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When blood is removed from the body and placed in a glass test tube, it clots fairly quickly , what is needed for this process Calcium ions are required for this process. Addition of EDTA or citrate prevents clotting by binding calcium.
Clotting can be initiated in vitro at a later time by adding back an excess of calcium ions.
The clotting time after recalcification can be shortened by adding an emulsion of negatively-charged phospholipids (PL).
The clotting time is further shortened to 21-32 sec by preincubation of the plasma with particulate substances such as kaolin (insoluble aluminum silicate).
The reaction initiated by kaolin, PL, and calcium is termed the activated partial thromboplastin time (aPTT) test.
the clotting time of recalcified plasma can be shortened to 11-12 sec by adding "thromboplastin" (a saline brain extract containing tissue factor, a lipoprotein described below).
The reaction initiated by thromboplastin and calcium is termed the prothrombin time (PT) test.
Many patients with inherited bleeding disorders have prolongation of the aPTT, the PT, or both.
A patient with a prolonged aPTT and a normal PT is considered to have a intrinsic" coagulation pathway
The name indicates that all of the components of the aPTT test, except kaolin, are "intrinsic" to the plasma.
a patient with a prolonged PT and a normal aPTT has a defect in the "extrinsic" coagulation pathway (tissue factor is "extrinsic" to the plasma).
Prolongation of both the aPTT and the PT suggests that the defect lies in a common pathway.
At each stage a precursor protein (zymogen) is converted to an active protease by cleavage of one or more peptide bonds in the precursor molecule
The types of components that can be involved at each stage include the following: (a) a protease (from the preceding stage) (b) a zymogen (c) a non-enzymatic protein cofactor (d) calcium ions (e) an organizing surface (provided by a phospholipid emulsion in vitro or by platelets in vivo)
The final protease generated is thrombin (factor IIa).
Thrombin converts the soluble protein fibrinogen into an insoluble fibrin gel, which is strengthened further by covalent cross-linking catalyzed by factor XIIIa.
The blood vessels act to prevent bleeding by three mechanisms vasocontriction, diversion and activation
A transient vasospasm, especially in the capillaries is the first response of a blood vessel to injury.
Blood is diverted from the injured vessel to collateral circulation where the vessels are intact.
The inner surface of normal vasculature is smooth and coated with anticoagulant factors.
When the endothelium is damaged collagen fibers are exposed and thromboplastin and vonWillebrand factor leak from the injured cells.
Activation occurs due to the contact of of platelets with these collagen fibers and the released vonWillebrand factor.
The coagulation system is activated when hen blood proteins contact tromboplastin leaking from damaged tissue cells.
Platelets (thrombocytes) are cellular fragments of megakaryocytes, mature cells located in the bone marrow.
As these cytoplasmic fragments are released they enter the circulation, where their mean survival time is approximately ten days.
The function of the platelet is primary hemostasis—the formation of a platelet plug. This is initiated by adhesion.
The cell membranes dissolve and viscous metamorphosis occurs as a fragile jellylike plug is formed (imagine sneezing right after a nosebleed stops—it’s the platelet plug that comes out).
This platelet mass is the substrate on which the coagulation system reacts to form a fibrin clot (scab).
The coagulation system is a series of enzymatic reactions that results in the formation of an insoluble fibrin mesh around the platelets.
This series of reactions is called the coagulation cascade
Most of the coagulation factors are protein-based enzymes that circulate in inactive form.
Factor I fibrinogen
Factor II prothrombrin
factor III tissue thromboplastinq
Factor IV calcium ions
Factor V proaccelerin
Factor VII proconvertin
Factor VIIIa vonWillebrand factor
Factor IX Christmas factor
Factor X Stuart factor
Factor XII Stuart factor
Factor XII Hageman factor
Factor XIII fibrin stabilizing factor
vonWillebrand factor (factor VIIIa) is part of factor VIII, but functions independently of the coagulation cascade.
vonwillerbrand factor-It is an adhesive protein produced by by the endothelial cells and the megakaryocytes. It facilitates the attachments of platelets to collagen fibers
There are three coagulation pathways, two that initiate coagulation (the intrinsic and extrinsic pathways) and the common pathway that completes the fibrin clot formation.
