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Cardiology > Anti-platelet, anti-coagulant and thrombolytic drugs > Flashcards

Anti-platelet, anti-coagulant and thrombolytic drugs Flashcards

1
Q

Which clotting factor is factor 2?

A

Thrombin

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2
Q

What kind of thrombus is a white thrombus? (Arterial/venous)

A

Arterial

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3
Q

What kind of thrombus is a red thrombus? (Arterial/venous)

A

Venous

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4
Q

Which organs do white thromboemboli generally tend to occlude the blood supply to?

A

Brain
Heart
Kidney

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5
Q

Where do red thromboemboli tend to lodge?

A

Pulmonary artery

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6
Q

What is the definition of thrombosis?

A

Pathological haemostasis

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7
Q

What kind of precursors are clotting factors 2, 7, 9 and 10?

A

Glycoprotein

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8
Q

What do the active factors 2a, 7a, 9a and 10a act as?

A

Serine proteases

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9
Q

What need to occur to allow transformation of precursors to clotting factors? E.g. prothrombin to thrombin.

A

Gamma carboxylation (of glutamate residues)

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10
Q

What process does Vitamin K allow to occur and what does this facilitate?

A

Gamma carboxylation, facilitating the conversion of precursors to active clotting factors e.g. prothrombin to thrombin

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11
Q

Which form of Vitamin K is required to allow gamma carboxylation to occur? (Oxidised/reduced)

A

Reduced form - a hydroquinone

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12
Q

Which enzyme converts vitamin K from it’s oxidised form to it’s reduced form?

A

Vitamin K reductase

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13
Q

Which enzyme does the drug warfarin target?

A

Vitamin K reductase

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14
Q

What can be used to counteract Warfarin when dose is too high?

A

Vitamin K

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15
Q

What drug may be added to dose of warfarin to produce rapid anticoagulant effect?

A

Heparin

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16
Q

What scale is used to ensure that the correct dose of warfarin has been given?

A

International normalised ratio

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17
Q

Why is haemorrhage more likely with warfarin in a patient with existing liver disease?

A

The liver produces clotting factors

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18
Q

Which molecule in the body acts to stop the coagulation cascade naturally?

A

Antithrombin 3

19
Q

How does antithrombin 3 act to stop the coagulation cascade?

A

It binds directly to the active site of active thrombin and inhibits it

20
Q

How does heparin work?

A

Heparin binds to antithrombin III, increasing its affinity for serine protease clotting factors (particularly Xa and IIa (thombin) to greatly increase their rate of their inactivation

21
Q

To inactivate factor 2a, what must heparin bind to?

A

Both antithrombin 3 and thrombin

22
Q

To inactivate factor 10, what must heparin bind to?

A

Antithrombin 3

23
Q

What clotting factor does low molecular weight heparin inhibit?

A

Factor Xa

24
Q

Where does excretion of LMWH occur?

A

Kidneys

25
Q

Which drug - heparin or LMWH - shows zero order kinetics?

A

Heparin

26
Q

Which drug - heparin or LMWH - shows first order kinetics?

A

LMWH

27
Q

Which drug - heparin or LMWH - is preferred in renal failure and why?

A

Heparin - LMWH excreted via renal system

28
Q

How does rivaroxiban work?

A

Directly inhibitis Xa

29
Q

When is rivaroxiban used in treatment?

A

After hip and knee surgeries to prevent formation of venous clot

30
Q

How do platelets adhere to surfaces with endothelial damage? Where does von Willebrand factor (vWF) come into this?

A

Endothelial damage exposes subendothelial molecules to which platelets adhere via surface glycoproteins (GPIb receptors)
Von Willebrand factor acts as a bridge

31
Q

What platelet derived substances is aggregation driven by?

A 
Adenosine diphosphate (ADP) 
5-hydroxytryptamine (5-HT)
Thromboxane A2 (TXA2) synthesis via the enzyme cyclo-oxygenase (COX)
32
Q

How is clopidogrel used to stop platelet aggregation?

A

Irreversibly binds to ADP receptors

33
Q

How is tirofiban used to stop platelet aggregation?

A

Blocks the GPIIb/IIIa receptors which allow bridge formation between platelets

34
Q

How is aspirin used to stop platelet aggregation?

A

Inhibits the COX enzyme irreversibly which stops the formation of thromboxane A2 (TXA2)

35
Q

What is the main adverse affect of aspirin?

A

Peptic ulcer formation

36
Q

What is the main clinical use for aspirin?

A

Thomboprophylaxis in patients at high cardiovascular risk

37
Q

Which antiplatelet drug is used intravenously with heparin to prevent MI in patients with unstable angina?

A

Tirofiban

38
Q

A fibrinolytic cascade exists endogenously which opposes the coagulation cascade. What is the main molecule involved in this?

A

Plasminogen, which is converted to plasmin

39
Q

How do thrombolytic drugs e.g. streptokinase, alteplase and duteplase work?

A

They activate plasminogen to plasmin

40
Q

Streptokinase is not an enzyme - what is it?

A

A protein extracted from cultures of streptococci

41
Q

Why is streptokinase ineffective after 4 days?

A

Because streptokinase is extracted from cultures of streptococci, the body forms antibodies against it

42
Q

How might haemorrhage caused by thrombolytic drugs be countered?

A

Tranexamic acid

43
Q

In which drug - streptokinase, alteplase or duteplase - is there a risk of allergic reaction?

A

Streptokinase

Cardiology (15 decks)

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