Coagulation Flashcards

(47 cards)

1
Q

What are the requirements for specimen collection for routine coagulation studies?

A

Anticoagulant: Light blue top tube with 3.2% buffered sodium citrate.

Purpose: Binds calcium to inhibit coagulation while preserving coagulation factors.

Fill requirement: Must be filled to the proper line to maintain a 9:1 ratio of blood to anticoagulant.

Order of draw: Collected after blood culture tubes and before any other tubes.

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

Why is the order of draw important when collecting coagulation specimens and CBCs?

A

Coagulation tests (light blue top) must be drawn before CBC (lavender top EDTA tube).

EDTA in the CBC tube can interfere with coagulation test results if drawn first.

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

How is a coagulation specimen processed in the lab, and what are PPP and PRP?

A

Processing: Spun at 3000 rpm for 15 minutes to separate plasma.

PPP (Platelet-Poor Plasma): Used for coagulation testing to avoid interference from platelets (which act as a phospholipid source).

PRP (Platelet-Rich Plasma): Contains higher platelet concentration, not suitable for coagulation tests.

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

For how long can a PT specimen be left in the lab without spinning? What about PTT? Why?

A

PT can be left up to 24 hours, and PTT can be left up to 4 hours. This is because the coagulation factors tested in PT are more stable than those in PTT.

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

How does a short draw affect PT and APTT results?

A

It falsely prolongs both PT and APTT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How long is a PT specimen valid after collection, and at what temperatures?

A

Room temperature (15-25°C): Up to 24 hours

Refrigerated (2-8°C): Up to 24 hours

Frozen (-20°C): Up to 2 weeks

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

How long is a PTT specimen valid after collection, and at what temperature?

A

It is stable at room temperature (15-25°C) for up to 4 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why does PT have longer stability compared to PTT?

A

The coagulation factors tested in PT are more stable than those tested in PTT.

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

What is INR, and how is it calculated?

A

INR (International Normalized Ratio) is the standardized method of reporting PT (Prothrombin Time) to account for variations between labs. It is calculated using the formula:
(Patient PT / Mean Normal PT)^ISI, where ISI (International Sensitivity Index) is provided by the reagent supplier.

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

What information is needed to calculate INR, and where do you find it?

A

You need:

Patient PT (from the test result).

Mean Normal PT (determined by the lab).

ISI (provided by the reagent supplier for each lot).

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

When do you need to re-calculate INR for the analyzer?

A

Recalculate when:

A new lot of Thromboplastin reagent is used.

The mean normal PT value changes.

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

Which clinical conditions cause both PT and PTT to be prolonged?

A

DIC (Disseminated Intravascular Coagulation) and Liver Disease.

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

Which conditions cause only PT to be prolonged?

A

Factor VII deficiency or Factor VII inhibitors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which conditions cause only PTT to be prolonged?

A

Hemophilia A/B/C, acquired FVIII inhibitor, VWD (Von Willebrand Disease), and Antiphospholipid syndrome.

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

Does FXIII deficiency prolong the PTT? Why or why not?

A

No, because FXIII is not part of the intrinsic pathway measured by the PTT.

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

Can VWD prolong the PTT? Explain.

A

Yes, if FVIII is significantly low, since VWF stabilizes FVIII. Low FVIII affects the intrinsic pathway (measured by PTT).

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

For patients on anticoagulant therapy, what is the risk when results are not within the therapeutic range? What is special about FXII?

A

The risk is bleeding uncontrollably. FXII is unique because its deficiency does not cause bleeding, as it can be bypassed as a contact factor by direct activation of FXI by thrombin.

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

What are mixing studies, and how are they interpreted? What follow-up actions are taken based on the results?

A

Principle: Mixing studies are performed when PT/PTT results are unexpectedly prolonged without a clear history. They differentiate between factor deficiencies and inhibitors.

Interpretation & Follow-Up:

If results remain prolonged after mixing: Suggests an inhibitor → follow up with an inhibitor assay (e.g., DRVVT).

If results normalize after mixing: Suggests a factor deficiency or factor antibody. Incubate for 1-2 hours at 37°C:

If results stay normal: Factor deficiency → perform factor assays.

If results become prolonged: Factor antibody → perform factor antibody assays.

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

What is the concentration of factor required for normal activity?

20
Q

What determines the severity of hemophilia?

A

The severity of the genetic mutation causing the factor deficiency and the level of activity of the deficient clotting factor.

21
Q

How are patients on unfractionated heparin therapy monitored, and why?

A

They are monitored using aPTT and platelet count. aPTT ensures the patient is in the therapeutic range (avoiding overdose/bleeding risks), and platelet count checks for Heparin-Induced Thrombocytopenia (HIT).

22
Q

How are patients on LMWH therapy monitored, and why is monitoring often unnecessary?

