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Coagulation > Exam 2 > Flashcards

Exam 2 Flashcards

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
Q

What side effects can heparin have and how can they be affect test results

A

platelet count is 40% lower, heparin induced thrombocytopenia

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26
Q

What conditions can lead to heparin resistance

A

inflammation
prolonged UFH therapy
platelets release platelet factor 4 which neutralizes heparin (shortens PTT)

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27
Q

What can cause falsely prolonged PTT levels

A

hypofibrinogenemia, factor deficiencies, present of LAC, FDP or paraproteins

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28
Q

What are the limits of chromogenic anti-Xa assay? and activated clotting time?

A

only reflects Xa binding to antithrombin, PTT is better because it gives a global impression
ACT- only for point of care and cardiac surgeries

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29
Q

What is the median ACT interval

A

98 seconds

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30
Q

How can we reverse the effects of heparin

A

protamine sulfate- from salmon perm, binds and neutralizes heparin
also fibrinolytic therapy

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31
Q

How does LMWH work

A

low molecular weight heparin
also a pentasacharride that binds antithrombin but shorter
less bridging, mostly Xa inhibition

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32
Q

Which heparin therapy is best at activating antithrombin? and Xa?

A

UFH-antithrombin

LMWH- Xa

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33
Q

What tests are used to measure LMWH

A

chromogenic anti-Xa assay,

not PTT because it mostly affects Xa

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34
Q

What does the chromogenic anti Xa heparin assay measure

A

measures leftover products and substrates after Xa is inhibited, the more substrates and products the less heparin present

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35
Q

What is fondaparinux and how does it work

A

synthetic formula of pentasacharride in UFH and LMWH
short like LMWH only inhibits Xa
raises antithrombin activity by 400

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36
Q

What test is used to measure the effectiveness of fondaparinux?

A

chromogenix anti Xa heparin assay

not PTT

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37
Q

How can fondaparinux overdose be reversed

A

rFVlla- can particially reverse effect

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38
Q

What are DTIs and what do they do

A

direct thrombin inhibitors
anticoagulants that dont need antithrombin to work
binds both free and clot bound thrombin

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39
Q

What lab tests are used to measure DTI effectiveness and how are they affected by it.

A

prolongs Thrombin time and PTT
Ecarin chromagenic assay- snake venom
plasma diluted thrombin time- patient plasma + normal plasma

40
Q

What are intravenous DTIs and give examples

How do they affect test results

A

argatroban and bivalirudin
used on patients with HIT
binds and activates free or clot bound thrombin
prolong everything

41
Q

What tests are used to monitor intravenous DTIs

A

PP, PT, PTT and ACT

all prolonged

42
Q

What is DOAC and how is it monitored, name the drug

A

Direct oral anticoagulants
no monitoring needed, no antithrombin needed, acts directly on X
prolongs PTT, TT and ECT
Dabigatran

43
Q

What do intravenous antiplatelet drugs do and what are they for

A

block fibrinogen or VWF from binding, reducing platelet aggregation
for percutaneous coronary intervention
primary hemostasis

44
Q

What are intravenous antiplatelet drugs coadministered

A

UFH and aspirin

45
Q

What kind of drugs are these

abciximab( ReoPro) , eptifibatide (integrillin) ,tirobaban hydrochloride ( Aggrastat)

A

Intravenous antiplatelet drugs

46
Q 
What kind of drugs are these
Aspirin
clopidogrel
prasugrel
ticargrelor
A

oral antiplatelet drugs

47
Q

What mechanism do antiplatelet drugs use

A

bind to ADP receptor on platelets (P2Y12) and suppress their aggregation

48
Q

What is aggregometry

A

reference for antiplatelet drugs

49
Q

What are the platelet counts for PPP and PRP and what do they stand for?

A

PPP- poor platelet count less than 10,000

PRP platelet rich plasma about 200,000

50
Q

What sodium citrate to blood volume ratio should there be if the HCT is elevated 55% or more

A

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
Q

What is the formula for sodium citrate adjustment for elevated HCT

A

C=(1.85x10^-3)(100-HCT)V
C= citrate volume ml
V= volume of whole blood
HCT= hematocrit in %

52
Q 
Describe how each of these affect test results
short draw
specimen clot
visible hemolysis
lipemia or icterus
tourniquet >1min
specimen @ 1-6C
specimen @ >25C
A

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
Q

How should hemostasis specimen be transported and stored

A

15-25C, ambient
because coag factors are heat labile (unstable)
PT- within 24hrs
PTT within 4 hrs

54
Q

When should coag specimen be spun down

A

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
Q 
How soon should these specimen get tested
PT no UFH
PTT no UFH
PT with UFH
Factor assay
optical platelet aggregometry
whole blood aggregometry
A 
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
Q

What is the bleeding time test? What is the normal range and what does it mean if it is prolonged

A

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
Q

How is platelet PRP aggregometry performed

A

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
Q

What are the 5 steps of platelet aggregation

A 
resting platelet stable baseline
shape change
primary aggregation 
secretion
secondary aggregation
59
Q

How is whole blood platelet aggregometry preformed

A

measures electrical impedance
platelets adhere to an electrode and impede a current
if impedance rises, platelet aggregation is rising, charge goes down

60
Q

How does platelet lumiaggregometry work

A

measures the secretion of ATP by platelets
luciferin-luciferase reagent creates cold chemiluminescence proportional to ATP
amplifies luminescence

61
Q

What is an agonist

A

used in platelet test for specific membrane binding sites on platelets

62
Q

List the platelet agonists that used to activate platelets in aggregometry

A 
Thrombin
TRAP-thrombin receptor activating peptide
ADP
Epinephrine
Collagen
Arachidonic acid
Ristocetin
63
Q

What specific deficiencies are arachidonic acid and ristocetin for

A

arachidonic acid-deficiencies in eicosanoid synthesis pathway
Ristocetin- abnormalities of VWF in VWD

64
Q

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

A
  • 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
Q

What are these abbreviations for

PT, PTT, FGB, TCT, ACT

A

prothrombin time, partial thromboplastin time, fibrinogen, thrombin clotting time, activated clotting time
finds coagulopathies- coag deficiencies

66
Q

What reagent is used in PT test?
What is the normal range?
What pathway does it monitor?
What factor is first activated?

A

thromboplastin: TF +phospholipids +Ca
12.6-14.6
Extrinsic pathway, and common
Factor VII

67
Q

IF a PT test is prolonged, what is the most likely reason?

What is PT used to monitor?

A

VII deficiency, V and X, FBG, insensitive to VIII, IX and XIII
Coumadin monitoring

68
Q

What is the PT procedure

What can PT diagnose

A

Thromboplastin+ PPP, timed until clot forms

multiple deficiencies in LIVER, vitamin K, cause prolonged PT

69
Q

How can we tell if a PT test is prolonged due to liver disease vs vitamin K deficiency

A

only factor VII is reduced when its a vitamin K deficiency

both reduced in liver disease

70
Q

What is the reagent in a PTT test?
What pathway does it measure?
What does it monitor?
What is the normal range?

A

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
Q

What factors prolong PTT, which ones don’tW

A

all deficiencies prolong it except for VII and XIII

72
Q

What can prolong a PTT other than coag factors

A

antibodies against coagulation factors, nonspecific inhibitors and interfering substances, could be vitamin K deficiency

73
Q

What is the normal range for a TCT
What reagent is in TCT and what does it cleave?
Also called TT

A

15-20s

reagent bovine thrombin- cleaves fibrinopeptides A and B-> forms detectable fibrin polymer

74
Q

Does TCT give qualitative or quantitative fibrinogen measurements
What are the possible results?
What is it used to monitor

A

both qualitative and quantitative
afibrinogenemia, hypofibrinogenemia ( <100)
dysfibrinogenemia- abnormal fibrinogen
monitors UFH to confirm prolonged PTT, can also find direct thrombin inhibitors

75
Q

What factors cause TCT to become prolong?

Which ones don’t

A

fibrinogen, thrombin

not XIII nor anything before thrombin

76
Q

What is the purpose of performing a mixing study?

A

to detect LACs and distinguish them from specific inhibitors and factor deficiencies

77
Q

What is an LAC? How can they affect lab tests

A

lupus anticoagulants- IgG immunoglobulins directed against phospholipid-protein complexes
NON SPECIFIC INHIBITORS-prolong PTT

78
Q

What are factor inhibitors? Why do they arise?

A

IgG immunoglobulins directed against specific coag factors

arise in response to factor concentration treatment,

79
Q

What is the most common specific inhibitor, what disease is it associated with?

A

anti factor VIII, hemophilia

80
Q

Name the tests involved in a mixing study

A

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
Q

Explain how a fibrinogen assay works

A

PPP 1:10 with Owren buffer
bovine thrombin to diluted specimen
FBG turns into fibrin

82
Q

What is the normal range for a fibrinogen assay

The __ FBG present the ____ the time it takes to form a clot

A

220-498
more FBG
lower time

83
Q

Name the reference ranges for high and low fibrinogen assays and what they might indicate

A

low-<200- liver disease
high>498 liver disease, pregnancy, chronic inflammation
afibrinogenemia- anatomic hemorrhage

84
Q

What is a single factor assay and when is it used?

A

after prolonged PTT but normal PT and TCT

mixing study if corrected after incubated and single factor deficiency is suspected

85
Q

What are the 3 factor deficiencies that accompany hemorrhage and what hemophilia are each associated with

A

VIII- most common, hemophilia A
IX- hemophilia B
XI- Rosenthal

86
Q

What is the purpose of the Nijmegan-Bethesda Assay

A

confirms and quantifies anti-factor VIII inhibitors

87
Q

What likely causes a PTT and PT to be prolonged but the TCT to be normal?

A

some single factor deficiency of the common pathway

deficiency of prothrombin, V or X

88
Q

What are factor XIII assays used for

A

if PT and PTT are normal but there is a factor XIII deficiency
poor wound healing, oozing wounds

89
Q

What are the fibrinolysis assays

A

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
Q

What are the 6 endpoint detection principles of coagulation in the lab

A

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
Q

What type of tests measure the entire coag cascade and are therefore not very specific

A

clot-based tests

92
Q

What tests are isolated to specific enzyme reactions

A

chromogenic tests

93
Q

What tests are affected by icterus/lipemic specimen? Which ones are not

A

affected- photo-optical

not affected- clot based

94
Q

When can POC test instruments be utilized

A

during clinical procedures or surgeries
bedside
self testing
infants

95
Q

What tests can POC instruments run

A

ACT-activated clotting time- for heparin monitoring during cardiac surgery
PT/INR-for monitoring coumadin

96
Q

What specimen is used in TEG tests?
What is being measured?
Adv and Disadv

A

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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