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MT2 > Coagulation Cascade > Flashcards

Coagulation Cascade Flashcards

1
Q

coagulation is also known as

A

clotting

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2
Q

the process by which blood changes from a liquid to a gel, forming a blood clot.

A

Coagulation

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3
Q

Coagulation - It potentially results in ________, the cessation of blood loss from a damaged vessel, followed by _______.

A

hemostasis ; repair

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4
Q

in coagulation,

cascades in that as _____ became activated, it in turn activated the next enzyme in _____

A

one enzyme ; sequence

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5
Q

Coagulation factors/ clotting factors:

A

glycoproteins synthesized in the liver (monocytes, ECs, and megakaryocytes: produce few amts)

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6
Q

8: enzymes that circulate in an inactive form

A

(zymogens)

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7
Q

bind, stabilize, and enhance the activity of their respective enzymes.

A

Cofactors

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8
Q

If zymogen activation is uncontrolled and generalized, the condition is called _______

A

disseminated intravascular coagulation (DIC)

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9
Q
  • ultimate substrate of the coagulation pathway
  • Large, stable globulin protein (mw 341,000)
  • Precursor of fibrin (Factor Ia), which forms clot
A

Fibrinogen (Factor I)

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10
Q

When fibrinogen is exposed to thrombin, 2 peptides split from the fibrinogen leaving _______

Monomers aggregate together to form ________

A

fibrin monomer ; polymerized fibrin clot

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11
Q

___________, whose level increases in inflammation, infection, and other stress conditions

A

acute phase reactant protein

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12
Q

Cross-linking of fibrin polymers by factor XIIIa covalently incorporates ________: a plasma protein involved in cell adhesion

A

fibronectin

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13
Q

renders the fibrin mesh resistant to fibrinolysis.

A

a2-antiplasmin

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14
Q
  • Stable CHON (mw 63,000)
  • Converted into thrombin by enzymatic action of thromboplastin in the presence of ionized calcium
  • Half life is almost 3 days
A

Factor II (Prothrombin)

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15
Q
  • Activated form of prothrombin
  • Inert precursor in the circulation
  • Consumed when fibrinogen is converted to fibrin
A

Factor IIa (Thrombin)

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16
Q

In factor IIa (thrombin), a unit will coagulate 1 mL of a ________ in 15 seconds at 28 degrees Celsius

A

standard fibrinogen solution

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17
Q
  • initiates aggregation of platelets
  • considered the key protease of the coagulation pathway
  • plays a role in coagulation (fibrin), in platelet activation, in coagulation control (binding to thrombomodulin to activate protein C), and in controlling fibrinolysis (activates TAFI)
A

Factor IIa (thrombin)

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18
Q

Nonplasma, contains lipoCHON complex from tissues

A

Tissue Thromboplastin (Factor III)

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19
Q

Tissue Thromboplastin (Factor III) is high concentration in

A

Brain, Lung, Vascular Endothelium, Liver, Placenta, Kidneys

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20
Q
  • These tissue types are capable of converting prothrombin to thrombin
  • Transmembrane receptor for factor VIIa
A

Tissue Thromboplastin (Factor III)

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21
Q

Necessary for the activation of thromboplastin and conversion of prothrombin to thrombin

A

Ionized Calcium (Factor IV)

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22
Q
  • Labile globulin CHON
  • Half life is 16 hrs
  • Consumed during clotting and essential in thromboplastin formation
  • Both activated by thrombin and then ultimately inactivated by the generation of thrombin
A

Factor V (Proaccelerin)

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23
Q

bound thrombin activates protein C, which inactivates Va to Vi

A

thrombomodulin

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24
Q
  • A beta globulin
  • Activation of tissue thromboplastin and acceleration of the production of thrombin from prothrombin
  • Reduced by vitamin k antigonists
A

Factor VII (Proconvertin)

