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Pharmacology > Anticoagulants > Flashcards

Anticoagulants Flashcards

1
Q

What is aspirin? What is it used for?

A 
COX I and II inhibitor
Used as a prophylactic treatment ("baby")
Following an MI, higher dose
Prevents cerebral ischemia and MI
Benefit is not clear in females
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2
Q

What is clopidogrel? What is it used for?

A

ADP receptor antagonist (stops ADP from binding to platelets)
Prevents ischemic stroke and MI (given routinely during stent insertion of an MI)

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3
Q

What are some examples of antithrombin III activators? What binds them?

A

Heparin and LMW heparin

Protamine sulfate binds them (can stop excessive bleeding)

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4
Q

What is rivaroxaban? What binds it?

A

An orally active direct factor Xa (prevents prothrombin conversion to thrombin) inhibitor
Bound by andexanet alfa (given to reverse excessive bleeding)

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5
Q

What is warfarin?

A

Coumarin. A competitive vitamin K antagonist

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6
Q

Why is vitamin K important?

A

It is an important cofactor needed in the synthesis of coagulation factors (II, VII, IX, X)

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7
Q

What is dabigatran? What binds it?

A

An orally active direct thrombin inhibitor

Bound by idarucizumab (given IV if excessive bleeding)

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8
Q

What is hemostasis?

A

The process of arresting the loss of blood from injured vessels.

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9
Q

What is a hemostatic plug?

A

A plug formed by aggregated platelets and then stabilized by cross-linked fibrin.

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10
Q

What is thrombosis?

A

The unwanted formation of a hemostatic plug or clot inside a blood vessel or heart chamber.

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11
Q

What is a thrombus?

A

A blood clot attached to a blood vessel that may obstruct flow or pieces can break off to plug capillaries.

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12
Q

What is an emboli?

A

A portion of a thrombus that breaks away. A clot floating around in the blood. Will get stuck in the capillaries and can do damage depending on where it lodges (heart, brain, lung)

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13
Q

What is the difference between arterial and venous clots?

A

Arterial are platelet rich and venous are red blood cell rich.

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14
Q

What is atherosclerosis?

A

A build up of plaque from excess cholesterol that may partially obstruct the flow of the artery. It will eventually damage the endothelium, forming a thrombus. Both will then block blood flow.

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15
Q

What can cause an arterial thrombic disorder?

A

Damaged endothelial layer due to atherosclerosis or physical damage caused by stenting or balloon angioplasty

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16
Q

What are the different effects caused by placement of the emboli in different areas?

A

Lodged in cerebral capillary, acute ischemic stroke
Lodged in coronary artery, acute MI
Lodged in lung capillaries, pulmonary embolism

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17
Q

What is venous thrombosis?

A

Involves red blood cells, not platelets (antiplatelet drugs won’t work) and related to stagnant flow in the veins and/or atria

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18
Q

What are the major sites that venous clots can form?

A 
Lower leg veins (deep vein thrombosis-DVT)
Right atria (if not contracting properly)
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19
Q

When is a time that venous clots may form?

A

Post surgery, long term bed rest, sitting (long plane rides)

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20
Q

Where do arterial clots usually form?

A

Carotid artery or coronary artery

21
Q

What are the steps of hemostasis?

A

Formation of a platelet plug (platelet adhesion, activation, aggregation), Coagulation (clot formation, stabilizes, thrombin increases fibrin formation) and fibrinolysis (clot dissolving to remove clot as wound heals)

22
Q

Which drugs are platelet inhibitors?

A

Aspirin, Clopidogrel and Abciximab

23
Q

Which drugs are anticoagulents?

A

Heparin, Warfarin, Dabigatran and Rivaroxaban

24
Q

Which drug is a thrombolytic agent?

A

Tissue plasminogen activator (tPA)

25
Q

What is the lifecycle of fibrin?

A

Fibrinogen is converted to fibrin by thrombin (produced by coagulation pathway). Fibrin is broken down by plasmin.

26
Q

What does prostaglandin I2 (PGI2) or prostacyclin do?

A

Secreted by the healthy endothelial cells to stabilize platelets by inhibiting mediator release and preventing GPIIb/IIIa receptor activation on platelets

27
Q

What are the steps to the formation of a platelet plug?

