Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > Drugs affecting blood coagulation, platelet aggregation and fibrinolysis > Flashcards

Drugs affecting blood coagulation, platelet aggregation and fibrinolysis Flashcards

0
Q

Haemostasis is most effective in small vessels. Name 3 types of small vessel:

A

Arterioles, capillaries and venules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What is haemostasis?

A

It is a balance BETWEEN the NORMAL function of blood and preventing BLOOD LOSS following vessel damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What process enlists the vasoconstriction of blood vessels, platelets, coagulation/clotting factors and inhibitors and fibrinolysis?

A

Haemostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

In the term fibrinolysis, what does fibrin and what does lysis mean?

A 
Fibrin = fibrin CLOT
Lysis = breakdown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

A ‘good’ clot is otherwise known as a stable haemostatic plug. Other than fibrin, blood coagulation and platelets, what other step needs to happen for this to form?

A

Vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is a thrombus?

A

A blood clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the two types of thrombosis?

A

Venous and arterial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is a fibrin framework made up of?

A

Platelets that other blood cells stick to

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Once the fibrin framework has attached to the vessel wall, causing a thrombus, what are the two main things this does?

A

Impedes blood flow

Reduces the perfusion (oxygen flow) of tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Does coagulation or platelet aggregation have a more important role in venous thrombosis?

A

Coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Does coagulation or platelet aggregation have a more important role in arterial thrombosis?

A

Platelet aggregation, although coagulation is also a factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a major cause of DVT?

A

Clotting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are fibrin strands made up of?

A

Red Blood Cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the term for the formation of a thrombus within a vessel?

A

Thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What usually causes venous thrombosis?

A

The pooling of blood in veins due to sluggish flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What usually causes arterial thrombosis?

A

Damaged vessels and atheromatous plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is an embolus?

A

It is a fragment or whole thrombus that has detached from the blood vessel wall - the clot has broken off and travelled somewhere else in the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

An embolus can travel through blood vessels before potentially blocking small blood vessels in the pulmonary, cardiac or central nervous system circulation.
What are the 3 treatable but potentially fatal results of this?

A

Pulmonary Embolism (stops blood flow returning to left side of heart)
Myocardial Infarction
Stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

In venous thrombosis, what should the drug aim to modify?

A

Coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

In arterial thrombosis, what should the drug aim to modify?

A

Platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is prophylaxis?

A

A drug that prevents the formulation of clots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is a common side effect of prophylaxis?

A

Bleeding - so it is important to monitor patients carefully and control the dosage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What (beginning with h) do we want to continue when giving drugs to inhibit thrombus formation?

A

Haemostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are heparin, LMWHs, hirodin and warfarin examples of?

A

Anticoagulants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What type of agent is tranexamic acid?

A

Anti fibrinolytic Agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What do fibrinolytic agent drugs tend to end in?

A

‘ase’

e.g. anistreplase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Heparin is present in our liver, lungs and mast cells. What is it?

A

A natural anti-coagulant made in our body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Are enoxoparin, dalteparin and tinzaparin examples of high or low molecular weight heparin?

A

Low MW

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which type of heparin is of low molecular weight and consequently has higher bioavailability?
Standard or unfractionated heparin?

A

Standard heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What does heparin activate?

A

Antithrombin (AT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the main 2 clotting factors that AT forms complexes with once it has been activated by heparin?

A

Thrombin and Factors Xa.

Antithrombin inactivates them (along with FIXa and XIa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Heparins increase the rate of c….. f…..

A

complex formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the 2 most important targets for anti-coagulant drugs?

A

Thrombin and Factor X (Factor 10)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Heparin is poorly absorbed by oral administration. What are the most common routes of administration for it?

A

Intravenous and subcutaneous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is a major risk factor of heparin?

A

Haemmorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

If a patient has mild haemorrhage from taking heparin, what should you do?

A

Cease administration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

In what situation would you give a patient protamine sulphate, so that it forms a complex with heparin to stop its anticoagulant effect?

A

Severe haemorrhage

37
Q

Which type of heparin (unfractionated or low molecular weight) does not affect platelet function?