The intrinsic pathway is initiated by the contact of blood components with abnormal endothelial surfaces (i.e. collagen fibers). This is a slow process and generally takes several minutes to complete.
The extrinsic pathway is very rapid, completing its action within seconds. This occurs when shed blood contact thromboplastin in the tissues surrounding the damaged blood vessel.
The intrinsic and extrinsic pathways merge to form the common pathway.
This part of the cascade converts fibrinogen to fibrin forming a protective scab
Coagulation must be followed by fibrinolysis the breakdown of fibrin—or we (and our animals) would be giant walking scabs.
The fibrinolytic system replaces fibrin with collagen, re-establishing the normal channel.
As fibrinolysis occur, fibrin degradation products are formed, coating platelets and interfering with further clotting.
Define hemostasis and list the four components Hemostasis is the formation of a solid clot from fluid blood while maintaining blood flow through a damaged vessel, resulting in repair/There are four components/ the blood vessels, plets,coagulation system and the fibrinolytic system.
What are common clinical signs of hemostatic abnormalities? Prolonged bleeding from minor trauma or surgery Petechiae, ecchymoses and purpura Hematomas and hemarthroses Nonspecific bleeding, such as epistaxis, melena, hematemesis and hematuria
Describe how the blood vessel prevents initiation of or contributes to hemostasis by three mechanisms—vasocontriction,diversion and activation.A transient vasospasm, especially in the capillaries,is the first response of a blood vessel to injury. Blood is diverted from the injured vessel to collateral cir,where the vessels are intact
Define ‘coagulation system”. is a series of enzymatic reactions that results in the formation of an insoluble fibrin mesh around the platelets
Differentiate between the methods of initiation of the intrinsic vs. extrinsic coagulation systems. The intrinsic pathway is initiated by the contact of blood components with abnormal endothelial surfaces.The extrinsic pathway is very rapid, This occurs when shed blood contact thromboplastin in the tissues surrounding the damaged blood vessel.
What is fibrinolysis and what is its purpose? the breakdown of fibrin.The fibrinolytic system replaces fibrin with collagen, re-establishing the normal channel. As fibrinolysis occur, fibrin degradation products are formed, coating platelets and interfering with further clotting.
Why is it important to test for the number of platelets? This platelet mass is the substrate on which the coagulation system reacts to form a fibrin clot (scab).
What test can evaluate platelet number AND function? Bleeding time is a method that evaluates both the quantity and function of platelets
What should be run with every test specimen in a coagulation system test? Regardless of the test selected, controls should always be run and used to evaluate the results
What is most common test for the intrinsic pathway? The activated partial thromboplastin time (APTT) is the most sensitive and specific in-clinic test for the intrinsic coagulation system.
What is the most common test for the extrinsic pathway? is prothrombin time (PT). Like the APTT, it is independent of thrombocytopenia and the results should be within 25% of the control results.
What occurs in DIC and what can cause it? results from the simultaneous overstimulation of the coagulation and fibrinolytic systems, causing the formation of microthrombi with concurrent hemorrhage.
thrombin time used to establish the presence of normal levels of fibrinogen/affected by the presence of fibrin split products,heprin or thromin antibodies
bleeding time evaluates plt function-vWF(regulates interaction of plt w/vessel walls)can be prolonged in severe hypofibrinogenimia
Activated partial thromboplastin time aPTT used when someone has the aPTT is often used as a starting place when investigating the cause of a bleeding or thrombotic ( episode.unexplained bleeding or clotting.The aPTT used to monitor heparin therapy.Deffact,XII,XI,X,IX,V, prothrombin,fibrinogen
Prothrombin time sensitive to def. of factors VII,X,II (prothrombin) and I(fibrinogen)
prothrombin time performed by adding tissue thromboplastin (tissue factor) and Ca++ to citrated plasma-tests the intrinsic pathway
laboratory assessment of coagulation platelet count-Prothrombin time and INR-aPTT-Bleeding time-thrombin time-Activated clotting time.