A

Damaged endothelium (exposed collagen) causes platelets to stick. The platelets are activated and release thromboxane A2 (TxA2), ADP and serotonin to excite other platelets which come to form the platelet plug. GPIIb/IIIa receptors are activated and bind fibrinogen linking platelets leading to more aggregation.

28
Q

How can we prevent platelet plug formation?

A

Possibly change prostaglandin levels (increase/maintain pro

29
Q

How do COX inhibitors (NSAIDS) work?

A

Irreversibly inhibits cyclo-oxygenase, an enzyme necessary in the formation of prostaglandins like TxA2 and PGI2

30
Q

What do TxA2 and PGI2 do?

A

TxA2 promotes aggregation of platelets
PGI2 increases stability of platelets (less likely to aggregate)
A balance between the two determines how “sticky” the platelets will be.

31
Q

How long would the effects of the COX inhibitor last for the platelet?

A

Platelets cannot generate new COX because they don’t have a nucleus. So for they would be without for their entire lifespan (7-10 days)
Vascular endothelial cells produce more COX and therefore PGI2 in response.

32
Q

What are some problems with platelet inhibitors?

A 
Problems associated with increased bleeding 
Hemorrhagic stroke (stroke from bleeding in brain), GI bleeding and easy bruising
33
Q

How does ADP affect platelet plug formation?

A

The binding of ADP to platelets activates the GP IIb/IIIa receptors, thus allowing fibrinogen to link the platelets and aggregate more.

34
Q

What does abciximab do?

A

Given IV. It is a monoclonal antibody against the GP IIb/IIIa receptor that is important to aggregate platelets.
By blocking this receptor, you prevent fibrinogen from joining platelets and thus stopping their aggregation and formation of the plug.

35
Q

How does coagulation work?

A

Two complex pathways of clotting factors convert prothrombin to thrombin. Thrombin then converts fibrinogen to fibrin (threads to hold and strengthen clot)
Without fibrin, the clot dissolves

36
Q

What are the two coagulation pathways?

A

Intrinsic pathway in which factors are released at the site of damage.
Extrinsic pathway in which tissue factors are released from somewhere else.

37
Q

What is low vitamin K associated with?

A

Bleeding disorders.

38
Q

What does antithrombin III do?

A

Naturally inactivates thrombin and factor Xa, decreasing fibrin formation.

39
Q

How does heparin work?

A

Leads to thrombin inactivation by binding to antithrombin and increasing its activity.
Less conversion of fibrin from fibrinogen.

40
Q

When is heparin used?

A

In prevention of arterial and venous thrombosis following surgery or thrombolytic treatment.
In treatment of pulmonary embolism and acute MI
Anticoagulant drug of choice in pregnancy.

41
Q

What is the difference between heparin and low molecular weight heparin?

A

Both are given parenterally (IV or deep subcutaneous)
LMWs are way more bioavailable, with predictable effects, longer half life and less frequent bleeding. Can be given to outpatients.

42
Q

Why is warfarin useful?

A

An oral anticoagulant (more convenient).

But requires constant monitoring/visits to a clinic to measure prothrombin/INR ratio

43
Q

How long do the anticoagulation effects of warfarin take?

A

8-12 hours to be effecttive. Start with heparin then switch to warfarin.

44
Q

How can you treat excessive bleeding or a warfarin overdose?

A

Administration of vitamin K, antidote

45
Q

What class of drugs are dabigatran and rivaroxaban?

A

Novel oral anticoagulents, orally active and more predictable than with warfarin (don’t have to be constantly monitored)

46
Q

When are novel oral anticoagulents used?

A

Percutaneous cardiac interventions, venous thromboembolism and post surgery hip/knee replacement

47
Q

What is tissue plasminogen activator (tPA)? What is it used for?

A

A fibrinolytic that activates tissue plasminogen.

Used to treat MI, massive pulmonary embolism and acute ischemic stroke. Earlier treatment is better.

48
Q

How does plasminogen work?

A

Converted to plasmin by streptokinase. Plasmin then degrades fibrin, dissolving the clot.

49
Q

What is the problem with fibrinolytic drugs?

A

Do not distinguish between fibrin of a beneficial hemostatic plug and unwanted thrombi. Can cause bleeding in an unknown lesion.

Pharmacology (11 decks)

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