A

Low Molecular Weight heparin does not affect platelet function.
It is more predicatable that unfractionated.

38
Q

In what situations would you use unfractionated heparin, given that it has lower bioavailability, inhibits platelet function and must be administered by intravenous infusion?

A

Surgical patients, late pregnancy, acute pulmonary embolism

39
Q

In what situation would you administer Low MW heparin, given it does not affect platelet function, has 100% bioavailability and is given just once daily?

A

Less serious circumstances - DVT, pulmonary embolism and pregnancy

40
Q

Warfarin is an oral anti-coagulant. What vitamin structure is it related to?

A

Vitamin K

41
Q

Which drug ANTAGONISES the vitamin K role (preventing the formation of clotting factors)?

A

Warfarin

42
Q

Warfarin stops vitamin K from converting 3 factors to active factors. Which factors are they?

A

2 (known as prothrombin), 7 and 9

Factors II, VII and IX

43
Q

What is needed to convert inactive proteins to active proteins in order to form coagulation/clotting?

A

Vitamin K-dependent carboxylase

Warfarin stops the vitamin K enzyme being produced

44
Q

Should we use heparin or warfarin first?

Why?

A

Heparin, as warfarin has a slow onset.

45
Q

How many days does it take for a patient to become fully anti-coagulated following the administration of Warfarin?

A

3 days

46
Q

Why does warfarin have such a slow onset?

A

Due to a variation in the half life of clotting factors - and all of these pre-existing factors need to be depleted

47
Q

Warfarin has many interactions with food.

Why?

A

Many foods have vitamin K, thus it can affect its absorption (prevent it)

48
Q

What can we use to monitor warfarin and to determine the risk of bleeding or clotting?

A

International Normalised Ratio

49
Q

If a patient is taking warfarin, in what situation would you give them vitamin K, clotting factors, whole blood and fresh frozen plasma?

A

Severe haemorrhage

50
Q

Why should you avoid giving warfarin to a woman in late pregnancy?

A

Risk of haemorrhage in new born

51
Q

Should you use heparin or warfarin in early pregnancy?

A

Heparin.

Warfarin can be teratogenic causing embryonic defect

52
Q

Warfarin has lots of drug interactions. What are the two potential consequences of this?

A

Enzyme induction - increased metabolism e.g. carbamazepine

Enzyme inhibition - reduced metabolism e.g. cimetidine

53
Q

Which new anti-coagulant inhibits factor Xa (10a)?

A

Rivaroxaban (Xarelto)

54
Q

Which new anti-coagulant inhibits thrombin?

A

Dabigatran (Pradaxa)

55
Q

If/when rivaroxaban and dabigatran become cheaper, they may replace warfarin as they are also given orally and in a fixed dose.
But unlike warfarin, what do they not require?

A

Routine monitoring - no increased risk of bleeding

56
Q

When a vessel is damaged, collagen is exposed. Platelets bind to the collagen and become activated, causing increased synthesis of TxA2 (thromboxane A2). This increases glycoprotein 2b and 3a receptor expression on platelets.
What does this result in?

A

The aggregation of platelets, so that they can stick together where the vessel is damaged

57
Q

What are the 3 targets for anti-platelet drugs?

By stopping these targets working, which will reduce the production of platelets and which increases the production?

A

Synthesis of THROMBOXANE A2 within the platelets - to reduce (needed for platelet production)

cAMP levels in platelets - to increase (needed to break down platelets)

Glycoprotein 2b and 3a receptors on platelets - to reduce

58
Q

Does cAMP reduce or increase platelet aggregation?

A

Reduce

59
Q

Do TxA2 and GP2b/3a reduce or increase platelet aggregation?

A

Increase

60
Q

The COX enzyme produces what, to increase cAMP levels to reduce platelet aggregation?

A

Prostacyclin

61
Q

What does aspirin target to prevent the synthesis of TXA2 and therefore platelet aggregation?

A

COX Enzyme

62
Q

What can aspirin do in relation to the blood and platelet aggregation?

A

It reduces platelet aggregation by inhibiting the COX enzyme.
Too much however can cause bleeding.

