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376 Cards in this Set
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- 3rd side (hint)
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name 5 inherited hemostasis disorders
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hemo A, B, C, von willebrand dz and ftxr XIII (13) defncy
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name the following hemostasis disorder that have the following: defncy of factor 13, sex linked recessive - almost exclusive in men, spontaneous bleeding into the joints & treated with commercial factor 13
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hemophilia A
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name the following hemostasis disorder that have the following: defcy in factor IX (9), sex linked recessive - almost exclusive in men, clinically identical in inheritance & symptoms to hem A, treated with factor IX concentrates
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hemophilia B
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name the following hemostasis disorder that have the following: defncy in factor XI (11), incomplete autosomal recessive, wide range of clinical severity, high incidence in Askenzai Jews, and only contact factor associated with bleeding
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hemophilia C
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name the following hemostasis disorder that have the following: primary defect in von WF, sually find secondary defncy of factor VIII (8), autosomal dominant - (both sexes), platelet adhension defect with prolonged bleeding time, & treated with cryo or DDABP (drug), factor VIII (8) concentrates do NOT contain vWF
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von willebrand disease
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name the following hemostasis disorder that have the following: automosal recessive, NOT detected by common coag tests, results in significant bleeding disorder & detect with 5M urea test
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factor XIII (13) defncy
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acquired disorders have inhibitors - usually IGG antibody directed against a ___ or ___
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specific factor or phospholipids
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describe some characteristics of Lupus anticoagulant (3)
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1. direct against phospholipids
2. seen in lupus erythematosis (about 5 - 10%), but also seen in malignancies, infections, drug therapy & other autoimmune disorders 3. use platelet neutralization techx to confirm presence (platelet phospholipid neutralizes antibody) |
hint: phospholipids, LE & platelet neutraliztx
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describe some characteristics of factor VIII (8) inhibitor (4) how it relates to the hemostatic mechx, its cofactor to, bleeding (+/-) and how APTT is important to the results
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Factor VIII (FVIII-C; antihemophilic globulin) is
1. IMPORTANT part of the hemostatic mechanism 2. participating as a COFACTOR in the second burst of THROMBIN generation, which leads to clot formation 3. An isolated deficiency of factor VIII-C is ass w/ a significant bleeding diathesis 4. APTT mixing studies differentiate factor defncy from inhibitors |
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describe some characteristics of vit K defncy
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functional defncy of factors: 2, 7, 9 & 10, PIVKA molecules (proteins in vit K absence) - present but not functional, vit K originates from diet & bacteria in gut, defncy seen in poor diet & with broad spect antibiotic use, same result observed in coumarin & dicoumoral theraphy
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describe some characteristics of liver disease (depending on severity)
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defncy factor: 1, 2, 5, 7, 9 & 10, factor 7 defncy most pronounced, decrease clearance of plasminogen activators & increase FDP due to fibrin (ogen) lysis
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describe some characteristics of DIC (4) ex: how is can be cause, which factors it can consume and positive lab tests
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secondary to sepsis or obstetric complications, thrombotic occlusion of microcirculation, RBC fragments, consumption of platelets & factor: 1, 5, 8 and high levels of FDP & D-Dimer
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why is sodium citrate the more preferred choice for routine coag studies and how does heparin & EDAT play a role in the coag system
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because factor 5 or 8 are more labile (undergoing or likely to undergo change; unstable: a labile compound) in sodium oxalate, herparin neutralizes thrombin & EDTA inhibits the thrombins actions on fibrinogen
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sodium oxalate
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labile for factor 5 & 8
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heparin
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neutralizes thrombin
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edta does what to fibrinogen
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inhibits thrombin act on fibrinogen
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what is the ration for anticoag to blood for coag procedures
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1:9 (anticoag to blood) - the anticoag supplied in this amount is sufficient to bind all the available calcium thereby preventing clotting
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what reagent is used in the PT test
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thromboplastin & calcium
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which test would be anormal in a patient with Stuart-Prower factor (factor X) defncy
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PTT & APTT
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name a characteristic of vit K
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it is required for carboxylation of glutamate residues of some coag factors
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vit K is necessary for activation of which vita K dependent clotting factors
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2, 7, 9 and 10
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what does the fibrinogen/fibrin degradation product test for (late + early products)
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the FDP test detects the late degradation products (fragement D & E) and not the early ones (frag X & Y)
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which of the following platelet aggrtx agents demo a monophasic aggrtx curve when used at optimal concentration
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collagen (it demo a single wave (monophasic) response preceded by a lag time
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what does INR test for
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(international normalized ration) it standardizes PT results - it help adjust for the different in thrmboplastin reagents made by diff manufacturers & used by various institutions - INR calc uses the international sensitivity index value & is used to monitor an oral antigcoag such as warfarin
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what is referred to as an endogenous activator of plasminogen
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tissue plasminogen activator
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what is an exogenous (not made in the body) that activates the plasminogen
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streptokinase
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tissue plasminogen activator (tPA) is an enogenous (produced in the body) activator of plasminogen - where is it released and what does it convert into
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it is released from the endothelial cells by the action of protein C and it converts plasminogen to plasmin
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which protein is the primary inhibitor of the fibrinolytic system
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a2-antiplasm (it inhibits plasmin by forming an 1:1 stoichiometeric complex with any free plasmin in the plasma & therefore prevents the binding of plasmin to fibrin & fibrinogen
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what is the test predictive value/result for d-dimer
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test has a negative predictive value - a nonspecific screening test widely used to rule out thrombosis (blood clot) or thrombotic (relating to, caused by or characterized by thrombosis)
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why should you reject a blood sample if it is not filled up correctly with the blood:coag ratio and how does that affect PT/APTT
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because the excess anticoag is an QNS sample binds to the reagent calcium, thereby resulting in a prolonged of PTT & APTT
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what is the correct storage time for both the PTT & APTT testing tube
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plasma sample for PT testing are stable for 24 hours at room temp if capped, refrigerating the same causes cold activation of factor 7 & therefore shortened PT results, the APTT samples are stable for 4 hours if stored at 4c
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in primary fibrinolysis, the fibrinolytic activity results in the response in
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spontaneous activation of fibrinolysis
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name some of the steps that happens in primarily fibrinolysis (4)
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1. rare pathological condtx which a spontaneous systemic firbinolysis occurs
2. plamin is formed in the absence of coag activation & clot formation 3. PF is associated with increased production of plasminogen & plasmin 4. decreased in plasmin removal from circulation & spontaneous bleeding |
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plasminogen defncy is associated with
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thrombosis
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plasminogen is important component of fibrinolytic system, why
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plasminogen is activated --> plasmin
which is needed for degradtio of fibrin clots to prevent thrombosis *when plasminogen is deficient, plasmin is not formed = causing a defect in clot lysing processes |
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name the 5 main hemostatic plug formation
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adhesions, aggregation, plug formation, consolidation & fibrin stabilization
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name the 5 major system involved in maintaining hemostasis
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vascular system, platelelts, coag system, fibrinolytic system & serin protease inhibitors
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name the 2 minor system involved in maintaining hemostasis
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kinin system & complement system
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hint: KfC (minus the f)
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which step does this happen in vasoconstriction, platelet adhension to exposed subendothelial cxt tissue, platelet aggretx to form initial plug @ injury site
