Term
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Definition
| thrombophilia, tendency to form blood clots abnormally |
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Term
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Definition
| tendency to form blood clots abnormally |
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Term
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Definition
| formation of blood clot or thrombus, usually considered to be under abnormal conditions within a blood vessel |
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Term
| Hypercoagulability physiological process |
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Definition
| Occurs when activation of blood coagulation exceeds the ability of the natural protective mechanisms to prevent fibrin formation and can form in any part of the cardiovascular system. The thrombus is composed of fibrin, platelets, and entrapped cells and the can differ in arterial and venous vessels. There is a difference between a clot in a thrombus in that a clot is a superficial lesion on an arm or a leg which is a normal response while thrombosis is inappropriate clotting. |
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Term
| how does a thrombus becomes a thromboembolus |
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Definition
| The thrombus enlarges and a piece of the thrombic material (embolus) may dislodge and travel though the circulatory system and lodge at a distant state which can obstruct blood flow at that site and cause a thromboembolus |
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Term
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Definition
| composed of platelets and fibrin (With some leukocytes and erythrocytes) usually forms in regions of disturbed blood flow at sites of epithelial damage. Atherosclerotic plaques are composed of lipids, fibrinous connective tissue, macrophages and smooth muscle cells, they can rupture which exposes thrombogenic material in sub-endothelium to blood and activates platelets and plasma coagulation factors. Fibrin formation turns into a thrombus and embolization can occur which can lead to a myocardial or cerebral infarction. The therapy for white thrombi is platelet inhibiting drugs, and thrombolytic therapy (preventative measures). |
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Term
| White thrombus risk factors |
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Definition
| hypercholesterolemia, hypertension, smoking, physical inactivity, obesity, and diabetes |
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Term
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Definition
| venous thrombus, composed of red blood cells trapped in fibrin mesh (contains few platelets and leukocytes) and usually forms in regions of slow or disrupted blood flow (venous segments exposed to trauma). They most commonly occur in veins or lower leg, in superficial veins of the legs it is called benign thrombophlebitis and in deep veins of the legs it is called deep vein thrombosis which is more serious and produces distal thrombi (which are less serious than thrombi in proximal veins). A potential complication of a DVT is a pulmonary embolism or venous thrombosis. |
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Term
| Red thrombus risk factors |
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Definition
| venous stasis, vessel wall damage, factor V-Leiden, deficiency of protease inhibitors, elevated Prothrombin levels, anti-phospholipid antibodies, hyperhomocysteinemia, decreased fibrinolytic activity, malignancy, and other miscellaneous risk factors |
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Term
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Definition
| formation of a thrombus, or blood clot, in the deep veins (usually a leg vein) |
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Term
| Deep Vein Thrombosis diagnosis |
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Definition
| clinical/laboratory diagnosis of venous thrombosis is unreliable and objective tests are needed to confirm diagnosis. Objective tests using radiologic procedures to visualize the thrombus can help to identify thrombi and venography, venous compression ultrasonography (CUS) and spiral computerized tomography (s-CT) can be used to confirm a DVT. Blood tests for biological markers of thrombin generation and fibrinolysis are often elevated in patients with DVT. Laboratory tests include: Prothrombin fragment 1.2, fibrinopepide A, thrombin-antithrombin complex, soluble fibrin monomer, D-dimer, tPA, and PAI-1. These tests are nonspecific and can be abnormal in a number of clinical conditions associated with excessive coagulation and/or fibrinolysis so they have a low specificity for DVT. D-Dimer assays have a high sensitivity and negative predictive value; negative results can be used to rule out DVT. |
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Term
| Clinical conditions from Deep Vein Thrombosis |
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Definition
| Pulmonary embolism (proximal DVTs embolize to the pulmonary circulation) |
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Term
| the role of heparin in the neutralization of activated coagulation factors by antithrombin. |
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Definition
| : LMWH catalyzes interaction of Antithrombin with F-Xa, which increases the activity of AT to neutralize serine proteases to prevent further clotting |
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Term
| Relationship of PC and PS to coagulation pathway |
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Definition
| activated PC neutralizes cofactors Va and VIIIa. PS is a cofactor for activated PC only in its free form (40%) |
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Term
| Deficiency in PC leads to thrombotic tendency |
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Definition
| : reduction in PC levels predisposes to venous thrombosis because it decreases the capacity to destroy Va and VIIIa which results in an increase in the generation of thrombin which generates fibrin and excess thrombin activates TAFI (anti-fibrinolytic effect) |
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Term
| Deficiency in PS leads to thrombotic tendency: |
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Definition
| : a decrease in free PS leads to prothrombotic tendencies due to inadequate PC inactivation of Va and VIIIa. |
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Term
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Definition
| inability of APC to prolong clotting tests when added to test system due to diminished ability to destroy Va, due to V-leiden resistant to APC inactivation because APC cleavage site is altered |
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Term
| APC resistance contribution to thrombophilia |
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Definition
