1. Bleeding time,clotting time, PT, and PTT
Dr. Ayham Abu Laila

2. Hemostasis or haemostasis
Is a complex process which causes the bleeding process to stop.
It refers to the process of keeping blood within a damaged blood vessel.

3. Hemostasis is maintained in the body via three mechanisms:
Vascular spasm - Damaged blood vessels constrict.
Platelet plug formation - Platelets adhere to damaged endothelium to form platelet plug (primary hemostasis) and then degranulate.
Blood coagulation - Clots form upon the conversion of fibrinogen to fibrin, and its addition to the platelet plug (secondary hemostasis).

4. THE CLOTTING MECHANISM
INTRINSIC
EXTRINSC
Collagen
Tisue Thromboplastin
XII XI
VII IX
VIII X V
FIBRINOGEN
(I)
PROTHROMBIN THROMBIN
(II)
(III)
FIBRIN

6. FIBRINOLYTIC PHASE
ANTICLOTTING MECHANISMS ARE ACTIVATED TO ALLOW CLOT DISINTEGRATION AND REPAIR OF THE DAMAGED VESSEL.

7. HEMOSTASIS DEPENDENT UPON: Vessel Wall Integrity
Adequate Numbers of Platelets
Proper Functioning Platelets
Adequate Levels of Clotting Factors
Proper Function of Fibrinolytic Pathway

8. So What Causes Bleeding Disorders?
VESSEL DEFECTS
PLATELET DISORDERS
FACTOR DEFICIENCIES

9. VESSEL DEFECTS VITAMIN C DEFICIENCY BACTERIAL & VIRAL INFECTIONS
ACQUIRED

10. PLATELET DISORDERS Causes
THROMBOCYTOPENIA (INADEQUATE NUMBER OF PLATELETS)
Causes
DRUG INDUCED
BONE MARROW FAILURE
HYPERSPLENISM
OTHER CAUSES

11. THROMBOCYTOPATHY )ADEQUATE NUMBER BUT ABNORMAL FUNCTION .( causes
UREMIA
INHERITED DISORDERS
MYELOPROLIFERATIVE DISORDERS
DRUG INDUCED(ASPIRIN, NSAIDS)

12. FACTOR DEFICIENCIES Acquired: Inherited: Anticoagulant therapy
HEMOPHILIA A
HEMOPHILIA B
VON WILLEBRAND’S DISEASE
Acquired:
Anticoagulant therapy
Liver diseases
DIC

13. LABORATORY EVALUATION
PLATELET COUNT
BLEEDING TIME (BT)
Clotting time (CT)
PROTHROMBIN TIME (PT)
Activated PARTIAL THROMBOPLASTIN TIME (APTT)

14. PLATELET COUNT (CBC) NORMAL 100,000 - 400,000 CELLS/MM3
< 100, Thrombocytopenia
50, ,000 Mild Thrombocytopenia
< 50,000 Sever Thrombocytopenia

15. BLEEDING TIME PROVIDES ASSESSMENT OF PLATELET COUNT AND FUNCTION
NORMAL VALUE
2-8 MINUTES

16. Clotting time - capillary method
Material
Sterile disposable pricking needle or lancet.
Stop watch
Dry glass capillary tube (narrow diameter 1 top 2 mm, minimum 10 cm long.)
Cotton Swab of absorbent cotton.
Spirit wetted, cotton swab.
70 % v/v ethyl alcohol

17. Clotting time of whole blood

18. Clotting Time - Slide Method
The surface of the glass tube initiates the clotting process. This test is sensitive to the factors involved in the intrinsic pathway
The expected range for clotting time is 4-10 min.

19. PROTHROMBIN TIME Measures Effectiveness of the Extrinsic Pathway
NORMAL VALUE
10-15 SECS

20. PT
The prothrombin time: is therefore the time required for the plasma to clot after an excess of thromboplastin and an optimal concentration of calcium have been added.
Measures the function of the Extrinsic Pathway.
Sensitive to Factors I, II, V, VII, X.
The PT evaluates patients suspected of having an inherited or acquired deficiency in these pathways.

21. THE CLOTTING MECHANISM
INTRINSIC
EXTRINSC
Collagen
Tisue Thromboplastin
XII XI
VII IX
VIII X V
FIBRINOGEN
(I)
PROTHROMBIN THROMBIN
(II)
(III)
FIBRIN

22. When is it ordered?
Used to monitor oral anticoagulant therapy (Warfarin / Coumadin).
When a patient who is not taking anti-coagulant drugs has signs or symptoms of a bleeding disorder.
When a patient is to undergo an invasive medical procedure, such as surgery, to ensure normal clotting ability.

23. An elevated prothrombin time may indicate the presence of:
Vitamin K deficiency
(Vitamin K is needed to make prothrombin and other clotting factors)
DIC
liver disease
a deficiency in one or more of the following factors:
I, II, V, VII, X.
Anticoagulant (warfarin)

24. INR A PT test may also be called an INR test.
INR (international normalized ratio) stands for a way of standardizing the results of prothrombin time tests, no matter the testing method.
So your doctor can understand results in the same way even when they come from different labs and different test methods.
Using the INR system, treatment with (anticoagulant therapy) will be the same. In some labs, only the INR is reported and the PT is not reported

25. An INR of 1.0 means that the patient PT is normal.
An INR greater than 1.0 means the clotting time is elevated.
INR of greater than 5 or 5.5 = unacceptable high risk of bleeding,whereas if the INR=0.5 then there is a high chance of having a clot.
Normal range for a healthy person is 0.9–1.3, and for people on warfarin therapy, 2.0–3.0, although the target INR may be higher in particular situations, such as for those with a mechanical heart valve.