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25
Q
  • produced primarily by hepatocytes, & microvascular ECs in lung and other tissues
  • activated by thrombin and inactivated by protein C
  • cofactor to factor IX
  • circulates bound to VWF
A

Factor VIII (Antihemophilic Factor)

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26
Q

unstable in plasma

A

Free factor VIII

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27
Q

During coagulation, thrombin cleaves factor VIII from VWF and activates it. Factor VIIIa binds to activated platelets and forms the _______

A

intrinsic tenase complex

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28
Q

Males with hemophilia A have diminished _______ but normal _______

A

factor VIII activity ; VWF levels

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29
Q

deteriorates more rapidly than the other coagulation factors in stored blood

A

Factor VIII (Antihemophilic Factor)

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30
Q

level drops to approximately 50% after 5 days

A

thawed component plasma

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31
Q

In factor VIII, Replacement therapy transfused according to the _________ of factor VIII

A

12-hour half-life

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32
Q

participates in platelet adhesion and transports the factor VIII

A

VWF

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33
Q

VWF-cleaving protease

A

ADAMTS-13

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34
Q

In TTP: inherited or acquired defective ADAMTS-13 enzyme activity is associated with the presence of ______

A

ultralarge VWF

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35
Q

individuals with VWD: diminished ________ levels

A

factor VIII activity

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36
Q

In factor VIII, _______ individuals have lower levels of VWF than other ABO types

A

Group O

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37
Q

an acute phase protein, as is factor VIII, and levels increase in ______, _____, ______, and _______.

A

pregnancy, trauma, infections, and stress.

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38
Q

Ag is procoagulant Ag as measured by immunological techniques using antibodies for factor VIII:C

A

Factor VIIIC

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39
Q

Ag is a related factor VII ag that was identified by immunological techniques employing heterologous Ab to VIII/vWF

A

Factor VIIIR

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40
Q

RCo demonstrates ristocetin cofactor activity, required for aggregation of human platelets induced by the antibiotic ristocetin

A

Factor VIIIR

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41
Q

synthesize by endothelial cells

A

Factor VIII/vWF

42
Q

Forms the final common pathway through which the products of both the intrinsic and extrinsic thromboplastin generating systems merge to form thromboplastin that converts prothrombin to thrombin

A

Factor X (Stuart Factor)

43
Q
  • A beta globulin
  • Found in serum
  • For thromboplastin-generating mechanism
  • Activated by the contact factor complex and by thrombin
A

Factor XI (Plasma Thromboplastin antecedent)

44
Q

Deficiencies of factor XI: __________

A

Rosenthal syndrome

45
Q
  • Stable factor, consumed in coagulation
  • Absorption of this factor and kininogen to negatively charged surfaces like glass and subendothelium exposed by blood vessel injury initiates the intrinsic coagulation pathway
  • Surface absorption alters and partially activates this factor to factor XIIa by exposing an active enzyme site
A

Factor XII (Hageman Factor)

46
Q

Produces stable fibrin clot in the presence of ionized Ca

A

Factor XIII (Fibrin-stabilizing factor)

47
Q

contact factors AKA _____________

A

intrinsic accessory pathway proteins

48
Q

contact factors include

A

factor XII, high-molecular-weight kininogen (HMWK, Fitzgerald factor), prekallikrein (pre-K, Fletcher factor)

49
Q

activated by contact with negatively charged foreign surfaces

A

Contact factors

50
Q

intrinsic contact factor complex:___________ is a cofactor to factor XIIa and prekallikrein

A

High-molecular-weight kininogen

51
Q

mechanism for activating coagulation in conditions where foreign objects such as mechanical heart valves or bacterial membranes and/or high levels of inflammation are present.

