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Coagulation > Exam 2 > Flashcards

Exam 2 Flashcards

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1
Q

Define thrombosis, deep vein and pulmonary embolisms

A

development of a blood clot in the veins or arteries that obstruct blood flow and cause tissue death
deep vein-not moving
PE-moving clot

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2
Q

What stage of coagulation do antiplatelet and anticoagulant drugs suppress or affect

A

anticoagulants- 2ndary

antiplatelets- 1ary

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3
Q

What could happen if antithrombotics are overused

A

uncontrolled bleeding, can be fatal

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4
Q 
Which are arterial and which are venous thrombosis
acute myocardial infarction 
deep vein thrombosis
ischemic cerebrovascular accident
pulmonary embolism
A

acute myocardial infarction- AT
deep vein thrombosis-VTE
ischemic cerebrovascular accident-AT
pulmonary embolism-VTE

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5
Q

How does coumadin work

A

it is a vitamin K antagonist, it slows the activity of the enzyme that reduces vitamin K

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6
Q

What are the vitamin K dependent factors?

A

II, VII, IX , X, proteins C, S and Z

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7
Q

What is the goal of coumadin therapy

A

reduces but does not eradicate thrombin generation.

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8
Q

In what order to the factors affected by coumadin decrease?

A

VII, because it has the shortest half life
IX
X
prothrombin

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9
Q

What are the risks of coumadin, how quickly does it start to affect coagulation?

A

cannot be taken during pregnancy
begins immediately, it takes 5 days for the factors to reach the correct therapeutic levels
patient is at risk of thrombosis, cannot take any anticoagulants

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10
Q

What happens if you take anticoagulants while also undergoing coumadin therapy?

A

can increase risk of skin necrosis

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11
Q

What tests are used to monitor coumadin therapy, what pathways are they monitoring

A

Prothrombin time- measures how extrinsic and common pathways are affected

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12
Q

What reagents are in prothrombin time (PT) test

A

tissue factor, phospholipid, ionic calcium- creates extrinsic tenase

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13
Q

What will happen to PT results during coumadin therapy

A

will be prolonged very soon because of short half life of factor VII

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14
Q

What is the INR sometimes added to PT

A

international normalized ratio, accounts for variations in thromboplastin reagents

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15
Q

What is the INR therapeutic range for a patient on coumadin?

A

2-3

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16
Q

What is the INR range for a patient with a mechanical heart valve?

A

2.5-3.5

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17
Q

What does an INR of over 5 mean?

A

increased risk of hemorrhage, critical result

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18
Q

What can be used it the PT test is compromised?

A

Chromogenic factor X assay
it inhibits any substances that could affect the test results
if patient has taken any other anticoagulants, inhibitors or have any deficiencies

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19
Q

What could a patient do to affect their coumadin therapy negatively? How are the test results affected?

A

cannot eat too much vitamin K, it decreases coumadin’s effectiveness
reduces INR

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20
Q

What is coumadin sensitivity and what causes it

A

gene mutations that affect vitamin K or affect enzymes that breakdown coumadin
makes patient react to smaller amounts of coumadin, must be given lower dosage

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21
Q

What is coumadin resistance and what causes it

A

if the coumadin receptors on patients cells are insufficient, makes coumadin useless and patient will less responsive to it
less effective, patient needs higher dosage

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22
Q

How can coumadin be reversed? What if its severe.

A

if overdose and excessive bleeding occurs,
patient will be given oral or IV vitamin K
if severe- patient needs substitute active coag factors from blood products like plasma

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23
Q

How does UFH work?

A

unfractionated heparin- made of polysaccharides that binds to plasma antithrombin and activates it.
new complex binds to and inactivates serine proteases IIa (thrombin), IXa, Xa and XII
stops clotting by activating antithrombin

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24
Q

What tests are used to monitor heparin therapy

A

PTT- partial thrombinplastin time and platelet count
Chromogenic anti-Xa assay
Activated clotting time

