bleeding time, clotting time pt and ptt2
TRANSCRIPT
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Hemostasisor haemostasis:
is a complex process which causes thebleeding process to stop. It refers to theprocess of keeping blood within adamaged blood vessel.
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Hemostasis is maintained in the bodyvia three mechanisms:
Vascular spasm- Damaged blood vesselsconstrict.
Platelet plug formation- Plateletsadhere to
damaged endothelium to form platelet plug(primary hemostasis) and then degranulate.
Blood coagulation- Clots form upon theconversion of fibrinogento fibrin, and itsaddition to the platelet plug (secondaryhemostasis).
http://en.wikipedia.org/wiki/Vasoconstrictionhttp://en.wikipedia.org/wiki/Platelethttp://en.wikipedia.org/wiki/Coagulationhttp://en.wikipedia.org/wiki/Fibrinogenhttp://en.wikipedia.org/wiki/Fibrinhttp://en.wikipedia.org/wiki/Fibrinhttp://en.wikipedia.org/wiki/Fibrinogenhttp://en.wikipedia.org/wiki/Coagulationhttp://en.wikipedia.org/wiki/Platelethttp://en.wikipedia.org/wiki/Vasoconstriction -
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THE CLOTTING MECHANISM
INTRINSIC
EXTRINSC
PROTHROMBIN THROMBIN
FIBRINOGE
N
FIBRIN(II) (III)
(I)V
X
Tisue ThromboplastinCollagen
VII
XII
XIIX
VIII
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FIBRINOLYTIC PHASE
ANTICLOTTING MECHANISMS ARE ACTIVATEDTO ALLOW CLOT DISINTEGRATION ANDREPAIR OF THE DAMAGED VESSEL.
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HEMOSTASIS
DEPENDENT UPON:
Vessel Wall Integrity
Adequate Numbers of Platelets
Proper Functioning Platelets
Adequate Levels of Clotting Factors
Proper Function of Fibrinolytic Pathway
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So What Causes Bleeding Disorders?
VESSEL DEFECTS
PLATELET DISORDERS
FACTOR DEFICIENCIES
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VESSEL DEFECTS
VITAMIN C DEFICIENCY
BACTERIAL & VIRAL INFECTIONS
ACQUIRED
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PLATELET DISORDERS
THROMBOCYTOPENIA(INADEQUATE NUMBER OF PLATELETS)
Causes DRUG INDUCED
BONE MARROW FAILURE
HYPERSPLENISM OTHER CAUSES
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THROMBOCYTOPATHY)ADEQUATE NUMBER BUT ABNORMALFUNCTION (.
causes UREMIA
INHERITED DISORDERS MYELOPROLIFERATIVE DISORDERS
DRUG INDUCED(ASPIRIN, NSAIDS)
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FACTOR DEFICIENCIES
Inherited:
1. HEMOPHILIA A
2. HEMOPHILIA B
3. VON WILLEBRANDSDISEASE
Acquired:
1. Anticoagulant
therapy
2. Liver diseases
3. DIC
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LABORATORY EVALUATION
PLATELET COUNT
BLEEDING TIME (BT)
PROTHROMBIN TIME (PT)
PARTIAL THROMBOPLASTIN TIME (PTT)
THROMBIN TIME (TT)
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PLATELET COUNT (CBC)
NORMAL 100,000 - 400,000CELLS/MM3
< 100,000Thrombocytopenia
50,000 - 100,000Mild Thrombocytopenia
< 50,000Sever Thrombocytopenia
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BLEEDING TIME
PROVIDES ASSESSMENT OF
PLATELET COUNT AND FUNCTION
NORMAL VALUE2-8 MINUTES
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PROTHROMBIN TIME
Measures Effectiveness of the Extrinsic
Pathway
NORMAL VALUE
10-15 SECS
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PT
The prothrombin time: is therefore the time required for the plasmato clot after an excess of thromboplastin and an optimalconcentration 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 oracquired deficiency in these pathways.
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THE CLOTTING MECHANISM
INTRINSIC
EXTRINSC
PROTHROMBIN THROMBIN
FIBRINOGE
N
FIBRIN(II) (III)
(I)V
X
Tisue ThromboplastinCollagen
VII
XII
XI
IX
VIII
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When is it ordered?
Used to monitor oral anticoagulant therapy (Warfarin /
Coumadin).
When a patient who is not taking anti-coagulant drugshas signs or symptoms of a bleeding disorder.
When a patient is to undergo an invasive medical
procedure, such as surgery, to ensure normal clottingability.
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An elevated prothrombin time may indicatethe 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)
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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
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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 ofbleeding,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.
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PARTIAL THROMBOPLASTIN TIME
Measures Effectiveness of the Intrinsic
Pathway
NORMAL VALUE
25-40 SECS
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PTT
Thepartial thromboplastin time (PTT) oractivated partial
thromboplastin time(aPTTorAPTT(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 majoranticoagulant.
