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OD2 (S1&2) > PHARM - Drugs That Modulate Haemostasis and Thrombosis - Week 6 > Flashcards

PHARM - Drugs That Modulate Haemostasis and Thrombosis - Week 6 Flashcards

1
Q

Define haemostasis.

A

Arrest of blood loss from damaged vessels

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2
Q

Define coagulation.

A

Formation of a fibrin clot in a blood vessel

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3
Q

Define thrombosis.

A

Pathological formation of a haemostatic plug in a blood vessel in the absence of blood loss

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4
Q

Name the two kinds of thrombi and where they occur.

A

Arterial thrombus (white)
Venous thrombus (red)

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5
Q

What are the three components of a white arterial thrombus?

A

Platelets and white blood cells in a fibrous mesh

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6
Q

What are aterial thrombi associated with?

A

Vessel wall damage (atherosclerosis)

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7
Q

What are venous thrombi associated with?

A

Blood stasis

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8
Q

What are the three components of a venous thrombus?

A

Fibrin, platelets, and red blood cells

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9
Q

What can happen to a venous thrombus?

A

Can break off and lead to an embolus lodged in the lungs (pulmonary embolism) or the brain (stroke)

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10
Q

Define a thromboembolus.

A

A blockage in a blood vessel caused by a dislodged thrombus.

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11
Q

Does damage to a blood vessel lead to vasodilation or vasoconstriction?

A

Vasoconstriction.

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12
Q

Is 5-HT a vasodilator or vasoconstrictor?

A

Powerful vasoconstrictor

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13
Q

Describe in three steps, the mechanism of vasoconstriction following blood vessel damage.

A

Collagen exposed on a damaged vessel wall.
Platelets stick to the collagen and activate
ADP and 5-HT released from platelets

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14
Q

Describe in 5 steps, the mechanism of platelet activation and adhesion.

A

ADP from activated platelets cause others to activate and morph
Granule contents (ADP/5-HT) are secreted
Mediators are synthesised (thromboxane)
Platelets aggregate and adhere via fibrinogen
Soft plug formed

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15
Q

Platelets aggregate and adhere via fibrinogen and bridge between which two receptors?

A

GPIIb an GPIIIa

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16
Q

Briefly describe in steps, how a platelet activates.

A

PLA2 cleaves phospholipids to release free arachidonic acid
COX enzymes convert arachidonic acid to TXA2
TXA2 mediates increased Ca2+, which induces adhesion and aggregation

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17
Q

Name 4 stimuli for platelet activation.

A

Collagen
Thrombin
Thromboxane
ADP

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18
Q

Describe the mechanism of fibrin deposition.

A

Thrombin cleaves fibrinogen into fibrin, which is an insoluble monomer

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19
Q

Is fibrin or fibrinogen soluble?

A

Fibrinogen

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20
Q

Is thrombin found in the plasma? Explain.

A

No, it is produced by activating prothrombin

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21
Q

How many cascade reactions are there in haemostasis? List them and note which is faster.

A

Two
Extrinsic and intrinsic
Extrinsic is faster

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22
Q

What factor is released in the extrinsic pathway?

A

Thromboplastin

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23
Q

What is the action of thromboplastin?

A

Converts factor VII to VIIa

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24
Q

What is the factor for the intrinsic pathway?

A

Exposed collagen (and negative charges, glass etc)

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25
Q

What factor controls cascade inhibition?

A

Enzyme inhibitors like antithrombin III

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26
Q

What is the action of plasmin?

A

Fibrinolysis

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27
Q

Describe the three components of Virchow’s triad.

A

Vessel damage
Blood stasis
Hypercoagulability

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28
Q

Name 2 common situations of blood stasis that leads to thrombus formation.

A

Atrial fibrillation
Deep vein thrombosis

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29
Q

Name a common cause of blood vessel damage that leads to thrombus formation.

A

Atherosclerosis

30
Q

What is a thrombus in coronary vessels called?

A

Myocardial infarction

31
Q

What is a thrombus in carotid arteries called?

A

Stroke

32
Q

Give an example of a procoagulant drug.

A

Vitamin K

33
Q

Give an example of an injectable anticoagulant and what kind of therapy that drug might be used for.

A

Heparin - used acutely for short term action

34
Q

Give an example of an oral anticoagulant and what kind of therapy that drug might be used for.

A

Warfarin - used for prolonged therapy

35
Q

What is the action of factor Xa?

A

Converts prothrombin into thrombin, which converts fibrinogen into fibrin

36
Q

What is the mechanism of action for heparin?

A

Enhances the activity of antithrombin III

37
Q

What is the action of antithrombin III?

A

A natural inhibitor of factor Xa and thrombin

38
Q

Consider light molecular weight heparins. How does their action differ to regular heparin (2)? Compare the anticoagulation effects.

