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MD2002 Arvin > Anticoagulant Drugs > Flashcards

Anticoagulant Drugs Flashcards

1
Q

What is haemostasis ?

A

The arrest of blood loss from damaged blood vessels

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2
Q

What are the main ways in which haemostasis occurs.

A
  • Vascularconstriction
  • Formation of a platelet plug
  • Formation of a blood clot as a result of blood coagulation
  • Growth of fibrous tissue into the blood clot to close the hole permanently
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3
Q

Is promotion of haemostasis ever necessary ? Using what drug ?

A

Rarely, using tranexamic acid

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4
Q

Which steps of thrombosis does drug therapy target ?

A
  • Blood clotting
  • Platelet adhesion and activation
  • Processes involved in fibrin removal
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5
Q

Identify an example of condition due to genetically determined deficiencies of clotting factors. How is this condition treated ?

A

Haemophilia

Treated with replacement therapy

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6
Q

What are possible causes of acquired clotting defects ? How are these treated ?

A

Liver Disease
Vitamin K deficiency
Ingestion of oral anti-coagulants

Treated with

  1. natural Vitamin K (phytomenadione) or
  2. synthetic preparation, menadiol sodium phosphate
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7
Q

What is the role of vitamin K in the treatment of clotting defects ?

A

Acts as co-factor for “the gamma-carboxylase enzymes which catalyze the posttranslational gamma-carboxylation of glutamic acid residues in inactive hepatic precursors of coagulation factors II (prothrombin), VII, IX and X”

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8
Q

What are all the clinical uses of vitamin K ?

A
  • Treatment and/or prevention of bleeding from excessive oral anticoagulant use
  • In babies to prevent haemorrhagic disease of the newborn
  • For Vitamin K deficiencies in adults
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9
Q

Identify antagonists of vitamin K.

A

Warfarin

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10
Q

How does warfarin inhibit vitamin K action ?

A

Prevents reduction of vitamin K

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11
Q

What is the onset of warfarin ? Why ?

A

Takes many hours to act because of time taken for degradation of factors

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12
Q

How may one cover for the slow onset of warfarin ?

A

Using heparin treatment

Giving loading dose of warfarin then go down to small dose to try and maintain plasma levels

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13
Q

What is the main side effect of warfarin ? How can this be treated ?

A

haemorrhage

Can be reversed by Vitamin K

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14
Q

How are patients’ response to the dose of warfarin measured ?

A

Prothrombin Time test, allows to calculate International Normalized Ratio (INR)

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15
Q

Identify factors which increase the effect of warfarin.

A
  • ↓ availability of Vitamin K
  • Broad-spectrum antibiotics
  • Liver disease
  • Drugs which:
  • impair platelet function
  • displace warfarin from their binding sites on plasma albumin
  • agents which inhibit microsomal enzymes in the liver

-Dietary factors

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16
Q

Identify factors which decrease the effect of warfarin.

A
  • Drugs which ↑ drug metabolism
  • Oral contraceptives
  • Dietary factors
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17
Q

What is the method of administration of warfarin ?

A

Orally

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18
Q

What is the method of administration of heparin ?

A

Injected

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19
Q

Give an example of heparin.

A

Dalteparin

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20
Q

What kind of molecule are heparins ?

A

sulphated glycosaminoglycans

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21
Q

What are the main two groups of heparin ? What is their main distinction ?

A

Unfractionated (UFH) or Low Molecular Weight (LMWH)

LMWH longer acting, don’t require monitoring

22
Q

Where is heparin found in the body ?

A

In mast cells, in plasma and in endothelial cells

23
Q

What is the onset of heparin ?

A

Starts acting almost immediately

24
Q

What is the main side effect of heparin ?

How can this be treated ?

