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AU 15 - Pharm Final > Hemostasis/Anti-coagulants > Flashcards

Hemostasis/Anti-coagulants Flashcards

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1
Q

Hemostasis

A

The process which causes bleeding to stop

Meaning to keep blood within a damaged blood vessel

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2
Q

What is the opposite of hemostasis?

A

Hemmorrhage

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3
Q

What are the steps of blood clot formation?

A

1) Vessel constriction
2) Platelet adhesion, activation, and aggregation
3) Cross-linking of fibrin through the coagulation cascade

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4
Q

What is produced by vascular epithelial cells upon injury?

A

Prostaglandin F 2a

Thromboxane A2

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5
Q

Prostaglandin F 2a

Thromboxane A2

A

Potent vasoconstrictors acting on smooth muscle helping to limit hemorrhage

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6
Q

What is exposed at an injury site and what does that allow?

A

Extracellular matrix
Allows platelets to bind to the matrix proteins collagen, fibronectin, and von Willebrand factor
Binding also leads to platelet activation

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7
Q

What is secreted by activated platelets?

A 
Thromboxane A2 (vasoconstriction)
Prostaglandin F 2a (vasoconstriciton)
ADP (platelet aggregation)
Serotonin (vasoconstriction and platelet aggregation)
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8
Q

What does platelet activation lead to?

A

A conformation change in an integrin receptor that allows it to bind fibrinogen (a plasma protein)
The platelets aggregate as a result of fibrinogen cross-linking

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9
Q

What is happening as platelet aggregation and activation is taking place?

A

Extrinsic and intrinsic coagulation pathways are initiated

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10
Q

Which is more important, the extrinsic or the intrinsic coagulation pathway?

A

Extrinsic

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11
Q

Factor VII

A

A serine protease that needs to be activated to become Factor VIIa

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12
Q

How does Factor VII become activated?

A

Once complexed with TF (tissue factor), VII can be activated by proteolytic cleavage by proteases such as thrombin, Xa, IXa, XIIa, and TF-VIIa itself

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13
Q

Tissue Factor (TF)

A

Present in the basement membrane (extracellular matrix of endothelial cells, subendothelium)
It is not exposed to the blood unless tissue is damaged

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14
Q

Once you have TF-VIIa, what happens?

A

It can activate Factors IX and X (but IX is more important)

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15
Q

What does the IXa-VIIIa complexes do?

A

Allow for the formation of Xa-Va complexes

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16
Q

Xa-Va complexes

A

Cleave prothrombin (II) to make thrombin (IIa) - producing an enzyme that will create a blood clot

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17
Q

Thrombin (factor IIa)

A

Cleaves fibrinogen and exposes binding sites, resulting in the formation of a fibrin mesh

Thrombin will also cleave and activate the clotting factors V, VIII, and XI

Thrombin also activates Factor XIII - an enzyme that cross links the fibrin mesh - creating a blood clot

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18
Q

Thrombosis

A

The formation or presence of a blood clot in a blood vessel

The vessel may be any vein or artery

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19
Q

What is a blood clot also referred as?

A

Thrombus

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20
Q

What is it called if a clot breaks loose and travels through the blood stream?

A

Thromboembolism

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21
Q

Antithrombin

A

Small protein molecule that inactivates several enzymes of the coagulation system
Produced in the liver

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22
Q

What can increase Antithrombin’s activity?

A

The anticoagulant drug Heparin

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23
Q

How does Heparin work?