A

Contact Factors

52
Q

_______ transforms ______, a glycoprotein that circulates bound to _____, into its active form _______, which cleaves HMWK to form ________

A

Factor XIIa ; pre-K ; HMWK ; kallikrein ; bradykinin

53
Q

contact factor complex (HMWK:pre-K:FXII) activates ______

A

factor XI

54
Q

Function: Required for coagulation factors to bind to phospholipid (formerly known as factor IV)

Associated Genetic Disorders: —

A

IV Calcium

55
Q

Function: Co-factor of X with which it forms the prothrombinase complex

Associated Genetic Disorders: Activated protein C resistance

A

V (proaccelerin, labile factor)

56
Q

Function: Unassigned – old name of Factor Va
Associated Genetic Disorders: –

A

VI

57
Q

Function: Activates IX, X
Associated Genetic Disorders: congenital factor VII deficiency

A

VII(stable factor, proconvertin)

58
Q

Function: Co-factor of IX with which it forms the tenase complex
Associated Genetic Disorders: Haemophilia A

A

VIII (Antihemophilic factor A)

59
Q

Function: Activates X: forms tenase complex with factor VIII
Associated Genetic Disorders: Haemophilia B

A

IX (Antihemophilic factor B or Christmas factor)

60
Q

Function: Activates II: forms prothrombinasecomplex with factor V

Associated Genetic Disorders: Congenital Factor X deficiency

A

X (Stuart-Prower factor)

61
Q

Function: Activates IX

Associated Genetic Disorders: Haemophilia C

A

XI(plasma thromboplastin antecedent)

62
Q

Function: Activates factor XI, VII and prekallikrein

Associated Genetic Disorders: Hereditary angioedema type III

A

XII (Hageman factor)

63
Q

Function: Crosslinks fibrin

Associated Genetic Disorders: Congenital Factor XIIIa/b deficiency

A

XIII (fibrin-stabilizing factor)

64
Q

Function: Binds to VIII, mediates platelet adhesion
Associated Genetic Disorders:von Willebrand disease

A

von Willebrand factor

65
Q

Function: Activates XII and prekallikrein; cleaves HMWK
Associated Genetic Disorders: Prekallikrein/Fletcher Factor deficiency

A

Prekallikrein/ Pre-K
(Fletcher factor)

66
Q

Function: Mediates cell adhesion

Associated Genetic Disorders: Glomerulopathy with fibronectin deposits

A

fibronectin

67
Q

Vitamin K–Dependent Prothrombin Group

A

Prothrombin (factor II), factors VII, IX, and X and the regulatory proteins protein C, protein S, and protein Z

68
Q

________ is a quinone found in green leafy vegetables and is produced by the intestinal organisms Bacteroides fragilis and Escherichia coli.

A

Vitamin K

69
Q

Makes them (Vit. K dependent prothrombin group) unable to participate in coagulation: __________

A

vitamin K deficiency or in the presence of warfarin/ coumadin

70
Q
  • assembled by the prothrombin grp
  • Composed of vitamin K–dependent serine protease, cofactor, and Ca2+
A

3 membrane complexes

71
Q

what are the 3 membrane complexes

A
  1. Extrinsic Tenase
  2. Intrinsic Tenase
  3. Prothrombinase
72
Q
  • FVIIa + TF (TF-bearing cells)
  • Activates FIX and X
A

Extrinsic tenase

73
Q
  • FIXa + VIIIa (Plt membrane)
  • Activates factor X much more efficiently than the TF:VIIa complex
A

Intrinsic tenase

74
Q
  • FXa + CfVa (Plt surface)
  • converts prothrombin to thrombin
A

Prothrombinase

75
Q

Cofactors in Hemostasis

tissue factor, factor V, factor VIII, and HMWK: _______

A

Coagulation cascade

76
Q

______ : Coagulation control cofactors

A

Thrombomodulin, protein S, and protein Z

77
Q

cofactor binds its particular _________. When bound to their cofactors, serine proteases gain _____ and increased _____

A

serine protease ; stability ; reactivity

78
Q
  • _________ : expressed by vascular ECs
    thrombin cofactor
  • _________ activate protein C and thrombin activatable fibrinolysis inhibitor (TAFI)
A

