LAB - Hemostasis Flashcards

1
Q

Prothrombin time

A

measures the time to form a clot when calcium and tissue thromboplastin (FIII or TF) are added to citrated plasma

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2
Q

what does Warfarin do t the vitamin K-dependent clottingfactors?

A
  • II, VII, IX, X
  • prevents y-carboxylation of terminal AAs which is required for binding to calcium and interaction with platelet phospholipid
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3
Q

rate of clotting in PT dependent on

A

the nature of tissue thromboplastin used (human brain more sensitive to levels of coag than is rabbit brain thromboplastin)

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4
Q

purpose of the international sensitivity index

A

allows each lab to express results as they would be had the international primary std thromboplastin of ISI = 1.0 been used

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5
Q

reagents used in PT

A
  • tissue thromboplastin = reconstitute; 15 mins
  • control: commercial lyophilized citrated plasma; reconstitute; 15 minutes
  • test plasma: from 3.2% sodium citrate; centrifuge at 2500 g for 10 mins; if not in use within 24 hrs, remove to plastic tubes and store at -20C for no longer than 2 weeks
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6
Q

KC1 analyzer

A
  • metal ball in testing cup attracted to a magnet within the instrument
  • cup rotates = ball remains attracted to magnet = stays in place if no clot
  • as thromboplastin is added to plasma = clot = contents of cup becomes more viscous = ball no longer attracted to magnet
  • timer stops
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7
Q

STart-4

A
  • metal ball in the cuvette oscillates between two magnets

- clot forms = viscosity increases = ball stops moving

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8
Q

causes of prolonged prothrombin times

A
  • factor def = II, V, VII, X, or fibrinogen
  • coag factor inhibitors
  • oral anticoag therapyu
  • vit k deficiency
  • DIC
  • liver damage
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9
Q

causes of shortened PT

A
  • multiple myeloma
  • myocardia infarction
  • drug therapy
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10
Q

PTT reagent contains a activator such as

A

MICRONIZED SILICA

- ALSO CONTAINS PHOSPHOLIPID (PF3)

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11
Q

aPTT = contact factors of intrinsic clotting cascade activated by the silica to the level of…

A

XIa

- subsequent addition of calcium chloride allow progression to a fibrin clot

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12
Q

causes of prolonged PTT times

A
  • deficiency of factors HMWK, PK, XII, XI, IX, VIII, X, V, prothrombin, fibrinogen

may be related to:

  • inherited factor def
  • anticoag therapy w/ heparin or warfarin
  • secondary fibrinolysis (DIC consuming factors)
  • liver disease = impaired synthesis
  • vitamin K deficiency

Or

  • pathological inhibitors (including lupus anticoagulant)
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13
Q

some reasons why PTT reference range could change

A
  • different Lot #’s = preparations of reagents vary
  • automated vs manual methods
  • test population = depends
  • means of detecting endpoint
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14
Q

In a mixing stud, correction of the clotting time cannot rule out a what…

A

delayed- reacting inhibitor

- results will provide direction on the next steps of testing to determine cause of prolonged PT or PTT

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15
Q

fibrinogen assay

A

dilutions of fibrinogen standard of known concentration and patient plasma are clotted ith n EXCESS amount of thrombin

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16
Q

reagents in a fibrinogen assay

A
  • standard
  • thrombin
  • control plasma
  • *reconstitute according to instructions**
  • test plasma
  • Owren’s Veronal buffer (pH 7.35)
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17
Q

T or F. Samples with high fibrinogen concentrations will have short clotting times

A

T

  • further dilute such plasmas (120 total), repeat test and multiply graph reading by 2
  • very low fibrinogen concentrations require less dilution
18
Q

how can thrombin be prevented from acting on fibrinogen

A

by heparin
- in anticoag patients
OR
by early fibrinogen and fibrin split products (patents with fibrinolysis); fibrinogen assay avoids these potential interferences through the use of excess thrombin

19
Q

testing for FVIII deficiency is based on …

A

the PTT method

20
Q

how does a FVIII specific assay work?

