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MLSCI 230 > Laboratory Evaluation of Hemostasis > Flashcards

Laboratory Evaluation of Hemostasis Flashcards

1
Q

petechiae and mucus membrane bleeding are signs of…

A

PLT/vascular defect (primary hemostasis)

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2
Q

ecchymosis, bleeding into joints, and hematuria are signs of…

A

coagulation defects (secondary hemostasis)

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3
Q

specimen requirements and handling for evaluation of hemostasis

A
  • clean venipuncture (avoid trauma; no TF release; prevent activation of clotting factors
  • avoid EDTA, heparin, and fluoride contamination (collect coag tubes first)
  • use anticoagulant (3.2% sodium citrate)
    > reversibly binds free calcium in sample
    > preserves factors V and VIII best
    > does not inhibit PLT function
  • clotted specimens useless; invert 4-5 times only
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4
Q

ratio of anticoagulant to blood in citrate tubes must be

A

1: 9
* *tubes must be filled completely when being collected**
- if too little = overanticoagulation and testing times will be falsely prolonged
- using butterfly needle = discard tube must be collected first (accounts for air vol in tubing)

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5
Q

if severe hemolysis occurs, the release of this occurs

A

erythrocytin

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6
Q

T or F. Factors V and VIII are stable

A

F! they are labile!! if not tested right away, remove plasma and freeze

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7
Q

bleeding disorders (3 categories)

A
  • vascular and PLT disorders
  • coag factor defs/abnormalities
  • fibrinolytic disorders
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8
Q

tests for PLT/vascular disorders (4)

A
  1. PLT count (automatic methods usually; impedance or flow cytometry)
  2. bleeding time (not done anymore)
  3. PLT aggregation tests
  4. Ristocetin cofactor tests
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9
Q

this detects qualitative abnormalities in patients who have a normal PLT count

A

PLT function tests

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10
Q

Platelet aggregometry/light transmission aggregometry

A
  • continuous measurement of light transmitted through a suspension of PLTs in plasma ; more aggregation = more light transmittance
  • variety of agonists to activate aggregation = thrombin, ADP, arachidonic acid, epinephrine, collagen, ristocetin
  • each agonist has a typical transmittance pattern
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11
Q

T or F. 0% Transmittance = 0% aggregation

A

T!

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12
Q

antibiotic that cases vWF to bind GP Ib/IX/V on platelets

A

Ristocetin

  • agglutination (not true aggregation)
  • requires presence of vWF (ristocetin cofactor) and GP Ib/IX/V
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13
Q

PLT Aggregation Test interpretation of results

A
  • Glanzmann Thrombasthenia: GPIIb/IIIa def; abnormal aggregation w all agonists except ristocetin
  • Von Willebrand Disease: normal aggregation with all except ristocetin
  • Bernard-Soulier syndrome: GPIb def; same as vW disease
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14
Q

Ristocetin cofactor test

A
  • differentiate between vW disease and Bernard-Soullier syndrome
  • done when PLT aggregometry is abnormal with ristocetin
  • repeat aggregometry using:
    > ristocetin
    > normal plts: ensures GPIb/IX/V is present
    > patient’s plasma: must provide vWF
  • still abnormal = vWF disease 9patient’s plasma did NOT provide vWF)
  • normal = Bernard-Soulier disease
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15
Q

confirmatory testing for ristocetin cofactor test

A

vWF antigen asay or GP Ib, IX, V receptors

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16
Q

factor abnormalities can be caused by:

A
  • decreased synthesis
  • production of dysfuncitonal coag factor molecule
  • excessive destruction of factors through acquired disorders
  • inactivation of factors through circulating inhibitors
17
Q

tests for coag factor abnormalities

A
  • prothrombin time
  • activate partial thromboplastin time
  • thrombin time
  • screening test for circulating inhibitors
  • fibrinogen assay
  • single facto assays
  • factor XIII screen/factor XIII assay
18
Q

clot-based testing

A
  • measures time from initiation of clotting to clot formation
    > endpt = clot
    > prolonged clotting time indicates coagulopathy
19
Q

Endpt clot detection methods: (2)