The intrinsic pathway The intrinsic pathway is activated when blood comes into contact with sub-endothelial connective tissues or with negatively charged surface that are exposed as a result of tissue damage.Kallikrien act. XII to XIIa on neg charg surf, facillitated by HMWK.
Platelets secrete Dense bodies;ADP;ATP;SERITONIN;Ca;CYTOPLASM;FACTOR XIII,ADHESIVE PROTIENS;FIBRINOGEN;FIBRONECTIN;vWF;growth modulators,PDGF,TGF-B,PF4,Coag factors-factor V, HMWK,fibrinogen, fac XI.protiens,
kallikrein produced can then also cleave factor XII, and a further amplification mechanism is triggered. The activated factor XII remains in close contact with the activating surface, such that it can activate factor XI, the next step in the intrinsic pathway.
EXPLAIN THE BASIC CONCEPTS / PURPOSES OF HEMOSTASIS process by which the body maintains the life flow of blood and prevents bleeding problems. Hemostasis is a complex sequence of interactions in the (1) blood vessels, (2) thrombocytes, (3) coagulation proteins of blood,
EXPLAIN THE BASIC CONCEPTS / PURPOSES OF HEMOSTASIS (4) fibrinolytic proteins of blood. This mechanism is able to retain blood within the injured vessel until the repair is completed.
EXPLAIN THE BASIC CONCEPTS / PURPOSES OF HEMOSTASIS The end product of hemostasis is the transformation of blood into a thrombus or clot. This is the culmination of a three step phenomenon consisting of (1) extravascular, (2) vascular, and (3) intravascular phases
LIST FIVE FACTORS WHICH AFFECT THE EFFECTIVENESS OR INEFFECTIVENESS OF HEMOSTASIS. ] Type of injury, bruise, cut, abrasion, etc.[2] Magnitude of the injury.[3] Size of the vessels involved and their ability to respond
LIST FIVE FACTORS WHICH AFFECT THE EFFECTIVENESS OR INEFFECTIVENESS OF HEMOSTASIS. ] Hydrostatic pressures within the blood vessels and tissues.[5] Availability, quantity, and quality of platelets, clotting factors, and inhibitors
Vascular Disorders Purpura: hemmorhage in skin, mucous memebranes and internal organs1. direct endothelial damage2. inherited disease of connective tissue3. Decreased strength of microcirculation
Vascular Disorders 4. disruption of small venules-increased pressure5. Microthrombi6. Vascular malignancy
Abnormal Platelet Morphology Wiskott-Aldrich-small pltsMay-Hegglin-lrge plts w/thrombocytopenia Alport’s Syndrome-Giant plts w/thrmbocytopBernard-Soulier- giant platelet syndrome
Thrombocytopenia decrease in the number of platelets1. Disorders of production
Thrombocytopenia 2. Disorders of Destruction3. Disorders of Platelet distribution and dilution
Purpura : hemmorhage in skin, mucous memebranes and internal organs
VASCULAR DISORDERS direct endothelial damage
VASCULAR DISORDERS inherited disease of connective tissue
VASCULAR DISORDERS Decreased strength of microcirculation
VASCULAR DISORDERS disruption of small venules-increased pressure
VASCULAR DISORDERS Microthrombi
VASCULAR DISORDERS Vascular malignancy
Abnormal Platelet Morphology Wiskott-Aldrich-small plteletsMay-Hegglin-lrg pl. w/thrombocytopenia Alport’s Syndrome-Giant plts w/thrbcytopBernard-Soulier-giant plt syndrome
Quantitative Platelet Disorders Thrombocytopenia: decrease in the number of platelets1. Disorders of production
Quantitative Platelet Disorders 2. Disorders of Destruction3. Disorders of Platelet distribution and dilution
Disorders of production Decrease in the production of megakaryocytes or ineffective platelet production may be acquired or hereditary
Disorders of production May be caused by: drugs, irradiation, chemicals, alcohol or infiltration of malignant cells
Disorders of production Nutritional disorders such as malnourishment, B-12 and Folate deficiency
Disorders of production Hereditary: Falconi’s syndrome, aplastic anemia, TAR syndrome, X-linked, Wiskott-Aldrich, May-Hegglin, Alport’s syndrome
Disorders of Destruction Drugs of Foreign substancesQuinidineSulfonamide Derivatives HeroinMorphine
Disorders of Destruction Snake venom Bacterial sepsis- bacterial Antigen attached to plateletAutoimmune of Isoimmune destruction of plts.
Disorders of Destruction Heparin-Induced ThrombocytopeniaMost common drug-induced thrombocytopenia with high risk of venous and arterial thrombosis due to antibody recognizing the heparin that is bound to PF4
Disorders of Destruction Immune and NonimmuneImmune will return to normal in 4 to 10 days after stopping therapy Antibody disappears in 2-3 months
Disorders of Destruction Nonimmune the plt. Count returns to normal within 5 days even if the therapy continues
Increased Utiliztation Accelerated consumptionImmune (Idiopathic) Thrombocytopenic Purpura ITPThrombocytopenic Purpura TTPThrombotic Thrombocytopenic Purpura TTP
Immune (Idiopathic) Thrombocytopenic Purpura Low plt. Count, Normal Bone Marrow, Absence of other causes of thrombocytopeniaAcute usually in children- usually caused by infections. Corrects itself in 2-4 weeks
Immune (Idiopathic) Thrombocytopenic Purpura Chronic in adults – usually caused by autoantibodyCaused by autoantibodies and diagnosed by autoantibody tests and ruling out other causes 1. Thrombocytopenia 2. Absences of other causes
Immune (Idiopathic) Thrombocytopenic Purpura 3. Absence of infections-HIVTreat with I.V. Immune Globulin
Thombocytopenic Purpura Decrease platelet counts Caused by : DICTraumaObstetrical complicationsSpepsis
Thrombotic Thrombocytopenic Purpura Caused by deficiency of Von Willebrand Factor-cleaving protease
Thrombotic Thrombocytopenic Purpura Characterized by Fluctuating ischemic vascular occlusion, hemolytic anemia, & thrombocytopenia
Thrombotic Thrombocytopenic Purpura Usually forms after viral infectionHUS is like TTP only occurs in children
Thrombocytosis Substantial increase in the circulating platelets over the normal 450 x 109 /L
Thrombocytosis Reactive thrombocytosis: chronic blood loss, chronic inflammatory diseases, chronic infections, drugs, aspelnic states, splenectomy, malignancy, rebound thrombocytosis, acute blood loss, exercise, hemolytic anemia
Qualitative Characteristics of Platelets Normal in number, but fail to function correctly
Qualitative Characteristics of Platelets Testing for plt. Function includes: BT, Clot retraction, platelet aggregation, platelet adhesiveness, and anitplatelet anibodies
Qualitative Characteristics of Platelets Types of Platelet Dysfunction:AcquiredDrug induced Hereditary
Qualitative Characteristics of Platelets Acquired:Caused by a blood plasma inhibitory substancePresence of fibrinolytic degradation products
Qualitative Characteristics of Platelets myeloproligerative Syndromes, parprotein disorders, autoimmune diseases, fibringoen Degadation Producst, anemia, Uremia, Drug inducedPlt. Membranes may be altered by drugs
Qualitative Characteristics of Platelets Autosomal hereditary bleeding disorder. Plat adhesion disorder with glycoproteins missing Giant plateletsMild thrombocytopenia
Qualitative Characteristics of Platelets Lacks the receptor for the vWF necessary for the plt to adhere to the subendothelium Plt aggregation is normal except with ristocetinClinical: Brusing, epistaxis, hypermenorrhagia, and petechiae
Qualitative Characteristics of Platelets Hereditary: Structural or biochemical Connective tissue (collagen)Failure of plts. To adhere to the subendothelium
Bernard-Soulier Syndrome Hereditary Autosomal hereditary bleeding disorder. Plat adhesion disorder with glycoproteins missing Giant plateletsMild thrombocytopenia
Bernard-Soulier Syndrome Hereditary Lacks the receptor for the vWF necessary for the plt to adhere to the subendothelium Plt aggregation is normal except with ristocetin
Bernard-Soulier Syndrome Hereditary Clinical: Brusing, epistaxis, hypermenorrhagia, and petechiae
Glanzmann’s Thrombasthenia and Essential Athrombia Hereditary Autosomal recessive Clinical: plt. Dysfunction, easy and spontaneous bruising, subcutaneous hematomas, petechiae
Glanzmann’s Thrombasthenia and Essential Athrombia Hereditary Glycoprotein complex IIb/IIIa Normal plt. Count with prolonged bleeding timeClot retraction is decreased
