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

antiplatelets and anticoagulants Flashcards

(50 cards)

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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)

Study These Flashcards
A

prophylaxis and treatment of MI, stroke and other vascular disorders

22
Q

adverse effects of antiplatelets (5)

Study These Flashcards
A

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

23
Q

MOA of alteplase, duteplase, reteplase & streptokinase

Study These Flashcards
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

Study These Flashcards
A

the stroke is not haemorrhagic

25
use of thrombolytic agents (alteplase etc. - 4)
MI; ischaemic stroke; arterial thrombosis; occaionally in DVT/PE
26
why should thrombolytic agents not be used after the initial dose
antibodies appear after the initial dose (around 4 days after) which can block the action of the drugs
27
adverse effects of thrombolytic agents
bleeding; reperfusion dysrhythmias; nausea/ vomiting; hypersensitivity reactions
28
MOA of tranexamic acid
inhibits plasminogen activation, preventing fibrinolysis (opposite to alteplase)
29
use of tranexamic acid
reduction of haemorrhage
30
why might heparin have to be distributed multiple times?
it has a short half life
31
MOA of heparin
accelerates action of antithrombin III - results in downregulating clotting factors IIa and Xa (also affects IXa, XIa & XIIa)
32
clinical uses of heparin (3)
treatment of vein thrombosis/PE; unstable angina; PAD
33
adverse effects of heparin (4)
bleeding; thrombocytopaenia; hypersensitivity reactions; osteoporosis
34
MOA of LMWH - enoxaparin, dalteparin, bemiparin
accelerate action of antithrombin III (inactivates factor Xa)
35
clinical uses of LMWH (4)
prophylaxis of VTE; treatment of DVT/PE; treatment of MI; treatment of angina
36
why use LMWH rather than heparin (3)
better bioavailability; longer half life; less likely to cause thrombocytopaenia, hypersensitivity and osteoporosis
37
how to treat LMWH overdose
protamine sulphate
38
what drug class if warfarin
anticoagulant
39
MOA of warfarin
Vit K antagonist - inhibits the reduction of vit K (thus preventing the carboxylation of glutamate residues in factors II/VII/IX/X)
40
clinical use of warfarin (2)
treat VT/PE; prophylaxis of embolism in AF & valvular heart disease
41
when should warfarin be given over DOACs
if mechanical heart valves are present
42
adverse effects of warfarin
bleeding - treat by giving vit K or prothrombin complex concentrates
43
what must be monitored for warfarin
INR (prothrombin time)
44
rivaroxiban; apixaban; dabigtran drug class
factor Xa inhibitors; DOACs
45
dabigatran MOA
direct inhibitor of clot-bound and free thrombin (factor IIa)
46
rivaroxiban, apixaban MOA
direct factor a inhibitors
47
cons of dabigatran
low bioavailaibility - 80% excreted renally
48
rivaroxiban; apixaban; dabigtran clinical use
prophylaxis of DVT/PE in ortho surgery; treatment of VTE; prophylaxis of stroke in AF
49
what should be given for a haemorrhagic stroke
anti hypertensives e.g. labetolol
50
what should be done if AF + acute coronary syndrome is present
triple therapy (e.g. fondaparinux, aspirin/clopidogrel, ticagrelor)

2D week 2 - stroke rehab (5 decks)

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