Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Boards.CP.Coagulation > Hemostasis Lab Testing > Flashcards

Hemostasis Lab Testing Flashcards

1
Q

What test measures the time required for anticoagulated whole blood to occlude a standard aperature (closure time)?

A

PFA-100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The aperture in PFA-100 is covered by 2 types of thin membranes, what are they and what are they used for?

A

Collagen and Epinephrine (Col/Epi)
-Sensitive to global platelet defects

Collagen and ADP (Col/ADP)
-Sensitive to Drug induced platelet defects (Aspirin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Besides platelet dysfunction, what might cause a prolonged Closure Time (PFA-100)?

A
  • Anemia (Hct <25%)

- Thrombocytopenia (<100)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What specimen type is used for Platelet Aggregometry and how is it prepared?

A

Platelet rich plasma

-slow centrifugation of whole blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What Agonists are used in Platelet Aggregometry? (5)

A
  • ADP
  • Epinephrine
  • Arachidonate
  • Collagen
  • Ristocetin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Platelet Aggregometry - Curve:

  • Biphasic
  • What causes the secondary wave?
A
  • ADP (Low Dose)
  • Epinephrine

-Platelet degranulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Platelet Aggregometry - Curve:

-Monophasic (primary aggregation only)

A
  • ADP (High Dose)
  • Collagen
  • Ristocetin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the most common cause of an Abnormal Agrregometry? What Agonists is used?

A

Medication

-Decreased aggregation with Arachidonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Abnormal Aggregometry in Glanzmann Thrombasthenia.

A

-Poor response to ALL agents EXCEPT Ristocetin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What causes an Absent Secondary phase with Epinephrine and ADP (Low)?

A
  • Storage pool defects

- Aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What Abnormality can you see in myeloproliferative neoplasms?

A

-Poor response to Epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What Abnormal Aggregometry pattern is the Hallmark dor von WIlledbrand Disease? what other syndrome has this pattern?

A

Response to everything EXCEPT Ristocetin

-Bernard-Soulier syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Activated Clotting Time (ACT):

  • Use
  • Setting
  • Specimen type
A
  • Point of care test to monitor high dose Heparin therapy
  • Cardiopulmonary bypass surgery
  • Whole blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Activated Partial Thromboplastin Time (aPTT):

-What is added to citrated plasma

A
  • Phospholipid
  • Contact activator of F12 (silica, kaolin, etc)
  • Excess calcium

*Time to clot is formation is the aPTT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Prolongation of the aPTT is caused by?

A
  • Factor deficiency

- Inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which pathways/factors are tested in aPTT?

A

Intrinsic Pathway
-12,11,9,8

Common Pathway
-5,10,2,1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Prolongation of both PT and aPTT is caused by what factor deficiencies?

A

Common Pathway

-1,2,5,10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

A factor generally must be what percentage to cause prolonged aPTT?

A

30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Elevation of what factor may shorten the aPTT?

A

F8 (VIII)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What factor is involved with an INcreased PT and a Normal aPTT? (clinical considerations;4)

A

Factor 7 (FVII)

  • Liver disease
  • Vit. K deficiency
  • Warfarin
  • Inherited factor deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

If mixing study fails to correct the aPTT, what should be suspected?

A

-Inhibitor

22
Q

If mixing study corrects the aPTT, what should be suspected?

A

-Factor deficiency

23
Q

What inhibitor shows immediate correction but prolongation of the incubated aPTT over time?

A

Anti-Factor8 (VIII) antibody.

24
Q

aPTT is used to monitor what?

A

Heparin therapy (unfractionated heparin)

25
Q

In circumstances where the aPTT is unreliable, what assay should be used to monitor Heparin therapy?

A

Factor Xa assay

26
Q

The anticoagulant (3.2% trisodium citrate) in collection tubes, ~0.5 mL, is intended to result in a whole blood to anticoagulant of ___, and a ratio of plasma to anticoagulant of ___, assuming a normal hematocrit (35-55%).

A
  • 9:1 (whole blood:anticoagulant)

- 5:1 (plasma: anticoagulant)

27
Q

How does a high hematocrit (>55%) affect the aPTT?

