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Coagulation 1 Flashcards

1
Q

What are the basic steps of the hemostasis?

A
  • Injury to cells
  • neurohumoral constriction of blood vessel
  • von Willebrand Factor VWF on ECM initiates cascade
  • Tissue factor
  • Thrombin then fibrin
  • wound heals then remove
  • t-PA tissue plasminogen activator and endothelian
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2
Q

How do endothelial cells maintain blood fluidity?

A
  • Regulate vessel tone >> secrete endothelin >> a potent vasoconstrictor
  • Prevent plt aggregation & promote vasodilation >> secrete prostacyclin, nitric oxide
  • Synthesize and secrete membrane associated heparin-like molecules (heparan sulphate) and thrombomodulin
  • Modulate fibrinolysis
    • synthesize tissue plasminogen activator t-PA
    • synthesis plasminogen activators inhibitors (PAIs)
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3
Q

How do anticoagulants work?

A

Prevent interaction with adhesive proteins like collagen, VWF, Tissue Factor

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4
Q

What is tissue factor?

A
  • Membrane protein located in smooth muscle, fibroblasts, and macrophages
  • is the trigger for initiation of coagulation
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5
Q

What are the prothrombotic properties of endothelial cells?

A
  • Synthesis, storage, and release of vWF
  • storage and relase of factor VIII
    • Weibel-Palade bodies
  • Synthesize tissue factor
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6
Q

What are the important parts of platelets?

A

The dense body and the alpha granule

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7
Q

What are the chemicals in the Dense Body of platelets?

A

ADP, ATP , serotonin, calcium

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8
Q

What are the chemicals in alpha granules of platelets?

A

VWF, Factor V, Platelet Factor 4 (PF4) , fibrinogen

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9
Q

What are the three As of coagulation?

A
  • Adhesion: to subendothelium mediated by vWF (especially at high shear rate) at site of injury
  • Activation: metabolic >> secretion, membrane shape change and surface GPIIb/IIIa alteration
  • Aggregation: fibrinogen cross-links GPIIb/IIIa, surface phospholipid exposed (coagulation matrix), and mechanical contraction (actomyosin)
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10
Q

Explain the Concept of Anti-platelet Therapy.

A

Inhibition of inappropriate platelet activation can prevent stroke, may prevent ischemic heart disease, retard coronary artery re-stenosis after coronary angioplasty or stenting

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11
Q

What are anti-platelet drugs?

A
  • Aspirin: irreversibly inhibits platelet cyclo-oxygenase-1 (COX-1)
  • Non-steroidal anti-inflammatory agents (e.g. ibuprofen): reversibly inhibit COX-1
  • Clopidogrel (Plavix): blocks ADP receptor
  • Abciximab (Reopro) and tirofiban (Aggrastat): block GPIIb/IIIa
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12
Q

Aspirin vs NSAIDs… which reversibly vs irreversibly block COX-1?

A
  • Aspirin >> irreversibly
  • NSAIDS >> reversibly
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13
Q

Where are the sites of synthesis and storage of

von Willebrand factor?

(hint: there are two for each)

A
  • Synthesized in Endothelial cell and stored in Weibel-Palade body
  • synthesized in megakaryocyte/platelet and stored in the alpha-granule
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14
Q

Explain the constituitive and stimulated secretion of vWF.

A
  • Constitutive:
    • from endothelium into plasma,mean (100%) = 10 ug/mL
    • normal range 40-240%
  • Stimulated:
    • from endothelium by thrombin, fibrin, histamine, and DDAVP
    • from platelet alpha- granules upon activation
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15
Q

What are the functions of vWF (class)?

A
  • Adhesion
    • Conformational change on binding to sub-endothelial collagens, esp. at high shear rates leads to binding to platelet GPIb
  • Aggregation
    • Binds platelet GPIIb/IIIa
  • FVIII binding
    • Protects FVIII from proteolytic cleavage
    • Brings FVIII to site of hemorrhage
    • FVIII:vWF ≈ 50:1 molar ratio (FVIII: vWF monomer)
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16
Q

Explain platelet activation.

A

When the endothelium is damaged, the normally isolated, underlying collagen is exposed to circulating platelets, which bind directly to collagen with collagen-specific glycoprotein Ia/IIa surface receptors.

This adhesion is strengthened further by von Willebrand factor (vWF), which is released from the endothelium and from platelets

vWF forms additional links between the platelets’ glycoprotein Ib/IX/V and the collagen fibrils.

