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Biochem Winter 2012 > Bloot Clotting and Blood Groups > Flashcards

Bloot Clotting and Blood Groups Flashcards

1
Q

Whawt is hemostasis

A

balance between maintaining blood flwo under normal conditions and clotting blood to minimize its loss when vascular injry ruptures a blood vessel

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2
Q

What does sealing a vascular rupture require?

A

requires responses on both the cellular and the molecular levels in teh form of aggregated PLATELETS and FIBRIN CLOTS respectively

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3
Q

What is the MOLECULAR RESPONSE (coagulation cascade)

A

produces FIBRIN CLOTS

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4
Q

What is the CELLULAR REPSONSE

A

Involves the role of PLATELETS

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5
Q

What are hemorrhagic disorders

A

Uncontrolled bleeding

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6
Q

What are THROMBOTIC disorders. What are examples?

A

produces THROMBOSIS (localized blodo clotting) that obstructs BF inside arterial and/or venous BV.

MI, stroke, Deep Vein Thrombosis

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7
Q

What’s first, cellular (platelet) or molecular (fibrin)

A

Platelet!

  1. Platelets- cover the big whole
  2. Fibrin- stop/slow flow with clot
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8
Q

What is the first response to vascular damage?

A

contraction of SM, which minimiezes flow via VASOCONSTRICTION

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9
Q

What is produced with endothelial damage?

A

Endothelin

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10
Q

What is endothelin

A

oligopeptide with powerful VASOCONSTRICTOR properties

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11
Q

What is the cellular response triggered by?

A
  1. exposure to collagen
  2. von Willebrand factor (vWF)
    this transproms the inactive and soluble platelets into platelets that adhere to rim of vascular tear
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12
Q

What happens with platelets during cellular response

A

platelets become sticky (via activation) to promote aggregation that blocks rupture.

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13
Q

What intitates moleuclar repsonse?

A

TF–> then produces FIBRIN CLOTS

fibrinogen –> fibrin clots

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14
Q

what happens once sealed –>

A

repair process begins b/c circulating blood contains factors that inhibit cellular and molecular responses, adn promote FIBRINOLYSIS (process of dissovling fibrin clots) and vasodialtion

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15
Q

Factor I

A

Fibrinogen

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16
Q

Factor II

A

Prothrombin

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17
Q

Factor III

A 
Tissue Factor (TF
or Thromboplastin
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18
Q

Factor IV

A

Ca 2+

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19
Q

HOw many serine proteases activate other factors?

A

7

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20
Q

Which factors are zymogen?

A

prothrombin
prekallikrein
Factors VII, IX-XII (7, 9-12)

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21
Q

Which factors are Activated forms?

A

Thrombin
kallikrein
Factors VIIa, IXa-XIIa

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22
Q

Which factor is NOT a protease

A

Factor VIII

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23
Q

Is there a factor VI?

A

No!

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24
Q

Which factors have only ONE form ?

A
  1. TF
    Phospholipids
    Calcium ions
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25
Q

What factors have inactive (zymogen) and active (active) fors?

A

Prothrombin, prekallikrein, and

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26
Q

Wich factor ahve three forms?

A

Factors V and VIII.

  1. inactive precursors (V and VIII)
  2. Active form (VA and VIIIa)
  3. Inactive degraded form (Vi and VIIIi)
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27
Q

what part is cleavage >

A

only activation

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28
Q

what vitamin is an imporant one in coag?

A

Vitamin K

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29
Q

what are the four variets of factors?

A
  1. 6 serine proteases
  2. 4 are cofactors
  3. 1 forms the fibrin clot
  4. 1 is the transglutaminase tha tcrosslinks the fibrin clot
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30
Q

What are teh 6 serine proteases (facotrs)

A 
thrombin
VIIa
IXa
Xa
XIa
XIIa
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31
Q

what are the 4 cofactors

A

TF
Ca2”
Va
VIIIa (8a)

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32
Q

What forms the fibrin clot

A

Fibrin

q

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33
Q

What is the translutaminase that crosslinks the fibrin clot

A

XIII (13)

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34
Q

what is the role of vWF

A
  1. stabilize Factor VIII by forming 1:1 complex hen factor is circulating
  2. role in platelet adhesion
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35
Q

What does the INTRINSIC pathway connect to and provide

A

It connects kallikrein-kinin pathway and provides cofactor HMWK and PK

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36
Q

What are the three pathways of the Molecular response

A
  1. Extrinsic
  2. Intrinsic
  3. Common
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37
Q

How is the Intrinsic Pathway activated?

