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Coagulation > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What diseases does arterial thrombosis include?

A

Acute myocardial infarction, CVA/strokes, heart attacks, PAD

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2
Q

What diseases does venous thromboembolic disease include?

A

DVT, pulmonary embolisms (PE)

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3
Q

Antithrombotic drugs

A

Prevent the formation of clots

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4
Q

Anticoagulants

A

suppress coagulation and reduce thrombin formation (affects secondary hemostasis)

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5
Q

Antiplatelet drugs

A

suppress platelet activation (affects primary hemostasis)

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6
Q

Fibrinolytic/thrombolytic drugs

A

Drugs used to break down clots that are already present (used to resolve DVT, PE, PAO, AMI, strokes)

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7
Q

What factors are affected by Coumadin?

A

Vitamin K dependent factors: II (prothrombin), VII, IX, X, Protein C/Z/S

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8
Q

In what order do the factors decrease after initiation of Coumadin therapy?

A

Factor VII decreases first (shortest half life)
IX
X
II (prothrombin has the longest half life)

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9
Q

What is Coumadin and how does it work?

A

Coumadin is an anticoagulant (blood thinner).
It is a vitamin K antagonist that slows the activity of the enzyme vitamin K epoxide reductase. The end goal is to reduce thrombin generation.

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10
Q

Can you take Coumadin while pregnant?

A

No. It causes birth defects.

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11
Q

What test is used to monitor Coumadin therapy? Why?

A

PT/INR. This is used because Prothrombin Time (PT) is sensitive to reductions of Factors II, VII, and X.

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12
Q

Coumadin PT/INR therapeutic range:

A

2-3

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13
Q

PT/INR range for patient with mechanical heart valve:

A

2.5-3.5

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14
Q

PT INR >5

A

Increased risk of hemorrhage - CRITICAL result!

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15
Q

What alternative test can be used to measure Coumadin therapy other than PT/INR?

A

chromogenic Factor X assay is used as an alternative when PT is compromised in Lupus, factor inhibitor, or coag factor deficiencies. It eliminates the necessity for normalization of test results using INR.

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16
Q

How do you reverse the effects of Coumadin?

A

Increase dietary Vitamin K in patient

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17
Q

Dietary Vitamin K ______ Coumadin’s effectiveness and ______ the INR.

A

decreases; reduces

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18
Q

What is UFH and how does it work?

A

UFH is unfractionated heparin, an anticoagulant.
It supports a pentasaccharide that binds plasma antithrombin with high affinity. It activates antithrombin to neutralize and inhibit serine proteases.

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19
Q

How do you reverse the affects of Heparin?

A

Protamine sulfate (protein extracted from salmon sperm)

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20
Q

What 3 tests are used to monitor UFH therapy? Why?

A

PTT - responds to all plasma-based heparin activities
chromogenic anti-Xa assay - fewer interferences, reflects only changes in antithrombin-Xa binding
ACT - used to monitor extremely high UFH doses that exceed other tests limits

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21
Q

Interferences to UFH therapy using PTT

A

Inflammation (PTT less sensitive to heparin’s effects), Prolonged UFH therapy (PTT below therapeutic range), release of PF4 can shorten PTT, and factor deficiencies can prolong PTT

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22
Q

Side effect of heparin use

A

HIT (heparin induced thrombocytopenia)

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23
Q

What factors are affected by UFH therapy?

A

All serine proteases -> Factor II, VII, IX, XI, XII, Pre-K

But especially factor IIa (thrombin) and Xa

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24
Q

What does UFH inactivate best? What does LMWH inactivate best?
T/F: They can activate both?

A

UFH inactivates thrombin best.
LMWH inactivates Factor Xa best.
True, UFH and LMWH can inactivate both.

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25
Q

What is LMWH? How does it work?

A

LMWH is low molecular weight heparin, produced from UFH. It has similar anticoagulant efficacy as UFH, but it primarily inactivates factor Xa with less thrombin-antithrombin binding. It has a shorter pentasaccharide sequence than UFH.

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26
Q

How do you measure LMWH therapy?

A

Through the Chromogenic Anti-Xa assay

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27
Q

Why can you use PTT to monitor UFH therapy, but not LMWH therapy?

