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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
What is LMWH? How does it work?
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.
26
How do you measure LMWH therapy?
Through the Chromogenic Anti-Xa assay
27
Why can you use PTT to monitor UFH therapy, but not LMWH therapy?
LMWH neutralizes factor Xa more avidly than thrombin. | UFH neutralizes thrombin more avidly, so PTT can be used.
28
What factors are affected by LMWH?
Factor Xa the most. | Can also inactivate IIa (thrombin). Just not as avidly.
29
What is fondaparinux and how does it work?
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.
30
What factors are affected by Fondaparinux?
Only factor Xa through antithrombin
31
What test is used to monitor Fondaparinux therapy? Why can you not use PTT?
Chromogenic anti-Xa heparin assay. | Cannot use PTT because Fondaparinux only inhibits factor Xa, not thrombin or serine proteases.
32
How to reverse fondaparinux effects?
rFVIIa (NovoSeven) | *protamine sulfate ineffective!
33
DOACs - what do they stand for? How do they work? How are they monitored? Give an example of one.
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")
34
DTIs: what does it stand for? how are they monitored? how do they work? give an example
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)
35
How do antiplatelet drugs work? Give 3 examples of antiplatelet drugs.
They inhibit aggregation of platelets and reduce formation of platelet plug. Ex. Aspirin, Clopidogrel, Prasugrel
36
VerifyNow Aspirin agonist
arachidonic acid
37
VerifyNow P2Y12 agonist
ADP
38
VerifyNow IIb/IIIa agonist
thrombin receptor-activating peptide
39
What is the reference method for antiplatelet drugs?
Aggregometry
40
PLT count for PPP (platelet poor plasma)
<10,000/uL
41
PLT count for PRP (platelet rich plasma)
~200,000/uL
42
Why do we adjust sodium citrate volume for elevated HCT?
There will be an increased anticoagulant-to-plasma ratio which can falsely prolong results for clot-based assays
43
What is the formula used to adjust anticoagulant volume with an elevated hematocrit?
``` C = (0.00185)(100-HCT)V C = volume of sodium citrate needed V = volume of blood HCT = patient's hematocrit in % ```
44
How will a short draw affect clot-based results?
PTT and PT are falsely prolonged because there is too much anticoagulant
45
How will a lipemic/icteric specimen affect clot-based results?
Optical instruments may fail to measure clots in cloudy/high colored specimens
46
How will a clot in a specimen affect clot-based results?
PT/PTT prolonged because everything is already clotted
47
How will tourniquet application of >1 minute affect clot-based assays?
It will falsely shorten clot-based results
48
How long do you have until you must test PT with no UFH?
24 hours
49
How long do you have to test PT or PTT with UFH present?
4 hours after centrifugation for 1 hour
50
How long do you have until you must test PTT with no UFH?
4 hours
51
What are platelet function tests used for?
to detect qualitative (functional) platelet abnormalities
52
What is the bleeding time test? Reference interval? Is it used today?
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
What are the 5 stages of platelet aggregation response?
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
How is aggregation measured in whole blood PLT aggregometry?
electrical impedance. | increased impedance = increased aggregation
55
What method of PLT aggregometry is associated with the measurement of secretion of ATP from PLTs?
Lumiaggregometry
56
What method of PLT aggregometry is associated with the measurement of electrical impedence?
Whole blood PLT aggregometry
57
What method of PLT aggregometry is associated with the measurement of qualitative PLT defects?
All platelet aggregometry tests
58
What method of PLT aggregometry is associated with the increase of light transmittance as PLT aggregates form?
platelet rich plasma aggregometry
59
What is an agonist?
A substance which initiates a response when combined with its receptor
60
What does PLT agonist Thrombin bind?
PAR-1 and PAR-2
61
What does PLT agonist ADP bind?
P2Y1 and P2Y12
62
What does PLT agonist epinephrine bind?
alpha adrenergic receptors
63
What does PLT agonist collagen bind?
GPIa/IIa
64
What coagulation pathways/factors are monitored by the PT?
Extrinsic Pathway and Common Pathway (Factor VII, X, V, and II)
65
What is the PT reagent and what is it made of?
Thromboplastin - made of tissue factor, phopholipids, and calcium chloride
66
What anticoagulant drug is monitored by the PT?
Coumadin
67
PT prolongation is most sensitive to which factor deficiency?
Factor VII
68
What is the PT reference interval?
12.6 - 14.6 seconds (will make a clot in this time frame after thromboplastin is added)
69
What is a prolonged PT result most likely due to?
