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coagulation Flashcards

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1
Q

extrinsic pathway

A

plasma-mediated, initiation of hemostasis
AKA primary hemostasis
key: tissue factor

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2
Q

intrinsic pathway

A

amplifies and propogates hemostasis
aka secondary hemostasis
key: thrombin

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3
Q

common pathway

A

results in an insoluble fibrin clot

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4
Q

hemostasis is regulated by interactions between what three factors

A

vessel walls, circulating platelets, and clotting proteins in the plasma (FFP)

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5
Q

fibrinolysis definition

A

the orderly breakdown of a stable clot

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6
Q

in normal hemostasis what predominates - anticoagulants or procoagulants?

A

anticoagulants

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7
Q

what elicits vasoconstriction, the first step of the clotting pathway

A

damage to the endothelium that exposes the underlying ECM will elicit a contraction

also can be triggered by thrmobin, hypoxia, and high fluid sheer stress

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8
Q

what are the three major biochemical and physical change stages when forming a platelet plug

A

adhesion
activation
aggregation

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9
Q

thrombocytes

A

thrombus/clot + cells

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10
Q

what is the normal concentration of platelets per microliter

A

150,000-400,000

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11
Q

at what concentration of platelet per microliter do you start spontaneously bleeding and when is it lethal

A 
<50,000 = spontaneous bleeding
<10,000 = lethal
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12
Q

what is the life of a platelet

A

8-12 days (so you need to stop your antiplatelets for 8-12 days - or give them platelets)

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13
Q

platelet inhibitors

A

adenosine, insulin, NO, PGE2 and PGI2

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14
Q

platelet activators

A

adrenalin, cholesterol, thrombopoeitin, vWF, PGE2(viaEP3)

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15
Q

platelet adhesion

A

exposure to the subendothelial matrix proteins allows platelets to undergo a conformational change to adhere to the vascular wall

aka - matrix activates it and makes it sticky

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16
Q

von Willebrand factor

A

produced in the endothelium and platelets, released by endothelial cells and activated by platelets and its primary function is to bind other proteins

it is a bridging molecule between the subendothelial matrix and platelets forming crosslinks

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17
Q

GPIb-V-IX complex

A

binds vWF allowing platelet adhesion and platelet plug formation at sites of vascular injury

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18
Q

bernard soulier syndrome

A

absence of GPIb-V-IV receptor

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19
Q

when is vWB factor mainly activated

A

in conditions of high blood flow and shear stress

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20
Q

vWB disease

A

1 in 100 individuals are deficient but it is only clinically significant in 1 in 10,000

deficiency of vWB factor shows primarily in organs with small vessels and is diagnoses by measuring the amount of vWB factor in a vWB factor antigen assay and the funtionality of vWB factor wiht binding assays

factor 8 is also measured

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21
Q

type 1 vWB disease

A

60-80%
failure to secrete vWB factor into circulation or cleared too quickly

this is mild and often undiagnosed until bleeding following surgery, easy bruising, or menorrhagia

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22
Q

type 2 vWB disease

A

15-30%

this is a qualitative defect of the vWB factor and so effects vary

could have a decreased ability to either bind GPIb or VIII

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23
Q

type 3 vWB disease

A

most severe, homozygous defective gene, complete absence of production of vWB factor - leads to extremely low levels of factor VIII since it does not exsist to protect it from proteolytic degradation

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24
Q

platelet type vWB disease

A

in this type the problem is actually a defect of the platelet’s GPIb receptor

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25
what are GPIIb/IIIa inhibitors?
they are a class of antiplatelets that block the ability of fibrinogen to form around aggregated platelets so no fibrinogen bridging of platelets to other platelets can occur examples - abciximab (reopro), etifibatide (integrilin), tirofiban (aggrastat)
26
what is different about abciximab than other antiplatelets?
it irreversibly binds to its receptor so it takes 24hours to restore platelet function and is eliminated by plasma proteases the other two (eptifibatide and tirofiban) reversibly bind to their receptors and it only takes 4-6 hours to restore platelet function and they are eliminated renally
27
platelet activation
occurs after platelets adhere to endothelial wall, and intracellular signaling pathways are activated when ligands bind to platelet receptors to begin a serious of physical/biochem changes platelets develop pseudopod-like membrane extensions to increase SA
28
platelet recruitment
mediated by other platelets releasing granular contents | this also activates them
29
thromboxane A2 inhibitors
aka cox inhibitors aspirin inhibits the ability of cox enzyme to synthesize the precursors of thromboxane within platelets naproxen is nonselective
30
P2Y12 receptor
amplify the response to ADP and draw forth the completion of aggregation
31
ADP receptor antagonist prodrugs
ticlopidine (ticlid) clopidogrel (plavix) prasurgrel (efient)
32
ADP receptor antagonists - direct acting
ticagrelor - brilinta | cangrelor - kengrexal
33
what is the last step of the formation of a platelet plug?
platelet aggregation
34
what does the glycoprotien IIb/IIIa do when activated
they are on platelet surface and they bind fibrinogen to provide for crosslinking with adjacent platelets
35
formation of blood clot after platelet adhesion, activation, and aggregation
soluble fibrinogen becomes insoluble fibrin via thrombin which is then crosslinked into a stable mesh
36
what is the key step in blood clotting
the conversion of fibrinogen (I) to fibrin (Ia) by thrombin (IIa)
37
when is the intrinsic pathway triggered
when blood contacts a negatively charged surface (like the exposed subendothelial collagen) begins with damage to blood vessels themselves primary complex forms on collagen and thrombin is generated by way of factor XII ends when merged into common pathway to activate factor X may be more involved with inflammation, amplification and propagation of the hemostatic response to maximize thrombin generation
38
when is the extrinsic pathway activated
when blood contacts cells outside the vascular endothelium nonvascular cells express tissue factor which initiate this pathway follows damage o blood vessel, factor VII comes into contact wiht tissue factor to form TF-VIIa complex that activates factor X to promote Xa which starts the common pathway
39
what designates the beginning of the common final pathway
the activation of factor X to promote prothrombin to form thrombin which turns fibrinogen into fibrin
40
most coagulation factors are enzymes with the exception of
vWB and tissue factor (III) which are glycoproteins
41
most coagulation factors are synthesized where with the exception of what
liver calcium (IV) - comes from diet vWB - synthesized from endothelial cells and platelets
42
which factors are vitamin k dependent for utilization
II, VII, IX, X
43
what is the activity of thrombin
converts fibrin to fibrinogen*** also: activates platelets and factor XIII (fibrin stabilizing factor) Converts factor V and VIII into active forms activates factor XI upregulates TF stimulates vascular endothelium to down regulate fibrinolytic activity
44
what all do you need to promote prothrombin to thrombin
Xa Va Calcium (IV) "prothrombin activator"
45
what is the role of fibrin in a blood clot
it creates covalent bonds and crosslinks all fibers to create meshwork in all directions of blood cells, platelets, and plasma which adhere to the surface of damaged blood vessel
46
why do cobwebs stop clotting
they are rich in vitamin K
47
when does clot lysis occur?
when plasminogen is activated to plasmin by t-PA which is released from teh tissue, vascular endothelium, plasma and urine
48
what is plasmin
an enzyme which digests fibrin, fibrinogen, factor V, factor VIII, prothrombin, and factor XII
49
what is an example of an exogenous plasminogen that can be used clinically to dissolve intravascular clots
streptokinase
50
thrombolytics
possess inherent fibrinolytic effects of enhances the body's fibrinolytic system by converting endogenous pro-enzyme plasminogen to the fibrinolytic enzyme plasmin more capable of dissolving newly form clots which are platelet rich and have weaker fibrinogen bonds
51
prothrombin time
evaluates the extrinsic pathway a sample of blood plasma is incubated with tissue factor in the presence of calcium it is particularly sensitive to 3 of the 4 vitk dependent factors (II, VII, and X)
52
what is the problem with prothrombin times
commercial PT reagents vary markedly in their responsiveness to warfarin-induced decreases in clotting factors and are not interchangeable between labs use INR for standardization
53
partial thromboplastin time
indicates the performance of the intrinsic pathway a sample of blood is triggered by adding an activator surface plus phospholipid and calcium
54
ACT
performed by mixing whole blood with an activated substance to initiate activation of the clotting cascade reliable for high heparin concentrations influenced by hypothermia, thrombocytopenia, coagulation deficiencies
55
viscoelastic testing - thromboelastometry (TEG) and rotational thromboelastometry (ROTEM)
a global assay for whole blood clotting including coagulation factors, inhibitors, anticoagulant drugs, platelets, and fibrinolysis
56
bleeding time
sensitive test of platelet function a small standardized incision is made in the underside of the forearm and the amount of time it takes for bleeding to stop is recorded
57
heparin concentration measurements
increasing concentrations of protamine are added to samples of heparin-containing blood and time to clot is measured. the sample in which heparin and protamine are most closely matched will clot first 1mg protamine will inhibit 1mg (100u) of heparin
58
platelet function test
centrifugation of patient blood to obtain platelet-rich plasma it is then analyzed in a cuvette at 37C placed between a light source and a photocell
59
what is the normal bleeding time
3-10 min
60
what is the normal platelet count
150,000-350,000 mm3
61
what is the normal prothrombin time
12-14sec
62
what is the normal INR
0.9-1.2
63
what is the normal aPTT
25-35s
64
what is the normal thrombin time
<30sec
65
what is the normal active coagulation time
80-150s
66
what is the normal level of fibrinogen
>150mg/dL

Advanced Pharm (11 decks)

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