A

LMWH neutralizes factor Xa more avidly than thrombin.

UFH neutralizes thrombin more avidly, so PTT can be used.

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28
Q

What factors are affected by LMWH?

A

Factor Xa the most.

Can also inactivate IIa (thrombin). Just not as avidly.

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29
Q

What is fondaparinux and how does it work?

A

It is a synthetic formulation of the active pentasaccharide sequence in UFH and LMWH. The only synthetic heparin.
It can ONLY inhibit factor Xa through antithrombin. It has no inhibitory effect on thrombin or other serine proteases.

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30
Q

What factors are affected by Fondaparinux?

A

Only factor Xa through antithrombin

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31
Q

What test is used to monitor Fondaparinux therapy? Why can you not use PTT?

A

Chromogenic anti-Xa heparin assay.

Cannot use PTT because Fondaparinux only inhibits factor Xa, not thrombin or serine proteases.

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32
Q

How to reverse fondaparinux effects?

A

rFVIIa (NovoSeven)

*protamine sulfate ineffective!

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33
Q

DOACs - what do they stand for? How do they work? How are they monitored? Give an example of one.

A

Direct oral anticoagulants - inhibit factor Xa whether it is free, clot-bound, or bound to coag factor IX. They DO NOT require antithrombin to express anticoagulant activity.
These are NOT monitored.
Example: Rivaroxaban (any drug ending with “xaban”)

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34
Q

DTIs: what does it stand for? how are they monitored? how do they work? give an example

A

Direct Thrombin Inhibitors - can be oral or intravenous. They bind and inactivate both free and clot-bound thrombin. DO NOT require antithrombin. Oral example: Dabigatran - not monitored
IV example: Argatroban - monitored through PTT/PT/TT/ACT (will prolong these)

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35
Q

How do antiplatelet drugs work? Give 3 examples of antiplatelet drugs.

A

They inhibit aggregation of platelets and reduce formation of platelet plug.
Ex. Aspirin, Clopidogrel, Prasugrel

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36
Q

VerifyNow Aspirin agonist

A

arachidonic acid

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37
Q

VerifyNow P2Y12 agonist

A

ADP

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38
Q

VerifyNow IIb/IIIa agonist

A

thrombin receptor-activating peptide

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39
Q

What is the reference method for antiplatelet drugs?

A

Aggregometry

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40
Q

PLT count for PPP (platelet poor plasma)

A

<10,000/uL

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41
Q

PLT count for PRP (platelet rich plasma)

A

~200,000/uL

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42
Q

Why do we adjust sodium citrate volume for elevated HCT?

A

There will be an increased anticoagulant-to-plasma ratio which can falsely prolong results for clot-based assays

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43
Q

What is the formula used to adjust anticoagulant volume with an elevated hematocrit?

A 
C = (0.00185)(100-HCT)V 
C = volume of sodium citrate needed 
V = volume of blood 
HCT = patient's hematocrit in %
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44
Q

How will a short draw affect clot-based results?

A

PTT and PT are falsely prolonged because there is too much anticoagulant

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45
Q

How will a lipemic/icteric specimen affect clot-based results?

A

Optical instruments may fail to measure clots in cloudy/high colored specimens

46
Q

How will a clot in a specimen affect clot-based results?

A

PT/PTT prolonged because everything is already clotted

47
Q

How will tourniquet application of >1 minute affect clot-based assays?

A

It will falsely shorten clot-based results

48
Q

How long do you have until you must test PT with no UFH?

49
Q

How long do you have to test PT or PTT with UFH present?

A

4 hours after centrifugation for 1 hour

50
Q

How long do you have until you must test PTT with no UFH?

51
Q

What are platelet function tests used for?

A

to detect qualitative (functional) platelet abnormalities

52
Q

What is the bleeding time test? Reference interval? Is it used today?

A

Small puncture wound made on arm; wound blotted every 30 seconds until bleeding stops –> duration of bleeding is recorded.
Reference interval is 2-9 minutes and it is not used today.

53
Q

What are the 5 stages of platelet aggregation response?

A
  1. Resting platelet (stable baseline)
  2. Shape change (raise in baseline)
  3. primary aggregation (declining)
  4. secretion (small plateau)
  5. secondary aggregation (further declining)
    * *KNOW FIGURE**
54
Q

How is aggregation measured in whole blood PLT aggregometry?

A

electrical impedance.

increased impedance = increased aggregation

55
Q

What method of PLT aggregometry is associated with the measurement of secretion of ATP from PLTs?

A

Lumiaggregometry

56
Q

What method of PLT aggregometry is associated with the measurement of electrical impedence?

A

Whole blood PLT aggregometry

57
Q

What method of PLT aggregometry is associated with the measurement of qualitative PLT defects?

A

All platelet aggregometry tests

58
Q

What method of PLT aggregometry is associated with the increase of light transmittance as PLT aggregates form?

A

platelet rich plasma aggregometry

59
Q

What is an agonist?

A

A substance which initiates a response when combined with its receptor

60
Q

What does PLT agonist Thrombin bind?

A

PAR-1 and PAR-2

61
Q

What does PLT agonist ADP bind?

A

P2Y1 and P2Y12

62
Q

What does PLT agonist epinephrine bind?

A

alpha adrenergic receptors

63
Q

What does PLT agonist collagen bind?

64
Q

What coagulation pathways/factors are monitored by the PT?

A

Extrinsic Pathway and Common Pathway (Factor VII, X, V, and II)

65
Q

What is the PT reagent and what is it made of?

A

Thromboplastin - made of tissue factor, phopholipids, and calcium chloride

66
Q

What anticoagulant drug is monitored by the PT?

67
Q

PT prolongation is most sensitive to which factor deficiency?

A

Factor VII

68
Q

What is the PT reference interval?

A

12.6 - 14.6 seconds (will make a clot in this time frame after thromboplastin is added)

69
Q

What is a prolonged PT result most likely due to?

A

Factor VII deficiency

could also be due to factor X or V deficiency

70
Q

How to determine if someone has liver disease or just a vitamin K deficiency through PT?

A

In liver disease, both factor V and factor VII levels will be decreased.
In Vitamin K deficiency, only factor VII is reduced.

71
Q

What factors is the PT not affected by? Why?

A

Factor VIII, IX, XI, XII, or XIII. These are the intrinsic pathway factors.

72
Q

What anticoagulant is monitored through the PTT?

73
Q

What reagent is used in PTT? What is it made of?

A

Partial thromboplastin - made of phospholipid and a negatively charged particulate activator such as silica

74
Q

What coagulation pathways/factors does the PTT measure?

A

Intrinsic pathway/common pathway (Factors 8/9/10/11/12/5/2)

75
Q

What factors will not affect the PTT?

A

VII and XIII

76
Q

What is the PTT reference interval? What is the PTT therapeutic range (someone on UFH)?

A

26-38 seconds reference

60-100 seconds UFH

77
Q

TCT reference interval

A

15-20 seconds

78
Q

What is the reagent used for TCT?

A

Commercially prepared bovine thrombin reagent

79
Q

What portion of the coagulation pathway does TCT measure?

A

Thrombin converting Fibrinogen –> Fibrin

80
Q

What will cause a prolonged TCT?

A

lack of fibrinogen, low fibrinogen, or dysfibrinogenemia (weird fibrinogen)

81
Q

LACs - what does it stand for and what are they?

A

Lupus anticoagulants - igG immunoglobulins that are directed against multiple phospholipid-protein complexes - i.e. they are nonspecific inhibitors

82
Q

Factor inhibitors

A

IgG immunoglobulins that are directed against specific coag factors

83
Q

What is the most common specific inhibitor? What disease patients are they found in?

A

Anti-Factor VIII - found in patients with severe hemophilia

84
Q

What is the purpose of performing a mixing study?

A

to distinguish LACs (nonspecific inhibitors) from specific inhibitors and factor deficiencies

85
Q

Order of testing in a mixing study

A

Prolonged PTT/PT –> TCT to detect if UFH is present –> PTT mixing study –> incubated mixing study (if needed) –> specific factor assay or LAC profile

86
Q

If a PTT mixing study corrects, what does that indicate? If it does not correct, what do you do?

A

If PTT mixing study corrects, it indicates a coag factor deficiency. If it does not correct, you move on to an incubated PTT mixing study

87
Q

If the TCT is normal, what does that indicate? If TCT is not normal, what does that indicate?

A

TCT is normal = no UFH interference

TCT abnormal = presence of UFH

88
Q

If the incubated mixing study corrects, what does that indicate? If it does not correct, what do you do?

A

If it corrects, it indicates a coag factor deficiency. If it does not correct, it indicates that an inhibitor may be present. If patient is bleeding, run factor activity assay. If patient is NOT bleeding, run a LAC profile.

89
Q

What is in a mixing study?

A

1:1 mixture of patient plasma and normal plasma

90
Q

Fibrinogen reference interval

A

220-498 mg/dL

91
Q

Hypofibrinogenemia and diseases associated with it

A

Decreased fibrinogen (<200 mg/dL), DIC and severe liver disease

92
Q

Hyperfibrinogenemia and diseases associated with it

A

Increased fibrinogen (>498 mg/dL), early liver disease/pregnancy/chronic inflammation

93
Q

Afibrinogenemia

A

lack of fibrinogen associated with anatomic hemorrhage

94
Q

Dysfibrinogenemia

A

abnormal fibrinogen species hydrolyzed by thrombin slower than normal

95
Q

What is the purpose of the Nijmegen-Bethesda Assay?

A

It quantifies the presence of anti-factor VIII inhibitors

96
Q

How does Factor XIII affect PT/PTT/TT results?

A

It does not affect them at all.

97
Q

What does a factor XIII deficiency lead to? When would you perform a factor XIII assay?

A

Perform Factor XIII assay when a patient presents with poor wound healing but a normal PTT, PT, FBG, and PLT count.
Factor XIII deficiency leads to oozing wounds

98
Q

List fibrinolysis assays and what increased levels indicate

A 
D-Dimer immunoassay (increased D-dimers = increased fibrinolysis)
Fibrin degradation product immunoassay (increased FDPs = increased fibrinolysis) 
Plasminogen assay (Increased plasminogen = increased fibrinolysis)
TPA assay (Increased TPA = decreased thrombosis)
PAI-1 assay (increased PAI-1 = increased thrombosis)
99
Q

Mechanical Clot End-Point Detection

A

uses two metal electrodes or steel ball to detect clots

100
Q

Photo-Optical Clot End-Point Detection

A

Detects change in optical density during clotting

*Most sensitive to lipemic and icteric specimens

101
Q

Viscoelastic Clot Detection

A

used in Global Hemostasis Assessment for whole blood clotting

102
Q

Chromogenic end-point detection

A

Uses a chromophore to measure activity of specific coag factors (increased factor concentration = more color released)

103
Q

Nephelometric end-point detection

A

Uses forward angle light scatter to measure clot formation

104
Q

Immunologic Light absorbance end point detection

A

Based on antigen-antibody reactions, but uses light absorbance end point

105
Q

Advantages of chromogenic tests

A

more specific than clot based assays, ability to measure proteins that do not clot

106
Q

Disadvantages of photo optical tests

Advantages of photo optical tests

A

disadv: icteric and lipemic specimens prolong the clotting time
adv: ability to observe graph of clot formation

107
Q

Disadvantage of clot based tests

A

not as specific as other types of tests

108
Q

instrument features to consider when selecting a coagulation instrument

A
  • reduced reagent/specimen volumes
  • reagent tracking
  • primary tube sampling
  • flagging
  • kinetics of clot formation
  • random access testing
109
Q

What are some POC coagulation tests and why would they be used?

A

ACT - used for heparin monitoring during cardiac surgery

PT/INR - monitoring coumadin for hospitalized patient/self testing for outpatient

110
Q

TEG: what specimen is used? what is being measured?

A

Whole blood is used for TEG.
Measures evalution of entire kinetic process of clotting formation (PLTs, WBC, RBC, coag factors, plasma proteins)
*provides real time information

111
Q

ROTEM: what specimen is used? what is being measured? disadvantage?

A

Whole blood specimen is used.
Also measures the entire clotting process, same as TEG.
Disadvantage is that it requires special skills, knowledge, and experience.

Coagulation (5 decks)

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