Blood Physiology Part 5 Flashcards

(34 cards)

1
Q

What does opposition of clot formation help?

A

helps to limit clot formation process and prevent it from spreading excessively.

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2
Q

What are the mechanisms that oppose clot formation?

A

• Tissue factor pathway inhibitor (TFPI)
2 Protein C system
3 Antithrombin Ill

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3
Q

What secretes Tissue factor pathway inhibitor (TFPI)?

A

Endothelial cells

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4
Q

How does TFPI oppose clot formation?

A

It binds to tissue factor-factor VIla complexes and inhibits the
ability of these complexes to generate factor Xa.

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5
Q

Thrombin can bind to an endothelial
cell receptor known as?

A

thrombomodulin.

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6
Q

What does the binding of thrombin to thrombomodulin cause ?

A

This binding eliminates all of thrombin’s clot- producing effects and causes the bound thrombin to bind a particular plasma protein, protein C

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7
Q

How does the protein C system oppose clot formation?

A

The binding to thrombin activates protein C, which, in combination with yet another plasma protein, then inactivates factors VIlla and Va.

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8
Q

How does antithrombin III oppose clot formation?

A

Antithrombin III inactivates thrombin and several other clotting factors

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9
Q

What greatly enhances the activity of antithrombin Ill ?

A

Binding to the heparin on the surface of
endothelial cells

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10
Q

What is the effect of the endothelial barrier between blood and subendothelial connective tissue?

A

It prevents platelet aggregation and the formation of tissue factor–factor VIIa complexes.

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11
Q

What is the function of PGI₂ and nitric oxide released by endothelial cells?

A

They inhibit platelet activation and aggregation.

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12
Q

What is the role of tissue factor pathway inhibitor secreted by endothelial cells?

A

inhibits the ability of tissue factor–factor VIIa complexes to generate factor Xa.

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13
Q

How does endothelial binding of thrombin via thrombomodulin help in anticoagulation?

A

activates protein C, which inactivates clotting factors VIIIa and Va.

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14
Q

What is the role of heparin molecules on endothelial plasma membranes?

A

They bind antithrombin III, which then inactivates thrombin and other clotting factors.

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15
Q

What is the function of tissue plasminogen activator secreted by endothelial cells?

A

catalyzes the formation of plasmin, which dissolves clots.

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16
Q

What is a fibrin clot?

A

fibrin clot is not designed to last forever. It is a temporary fix until permanent repair of the vessel
occurs. •

17
Q

What is the fibrinolytic system?

A

• The fibrinolytic system is the principal effector of clot removal.

18
Q

What does tge fibrinolytic system constitute?

A

a plasma proenzyme, plasminogen, which can be activated to the active enzyme plasmin by protein plasminogen activators. Once formed, plasmin digests fibrin, thereby dissolving the clot.

19
Q

What secretes Tissue plasminogen activator (t-PA)

A

The endothelial cells

20
Q

What happens during clotting?

A

both plasminogen and t-PA bind to fibrin and become incorporated throughout the clot.

21
Q

Why is the The binding of t-PA to fibrin crucial?

A

because t-PA is a very weak enzyme in
the absence of fibrin.

22
Q

What dissolves a clot after it is formed.?

A

Thrombolytic therapy

23
Q

What significantly reduces myocardial
damage and mortality?

A

Intravenous administration of recombinant t-PA within a few hours after myocardial infarction

24
Q

Recombinant t-PA has also been in reducing???

A

brain damage following a stroke caused by blood vessel occlusion

25
Why is t-PA application limited?
because of increased risk of hemorrhagic transformation beyond the time window
26
What is ischemic stroke?
Ischemic stroke is an emergency condition in clinic, characterized by a sudden loss of blood flow to an area of brain because of blockage of thrombus.
27
What is s the currently used intravenous thrombolytic agent for acute ischemic stroke?
tPA (tissue-type plasminogen activator)
28
Is tpA treatment safe?
Yes it is But its efficiency is greatly restricted by the short time window of 3 to 4.5 hours after onset of symptoms.
29
What is the major challenge for tPA treatment ?
hemorrhagic transformation (HT), particularly for the patients who received a delayed administration of tPA.
30
What is needed to counteract hemorrhagic transformation (HT?
an adjunctive remedy is needed to counteract HT after tPA treatment
31
What underlies HT after tPA ?
Blood brain barrier disruption
32
What happens to the blood-brain barrier (BBB) after delayed tPA treatment?
It becomes disrupted, leading to bleeding and worsened injury due to excessive degradation of tight and adherens junction proteins
33
What are the two main categories of hemostatic disorders?
Thromboembolic disorders and bleeding disorders
34
What are examples of thromboembolic disorders?
• Cerebral infarction • Myocardial infarction • Deep venous thrombosis