A
  • visual (manual): time stos when a clot is seen
  • automated
    > optical endpt - change in absorbance
    > mechanical - measures viscosity
    > electrical circuit completed as a clot forms
20
Q

prothrombin time (PT)

A
  • screens for factor deficiecies in extrinsic and common pathway; presence of circulating inhibitors
    > factors VII, X, V, prothrombin and fibrinogen
  • measures time for clot to form when reagent containing tissue thromboplstin, phospholipids, and Ca 2+ are added to plasma = activates VII => common pathway
  • also used to monitor oral anticoagulant therapy (warfarin/Coumadin)
21
Q

PT is reported as …

A

international normalized ratio (INR)

  • corrects for variability in thromboplastin used
  • PT results around the world are standardized; critical for monitoring patients on Coumadin
21
Q

PT is reported as …

A

international normalized ratio (INR)

  • corrects for variability in thromboplastin used
  • PT results around the world are standardized; critical for monitoring patients on Coumadin
22
Q

aPTT

A
  • screens for factor deficiencies and inhibitors in the intrinsic and common pathways
    > prolong in defs of PK, HMWK, XII, XI, IX, VIII, V, prothrombin, fibrinogen
  • plasma incubated with reagent that contains activator and phospholipid
  • contact factors activated and XIa formed
  • addition of Ca 2+ allows progression to formation of fibrin clot
  • used to monitor heparin anticoag therapy - ref range varies with each lot # of reagent
23
Q

inhibitor screen

A
  • normal plasma added to patient plasma to see if there s a correction of a prolonged PT/PTT result
    > corrected = factor def (normal plasma provides missing factor)
    > no correction = inhibitor is present (inhibits factors in both plasmas)
  • additional test to: determine type and specificity of inhibitor + identify factor that is deficient
  • inhibitors can be against specific factors, or non-specific
24
Q

thrombin time

A
  • measures time needed for thrombin to convert fibrinogen to a fibrin clot
    > directly activates fibrinogen to bypass previous steps in coagulation pathways
  • uses dilute thrombin reagent
  • detects deficient/defective fibrinogen and thrombin inhibitors [heparin and fibrin degradation products (FDPs)]
  • also prolonged due to oral direct thrombin inhibitor therapy
24
Q

thrombin time

A
  • measures time needed for thrombin to convert fibrinogen to a fibrin clot
    > directly activates fibrinogen to bypass previous steps in coagulation pathways
  • uses dilute thrombin reagent
  • detects deficient/defective fibrinogen and thrombin inhibitors [heparin and fibrin degradation products (FDPs)]
  • also prolonged due to oral direct thrombin inhibitor therapy
24
Q

thrombin time

A
  • measures time needed for thrombin to convert fibrinogen to a fibrin clot
    > directly activates fibrinogen to bypass previous steps in coagulation pathways
  • uses dilute thrombin reagent
  • detects deficient/defective fibrinogen and thrombin inhibitors [heparin and fibrin degradation products (FDPs)]
  • also prolonged due to oral direct thrombin inhibitor therapy
25
Q

fibrinogen assay

A
  • measures clotting when exces thrombin is added
    > clotting time inverself proportional to amount of fibrinogen
  • modification of thrombin time procedure = excess thrombin neutralizes heparin and FDPs
  • results are read from a standard graph
    > prepared by testing known concentrations of fibrinogen
26
Q

single factor assays (ex: FVIII)

A
  • patient plasma is added to factor deficient plasma and tested using PT or PTTT
  • measure ability of patient plasma to correct factor def plasma
    > patient plasma provides deficient factor
    > results are compared to normal plasma
27
Q

T or F. Factor XIII deficiency is not detected by PT or PTTT

A

T!

  • endpt is before fibrin crosslinking
  • factor XIII stabilizes fibrin clot by converting hydrogen bonds into covalent bonds
  • measures time for a fibrin clot to disolve in 5M urea or 1% monochloroacetic acid
  • if XIII def, clot dissolves <1 hr in monochloroacetic acid or <24 hrs in 5M urea
  • factor XIII assay performed to confirm deficiency/identify functional abnormalities

MLSCI 230 (36 decks)

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