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Bleeding time,clotting time,

PT, and PTT

Dr. Ayham Abu Laila

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.

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).

THE CLOTTING MECHANISM


INTRINSIC
Collagen

EXTRINSC
Tisue Thromboplastin

XII
XI
IX
VIII

VII

X
FIBRINOGEN
(I)

V
PROTHROMBIN
(II)

THROMBIN
(III)

FIBRIN

FIBRINOLYTIC PHASE
ANTICLOTTING

MECHANISMS ARE
ACTIVATED TO ALLOW CLOT
DISINTEGRATION AND REPAIR OF THE
DAMAGED VESSEL.

HEMOSTASIS
DEPENDENT

UPON:

Vessel Wall Integrity


Adequate Numbers of Platelets
Proper Functioning Platelets
Adequate Levels of Clotting Factors
Proper Function of Fibrinolytic Pathway

So What Causes Bleeding


Disorders?

VESSEL DEFECTS

PLATELET DISORDERS

FACTOR DEFICIENCIES

VESSEL DEFECTS

VITAMIN C DEFICIENCY
BACTERIAL & VIRAL INFECTIONS
ACQUIRED

PLATELET DISORDERS
THROMBOCYTOPENIA
(INADEQUATE NUMBER OF PLATELETS)

Causes

DRUG INDUCED
BONE MARROW FAILURE
HYPERSPLENISM
OTHER CAUSES

THROMBOCYTOPATHY
)ADEQUATE NUMBER BUT ABNORMAL
FUNCTION .(

causes

UREMIA
INHERITED DISORDERS
MYELOPROLIFERATIVE DISORDERS
DRUG INDUCED(ASPIRIN,

NSAIDS)

FACTOR DEFICIENCIES

Inherited:
1.

HEMOPHILIA A

2.

HEMOPHILIA B

3.

VON WILLEBRANDS
DISEASE

Acquired:

1.

Anticoagulant
therapy

2.

Liver diseases

3.

DIC

LABORATORY EVALUATION
PLATELET

COUNT
BLEEDING TIME (BT)
Clotting time (CT)
PROTHROMBIN TIME (PT)
Activated PARTIAL THROMBOPLASTIN
TIME (APTT)

PLATELET COUNT (CBC)


NORMAL

100,000 - 400,000

CELLS/MM3

Thrombocytopenia

100,000>

Mild Thrombocytopenia100,000 - 50,000


Sever Thrombocytopenia 50,000>

BLEEDING TIME
PROVIDES ASSESSMENT OF

PLATELET COUNT AND FUNCTION

NORMAL VALUE
2-8 MINUTES

Clotting time - capillary method

Material

1.

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

2.
3.
4.
5.
6.

Clotting time of whole blood

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.

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

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.

THE CLOTTING MECHANISM


INTRINSIC
Collagen

EXTRINSC
Tisue Thromboplastin

XII
XI
IX
VIII

VII

X
FIBRINOGEN
(I)

V
PROTHROMBIN
(II)

THROMBIN
(III)

FIBRIN

?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.

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)

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

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 0.91.3, and for
people on warfarin therapy, 2.03.0, although the target
INR may be higher in particular situations, such as for
those with a mechanical heart valve.

PARTIAL THROMBOPLASTIN TIME

Measures Effectiveness of the Intrinsic


Pathway

NORMAL VALUE
25-40 SECS

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

THE CLOTTING MECHANISM


INTRINSIC
Collagen

EXTRINSC
Tisue Thromboplastin

XII
XI
IX
VIII

VII

X
FIBRINOGEN
(I)

V
PROTHROMBIN
(II)

THROMBIN
(III)

FIBRIN

Normal

PTT times require the


presence of the following coagulation
factors:
I, II, III, IV, V, VI, VIII, IX, X, XI, & XII

?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.

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

THE CLOTTING MECHANISM


INTRINSIC
Collagen

EXTRINSC
Tisue Thromboplastin

XII
XI
IX
VIII

VII

X
FIBRINOGEN
(I)

V
PROTHROMBIN
(II)

THROMBIN
(III)

FIBRIN

FACTOR DEFICIENCIES

Inherited:
1.

Acquired:

1.

Anticoagulant
therapy

2.

Liver diseases

3.

DIC

HEMOPHILIA A

2.

HEMOPHILIA B

3.

VON
WILLEBRANDS
DISEASE

HEMOPHILIA A (Classic Hemophilia)


80-85% of all Hemophiliacs
Deficiency of Factor VIII
Lab Results - Prolonged PTT

HEMOPHILIA
10-15%

B (Christmas Disease)

of all Hemophiliacs
Deficiency of Factor IX
Lab Test - Prolonged PTT

VON

WILLEBRANDS 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

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.

1.
2.

ANTICOAGULANTS

Coumadins (Vitamin K antagonists)


Heparin

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 .

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.

Liver Disease

Liver Disease can Result in Reduced


Production of Coagulation
Factors
(I,II,V,VII,IX,X).

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

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.

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

Condition

Prothrombi
n
time

Partial
thromboplastin
time

Bleeding
time

Platelet
count

Von Willebrand disease

unaffected

prolonged

prolonged

unaffected

Vitamin K deficiency or
Warfarin

prolonged

prolonged

unaffected unaffected

Uremia

unaffected

unaffected

prolonged

Haemophilia

unaffected

prolonged

unaffected unaffected

Factor V deficiency

prolonged

prolonged

unaffected unaffected

Aspirin

unaffected

unaffected

prolonged

unaffected

Thrombocytopenia

unaffected

unaffected

prolonged

decreased

End-stage Liver failure

prolonged

prolonged

prolonged

decreased

Disseminated intravascular
coagulation

prolonged

prolonged

prolonged

decreased

Bernard-Soulier syndrome

unaffected

unaffected

prolonged

decreased

unaffected

THANK YOU

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