26. PARTIAL THROMBOPLASTIN TIME
Measures Effectiveness of the Intrinsic
Pathway
NORMAL VALUE
25-40 SECS

27. PTT
The partial thromboplastin time (PTT) or activated partial thromboplastin time (aPTT or APTT( is a performance indicator measuring the efficacy of both the "intrinsic" and the common coagulation pathways.
It is also used to monitor the treatment effects with heparin a major anticoagulant.
Kaolin cephalin clotting time (KccT) is a historic name for the activated partial thromboplastin time

28. THE CLOTTING MECHANISM
INTRINSIC
EXTRINSC
Collagen
Tisue Thromboplastin
XII XI
VII IX
VIII X V
FIBRINOGEN
(I)
PROTHROMBIN THROMBIN
(II)
(III)
FIBRIN

29. Normal PTT times require the presence of the following coagulation factors:
I, II, III, IV, V, VI, VIII, IX, X, XI, & XII

30. When is it ordered?
When a patient presents with unexplained bleeding or bruising,
It may be ordered as part of a pre-surgical evaluation for bleeding tendencies,
When a patient is on intravenous (IV) or injection heparin therapy, the APTT is ordered at regular intervals to monitor the degree of anticoagulation.

31. Prolonged APTT may indicate:
use of heparin.
antiphospholipid antibody:especially lupus anticoagulant, which paradoxically increases propensity to thrombosis
coagulation factor deficiency ,
e.g hemophilia
DIC
Liver disease

32. THE CLOTTING MECHANISM
INTRINSIC
EXTRINSC
Collagen
Tisue Thromboplastin
XII XI
VII IX
VIII X V
FIBRINOGEN
(I)
PROTHROMBIN THROMBIN
(II)
(III)
FIBRIN

33. FACTOR DEFICIENCIES Inherited: Acquired: Anticoagulant therapy
HEMOPHILIA A
HEMOPHILIA B
VON WILLEBRAND’S DISEASE
Acquired:
Anticoagulant therapy
Liver diseases
DIC

34. HEMOPHILIA A (Classic Hemophilia)
80-85% of all Hemophiliacs
Deficiency of Factor VIII
Lab Results - Prolonged PTT

35. HEMOPHILIA B (Christmas Disease)
10-15% of all Hemophiliacs
Deficiency of Factor IX
Lab Test - Prolonged PTT

36. VON WILLEBRAND’S DISEASE
Deficiency of VWF & amount of Factor VIII
Factor VIII is bound to vWF while inactive in circulation; Factor VIII degrades rapidly when not bound to vWF
Lab Results - Prolonged BT, PTT

37. ANTICOAGULANTS ANTICOAGULANTS
An anticoagulant is a substance that prevents coagulation; that is, it stops blood from clotting
This prevents deep vein thrombosis, pulmonar embolism, myocardial infarction and stroke.
ANTICOAGULANTS
Coumadins (Vitamin K antagonists)
Heparin

38. Coumadins
These oral anticoagulants that antagonize the effects of vitamin K.
Examples include warfarin. It takes at least 48 to 72 hours for the anticoagulant effect to develop. Where an immediate effect is required, heparin must be given concomitantly.
Monitored by PT times
These anticoagulants are used to treat patients with deep-vein thrombosis (DVT), pulmonary embolism (PE), atrial fibrillation (AF), and mechanical prosthetic heart valves.

39. Heparin Heparin is a biological substance.
It works by activating antithrombin III, which blocks thrombin from clotting blood.
Heparin Therapy is Monitored by PTT times
Low molecular weight heparin is a more highly processed product that is useful as it does not require monitoring of the APTT coagulation parameter (it has more predictable plasma levels) and has fewer side effects.

40. Liver Disease
Liver Disease can Result in Reduced Production of Coagulation Factors (I,II,V,VII,IX,X).

41. DIC
Disseminated intravascular coagulation (DIC is a pathological activation of coagulation) blood clotting) mechanisms that happens in response to a variety of diseases
DIC leads to the formation of small blood clots inside the blood vessels throughout the body
The small clots also disrupt normal blood flow to organs (such as the kidneys), which may malfunction as a result

42. As the small clots consume coagulation proteins and platelets, normal coagulation is disrupted and abnormal bleeding occurs from the skin the gastrointestinal tract, the respiratory tract and surgical wounds.
The PT and APTT are usually very prolonged and the fibrinogen level markedly reduced
High levels of fibrin degradation products, including D-dimer, are found owing to the intense fibrinolytic activity stimulated by the presence of fibrin in the circulation.

43. Definitive diagnosis depends on the result of DIC:
Thrombocytopenia) prolonged bleeding time)
Prolongation of prothrombin time and activated partial thromboplastin time
A low fibrinogen concentration
Increased levels of fibrin degradation products

44. Partial thromboplastin time Prothrombin time Condition
Platelet count  
Bleeding time  
Partial thromboplastin time  
Prothrombin time  
Condition  
unaffected
prolonged
Von Willebrand disease
Vitamin K deficiency or Warfarin
Uremia
Haemophilia
Factor V deficiency
Aspirin
decreased
Thrombocytopenia
End-stage Liver failure
Disseminated intravascular coagulation
Bernard-Soulier syndrome

45. THANK YOU