Pharmacology of stable coronary artery Flashcards

1
Q

drugs can help by

A

reducing heart rate, reducing myocardial contractility, afterload

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2
Q

purpose of drug treatment

A

relieve symptoms, halt the disease process, regression of disease process, prevent myocardial infarction, prevent death

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3
Q

vasodilators

A

calcium channel blockers, nitrates- oral and sublingual

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4
Q

rate limiting drugs

A

beta adrenoceptor antagonists, calcium channel blockers, ivabradine

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5
Q

common beta blockers used

A

bisoprolol, atenolol

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6
Q

beta blockers

A

reversible antagonists of the B1 and B2 receptors, newer drugs are cardioselective acting primarily on the B1 receptors, block the sympathetic system

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7
Q

beta blockers decrease what three determinants of myocardial oxygen demand

A

heart rate, contractility, systolic wall tension and also allow improved perfusion of the subendocardium by increasing diastolic perfusion time. this increases the exercise threshold at which angina occurs

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8
Q

contraindications of beta blockers

A

asthma, peripheral vascular disease (relative contraindication), raynauds syndrome, heart failure (those patients who are dependent on sympathetic drive), existing bradycardia/ heart block

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9
Q

adverse drug reactions of beta blockers

A

tiredness/ fatigue, lethargy, impotence, bradychardia, bronchospasm, rebound- sudden cessation of beta blocker therapy may precipitate myocardial infarction

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10
Q

drug- drug interactions

A

primarily pharmacodynamic

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11
Q

what happens when beta blockers with verapamil or diltiazem

A

bradycardia or cardiac failure

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12
Q

what happens when beta blockers with insulin or oral hypoglycaemics

A

exaggerate and mask hypoglycaemic actions

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13
Q

what happens when beta blockers with other hypotensive drugs

A

hypotension

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14
Q

examples of calcium channel blockers

A

diltiazem, verapamil, amlodipine

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15
Q

calcium channel blockers

A

prevent calcium influx into myocytes and smooth muscle lining arteries and arterioles by blocking the L type calcium channel

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16
Q

rate limiting calcium channel blockers

A

CCBs like diltiazem and verapamil reduce heart rate and force of contraction

17
Q

vasodilators calcium channel blockers

A

CCBs like amlodipine reduce BP and after load

18
Q

why never use nifedipine immediate release

A

may precipitate acute MI or stroke

19
Q

post MI CCB use

A

may increase morbidity and mortality in patients with impaired LV function

20
Q

unstable angina CCB use

A

evidence that dihydropyridines may increase infarction rate and death in the unstable patient

21
Q

adverse drug reactions CCBs

A

ankle oedema, headache, flushing, palpitation

22
Q

nitrovasodilators examples

A

glyceryl trinitrate GTN, isosorbide mononitrate, isosorbide dinitrate

23
Q

how do nitrovasodilators work

A

relax almost all smooth muscle by releasing NO which then stimulates the production of cGMP which produces smooth muscle relaxation. reduce preload and after load so reduce myocardial oxygen consumption

24
Q

how do nitrovasodilators relieve angina

A

arteriolar dilatation and so reducing cardiac after load and thus myocardial work and oxygen demand. peripheral venodilatation and so reducing venous return, cardiac preload and thus myocardial workload

25
Q

tolerance of nitrate therapy is overcome by

A

giving asymmetric doses of nitrate 8am and 2pm which incorporates a nitrate free period

26
Q

adverse reactions to nitrates

A

headache- increase dose slowly, hypotension- GTN syncope

27
Q

second line therapy for angina

A

nicorandil, ivabradine, ranolazine

28
Q

nicorandil

A

significant effect. activates ATP sensitive potassium channels allowing entry of potassium into cardiac myocytes and inhibiting calcium influx and so has a negative isotropic action. induces relaxation of vascular smooth muscle and has coronary vasodilator properties

29
Q

ivabradine

A

selective sinus node If channel inhibitor, inhibits the If pacemaker current in the sinoatrial node and reduces heart rate. decreases heart rate means decreases myocardial oxygen demand . used for the symptomatic treatment of chronic stable angina in adults with normal sinus rhythm and heart rate greater than 70bpm. reduces myocardial infarction

30
Q

ranolazine

A

inhibits persistent or late inward sodium current in heart muscle, this leads to reduction in intracellular calcium levels this results in reduced heart wall tension and reduced oxygen requirements

31
Q

do not use ranolazine with

A

clarithromycin, erythromycin or ketoconazole because these antibiotics and antifungal significantly inhibit CYP3A4

32
Q

antiplatelet therapy

A

combined with aspirin or P2Y12 inhibitors results in a significant reduction in serious vascular events, non fatal myocardial infarction, non fatal stroke and vascular mortality

33
Q

anti platelet agents eg aspirin

A

prevent the formation of platelet aggregates which are important in the pathogenesis of angina, unstable angina and acute MI. aspirin is a potent inhibitor of platelet thromboxane production which stimulates platelet aggregation

34
Q

P2Y12 inhibitors block what

A

platelet P2Y receptor which plays a key role in platelet activation and the amplification of arterial thrombus formation

35
Q

cholesterol lowering agents examples

A

HMG CoA reductase inhibitors -atorvastatin, simvastatin