A
  • ability of dilutions of patient plasma to correct the prolonged PTT of factor VIII deficient (substrate) plasma is measured
  • clotting time compared to those obtained when dilutions of normal plasma of known factor conctn (Std plasma) are similarly added to FVIII deficient plasma
21
Q

decrased FVIII

A
  • hemophilia
  • vWD
  • DIC
  • liver disease
22
Q

increased FVIII

A
  • inflammation with increased acute phase reactant

- immediately following surgery

23
Q

primary fibrinolysis

A
  • high levels of plasmin
  • unopposed by antiplasmins
  • circulating fibrinogen cleaved by plasmin = FDPs
24
Q

secondary fibrinolysis

A
  • inappropriate activity of the fibrinolytic system
  • increased activity due to the formation of intravascular clots
  • fibrin clots will be the target of plasmin = FDPs and D-dimer fragments
24
Q

secondary fibrinolysis

A
  • inappropriate activity of the fibrinolytic system
  • increased activity due to the formation of intravascular clots
  • fibrin clots will be the target of plasmin = FDPs and D-dimer fragments
25
Q

this test is helpful in distinguishing between primary and secondary fibrinolysis

A

D-dimer test

26
Q

thrombolytic therapy required by patients with…

A

potentially life-threatening clots such as DVT, PE, and blocked coronary arteries

27
Q

difference between anticoagulant therapy and thrombolytic therapy

A
  • anticoags = prevent inappropriate clotting
  • thrombolytic therapy = dissolve existing clots
    > streptokinase, urokinase, rTPA
    > promote generation of plasmin for clot lysis = thrombin time to monitor
28
Q

why is thrombin time useful for monitoring thrombolytic therapy

A
  • reflects fibrinogen levels
    > risk of therapy is that plasmin generated will indiscriminately lyse both fibrin and fibrinogen; hemorrhage if fibrin is depleted
  • thrombin time responds to presence of FDPs, which are indicators that thrombolysis is taking place
29
Q

compared to thrombin time, this is a more specific indicator of clot lysis

A

D-Dimer test

- recognizes fragments form cross-linked fibrin degradation

30
Q

D-Dimer Test

A

latex particles coated with monoclonal antibody to D-Dimer (mouse anti-human D-dimer) will specifically detect D-dimers in test plasma

31
Q

test sample for D-Dimer test

A

fresh, citrated, EDTA or heparinized plasma

32
Q

Notes for D-Dimer Test

A
  • do not allow mixtures to dry
  • read at exactly three minutes
  • serum can be used but plasma is preferred as D-Dimers may get trapped within the clot
  • false positive can occur in presence of rheumatoid factor
33
Q

increased levels of D-Dimers are seen in:

A
  • DVT
  • PE
  • DIC
  • hemorrhage
  • surgical patients
  • cancers and cirrhosis
34
Q

what is thrombin time?

A

measures the time taken to form a fibrin clot when thrombin acts on fibrinogen in a plasma sample

  • fibrin formation is triggered when thrombin is added to the patient plasma (bypasses prior steps in cascade)
  • thrombin time affected by low fibrinogen (hypo-), dysfunctional fibrinogen (dys-), and the presence of circulating anticoags (heparin and FDPs)
35
Q

a prolonged TT may be due to

A
  • decreased levels of fibrinogen (acquired or inherited)
  • abnormally functioning fibrinogen
  • thrombin inhibitors (FDPs, heparin)
36
Q

FXIII

A

converts hydrogen bonds b/w fibrin monomers to covalent bonds

37
Q

FXIII screening test

A
  • if absent, clots are soluble in 1% monochloroacetic acid = should take more than 1 hr for clot to dissolve OR 5M urea (more than 24 hrs)
38
Q

abnormal clot solubility (disappearance of clots) seen in

A
  • inherited lack of FXIII (or abnormal)
  • DIC
  • liver disease
39
Q

what are potential complications for DVT?

A
  • amputation
  • chronic illness => post-thrombotic sybdrome
  • could dislodge and travel to lungs = PE (fatal if large and blocks blood flow to lungs)
40
Q

in those at risk for DVT, how can it be prevented?

A
  • compression socks
  • healthy diet
  • no smoking
  • anticoags therapy
  • adequate hydration for fluid blood
  • exercise
41
Q

two substances responsible for a prolonged thrombin time, but do not affect fibrinogen

A
  • heparin
  • FDP
  • *thrombin in excess in fibrinogen assay**