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Cardiology > Thrombolytics; Anticoagulants; Antiplatelet Drugs > Flashcards

Thrombolytics; Anticoagulants; Antiplatelet Drugs Flashcards

1
Q

What is haemostasis?

A

Arrest of blood loss. Physiological response to bleeding/haemorrhage. Pathological response to damaged blood vessel.

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2
Q

What can abnormalities in haemostasis lead to?

A
  • haemorrhage

- thrombosis

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3
Q

What are the stages in haemostasis

A
  • local vasoconstriction (loss of blood supply)
  • adhesion + activation of platelets at site of injury (platelet plug) (primary haemostasis)
  • formation of fibrin clot (blood coagulation) (secondary haemostasis)
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4
Q

What is thrombosis?

A
  • pathological formation of solid blood constituents within the blood vessel
  • occurs in the absence of previous bleeding
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5
Q

Name + describe the 3 components of Virchow’s Triad

A

1) injury to blood vessel wall (loss of surface/inflammation)
2) abnormal blood flow (stasis/turbulence)
3) increased coagulability of the blood (formed by platelets/coagulation proteins that increase blood viscosity)

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6
Q

What conditions can increase the coagulability of blood?

A
  • pregnancy
  • contraceptive pill
  • leukaemia
  • dehydration
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7
Q

What 3 factors influence a clot formation? (hint: each of these factors can be treated by thrombolytic drugs)

A

1) platelets
2) coagulation cascade
3) fibrinolytic cascade

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8
Q

Describe an arterial thrombus

A
  • white
  • mainly platelets surrounded by fibrin mesh
  • forms embolus + detaches from site of origin (e.g. left heart/carotid artery)
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9
Q

Describe a venous thrombus

A
  • red
  • white fibrin head
  • jelly like tail composed of blood cells
  • fibrin + red blood cell rich
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10
Q

Where do embolus that detach from arterial thrombus usually occur?

A

brain (stroke)

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11
Q

Where do embolus that detach from venous thrombus usually occur?

A

lungs (pulmonary embolus)

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12
Q

Are platelets nucleated?

A

No, they are a nucleate cell fragments

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13
Q

What factor influences the formation of fibrin in a clot formation?

A

thrombin (clotting factor 2a)

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14
Q

What factor influences the conversion of prothrombin to thrombin?

A
  • clotting factor 10a

- proteolytic cleavage of prothrombin by 10a produces thrombin

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15
Q

What are the names of the 2 pathways that can form clotting factor 10a?

A

1) contact (intrinsic) pathway

2) in vivo

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16
Q

What clotting factors are associated with the contact pathway?

A

clotting factors 11a + 12a

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17
Q

What clotting factor is associated with the in vivo pathway?

A

clotting factor 7a

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18
Q

Where are clotting factors synthesised?

A

liver (Prof Fleming’s thrombosis lecture)

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19
Q

Describe the stages in platelet activation in response to endothelial damage (in the formation of a fibrin clot)

A
  • platelets adhere to damaged site
  • aggregation of platelets
  • secretion of preformed mediators from platelet granules (e.g. ADP/5-HT/coagulation factors)
  • synthesis of other mediators (e.g. TXA2)
  • further aggregation
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20
Q

The platelet membrane provides a surface allowing what to be brought together?

A

-clotting factors

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21
Q

How can clotting factors attach themselves to the platelet membrane?

A

-they become carboxylated

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22
Q

What charge does the platelet membrane have?

A

-negative charge

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23
Q

What clotting factor facilitates prothrombin and clotting factor 10a to be brought together (to form thrombin)?

A
  • clotting factor 5a
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24
Q

How are clotting factors 2/7/9/10 related to their active form?

A

they are GLYCOGEN PRECURSORS of 2a/7a/9a/10a

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25
Q

What is another name for these clotting factors? (2/7/9/10)

A

serine proteases

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26
Q

What needs to happen to the clotting factor precursors for them to become activated?

A
  • post-translational modification (e.g. gamma carboxylation)
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27
Q

What does the carboxylase enzyme that mediates gamma carboxylation require to work?

A

vitamin k in its reduced from

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28
Q

Give an alternative name for vitamin K in its reduced form

A

-hydroquinone

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29
Q

What is vitamin K in its oxidised form called?

A

-epoxide

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30
Q

What enzyme converts oxidised vitamin k to reduced vitamin k?

A
  • vitamin k reductase
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31
Q

What does warfarin do?

A
  • blocks vitamin K reductase
  • prevents formation of hydroquinone
  • prevents gamma carboxylation of clotting factors and subsequent coagulation
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32
Q

What type of drug is warfarin?

