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2D week 2 - stroke rehab > antiplatelets and anticoagulants > Flashcards

antiplatelets and anticoagulants Flashcards

1
Q

function of anticoagulants

A

slow down clotting, by reducing fibrin formation and preventing clots
from forming and growing

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2
Q

examples of anticoagulants

A

heparin, warfarin

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3
Q

function of antiplatelets

A

prevent platelets from clumping and also prevent clots from forming
and growing

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4
Q

examples of antiplatelets

A

aspirin, clopidogrel, ticagrelor, prasugrel

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5
Q

examples of DOACs

A

apixaban, rivaroxaban, dabigatran

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6
Q

what factors does warfarin act on?

A

II, VII, IX, X

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7
Q

what factors do DOACs work on

A

II, X

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8
Q

when should warfarin be given over DOACs

A

if the patient has mechanical heart valves

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9
Q

how does platelet aggregation occur

A

inter alia linking of platelets by fibrinogen binding to platelet GPIIb/GPIIIA receptors

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10
Q

what stage do anticoagulants act on

A

they inhibit the activation of clotting factors and tissue factors

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11
Q

what is the action on fibrinolytic agents (alteplase, reteplase)

A

they upregulate the activation of plasminogen to plasmin which acts to break down fibrin

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12
Q

how do clots form (pathway)

A

platelet adhesion activation aggregation -> activation of clotting factors/tissue factors -> fibrin framework arises allowing a thrombus to form

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13
Q

what do antifibrinolytic agents act on and when would they be used?

A

inhibit plasminogen turning into plasmin - allows clots to form; used to stop excessive bleeding

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14
Q

clotting cascade (draw it out)

A

https://www.osmosis.org/answers/coagulation-cascade

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15
Q

aspirin mechanism of action

A

irreversibly inactivates COX-1; alters the balance between thromboxane A2 and PGI2 in the vascular endothelium axis

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16
Q

clinical uses of aspirin

A

treatment of acute coronary syndrome; stroke (300mg loading dose); secondary prevention of arterial thrombosis (long term) after CV events; analgesia (much higher dose)

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17
Q

adverse effects of aspirin

A

GI bleed (due to PGs action in mucous barrier building); bronchospasm

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18
Q

MOA of clopidogrel

A

irreversibly inhibit the binding of ADP to the receptor on platetlets, inhibiting ADP-mediated platelet activation and GP IIb/IIIa mediated platelet aggregation

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19
Q

MOA of prasugrel

A

irreversibly inhibit the binding of ADP to the receptor on platetlets, inhibiting ADP-mediated platelet activation and GP IIb/IIIa mediated platelet aggregation

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20
Q

MOA of ticagrelor

A

reversible, non-competitive, P2Y12 inhibitor

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21
Q

clinical use of antiplatelets (clopidogrel, ticagrelor etc. - 3)

A

prophylaxis and treatment of MI, stroke and other vascular disorders

22
Q

adverse effects of antiplatelets (5)

A

bleeding; GI discomfort; rashes; neutropoenia; dyspnoea (rare)

23
Q

MOA of alteplase, duteplase, reteplase & streptokinase

A

activate plasminogen (acting as an enzyme) to form plasmin which digests fibrin and fibrinogen which dissolves the clot

24
Q

what must be checked before thrombolysis

A

the stroke is not haemorrhagic

25
Q

use of thrombolytic agents (alteplase etc. - 4)

A

MI; ischaemic stroke; arterial thrombosis; occaionally in DVT/PE

26
Q

why should thrombolytic agents not be used after the initial dose

A

antibodies appear after the initial dose (around 4 days after) which can block the action of the drugs

27
Q

adverse effects of thrombolytic agents

A

bleeding; reperfusion dysrhythmias; nausea/ vomiting; hypersensitivity reactions

28
Q

MOA of tranexamic acid

A

inhibits plasminogen activation, preventing fibrinolysis (opposite to alteplase)

29
Q

use of tranexamic acid

A

reduction of haemorrhage

30
Q

why might heparin have to be distributed multiple times?

A

it has a short half life

31
Q

MOA of heparin

A

accelerates action of antithrombin III - results in downregulating clotting factors IIa and Xa (also affects IXa, XIa & XIIa)

32
Q

clinical uses of heparin (3)

A

treatment of vein thrombosis/PE; unstable angina; PAD

33
Q

adverse effects of heparin (4)

A

bleeding; thrombocytopaenia; hypersensitivity reactions; osteoporosis

34
Q

MOA of LMWH - enoxaparin, dalteparin, bemiparin

A

accelerate action of antithrombin III (inactivates factor Xa)

35
Q

clinical uses of LMWH (4)

A

prophylaxis of VTE; treatment of DVT/PE; treatment of MI; treatment of angina

36
Q

why use LMWH rather than heparin (3)

A

better bioavailability; longer half life; less likely to cause thrombocytopaenia, hypersensitivity and osteoporosis

37
Q

how to treat LMWH overdose

A

protamine sulphate

38
Q

what drug class if warfarin

A

anticoagulant

39
Q

MOA of warfarin

A

Vit K antagonist - inhibits the reduction of vit K (thus preventing the carboxylation of glutamate residues in factors II/VII/IX/X)

40
Q

clinical use of warfarin (2)

A

treat VT/PE; prophylaxis of embolism in AF & valvular heart disease

41
Q

when should warfarin be given over DOACs

A

if mechanical heart valves are present

42
Q

adverse effects of warfarin

A

bleeding - treat by giving vit K or prothrombin complex concentrates

43
Q

what must be monitored for warfarin

A

INR (prothrombin time)

44
Q

rivaroxiban; apixaban; dabigtran drug class

A

factor Xa inhibitors; DOACs

45
Q

dabigatran MOA

A

direct inhibitor of clot-bound and free thrombin (factor IIa)

46
Q

rivaroxiban, apixaban MOA

A

direct factor a inhibitors

47
Q

cons of dabigatran

A

low bioavailaibility - 80% excreted renally

48
Q

rivaroxiban; apixaban; dabigtran clinical use

A

prophylaxis of DVT/PE in ortho surgery; treatment of VTE; prophylaxis of stroke in AF

49
Q

what should be given for a haemorrhagic stroke

A

anti hypertensives e.g. labetolol

50
Q

what should be done if AF + acute coronary syndrome is present

A

triple therapy (e.g. fondaparinux, aspirin/clopidogrel, ticagrelor)

2D week 2 - stroke rehab (5 decks)

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