These adhesions also activate the platelets

17
Q

What are the functions of vWF (wiki)

A
  • Factor VIII is bound to vWF while inactive in circulation; factor VIII degrades rapidly when not bound to vWF. Factor VIII is released from vWF by the action of thrombin.
  • vWF binds to collagen, e.g., when it is exposed in endothelial cells due to damage occurring to the blood vessel.
  • vWF binds to platelet gpIb when it forms a complex with gpIX and gpV; this binding occurs under all circumstances, but is most efficient under high shear stress (i.e., rapid blood flow in narrow blood vessels, see below).
  • vWF binds to other platelet receptors when they are activated, e.g., by thrombin (i.e., when coagulation has been stimulated).
18
Q

What is Factor

I

II

III

IV

V

VII

VIII

IX

X

XI

XII

XIII

also know: prekallikrein and high molecular weight kininogen

A

I = fibrinogen

II = prothrombin

III = tissue factor or thromboplastin

IV = Ca++

V = proaccelerin

VII = proconvertin

VIII = antihemophilic A

IX = antihemophilic B

X = stuart factor

XI = plasma thromboplastin antecedent

XII = hageman factor

XIII = fibrin stablizing factor

19
Q

fyi

What factors are enzymes?

What factors are cofactors?

What are miscellaneous factors?

A

What factors are enzymes?

Factor IIa
Factor VIIa
Factor IXa
Factor Xa
Factor XIa
Protein C
tPA
plasmin

What factors are cofactors?

Tissue factor
Factor V
Factor VIII
Protein S

What are miscellaneous factors?

Fibrinogen
Factor XIII
Alpha2-antiplasmin
PAI-1
Antithrombin

20
Q

What factors are vitamin K dependent?

A

Factor 2
Factor 7
Factor 9
Factor 10

21
Q
A

Thrombin is a master conductor

22
Q

What is the function of Factor XIII?

A

In the coagulation cascade, factor XIIIa functions to stabilize the fibrin clot by crosslinking the Lysine and glutamine side chains of α- and γ-chains of fibrin to form homopolymers

23
Q

What is the quaternary complex?

A

Enzyme

Co-factor

phospholipid surface

Ca ions

24
Q

What are endogenous anti-coagulants?

A

mostly endothelial derived molecules (heparin-like)

or proteins (thrombomodulin, t-PA, PAI-1)

25
Q

In anticoagulation therapy…

What decreases procoagulant factors?

What inhibits thrombin?

What are fibrolytic agents to lyse clot?

A
  • decrease procoagulant factors:
    • Oral vitamin K antagonist Coumadin
    • decreases factors II,VII,IX,X (a.k.a. “blood thinner”)
  • Inhibit action of thrombin (and factor Xa)
    • Heparin and derivatives
    • R-hirudin
  • Fibrinolytic agents to lyse clot
    • endogenous:
    • t-PA
    • urokinase
    • streptokinase
26
Q

What are the anticoagulant mechanisms?

A

Antithrombin system

Protein C system

Fibrinolytic system

27
Q

What are the components of the following anticoagulant mechanisms…

Antithrombin system?

Protein C system?

Fibrinolytic system?

A
  • Antithrombin system
    • antithrombin III + heparins
  • Protein C system
    • thrombomodulin
    • protein C
    • protein S
  • Fibrinolytic system
    • plasminogen activators
    • plasmin
    • plasminogen activator inhibitors
    • plasmin neutralizers
28
Q

What happens in the antithrombin system?

A
  • Antithrombins plus endogenous heparin-like molecules inactivate Thrombin IIa
  • Neutralizing Thrombin IIa downregulates
    • IXa
    • Xa
    • XIa
    • XIIa
29
Q
A
30
Q

In the protein C system…

What is thrombomodulin? What does it do?

What is Protein C? What does it do?

What is Protein S? What does it do?

A

Thrombomodulin is an endothelial membrane bound protein. It binds thrombin + protein C >> activated proteinC

Protein C is a vit K dependent protein

Protein S is a vit K dependent protein and a co-factor for Protein C

Activated Protein C + PrS >> inactivates factor Va and VIIIa

31
Q
A
32
Q

Explain the events of the fibrolytic system.

A
  • Three proteins
    • t-PA Tissue Plasminogen activator
    • u-PA Urokinase
    • Streptokinase
  • convert plasminogen (produced in the liver) to plasmin-serine protease
  • cleaves fibrin
33
Q

What is the role of Plasminogen Activator Inhibitor PAI-1?

What is the role of alpha-2 antiplasmin?

A

PAI-1 inactivates excess t-PA

alpha-2 antiplasmin inactivates plasmin that escapes into the plasma

34
Q
A
35
Q
A
36
Q
A

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