Hereditary Storage Pool Defect Secondary aggregation disorder -Aspirin-like disorder/ingestion
Bleeding Disorders Related to Blood Clotting 1. Defective Production2. Excessive Destruction3. Pathological Inhibition
Defective Production Vitamin K deficiency Synthesis of vitamin K and dependant factors because of disease or drugs
Defective Production Neonates, malabsorption, biliary obstruction, oral anticoagulantsII VII IX X Vitamin K dependant
Severe Liver Disease Liver is the primary synthesis of coag factorsDecrease plasma levels of fibrinogenPT long, APTT variable
Hereditary Clotting Defects Hemophilia:Severe hemorrhage from deficiency of factor VIIIEither gene deletion or point mutationCorrected by the infusion of factor VIII
Hereditary Clotting Defects Hemophilia B: Factor IXDeficient low-molecular weight procoagulant portionvWB is decreased HMW and LMWKNOW THE INHERITANCE!
Von Willebrands Disease Prolonged bleeding time and autosomal inheritance pattern Hereditary or acquired-type 1 is most common true disease has deletion of the vWF genePsudeo-von willebrand will have abnormal receptor the vWF
Von Willebrands Disease One of the most common disorders of coagProlonged BT and Decreased factor VIII procoagulant activity vWF binds to the platelet and to the damaged wall to form bridge
Von Willebrands Disease Clinical: mucosal bleeding with epixtaxis, menorrhagia, and gastrointestinal bleeding (most common)Type 1 is the most commonAll show low ristocetin cofactor activity
Von Willebrands Disease Laboratory findings: BT: Mild to moderate prolongedPlt retention: typically decreased
Von Willebrands Disease Plt agglutination: ristocetin-abnormalvWF antigen tested with immunoelectrophoresisPT and APTT normal
Hereditary Clotting Defects Hemophilia B factor IX is deficientChristmas Factor
Hereditary Clotting Defects Hereditary fibrinogen deficiency is usually asymptomatic (fibrinogen usually is)
Hereditary Clotting Defects Factor XII deficiency = no bleedingFactor XIII deficiency = spontaneous abortion and poor wound healing
Disorders of Destruction and Consumption Damage may be caused to organs by thrombosisSnake bites may cause degradation
Disorders of Destruction and Consumption Consumption problems may occur with obstetrical complications, trauma, burns, prostatic and pelvic surgery, shock, advanced malignancy, septicemia and intravascular hemolysis
General Features of Fibrinolysis Primary fibrinolysis is associated the gross activation of the fibrinolytic mechanism with subsequent fibrinogen and coagulation factor consumptionNo evidence of fibrin deposits
General Features of Fibrinolysis Occurs when plasminogen enters the circulatory system as a result of trauma, surgery, and malignanciesThe secondary is the same as DIC but different from primary in that fibrin is formed in DIC/secondary
Disseminated Intravascular Coagulation DIC/secondary fibrinolysisComplication of many diseasesConsumption coagulopathy or defibrination syndromeHypofibrinogenemia characterizes DIC
Disseminated Intravascular Coagulation Gram negative bacteria can trigger DIC with endotoxin productionSnake bites Malaria Incompatible transfusion productsLiver and renal disease
Disseminated Intravascular Coagulation LymphoproliferationShock, hypothermia, tissue damage, MI, Eclampsia
Disseminated Intravascular Coagulation Hemostatic mechanism breakdownInvolves the coagulation factors, platelets, vascular endothelial cells, fibrinolysis, and plasma inhibitorsoccurs when procogulants outweigh the anticoagulants
Disseminated Intravascular Coagulation Characterized by the excess thrombin formation, converting fibrinogen to Fibrin, platelet consumption and then depositionCoagulation Factors are decreased and hemorrhage in uncontrolled