A

by the extrinsic pathway

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38
Q

What does the EXTRINSIC involve

A

PL,
Ca 2+
VII
TF

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39
Q

What doe INTRINSIC pathway involve

A 
PL
Ca2+
VIII
IX
XI
XII
vWF, HMWK, and PK also conribute
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40
Q

What does the COMMON pathway involve

A 
PL
Ca2+
V
X
XIII
Prothrombin
Fibrinogen
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41
Q

What is another name for TF?

A

Thromboplastin or Factor III

42
Q

What happens when vascular inury

A

TF is exposed and as an integral membrane glycoprotein, it is tightly assocaited with membrane PL

43
Q

What converts VII to VIIA?

A

Autoactivation produces some factor VIIa that is found circulating in the blood
This small amt participated
Cascade initates and then Factor Xa provides positive feedback by concerting more factor VII to VIIa

44
Q

To fully activate VIIa, it must be assembled with

A

TF, Ca ions, PL, in a membrane assocaited cmpelx called EXTRINSIC TENASE

45
Q

What is extrinsic tease

A

Complex with VIIa, TF, Ca ions, and PL that coverts Factor X to Xa

46
Q

what factors are in the Common pathway?

A

V, X, XIII

as well as prothrombin (II) and fibrinogen (I)

47
Q

What needs to assemble with Xa to fully activate it

A

Va in teh presence of PL and Ca ions to form a mebrana ss. complex called PROTHROMBINASE

48
Q

What is prothrombinase fnc

A

itconversts Prtothrombin to throbin, which in turn converts fibrinogen to fibrin

49
Q

What does Thrombin activate?

A

converts Factor XIII to XIIIa which in turn cross-links fibrin to form hard clot

50
Q

what can initiate Intrinsic Pathway

A

by extrinsic pathwy or by negatively charged surfaces such as PL on activated platelets

In vitro- pathway initiated by negatively charged surfaces such as powdered glass, kaolin, or dextran sulfate

51
Q

What is Factor XII

A

Hageman Factor

binds to negatively charged surfaces and undergoes conformational change that increases its proteolytic activity to convert factor XI to XIa up to 100,000 fold

52
Q

What factor in the intrinsic pathway does Extrinsic Tenase Activate

53
Q

WHAT IS THE difference between hard clot and soft clot

A

soft clot- fibrin monomers no longer soluble and polymerize to form fibrin clot

hard clot- Thrombin converts facor 13–>13a–> then cross-links fibrin to form a hard clot

54
Q

WHAT IS THE difference between hard clot and soft clot

A

soft clot- fibrin monomers no longer soluble and polymerize to form fibrin clot

hard clot- Thrombin converts facor 13–>13a–> then cross-links fibrin to form a hard clot

55
Q

WHAT IS THE difference between hard clot and soft clot

A

soft clot- fibrin monomers no longer soluble and polymerize to form fibrin clot

hard clot- Thrombin converts facor 13–>13a–> then cross-links fibrin to form a hard clot

56
Q

WHAT IS THE difference between hard clot and soft clot

A

soft clot- fibrin monomers no longer soluble and polymerize to form fibrin clot

hard clot- Thrombin converts facor 13–>13a–> then cross-links fibrin to form a hard clot

57
Q

WHAT IS THE difference between hard clot and soft clot

A

soft clot- fibrin monomers no longer soluble and polymerize to form fibrin clot

hard clot- Thrombin converts facor 13–>13a–> then cross-links fibrin to form a hard clot

58
Q

WHAT IS THE difference between hard clot and soft clot

A

soft clot- fibrin monomers no longer soluble and polymerize to form fibrin clot

hard clot- Thrombin converts facor 13–>13a–> then cross-links fibrin to form a hard clot

59
Q

What does serine protease thrombin do?

A

converts solutible fibrinogen MONOMERS into FIBRIN POLYMERS

this is key step in clotting process- formation of soft fibrin clot

60
Q

What does serine protease thrombin do?

A

converts solutible fibrinogen MONOMERS into FIBRIN POLYMERS

this is key step in clotting process- formation of soft fibrin clot

60
Q

How dos TFPI inhibit thromboses?

