Bleeding time,clotting time, PT, and PTT

Slides:



Advertisements
Similar presentations
Hemostasis Shaina Eckhouse 10/12/2010.
Advertisements

Basic coagulation techniques and Quality control issues
Chapter 12 Disorders of Hemostasis
Diagnosis and Management of Hemorrhage in Oral Surgery
Initiation substances activate s by proteolysis a cascade of circulating precursor proteins which leads to the generation of thrombin which in turn converts.
ANAESTHESIA AND ANTICOAGULANTS
HAEMATOLOGY MODULE: COAGULATION DISORDERS 1 Adult Medical-Surgical Nursing.
Vascular Pharmacology
Gatmaitan, Raymond Vincent Golpeo, Kirsten C.
MLAB 1227: Coagulation Keri Brophy-Martinez
Dr msaiem Acquired Coagulation Disorders Dr Mohammed Saiem Al-dahr KAAU Faculty of Applied Medical Sciences.
Week 6: Secondary Hemostasis Plasmatic factors Plasmatic factors Intrinsic pathway Intrinsic pathway Extrinsic pathway Extrinsic pathway Specimen Specimen.
Anticoagulation in the Acute Care Population Aimee Ring PT, DPT, GCS.
Interactive Session on Clotting Profile Dr P T R Makuloluwa MBBS (Col), MD (Anaesthesiology), FRCA (Lond)
Lecture NO- 12- Dr: Dalia Kamal Eldien.  Coagulation: Is the process by which blood changes from a liquid to a clot. Coagulation begins after an injury.
Bleeding time,clotting time, PT, and PTT
Bleeding time,clotting time, PT, and PTT
Hemostasis and Blood Coagulation
MLAB Coagulation Keri Brophy-Martinez
General Approach of Haemostasis
Dr Mahvash Khan MBBS, MPhil. ◦ Occurs inside the blood vessels, it is also called fibrinolysis ◦ Occurs due to a substance known as plasmin (fibrinolysin)
WARFARIN AN OVERVIEW.
Bleeding Disorders Dr. Farjah H.AlGahtani
Approach to Bleeding Disorders
Scheme of Coagulation F XIIF XIIa F XIF XIa F IX F X F IXa F VIIaF VII Extrinsic System Tissue damage Release of tissue thromboplastine (F III) Intrinsic.
1 HAEMOSTASIS. 2 Definition Haemostasis is a complex sequence of physical and biochemical changes induced by damage to tissues and blood vessels, which.
APPROACH TO BLEEDING DISORDERS. History of Bleeding Spontaneous vs. trauma/surgery-induced Ecchymoses without known trauma Medications or nutritional.
MIXING STUDIES General Approach of Haemostasis
Coagulation Concepts A review of hemostasis Answers are in the notes pages.
  The prothrombin time is therefore the time required for the plasma to clot after an excess of thromboplastin and an optimal concentration of calcium.
BLEEDING DISORDERS LCDR ART GEORGE.
Investigation of Haemostasis MS. c. program Lab-9.
To understand blood coagulation tests it is helpful to have a basic understanding of the role of the different blood clotting factors and the coagulation.
Activated Partial Thromboplastin Time (aPTT)
HEMOSTASIS When blood vessels are cut or damaged, the loss of blood from the system must be stopped before shock and possible death occur. This is accomplished.
Coagulation Modifier Agents Lilley Pharmacology Text: Chapter 26 Original Text modified by: Anita A. Kovalsky, R.N., M.N.Ed. Professor of Nursing Original.
Intrinsic pathway Extrinsic pathway Common pathway The extrinsic pathway was required the addition of an exogenous trigger (originally provided by tissue.
Hemostasis and Coagulation Hemostasis Hemostasis is the maintenance of circulating blood in the liquid state and retention of blood in the vascular system.
Haemostasis. Indications for hemostasis test – Identify patients presenting with bleeding that have a correctable bleeding tendency – Identify patients.
1. Normal haemostasis Haemostasis is the process whereby haemorrhage following vascular injury is arrested. It depends on closely linked interaction.
Hemostasis Is a complex process which causes the bleeding process to stop. It refers to the process of keeping blood within a damaged blood vessel. Dependent.
Anticoagulants Course: Pharmacology I Course Code: PHR 213 Course Instructor: Sabiha Chowdhury Lecturer Department of Pharmacy BRAC University.
Chapter 17 Coagulation Testing
Chapter 23. Bleeding disorders associated with coagulopathy
Bleeding Tendency Dr. Mervat Khorshied Ass. Prof. of Clinical and Chemical Pathology.
Fibrinolysis, anticaogulants, related aspects. Learning objectives Learning objectives Clot retraction Clot retraction Fibrinolysis Fibrinolysis Thromboses,
Platelets. Fig Hemostasis the process by which the bleeding is stopped from broken vessels. steps involved: Vascular spasm. Platelets plug formation.
Bleeding disorders Deficiency of any of the clotting factors leads to excessive bleeding Most common and important bleeding disorders are due Vitamin K.
Approach To Bleeding Disorders In Neonates
MLAB Coagulation Keri Brophy-Martinez
Secondary Haemostasis
Lec. 12….
General Approach of Haemostasis
General Principles of Hemostasis Kristine Krafts, M.D.
Bleeding disorders Dr. Feras FARARJEH.
General Approach in Investigation of Hemostasis
The normal haemostasis process involves three stages: 1
Hemostasis.
and anti-thrombotic pharmocology Tom Williams
Coagulation Cascade of the Newborn
Coagulation Disorders
Steps in clotting mechanism
ANTICOAGULANTS Dr. A. Shyam Sundar. M.Pharm., Ph.D,
Intrinsic pathway Formation of prothombin activator is the central event in the clotting pathway For its formation the pathway that is initiated by.
Bleeding disorders Dr. Feras FARARJEH.
Hematology and Coagulation Procedures
General Principles of Hemostasis Kristine Krafts, M.D.
Drugs Affecting Blood.
Hemostasis and Coagulation
Presentation transcript:

Bleeding time,clotting time, PT, and PTT Ostadrahimi MD,PhD

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.

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

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

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

LABORATORY EVALUATION PLATELET COUNT BLEEDING TIME (BT) PROTHROMBIN TIME (PT) PARTIAL THROMBOPLASTIN TIME (PTT) THROMBIN TIME (TT)

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

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

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 EXTRINSC Collagen Tisue Thromboplastin XII XI VII IX VIII X V FIBRINOGEN (I) PROTHROMBIN THROMBIN (II) (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 0.9–1.3, 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.

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 EXTRINSC Collagen Tisue Thromboplastin XII XI VII IX VIII X 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, 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 EXTRINSC Collagen Tisue Thromboplastin XII XI VII IX VIII X V FIBRINOGEN (I) PROTHROMBIN THROMBIN (II) (III) FIBRIN

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

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 Lab Test - Prolonged PTT

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

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

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

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

THANK YOU