Factor VII deficiency | could also be due to factor X or V deficiency
70
How to determine if someone has liver disease or just a vitamin K deficiency through PT?
In liver disease, both factor V and factor VII levels will be decreased. In Vitamin K deficiency, only factor VII is reduced.
71
What factors is the PT not affected by? Why?
Factor VIII, IX, XI, XII, or XIII. These are the intrinsic pathway factors.
72
What anticoagulant is monitored through the PTT?
UFH
73
What reagent is used in PTT? What is it made of?
Partial thromboplastin - made of phospholipid and a negatively charged particulate activator such as silica
74
What coagulation pathways/factors does the PTT measure?
Intrinsic pathway/common pathway (Factors 8/9/10/11/12/5/2)
75
What factors will not affect the PTT?
VII and XIII
76
What is the PTT reference interval? What is the PTT therapeutic range (someone on UFH)?
26-38 seconds reference | 60-100 seconds UFH
77
TCT reference interval
15-20 seconds
78
What is the reagent used for TCT?
Commercially prepared bovine thrombin reagent
79
What portion of the coagulation pathway does TCT measure?
Thrombin converting Fibrinogen --> Fibrin
80
What will cause a prolonged TCT?
lack of fibrinogen, low fibrinogen, or dysfibrinogenemia (weird fibrinogen)
81
LACs - what does it stand for and what are they?
Lupus anticoagulants - igG immunoglobulins that are directed against multiple phospholipid-protein complexes - i.e. they are nonspecific inhibitors
82
Factor inhibitors
IgG immunoglobulins that are directed against specific coag factors
83
What is the most common specific inhibitor? What disease patients are they found in?
Anti-Factor VIII - found in patients with severe hemophilia
84
What is the purpose of performing a mixing study?
to distinguish LACs (nonspecific inhibitors) from specific inhibitors and factor deficiencies
85
Order of testing in a mixing study
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
If a PTT mixing study corrects, what does that indicate? If it does not correct, what do you do?
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
If the TCT is normal, what does that indicate? If TCT is not normal, what does that indicate?
TCT is normal = no UFH interference | TCT abnormal = presence of UFH
88
If the incubated mixing study corrects, what does that indicate? If it does not correct, what do you do?
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
What is in a mixing study?
1:1 mixture of patient plasma and normal plasma
90
Fibrinogen reference interval
220-498 mg/dL
91
Hypofibrinogenemia and diseases associated with it
Decreased fibrinogen (<200 mg/dL), DIC and severe liver disease
92
Hyperfibrinogenemia and diseases associated with it
Increased fibrinogen (>498 mg/dL), early liver disease/pregnancy/chronic inflammation
93
Afibrinogenemia
lack of fibrinogen associated with anatomic hemorrhage
94
Dysfibrinogenemia
abnormal fibrinogen species hydrolyzed by thrombin slower than normal
95
What is the purpose of the Nijmegen-Bethesda Assay?
It quantifies the presence of anti-factor VIII inhibitors
96
How does Factor XIII affect PT/PTT/TT results?
It does not affect them at all.
97
What does a factor XIII deficiency lead to? When would you perform a factor XIII assay?
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
List fibrinolysis assays and what increased levels indicate
``` 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
Mechanical Clot End-Point Detection
uses two metal electrodes or steel ball to detect clots
100
Photo-Optical Clot End-Point Detection
Detects change in optical density during clotting | *Most sensitive to lipemic and icteric specimens
101
Viscoelastic Clot Detection
used in Global Hemostasis Assessment for whole blood clotting
102
Chromogenic end-point detection
Uses a chromophore to measure activity of specific coag factors (increased factor concentration = more color released)
103
Nephelometric end-point detection
Uses forward angle light scatter to measure clot formation
104
Immunologic Light absorbance end point detection
Based on antigen-antibody reactions, but uses light absorbance end point
105
Advantages of chromogenic tests
more specific than clot based assays, ability to measure proteins that do not clot
106
Disadvantages of photo optical tests | Advantages of photo optical tests
disadv: icteric and lipemic specimens prolong the clotting time adv: ability to observe graph of clot formation
107
Disadvantage of clot based tests
not as specific as other types of tests
108
instrument features to consider when selecting a coagulation instrument
- reduced reagent/specimen volumes - reagent tracking - primary tube sampling - flagging - kinetics of clot formation - random access testing
109
What are some POC coagulation tests and why would they be used?
ACT - used for heparin monitoring during cardiac surgery | PT/INR - monitoring coumadin for hospitalized patient/self testing for outpatient
110
TEG: what specimen is used? what is being measured?
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
ROTEM: what specimen is used? what is being measured? disadvantage?
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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