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N929 Pharmacology II > Coagulation & dissolution of a blood clot > Flashcards

Coagulation & dissolution of a blood clot Flashcards

1
Q

Steps to blood clotting (general)

A

Vasoconstriction, platelet aggregation, clot strengthening, and clot dissolution

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2
Q

Normal hemostasis for coagulation is

A

a balance between generation of hemostatic clots and uncontrolled thrombus formation

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3
Q

The extrinsic pathway is

A

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

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4
Q

The intrinsic pathway

A

amplifies and propagates hemostasis
AKA- secondary hemostasis
Key: thrombin

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5
Q

The common pathway results

A

in an insoluble fibrin clot

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6
Q

Preoperative coagulation testing should be based on

A

patient’s history and planned surgery

patient’s history is why you should check lab values

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7
Q

Agents that impact the coagulation cascade include

A

antiplatelets, anticoagulants, thrombolytics, procoagulants

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8
Q

There are more than ____ substances that affect blood coagulation

A

50

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9
Q

At normal homeostasis, _____ predominates but when a vessel is ruptured, _______ are activated

A

anticoagulants; procoagulants

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10
Q

Fibrinolysis is

A

the orderly breakdown of a stable blood clot

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11
Q

Hemostasis is regulated by interactions between

A

the blood vessel walls, circulating platelets, and clotting proteins in the plasma

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12
Q

Normally, vascular endothelium provides a

A

non-thrombogenic surface- antiplatelet or profibrinolytic surface

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13
Q

Damage to the endothelium exposes

A

the underlying extracellular matrix and elicits a contraction (vasoconstriction)

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14
Q

Thrombin, hypoxia, and high fluid sheer stress can

A

also induce prothrombotic endothelial changes

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15
Q

When platelets are exposed to the extracellular matrix in damaged endothelium they undergo

A

a series of biochemical and physical alterations

adhesion, activation, and aggregation

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16
Q

Normal concentration of platelets is

A

150,000-400,000 per microliter
spontaneous bleeding <50,000 micrograms/L
Lethal <10,000 micrograms/L

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17
Q

The life of a platelet is

A

8-12 days

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18
Q

Platelets are formed in

A

the bone marrow

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19
Q

A thrombocyte is a

A

thrombus/clot+ cells

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20
Q

Platelet adhesion occurs due to

A

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

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21
Q

Von willebrand factor is produced in the

A

endothelium and platelets

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22
Q

vWF is released by

A

endothelial cells and by activated plateletes

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23
Q

vWF’s primary function is to

A

bind other proteins
it is particularly important as a bridging molecule between the subendothelial matrix and platelets forming a cross links
glycoprotein IIb/IIIa; glycoprotein Ib/factor IX/factor V receptor complex

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24
Q

The GPIb-V-IX complex binds

A

von Willebrand factor, allowing platelet adhesion and platelet plug formation at sites of vascular injury

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25
Q

Absence of GP1b-V-IV receptor is known as

A

Bernard Soulier syndrome

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26
Q

Von Willebrand factors is mainly activated in conditions of

A

high blood flow and shear stress

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27
Q

Deficiency of vWF shows primarily in

A

organs with small vessels such as skin, GI, and uterus

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28
Q

Von willebrands disease is diagnosed by

A

measuring the amount of vWF in a vWF antigen assay and the functionality of vWF with binding assays
factor VIII is also measured

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29
Q

Type 1 vWD is a

A

failure to secrete vWF into circulation or vWF being cleared more quickly than normal; mild, often undiagnosed until bleeding following surgery, easy bruising, or menorrhagia

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30
Q

Type 2 vWD is a

A

qualitative defect and bleeding varies- decreased ability to bind to GPib
decreased ability to bind to VIII

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31
Q

Type 3 vWD is

A

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

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32
Q

Platelet type Von Willebrand disease is

A

a defect of the platelet’s GPIb receptor

vWF is normal, the platelet receptor GPIb is abnormal

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33
Q

We need to figure out which type of Von Willebrand’s disease they have in order to

A

know how to treat them

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34
Q

What medications are GPIIb/IIIa inhibitors?

A

considered a class of antiplatelets; includes abciximab, integrilin, and aggrastat

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35
Q

GpIIb/IIIa inhibitors work by

A

blocking the ability of fibrinogen to form around the aggregated platelets
as a result, no fibrinogen bridging of platelets to other platelets can occur

36
Q

Platelet activation causes platelets to

A

develop pseudopod-like membrane extensions to increase platelet surface area

37
Q

Platelet recruitment occurs when

A

platelets release granular contents resulting in recruitment and activation of additional platelets

38
Q

Medications that are thromboxane A2 inhibitors include:

A

aspirin- inhibits the ability of COX enzyme to synthesize the precursors of thromboxane within platelets
Naproxen- nonselective COX inhibitor

39
Q

P2Y12 receptors further amplify

A

the response to ADP and draw forth the completion of aggregation

40
Q

ADP receptor antagonist medications include:

A

prodrugs: ticlopidine, clopidogrel (Plavix), and prasugrel (Efient)
direct acting: ticagrelor (brilinta) and cangrelor (kengrexal)