A

Has the same effect of factor Xa, but less effect on thrombin
Anticoagulant effects are similar

39
Q

How is heparin administered and what charge does it have?

A

Injected and largely negative

40
Q

What is the half-life of low molecular weight heparin and what is a benefit of this?

A

Longer elimination half life
Used for patient self-administration

41
Q

Are injectable coagulants available orally?

A

no

42
Q

How can you monitor anticoagulant effects of heparin?

A

Measuring activated partial thromboplastin time.

43
Q

Define the activated partial thromboplastin time.

A

Time for clot formation in citrated plasma after the addition of Ca2+, contact activator and phospholipid

44
Q

What is activated partial thromboplastin time a measure of?

A

Intrinsic pathway

45
Q

Name three adverse effects of heparin and a mechanism why.

A

Haemorrhage (self explanatory)
Thrombocytopaenia (platelet deficiency)
Osteoporosis (mechanism unknown)

46
Q

What four clotting factors is vitamin K essential for the formation of? What is required of these factors after synthesis? How does vitamin K play a role here?

A

Factors II, VII, IX, and X
Gamma carboxylation
Reduced vitamin K is a cofactor in the carboxylation of glutamate

47
Q

How do oral anticoagulants work (mechanism of action)?

A

Inhibits the reduction of vitamin K, inhibiting the gamma carboxylation of glutamate in factors II, VII, IX, and X

48
Q

Does warfarin have a rapid or delayed onset of action?

A

Delayed

49
Q

Can warfarin inhibit factors that are already active?

A

Noh

50
Q

What does warfarin bind to once absorbed orally?

A

Plasma proteins

51
Q

Is warfarin rapidly or slowly absorbed orally?

A

Rapidly

52
Q

Name 4 adverse effects of warfarin and why if applicable.

A

Haemorrhage
Vitamin K deficiency
Hepatic disease (impaired synthesis of clotting factors)
Hypermetabolic states (increased metabolism of clotting factors)

53
Q

Name three possible drug interactions that can occur with warfarin and the mechanism involved.

A

Impaired platelet aggregation
-aspirin
Competition for plasma protein binding
-NSAIDs
Competition for cytochrome p540 pathway
-cimetidine

54
Q

What four things can reduce warfarin activity?

A

Pregnancy
Drug interactions
-induction of liver enzymes/chronic alcohol use
Vitamin K supplements

55
Q

Define prothrombin time and what it measures.

A

Time for clot formation of plasma after addition of Ca2+ and tissue factors
Measures extrinsic pathway

56
Q

Define international normalised ratio.

A

Ratio of patient thrombin time to normal thrombin time

57
Q

Define NDACs.

A

Non-vitamin K dependent anticoagulant agents

58
Q

Do NDACs have a high or low molecular weight?

A

Low

59
Q

Are NDACs orally available or injected?

A

Orally available.

60
Q

Do NDACs have a more or less predictable dose-response? What does this result in?

A

More predictable
Results in reduced laboratory monitoring required

61
Q

In what three ways can NDACs have an anticoagulant effect?

A

Indirect factor Xa inhibitor
Direct factor Xa inhibitor
Direct thrombin inhibitor

62
Q

Name three drugs that affect platelet activation and adhesion.

A

ADP receptor antagonists
Thromboxane synthesis inhibitors
Glycoprotein IIb/IIIa receptor antagonists

63
Q

What are the guidelines for the use of platelet inhibitors (2)?

A

As an adjunctive therapy with aspirin
In patients intolerant to aspirin

64
Q

What is thromboxane a potent activator of?

A

Platelets

65
Q

Where are thromboxanes synthesised, from what, and by what?

A

In platelets from arachidonic acid by cyclo-oxygenase

66
Q

In what three ways does aspirin mediate anticoagulation and how?

A

Reduces thromboxane synthesis
Decreases platelet aggregation
Decreases vasoconstriction
Is an irreversible cyclo-oxygenase inhibitor

67
Q

Describe low dose aspirin therapy (3). What does it preserve and how?

A

Platelets are exposed to aspirin as they circulate in the portal vein.
Aspirin causes irreversible inhibition of COX in exposed platelets.
This decreases platelet aggregation.
Endothelial production of prostaglandin I2 is preserved.
-beneficial vasodilation is preserved.

68
Q

How do fibrinolytic drugs work?

A

Activates plasminogen

69
Q

Describe why some fibrinolytic drugs are single use.

A

Are antigenic so single use like streptokinase

70
Q

What kind of drug is alteplase and is it single use?

A

It is a fibrinolytic drug that is not single use because it is not antigenic.

71
Q

What is alteplase more active on?

A

On fibrin-bound plasminogen so it is clot selective.

OD2 (S1&2) (174 decks)

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