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primary hemostasis
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hint: A+A happens here
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which step does this happen in coag factors interact on platelet surface to produce fibrin, fibrin stabilization by factor 13 (XIII)
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secondary hemostasis
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which step does this happen in release tissue plasminogen activator, conversion of plasminogen to plasmin, conversion of fibrin to fibrin degradation products (fibrin split products)
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firbrinolysis
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name the 3 principal mech of platelet adhesion
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vWF, collagen fibers, platelet membrane glycoprotein Ib
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what is vWF function
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protein systhz in endothelial cells & megakarocytes primarily bind to platelet membrane receptor GPIb, to promote adhesion & carrier for factor 8, provides stability in circulation
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fibrin formation
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firbrinogen
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promotes platelet adhesion
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vWF
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name the two factors that are cofactor in fibrin formation
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factor 5 or 8
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cellular adhesion molecule, promotes platelet spreading
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fibronectin
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activation of the intrinsic pathway via contact
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HMWK high molecular weight kininogen
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inhibits plasm
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a2-antiplasmin
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precursor to plasmin, function in fibrinolysis
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plasminogen
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promotes platelet aggregation (dense granules)
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ADP (nometabolic)
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primary & secondary messenger regulates platelet activation/aggregation
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calcium (dense granules)
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promotes vasocontriction
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serotonin (dense granules)
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regulates blood flow in damaged vessel, increases concentration of biochem to promote platelet activation events
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vasoconstriction
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signal intracellular activation, leading to platelet plug formation
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platelet shape change
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platelet to platelet interaction mediated by fibrinogen, ca2+. & platelet membrane activated glycoprotein IIb/IIa complex
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platelet aggregation
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adhesion & aggregation of platelet to the site of injury
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platelet plug
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release chemical constituents contains in various granules, amplifies platelet response
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platelet secretion
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platelet plug stabilized by formation of fibrin mesh over the platelet aggregates
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stabilization
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factor I
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fibrinogen
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factor 2
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prothrombin
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factor 3
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tissue thromboplastin (tissue factor)
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factor 4
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ionized ca2+
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factor 5
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labile factor (proaccelerin)
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factor 6
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not assigned
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factor 7
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stable factor (serum prothrombin conversion accelerator proconvertin)
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factor 8
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anti-hemophilic factor A
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factor 9
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christmas factor
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factor 10
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stuart prower factor
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factor 11
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plasma thromboplastin antecedent (PTA)
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factor 12
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hageman factor
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factor 13
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fibrin stabilizing factor
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HMWK or HK
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high molecular weight kininogen (fitzgerald factor)
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PK
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prekallikrein (fletcher factor)
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which factor does this relate to: hemophilia b
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factor IX - christmas factor
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which factor does this relate to: hemophilia a
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factor 8 - antihemophliic factor
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which factor does this relate to: hemophilia c
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factor 11 - PTA - plasma thromboplastic antecedent
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which factor does this relate to: needed for glass activation factor, not requried in vivo, no clinical signs of defncy
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XII - hagemant factor
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stabilizes fibrin clot, defncy leads to poor wound healing, assay by urea solubility test
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13 - fibrin stabilizing factor
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which factor does this relate to: converted to fibrin by thrombin, normal = 200 - 400 mg/dL
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I - fibrinogen
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which factor does this relate to: precursor of thrombin
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II - prothrombin
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which factor does this relate to: molecular weight lipoprotein present in all tissue, liberated by trauma
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III - tissue thromboplastin
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which factor does this relate to: bound by sodium citrate, must be replaced by reagents
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IV - Ca 2+
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which factor does this relate to: deteriorates at room temp
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V - labile factor
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which factor does this relate to: defncy - hemophilia A, most common inherited bleeding abn. labile
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VIII - antihemophilic factor
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name the coagulation factors from 1 - 13 (note NO factor 6)
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(FPT--CLS---AXS---PHF) fibrinogen, prothrombin, tissue thromboplastin, Ca 2+, labile factor, stable factor, antihemophilic factor, x-mas factor, stuart prower factor, plasma thromboplastin antecedent, hagement factor & fibrin stabilizing factor
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in plasma coag factors: based on the function which factor is the substrate (1)
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factor I - fibrinogen
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in plasma coag factors: based on the function which factor is the co-factors that accelerate emz rtx (4)
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factors 3, 5 & 8 including factor HMWK (high molecular weight kininogen)
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in plasma coag factors: based on the function which factor is the serine proteases - cleave peptide bonds
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factors 2, 7, 9, 10, 11 and 12
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in plasma coag factors: based on the function which factor is the transmidase
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factor 13 only
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which tube of blood for coag is preferred 3.8 or 3.2 %
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3.2% (Ca 2+ is needed for both coag & platelet aggrtx studies
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what is the anticoag ratio
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9:1 (blood:anticoag)
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which coag tube is better to use plastic or glass and why
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use plastic tubes or siliconized glassware because glass activates factor 12 and platelets will adhere to glass
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should hemolyzed sp be used and why not
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hemolyzed samples should not be used to platelet aggrtx studies because red cell contains ADP
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why shouldnt lipemic samples be used for coag & aggrtx studies
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may obscure changes in optical density
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why shouldnt you use the first tubes using evacuated vacutainers for coag samples
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because of contamination with tissue thromboplastin (activates coag) as needle pierces skin (if only test ordered is caog studies, draw small amount in a tube that is discarded)
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name three of the clotbusters
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streptokinase, urokinase & tissue plasminogen activator (strep UR TP activator)
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what does the PT screen for
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extrinsic & common pathway
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what factors does the PT measures
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factor 1, 2, 5, 7 & 10