| in vivo- inadequate Va inactivation leads to increased production of thrombin and possibly thrombosis, clot based mutation |
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Term
| Two side effects of heparin therapy |
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Definition
| HIT (heparin induced thrombocytopenia) or bleeding |
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Term
| Hematology procedures to monitor and limit heparin complications |
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Definition
| UFH (via IV or sub cutaneous) is monitored by aPTT (therapeutic range x patient’s baseline aPTT before heparin therapy) and LMWH is monitored by anti-F-Xa assay (If necessary). |
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Term
| Un-fractioned heparin (UFH) anticoagulant mechanism |
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Definition
| catalyzes inhibition of clotting proteases |
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Term
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Definition
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Term
| Low molecular weight heparin anticoagulant mechanism |
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Definition
| catalyzes interaction of AT and Xa |
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Term
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Definition
| does not require routine laboratory monitoring, but if monitored it is done with anti-Xa assay |
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Term
| Coumadin and decreasing risk for thrombosis |
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Definition
| inhibits coagulation by interfering with vitamin K action in the liver which blocks vitamin K dependent carboxylation of target proteins resulting in release of nonfunctional molecules in the plasma (des-carboxy proteins) |
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Term
| Oral anticoagulation monitoring |
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Definition
| PT/INR, administered 4-5 days before therapeutic anticoagulation is achieved and weaning off heparin |
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Term
| Arterial Thrombi Laboratory Tests |
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Definition
| White thrombi- the standard laboratory tests of hemostasis are neither sensitive not specific (aPTT, PT, etc.), the new potential tests are sensitive yet still not specific. Examples are: hyperhomocysteinemia, elevated lipoprotein (a), elevated fibrinogen (can be elevated in pregnancy), elevated d-dimer, elevated PAI-1 or decreased t-PA, elevated high sensitivity, CRP. |
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Term
| Venous Thrombi Laboratory tests |
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Definition
| red thrombi- similar features and laboratory test results are found in other conditions. Objectives tests: radiologic procedures to visualize thrombus, venography to confirm DVT, lung scanning to confirm PE, blood tests for biological markers, lab tests (prothrombin fragment, FPA, TAT complex, soluble fibrin monomer, d0-dimer, tPA and PAI-1) all non specific and can be abnormal in a number of clinical conditions |
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Term
| Clinical manifestations suggestive of inherited thrombophilia |
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Definition
| (1) venous thromboembolism at a young age (prior to 45) (2) recurrent venous thromboembolism (3) family history of venous thromboembolism and (4) thrombosis in an unusual site (cervical or visceral veins) |
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Term
| Why patients aren’t diagnosed with inherited thrombophilia |
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Definition
| : the defect does not lead to thrombosis, and not all people with thrombophilia experience a thrombotic event, many do not develop thrombosis unless some other risk is present |
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Term
| Clotting assay for APCR diagnosis |
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Definition
| APCR is characterized by APC’s inability to prolong clotting assays when performed in vitro. Required along with molecular assay because 10%of individuals do not have the FVL mutation |
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Term
| Molecular assay for APCR diagnosis |
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Definition
| 90% of APCR are due to a single point mutation of the V gene involving replacement of Arg with Gln (factor V leiden). Mutant V molecule is resistant to APC inactivation. Confirmatory test for FVL is PCR-based molecular assay, also confirms mutations other than FVL. |
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Term
| Increased levels of prothrombin |
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Definition
| directly contributes to an increased thrombic risk by causing increased thrombin generation and decreased fibrinolytic activity can occur because of enhanced activation of TAFI. |
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Term
| Increased levels of fibrinogen |
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Definition
| due to fibrinogen resistance to lysis by plasmin or reduced plasminogen activation |
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Term
| Deficiencies of plasminogen or plasminogen activator |
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Definition
| decreased of both protein concentration and functional ability or normal antigen levels but reduced functional activity |
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Term
| Increased levels of plasminogen activator inhibitor |
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Definition
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Term
| Secondary disorders leading to thrombosis |
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Definition
| acquired fibrinolytic defects, anti-phospholipid antibody syndromes (APLS), HIT, malignancy, pregnancy and oral contraceptives, post-operative state and trauma |
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Term
| Treatment of a thrombotic event |
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Definition
| Low-dose heparin, corticosteroids to normalize clot times |
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Term
| INR to standardize PT times |
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Definition
| A patient PT on oral anticoagulation is inserted into a formula which includes ISI, the outcome is the INR. INR is independent of the reagents and methods to determine PT and allows for better assessment of long-term oral anticoagulant therapy. |
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Term
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Definition
| (patients PT/mean normal PT)^ISI |
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Term
| Use of thrombolytic therapy |