A

LMWH is typically not monitored due to its safety and predictable dosing. If needed, a FXa assay can be used.

23
Q

How is a patient on Coumadin monitored? Why?

A

They are monitored using the PT results because FVII is affected the earliest (it has the shortest half-life) and therefore gives the fastest information on the effectiveness of the drug dosage.

24
Q

What does aspirin do?

A

It stops platelets from aggregating at the point of plaque formation and causing arterial thrombosis by irreversibly acetylating a platelet enzyme needed to produce thromboxane A2 (which is a platelet agonist).

25
What type of disorder is vWD? What are the findings?
It is an autosomal dominant or recessive disorder caused by dozens of germline mutations of VWF. The findings depend on the type of VWD: Quantitative VWF abnormality: reduced plasma concentration of VWF and FVIII. Qualitative VWF abnormality: reduced functionality of VWF, affecting platelet adhesion and aggregation.
26
What assay can be used to confirm suspected vWD diagnosis?
A VWF:RCo : VWF:Ag assay. VWF:RCo assesses VWF activity (platelets aggregate only if VWF is active). VWF:Ag assesses the quantity of VWF.
27
What is the difference between BSS and Glanzmann Thrombasthenia?
BSS (Bernard-Soulier Syndrome): Disorder of platelet adhesion due to missing or dysfunctional GP Ib/IX/V receptor (binds to VWF). Glanzmann Thrombasthenia: Disorder of platelet aggregation due to defective/low levels of GP IIb/IIIa receptor (binds fibrinogen & VWF).
28
Why might a patient be prescribed an anticoagulant? Provide examples.
Purpose: To suppress coagulation and reduce thrombin formation. Examples of conditions: Ischemic Heart Disease, Deep Vein Thrombosis (DVT), Pulmonary Embolism (PE).
29
What happens if there is a factor deficiency in the coagulation process?
The coagulation process is impaired (mildly or severely). Risk: Uncontrollable bleeding, especially during trauma or medical procedures.
30
Which factor is deficient in Hemophilia A?
Factor 8
31
Which factor is deficient in Hemophilia B?
Factor 9
32
Which factor is deficient in Hemophilia C?
Factor 11
33
What are the two types of Immune Thrombocytopenic Purpura (ITP)?
Acute ITP: Primarily seen in children, following viral infections or vaccinations. Chronic ITP: Mostly seen in adults, with an insidious cause.
34
What can cause drug-induced ITP?
Following the use of drugs like penicillin, acetaminophen, carbamazepine, and/or heparin.
35
How are platelets destroyed in ITP?
Antibody-coated platelets are removed from circulation and destroyed by reticuloendothelial cell macrophages (primarily in the spleen).
36
What is the mechanism of ITP at the molecular level?
Autoantibodies are made against platelet surface proteins (GPIIb, GPIIIa, and/or GPIa/IIa). These antibodies coat platelets, forming immune complexes on their surface. Increased splenic destruction by macrophages occurs.
37
Where does the destruction of antibody-coated platelets primarily occur in ITP?
In the spleen, where macrophages with Fc receptors phagocytose the platelets.
38
What diseases are associated with Secondary Thrombocytopenia?
CLL (Chronic Lymphocytic Leukemia), SLE (Systemic Lupus Erythematosus), and Malaria.
39
What causes Post-Transfusion Purpura?
Transfusion with products containing incompatible platelets, leading to anti-platelet antibodies that cross-react with both transfused and the patient’s own platelets, causing thrombocytopenia.
40
What is Heparin-Induced Thrombocytopenia (HIT)?
An adverse effect of heparin treatment where IgG antibodies form against heparin–platelet factor 4 complexes, leading to platelet activation, thrombocytopenia, and microvascular thrombi.
41
How long does a patient typically need to be on UFH (Unfractionated Heparin) to develop HIT?
More than 5 days.
42
What is the incidence rate of HIT?
0.5% to 5% of patients receiving heparin.
43
What is Thrombotic Thrombocytopenic Purpura (TTP) characterized by?
MAHA (Microangiopathic Hemolytic Anemia) Thrombocytopenia Neurologic abnormalities
44
Why do UL-VWF multimers accumulate in TTP?
Due to deficiencies or dysfunction of ADAMTS13.
45
How do UL-VWF multimers contribute to thrombosis in TTP?
They are more efficient at binding platelets (PLTs) and do so spontaneously under high shear stress. This forms platelet aggregates or thrombi in small blood vessels.
46
Why does TTP result in thrombocytopenia?
Increased thrombi formation consumes platelets, leading to low platelet counts.
47
What is the role of ADAMTS13 in normal physiology?
ADAMTS13 cleaves UL-VWF multimers to prevent excessive platelet aggregation.