41
Q

_____ completes the formation of a platelet plug

A

platelet aggregation

42
Q

Activators released during the activation phase

A

recruit and amplify the response of additional platelets to the site of injury

43
Q

Newly activated glycoprotein IIb/IIIa receptors on the platelet surface bind

A

fibrinogen to provide for cross-linking with adjacent platelets

44
Q

The key step in blood clotting is

A

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

45
Q

Soluble fibrinogen is converted to

A

insoluble fibrin

46
Q

Following platelet adhesion, activation, and aggregation, the

A

blood clot begins to form
the plasma protein fibrinogen breaks down to produce fibrin which becomes cross-linked into a stable mesh
coagulation factors are then activated and initiate the coagulation cascade

47
Q

The classic description of coagulation includes initiation of

A

the coagulation cascade via the intrinsic or extrinsic pathway

48
Q

The intrinsic pathway is triggered when

A

blood contacts a negatively charged surface (i.e. exposed subendothelial collagen)

49
Q

The extrinsic pathway is activated when

A

blood contacts cells outside the vascular endothelium

-nonvascular cells express a membrane protein called tissue factor (III) which initiates this pathway

50
Q

The common final pathway is where

A

the intrinsic and extrinsic pathways converge with the activation of factor X

51
Q

Most coagulation factors are _____ with some exceptions_____

A

enzymes; vWF and tissue factor (III) are glycoproteins)

52
Q

Most coagulation factors are synthesized

A

via the liver except for calcium (IV) comes from diet & von Willebrand is synthesized in endothelial cells and platelets

53
Q

Factors ___, ____, ___, and _____ are Vitamin K dependent for utilization

A

II, VII, IX, and X

54
Q

The intrinsic pathway of coagulation begins with

A

damage to the blood vessels themselves

55
Q

Formation of the primary complex on collagen and thrombin generation by way of factor

A

XII and ultimately merges to the common pathway and activates factor X

56
Q

The intrinsic pathway is also known as the

A

contact activation system

57
Q

The extrinsic pathway is also known as the

A

tissue factor pathway

58
Q

The extrinsic pathway is the initial step in

A

plasma-mediated hemostasis

59
Q

Following damage to the blood vessel,

A

factor VII comes into contact with tissue factor and forms an activated TF-VIIa complex

60
Q

The TF-VIIa circulating the plasma activates

A

factor X to promote the conversion of X to Xa

61
Q

The common pathway of coagulation depicts

A

thrombin generation and subsequent fibrin formation- prothrombin II is cleaved by activated factor X to produce thrombin IIa

62
Q

Factor X takes

A

prothrombin and turns it into thrombin

63
Q

Prothrombin gets activated to

A

thrombin

64
Q

Thrombin activates

A

fibrinogen to form fibrin

65
Q

Fibrin creates

A

covalent bonds and cross-linking of fibers create a meshwork in all directions of blood cells, platelets, and plasma which adhere to the surface of damaged blood vessel

66
Q

After a clot is formed, the

A

actin and myosin of the platelets trapped in the fibrin mesh interact in a manner like that in muscle contraction

67
Q

Clot lysis occurs when

A

plasminogen (normally found in the blood) is activated to plasmin

68
Q

Tissue plasminogen activator

A

is released from the tissue, vascular endothelium, plasma, and urine to activate clot lysis

69
Q

Plasmin is an

A

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

70
Q

Exogenous plasminogen activators such as

A

streptokinase are used clinically to dissolve intravascular clots

71
Q

Thrombolytics are

A

more capable of dissolving newly formed clots (platelet rich and weaker fibrinogen bonds)
-older clots have more cross-linking and re more compacted= more difficult to dissolve

72
Q

Thrombolytics possess inherent

A

fibrinolytic effects or enhance the body’s fibrinolytic system by converting endogenous pro-enzyme plasminogen to the fibrinolytic enzyme plasmin

73
Q

Prothrombin time evaluates the

A

evaluates the extrinsic pathway

sensitive to factors II, VII, and X

74
Q

Partial thromboplastin time indicates the

A

indicates the performance of the intrinsic pathway

75
Q

ACT is

A

reliable for high heparin concentrations

influenced by hypothermia, thrombocytopenia, and coagulation deficiencies

76
Q

Visoelastic testing

A

TEG & Rotem- global assay for whole blood clotting including coagulation factors, inhibitors, anticoagulant drugs, platelets, and fibrinolysis

77
Q

Platelet function tests

A

involve centrifugation of platelet blood to obtain platelet-rich plasma

78
Q

Heparin concentration measurements

A

increasing concentrations of protamine are added to samples of heparin containing blood and time to clot is measured

79
Q

Bleeding time

A

incision is made on the forearm and the amount of time it takes for bleeding to stop is recorded

80
Q

ACT normal value

A

80-150 seconds

81
Q

Fibrinogen normal value

A

> 150 mg/dL

82
Q

aPTT normal values

A

25-35 seconds

83
Q

Thrombin time normal values

A

<30 seconds

84
Q

INR normal values

A

0.9-1.2

85
Q

Prothrombin time normal values is

A

12-14 seconds

86
Q

Bleeding time is

A

3-10 minutes

87
Q

Platelet count is

A

150,000-400,000

N929 Pharmacology II (16 decks)

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