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coagulation Flashcards

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
Q

what are GPIIb/IIIa inhibitors?

A

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)

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26
Q

what is different about abciximab than other antiplatelets?

A

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

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27
Q

platelet activation

A

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
Q

platelet recruitment

A

mediated by other platelets releasing granular contents

this also activates them

29
Q

thromboxane A2 inhibitors

A

aka cox inhibitors

aspirin inhibits the ability of cox enzyme to synthesize the precursors of thromboxane within platelets

naproxen is nonselective

30
Q

P2Y12 receptor

A

amplify the response to ADP and draw forth the completion of aggregation

31
Q

ADP receptor antagonist prodrugs

A

ticlopidine (ticlid)
clopidogrel (plavix)
prasurgrel (efient)

32
Q

ADP receptor antagonists - direct acting

A

ticagrelor - brilinta

cangrelor - kengrexal

33
Q

what is the last step of the formation of a platelet plug?

A

platelet aggregation

34
Q

what does the glycoprotien IIb/IIIa do when activated

A

they are on platelet surface and they bind fibrinogen to provide for crosslinking with adjacent platelets

35
Q

formation of blood clot after platelet adhesion, activation, and aggregation

A

soluble fibrinogen becomes insoluble fibrin via thrombin which is then crosslinked into a stable mesh

36
Q

what is the key step in blood clotting

A

the conversion of fibrinogen (I) to fibrin (Ia) by thrombin (IIa)

37
Q

when is the intrinsic pathway triggered

A

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
Q

when is the extrinsic pathway activated

A

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
Q

what designates the beginning of the common final pathway

A

the activation of factor X to promote prothrombin to form thrombin which turns fibrinogen into fibrin

40
Q

most coagulation factors are enzymes with the exception of

A

vWB and tissue factor (III) which are glycoproteins

41
Q

most coagulation factors are synthesized where with the exception of what

A

liver

calcium (IV) - comes from diet
vWB - synthesized from endothelial cells and platelets

42
Q

which factors are vitamin k dependent for utilization

A

II, VII, IX, X

43
Q

what is the activity of thrombin

A

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
Q

what all do you need to promote prothrombin to thrombin

A

Xa
Va
Calcium (IV)
“prothrombin activator”

45
Q

what is the role of fibrin in a blood clot

A

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
Q

why do cobwebs stop clotting

A

they are rich in vitamin K

47
Q

when does clot lysis occur?

A

when plasminogen is activated to plasmin by t-PA which is released from teh tissue, vascular endothelium, plasma and urine

48
Q

what is plasmin

A

an enzyme which digests fibrin, fibrinogen, factor V, factor VIII, prothrombin, and factor XII

49
Q

what is an example of an exogenous plasminogen that can be used clinically to dissolve intravascular clots

A

streptokinase

50
Q

thrombolytics

A

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
Q

prothrombin time

A

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
Q

what is the problem with prothrombin times

A

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
Q

partial thromboplastin time

A

indicates the performance of the intrinsic pathway

a sample of blood is triggered by adding an activator surface plus phospholipid and calcium

54
Q

ACT

A

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
Q

viscoelastic testing - thromboelastometry (TEG) and rotational thromboelastometry (ROTEM)

A

a global assay for whole blood clotting including coagulation factors, inhibitors, anticoagulant drugs, platelets, and fibrinolysis

56
Q

bleeding time

A

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
Q

heparin concentration measurements

A

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
Q

platelet function test

A

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
Q

what is the normal bleeding time

A

3-10 min

60
Q

what is the normal platelet count

A

150,000-350,000 mm3

61
Q

what is the normal prothrombin time

A

12-14sec

62
Q

what is the normal INR

A

0.9-1.2

63
Q

what is the normal aPTT

A

25-35s

64
Q

what is the normal thrombin time

A

<30sec

65
Q

what is the normal active coagulation time

A

80-150s

66
Q

what is the normal level of fibrinogen

A

> 150mg/dL

Advanced Pharm (11 decks)

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