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what does PT monitor
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oral anticoagulants (warfarin, coumarin, dicoumarol)
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what reagent does PT use
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tissue thromboplastin & CaCl2
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what is PT sensitive to
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vitamin K
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what is the reference range for PT
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reference range: <14 second
therapeutic goal: 2.0 - 3.5 |
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what does the APPT screen for
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instrinsic & common pathway
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what does the APTT measure
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all factors except 7 and 13
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what does APTT monitor
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monitors heparin therapy
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what are the reagents used for APTT
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activator (kaolin, celite or ellagic acid), platelet phospholipid (PF3), & CaCl2
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what the reference range for APTT
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reference range: 20 - 40 seconds
therapeutic goal: 1.5 - 2.5 times "normal" or use heparin response curve |
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APTT = 2 TT remind you of an
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H = heparin
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PT =
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coumarin, vit K factors
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what does fibrinogen assay measure
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quantitative measure of factor I
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what is the reference range for fibrinogen assay
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reference range: 200 - 400 mg/dl
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what does the thrombin time (aka thombin clotting time)
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does not measure intrinsic/extrinsic pathway, affected by the decrease FIBRINOGEN levels & presence of heparin & other anit-thrombin
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what is the reference range for thrombin time
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reference range: <20 second
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what does bleeding time measure
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platelet functions & numbers
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what are the three different types of bleeding time location
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Duke - earlobe: normal 0-6 mins
Ivy - forearm, normal 1-6 mins Template - forearm, normal 2 - 9.5 mins |
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name an example that cause bleed time to be prolonged
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prolonged with aspirin (effects last 7-10 days) and other drugs
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what does clot retraction evaluate (infrequently used)
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evaluates platelet function, fibrinogen, red cell volume
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based on the clot retraction testing, what would be an abnormal platelet count
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<100,000 mm3
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what two things would cause a DECREASE in clot retraction
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anemia & hypofibrinogenmia
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what would cause an INCREASE in clot retraction
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rapid dissolution of clot = INCREASE fibrinolytic activity (ex: DIC)
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what happens in clot retraction with Glanzmann Thrombasthenia
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no clot retraction
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define Glanzmann thrombasthenia and how does it effect coag system
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is a genetic platelet disorder in which the platelet glycoprotein IIb/IIIa (GP IIb/IIIa) complex is either deficient or present but dysfunctional. The genes of both of these proteins are on chromosome 17, and 50% activity of each protein is enough to support normal platelet aggregation. Defects in the GP IIb/IIIa complex leads to defective platelet aggregation and subsequent bleeding
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differentiating platelet disorders - Glanzman assay checks out what
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abnormal aggrtx (all agents decrease) & vWF normal
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differentiating platelet disorders - Bernard Soulier assy checks out what
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morph: giant platelets, abnormal ADHESION, (ristocetin decrease) & vWF normal
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differentiating platelet disorders - von willebrand assay checks out what
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abnormal adhension (ristocetin decrease) & vWF abnormal
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what is ristocetin
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It causes platelet agglutination and blood coagulation and is used to assay those functions in vitro, e.g., to diagnose von Willebrand disease (vWD) or the Bernard-Soulier syndrome. Platelet agglutination caused by ristocetin can occur only in the presence of large multimers of von Willebrand factor, so if ristocetin is added to blood lacking the factor/receptor - it will not coagulate
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what can cause an abnormal bleeding time
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prolonged with: 1. platelet abn, 2. vascular disease & 3. aspirin
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what is important about clot retraction
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decrease with thrombocytopenia & qualitative platelet defects, rarely performed
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what is important about platelet aggrtx
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test of platelet adhesion, aggrtx, & secretion, detect qualitative platelet defects
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what is important about prothrombin time
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detect defncy in extrinsic & common pathway. used to monitor coumadin therapy, report in INR 2.0 - 3.5 >5 increase in bleeding
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what is important about activated partial thromboplastin time
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detect defncy in intrinsic & common pathway, most common test to monitor heparin theraphy
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what is important about activate coag time (act)
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use for bedside monitoring of heparin therapy
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what is important about thrombin clotting time (tct)
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little used test to monitor heparin therapy
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what is important about fibrinogen
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estimtx of fibrinogen level
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what is important about urea solubility
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factor 13 screening test (fibrin stabilizing factor)
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what is important about d-dimer
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Pos + = dic, deep vein thrombosis, pulmonary embolism, & after lytic therapy
Neg - = primary fibrinolysis |
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what is important about fdp/fsp
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present in dic, primary fibrinolysis, deep vein thrombosis, pulmonary embolism, after lytic therapy
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what is important about plasminogen & how does it react with lytic therapy, DIC and primary fibrinolysis
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precursor of plasmin, decrease folloing lytic therapy (clot busting drug delivered to veins), DIC, primary fibrinolysis
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what is important about anti-thrombin III (AT-III)
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heparin cofactor, defncy associated with thrombosis
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what is important about protein C & protein S
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inhibitors of coagulation, deficiency ass with thromboembolic disorders
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define fibrinolysis
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is normal body process that occur continuously to keep naturally occurring blood clots from growing & causing problems, however, the break down of fibrin can increase under certain conditions
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whats the diff from primary to secondary fibrinolysis
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primary fibrinolysis - norm blood clots
secondary fibrinolysis - breakdown of blots & poss abn bleeding due to another medical disorder |
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name that factor deficiency & treatment - factor I
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a/hypo/dys-fibrinogenemia
cryo (contains: 8, fibrinogen, vwf, 13) |
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name that factor deficiency & treatment - factor 2
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prothrombin defncy
ffp (contains: coag fxtr, fibrinolytic & complement factors) |
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name that factor deficiency & treatment - factor 5
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labile factor defncy (owen's dz)
ffp (contains: coag fxtr, fibrinolytic & complement factors) |
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name that factor deficiency & treatment - factor 7
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factor 7 defncy, plasma or prothrombin complex
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name that factor deficiencies & treatment - factor 8 (hem A)
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hemophilia a
cyro, factor 8 concentrate, 1-desamino-8-d-arginine vasopressin (DDAVP) one of the most common inherited coag disorders, sex linked recessive occur in men, mothers are carriers |
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name that factor deficiencies & treatment - factor 8 (vwd)
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cryo, 1-desamino-8-d-arginine vasopressin (DDAVP) - defncy in VW factor (part of factor 8 complex) autosomal dominant, bother sexes are affected
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name that factor deficiencies & treatment - factor 9
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christmas = hemophilia B, plasm or commercial concentrates
sex linked recessive |
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name that factor deficiencies & treatment - factor 10
