Antiplatelet and Anticoagulant drugs Flashcards

1
Q

What is hemostasis?

A

The process of stopping bleeding while maintaining blood flow.

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2
Q

What are the four steps of hemostasis?

A

1) Vasoconstriction
2) Primary Hemostasis
3) Secondary Hemostasis
4) Fibrinolysis

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3
Q

Which molecule causes vasoconstriction at the injury site?

A

Endothelin (released from endothelial cells).

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4
Q

What do platelets bind to at the injury site?

A

von Willebrand factor (vWF) & collagen.

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5
Q

What happens when platelets are activated?

A

They change shape, degranulate, and release ADP & TXA2.

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6
Q

What is the role of ADP & TXA2?

A

They recruit & aggregate more platelets to form a platelet plug.

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7
Q

What stabilizes the platelet plug?

A

Fibrin (formed via coagulation cascade).

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8
Q

Which key coagulation factors are involved?

A

Factor X, Factor II (thrombin), and Factor I (fibrinogen).

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9
Q

What enzyme breaks down the clot?

A

Plasmin.

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10
Q

Which enzyme activates plasmin from plasminogen?

A

Tissue plasminogen activator (t-PA).

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11
Q

What causes arterial thrombosis?

A

Atherosclerotic plaque rupture or erosion.

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12
Q

Which process is primarily involved in arterial thrombosis?

A

Platelet activation.

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13
Q

What conditions are associated with arterial thrombosis?

A

Heart attacks (myocardial infarction), strokes, peripheral vascular disease.

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14
Q

What type of drugs are used for prevention/treatment arterial thrombosis?

A

Antiplatelet drugs (e.g., aspirin, clopidogrel).

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15
Q

What causes venous thrombosis?

A

Thrombophlebitis (inflammation of vein walls) or static blood flow.

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16
Q

Which process is primarily involved in venous thrombosis?

A

Activation of the coagulation cascade.

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17
Q

What conditions are associated with venous thrombosis?

A

Deep vein thrombosis (DVT) and pulmonary embolism.

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18
Q

What type of drugs are used for prevention/treatment of venous thrombosis?

A

Anticoagulants (e.g., heparin, warfarin, rivaroxaban).

19
Q

What enzyme produces TxA2?

A

COX-1 enzyme from arachidonic acid.

20
Q

What is the function of TxA2?

A

Promotes platelet activation and aggregation.

21
Q

How does aspirin affect TxA2?

A

Aspirin irreversibly inhibits COX-1, preventing TxA2 synthesis and reducing platelet activation.

22
Q

Where is Adenosine Diphosphate released from?

A

Activated platelets.

23
Q

What is the function of Adenosine Diphosphate in platelet activation?

A

Binds to ADP receptors to mediate calcium release and enhance platelet activation.

24
Q

How does clopidogrel (Plavix) work?

A

Antagonizes ADP receptors on platelets, preventing ADP-mediated activation.

25
Q

What is the role of Factor X in the coagulation cascade?

A

Links the intrinsic and extrinsic pathways to the common pathway by converting to active Xa.

26
Q

How is thrombin (Factor IIa) generated?

A

Factor Xa activates prothrombin (Factor II) to thrombin (Factor IIa).

27
Q

What is the function of thrombin?

A

Converts fibrinogen (Factor I) into fibrin, forming a stable clot.

28
Q

How does the coagulation cascade contribute to thrombosis?

A

Converts soluble fibrinogen to insoluble fibrin strands, stabilizing the platelet plug into a thrombus.

29
Q

What happens in pathological conditions with excessive coagulation activation?

A

Can lead to harmful clot formation, increasing the risk of stroke, heart attack, or deep vein thrombosis.

30
Q

What are the advantages of warfarin?

A

Oral administration.
Has an antidote (vitamin K).

31
Q

What are the disadvantages of warfarin?

A

Delayed onset (72hrs to peak).
Requires monitoring (PT-INR).
Many drug/food interactions.
Variable effectiveness between patients.

32
Q

What are the advantages of rivaroxaban?

A

Fixed dosing, no monitoring needed.
Few drug interactions.
Rapid onset.
Predictable effect.

32
Q

What is the mechanism of warfarin?

A

Inhibits vitamin K-dependant clotting factors

33
Q

What are the disadvantages of rivaroxaban?

A

No readily available antidote.
Still carries bleeding risk.

34
Q

What is the mechanism of rivaroxaban?

A

Direct factor Xa inhibitor

35
Q

What are the advantages of heparin?

A

Immediate effect.
Can be used in kidney/liver disease.
Has an antidote (protamine).

36
Q

What are the disadvantages of heparin?

A

Requires injection/IV.
Short half-life (1hr).
Risk of thrombocytopenia.
Allergic reactions possible (animal product).

37
Q

What is the mechanism of heparin?

A

Enhances antithrombin activity to inhibit factor Xa and thrombin

38
Q

What conditions are antiplatelet drugs used to prevent?

A

Arterial thrombosis (e.g., stroke, heart attack, coronary artery disease).

39
Q

What conditions are anticoagulant drugs used for?

A

Deep venous thrombosis (DVT).
Atrial fibrillation.
Pulmonary embolism.
Mechanical heart valves.
Knee/hip replacement therapy.
Myocardial infarction.

40
Q

What is the bleeding risk for patients on anticoagulants and antiplatelet drugs?

A

Prolonged bleeding after dental procedures.

41
Q

Why should NSAIDs be avoided with anticoagulants and antiplatelet drugs?

A

Increased risk of gastrointestinal bleeding.

42
Q

What can alter warfarin levels?

A

Antibiotics, antifungals, and pain meds can affect warfarin levels, requiring dose adjustments.

43
Q

Key Takeaways for Dental Practice

A

Assess bleeding risk before procedures.
Coordinate with physicians for patients on anticoagulant therapy.
Consider local hemostatic measures (e.g., sutures, tranexamic acid) for surgical procedures.
Educate patients on bleeding risks and signs of complications.
May require medication adjustment/discontinuation
Consider alternative pain medications to NSAIDs
Be aware of herbal supplements that affect bleeding risk