1. COGULATION
PROFILE
Bleeding time, clotting time,
PT, and PTT
Presented By
HUSSAIN AKHTAR

2. WHAT IS COAGULATION?
Coagulation is a complex process by which blood forms clots.
Blood must be remain fluid with in the vasculature and yet clot
quickly when expose to non endothelial surface at a site of
vascular injury.
It is an important part of haemostasis (the cessation of blood
loss from a damaged vessel), where in a damaged blood vessel
wall is covered by a platelet and fibrin-containing clot to stop
bleeding and begin repair of the damaged vessel.
Disorders of coagulation can lead to an increased risk of
bleeding (hemorrhage) or clotting (thrombosis).

3. Hemostasis is maintained in the body via three
mechanisms:
Vascular spasm - Damaged blood vessels.
constrict
Platelet plug formation - Platelats 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. Factor I Fibrinogen Factor VIII Antihemophilic
globulin
Factor II Prothrombin Factor IX Partial
thromboplastin
component
Factor III Thromboplastin Factor X Stuart-Prower
factor
Factor IV Calcium Factor XI Plasma
thromboplastin
antecedent
Factor V Labile or
proaccelerin
Factor XII Hageman factor
Factor VII Stable factor or
proconvertin
Factor XIII Fibrin-
stabilizing factor

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

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
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 Inherited:
1. HEMHHHHOPHILIA A
2. HEMOPHILIA B
3. VON WILLEBRAND’S
DISEASE
 Acquired:
1. Anticoagulant therapy
2. Liver diseases
3. 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
< 100,000 Thrombocytopenia
50,000 - 100,000 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
1. Sterile disposable pricking needle or lancet.
2. Stop watch
3. Dry glass capillary tube (narrow diameter 1 top 2 mm,
minimum 10 cm long.)
4. Cotton Swab of absorbent cotton.
5. Spirit wetted, cotton swab.
6. 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 TIMEPROTHROMBIN TIME
Measures Effectiveness of the ExtrinsicMeasures Effectiveness of the Extrinsic
PathwayPathway
NORMAL VALUENORMAL VALUE
10-15 SECS10-15 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
PROTHROMBIN THROMBIN
FIBRINOGEN
FIBRIN(II) (III)
(I)
V
X
Tisue ThromboplastinCollagen
VII
XII
XI
IX
VIII

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 VALUENORMAL VALUE
25-40 SECS25-40 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
PROTHROMBIN THROMBIN
FIBRINOGEN
FIBRIN(II) (III)
(I)
V
X
Tisue ThromboplastinCollagen
VII
XII
XI
IX
VIII

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

33. FACTOR DEFICIENCIES
 Inherited:
1. HEMOPHILIA A
2. HEMOPHILIA B
3. VON
WILLEBRAND’S
DISEASE
 Acquired:
1. Anticoagulant
therapy
2. Liver diseases
3. 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
 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
1. Coumadins (Vitamin K antagonists)
2. Heparin

38. Coumadin's
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. Pre-analytic errors
 Problems with blue-top tube
 Partial fill tubes
 Vacuum leak and citrate evaporation
 Problems with phlebotomy
 Heparin contamination
 Wrong label
 Slow fill
 Underfill
 Vigorous shaking
Biological effects
•Hct ≥55 or ≤15
•Lipemia, hyperbilirubinemia,
hemolysis
Laboratory errors
•Delay in testing
•Prolonged incubation at 37°C
•Freeze/thaw deterioration