Stable Ischaemic Heart Disease and Angina Therapy Flashcards

1
Q

what are the risk factors for SIHD and angina?

A
> hypertension
> smoking
> hyperlipidaemia
> hyperglyaemia
> male
> post-menopausal females
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2
Q

what is the purpose of drug treatment?

A
> relieve symptoms
> halt disease process
> regress the disease process
> prevent myocardial infarction
> prevent death
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3
Q

in an atheroma plaque what layer of artery is affected the most?

A

the intimal area

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4
Q

how does stable angina arise?

A

a mismatch between myocardial blood/oxygen supply and demand

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5
Q

how do drugs correct the supply and demand imbalance of oxygen in the myocardium?

A
Decrease myocardial oxygen demand:
> reduction of the heart rate
> reduction of the myocardial contractility
> reduction of afterload
Increase supply of oxygen to myocardium
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6
Q

name 2 beta blocker used

A

> bisprolol

> atenolol

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7
Q

what are beta blockers?

A

reversible antagonists for beta1 and 2 receptors

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8
Q

what three things do beta blockers decrease?

A

> heart rate
contractility
systolic wall tension

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9
Q

how do beta blockers improve perfusion of the sub-endocardium

A

by increasing diastolic perfusion time

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10
Q

what do beta blockers protect cardiomyocytes from during ischemic episodes?

A

oxygen free radicals

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11
Q

how do beta blocker increase the threshold at which angina occurs?

A

they reduce the heart rate, force of contraction and blood pressure so the balance point at which demand for oxygen outstrips the supply.

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12
Q

what is rebound phenomena?

A

sudden cessation of beta blocker therapy may precipitate myocardial infarction

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13
Q

what are the contraindications for beta blockers?

A
> asthma
> peripheral vascular disease
> raynauds syndrome
> heart failure (dependant on sympathetic system)
> bradycardia/heart block
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14
Q

what adverse drug reaction can occur due to beta blockers?

A
> tiredness
> lethargy
> impotence
> bradycardia
> bronchospasm
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15
Q

what drug-drug interactions with beta blockers can cause hypotension?

A

other hypotensive agents

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16
Q

what drug-drug interactions with beta blockers cause bradycardia?

A

other rate limiting drugs such as verapamil or diltiazem

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17
Q

what drug-drug interactions with beta-blocker cause cardiac failure?

A

negatively inotropic agents such as verapamil, diltiazem or disopyramide

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18
Q

what drug-drug interactions with beta blockers agonise antihypertensive actions?

A

NSAIDs

19
Q

what are the drug drug interaction of beta-blockers and insulin/oral hypoglycaemics?

A

they exaggerate and mask hypoglycaemic actions of insulin or oral hypoglycaemics

20
Q

name three calcium channel blocker

A

> diltiazem
verapamil
amlodipine

21
Q

what is the action of calcium channel blockers?

A

they prevent calcium influx into myocytes and smooth muscle lining the arteries and arterioles by blocking the l-type calcium channels. this reduces vascular tone, afterload, heart rate and myocardial oxygen requirements.

22
Q

what are the effects of rate limiting calcium channel blocker?

A

they reduce heart rate and force of contraction

23
Q

what are the effects of vasodilating calcium channel blockers

A

they produce a reflex tachycardia

24
Q

why should you never use nifedipine immediate release?

A

there is evidence that the use of rapidly acting vasodilatory CCBs may precipitate and MI or stroke

25
Q

what are the contraindications of calcium channel blockers?

A

post MI (may increase morbidity and mortality) and unstable angina (increase infarction rate and death).

26
Q

name some adverse drug reaction from calcium channel blockers

A

> ankle oedema
headache
flushing
palpitations

27
Q

name three nitrovasodilators and their administration methods

A

> glyceryl trinitrate (sublingual, buccal, transdermal)
isosorbide mononitrate (sustained release formulation, tablets)
isosorbide dinitrate (sustained release formulation, tablets)

28
Q

describe the pharmacology of nitrovasodilators

A

they relax almost all smooth muscle by releasing NO which then stimulates the release of cGMP which produces smooth muscle relaxation.

29
Q

what is the effect of nitrovasodilators on preload and afterload?

A

they reduce preload and afterload

30
Q

how do nitrates relieve angina?

A

> arteriolar dilation (reduce cardiac afterload)
peripheral veno-dilation (reducing venous return, afterload)
relieves coronary vasospasm
redistributes myocardial blood flow to ischaemic areas

31
Q

what nitrate is used for prophylaxis?

A

oral nitrates given as a once a day sustained release

32
Q

what is used to rapidly treat angina pain?

A

GTN

33
Q

what is the main treatment of unstable angina?

A

intravenous nitrates used in combination with heparin

34
Q

how can tolerance to nitrates be overcome?

A

> giving asymmetric doses of nitrate 8am and 2pm

> using a sustained release preparation which incorporates a nitrate free period

35
Q

what adverse drug reactions can occur with nitrates?

A

> headache

> hypotension: GTN syncope

36
Q

what does nicorandil activate?

A

silent potassium channels

37
Q

what is the affect of nicorandil?

A

it allows entry of potassium into cardiac myocytes inhibiting the calcium influx, having a negative inotropic action.

38
Q

what problems arise due to nicorandil?

A

bowel ulceration

39
Q

what channel does ivabradine inhibit?

A

sinus node If channel

40
Q

what is the affect of ivabradine?

A

it slows diastolic depolarisation slope of the SA-node resulting in a reduction in heart rate and myocardial oxygen demand

41
Q

what does aspirin inhibit?

A

platelet thromboxane production

42
Q

what are the indications for aspirin?

A

> adults who are unable to tolerate/with a contraindication for the use of beta blockers
in combination wit beta blockers in patients inadequately controlled with an optimal beta-blocker dose

43
Q

what does clopidogrel inhibit?

A

ADP receptor activated platelet aggregation

44
Q

name three HMG CoA reductase inhibitors

A

> simvastatin
pravastatin
atorvastatin