Disseminated Intravascular Coagulation Thrombin activation initiates a number of coagulation activation:Fibrinogen to Fibrin _________________Activation of of factor XIII _____Stimulation of Platelets __Activation of factors V and VIII _________Activation of Protein C _______________
Disseminated Intravascular Coagulation activators Plasmin then destroys fibrin, fibrinogen, factors V and VIII Plasmin degrades fibrinogen to FSP acting much like a heparin.The FSP coat the plts. And they fail to activate
Disseminated Intravascular Coagulation The thrombi formed deposit in the microvasculature and cause the secondary fibrinolysisDamaged renal cells release plasminogen
Disseminated Intravascular Coagulation The body tries to stop the coagulation with its two major inhibitor systems: Antithrombin and Protein C & S
Disseminated Intravascular Coagulation Acute DIC : clotting and fibrinolytic activated at the same time performing at an unusually high rateFactor VIII:C may be used as a marker of a high degree of DIC
Disseminated Intravascular Coagulation Protein C : controls thrombin formation by controlling factors Va and VIII:CProtein C also increases fibrin degradation (anticoagulant-thrombi
Disseminated Intravascular Coagulation Thrombin being activated in DIC may also trigger the Protein C activationProtein C is accelerated by Protein S
Disseminated Intravascular Coagulation Chronic DIC is more common than acute DICChronic DIC may have predominate thrombi and cause DVT
Disseminated Intravascular Coagulation Acute DIC is more severe and often life threatening
Disseminated Intravascular Coagulation Clinical: petechiae, purpura, hemorrhagic bullae, surgical wound bleeding, venipuncture site bleed, arterial line oozing, and subcutaneous hematomas
Disseminated Intravascular Coagulation Laboratory testing: PT and APTT prolongedThrombin time prolongedIncrease in D-dimer
Disseminated Intravascular Coagulation Fibrinogen and platelet count vary but usually decreased due to consumptionFSP present
Disorders Related to Evaluated Fibrin Split Products Normal values: Serum: < 10ug/ml urine: < 0.25ug/mlHigh levels of FSP are found in renal diseaseUrine will be 50.0ug/ml in kidney diseaseExercise and stress elevate FSP
The Hypercoagulable State Thrombi forming because coagulation is enhanced and fibrinolysis is impairedMajor inherited inhibitor disease states are AT-III deficiency and Protein S & C deficiency
The Hypercoagulable State General features: Vascular damage and blood flowPlatelets-stasis settling and increased number of plts. Releasing factors to clot *Qualitative alterations may cause the plts to malfunction
The Hypercoagulable State Factor V mutation is the most common factor cause of thrombophiliaFactor V is both procoagulant and antithrombotic
The Hypercoagulable State Evaluate with: Prothombin Time-prolongedAPTT-prolongedLupus Anticoagulant screening Factor VIII and fibrinogenAPC assayProtein S and Protein CD-dimerCRP Mixing studies- do not correct/prolonged
The Hypercoagulable State Circulating AnticoagulantsSpecificNonspecificNonspecific are usually not associated with bleeding
The Hypercoagulable State Specific: Lupus AnticoagulantFound in patients with SLEMost common acquired of the specific inhibitorsExhibits anticoagulant effectRarely associated with bleeding only with hypothrombocytic states
The Hypercoagulable State May see spontaneous abortion and intrauterine deathInterferes with phospholipid dependant coagulationACA Anticardiolipin Antibodies bind to phospholipids cardiolipin Mechanism of action is unclear on either ACA or LA
The Hypercoagulable State Specific factors: Factor VIII inhibitor- most common of the specificFactor IX inhibitorFactor V inhibitor Fibrinogen, fibrin, and factor XIII inhibitorFactor II, VII, IX, & X inhibitors Factor XI and XII inhibitors
Inpaired Fibrinolysis Genetic and AcquiredProtein C deficienciesAPC resistanceProtein S deficiency Congenital Protein S deficiencyAntithrombin III deficiency Decreased levels of AT-IIIHeparin cofactor deficiency
Created by: wannabeaclt