A

Haemorrhage

May be reversed by protamine

25
What is the mechanism of action of heparin ?
- Antithrombin forms a 1:1 complex with thrombin by binding to active site, thus inhibiting thrombin - Heparin acts on antithrombin III (naturally-occurring inhibitor of thrombin) and other serine proteases in the coagulation cascade (XIIa, XIa, IXa, & Xa) (brings ATIII to activated factors) - As a result, heparin accelerates the rate of this inhibition (thus prevents fibrin formation)
26
Which chemical property of heparin relates to its mechanism of action in preventing blood clotting ?
Electronegative charge
27
Identify two direct factor Xa inhibitors ?
Rivaroxaban or apixaban
28
What is the route of adminsitration of direct factor Xa inhibitors ?
Orally
29
How is response to direct factor Xa inhibitors measured ?
Does not require PT/INR monitoring (Meaningless for these drugs!)
30
What is the onset of direct factor Xa inhibitors ?
Rapid onset of action compared to warfarin, just takes a few hour
31
What is the duration of effect of direct factor Xa inhibitors ? How long does it take before factor Xa normal activity comes back to normal ?
8-12 hours | 24 hours
32
What is the main side effect of direct factor Xa inhibitors ? How is this treated
Haemorrhage | No antidote
33
Are anti-platelets and anti-coagulants the same ?
No
34
Identify two examples of anti-platelet drugs.
Aspirin | Clopidogrel
35
How do aspirin and Clopidogrel respectively inhibit platelet
ASPIRIN Inhibits cyclooxegenase Stops production of thromboxanes which would normally increase expression of receptors that lead to aggregation CLOPIDOGREL Inhibits P2Y12 purinergic receptors Inhibits ADP-induced platelet aggregation
36
What is the general function of Antiplatelet drugs ?
Decrease platelet aggregation and thereby inhibit thrombus formation
37
What is Fibrinolysis ?
Breaking down of thrombus
38
When is fibrinolysis induced ?
When the intrinsic coagulation system is activated
39
Describe the mechanism of fibrinolysis.
- Generation of plasminogen activators - Plasminogen activators release active enzyme plasmin from plasminogen precursor - Plasmin digests not only fibrin but other blood proteins such as factors II, V & VII
40
What is plasminogen ?
Inactive pro-enzyme deposited in the fibrin strands within a thrombus
41
What is plasmin ?
Trypsin-like enzyme acting on ARG-LYS bonds
42
How is plasmin which escapes into circulation removed after having fulfilled its function ?
Plasmin which escapes into the circulation is inactivated by various plasmin inhibitors
43
Give examples of fibrinolytic agents.
Streptokinase, Alteplase
44
What kind of organic molecule is streptokinase ?
Non-enzymatic protein
45
How does streptokinase lead to fibrinolysis ?
Acts indirectly by forming a stable complex with plasminogen. This activates enzymatic activity of plasminogen by inducing a conformational change.
46
Give an example of Tissue Plasminogen Activator. How is this plasminogen activator synthesised ?
ALTEPLASE | Synthesised in vivo by endothelial cells, but can also be made by recombinant technology
47
How is Alteplase clot selective (does not just activate plasminogen in the plasma) ?
Because Alteplase's enzymatic activity is enhanced more in the presence of fibrin-bound plasminogen than plasma plasminogen
48
Overall, what are the main groups of drugs which target thrombosis ? What process does each of these inhibit/activate ?
1. Anticoagulants (Heparin, Warfarin, Factor Xa inhibitors): Inhibits activation of clotting factors (XIIa, IXa, XIa, Xa) 2. Antiplatelet agents (Aspirin, Clopidogrel): Inhibits platelet adhesion, activation, aggregation 3. Fibrinolytic agents (Streptokinase, Alteplase): Enhances conversion of Plasminogen into Plasmin (which digests fibrin and blood proteins)
49
What are some therapeutic uses of anticoagulants ?
VENOUS THROMBOEMBOLISM ``` TREATMENT AND PROPHYLAXIS OF – DVT – Pulmonary embolisms – Thromboembolism from atrial fibrillation – Prosthetic heart valves – Clotting during kidney dialysis ```
50
What specific anticoagulants are given for venous thromboembolisms ?
– Heparin for short-tem action | – Oral anticoagulants for prolonged therapy
51
What are some therapeutic uses of antiplatelet agents and fibrinolytic agents ?
FIBRINOLYTIC AGENTS + ASPIRIN -therapy of acute myocardial infaraction (within 4-6 hours of onset) ASPIRIN -can reduce the risk of occlusive cardiovascular disease in patients already diagnosed as being at risk

MD2002 Arvin (110 decks)

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