A

anti-coagulant

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33
Q

What are anti-coagulants used for?

A
  • prevention of VENOUS thrombosis + embolism

e. g. DVT/ post-op thrombosis/ artificial heart valves/ atrial fibrillation

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34
Q

What is the risk of taking anti-coagulants?

A

-haemorrhage

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35
Q

Does warfarin block vitamin k reductase in vivo or in vitro? (or in both?)

A
  • warfarin blocks vit k reductase in vivo only.

- this is because vitamin k is needed for warfarin to work - outwith the body on exogenous surfaces there is no vit k

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36
Q

How is warfarin administered?

A

-orally

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37
Q

What is warfarin’s onset of action?

A

2-3 days (allows time for activated clotting factors to be cleared)

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38
Q

What other anti-coagulant drug can be added to warfarin to give a more rapid effect?

A

-heparin

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39
Q

What is the half life of warfarin?

A

40 hours

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40
Q

Is the therapeutic index of warfarin low/high?

A

-low

fine balance between therapeutic dose and haemorrhage-causing dose

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41
Q

The effect of warfarin must be monitored on a regular basis - what is the name given for this?

A
  • international normalised ratio (INR)
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42
Q

What factors can increase the risk of haemorrhage (if patient is given warfarin)?

A
  • liver disease (decreases clotting factors - as they are synthesised in liver)
  • high metabolic rate (high clearance of clotting factors)
43
Q

What drug interactions with warfarin increase the risk of haemorrhage?

A
  • drugs that inhibit platelet function (NSAIDS/aspirin)
  • drugs that inhibit hepatic metabolism of warfarin
  • drugs that decrease availability of vitamin K
44
Q

What factors can increase the risk of thrombosis (lessen warfarin action?

A
  • physiological state (e.g. pregnancy)

- vitamin K consumption (e.g. in certain foods)

45
Q

What drug interactions with warfarin increase the risk of thrombosis?

A
  • drugs that increase the hepatic metabolism of warfarin
46
Q

If a patient overdoses on warfarin - what counteractive treatment can be given?

A
  • vitamin K

- increase concentration of plasma clotting factors

47
Q

What is antithrombin 3?

A
  • important inhibitor of coagulation that neutralises all protease factors in the coagulation cascade (clotting factors 2/7/9/10) by binding to their active site
48
Q

What is heparin’s role in relation to antithrombin 3?

A
  • heparin binds to antithrombin 3
  • this increases antithrombin 3’s affinity for serene proteases (clotting factors)
  • greatly increases rate of inactivation
49
Q

Which two clotting factors are particularly inhibited by antithrombin 3?

A

Factors 10a + 2a

50
Q

Does heparin have to bind to the active site of both antithrombin 3 and factor 2a in order for 2a to be inactivated?

A

yes

51
Q

Does heparin have to bind to the active site of both antithrombin 3 and factor 10a in order for 10a to be inactivated?

A

no, heparin only has to bind to antithrombin 3 in order for 10a to be inactivated

52
Q

What is heparin + where is it derived from?

A
  • a naturally occurring sulphated glycosaminoglycan
  • of variable molecular size
  • extracted from beef lung/hig intestine
53
Q

What are the dosage units for heparin?

A
  • dosage is specified in units of activity instead of mass

- this is because preparations of heparin have variable potency

54
Q

What serine protease(s) does low molecular weight heparin (LMWH) inhibit?

A
  • factor 10a

- NOT factor 2a

55
Q

Give an example of a LMWH

A
  • enoxaparin

- dalteparin

56
Q

How are LMWHs administered?

A
  • subcutaneously
57
Q

How is heparin administered?

A
  • IV (immediate onset)

- subcutaneously (1 hour onset)

58
Q

What is an in vitro clotting test and what is it used for?

A
  • determines the optimum dosage of heparin

- not used for LMWH

59
Q

What drug displays 0 order kinetics (rate of elimination not determined by concentration of drug)?

A
  • heparin
60
Q

What drug displays 1st order kinetics (rate of elimination is dependent on the concentration of the drug)?

A
  • LMWH
61
Q

How are LMWHs excreted from the body?

A
  • via the renal system
62
Q

Which anticoagulant drug is preferred in renal failure?

A
  • heparin
63
Q

What drug can be given if patient overdoses on heparin?

A
  • protamine sulphate
64
Q

Adverse effects of heparin/LMWH?

A
  • haemorrhage
  • osteoporosis
  • hypoaldosteronism
  • hypersensitivity reactions
65
Q

Dabigatran is an example of what?