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25
What side effects can heparin have and how can they be affect test results
platelet count is 40% lower, heparin induced thrombocytopenia
26
What conditions can lead to heparin resistance
inflammation prolonged UFH therapy platelets release platelet factor 4 which neutralizes heparin (shortens PTT)
27
What can cause falsely prolonged PTT levels
hypofibrinogenemia, factor deficiencies, present of LAC, FDP or paraproteins
28
What are the limits of chromogenic anti-Xa assay? and activated clotting time?
only reflects Xa binding to antithrombin, PTT is better because it gives a global impression ACT- only for point of care and cardiac surgeries
29
What is the median ACT interval
98 seconds
30
How can we reverse the effects of heparin
protamine sulfate- from salmon perm, binds and neutralizes heparin also fibrinolytic therapy
31
How does LMWH work
low molecular weight heparin also a pentasacharride that binds antithrombin but shorter less bridging, mostly Xa inhibition
32
Which heparin therapy is best at activating antithrombin? and Xa?
UFH-antithrombin | LMWH- Xa
33
What tests are used to measure LMWH
chromogenic anti-Xa assay, | not PTT because it mostly affects Xa
34
What does the chromogenic anti Xa heparin assay measure
measures leftover products and substrates after Xa is inhibited, the more substrates and products the less heparin present
35
What is fondaparinux and how does it work
synthetic formula of pentasacharride in UFH and LMWH short like LMWH only inhibits Xa raises antithrombin activity by 400
36
What test is used to measure the effectiveness of fondaparinux?
chromogenix anti Xa heparin assay | not PTT
37
How can fondaparinux overdose be reversed
rFVlla- can particially reverse effect
38
What are DTIs and what do they do
direct thrombin inhibitors anticoagulants that dont need antithrombin to work binds both free and clot bound thrombin
39
What lab tests are used to measure DTI effectiveness and how are they affected by it.
prolongs Thrombin time and PTT Ecarin chromagenic assay- snake venom plasma diluted thrombin time- patient plasma + normal plasma
40
What are intravenous DTIs and give examples | How do they affect test results
argatroban and bivalirudin used on patients with HIT binds and activates free or clot bound thrombin prolong everything
41
What tests are used to monitor intravenous DTIs
PP, PT, PTT and ACT | all prolonged
42
What is DOAC and how is it monitored, name the drug
Direct oral anticoagulants no monitoring needed, no antithrombin needed, acts directly on X prolongs PTT, TT and ECT Dabigatran
43
What do intravenous antiplatelet drugs do and what are they for
block fibrinogen or VWF from binding, reducing platelet aggregation for percutaneous coronary intervention primary hemostasis
44
What are intravenous antiplatelet drugs coadministered
UFH and aspirin
45
What kind of drugs are these | abciximab( ReoPro) , eptifibatide (integrillin) ,tirobaban hydrochloride ( Aggrastat)
Intravenous antiplatelet drugs
46
``` What kind of drugs are these Aspirin clopidogrel prasugrel ticargrelor ```
oral antiplatelet drugs
47
What mechanism do antiplatelet drugs use
bind to ADP receptor on platelets (P2Y12) and suppress their aggregation
48
What is aggregometry
reference for antiplatelet drugs
49
What are the platelet counts for PPP and PRP and what do they stand for?
PPP- poor platelet count less than 10,000 | PRP platelet rich plasma about 200,000
50
What sodium citrate to blood volume ratio should there be if the HCT is elevated 55% or more
9:1 ratio must compensate to avoid falsely prolonged results, there is too much anticoagulant vs coagulation factors if this discrepancy is not adjusted
51
What is the formula for sodium citrate adjustment for elevated HCT
C=(1.85x10^-3)(100-HCT)V C= citrate volume ml V= volume of whole blood HCT= hematocrit in %
52
``` Describe how each of these affect test results short draw specimen clot visible hemolysis lipemia or icterus tourniquet >1min specimen @ 1-6C specimen @ >25C ```
short draw- PT and PTT false prolonged specimen clot-unacceptable visible hemolysis-unpredictable results lipemia or icterus-optical instruments cant see through color tourniquet >1min- elevated VWF and fibrinogen, falsely short clot results specimen @ 1-6C-precipitation of VWF multimers, activation of plts, VII, destruction of plt integrity specimen @ >25C- deteriorates V and VIII