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Definition
| reestablish vascular perfusion |
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Term
| Monitoring of thrombolytic therapy |
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Definition
| monitored by decrease in plasma fibrinogen and increase in FDPs (lytic state which can also induce hypercoaguability) |
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Term
| a platelet fibrin mass that forms within a vessel is known as |
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Definition
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Term
| Rupture of plaque in an artrey may results in |
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Definition
| formation of white thrombi |
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Term
| What clinical manifestation is more likely to be found in a person with an inherited thrombophilia than in a person with an acquired thrombophilia? |
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Definition
| venous embolism at a young age |
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Term
| A patient diagnosed with DVT. Four days later a thrombus is found in his lung, this is |
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Definition
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Term
| What type of laboratory test results for AT will a patient with a type I deficiency of AT have? |
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Definition
| decreased antigenic and decreased functional activity |
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Term
| An inhereited abnormality in the factor V molecule that renders it resistant to inactivation by protein C is known as |
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Definition
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Term
| a deficiency or defect in protein C can lead to thrombosis due to |
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Definition
| inability to inactivate factors Va and VIIIa |
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Term
| Patients who recieve UH as treatment for a thrombus should be monitored periodically for the complication of HIT. What laboratory test should be used to monitor the patient? |
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Definition
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Term
| Therapy with LMWH is best monitored using what laboratory test? |
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Definition
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Term
| The best test to monitor coumadin therpy is the |
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Definition
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Term
| A patient with thrombophilis has a decreased functional and antigenic activity of protein C. What is the diagnosis? |
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Definition
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Term
| Why is following up an abnormal clottin assay for APCR with a molecular test recommended? |
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Definition
| 10% of individuals with APCR do not have the FVL mutation |
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Term
| WHy does a patient with a thrombotic incident receive both heparin and coumadin for 4-5 days after the incident? |
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Definition
| coumadin takes this lon to produce its full anticoagulant action |
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Term
| The value of using the INR to report the PT is |
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Definition
| it reduces the interlaboratory variability in monitoring oral anticoagulants |
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Term
| A patient with a myocardial infarction is admitted to the ER. The physician starts the patient on strepokinase. She calls the laboratory and wants you to sugest a test to ensure the a lytic state is induced by the therpy. What test will you suggest |
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Definition
| A baseline TT and TT after 3-4 hours of therpy |
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Term
| What physiologic protein's anticoagulant effec is accelerated by heparin |
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Definition
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Term
| A patient has hyperhomocysteinemia. What laboratory test an be helpful in estabishing the etiology of his disease? |
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Definition
| molecular tests for MTHFR and CBS |
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Term
| Which of the following conditions is not associated with an icnreased tendency for thrombosis |
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Definition
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Term
| A 30 year olf patient is diagnosed with a DVT. This is his third episode of DVTs. He is currently hospitalized and recieveing herpain therapy. The physician orders a thrombotic risk battery of tests. What is the most approproate action that the laboratory should take? |
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Definition
| call the physician and explain that testing will not be accurate durin anticoagulant therpy and during a thrombotic episode |
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Term
| A patient is on coumadin for treatment of DVT. He returns to the doctor with skin necrosis. What protein deficieny should be tested for after coumadin therpay is finished? |
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Definition
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Term
| why would defects of fibrinolysis result in hypercoagulability? |
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Definition
| delicate balance between clot-promoting factors and clot-inhibiting factors has been disturbed, and clot-promoting factors dominate the clinical picture |
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Term
| Why is thrombotic disease associated with hereditary thrombophilis considered a multigene (or multirisk factor) disease? |
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Definition
| thrombophilia gene does not cause thrombtic episodes, need a second genetic or acquired predisposing factor, only diagnosed when family screening is done for another family member who has had thrombosis |
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Term
| Why are both immunologic and functional assays recommended when screening a patient suspected of having a familial thrombophilic defect? |
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Definition
| defects can be quantitative or qualitative, immunologic assays will miss qualitative defects because normal antigen levels but reduced functional levels. Functional assays are better |
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Term
| Why should heparin therapy overlap initiation of oral anticoagulant therapy when treating a patient with an acute thrombosis? |
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Definition
| Oral anticoagulants decrese functional levels or procoagulant proteins and anticoagulant proteins but action is not immediate depends on proteins half life. Heparin needs to be continued as to not aggravate the already out of balance hemostatic system until coumadin effect can be achieved |
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Term
| An increased tendency to form venous thromboemboli is called: |
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Definition
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Term
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Definition
| a piece of thrombotic material released from a thrombus into the circulatory system |
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Term
| All of the following are considered risk factors for the formation of venous thrombi EXCEPT |
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Definition
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Term
| Which of the following statements concerning the laboratory diagnosis of DVT is correct? |
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Definition
| Radiologic procedures to visualize the thrombus may aid in the identification of thrombi. |
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Term
| Heparin catalyzes the anticoagulant action of which plasma coagulation inhibitor? |
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Definition
| antithrombin and heparin cofactor II |
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Term
| Protein S deficiency predisposes to thrombosis because: |
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Definition
| There is inadequate protein C inactivation of Va and VIIIa. |
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Term
| Antithrombin deficiency as a cause of inherited thrombophilia may be due to: |
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Definition
| synthesis of reduced amounts of antithrombin (a quantitative deficiency) and production of a normal quantity of a nonfunctional protein |
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Term
| Activated Protein C Resistance (APCR) contributes to a thrombophilic tendency by: |
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Definition
| decreased destruction of factor Va by activated protein C |
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Term
| The major advantage of using low-molecular weight heparin vs. unfractionated heparin is: |
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Definition
| LMWH has a more predictable dose-response profile and LMWH does not usually require routine laboratory monitoring. |
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Term
| The best test for monitoring oral anticoagulant therapy is: |
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Definition
| International Normalized Ratio (INR) |
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Term
| What are the risk factors for formation of a venous thrombi |
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Definition
| deficiency of protein C or protein S, elevated prothrombin levels, and elevated plasminogen activator inhibitor (PAI-1) levels |
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Term
| C-reactive protein, an acute phase reactant used as a marker of inflammation, is useful in the diagnosis of: |
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Definition
| arterial thrombotic disease |
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Term
| All of the following are suggestive of an inherited thrombophilia EXCEPT: |
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Definition
| development of heparin-induced thrombocytopenia (HIT) |
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Term
| What is suggestive of an inherited thrombophilia |
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Definition
| venous thromboembolism at a young age (prior to age 45), family history of venous thromboembolism, and recurrent venous thromboembolism |
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Term
| A patient is being evaluated in the coagulation laboratory. The protein C level determined by a clot-based assay was 50%; the protein C level determined by an immunoassay was 50%. What do these results indicate? |
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Definition
| The patient has protein C deficiency, type I. |
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Term
| Which of the following statements best describes the inherited condition of Activated Protein C Resistance (APCR)? |
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Definition
| It may be due to mutations at either of the two APC cleavage sites of factor V. |
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Term
| The Prothrombin Gene mutation 20210 predisposes to thrombosis by what mechanism? |
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Definition
| increased synthesis of prothrombin |
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Term
| All of the following statements concerning the association of thrombotic disease with disorders of fibrinolysis are true EXCEPT: |
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Definition
| Abnormalities of fibrinolysis associated with thrombosis may be due to decreased plasminogen activator inhibitor. |
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Term
| The association of thrombotic disease with disorders of fibrinolysis |
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Definition
| Hereditary disorders of fibrinolysis are less common than hereditary disorders of procoagulants or coagulation inhibitors, Abnormalities of fibrinolysis associated with thrombosis may be due to abnormalities of fibrinogen structure and Abnormalities of fibrinolysis associated with thrombosis may be due to decreased concentration or functional activity of plasminogen. |
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Term
| The most common cause of an acquired fibrinolytic defect predisposing to thrombosis is: |
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Definition
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Term
| When treating a patient with an acute thrombotic episode, heparin therapy typically "overlaps" coumadin therapy because: |
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Definition
| It allows the thromboplastins produced by different manufacturers to be standardized, resulting in standardization of PT monitoring of oral anticoagulation. |
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Term
| The major clinical benefit of using thrombolytic therapy for a patient with a thrombotic event is: |
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Definition
| to quickly reestablish vascular perfusion |
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