A
  • a new orally active drug that acts as a direct inhibitor of thrombin
66
Q

What does rivaroxaban do?

A
  • directly inhibit factor 10a
67
Q

What circumstances are dabigatran/rivaroxaban used in?

A
  • patients undergoing hip/knee replacement (prevent DVT)
68
Q

Upon endothelial damage, platelet aggregation is driven by platelet-derived substances - name these.

A
  • adenosine diphosphate (ADP)
  • 5 - hydroxytryptamine (5-HT)
  • coagulation factors (excreted from platelet granules)
69
Q

What enzyme mediates the synthesis of thromboxane A2 (TXA2)?

A
  • cyclooxygenase 1 (COX-1)
70
Q

ADP/5 HT/ TXA2 act on the cell surface receptors of platelets causing expression what what receptors?

A
  • GP 2b/3a receptors
71
Q

What do GP 2b/3a receptors do?

A
  • cross link platelets via fibrinogen
72
Q

What does ADP bind to on the platelet surface?

A
  • P2Y12 receptor
73
Q

What drugs blocks ADP from binding to P2Y12?

A
  • clopidogrel
74
Q

How does P2Y12 bond to clopidogrel?

A
  • via a disulphide bond
75
Q

What does clopidogrel do?

A
  • irreversibly inhibits P2Y12
76
Q

What kind of drug is clopidogrel?

A
  • anti-platelet drug
77
Q

What does aspirin (another anti-platelet drug) do?

A
  • irreversibly blocks COX1 (in platelets/endothelial cells)
  • prevents synthesis of TXA2
  • prevents COX1 from converting arachidonic acid into cyclic-endoperoxidase (in the synthesis of TXA2)
78
Q

Is aspirin first line treatment for preventing arterial thrombosis?

A
  • yes
79
Q

Why is clopidogrel used to treat arterial thrombosis?

A
  • used if patient is intolerable to aspirin
80
Q

Is clopidogrel used alongside aspirin?

A
  • yes (has synergistic effect)
81
Q

What does tirofiban do?

A
  • blocks cross bridging between Gp 2b/3a receptors on platelets (prevents platelet aggregation)
  • anti-platelet drug
82
Q

Is tirofiban long/short term treatment?

A
  • short term
83
Q

What circumstances is tirofiban given in?

A
  • prevents MI in patients with unstable angina
84
Q

What other drugs are given alongside tirofiban?

A
  • aspirin

- heparin

85
Q

How is tirofiban administered?

A
  • IV
86
Q

Once a fibrin clot is formed, how is it dissolved?

A
  • by a process called fibrinolysis

- fibrinolysis opposes the coagulation cascade

87
Q

What substance converts fibrin to fibrin fragments?

A
  • plasmin
88
Q

How is plasmin produced?

A
  • by converting plasminogen
89
Q

What aids conversion of plasminogen - plasmin?

A
  • endogenous tissue plasminogen activator (tPA)
90
Q

Name 3 drugs which activate plasminogen?

A
  • streptokinase
  • alteplase
  • duteplase
91
Q

Streptokinase/ alteplase/ duteplase are examples of which kind of drug?

A
  • fibrinolytics
92
Q

What circumstances are fibrinolytics used?

A
  • reopen occluded arteries in acute MI/stroke/ less threatening venous thrombosis or pulmonary embolism
93
Q

How are fibrinolytics administered?

A
  • IV

- percutaneous coronary intervention (PCI)

94
Q
  • What other drug is given alongside fibrinolytics to make them more beneficial?
A
  • aspirin
95
Q

Where is streptokinase derived?

A
  • it is a protein derived from cultures of streptococci
96
Q

What blocks streptokinase’s action (and how long after beginning treatment does this occur?)

A
  • antibody production

- 4 days

97
Q

What name is given to alteplase + duteplase? (clue rt -PA)

A
  • recombinant tissue plasminogen activator (rt - PA)
98
Q

Are alteplase/duteplase more effective on fibrin bound plasminogen or plasma plasminogen?

A
  • fibrin bound plasminogen
99
Q

Are alteplast/duteplast selective?

A
  • yes, they show selectivity for clots
100
Q

How are alteplast/duteplast administered?

A
  • IV infusion
101
Q

Do alteplast/duteplast have a long/short half life?

A
  • short
102
Q

What is given to a patient if they overdose on fibrinolytics?

A
  • tranexamic acid
103
Q

What does tranexamic acid do?

A
  • inhibits plasminogen activation

- no conversion to plasmin

104
Q

Name the vitamin K dependent clotting factors

A
  • clotting factor 2/7/9/10

Cardiology (6 decks)

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