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stuart prower factor defncy - ffp or prothrombin complex
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name that factor deficiencies & treatment - factor 11
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hemophilia C - ffp
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name that factor deficiencies & treatment - factor 12
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hageman trait - no treatment & no bleeding disorders
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name that factor deficiencies & treatment - factor 13
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fibrin-stabilizing factor defncy - plasma or lyophilized placental factor 13
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1. idiopathic thrombocytopenic purpura (ITP) can cause severe ___
2. how would that affect the pat's platelet 3. what happens to megakarocytes in normal cellularity |
most common disorders causing severe isolated thrombocytopenia & cause by an autoantibody to pat's platelets (increase megakkaryocytes with norm cellularity)
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name 7 examples of congential disorders ass with decrease platelet productions
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alport synd, chediak higashi, hermansky-pudlak, may hegglin anomaly, tar synd & wiskott aldrich (herMay ate TAR w/ al & che)
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these following factors affect which acquired conditions:
mild 2, 7, 9, 10 mod 5, 8 severe also 1 |
liver disease
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these following factors affect which acquired conditions:
factor: 2, 7, 9 & 10 |
vit K defncy & coumadin therapy
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these following factors affect which acquired conditions:
factor: 1, 5, 8 and platelets |
disseminated intravascular coag
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these following factors affect which acquired conditions:
factor 1, 5 & 8 |
primary fibrinolysis
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thrombolytic therapy - whats the purpose
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to activate fibrinolytic syste, used to treat acute MI, deep vein thrombosis, pulmonary emboli
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thrombolytic therapy - what drugs are used
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streptokinase, urokinase, tissue plasminogen activator (TPA), pro-urokinase (pro-uk), aclated plasminogen streptokinase activated complex (apsac)
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thrombolytic therapy - whats the baseline tests/studies
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pt, aptt, cbc & fibrinogen
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thrombolytic therapy - what happens when changes induced by therapy
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DECREASE in fibrinogen, plasminogen, a2-antiplasmin, factors: 5, 7, 9, 11, 12
INCREASE in plasmin, FDP, d-dimer, aptt, pt & prothrombin time |
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thrombolytic therapy - what are some precautions
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limit venipuncture, apply pressure following venipuncture to stop bleeding
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what is thrombolytic therapy
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treatment to breakup clots inside the body (blood vessels)
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what is MI
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death/damage to heart muscles (result from coronary thrombosis)
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what is DVT
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formation of thrombus w/in the deep veins (leg/pelvis)
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what is PE
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emobolism of pulmonary artery - blood clot originating from the vein of leg/pelvis
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what is FDP
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aka crime evidence - are substx left behind when clots dissolve in the blood
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what is the difference between heparin & coumadin when it comes to administration & action of the drug
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hep - subcutaeous or iv & antithrombin effect
cou- oral & vit K antagonist |
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what is the difference between heparin & coumadin when it comes to effect & duration
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hep: immediate & short
cou: slow acting & long |
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what is the difference between heparin & coumadin when it comes to testing for monitoring
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hep: APTT (in)
cou: PT (ex) |
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what is the difference between heparin & coumadin when it comes to reversed by what & other info needed to know
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hep: reversed by protamine sulfate & requires AT-III to be effective
cou: reverse by vit K with DECREASE in production: 2, 7, 9, 10 |
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how is the liver and vit K related to one another
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liver uses vit K to make blood clotting proteins, vit K plays important role in your bodys natural clotting process
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what would change in blood in room temp do to: MCV
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increase - due to RBC sweeling
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what would change in blood in room temp do to: HCT
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increase - due to INCREASE in MCV
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what would change in blood in room temp do to: MCHC
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(opposite of MCV/HCT) decrease due to increase in HCT
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what would change in blood in room temp do to: osmotic fragility
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increase
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what would change in blood in room temp do to: wbc count
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decrease
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what would change in blood in room temp do to: wbc morphology
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necrobiotic cells, karyorrhexis (nuclear distintegration), degranulation, vacuolization
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lab finding for the following coag abn would indicate which disease:
decrease in factor 8 APTT prolonged PT normal BT = normal Plate count = normal |
hemophillia A
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lab finding for the following coag abn would indicate which disease:
APTT prolonged PT normal BT = normal Plate count = normal |
hemophilia B (sex linked & xmas disease)
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lab finding for the following coag abn would indicate which disease:
BT = proloned Plate aggrtx = abn w/ristocentin factor 8 may decrease APTT = may be prolonged PT = normal Plate count = norm |
VW Disease
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lab finding for the following coag abn would indicate which disease:
Clot retraction = abnormal BT = prolonged Plate count = normal Plat aggrtx = abn w/ADP, collagen, thrombin, epinephrine |
glanzmann's thrombasthenia (disorder of platelet function cz by abn/fefncy of the membrane GP IIb/IIa complex
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lab finding for the following coag abn would indicate which disease:
BT = prolonged Giant platelets Plate count = decrease Clot retraction = normal |
Bernard soulier synd (disorder cz by defncy of platelet GPIb/IX complex - goes h2h/gpv)
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what is the function of GPIIb/IIa
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protein that are heterodimers - chrom 17
mediates the binding of fibrinogen, vwf, & fibronection --> activates platelets serves 2 connect adhesive protein to contractile protein of the platelet after activation thereby facilitating clot retraction, ca2+ act as a stabilizer to the complex |
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what would happen if tech ran for PT & APTT and the the sample was clotted, what would happen to the results of PT & APTT
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in vitro, blood clots results in CONSUMPTION of the clotting factors & therefore PROLONG of PT/APTT. if the clotting factors have been activated but the clot formation is INCOMPLETE, it may result in SHORTENING the PT/APTT
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a plasma sample submitted to the lab for PT testing has been stored for 25 hours at 4c, the PT result is SHORTENED, what is the probably cause
|
activation of factor 7 due to exposure to cold temp (samples for eval for PT are stable for 24 hours if kept at room temp - prolonged exposure to cold will activate factor 7 resulting in a DECREASE in PT results
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the APTT results are not elevated in pat getting heparin, which factor may be associated with the lack of response to heparin therapy in this patient
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anti-thrombin defncy - AT defncy is patient getting heparin therapy may lead to heparin RESISTANCE & therefore lack of PROLONGATION of APTT results, AT is heparin COFACTOR & as such INCREASE heparin activity by 1000-fold, the defncy of AT is associated with a POOR RESPONSE to heparin therapy
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why should heparin be monitored so closely
|
heparin has a half life and is decreased in extended thrombosis & the anticoag activites of heparin change based upon nonspecific binding of heparin to plasma protein
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what kind of test can monitor heparin (3)
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APTT or activated clotting time (ACT) and platelet count - since decrease in platelet count to 50% below the baseline value is important & may be ass with HIT
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Heparin-induced thrombocytopenia (HIT)
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what is the proper protocol to eva patients receiving heparin therapy
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a baseline APTT & platelet count, APTT testing every 6 hours til the target is reached
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60yo patient was admitted to the hospital for a LIVER BIOPSY, the coag revealed PT = prolong with INR = 4.5, what is the most appropriate course of action
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cancel the procedure & start the patient on vit K therapy, repeat the PT test 4 days after starting vit K admin, & cancel the biopsy until the patient's PT returns to normal
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why is vit K therapy important to a patient that is going to have a liver biopsy with PT= prolong and a HIGH INR & how is vit K related to the liver
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liver biopsy in a patient with PT = prolonged and high INR could be LIFE THREATENING, in this patient, the PROLONG PT is likely caused by the liver disease, vit K is stored in the liver & is essential for activation of factors: 2, 7, 9 & 10 for its absorption. in liver disease characterize by obstruction, bile is not secreted into the GI tract & therefore vit K is poorly absorbed.