A

It blocks EXTRINSIC TENASE .

It has NO effect on Factor VIIa alone
it only blocsk VIIa when it assembles with TF, factor Xa and Calcium ions on a PL surface

61
Q

How does antithrombin inhibit thromboses?

A

Though Protein C Pathway: It inhibits the common and intrinsic pathways by forming a 1:1 complex with either thrombin of factor Xa to inactivate these serine proteases.

Antithrombin can also inactivate KALLIKREIN as well as Factor 9a, 11a, 12a in vitro

Only inhibition of Xa are fast enought to be physiologically significant

62
Q

How does heparin contribute to the reaction between thrombin and antithrombin?

A

Reaction is markedly accelerated (2,000x faster) int eh presence of heparin.

63
Q

What is heparin

A

It’s a polysacchardie having numerous negative hcarges (carboxylates and sulfates).

Heparain in syntheized by cells linign the BC walls of many tissues. It is used therapeutically as an anticoagulant; it must be administered parentaerally and its efect only lasts a few hours

64
Q

How long does the effect of heparin last?

A

only a few hours

65
Q

What is the role of NO, PGI2 and ADPase

A

Inhibits platelet activation

66
Q

What is the role of Throbmbin + Thrombomodulin?

A

Thorugh PRotein C pathway it inhibits INTRINSIC TENASE and PROTHROMBINASE

67
Q

What does Antithrombin + heparin

A

Inhibits thrombin and Factor Xa

68
Q

Wha tdoes Tsisue Factor Pathway Inhbitior (TFPI) do?

A

Inhibits EXTRINSIC TENASE

69
Q

What deosplasminogen activators tPA and uPA do

A

release plasmin–> degrades fibrin clots

70
Q

What is the general role of the protein C pathway

What two surfaces does this pathway occur on?

A

primarily prevents thrombosis in healthy capillaries and small BV

This pathway occurs on Endothelial CElls and ACTIVATEDPLATELETS

71
Q

What is Protein C (PC)

A

inactive form of a serine protease.

72
Q

Lumen side of the vascular endothelium that expresses teh surface glycoprotein thrombomodulin

A

Thrombomodulin modifies the substrate specificity of circulating throbin by forming a 1:1 cmplex with it

Thrombin is ineffective in clot formation

73
Q

Describe the Protein C pathway on endothelial cell surface

A

TM + Thrombin –> covert PC to APC –> forms 1:1 complex with PS –> APC and PS ass. with PL via a bridging ions

74
Q

What is the role of membrane assocaited comlex APC and PS (3)

A
  1. degrads factor 8a to factor 8i in the intrinsic tenase compelx
  2. degrades factor Va to factor Vi in teh Prothrombinase complex
  3. Degradation of these essential cofactor proteins indirectly inhibits the actiity of hte respective serine proteases in both complexes, factor 9a and 10a
75
Q

What is associated with deficiencies in eitehr PC or PS?

A

Increased thrombosis, demosnstrating these proteisn are improtant in hemostasis

76
Q

What is Factor V Leiden?

A

Single Nucleotide mutation in the Factor V gene (Arg506–>Gln)

common muation in northern Europeans (heteroxygous incidence of 5-10%)

B/c APC-mediated inactivatino of Factor V-Leiden is lsower than normal the risk for venous thrombosis is increased for patients with this mutation

77
Q

What is Plasmin

A

Serine protease that hydrolyzes peptide bonds in the rod-segment of fibrin to break up the fibrin clot (resulting chunks of protein are called fibrin split products)

78
Q

Where does Plasmin come from?

A

proteolytic cleavage of an inactive precursor, PLASMINOGEN , be the serine protease tissue plasmimogen activator (tPA)

79
Q

How is tPA used therapeutically?

A

produced by recombinatn DNA methods has found use as thrombolytic agent in early treatment of MI

80
Q

What is Urokinase and its role?

A

also a serine protease. An activator of plasminogen which is produced in teh kidney and excreted into the urine; believed to dissolve fibrin clots in teh epithelila cell lining excretory ducts

81
Q

What are the two ways to inhibit FIBRINOLYSIS?

