pharmacology of stable coronary disease Flashcards

1
Q

benefits of beta blockers

A

reduces myocardial workload
decreases contractility
decreases systolic wall tension- improve relaxation
increases diastolic perfusion time
reduces rate of ischaemic events and mortality

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2
Q

mechanisms of action of calcium channel blockers

A

prevents calcium influx into myocyte and smooth muscle by blocking L type channels.

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3
Q

name a few calcium channel blockers

A

amlodipine, felodipine, nifedipine

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4
Q

name a few calcium channel blockers

A

amlodipine, felodipine, nifedipine

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5
Q

side effects of calcium channel blockers

A

brachycardia, oedema, hypotension, headache, flushing

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6
Q

benefits of calcium channel blockers

A

slows heart rate, reduce contractility, reduce after load, increase diastolic perfusion time, ini

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7
Q

mechanism of vasodilators

A

nitric oxide relaxes smooth muscle, non selective

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8
Q

benefits of vasodilators

A

reduce preload and afterloac therefore reduces myocardial workout, improves coronary flow, doesn’t reduce mortality

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9
Q

what is nicorandil

A

(vasodilator) activates ATP sensitive potassium channels causing potassium influx can lead to GI ulcerations

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10
Q

what is ivabradine

A

inhibits the funny channels in the sinoatrial node. only works when patient is in the sinus rhythm

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11
Q

what is ranolazine

A

(sodium channel inhibitor) inhibits late sodium current in myocardial cells, rapid delay of potassium rectifier current.

reduces oxygen demand due to reduced wall stress

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12
Q

name 4 anti platelet drugs

A

aspirin, clopidogrel, ticagrelor, prasugrel

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13
Q

NSTEMI

A

predictable, plaque rupture but blood still flows and you get a ST depression

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14
Q

STEMI

A

complete blockage, ST elevation and rise in troponin

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15
Q

how do you increase myocardial oxygen supply

A

coronary vasodilation, correct hyperaemia, stop platelet aggregation

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16
Q

how do you decrease myocardial oxygen demand

A

reduce heart rate, reduce blood pressure, reduce preload, reduce contractility and wall stress

17
Q

initial management of STEMI and unstable angina

A

morphine, oxygen, nitrates, aspirin, clopidogrel

18
Q

antiplatelets and their agents

A

aspirin- thromboxane A2 inhibitor (inhibits platelet activation)
clopidogrel/ticagrelor/prasugrel (inhibits ADP activation of PY212 receptor)

Fondaparinux ( converts fibrinogen to fibrin) to reduce clots

18
Q

antiplatelets and their agents

A

aspirin- thromboxane A2 inhibitor (inhibits platelet activation)
clopidogrel/ticagrelor/prasugrel (inhibits ADP activation of PY212 receptor)

Fondaparinux ( converts fibrinogen to fibrin) to reduce clots

19
Q

fibrin specific agents

A

altepase, tenecteplase
All catalyse conversion of plasminogen to plasmin in the absence of fibrin

20
Q

non- fibrin specific agents

A

streptokinase- low bleeding risk catalyse systemic fibrinolysis