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what is the proper storage for APTT sample and what temp should it be kept at and when should it be tested and what would happen to factor 5 & 8 and what wold happen tot he APTT results
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samples for APTT should be centrifuged & tested within 2 HOURS after collection, however the sample is table for 4 hours if stored at 4c, factors 5 & 8 are cofactors necessary for FIBRIN formation --however both are both LABILE, storage beyong 4 hours causes falsely elevated APTT results
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name some of the other "new" brand names for anticoag drugs besides heparin & wafarin and what would some of the effects of these drugs do to the lab tests
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ex: hirduin, which inhibits thrombin and danapariod which inhibits factors Xa -- some of these new drugs have antithrombin effect and therefore increases PT, APPT & TT results
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what would cause a platelet aggregation to be falsely negative
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HIT testing may give false negative result due to the neutralization of antibody to heparin
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neutralization
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what is the anticoag to blood ratio formula (this should be adjust with patient with severe anemia)
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(0.00185)(V)(100-H) = C
V = volume of blood H = HCT C = volume of antiCoag |
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if one performs an APTT on a patient with HIGH DOSE WARFARIN therapy, we would expect that the result would be
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increase because of other factor deficiencies
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prolong bleeding time & giant platelets best describes
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Bernard Soulier syndrom
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which of the following wold one suspect in AFIBRINOGENEMIA
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BT = abnormal
Reptilase time = abnormal TT = abnormal |
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which disease cause: an immune medicated condition characterize by a LOW PLATELET count & found primarily in CHILDREN
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idiopathic thrombocytopenia purpura
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what is idiopathic thrombocytopenia purpura
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an immune mediated disorder characterized by an abrupt onset & spontaneous remission in several weeks, it is found primarily in children
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what is thrombotic thrombocytopenia purpura
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is a NON-IMMUNE mediated condtx usually characterized by MICROANGIOPATHIC anemia, thrombocytopenia, fever, renal disease & neurological abnormalities
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what is May Hegglin
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is a NONIMMUNE mediated condtx characterize by THROMBOCYTOPENIA with small HYPOGRAULAR platelets
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describe conditions ass w/ Wiscott Aldrich, its characterize by which defncy cell, decrease in --- and how it affect dense bodies
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1. an IMMUNOLOGIC condition
2. characterize by immune defncy (T & B cells) 3. thrombocytopenia w/ severely shortened platelet survival 4. platelet with absent dense bodies are ass with this disease |
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arterial events are drive by
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platelets driven (arthlerosclerosis, prosthetic heart devices)
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venous events are caused by these (2 things)
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1. blood flow problems (superficial or deep vein thrombosis) & clot inhibitors defncy
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name 2 clot inhibitor deficiency (about 20%)
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1. antithrombin III
2. protein C |
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1. name some characteristics of Antithrombin III (3) when it comes to active coag protease
2. where is it produced 3. its activated by ____ |
1. principle antagonist of active coag proteases
2. produced in the LIVER 3. activated by HEPARIN SULFATE on the endothelial cells & by heparin as therapeutic drug |
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name some characteristics of protein C (4)
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1. vit K dependent serine protease
2. activated by THROMBOMODULIN on the endothelial cell 3. requires PROTEIN S cofacter 4. INACTIVATES factor 5 & 8 |
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name some characteristics of Protein S (4)
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1. vit K dependent
2. Co-factor for Protein C 3. bound & FREE state 4. only free protein S is functional so measure TOTAL & FREE |
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name some characteristics of Factor 5 Leiden (3)
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1. MUTANT factor 5
2. RESIST of action of protein C & S 3. activated Protein C Resistance Test |
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name some characteristics of Antiphospholipid syndrome (3)
|
any of 3 classes of antibodies
1. anticardiolipin antibodies 2. Lupus anticoag 3. Specific antibody (ex: beta 2 glycoprotein) |
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name some characteristics of Prothrombin mutation (5)
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1. mutation at position 20210
2. first described in 1996 3. 1-2% general population are heterozygotes 4. result in INCREASE thrombin formation 5. INCREASE in risk of thrombotic even |
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what would the result be for primary vs secondary (dic) when it comes to platelet count
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primary - normal
secondary (dic) - DECREASE |
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what would the result be for primary vs secondary (dic) when it comes to red cell morphology
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primary - normal
secondary (dic) - RBC fragments |
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what would the result be for primary vs secondary (dic) when it comes to PT & APTT
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primary - ABNORMAL
secondary (dic) - ABNORMAL |
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what would the result be for primary vs secondary (dic) when it comes to protamine sulfate
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primary - NEGATIVE
secondary (dic) - POSITIVE |
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what would the result be for primary vs secondary (dic) when it comes to FDP
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primary - POSITIVE
secondary (dic) - POSITIVE |
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what would the result be for primary vs secondary (dic) when it comes to euglobulin clot lysis test
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primary - POSITIVE
secondary (dic) - negative |
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what would the result be for primary vs secondary (dic) when it comes to D-dimer
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primary - negative
secondary (dic) - POSITIVE |
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what would the result be for primary vs secondary (dic) when it comes to platelet count
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primary - normal
secondary (dic) - DECREASE |
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what would the result be for primary vs secondary (dic) when it comes to red cell morphology
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primary - normal
secondary (dic) - RBC fragments |
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what would the result be for primary vs secondary (dic) when it comes to PT & APTT
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primary - ABNORMAL
secondary (dic) - ABNORMAL |
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what would the result be for primary vs secondary (dic) when it comes to protamine sulfate
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primary - NEGATIVE
secondary (dic) - POSITIVE |
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what would the result be for primary vs secondary (dic) when it comes to FDP
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primary - POSITIVE
secondary (dic) - POSITIVE |
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what would the result be for primary vs secondary (dic) when it comes to euglobulin clot lysis test
|
primary - POSITIVE
secondary (dic) - negative |
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what would the result be for primary vs secondary (dic) when it comes to D-dimer
|
primary - negative
secondary (dic) - POSITIVE |
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thrombin has many functions, name some that are related to factor 5 & 8, platelets and throm-bom-o-dulin
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1. feed back to "potentiate" factors 5 & 8
2. recruits & aggrtx platelets 3. turns on e. cell THROMBOMODULIN (receptor/activator for Protein C & S system) to INACTIVATE factor 5 & 8) |
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what does aspirin do to platelet aggtrx curve
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aspirin inhibits secondary wave of aggtrx (DESTROYS CYCLO-O-XY-GENASE) --it keeps the curve at a HIGH constant and doesnt dip (normal PA curve starts out HIGH and eventually dips low)
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what would cause an ABNORMAL RICTOCETIN-induce aggrtx (2)
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1. Bernard Soulier
2. vo Willebrand |
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differentiating platelet disorder - in Glanzmann what would the assay test look like
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1. Abn aggtrx
2. all agents DECREASE (adp, collagent etc) 3. vWf - normal |
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differentiating platelet disorder - in Bernard Soulier what would the assay test look like
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1. Abn ADHENSION
2. DECREASE - RISTOCETIN 3. vWf - normal |
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differentiating platelet disorder - in vW what would the assay test look like
|
1. Abn ADHENSION
2. DECREASE - RISTOCETIN 3. vWf - ABNORMAL |
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what is the range for Factor Assay and what does it measure
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1. range 40-150% = normal --this test is used for PT/APTT tests performed with SPECIFIC FACTOR DEFICIENT plasma
2. % activity & amount of correction w/ normal plasma determined |
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what does the Stypven time test with and what type of test is it used for & which defncy factors would be prolonged
|
1. Russell's viper venom
2. diff factor 7 defncy from common pathway defncy a. factor 7 deficient plasma = normal b. deficiency of factor 10, 5, 2 = prolonged |
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between the Stypven time and Reptilase time, what venom does each test uses
|
1. Stypven time = russell viper venom
2. Reptilase time = snake vemon |
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what is use in Reptilase Time and what does it test for
|
snake venom emz - this test sim to Thrombin time, but is NOT inhibited by HEPARIN (good to use for patient on herparin) rr: 18-22 seconds)
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in fibrinolysis testing - FDP/FSP uses what type of testing and what would it be positive for
|
it uses latex beads coated with ANTI-FIBRINOGEN and positive screen = DIC
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in fibrinolysis testing - latex D-Dimer uses what type of antibody and what would it be positive for
|
monoclonal antibody to crx link D FRAGMENT, positive = DIC, DVT, & PE
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thrombotic thrombocytopenic purpura (TTP) is characterized by
|
increase platelet aggregation
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thrombocytopenia & hyper-plenism have what is common
|
HYPER-plenism - in this condition up to 90% of platelets can be sequestered in the SPLEEN, causing DECREASE in circulatory PLATELETS
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name some examples (3) that can be can cause THROMBOCYTOSIS (increase in platelet)
|
postsplenectomy, acute blood loss & increase proliferation of pluripotential stem cells
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what is thrombotic thrombocytopenic purpura
|
quantitate platelet disorder ass w/increase platelet activation & aggregation = thrombocytopenia, the PT & APTT = normal in TTP
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aspirin prevents platelet aggrtx by inhibiting the action of which emz
|
cyclo-OXYGENASE
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if aspirin inhibits CYCLO-OXYGENASE, what step would that interfere next in the platelet aggrtx
|
this inhibits prevents the formation of THRMOBOXANE A2 (TXA2) which serves as a potent platelet aggrtx
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|
normal platelet adhesion depends upon
|
glyco-protein Ib
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glyco-protein Ib teams up with ___ for normal platelet aggrtx
|
glyco-protein Ib is a platelet RECEPTOR for VWF, both are necessary for the normal platelet adhesion. other proteins plays a role in platelet adhesion are GLYCO-PROTEI 5 & 9 (V & IX)
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|
what test result is normal in a patient with classical VWD
|
platelet count & red cell morph is normal
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|
what is VWD
|
inherited, qualitative PLATELET disorder resulting in INCREASE in BLEEDING, APTT = P, and DECREASE factor VIII:C & VWF levels
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|
define thrombocytopenia
|
persist DECREASE in blood PLATELET that is often ass w/ HEMORRHAGIC conditions
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|
Bernard Soulier is associated with
|
1. thrombocytopenia
2. giant platelets |
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|
what is B. Soulier defncy in & name some of the test assay results (ex: Platelet aggrtx & BT)
|
GLYCOPROTEIN IB - B Soulier syndrome,
1. platelet aggrtx to ADP = NORMAL 2. BT = P 3. factor 8 assay is NOT indicated for this diagnosis |
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|
when performing platelet aggregation studies, which set of platelet aggrtx results would most likely be ass with B. Souiler syndrome
|
1. Platelet aggrtx = N = ADP, Collagem & Epinephrine
2. DECREASE/ABN aggrtx to RISTOCETIN |
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|
when performing platelet aggregation studies, which set of platelet aggrtx results would most likely be ass with Glanzmann thrombasthemia
|
1. Platelet aggrtx = ABN = ADP, Colalgen & Epinephrine
2. Ristocetin = N |
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|
which of the following is a characteristic of acute IDIOPATHIC THROMBOCYTOPENIC PURPURA
|
it is characterized by abrupt onset & spontaneous remission within a few weeks
|
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|
what is acute IDIOPATHIC THROMBOCYTOPENIC PURPURA & how/what is it caused by
|
AITP - IMMUNE mediated disorder found PO in children, it is commonly ass/ w infection (primarily VIRAL)
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|
TTP APTT results differ from DIC that is
|
APTT = N = TTP (thrombotic thrombocytopenia purpura)
APTT = P = DIC |
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|
what are the lab results for DIC (PT, APTT, PC & smear)
|
PT = P
APTT = P PC = DECREASE Smear = SCHISTOCYTES |
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|
what are the lab results for TTP (PT, APTT, PA & smear)
|
(thrombotic thrombocytopenia purpura)
PT = N APTT = N Smear = schistocytes, result from MICROANGIOPATHIC hemolytic anemia PA = INCREASE resulting in thrombocytopenia |
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|
several hours after birth, a baby boy develops petechaie & purpura & hemorrhagiv diathesis - the PC 18x10 9/L, explain the low platelet count
|
ISOIMMUNE NEONATAL THROMBOCYTOPENIA
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|
what is ISOIMMUNE NEONATAL THROMBOCYTOPENIA and what causes it
|
INT is sim to HDN - it results from immunization of the mom by FETAL PLATELET ANTIGEN. the maternal antibody produced is most often directed against the platelet A1 (P1A1) antigen on the fetal red cells. the mom AB crx the placenta = thrombocytopeina (rare with P1A2)
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|
what is usually associated with post transfusion purpura (PTP)
|
immune mediated thrombocytopenia/ALLOANTIBODIES
|
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|
what is post transfusion purpura (PTP)
|
an alloantibody mediated thrombocytopenia - which occurs about 1 week after transfusion w/ PLATELET contaminated products. PTP is beleived to result from ANAMNESTIC immune response - in the majority of cases the alloantibody produced is against platelet antigen A1 (P1A1) aka HPA-1a
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|
hemolytic uremic syndrome (HUS) is ass with
|
e. coli 0157:H7
|
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|
what is hemolytic uremic syndrome (HUS) & what is it characteristics
|
caused by E COLI 0157 (contaminated foods), commonly seen in chlidren. the clinical symp: fever, diarrhea, THROMBOCYTOPENIA, microangiopathic hemolytic anemia & renal failure
|
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|
storage pool defnct are defect of
|
platelet granules (most commonly, a decrease in platelet dense granules is present with DECREASE in ADP, ATP, Ca 2+ & Serotonin from platelet dense granules
|
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|
lumi aggregation measures
|
platelet aggrtx & ATP realease
|
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|
how is platelet aggrtx & ATP release measured
|
PA = measure by impedance
ATP release = measured by addition of LUCIFERIN to blood sample (there are NOT ATP in storage pool defncy) |
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|
neurological finding may be commonly ass w/
|
TTP is characterized by: neru problems, fever, thrombocytopenia, microangiopathic hemolytic anemia & renal failure
|
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|
what is Hypersplenism
|
Hypersplenism is a disorder that causes the spleen to rapidly and prematurelydestroy blood cells.
|
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|
what kind of disease is acquired thrombotic thrombocytopenic purpura, what kind of autoantibody is it associated with & what would happen to results: thrombocy2penia, plasma vwf & PA
|
autoimmune disease - ass w/ autoantibodies produced against vWF cleaving emz (ADAMTS-13), this defncy would cause thromboocytopenia = increase
plasma vWf = increase PA = increase |
|
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|
hereditary hemorrhagic telangiextasia is a disorder of
|
(aka: Osler Weber Rendu synd) connective tissue disorder ass w/ TELANGIECTASES of the mucous membranes & skin
|
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|
|
name some of the symptoms of hereditary hemorrhagic telangiextasia
|
connective tissue disorder that develop lesions on tongue, lips, palate, face, hands, nasal mucosa & throughout the GI tract - this disorder is autosomal dominant conditions that is usually manifests itself in adolescence or early adulthood
|
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|
what is a classic characteristic of hem A when it comes to bleeding (+/-), how it relates to factor VIII:C, BT & PT results
|
mild to serve bleeding episodes - depends upon the concentration of factor VIII:C (sex link dz)
BT = N PT = N |
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|
|
PT = P
APTT = P PC = DECREASE BT = INCREASE |
DIC (diffuse intravascular generation of thrombin ---> fibrin) as a result, coag factors & platelets are CONSUMED, resulting in
Platelet = DECREASE PT/APTT/BT = INCREASE |
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|
which predisposing condition can develop for DIC
|
adeno-carinoma - it can liberate procoagulant (thromboplastic - a clot) subtx that can activate prothrombin intravascularly
|
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|
|
what is ITP
|
a thrombocytopenia caused by an AUTOANTIBODY
|
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|
|
what is PTP (post transfusion purpura)
|
is a thrombocytopenia caused by an ALLOANTIBODY directed vs antigen positive transfused platelets
|
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|
|
what is HIT (heparin induce thrombocytopenia)
|
results from an ANTIBDOY to HEPARIN-PF4 complex causing thrombocytopenia in 1-5% in patients who are on heparin therapy (thrombosis may occur)
|
|
|
|
what is adeno-carinoma
|
cancer that originates in glandular tissue & also in epi tissue
|
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|
|
factor 12 defency is associated with
|
(hagemen) increase thrombosis. 13 also plays a role in the FIBRINOLYTIC system by activating
plasminogen ---> plasmin hermorrhagic manifestations are NOT ass w/ 12 defny cz thrombin generated by the EXTRINSIC pathway can activate factor 11 to 11a and factor 7a/TF ---> factor 9 to 9z |
