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Cogulation Profile: Bleeding Time, Clotting Time, PT, and PTT
Cogulation Profile: Bleeding Time, Clotting Time, PT, and PTT
PROFILE
Presented By
DR ARPANA HAZARIKA
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).
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).
Antihemophilic Factor VIII Fibrinogen Factor I
globulin
Partial Factor IX Prothrombin Factor II
thromboplastin
component
Stuart-Prower Factor X Thromboplasti Factor III
factor n
Plasma Factor XI Calcium Factor IV
thromboplastin
antecedent
Hageman factor Factor XII Labile or Factor V
proaccelerin
Fibrin- Factor XIII Stable factor or Factor VII
stabilizing factor proconvertin
THE CLOTTING MECHANISM
INTRINSIC EXTRINSC
Collagen Tisue Thromboplastin
XII
XI VII
IX
VIII
X
V FIBRINOGEN
(I)
PROTHROMBIN THROMBIN
(II) (III) FIBRIN
FIBRINOLYTIC PHASE
VESSEL DEFECTS
PLATELET DISORDERS
FACTOR DEFICIENCIES
VITAMIN K DEFIECIENCY
ANTI COAGULANT OVERDOSE
DISSEMINATED INTRAVASCULAR CLOTTING
VESSEL DEFECTS
VITAMIN C DEFICIENCY
BACTERIAL & VIRAL INFECTIONS
TOXIC EFFECT OF DRUGS AND CHEMICALS
ALLERGIC PURPURA
CONNECTIVE TISSUE DISEASES
PLATELET DISORDERS
l PURPURA-purpura is a group of disorder occuring due
to various disorder.The term purpura
l Is derived from purple coloured petichial haemorrhages
and bruises in the skin
THROMBOCYTOPENIC PURPURA
(INADEQUATE NUMBER OF PLATELETS)
Decrease in platelet count below 1.5 lac/mm3
is called thrombocytopenia
THROMBOCTOPENIC PURPURA MAY BE
PRIMARY THROMBOCYTOPENIC
PURPURA[Idiopathic]
SECONDARY THROMBOCYTOPENIA
Secondary thrombocytopenic purpura-The causes of
Platelet deficiency are
Bone marrow depression due to effect of various
cytotoxic drugs.Whole body irradiations and
hypoplastic and aplastic anaemia
Leukemia and secondary deposits of malignancies in
The bone marrow
Acute septicemia,toxaemia and uremia
Hypersplenism
Non thrombocytopenic purpura l
Non thrombocytopenic purpura occur due to vessel
Wall defect
THROMBOCYTOPATHY
) ADEQUATE NUMBER BUT ABNORMAL FUNCTION )
causes
UREMIA
INHERITED DISORDERS
MYELOPROLIFERATIVE DISORDERS
DRUG INDUCED(ASPIRIN, NSAIDS)
FACTOR
Inherited:
DEFICIENCIES
Acquired:
NORMAL VALUE
2-8 MINUTES
Clotting time - capillary method
Material
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.
V FIBRINOGEN
(I)
PROTHROMBIN THROMBIN
(II) (III) FIBRIN
When is it ordered?
Used to monitor oral anticoagulant therapy (Warfarin /
Coumadin).
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.
V FIBRINOGEN
(I)
PROTHROMBIN THROMBIN
(II) (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,
1. HEMOPHILIA A 1. Anticoagulant
therapy
2. HEMOPHILIA B
2. Liver diseases
3. VON
WILLEBRAND’S 3. DIC
DISEASE
HEMOPHILIA A (Classic Hemophilia)
80-85% of all Hemophiliacs
Deficiency of Factor VIII
Lab Results - Prolonged PTT
HEMOPHILIA B (Christmas Disease)
10-15% of all Hemophiliacs
Deficiency of Factor IX
ANTICOAGULANTS
1. Coumadins (Vitamin K antagonists)
2. Heparin
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.
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: