Coagulation Testing, Disorders, Treatment Flashcards
PT (Prothrombin Time): Purpose
identifies deficiency in EXTRINSIC + COMMON pathway (fibrinogen, II/ prothrombin, V, VII, X)
The PT reagent contains (3)
thromboplastin, phospholipid, and calcium
PTT (Partial Thromboplastin Time): Purpose
- identifies deficiency in INTRINSIC + COMMON pathway (all factors except VII and XIII)
- monitors unfractioned heparin treatment + some thrombin inhibitors
Mixing Studies: Purpose
Determines if abnormal PT/PTT is due to factor deficiency OR an inhibitor
Mixing Studies: Principle
- mix patient plasma + normal control (has all coag factors)
- test PT or PTT
Corrected = factor deficiency
Uncorrected = perform inhibitor screen
Inhibitor Screen: Purpose
Determines if inhibitor is immediate OR delayed
Inhibitor Screen: Principle
- (In 1:1 AND 4:1 patient ratios) = mix patient plasma + Normal control (has all coag factors)
- test PT/ PTT 3 times:
1. Mixed: Immediately
2. Mixed: after 1 HOUR of incubation at 37 degrees
3. Separately: after 1 HOUR of incubation at 37 degrees
What does it mean if PT/PTT of an inhibitor screen is prolonged immediately after patient plasma + Normal control are mixed ?
- Inhibitor screen = POS
- Inhibitor reacts IMMEDIATELY
What does it mean if PT/PTT of an inhibitor screen is prolonged after 1 HOUR of (patient plasma + Normal control) being mixed when it was normal after being immediately mixed ?
- Inhibitor screen = POS
- Inhibitor is delayed reacting
How can heparin be removed before performing an inhibitor screen ? Why is this done ?
- remove Heparin using Hepzyme
- Heparin causes FALSE POS inhibitor screen
- prolongs PT/ PTT
Why is patient plasma and Normal control incubated SEPARATELY for 1 hour at 37 degrees as part of the Inhibitor Screen ? What should the results be ?
- separate incubation ensures clotting factors did not degrade during incubation
- Normal control = POS
- patient plasma = neg
Why does the inhibtor screen use 1:1 AND 4:1 patient to Normal control ratios ?
4:1 ratio increases sensitivity to inhibitors
Single Factor Assay: Purpose
Determines which factor(s) patient is deficient in
Single Factor Assay: Principle
- mix patient plasma + plasma deficient in a single factor
- test PT or PTT
- compare results to standard graph to determine factor concentration
If patient plasma corrects PT/ PTT in a Single Factor Assay, what does this mean ?
Recall: patient plasma + plasma deficient in a known factor are mixed
Corrected = patient corrects deficient plasma; patient is not deficient in particular factor
Uncorrected = patient unable to correct deficient plasma; patient is deficient in the same known factor
Fibrinogen Testing: Purpose
Determines levels of fibrinogen in plasma
Fibrinogen Testing: Principle
- EXCESS thrombin + patient sample
- level of plasma fibrinogen is INVERSELY proportional to clotting time
NOTE: excess thrombin neutralizes anti-thrombin activity (FDPs)
Why is thrombin added in EXCESS in fibrinogen testing ?
To neutralize anti-thrombin activity (ie. FDPs)
TT (Thrombin Time): Purpose
- Detect DECREASED levels of fibrinogen, DYSFIBRINOGENEMIA, or THROMBIN INHIBITORS (ie. FDPs, D-dimers)
- Monitor/ evaluate DIC, heparin therapy, fibrinogen diseases
TT: Principle
Thrombin Time:
- dilute BOVINE thrombin + patient sample to bypass previous steps of coag cascade
- measures time to convert fibrinogen to insoluble fibrin crosslinks
D-Dimer: Purpose
To rule out DIC
D-Dimer: Principle
- turbidimetric IMMUNOASSAY (DIRECTLY proportional)
- MONOCLONAL Abs specific to D-dimers coat latex particles
- D-dimers DIRECTLY bind to Abs = AGGLUTINATION = increased turbidity = INCREASED ABSORBANCE measured
Reptilase Time: Purpose
To detect HEPARIN, DYSFIBRINOGENEMIA, or FIBRINOGEN DEFICIENCY
Reptilase Time: Principle
reptilase (enzyme) = converts fibrinogen to fibrin + NOT INHIBITED by heparin = clot forms
- compares results to PROLONGED thrombin time (TT)
What does it mean if TT = prolonged and Reptilase Time = equally prolonged ?
Fibrinogen Deficiency
- there is no fibrinogen in the first place; reptilase cannot form fibrin
NOTE = prolonged TT cannot be due to heparin because reptilase is not affected by heparin, which is also prolonged in this case
What does it mean if TT = prolonged and Reptilase Time = MORE PROLONGED ?
DYSFIBRINOGENEMIA
What does it mean if TT = prolonged and Reptilase Time = NORMAL ?
HEPARIN is present
- but reptilase is unaffected by the anticoagulant
Bleeding Time: Purpose
To test ability of PLTs to undergo PRIMARY HEMOSTASIS
Bleeding Time: Principle
- IN VIVO
- DO NOT DO if PLT <80 x10^9/L
- shallow skin-wound is made on patient
- time to stop bleeding is measured
Which coagulation tests use Turbidimetric end-point clot detection ?
- PT
- PTT
- TT
- Fibrinogen
Platelet Aggregometry: Purpose
To assess PLT function (secretion, aggregation, adhesion w/ ristocetin)
Platelet Aggregometry: Principle
- DO NOT DO if PLT <50 x10^9/L
- PLT-RICH plasma is stirred in AGGREGOMETER with diff agonists:
1. ADP + collagen + EPO + arachidonic acid = tests GPIIb/ IIIa and fibrinogen function
2. Ristocetin = tests GPIb and vWF function
NOTE: agonists initiate PLT aggregometry
Interferences in PLT Aggregometry
- gross lipemia
- aspirin
- PLT <50 x10^9/L
Ristocetin Co-factor Assay: Purpose
- To ensure vWF is present for coagulation
- Differentiate VonWillebrand Disease from Bernard Soulier
Ristocetin Co-factor Assay: Principle
- mix patient plasma with Normal PLTs + Ristocetin
- Ristocetin induces vWF to attach to GPIb receptors on Normal PLTs = aggregation
How to differentiate Unfractioned Heparin (UFH) from Low Molecular Weight Heparin (LMWH) ?
Both:
- indirect anticoagulants
UFH:
- inhibits all serine proteases (plasmin, IIa, IXa, Xa, XIa, XIIa) EXCEPT VII and Kallikrein
- monitored by aPTT or anti-Xa assay
LMWH:
- inhibits Xa
- monitored by anti-Xa assay ONLY
Heparin is a cofactor of __.
Heparin is a cofactor of ANTI-THROMBIN.
Coumadin: what does it do ? How is it monitored ?
- used in ANTICOAGULANT THERAPY
- acts on LIVER = IMPAIRS production of vit-K DEPENDENT factors (II, VII, IX, X “2790” and Protein C/ S/ Z)
- Monitored by PT (INR= 2.0 - 3.0)
Fondaparinoux: what does it do ? How is it monitored ?
- COMBINES with ENHANCES anti-thrombin activity
- inhibits Xa
- monitored by anti-Xa
Dabigatran: what does it do ? How is it monitored ?
- DIRECT THROMBIN INHIBITOR (both free and clot-bound)
- not monitored
Direct Xa Inhibitors: what do they do ? How are they monitored ?
- DIRECTLY INHIBITS Xa (free, bound to IXa, and clot-bound Xa)
- monitored by anti-Xa
What is Thrombolytic Therapy ? Give examples.
Removes pathological clots:
- recombinant TPA & purified UROKINASE = treats MI, embolic/ thrombotic stroke, pulmonary embolisms
- STREPTOKINASE = plasminogen activator but can induce immune/ allergic response
TPA = Tissue Plasminogen Activator
Tube/ anticoagulant requirements for coagulation testing ?
- Sodium citrate (light blue top)
- Filled to capacity
- 1:9 anticoagulant to blood
Why is Sodium Citrate the preferred anticoagulant for coagulation testing ?
- Preserves V and VIII (labile factors)
- Stabilizes pH
- Does not inhibit PLT function
- Anticoagulant reversed when Ca2+ is added
Interferences in Coagulation Testing
- clotted samples
- insufficient tube volume
- EDTA collection
- anticoagulants therapy (heparin, coumadin)
- hemolysis
- lipemia
- cold temp
- hot temp
How does cool temp storage interfere with coag testing ?
prematurely activates VII and PLTs during transport/ storage
How does hot temp interfere with coag testing ?
deteriorates factors V and VIII (heat-labile)
How does gross lipemia interfere with coag testing ?
interferes with testing that use end-point detection (PT, PTT, TT, Fibrinogen)
- increase turbidity = falsely decrease
How does EDTA interfere with coag testing ?
- EDTA does not preserve factor V
- prolongs tests
- chelates Ca2+ needed for coagulation cascade
How does insufficient tube volume interfere with coag testing ?
too much Sodium Citrate anticoagulant = tests falsely prolonged
How does Turbidimetric End-point detection work in coag testing ?
- fibrin clot forms = optical density increases/ transmittance decreases
- when optical density > baseline = timer stops to indicate cot formation
How does hemolysis interfere with coagulation testing ?
- severe hemolysis = falsely decrease PT and PTT
- coagulation prematurely starts before testing
- check clots in hemolyzed samples
Thrombocytopenia due to decreased/ defective production (3)
- Megakaryocyte hypoplasia:
- inadequate megakaryocytes in BM
- congenital (Fanconi’s), mutations, drugs, infection, injury to BM (radiation, chemotherapy) - Replacement of BM with fibrosis
- Primary Myelofibrosis or Hairy Cell - Inadequate megakaryrocytes in PBS:
- megaloblastic anemia (impaired DNA synthesis) or MDS
- normal marrow but peripheral blood cytopenia
Causes of Thrombocytopenia (3). Give examples.
- Defective Production (hypoplasia, PMF, MDS)
- Increased Consumption (TTP, HUS, DIC)
- Increased Destruction by Antibodies (ITP, Drug-induced, HIT)
ITP
Idiopathic Thrombocytopenic Purpura:
- thrombocytopenia due to increased destruction
- IgG binds to PLT GPIa or IIIb/IIa (surface glycoproteins) = removed by spleen
- megakaryocyte fragments, Large PLTs (?increased BM production/ early BM release)
Drug-Induced Thrombocytopenia
- Penicillin, quinidine
- anti-drug Ab binds to PLT glycoproteins via Fab region IN THE PRESENCE OF DRUG
- Fc region binds to Fc receptors on phagocytes = removal by spleen - Procainamide, gold salts
- autoAb bind to PLT glycoproteins WITHOUT drug present
Heparin-Induced Thrombocytopenia (HIT)
- type of Drug-induced Thrombocytopenia
- (unfractioned) heparin binds to PF4 on PLT = conformational change exposes new epitopes = Ab formation against PF4/heparin complex
- Fc region binds to PLT Fc receptors = activation and aggregation = decreased PLT count
Which part of the anti-drug Ab causes PLT activation/ aggregation in HIT ?
Fc region = binds other PLTs = activation/ aggregation
Cause of TTP
Thrombotic Thrombocytopenic Purpura:
- ADAMTS13 deficiency
- insufficient ADAMTS13 enzyme to cleave vWF multimers
Cause of HUS
Hemolytic Uremic Syndrome:
- viral/ bacterial infection
Ie. Shigella or E. coli O:157
Cause of DIC
Disseminated Intravascular Coagulation:
- secondary to systemic disease
Ie. infection, trauma, TRANSFUSION REACTION
How to confirm TTP
Molecular genetic testing = ADAMTS13 deficiency
ADAMTS13 activity test
PBS = poly, schisto, sphero, nRBC
How to confirm HUS
Blood culture = Shigella or E. coli O:157
PBS = poly, schisto, sphero, nRBC
How to differentiate DIC from TTP and HUS
DIC:
Transfusion history
PBS = poly, schisto, NO SPHERO, nRBC
PT/ PTT = PROLONGED
Fibrinogen = decreased (clot formation)
D-dimer = increased (fibrinolysis)
NOTE: all will have decreased PLT, (PBS = poly, schisto)
Differentiate ET from Reactive Thrombocytosis
Essential Thrombocytosis:
- stem cell disorder
- splenomegaly
- abnormal PLTs/ function
- clustering megakaryocytes in BM
Reactive Thrombocytosis:
- hemorrhage
- splenectomy
What is Bernard Soulier Syndrome ?
Deficient/ defective GPIb from PLT surface
- PLTs cannot bind vWF = DEFECTIVE ADHESION
Bernard Soulier Syndrome (PBS, BM, PT/PTT. PLT, BT, PLT aggregation)
PBS= giant PLTs
BM= normal/ increased megakaryocytes
PT/ PTT = normal
PLT = mild DECREASE
BT= increased (defective adhesion)
PLT aggregation:
ADP, EPO, collagen, a.a.= normal
Ristocetin= ABNORMAL
What is Glanzmann’s Thrombasthenia
GPIIb/ IIIa deficient or defective
- PLTs cannot bind fibrinogen and vWF = DEFECTIVE AGGREGATION
Inheritance pattern for Bernard Soulier and Glanzmann’s Thrombasthenia
Autosomal recessive
Glanzmann’s Thrombasthenia (PBS, BM, PT/ PTT, PLT, BT, PLT aggregation)
PBS/ BM= normal PLTs and megakaryocytes
PT/PTT= normal
BT= increased (defective aggregation)
ADP, EPO, collagen, a.a.= abnormal
Ristocetin= normal
Which coagulation disorder is associated with albinism ?
Dense granule deficiency
What does Dense granule deficiency affect ?
PLT aggregation
Alpha granule deficiency (PT/ PTT, PLT, BT)
PT/ PTT= normal
PLT= agranular, large, mild decrease
BT= increased (defective adhesion/ aggregation; primary hemostasis)
Inheritance pattern of vWD. What is vWD ?
WonWillebrand Disease = AUTOSOMAL DOMINANT
- mutation of vWF gene= quantitative/ qualitative defect
- DEFECTIVE PLT ADHESION
vWD (PT, PTT, PLT, BT, PLT aggregation). What other tests can be done ?
PT = normal
PTT = normal OR increased
PLT= normal
BT= increased (defective adhesion)
ADP, collagen, EPO, a.a.= normal
Ristocetin= abnormal
vWF antigen assay= decreased
FVIII assay = decreased (vWF needed to stabilize FVIII in plasma)
vWD vs Bernard Soulier: Ristocetin cofactor assay results
vWD= abnormal (no vWF)
Bernard Soulier= normal (has vWF to bind GPIb receptors supplied by normal PLTs)
RECALL: Ristocetin cofactor assay tests patient plasma with NORMAL PLTs
How does liver disease affect coagulation ?
Affects factors synthesized in liver:
- vit K dependent factors (II/ prothrombin, VII, IX, X, Protein C/S/Z)
- Dysfibrinogenemia
Hemophilia A: cause and lab results (factor assay, PT, PTT, TT, BT)
- FVIII deficiency
- X-linked recessive
FVIII assay = decreased
PT= normal
PTT= abnormal
TT= normal
BT= normal
Hemophilia B: cause and lab results (factor assay, PT, PTT, BT, TT)
- Factor IX deficiency
FIX assay= DECREASED
PT= normal
PTT= INCREASED
BT= normal
TT= normal
Hemophilia C: cause and lab results (factor assay, PT, PTT, BT, TT)
- FXI deficiency
FXI assay= DECREASED
PT= normal
PTT= INCREASED
TT = normal
Afibrinogenemia/hypofibrinogenemia: cause, effect and lab results
- Fibrinogen < 0.5 g/L = autosomal recessive
- PLT adhesion/ aggregation= abnormal
PT, PTT, TT, BT= INCREASED
Dysfibrinogenemia: cause, effect, and lab results
- AUTOSOMAL DOMINANT or acquired
- ALTERED fibrinogen STRUCTURE = defective clot formation AND fibrinolysis
- results in THROMBOPHILIA
PT= normal
PTT= normal
TT= INCREASED
Reptilase= MORE PROLONGED*
*NOTE: deformed fibrinogen can’t even bind to reptilase
FXII deficiency: effects, and lab results (factor assay, PT, PTT, TT, BT)
- no clinical bleeding
FXII assay= DECREASED
PT, TT, BT= normal
PTT= INCREASED
HMWK or PK deficiency: cause, effects, and lab results (factor assay, PT, PTT, TT, BT)
- no clinical bleeding
Factor assays= DECREASED
PT, TT, BT= normal
PTT= INCREASED
Factors II, V, X deficiency: lab results (PT, PTT, TT, BT)
- all are factors in common pathway
PT/, PTT= increased
TT, BT= normal
FVII deficiency: lab results (PT, PTT, TT, BT)
PT= INCREASED
PTT, TT, BT= normal
Factor XIII deficiency: clinical effects and lab testing ?
- decreased formation of insoluble clots = defective wound healing
- [XIII] measured by immunoassay/ chromogenic assay (NADPH consumption)
PT/ PTT= normal
Factor V Leiden: cause, effect, and lab testing
- AUTOSOMAL DOMINANT
- mutation = arginine to glutamine
- resistance to activated Protein C (aPC)= FV not inhibited despite high concentrations of thrombin = THROMBOPHILIA
Anticlot Protein C Resistance assay
Molecular genetics/ PCR
Prothrombin G20210A mutation: cause, effect and lab testing
- prothrombin gene = guanine to ADENINE
- increased [prothrombin] = increased risk of thrombosis
Molecular genetics/ PCR
Protein C/ S deficiency: cause, effects and lab testing
- AUTOSOMAL DOMINANT or acquired
- increased risk of Deep-Vein Thrombosis (DVT), pulmonary embolism and stroke
- cutaenous hemorrhage, tissue NECROSIS, and DIC
Clot based assay
Antigenic assay to measure levels
Lupus Anticoagulant Syndrome: cause and clinical effects
- anti-phospholipid autoAb form = bind to phospholipids (PF3) in PTT reagent = interferes with prothrombin activation
- PROLONGS COAG TESTING
Lupus Anticoagulant Syndrome: lab results (PT, PTT, TT, Mixing Studies, DRVVT)
PT= normal
PTT= INCREASED
TT= normal
Mixing studies= no correction with normal plasma
DRVVT= POSITIVE
DRVVT= Dilute Russel Viper Venom Time
DRVVT: principle
- viper venom activates factor X
- reagent has low [phospholipid]
PROLONGED/ POSITIVE= Lupus Anticoagulant (LAC) in patient plasma interferes with prothrombin activation
Normal= no LAC
Follow-up testing after POSITIVE DRVVT
- Use reagent with EXCESS PHOSPHOLIPIDS to neutralize LAC = normal clotting time = LAC positive
- Mixing study 1:1 of patient plasma and Normal plasma = uncorrected = LAC positive
Which of the following would lead to a prolonged bleeding time?
a.
A platelet count of 155 x 10^9/L
b.
Von Willebrand disease
c.
Fibrinogen value of 1.2 g/L
d.
Hemophilia A
b.
Von Willebrand disease
Prolonged PT and PTT: DIC, primary/ hyper fibrinoloysis, both or neither ?
DIC and hyper/primary fibrinoloysis
Increased D-dimers: DIC, primary/ hyper fibrinoloysis, both or neither ?
DIC and hyper/primary fibrinoloysis
Elevated plasmin: DIC, primary fibrinoloysis, both or neither ?
DIC and hyper/primary fibrinoloysis
Platelet count is normal: DIC, primary/ hyper fibrinoloysis, both or neither ?
ONLY hyperfibrinolytic states (primary fibrinolysis)
Factor XIII levels are elevated: DIC, primary fibrinoloysis, both or neither ?
Neither
Schistocytes can be seen on the smear: DIC, primary fibrinoloysis, both or neither ?
ONLY Disseminated Intravascular Coagulation (DIC)
Fibrinogen degradation products are elevated: DIC, primary fibrinoloysis, both or neither ?
Both
Which of the following is true about the aPTT test?
a.
It will be abnormal with a factor XIII deficiency
b.
It is used to monitor coumadin therapy
c.
It will be prolonged with abnormal platelet function
d.
It will be prolonged in Von Willebrand deficiency
d.
It will be prolonged in Von Willebrand deficiency
Thrombocytopenia on PBS: HUS, TTP, both or neither ?
Both
Most commonly in children: HUS, TTP, both or neither ?
ONLY Thrombotic Thrombocytopenic Purpura (TTP)
Can be congenital or acquired: HUS, TTP, both or neither ?
ONLY Thrombotic Thrombocytopenic Purpura (TTP)
Microangiopathic hemolytic anemia with schisto and poly: HUS, TTP, both or neither ?
Both
Clotting factors are decreased (used up): HUS, TTP, both or neither ?
Neither
Toxins damage renal glomerular capillaries: HUS, TTP, both or neither ?
ONLY Hemolytic Uremic Syndrome (HUS)
Abnormally large vWF multimers are implicated: HUS, TTP, both or neither ?
ONLY Thrombotic Thrombocytopenic Purpura (TTP)
Autoantibodies to ADAMTS 13 can occur: HUS, TTP, both or neither ?
ONLY Thrombotic Thrombocytopenic Purpura (TTP)
Prolonged PT and APTT: HUS, TTP, both or neither ?
Neither
Which of the following can cause a prolonged APTT?
a.
Decreased levels of factor XIII
b.
Decreased levels of factor VII
c.
Decreased levels of factor XI
d.
In-vitro hemolysis
c.
Decreased levels of factor XI
Crit: PLT
inpatient: <10 x10^9/L
outpatient: <20 x10^9/L
Crit: PTT
> 120 sec
Crit: Fibrinogen
Which statement about the fibrinogen assay is most correct?
a.
Clotting time is proportional to the amount of thrombin in the plasma
b.
An abnormal result is seen in patients on heparin therapy
c.
Concentrated thrombin reagent is added to dilute plasma
d.
Patient plasma is mixed 1:1 with fibrinogen-deficient plasma
c.
Concentrated thrombin reagent is added to dilute plasma
- Mode of action of heparin as an anticoagulant in the human body
- List which coagulation factors are inhibited by UFH
- Heparin is a cofactor for Antithrombin
- Heparin binds to AT, changes its conformation, and accelerates the rate of inactivation of coagulation factors by AT
- UFH inhibits all the serine proteases except VII and Kallikrein
- serine proteases: XIIa, XIa, IXa, Xa and IIa (and plasmin)
Which of the following can be ruled out if a patient has a D-dimer result of 8.0 mg/L?
a.
Disseminated intravascular coagulation
b.
Deep Vein thrombosis
c.
Pulmonary embolism
d.
None of the above
d.
None of the above
Thrombocytosis is typically seen in which of the following?
a.
Acute leukemia
b.
Post-splenectomy
c.
Essential Thrombocythemia
d.
Ineffective thrombopoiesis
b.
Post-splenectomy
c.
Essential Thrombocythemia
In heparin-induced thrombocytopenia (HIT), patients on heparin develop antibodies to:
a.
Self platelet Fc receptor antigens, causing platelet activation
b.
Phospholipids, which interferes with the activation of thrombin
c.
pf3, which causes PLT aggregation and activation
d.
Heparin in complex with pf4, leading to activation
d.
Heparin in complex with pf4, leading to activation
A patient specimen is received from an outside laboratory for coagulation testing. The history provided indicates the patient is on Coumadin (warfarin). The following results are obtained:
PT: no clot detected
PTT: no clot detected
The specimen is retested and the results check. You bring the results to your supervisor, who instructs you to perform a fibrinogen assay. Will the fibrinogen assay be useful?
Yes. A fibrinogen assay would be useful. The patients history indicates coumadin therapy and coumadin acts by inhibiting fibrinogen function
Which clotting factors would be affected by coumadin therapy? Select all that apply:
a.
Factor XIII
b.
Factor V
c.
Factor VIII
d.
Factor IX
d.
Factor IX
A Bleeding Time of >9 minutes could be expected in which of the following disorders? Select all that apply:
a.
Abnormal vascular function
b.
Marked thrombocytopenia
c.
Glanzman’s thrombasthenia
d.
Hemophilia A
a.
Abnormal vascular function
b.
Marked thrombocytopenia
c.
Glanzman’s thrombasthenia
How is the fibrinogen concentration of a sample determined in the fibrinogen assay?
The instrument compares the clotting time to a calibration curve
Which statement about the quantitative D-dimer assay is correct?
a.
The normal reference range is >0.5 g/L
b.
The result is abnormal when FDP’s are decreased
c.
Micro-latex particles in the reagent are coated with monoclonal antibodies to D-dimer
d.
The presence of D-dimers is detected by clot formation
c.
Micro-latex particles in the reagent are coated with monoclonal antibodies to D-dimer
In the APTT test, what happens during the initial incubation after the APTT reagent is added to the test plasma?
a.
Factor VII and the extrinsic pathway are activated
b.
Factors IX and VIII are activated
c.
Factor XI and XII are activated
d.
Factor X and V are activated
c.
Factor XI and XII are activated
Which of the following is correct with respect to specimen collection for coagulation testing?
a.
Mix the sample well with vigor
b.
Draw coagulation specimens after an EDTA tube
c.
Use a 1:9 dilution of anticoagulant to blood
d.
Make sure the vacutainer tube is filled 70% capacity
c.
Use a 1:9 dilution of anticoagulant to blood
Follow-up for Hct > 0.55 L/L
- there is excess anticoagulant = extra citrate will bind the calcium in the test reagent and falsely prolong the clotting time
- specimen should be recollected with less anticoagulant and the tests repeated