63
Q

What does Epoprostenol target to prevent platelet aggregation?
The COX Enzyme, synthesis of TXA2 or Expression of GP2b/3a

A

GP2b/3a

64
Q

Aspirin irreversibly blocks platelet COX enzyme, reducing the synthesis of what?

A

Thromboxane (TxA2)

65
Q

Aspirin can reduce platelet aggregation for 7-10 days.
Why is this?
What occurs after 7-10 days for platelet aggregation function to return?

A

Platelets have no nuclei and therefore cannot synthesise more COZ enzyme.

After 7-10 days, new platelets are made.

66
Q

Why do we use low doses of aspirin?

What do we need to avoid reducing?

A

Prostacyclin (PGI2).

67
Q

Dipyridamole inhibits the phosphodiesterase (PDE) enzyme, preventing the breakdown of cAMP in platelets.
What does this result in?

A

Platelet aggregation DECREASES as more cAMP is present.

68
Q

Dipyridamole blocks adenosine uptake into platelets, red cells and endothelial cells, what does this result in?

A

Inhibited TXA2 synthesis

69
Q

What anti-platelet drug works by reducing synthesis?

A

Aspirin

70
Q

What anti-platelet drug works by raising cAMP?

A

Dipyridamole

71
Q

What anti-platelet drug works by reducing receptors?

A

Clopidogrel

72
Q

Clopidogrel blocks the activation of a certain receptor complex that is important for platelet aggregation and cross-linking platelets with fibrin.
What is the name of this pathway?
What receptor does it inhibit?

A

It inhibits the ADP RECEPTOR to BLOCK the G2b/3a PATHWAY

73
Q

What drug inhibits the ADP receptor to block the glycoprotein 2a/3b pathway?

A

Clopidogrel

74
Q

Which drug targets the synthesis of thromboxane A2 within the platelets?
Does it increase or reduce platelet aggregation?

A

Aspirin. It reduces platelet aggregation

A = A2

75
Q

Which drug targets cAMP levels in platelets?

Does it reduce or increase platelet aggregation?

A

Dipyridamole. It increases platelet aggregation.

D comes after C.

76
Q

Which drug targets glycoprotein 2a/3b receptors on platelets?
Does it reduce or increase platelet aggregation?

A

Clopidogrel. It reduces platelet aggregation.

Has a G in it.

77
Q

What does the following mechanism do?:

Plasminogen is made active into plasmin, producing fibrin and FDPs

A

Clot bust!

78
Q

When plasminogen is activated, what does it turn into?

A

Plasmin

79
Q

What are fibrinolytic drugs used for?

A

To dissolve a pre-existing clot or thrombus in an acute situation.
This releases the blood flow back into tissues.

80
Q

Within what time scale are fibrinolytic drugs most effective?

A

Recent thrombi - within 6 hours

81
Q

What are the 2 risks of using fibrinolytic drugs?

A

Danger of haemorrhage

Risk of emboli

82
Q

Why do fibrinolytic drugs increase a danger of haemorrhage?

A

If they result in too much bleeding, the body’s clotting factors may have already been used up on the original clot

83
Q

How are fibrinolytic drugs administered?

A

By I.V. or intracoronary - so they get into the circulation immediately

84
Q

What do fibrinolytic drugs tend to end in?

A

‘ase’ - alteplase, reteplase, steptokinase.

They all have specific uses but are all fast acting for emergency situations

85
Q

What does alteplase convert and what does it mimic?

A

It converts inactive plasminogen to active plasmin.

It mimics fibrinolysis.

86
Q

What complex does alteplase bind to?

A

Fibrin strands bound to plasminogen

87
Q

Once alteplase has bound to fibrin strands that are bound to the plasminogen, and has converted it to plasmin, what does the plasmin do?

A

The plasmin digests the fibrin, dissolving the clot

88
Q

When are anti-fibrinolytic drugs used?

A

Situations with risk of bleeding

89
Q

What does tranexamic acid do?

A

Counteract risk of bleeding

90
Q

Tranexamic acid reduces the activation of plasminogen to plasmin. This prevents the digestion of fibrin. What is the result of this?

A

It prevents the digestion of fibrin strands and ensures blood clots are not dissolved. This prevents bleeding.

Pharmacology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions