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Cardiovascular > Anticoagulant, Antiplatelet and Thrombolytic Drugs > Flashcards

Anticoagulant, Antiplatelet and Thrombolytic Drugs Flashcards

1
Q

what is haemostasis?

A

arrest of blood loss from a damaged vessel

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2
Q

describe the sequence of haemostasis

A

vascular wall damage exposing collagen and tissue factor
primary haemostasis
- local vasoconstriction
- platelet adhesion, activation and aggregation
activation of blood clotting and the formation of a stable clot

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3
Q

what do activated platelets do?

A

extend pseudopodia

synthesise and release thromboxane A2 (TXA2)

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4
Q

what does TXA2 bind to?

A

platelet GPCR TXA2 receptors causing mediator release
vascular smooth muscle cells TXA2 receptors causing vasoconstriction that is augmented by mediator 5-HT binding to smooth muscle GPCR 5-HT receptors

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5
Q

what happens when ADP binds to platelet GPCR purine receptors?

A

they act locally to activate further platelets
aggregate platelets into a ‘soft plug’ at the site of injury
expose acidic phospholipids on the platelet surface that initiate coagulation of blood and solid clot formation

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6
Q

how is inactive factor X converted to the active fator?

A

by tenase

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7
Q

how is inactive factor II (prothrombin) converted to active factor IIa (thrombin)?

A

by prothrombinase

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8
Q

how is a solid clot formed?

A

because fibrinogen is converted by thrombin to fibrin

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9
Q

what is a thrombosis?

A

pathological haemostasis

a haemotological plug in the absence of bleeding

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10
Q

what are the predisposing factors to thrombosis?

A

Virchow’s triad

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11
Q

what are the 3 factors of virchow’s triad?

A

injury to vessel wall
abnormal blood flow
increased coagulability of the blood

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12
Q

what is an arterial thrombus?

A

a white thrombus

mainly platelets in a fibrin mesh

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13
Q

how does an arterial thrombus form an embolus?

A

if it detaches from the left heart or carotid artery and lodges in an artery in the brain (or another organ)

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14
Q

how is an arterial thrombus primarily treated?

A

with antiplatelet drugs

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15
Q

what is a venous thrombus?

A

a red thrombus

white head, jelly-like red tail, fibrin rich

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16
Q

how does a venous thrombus form an embolus?

A

if it detaches and lodges in the lung (pulmonary embolism)

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17
Q

how is a venous thrombus primarily treated?

A

with anticogulants

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18
Q

what do the precursors of the active factors require?

A

vitamin K in its reduced form

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19
Q

when are anticoagulants used?

A 
in the prevention and treatment of venous thrombosis and embolism
DVT 
prevention of post-operative thrombosis 
patients with artificial heart valves
atrial fibrillation
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20
Q

what is the main risk with anticoagulants?

A

haemorrhage

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21
Q

what is warfarin?

A

an anticoagulant
structurally related to vit K with which it competes for binding to hepatic vit K reductase preventing production of the active hydroquinone

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22
Q

what does warfarin do?

A

renders factors II, VII, IX and X inactive

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23
Q

how is warfarin administered?

A

orally (slower onset of action than heparin)

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24
Q

how can the overdose of warfarin be treated?

A

with administration of vit K1 or concentrate of plasma clotting factors (IV)

25
Q

which factors potentiate warfarin action?

A

liver disease
high metabolic rate
drug interactions

26
Q

how does liver disease potentiate warfarin action?

A

decreased clotting factors

27
Q

how does a high metabolic rate potentiate warfarin?

A

increased clearance of clotting factors

28
Q

which drug interactions can potentiate warfarin?

A

agents that inhibit metabolism of warfarin
drugs that inhibit platelet function
drugs that inhibit reduction, or decrease availability of vit K

29
Q

which factors lessen warfarin action?

A

pregnancy
hypothyroidism
vit K consumption
drug interactions

30
Q

how does pregnancy lessen warfarin action?

A

increased clotting factor synthesis

31
Q

how does hypothyroidism lessen warfarin action?

A

decreased degradation of clotting factors

32
Q

which drug interactions lessen warfarin action?

A

agents that increase hepatic metabolism of warfarin

33
Q

what is the role of antithrombin III?

A

an inhibiter of coagulation which neutralises all serine protease factors in the coagulation cascade by binding to their active site

34
Q

how does heparin act?

A

it binds to antithrombin III, increasing its affinity for serine protease clotting factors to greatly increase their rate of inactivation

35
Q

name LMWHs

A

enoxaparin and dalteparin

36
Q

what is the exception to when LMWHs are prefered?

A

renal failure

37
Q

how do LMWHs act?

A

they inhibit factor Xa but not thrombin (IIa)

38
Q

how is heparin administered?

A

IV or SC

LMWH = SC

39
Q

what is required for heparin but not for LMWHs?

A

an in vitro clotting test to determine optimum dosage

40
Q

what are the adverse effects of heparin and LMWHs?

A 
haemorrhage 
more rarely
osteoporosis 
hypoaldosteronism 
hypersensitivity reactions
41
Q

what is dabigatran etexilate?

A

a new orally active agent that acts as a direct inhibiter of thrombin

42
Q

what is rivaroxaban?

A

a new orally active agent that acts as a direct inhibiter of factor Xa

43
Q

what are the advantages of the new orally active agents?

A

convenience of administration

predictable degree of anticoagulation

44
Q

what is the major disadvantage of new orally active agents>

A

no specific agent is available to reduce haemorrhage in overdose

45
Q

describe the use of orally active inhibitors

A

used to prevent venous thrombosis in patients undergoing hip and knee replacements

46
Q

what are anti-platelet drugs used for?

A

in the treatment of arterial thrombosis

47
Q

what are the main antiplatelet drugs?

A

aspirin
clopidogrel
tirofiban

48
Q

describe the mechanism of action of aspirin

A

irreversibly blocks cycloxygenase (COX) in platelets, preventing TXA2 synthesis, but also COX in endothelial cells inhibiting production of antithrombotic prostaglandin I2 (PGI2)
balance is shifted in favour of an antithrombotic effect because endothelial cells can synthesise new COX enzyme whereas enucleate platelets cannot. TXA2 synthesis does not recover until affected platelets are replaced (7-10 days)

49
Q

describe the use of aspirin

A

Used orally, mainly for thromboprophylaxis in patients at high cardiovascular risk

50
Q

what is the main adverse effect of aspirin?

A

GI bleeding

ulceration

51
Q

describe the mechanism of action of clopidogrel

A

Links to P2Y12 receptor by a disulphide bond producing irreversible inhibition

52
Q

describe the use of clopidogrel

A

mainly in patients intolerant to aspirin
cost is an issue
administered orally
when combined with aspirin, has a synergistic action

53
Q

when is tirofiban given?

A

IV in short term to prevent MI in high risk patients with unstable angina (with aspirin and heparin)

54
Q

when are fibrinolytics used?

A

principally to reopen occluded arteries in acute MI or stroke
less frequently, life threatening venous thrombosis or PE
have an additive beneficial effect with aspirin

55
Q

how are fibrinolytics administered?

A

IV within as short a period as possible of the event

PCI is superior if available promptly

56
Q

describe the use of streptokinase

A

reduces mortality in acute MI but action blocked after 4 days by the generation of antibodies
may cause allergic reactions- not given to patients with recent streptococcol infections

57
Q

what are alteplase and duteplase?

A

recombinant tissue plasminogen activators

more effective on fibrin bound plasminogen than plasma plasminogen and show selectivity for clots

58
Q

describe the use of alteplase and duteplase

A

do not cause allergic reactions

given by IV infusion

59
Q

what is the major adverse effect of fibrinolytics?

A

haemorrhage that may be controlled by oral tranexamic acid which inhibits plasminogen activation

Cardiovascular (31 decks)

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