam antibiotics, chloramphenicol, clofibrate, heparin, methyldopa, neomycin, quinidine, quinine, sulphonamides, and salicylates.
- This is one of the screening tests for coagulation.
- This test evaluates the extrinsic pathway defect.
- This test also finds a common pathway defect.
- This test is done For the screening of prothrombin deficiency.
- PT is also used to evaluate dysfibrinogenemia.
- PT is done to monitor the heparin and coumarin effect.
- In the case of bruises and abnormal bleeding.
- In the case of Vit.K deficiency.
- This is advised as a liver function test.
- To monitor the Warfarin therapy.
- Prothrombin is a protein produced by the liver. Its molecular weight is 71,600 Daltons.
- Prothrombin helps in the clotting mechanism.
- Prothrombin production depends upon the adequate intake amount of Vit.K and its absorption.
- It is the most abundant and has a long half-life of the vit.K dependant clotting proteins, and circulate as a zymogen to serine protease.
- On clotting, prothrombin is converted into thrombin.
- Prothrombin Thrombin.
- Factor II, VII, IX, and X depend upon the Vit.K for biosynthesis.
- PT is prolonged by the abnormality in :
- Factors I, II, VII, X deficiency.
- Warfarin, liver diseases, and vit.K deficiency.
- PT measures :
- Extrinsic pathway (Activated VIIa)
- Tissue factor.
- Common pathway ( factor X, V, II, and fibrinogen ).
- The first stage is an aggregation of platelets to plug the damaged blood vessels
- The second stage is by activation of clotting factors.
- The first phase of the activation of the intrinsic pathway.
- At the same time, the extrinsic pathway is activated.
- Now by common pathway factor X is activated by the proteases formed by the intrinsic and extrinsic pathway.
- The fourth phase is the conversion of prothrombin to thrombin in the presence of Factor X, Factor V, phospholipids, and calcium.
- Thrombin converts fibrinogen to fibrin.
- Fibrin is converted into a stable gel.
- XIII cross-links the fibrin and forms the clot.
- PT = 11 to 13 seconds, (normally PT is 85% to 100%)
- (This may vary from lab to lab).
- This should be compared with the control which will be around 11 to 14 seconds.
- Anticoagulant therapy response = 1.5 to 2 times of the control value.
- Critical value = >20 seconds
- INR is an international normalized ratio. = 0.8 to 1.1
Increased Prothrombin Time is seen in:
- Deficiency of factor II (prothrombin), V, VII, and X.
- Liver diseases, like cirrhosis, and hepatic failure.
- The factor I, II, V, VII, IX, and X are produced in the liver.
- Biliary obstruction. There is a lake of the bile which is needed for the fat-soluble vitamins like Vit.A, D, E, and K for their absorption.
- Synthesis of factor II, VII, and X depends upon the vitamin K.
- If the patients respond to Vit.K therapy in 1 to 3 days means that there is no liver cell damage rather there is a biliary obstruction.
- If there is no response to Vit.k therapy then the patient has severe liver cell injury.
- Sprue, celiac disease, and chronic diarrhea.
- Vit.K deficiency, even in the newborn of the mother with Vit.K deficiency.
- Hemorrhagic disease of the newborn.
- Anticoagulant therapy (Warfarin and Coumadin).
- D I C.
- Factor 1 deficiency (Hypofibrinogenemia).
- Circulating anticoagulants is seen in lupus disease.
- Premature newborn.
- Salicylates intoxication.
- Massive blood transfusion.
Summary of PT, PTT
- Abnormal PTT alone
- Bleeding due to deficiency of factor V11, IX, and XI.
- Abnormal PT only
- Factor VII deficiency.
- Abnormal PT and PTT both
- Anticoagulant therapy.
- D I C.
- Vit.K deficiency.
- Liver diseases.
- Massive blood transfusion.
- Rarely due to Dysfibrinogenemia, and deficiency of factor X, V, and II.
|Clinical condition||Prothrombin time||Thrombin time||APTT||Platelets count|
|Heparin therapy||prolonged mild||prolonged||prolonged||normal (may be low)|
|Liver disease||prolonged||normal (rarely prolonged)||prolonged||low|
|Blood transfusion, massive||prolonged||normal||prolonged||low|
- Please for more information see PTT and APTT.