53
How should hemostasis specimen be transported and stored
15-25C, ambient because coag factors are heat labile (unstable) PT- within 24hrs PTT within 4 hrs
54
When should coag specimen be spun down
within 1 hour if patient of UFH or if specimen can't be resulted quickly -> plasma can be frozen, tested within an hour of thawing
55
``` How soon should these specimen get tested PT no UFH PTT no UFH PT with UFH Factor assay optical platelet aggregometry whole blood aggregometry ```
``` PT no UFH- within 24hrs PTT no UFH- within 4hrs PT with UFH- spin in 1 hr, test in 4hrs Factor assay-4hrs optical platelet aggregometry-spin in 30min, test in 4hrs whole blood aggregometry-4hrs ```
56
What is the bleeding time test? What is the normal range and what does it mean if it is prolonged
not used anymore- patient was cut, wound blotted every 30s, duration of bleeding was measured, 2-9 min prolonged-functional platelet disorder, vascular disorder
57
How is platelet PRP aggregometry performed
with PRP-light transmittance, near 0% transmittance agonist added as platelet activator intensity of light transmitted increases at first then increases as more aggregation occurs more platelet aggregation makes more light pass through PRP, should be 40% + if low, platelet function deficiency
58
What are the 5 steps of platelet aggregation
``` resting platelet stable baseline shape change primary aggregation secretion secondary aggregation ```
59
How is whole blood platelet aggregometry preformed
measures electrical impedance platelets adhere to an electrode and impede a current if impedance rises, platelet aggregation is rising, charge goes down
60
How does platelet lumiaggregometry work
measures the secretion of ATP by platelets luciferin-luciferase reagent creates cold chemiluminescence proportional to ATP amplifies luminescence
61
What is an agonist
used in platelet test for specific membrane binding sites on platelets
62
List the platelet agonists that used to activate platelets in aggregometry
``` Thrombin TRAP-thrombin receptor activating peptide ADP Epinephrine Collagen Arachidonic acid Ristocetin ```
63
What specific deficiencies are arachidonic acid and ristocetin for
arachidonic acid-deficiencies in eicosanoid synthesis pathway Ristocetin- abnormalities of VWF in VWD
64
Match the agonist to the binding site: Agonists: thrombin, arachidonic acid, collagen, epinephrine, ADP, TRAP Binding sites: alpha adrenergic, PAR1 and PAR2, GPIa/IIa and GPVI, thromboxane receptor
* Thrombin- cleaves PAR-1 and PAR-2 * ADP- binds P2Y1 and P2Y12 * Epinephrine- binds alpha-adrenergic receptors * Collagen-binds GPIa/IIa and GPVI, no primary aggregation * Arachidonic acid-becomes thromboxane A2 binds thromboxane receptor
65
What are these abbreviations for | PT, PTT, FGB, TCT, ACT
prothrombin time, partial thromboplastin time, fibrinogen, thrombin clotting time, activated clotting time finds coagulopathies- coag deficiencies
66
What reagent is used in PT test? What is the normal range? What pathway does it monitor? What factor is first activated?
thromboplastin: TF +phospholipids +Ca 12.6-14.6 Extrinsic pathway, and common Factor VII
67
IF a PT test is prolonged, what is the most likely reason? | What is PT used to monitor?
VII deficiency, V and X, FBG, insensitive to VIII, IX and XIII Coumadin monitoring
68
What is the PT procedure | What can PT diagnose
Thromboplastin+ PPP, timed until clot forms | multiple deficiencies in LIVER, vitamin K, cause prolonged PT
69
How can we tell if a PT test is prolonged due to liver disease vs vitamin K deficiency
only factor VII is reduced when its a vitamin K deficiency | both reduced in liver disease
70
What is the reagent in a PTT test? What pathway does it measure? What does it monitor? What is the normal range?
reagent- phospholipid + neg charged activator like silica intrinsic pathway via contact with neg charged surface monitors UFH 26-38 normal 60-100 if on UFH
71
What factors prolong PTT, which ones don'tW
all deficiencies prolong it except for VII and XIII
72
What can prolong a PTT other than coag factors
antibodies against coagulation factors, nonspecific inhibitors and interfering substances, could be vitamin K deficiency
73
What is the normal range for a TCT What reagent is in TCT and what does it cleave? Also called TT
15-20s | reagent bovine thrombin- cleaves fibrinopeptides A and B-> forms detectable fibrin polymer