Thrombomodulin ; thrombomodulin and thrombin

79
Q
  • _______ : a coagulation regulatory protein
  • ______ : fibrinolysis inhibitor
A

Protein C
TAFI

80
Q

cofactor to protein C and TFPI

A

Protein S

81
Q

cofactor to Z-dependent protease inhibitor (ZPI)

A

Protein Z

82
Q
  • activated partial thromboplastin time (aPTT): laboratory test that detects the absence of one or more of these factors
  • Deficiency=prolong test
A

Intrinsic pathway

83
Q

Prothrombin time test (PT): test used to measure the integrity of the extrinsic pathway

A

Extrinsic Pathway

84
Q

This system on activation by factor XIIa generates bradykinin, so named because of the slow contraction of smooth muscle it induces. First, kallikrein is formed from plasma prekaallikrein by the action of prekallikrein activator which is a fragment of factor XIIa. Kallikrein then acts on high molecular weight kininogen to form bradykinin.

A

Kinin System

85
Q

maintain a complex and delicate balance between thrombosis and abnormal bleeding

A

COAGULATION REGULATORY MECHANISMS

86
Q
  • Kunitz-type serine protease inhibitor
  • TFPI: Principal regulator
  • Kunitz-2 binds to and inhibits factor Xa
  • Kunitz-1 binds to and inhibits VIIa:TF
  • inhibits coagulation: 1st binding and inactivating Xa, TFPI:Xa complex then binds to TF:VIIa
    -forming a quaternary complex and preventing further
    activation of X and IX
  • Protein S: cofactor of activated protein C and TFPI and enhances factor Xa inhibition
A

Tissue Factor Pathway Inhibitor (TFPI)

87
Q
  • Triggered by thrombin binds the EC membrane protein thrombomodulin
  • Revises thrombin’s function from a procoagulant enzyme to an anticoagulant
  • EC protein C receptor (EPCR):transmembrane protein that binds both protein C and APC adjacent to the thrombomodulin-thrombin complex
  • Augments the action of thrombin-thrombomodulin at least fivefold in activating protein C to a serine protease
  • APC dissociates from EPCR and binds its cofactor, free plasma protein S
  • Stabilized APC-protein S complex hydrolyzes and inactivates factors Va and VIIIa
  • Protein S: cofactor that binds and stabilizes APC
  • Chronic acquired or inherited protein C or protein S deficiency or its mutation: may be associated with recurrent venous thromboembolic disease
  • purpura fulminans: neonates who completely lack protein C
A

Protein C Regulatory System/protein C anticoagulant system

88
Q
  • Antithrombin (AT): first of the coagulation regulatory proteins to be identified
    = first to be assayed
    = binds and neutralizes thrombin (factor IIa) and factors
    = IXa, Xa, XIa, XIIa, prekallikrein, and plasmin
    = binds thrombin, forming an inactive thrombin-antithrombin complex (TAT)
  • Heparin cofactor II: inactivates thrombin
  • both require heparin for effective anticoagulant activity
A

Antithrombin and Other Serine Protease Inhibitors (Serpins)

89
Q
  • ______ : mast cell granules, EC heparan sulfate
  • ________ :inactivation of thrombin
  • _________ : inactivates factor Xa
A

Heparin
Unfractionated heparin
low-molecular-weight AND pentasaccharide heparins

90
Q
  • ZPI: in the presence of its cofactor, _____, is a potent inhibitor of factor Xa
    -_____ : vitamin K–dependent plasma glycoprotein
  • increases the ability of ZPI to inhibit factor Xa
  • also inhibits factor Xia in the presence of heparin
A

protein Z
Protein Z

91
Q
  • ___________: nonspecific, heparin-binding serpin
  • inhibits a variety of proteases, including APC, thrombin, factor Xa, factor XIa, and urokinase
  • can function as an anticoagulant (inhibits thrombin), as a procoagulant (inhibits thrombin-thrombomodulin and APC), or as a fibrinolytic inhibitor
A

