Anti-platelet, anti-coagulant and thrombolytic drugs

Question 1

Which clotting factor is factor 2?

Answer 1

Thrombin

Question 2

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

Answer 2

Arterial

Question 3

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

Answer 3

Venous

Question 4

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

Answer 4

Brain
Heart
Kidney

Question 5

Where do red thromboemboli tend to lodge?

Answer 5

Pulmonary artery

Question 6

What is the definition of thrombosis?

Answer 6

Pathological haemostasis

Question 7

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

Answer 7

Glycoprotein

Question 8

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

Answer 8

Serine proteases

Question 9

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

Answer 9

Gamma carboxylation (of glutamate residues)

Question 10

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

Answer 10

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

Question 11

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

Answer 11

Reduced form - a hydroquinone

Question 12

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

Answer 12

Vitamin K reductase

Question 13

Which enzyme does the drug warfarin target?

Answer 13

Vitamin K reductase

Question 14

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

Answer 14

Vitamin K

Question 15

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

Answer 15

Heparin

Question 16

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

Answer 16

International normalised ratio

Question 17

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

Answer 17

The liver produces clotting factors

Question 18

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

Answer 18

Antithrombin 3

Question 19

How does antithrombin 3 act to stop the coagulation cascade?

Answer 19

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

Question 20

How does heparin work?

Answer 20

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

Question 21

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

Answer 21

Both antithrombin 3 and thrombin

Question 22

To inactivate factor 10, what must heparin bind to?

Answer 22

Antithrombin 3

Question 23

What clotting factor does low molecular weight heparin inhibit?

Answer 23

Factor Xa

Question 24

Where does excretion of LMWH occur?

Answer 24

Kidneys

Question 25

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

Answer 25

Heparin

Question 26

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

Answer 26

LMWH

Question 27

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

Answer 27

Heparin - LMWH excreted via renal system

Question 28

How does rivaroxiban work?

Answer 28

Directly inhibitis Xa

Question 29

When is rivaroxiban used in treatment?

Answer 29

After hip and knee surgeries to prevent formation of venous clot

Question 30

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

Answer 30

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

Question 31

What platelet derived substances is aggregation driven by?

Answer 31

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

Question 32

How is clopidogrel used to stop platelet aggregation?

Answer 32

Irreversibly binds to ADP receptors

Question 33

How is tirofiban used to stop platelet aggregation?

Answer 33

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

Question 34

How is aspirin used to stop platelet aggregation?

Answer 34

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

Question 35

What is the main adverse affect of aspirin?

Answer 35

Peptic ulcer formation

Question 36

What is the main clinical use for aspirin?

Answer 36

Thomboprophylaxis in patients at high cardiovascular risk

Question 37

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

Answer 37

Tirofiban

Question 38

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

Answer 38

Plasminogen, which is converted to plasmin

Question 39

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

Answer 39

They activate plasminogen to plasmin

Question 40

Streptokinase is not an enzyme - what is it?

Answer 40

A protein extracted from cultures of streptococci

Question 41

Why is streptokinase ineffective after 4 days?

Answer 41

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

Question 42

How might haemorrhage caused by thrombolytic drugs be countered?

Answer 42

Tranexamic acid

Question 43

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

Answer 43

Streptokinase