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A

Enhances the binding of antithrombin to Factor II and Factor X

24
Q

Protein C

Study These Flashcards
A

The activated form plays an important role in regulating coagulation

25
How does APC (Activated Protein C) regulate coagulation?
Primarily by inactivating proteins Factor Va and Factor VIIIa
26
What promotes the activation of Protein C?
The presence of Thrombomodulin and Endothelial Protein C Receptors (EPCR)
27
Tissue Factor Pathway Inhibitor
A single chain polypeptide which can reversibly inhibit Factor Xa While Factor Xa is inhibited, Xa-TFPI can also inhibit the FVIIa-tissue factor complex
28
Fibrinolysis
The process that prevents blood clots from gorwing and becoming problematic
29
Tissue plasminogen activator (tPA)
Secreted by endothelial cells | Clot dissolver used to treat heart attacks
30
Urokinase
Clot dissolver used to treat heart attacks
31
Disseminated Intravascular coagulation
Pathological process characterized y the widespread activation of the clotting cascade that results in the formation of blood clots in the small blood vessels throughout the body This leads to compromise of tissue blood flow and can ultimately lead to multiple organ damage In addition, as the coagulation process consumes clotting factors and platelets - normally clotting is disrupted and severe bleeding can occur form various sites
32
Fibrinolytics
Used to lyse thrombi/clot to recanalize the occluded blood vessel Work by activating the Fibrinolytic system
33
Anti-coagulant drugs
Agents that prevent the formation of blood clots by affecting the blood coagulation factors The mechanism of action varies depending on the agent
34
What disease are anti-coagulant used to treat?
Used to threat thrombotic and thromboembolic diseases such as stroke, myocardial ifarction, deep vein thrombosis, and pulmonary embolism
35
Heparin
Widely used as an injectable anticoagulant and has the highest negative charge density of any known biological molecule Can also be used to form an inner anticoagulant surface on various experimental and medical devices such as test tubes and renal dialysis machines
36
Indirect thrombin inhibitors
Act on antithrombin (AT) | Heparin binds to AT and increases its activity 1000 fold
37
What is an adverse effect of heparin?
Bleeding
38
Fondaparinux
An indirect thrombin inhibitor | Works the same as heparin
39
What are some examples of Direct Thrombin Inhibitors
Hirudin Bivalirudin Argatroban
40
Hirudin
Naturally occurring peptide in the salivary glands of medicinal leeches that has a blood anticoagulant property This is fundamental for the leeches' alimentary habit of hematophagy since it keeps the blood flowing after the initial phlebotomy performed by the worm on the host's skin
41
Bivalirudin
Specific and reversible direct thrombin inhibitor (DTI) | Chemically, it is a smaller synthetic version of hirudin
42
Argatroban
Anticoagulant that is a small molecule direct thrombin inhibitor
43
What are the two ways DTIs can bind to Thrombin and inhibit it?
1) Bind to both the active site and exosite 1 (bivalent) | 2) Bind to just the active site (univalent)
44
What are the two types of oral direct thrombolytics?
Thrombin Inhibitors | Coumarin anticoagulants
45
What is required for thrombin (and other clotting enzymes) to become catalytically competent?
They must undergo a carboxylation reaciton
46
What is required for the carboxylation reaction of thrombin?
The oxidation of Vitamin K
47
How do Coumarin anticoagulants work?
They block the conversion of vitamin K back to the reduced form - without this conversion, the body runs out of reduced vitamin K and thrombin will not become enzymatically active
48
What must you balance when prescribing Warfarin?
Must balance the threat of stroke versus intracerebral hemorrhage
49
Many drugs interact with Warfarin, which ones are serious?
Those that increase the anticoagulant effect and increase bleeding
50
What are the antidotes for Warfarin overdose?
Vitamin K | Aqua Mephyton
51
What are the antidotes for Heparin overdose?
Protamine Sulfate
52
Thromboxane A2
A type of thromboxane that is produced by activated platelets and has prothrombotic properties - it stimulates activation of new platelets as wells as increases platelet aggregation
53
How does Thromboxane A2 work?
Increases the expresison of the glycoprotein complex GPIIb/IIIa on the cell membrane of platelets - the same effect is also achieved by ADP in platelet stimulation
54
What anticoagulants work by blockage of platelet Aggregation?
``` Aspirin Clopidogrel Ticlopidine Epifibatide Tirofiban ```
55
Aspirin mechanism
Inhibits Thromboxane A2 synthesis
56
Clopidogrel and Ticlopidine mechanism
Blockage of ADP synthesis
57
Epifibatide and Tirofiban mechanism
Blockage of GPIIb/IIIa

AU 15 - Pharm Final (7 decks)

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