Protein C inhibitor

92
Q
  • The systematic, accelerating hydrolysis of fibrin by bound plasmin
  • TPA and UPA activate fibrin-bound plasminogen several hours after thrombus formation, degrading fibrin and restoring normal blood flow during vascular repair
  • Two activators of fibrinolysis: TPA and UPA
  • released in response to inflammation and coagulation
A

FIBRINOLYSIS

93
Q
  • Kringles: single-chain protein possessing five glycosylated loops
    = Enable plasminogen, along with TPA and UPA, to bind - – fibrin during polymerization
  • Fibrin bound plasminogen becomes plasmin
  • Plasmin: digests fibrin polymer
    = restores blood vessel patency
  • Free plasmin is capable of digesting plasma fibrinogen, factor V, factor VIII, and fibronectin, causing a potentially fatal primary fibrinolysis
    = plasma a2-antiplasmin rapidly binds and inactivates any
    free plasmin
A

Plasminogen and Plasmin

94
Q

Plasminogen Activation

A

TPA - tissue plasminogen activator
UPA - urokinase plasminogen activator

95
Q

hydrolyzes fibrin-bound plasminogen and initiates fibrinolysis by converting plasminogen to plasmin

A

TPA

96
Q
  • Urinary tract epithelial cells, monocytes, and macrophages: secretor
    = incorporated into the mix of fibrin-bound plasminogen
    and TPA at the time of thrombus formation
    = Does not bind firmly to fibrin
A

UPA

97
Q

control of fibrinolysis

A
  1. Plasminogen Activator Inhibitor 1 (PAI-1)
  2. a2-Antiplasmin
  3. Thrombin-Activatable Fibrinolysis Inhibitor (TAFI)
98
Q
  • principal inhibitor of plasminogen activation
  • Inactivating TPA and UPA
  • Platelets store a pool of PAI-1, accounting for more than half of its availability and for its delivery to the fibrin clot
  • Normal: PAI-1 > TPA
  • Fibrinolysis: TPA > PAI-1
  • PAI-1 deficiency: associated with chronic mild bleeding due to increased fibrinolysis
  • acute phase reactant
  • Increased PAI-1 levels correlate with reduced fibrinolytic activity and increased risk of thrombosis
A

Plasminogen Activator Inhibitor 1 (PAI-1)

99
Q
  • Primary inhibitor of free plasmin
  • therapeutic lysine analogues (tranexamic acid and e-aminocaproic acid): antifibrinolytic through their affinity for kringles in plasminogen and TPA
A

a2-Antiplasmin

100
Q
  • activated by the thrombin-thrombomodulin complex
  • antifibrinolytic enzyme: cleaves exposed carboxy-terminal lysine residues from partially degraded fibrin
    = preventing the binding of TPA and plasminogen to
    fibrin
    = blocks the formation of plasmin
  • Increased thrombin formation=increased TAFI activation =decreased fibrinolysis
A

Thrombin-Activatable Fibrinolysis Inhibitor (TAFI)

101
Q
  • Plasmin cleaves fibrin and produces a series of identifiable
  • fibrin fragments: X, Y, D, E, and D-D
  • inhibit hemostasis and contribute to hemorrhage by preventing platelet activation and by hindering fibrin polymerization
  • Fragments X, Y, D, and E: produced by digestion of either fibrin or fibrinogen by plasmin
  • D-dimer: specific product of digestion of cross-linked fibrin only
    = marker of thrombosis and fibrinolysis
    = D-dimer immunoassay is used to identify chronic and acute DIC and to rule out venous thromboembolism
A

Fibrin Degradation Products and D-Dimer

102
Q

Fibrin and fibrinogen degradation products (FDP) are protein fragments resulting from the action of plasmin on fibrin and fibrinogen.

A

Fibrinolysis

MT2 (45 decks)

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