Kaolin cephalin clotting time (KccT) is a historic name for
the activated partial thromboplastin time
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THE CLOTTING MECHANISM
INTRINSIC
EXTRINSC
PROTHROMBIN THROMBIN
FIBRINOGE
N
FIBRIN(II) (III)
(I)V
X
Tisue ThromboplastinCollagen
VII
XII
XI
IX
VIII
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Normal PTT times require the presence ofthe following coagulation factors:
I, II, III, IV, V, VI, VIII, IX, X, XI, & XII
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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.
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Prolonged APTT may indicate:
use ofheparin.
antiphospholipid antibody:especiallylupus anticoagulant,
which paradoxically increases propensity tothrombosis
coagulation factor deficiency ,
e.g hemophilia DIC
Liver disease
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FACTOR DEFICIENCIES
Inherited:
1. HEMOPHILIA A
2. HEMOPHILIA B
3. VON WILLEBRANDSDISEASE
Acquired:
1. Anticoagulant
therapy
2. Liver diseases
3. DIC
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HEMOPHILIA A (Classic Hemophilia)
80-85% of all Hemophiliacs
Deficiency of Factor VIII
Lab Results - Prolonged PTT
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HEMOPHILIA B (Christmas Disease)10-15% of all Hemophiliacs
Deficiency of Factor IX
Lab Test - Prolonged PTT
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VON WILLEBRANDS DISEASEDeficiency of VWF & amount of Factor VIII
Factor VIII is bound to vWF while inactive in
circulation; Factor VIII degrades rapidly when notbound to vWF
Lab Results - Prolonged BT, PTT
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Coumadins
These oral anticoagulants that antagonize the effects of
vitamin K.
Examples include warfarin. It takes at least 48 to 72hours for the anticoagulant effect to develop. Where animmediate effect is required, heparinmust be givenconcomitantly.
Monitored by PT times
These anticoagulants are used to treat patients withdeep-vein thrombosis(DVT), pulmonary embolism(PE),atrial fibrillation(AF), and mechanical prosthetic heartvalves.
http://en.wikipedia.org/wiki/Vitamin_Khttp://en.wikipedia.org/wiki/Warfarinhttp://en.wikipedia.org/wiki/Heparinhttp://en.wikipedia.org/wiki/Deep-vein_thrombosishttp://en.wikipedia.org/wiki/Pulmonary_embolismhttp://en.wikipedia.org/wiki/Atrial_fibrillationhttp://en.wikipedia.org/wiki/Prosthetic_heart_valvehttp://en.wikipedia.org/wiki/Prosthetic_heart_valvehttp://en.wikipedia.org/wiki/Prosthetic_heart_valvehttp://en.wikipedia.org/wiki/Prosthetic_heart_valvehttp://en.wikipedia.org/wiki/Atrial_fibrillationhttp://en.wikipedia.org/wiki/Pulmonary_embolismhttp://en.wikipedia.org/wiki/Deep-vein_thrombosishttp://en.wikipedia.org/wiki/Deep-vein_thrombosishttp://en.wikipedia.org/wiki/Deep-vein_thrombosishttp://en.wikipedia.org/wiki/Heparinhttp://en.wikipedia.org/wiki/Warfarinhttp://en.wikipedia.org/wiki/Vitamin_K -
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Heparin
Heparin is a biological substance.
It works by activating antithrombin III, which blocksthrombin from clotting blood.
Heparin Therapy is Monitored by PTT times
Low molecular weight heparinis a more highlyprocessed product that is useful as it does not requiremonitoring of the APTT coagulation parameter (it hasmore predictable plasma levels) and has fewer side
effects.
http://en.wikipedia.org/wiki/Antithrombin_IIIhttp://en.wikipedia.org/wiki/Low_molecular_weight_heparinhttp://en.wikipedia.org/wiki/Low_molecular_weight_heparinhttp://en.wikipedia.org/wiki/Antithrombin_III -
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Liver Disease
Liver Disease can Result in ReducedProduction of Coagulation Factors
(I,II,V,VII,IX,X).
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DIC
Disseminated intravascular coagulation ( DICis apathological activation ofcoagulation)blood clotting)mechanisms that happens in response to a variety ofdiseases
DIC leads to the formation of small blood clots inside theblood vessels throughout the body
The small clots also disrupt normal blood flow to organs
(such as the kidneys), which may malfunction as a result
http://en.wikipedia.org/wiki/Coagulationhttp://en.wikipedia.org/wiki/Kidneyhttp://en.wikipedia.org/wiki/Kidneyhttp://en.wikipedia.org/wiki/Coagulation -
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As the small clots consume coagulation proteins andplatelets, normal coagulation is disrupted and abnormalbleeding 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.
http://en.wikipedia.org/wiki/D-dimerhttp://en.wikipedia.org/wiki/D-dimerhttp://en.wikipedia.org/wiki/D-dimerhttp://en.wikipedia.org/wiki/D-dimerhttp://en.wikipedia.org/wiki/D-dimer -
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Definitive diagnosis depends on the result of DIC:
Thrombocytopenia)prolonged bleeding time)
Prolongation ofprothrombin timeandactivated partialthromboplastin time
A lowfibrinogen concentration
Increased levels offibrin degradation products
PlateletBleedingPartial
Prothrombi
http://en.wikipedia.org/wiki/Platelet_counthttp://en.wikipedia.org/wiki/Bleeding_timehttp://en.wikipedia.org/wiki/Partial_thromboplastin_timehttp://en.wikipedia.org/wiki/Prothrombin_timehttp://en.wikipedia.org/wiki/Disseminated_intravascular_coagulationhttp://en.wikipedia.org/wiki/Disseminated_intravascular_coagulationhttp://en.wikipedia.org/wiki/Disseminated_intravascular_coagulationhttp://en.wikipedia.org/wiki/Disseminated_intravascular_coagulationhttp://en.wikipedia.org/wiki/Prothrombin_timehttp://en.wikipedia.org/wiki/Partial_thromboplastin_timehttp://en.wikipedia.org/wiki/Bleeding_timehttp://en.wikipedia.org/wiki/Platelet_count -
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Platelet
count
Bleeding
timethromboplastin
time
Prothrombi
n timeCondition
unaffectedprolongedprolongedunaffectedVon Willebrand disease
unaffectedunaffectedprolongedprolongedVitamin K deficiencyor
Warfarin
unaffectedprolongedunaffectedunaffectedUremia
unaffectedunaffectedprolongedunaffectedHaemophilia
unaffectedunaffectedprolongedprolongedFactor Vdeficiency
unaffectedprolongedunaffectedunaffectedAspirin
decreasedprolongedunaffectedunaffectedThrombocytopenia
decreasedprolongedprolongedprolongedEnd-stage Liver failure
decreasedprolongedprolongedprolongedDisseminated intravascularcoagulation
decreasedprolongedunaffectedunaffectedBernard-Soulier syndrome
http://en.wikipedia.org/wiki/Platelet_counthttp://en.wikipedia.org/wiki/Platelet_counthttp://en.wikipedia.org/wiki/Bleeding_timehttp://en.wikipedia.org/wiki/Bleeding_timehttp://en.wikipedia.org/wiki/Partial_thromboplastin_timehttp://en.wikipedia.org/wiki/Partial_thromboplastin_timehttp://en.wikipedia.org/wiki/Prothrombin_timehttp://en.wikipedia.org/wiki/Prothrombin_timehttp://en.wikipedia.org/wiki/Von_Willebrand_diseasehttp://en.wikipedia.org/wiki/Vitamin_K_deficiencyhttp://en.wikipedia.org/wiki/Warfarinhttp://en.wikipedia.org/wiki/Uremiahttp://en.wikipedia.org/wiki/Haemophiliahttp://en.wikipedia.org/wiki/Factor_Vhttp://en.wikipedia.org/wiki/Aspirinhttp://en.wikipedia.org/wiki/Thrombocytopeniahttp://en.wikipedia.org/wiki/Bernard-Soulier_syndromehttp://en.wikipedia.org/wiki/Bernard-Soulier_syndromehttp://en.wikipedia.org/wiki/Bernard-Soulier_syndromehttp://en.wikipedia.org/wiki/Bernard-Soulier_syndromehttp://en.wikipedia.org/wiki/Thrombocytopeniahttp://en.wikipedia.org/wiki/Aspirinhttp://en.wikipedia.org/wiki/Factor_Vhttp://en.wikipedia.org/wiki/Haemophiliahttp://en.wikipedia.org/wiki/Uremiahttp://en.wikipedia.org/wiki/Warfarinhttp://en.wikipedia.org/wiki/Vitamin_K_deficiencyhttp://en.wikipedia.org/wiki/Von_Willebrand_diseasehttp://en.wikipedia.org/wiki/Disseminated_intravascular_coagulationhttp://en.wikipedia.org/wiki/Disseminated_intravascular_coagulationhttp://en.wikipedia.org/wiki/Prothrombin_timehttp://en.wikipedia.org/wiki/Prothrombin_timehttp://en.wikipedia.org/wiki/Disseminated_intravascular_coagulationhttp://en.wikipedia.org/wiki/Partial_thromboplastin_timehttp://en.wikipedia.org/wiki/Partial_thromboplastin_timehttp://en.wikipedia.org/wiki/Disseminated_intravascular_coagulationhttp://en.wikipedia.org/wiki/Bleeding_timehttp://en.wikipedia.org/wiki/Bleeding_timehttp://en.wikipedia.org/wiki/Disseminated_intravascular_coagulationhttp://en.wikipedia.org/wiki/Platelet_counthttp://en.wikipedia.org/wiki/Platelet_count -
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