|
|
|
BT = P
PC = N PT = N APTT = P |
vWd (platelet ADHESION disorder ass w/ decrease in VWF & factor 8 causing prolong BT & APTT
|
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|
BT = N
APTT = P |
hem A & hem B
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|
|
glansmann thrombasthenia (a platelet aggrtx defect) would have what kind of APTT result
|
APTT = N
|
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|
|
when performing a factor 8 activity assay, a pat plasma is mixed with
|
factor 8 deficient plasma
|
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|
|
what is coag factor assay based on
|
they are based upon the ability of pat's plasma to correct any specific factor deficient plasma (normal range 50 - 150%)
|
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|
|
the most suitable product for treatment of factor 8 defncy
|
factor 8 concentrate (human or recombinant) - FFP contains factor 8 however, it is NO longer used as the PRIMARY treatment for factor 8 defncy
**PROTHROMBIN complex concentrate is used for patient with factor 8 INHIBITOR |
|
|
|
BT = P
PA = Abnormal |
afibrinogenemia - rare inherited blood disorder in which the blood does not clot normally due to lack or malfunction of fibrinogen
- both platelet functions (BT = P & PA = Abnormal) |
|
|
|
___ this plasma protein is essential for platelet aggrtx & fibrin formation
|
fibrinogen
|
|
|
|
PT = N
APTT = P BT = INCREASE PC = N PA to Ristocetin = abnormal |
vWD (platelet count is NOT affected in VWF defncy)
|
|
|
|
which results are ass w/ Hem A (APTT & PT)
|
APTT = P
PT = N (hint: factor 8 is in the IN pway, not in the EX pway - so it would not be affected) |
|
|
|
fibrin monomers are increased in which condtx
|
increase fibrin monomers result from coag activation. DIC is an acquired contx ass w/ spontaneous activation of coag & fibrinolysis. in PRIMARY fibrinolysis the FIBRNOLYTIC system is ACTIVATED & FIBRIN MONOMERS = N
|
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|
|
what would cause a multiple factor defncy and why
|
liver disease because most of the clotting factors are made in the liver
|
|
|
|
an inherited disorder of coat is commonly ass w/
|
single factor defncy
|
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lupus anticoagulant is directed against
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phospholipd dependent coag factor
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dysfirbrinogenemia results from a defect of what
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an abnormal fibrinogen molecule
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PT = N
APTT = N in patient w/ a poor wound healing may be ass w |
factor 13 defncy can lead to impaired would healing & may cause severe bleeding problems - 13 = fibrin stabilizing factor that changes the fibrinogen bonds in fibrin polymers to stable covalent bonds. factor is NOT inv in the process of fibrin formation, therefore PT & APTT is NORMAL
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fletcher factor (prekallikrein) defncy may be ass with
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thrombosis - prekalli is a CONTACT factor, activated prekalli is name kallikrein & is inv in activation of factor 12 to 12a, like 12 defncy - fletcher factor defncy may be ass w/ thrombosis
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one of the complications ass w/ hem A is
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hemarthrosis (hemorrage of the joints that are caused be severe bleeding diathesis)
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what is the most common subtype of classic vWD
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type I
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name the 4 different subtype of VWD & their own characteristics
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Type 1 - most common (70-80%) ass w/ mild bleeding
Type 3 - inv the TOTAL ABSENT of the vW molecule = severe bleeding Type 2A (10 - 12%) & 2B (3 - 6%) = defncy of intermediated or high molecular weight protion of the vW molecule |
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define dysfibrinogenemia
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group of autosomal (non sex chrom) dominant disorder of qual abn fibrinogens
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define fletcher factor
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a prekallikrein inv w/ blood clotting act by enhancing the activity of factor Hageman (12)
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what is a characteristic of antithrombin (AT) (3)
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1. its a cofactor to HEPARIN
2. most important naturally occurring physiological inhibitor of blood coag 3. it represents about 75% of antithrombotic activity & is an a2 globuli made by the liver |
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which lab test is affected by heparin therapy
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thrombin time (heparing is an anti-THROMBIN drug & therefore INCREASE the TT test
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does heparin have an affect on fibrinogen assay or bleeding time
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no effect on either test
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how does Reptilase relates itself to fibrinogen and is it affect heparin
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Reptilase is a thrombin like snake venom protease that converts fibrinogen to fibrin. RT has not affect by heparin
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how is an APTT = abnormal cause by
pathological circulating anticoag affected/corrected |
not corrected with normal plasma. these anticoag are pathological subtx & are endogenously produced. they are either direct against a specific clotting factor or vs a group of factors.
APTT = P due to a factor defncy is corrected when mixed w/ normal plasma |
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the lupus anticoag is directed vs
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LA reacts against phospholipids rather than clotting proteins & therefore interferences w/ phospholipid dependent coag assay
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why is'nt coumadin recommended for pregnant/breast feeding mothers
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coumadin crx the placenta & is present in human milk. warfarin is a vitamin K antagonist drugs that retards sythz of the active form of vit K dependents (2,5,7,9,10). Antithrombin is heparin cofactor. INR is used to monitor dosage
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antithrombin is a cofactor to
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heparin
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name some characteristic for Protein C (2)
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1. its activity is enhanced by Protein S (protein S functions as a COFACTOR to protein C)
2. activated protein C inactivates factor 5a & 8a |
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what type is appropriate screening test for the diagnosis of lupus anticoag
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Diluted Russell's viper venom test (DVVT)
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thrombin time eva
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fibrinogen
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FDP & D dimer eva
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fibrinogen & FDP
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Russells viper venom reagent contains which factors that are strongly dependent on phospholipids
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factor 5 & 10, activating emz that are strongly phospholipid dependent
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Russells viper venom reagent contains (3)
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1. RVV
2. ca 2+ ions 3. phospholipids in the present of LA, the reagent's phospholipid is partially neutralize causing a PROLONGATION of clotting time |
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which is most commonly disease ass with activated protein C resistance (APCR)
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thrombosis
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what is activated protein C resistance (APCR)
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hemostatic disorder characterize by POOR ANTICOAG response to activate protein (this is the most common inherited thrombosis - main cause: gene mutation of factor 5)
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50YOM, been on heparin for the past 7 days, which combo of test is expected to be abnormal
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PT, APTT & TT
patient receiving heparin therapy the PT, APTT, TT are all PROLONGED quantative fibrinogen assay is NOT affected by heparin |
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what does heparin do and which factors does it affect
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heparin is a therapeutic anticoag w/ an ANTI-THROMBIN activity, it inhibits factors: 12a, 11a, 10a, 9a (all the beginning IN pway)
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Mrs Smith with lab results with NO BLEEDING history
APTT = P APTT: results on a 1:1 mixture of pat plasma + normal plasma are Preincubation: APTT = P 2 hour incubation: APTT = P |
Lupus anticoag
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I am associated w/ bleeding
APTT = prolonged 1: preincubation: could be corrected after mixing pat plasma + normal plasma what disease am i |
factor 8 defncy
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I am a bleeder
I am sensitive to: time & temp APTT = P 1. preincubation: may be corrected immediate after mixing 2. 2hour incubation: become ABNORMAL/Prolonged after incuation who am I |
factor 8 inhibitor
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I don't bleed
APTT = P 1. preincubation: APTT = P 2. 2 hour incubation APTT = P who am I |
lupus anticoag
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what symptoms or test diff lupus anticoag & factor 8 inhibitor
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lupus anticoag = bleeder
factor 8 inhibitor = NO BLEEDING same APTT = P 1. preincubation APTT = P 2. 2 hour incubation APTT = P |
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thrombin thrombomodulin complex is needed for activation of
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Protein C
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what is thrombomodulin (TM) and how does it relate to thrombin & protein C
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TM is a transmembrane protein that accelerates protein C activation 1000 fold by forming a complex with thrombin
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what happens when thrombin binds to TM thrombomodulin