74
Does TCT give qualitative or quantitative fibrinogen measurements What are the possible results? What is it used to monitor
both qualitative and quantitative afibrinogenemia, hypofibrinogenemia ( <100) dysfibrinogenemia- abnormal fibrinogen monitors UFH to confirm prolonged PTT, can also find direct thrombin inhibitors
75
What factors cause TCT to become prolong? | Which ones don't
fibrinogen, thrombin | not XIII nor anything before thrombin
76
What is the purpose of performing a mixing study?
to detect LACs and distinguish them from specific inhibitors and factor deficiencies
77
What is an LAC? How can they affect lab tests
lupus anticoagulants- IgG immunoglobulins directed against phospholipid-protein complexes NON SPECIFIC INHIBITORS-prolong PTT
78
What are factor inhibitors? Why do they arise?
IgG immunoglobulins directed against specific coag factors | arise in response to factor concentration treatment,
79
What is the most common specific inhibitor, what disease is it associated with?
anti factor VIII, hemophilia
80
Name the tests involved in a mixing study
prolonged PTT/PT-> prolonged TCT Mixing study- patient plasma + platelet poor normal plasma (PNP) corrected mix-> factor deficiency uncorrected mix-> incubated mix uncorrected incubated->inhibitor if bleeding LAC if not bleeding corrected incubated->factor deficiency
81
Explain how a fibrinogen assay works
PPP 1:10 with Owren buffer bovine thrombin to diluted specimen FBG turns into fibrin
82
What is the normal range for a fibrinogen assay | The __ FBG present the ____ the time it takes to form a clot
220-498 more FBG lower time
83
Name the reference ranges for high and low fibrinogen assays and what they might indicate
low-<200- liver disease high>498 liver disease, pregnancy, chronic inflammation afibrinogenemia- anatomic hemorrhage
84
What is a single factor assay and when is it used?
after prolonged PTT but normal PT and TCT | mixing study if corrected after incubated and single factor deficiency is suspected
85
What are the 3 factor deficiencies that accompany hemorrhage and what hemophilia are each associated with
VIII- most common, hemophilia A IX- hemophilia B XI- Rosenthal
86
What is the purpose of the Nijmegan-Bethesda Assay
confirms and quantifies anti-factor VIII inhibitors
87
What likely causes a PTT and PT to be prolonged but the TCT to be normal?
some single factor deficiency of the common pathway | deficiency of prothrombin, V or X
88
What are factor XIII assays used for
if PT and PTT are normal but there is a factor XIII deficiency poor wound healing, oozing wounds
89
What are the fibrinolysis assays
D-Dimer Immunoassay-increased with DIC, systemic fibrinolysis, DVT, PE Fibrin degradation product immunoassay-measures fibrin split products Plasminogen Assay-hyper-too much clot degradation (trauma, inflammation), hypo-not enough Tissue Plasminogen Assay: increased- fibrinolysis, inflammation, pregnancy, decreased: thrombolytic therapy, hepatitis, cancer Plasminogen activator inhibitor- decreased: MI, stroke, DVT risk, increased: thrombosis
90
What are the 6 endpoint detection principles of coagulation in the lab
mechanical- 2 metal electrodes in plasma or steel ball photo-optical- optical density during clotting nephelometric-forward angle light scatter chromogenic- uses chromophore to measure specific coag factors immunologic- antigen-antibody reactions measured with light absorbance viscoelastic- global hemostasis assessment, whole blood clotting
91
What type of tests measure the entire coag cascade and are therefore not very specific
clot-based tests
92
What tests are isolated to specific enzyme reactions
chromogenic tests
93
What tests are affected by icterus/lipemic specimen? Which ones are not
affected- photo-optical | not affected- clot based
94
When can POC test instruments be utilized
during clinical procedures or surgeries bedside self testing infants
95
What tests can POC instruments run
ACT-activated clotting time- for heparin monitoring during cardiac surgery PT/INR-for monitoring coumadin
96
What specimen is used in TEG tests? What is being measured? Adv and Disadv
whole blood clot formation measures entire kinetic process of clot formation adv: evaluates everything else in blood WBCs, proteins, coag factors disadv: operator dependent, need training, high skill

Coagulation (7 decks)

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