A
  1. Plasminogen Activator Inhibitor, PAI
    inactivates tPA and urokinase, thereby inhibitng the conversion of plasminogento plasmin, which in turn ihhibits fibrinoylysis
  2. alpha-2 Plasmin inhibitor (alpha-2-antiplasmin) rapidly inhibits plasmin by formation of a 1:1 complex.

It also preents plasminogen bindign to newly formed fibrin clot.
alpha 2 plasmin is linked to fibrin during coagulation by factor 13a, making fibrin more resistant to breakdown by plasmin

82
Q

What is the role of APC (activated protein C)?

A

Stimulates Fibrinolysis by inactivating PAI01

Inhibiting the inhibitor leads to activation

83
Q

What causes Hemophilia A?

A

Deficiency of Factor VIII

84
Q

Describe Hem A

A

X liked
1/5,000 mean
Queen Victoria was a carreir who passed it on to royal families of PRussia, Russia, Spain

85
Q

What causes Hemophilia B? What is aka

A

Christmas Disease

Deficieny in Factor IX

Defect to Intrinsic TEnase Complex

Tx: Facotr VIII purified from blood

86
Q

Dx Hem B

A

X linked
1/ 30,000 men

Defect to INTRINSIC TENASE COMPLEX

IX purified from blood

87
Q

vWF Disease

A

caused by absence of defect in vWF

Expereince bleeding disorders arising from reduced platelet adhesion,

Most common inherited, autosomal wild type,

88
Q

What is the role of vWF? (2)

A
  1. Prevents degradation of Factor 8

2. Acts as a mediator between collagen and GP Ib-V-IX

89
Q

What is the Bournard-Soulier Syndrome?

A

Cause; Mutation in GP Ib-IX-V receptor that often decreases expression of collagen –> which binds vWF –> which in turn binds to GP IB-IX-V expressed on platelet surface.

Rare disease demsntrates improtance of platelet adhesion to blood clotting

rare (incidence is <1/1,000,000)

90
Q

What is Glanzmann’s Thrombasthenia

A

Mutation in genes that encode GP IIB or GP IIIa- cause qualitative or quantitative abnormalities

rare autosomal recessive bleeding disorder that is

severely reudced or absent platelet AGGREGATION in response to physiological agonists, such as ADP, Thrombin or collagen

91
Q

What are physiological agonists to platelet AGGREGATION

A
  1. ADP
  2. Thrombin
  3. Collagen
92
Q

Antithrombin Deficeinces

A

predispose affected individuals to serious venous and arterial thrombotic disease.

An autosomal domiannt trait, inherited antithrombin deficeinty has a prevelence between 2 in 10,000 and 5 in 10,000 persons

93
Q

What can Actute Arterial Thrombosis cause?

A

Platelet Rich
Most MI and Strokes:

Antiplatelet drugs and fibrinolysis activators are primary therapies

94
Q

What can venous thromboembolism cause?

A

Fibrin Rich
3rd leading cause of CV-asocaited death

Therapy: anticoagulants

95
Q

What is the primary tirgger for arterial thrombosis?

A

rupture of atherosclerotic plaque

they are platelet rich.

96
Q

What are the three possible stesp taht drugs could inhibit for arterial thrombosis?

A

Platelet adhesion
Platelet Activtion
Platelet Aggregation

97
Q

What are ways you can inhibit Arterial Thrombosis (process and drug)

A
  1. Irreversibly inhibit platelet ACTIVATION with ASPIRIN-
  2. Irreversibly inhibit plaletet activation with CLOPIDOGREL (Plavix and Iclid)
  3. Inhibit Platelet AGGREGATION with GPIIb/IIIa R antagonists (Eptifibatide , tirofiban, fab fragment abciximab
  4. activation of fibrinolysis is also a therapy
98
Q

HOw does Aspirin inhibit Platelet Activation?

A

It Acetylates one specific His o sterically hinder substrate entry into active site of COX-1, which is needed to produce Thromboxane A2 (act. platelet and is vasoconstrictor)

99
Q

How does clopidogrel (Plavix) and ticlopidine (Ticlid) inhibit platelet activation?

A

blocks ADP R –> inhigibts platelet aggregation

100
Q

How does eptifibatide (Integrilin) or Tirogiban (Aggrastat) or Fab Frabmetn abciximab (ReoPro) work to inhibt plaetl agregation?

A

They are GPIIb/IIIa R Atagonists

Biochem Winter 2012 (10 decks)

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