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it loses its clotting function, inc activation of factor 5 & 8. activated protein C deactivates factors 5a and 8a
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what test is commonly used to monitor warfarin therapy
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INR
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what clotting factor (cofactors) are inhibited by Protein S
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factor 5a & 8a are deactivated by protein S and activated by protein C
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what drug promotes fibrinolysis
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urokinase is a thrombolytic drug commonly used to treat acute arterial thrombosis, venous thromboembolism, MI & clotted catheters
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whats the diff between warfarin, heparin & aspirin
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warfarin & heparin = anticoag drug
aspirin = prevents PLATELET AGGREGATION by inhibiting cyclo-oxygenase |
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diagnosis of LA is confirmed by what criteria
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neutralization of the antibody by high concentration of platelets (LA is not sensitive to time & temp unlike factor 8 inhibitor)
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what is a characteristic of low molecular weight heparin
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has a LONGER half life than unfractionated heparin
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low molecular weight heparin is derived from & what causes it to have a longer half life
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small glyco-samino-glycan that is derived from unfractional heparin (UFH) - LMWH has a low affinity for plasma proteins & endothelial cell therefore has a longer half life
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low molecular weight heparin has an inhibitory effect what which factors
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10a & 2a and does not require monitoring unless patient is kid
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which test is most likely to be abnormal in patient taking aspirin
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bleeding time (aspiring: anti-PLATELET drug therefore preventing platelet aggrtx causing BT = P
PC = N platelet morph = N clotting factors = no affect |
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what is ass with antithrombin defncy
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thrombosis
antithrombin is a physiological anticoag that inhibits factors: 2a, 9a, 11a, & 13a thrombotic events may be primarily (in the absent of trigger factor) or may be ass w/ other risk factors (pregny/surgery) |
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what is ass w/ thrombotic event
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decrease in Protein C
Protein C is a physiological ihibitor of coag, it is activated by thrombin-thrombomodulin complex |
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bleeding would be ass w/ (3)
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increased fibrinolysis
afibrinogenemia & ITP |
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aspiring resistance may be ass w/
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thrombosis - up to 22% of pat taking aspirin become resistance to aspirin's anti-platelet effect. people who are aspirin resistance have a higher rate of thrombosis (heart attack & strokes)
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TT = P
Reptilase time = N |
heparin therapy (anti-THROMBIN drug)
RT = sim thrombin like snake venom protease that is able to CLOT FIBRINOGEN & has no affect on heparin or LMWH |
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name two disorder that would cause a
Reptilase time = P |
1. hypofibrinogenemia
2. antifibrinogenemia |
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screening test for thrombophilia should be performed when
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on patients with thrombotic events occurring at a young age
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Prothrombin G20210A is characterized by what cause
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single MUTATION of prothrombin molecule/thrombosisand common cause of inherited HYPERCOAGULABILITY (behind factor 5 Leiden)
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what would Prothrombin G20210A do to plasma prothrombin
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Prothrombin G20210A is single point mutation of the PROTHROMBIN gene, resulting
Plasma prothrombin = Increase (concentration) & thereby a risk for thrombosis |
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Factor 5 Leiden promotes thrombosis by preventing
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deactivation of factor 5a
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what does factor 5, 5a & protein C have in common
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factor 5 Leiden is a single point mutation in the factor 5 gene that inhibits factor 5a inactivation by protein C, activated protein C enhances deactivation of factor 5a & 8a
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the incidence of antiphospholipids antibodies in the general population is
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2%
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which test is helpful in the diagnosis of aspirin resistance
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platelet aggregation
in aspirin resistance, PA is not inhibited by aspirin ingestion, aspirin resistance has no effect on PC & morphology |
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what complication may occur as a result of DECREASE tissue factor pathway inhibitor (TFPI)
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increased thrombotic risk
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factor 8 inhibitors occurs in ___ % of patient in F8 defncy
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10-20 %
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what is commonly caused after a patient with factor 8 defncy receives factor 8 replacement
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their body produces factor 8 inhibitors (antibodies)
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which therapy & resulting mode of action are appropriate for the treatment of a pat with HIGH TITER to factor 8 inhibitors
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recombinant factor 7a (rVIIa) to activate the common pathway
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the Bestheda assay is used for which determination
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factor 8 inhibitor titer
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B8
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hyper-homo-cystein-emia may be a risk factor for
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thrombosis
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what is hyper-homo-cystein-emia
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abn large level of homocyteine (amino acid) in the blood
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hirudin may be used for treatment of what
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DVT (hirudin alternative to heparin) & can be used for thromboembolism in patients who have developed heparin induce thrombocytopenia
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reaction of these two things are ass w/ heparin induced thrombocytopenia (HIT) results in
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antibodies to heparin + PF4 complex
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which drug may be ass w/ DVT deep vein thrombosis
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oral contraceptives are acquired risk factors for thrombosis (aspiring & plavix are anti-platelet drugs & tPa is a fibrinolytic drug use for treatment of thrombosis)
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elevated plasma homocysteine is a risk factor for
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the development of venous thrombosis (homocysteine is inherited/acquired) acquired homo cz = dietary def in vit B6, B12 & folic acid
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which lab test is used to screen activated protein C reistance
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modified APTT with & w/out activated protein C
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ecarin clotting time may be used to monitor
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hirudin therapy (ECT = a snake venom based clotting assay)
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which test may interfere w/ the activated protein C resistance (APCR) screen test & why
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lupus anticoag because APCR screening assay is based on the APTT ratio & with LA having a PROLONGED APTT, that wold render a invalid test
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thrombophilia may be ass with what disorder
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hyperfibrinogenemia
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name 3 disease are associated with bleeding
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factor 8 inhibitors
hypofibrinogenemia arfibrinogenemia |
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fibrinogen is an acute phase reactant and may be increased when
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inflammatio, stress, obseity, smoking & meds (ex oral contraceptives)
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heparin is monitor by
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APTT
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warfarin therapy is monitor by
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INR
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fibrinolytic therapy is monitor by
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D-dimer & fibrinogen assay
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name two disorder that can be caused by immune processed cause by the production of antibodies to heparin PF4 complex
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heparin induce thrombocytopenia & thrombosis --this immune complex binds to platelet fc receptors cz platelet activation & formation of platelet microparticles that in turn INDUCE hyper-COAGULABILITY & THromBocytopenia
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what is thrombo-philia
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is the propensity 2 dev THROMBOSIS (blood clots) due to abnormal in system of coagulation (process by which blood form clots) ==hypercoagulability==
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