A
  • Less plasma
  • sample over coagulated
  • Clotting time prolonged
28
Q

What assay can be used to monitor either unfractionated or low molecular weight heparin?

A

Anti-Xa assay (Heparin antifactor Xa assay)

29
Q

How is the Anti-Xa assay set up?

A

Patient plasma is added to known amount of factor Xa with excess antithrombin

30
Q

What is the MOA of the Anti-Xa assay?

A
  • Heparin from patient plasma stimulates antithrombin to inhibit factor Xa
  • Quantity of the residual factor Xa is measured with a chromogenic substrate
  • Residual Xa is subtracted from the initial Xa to determine the anticoagulant concentration
31
Q

T/F: The anti-Xa assay is not affected by underfilled collection tubes and is unaffected by abnormal factor levels.

A

True

32
Q

What assay is performed to determine the titer of anti-fVIII antibody?

A

Bethesda assay (factor VIII inhibitor assay, anti-fVIII antibody assay)

33
Q

What factor generates D-dimer?

-Mechanism>

A

Factor XIII

-Covalently linking the D regions of fibrin molecules

34
Q

What dissolves fibrin clots?

A

Plasmin

*Incapable of breaking up D-dimers

35
Q

What does the presence of D-dimers indicate?

A

Fibrin has been formed and then degraded

36
Q

When are D-dimers and fibrin degradation products (FDPs) increased? (5)

A
  • Thrombosis
  • Significant bleeding
  • A. fib
  • CHF
  • Cirrhosis
37
Q

What factor assays are PTT based? (4)

A

8, 9, 11, 12

  • FVIII
  • FIX
  • FXI
  • FXII
38
Q

What factor assays are PT based? (3)

A

2, 7, 10

  • FII
  • FVII
  • FX
39
Q

What factor assay can be either PT or PTT based?

A

5 (FV)

40
Q

Choice of factor assay depends upon screening test findings:

-Prolonged aPTT, Normal PT (4)

A

8, 9, 11, 12

  • FVIII
  • FIX
  • FXI
  • FXII
41
Q

Choice of factor assay depends upon screening test findings:
-Normal aPTT, Prolonged PT (1)

*what should also be considered?

A

7 (FVII)

*1,2,5,10 (common pathway), because PTT is insensitive to mild to moderate common factor deficiencies. Thus can sometimes produce a prolonged PT with normal PTT

42
Q

Choice of factor assay depends upon screening test findings:

-Prolonged aPTT, Prolonged PT

A

1,2,5,10 (common pathway)

43
Q

T/F: The lower the fibrinogen, the longer the clotting time.

A

True

44
Q

How is the Prothrombin Time (PT) set up?

A

A source of Tissue Factor and phospholipid (thromboplastin) is added to Citrated plasma with excess Calcium
-The time to clot formation is the PT

45
Q

What causes prolongation of the PT?

A
  • Factor 7 deficiencies
  • Factors 2,5,10 or Fibrinogen (common factor deficiencies)
  • Inhibitors
46
Q

PT or aPTT, which is more sensitive to common pathway deficiencies (F2,5,10)?

A

PT

47
Q

The PT forms the basis of INR, which is used to monitor what?

A

Warfarin (coumadin) therapy

48
Q

What is the Chromogenic Factor X assay useful for?

*different than Anti-Xa assays)

A

Monitoring warfarin in the presence of:

  • Lupus anticoagulant
  • Hirudin
  • Argatroban
49
Q

For the Thrombin Time (TT), thrombin is added to patient plasma and the time to clot formation is the TT. What causes a prolongation of the TT?

A
  • Fibrinogen deficiencies
  • Defective fibrinogen (dysfibrinogenemia)
  • Inhibitors (Heparin, Hirudin, Argatroban, or FDPs)
50
Q

If the TT is prolonged, the presence of Heparin can be confirmed by what? (2)

A
  • Reptilase time is normal in presence of Heparin

- 1:1 mix will fail to correct in presence of Heparin

Boards.CP.Coagulation (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions