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Semester 2 > SIHD and Angina - Therapy > Flashcards

SIHD and Angina - Therapy Flashcards

1
Q

Here are the learning outcomes

A
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2
Q

What are the acute coronary syndromes and the stable coronary artery diseases?

A

Acute:

Myocardial infarction (STEMI/NSTEMI)

Unstable angina pectoris

Stable:

Angina pectoris

Silent ischaemia

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3
Q

How does SCAD (stable coronary artery disease) arise?

A

•mismatch between myocardial blood/ oxygen supply and demand

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4
Q

What causes the onset of ischaemia in demand ischaemia vs Supply ischaemia?

A
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5
Q

What are the determinants of demand?

A

Heart rate

Systolic blood pressure

Myocardial wall stress

Myocardial contractility

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6
Q

What are the seterminants of supply?

A

Coronary artery diameter and tone

Collateral Blood flow

Perfusion pressure

Hear rate (duration of distole)

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7
Q

What does hyperlipidaemia result in the deposition of?

A

Cholesterol esters

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8
Q

Where is the accumulation of foam cells in atherosclerosis?

A

Subendothelial

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9
Q

What is the cause of disease in atherosclerosis?

A

Fibrous plaques that project into the arterial lumen reducing blood flow

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10
Q

How can drugs overcome the deman/suppply imbalance?

A
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11
Q

What is the purpose of drug treatment in stable coronary artery disease?

A

To releive symptoms

Halt the disease process

Regression of the disease process

Prevent myocardial infarction

Prevent death

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12
Q

Here is a summary of all the potental drug therapies for stable coronary artery disease

A
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13
Q

From summary of drugs for stable ischaemic heart disease, what is are the rate limiting drugs?

A

Beta blockers

Ivabradine

Calcium channel blockers

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14
Q

What are the vasodilators used in the treatment of stable ischaemic heart disease?

A

Calcium channel blockers

Nitrates

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15
Q

Give examples of beta blockers

A

Bisoprolol and atenolol

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16
Q

What receptors do beta blockers block?

A

Reversible antagonists of beta 1 and beta 2 receptors

Newer drugs are cardioselective acting on the beta 1 receptors

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17
Q

How do beta blockers serve to decrease demand?

A

Reduce heart rate, reduce contractility, reduce systolic wall tension, decreases blood pressure, protects cardiomyocytes from oxygen free radicalsf ormed during ischaemic episodes

•Also allow improved perfusion of the subendocardium by increasing diastolic perfusion time

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18
Q

What are the contraindications for beta blockers?

A

Asthma

Peripheral vascular disease

Raynauds syndrome

Heart failure (those patients who are dependatn on sympathetic drive)

Bradycardia / heart block

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19
Q

What are the adverse drug reactions of beta blockers?

A
  • Tiredness /fatigue
  • Lethargy
  • Impotence
  • Bradycardia
  • Bronchospasm
  • Rebound –

–Sudden cessation of beta blocker therapy may precipitate myocardial infarction

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20
Q

What are the drug drug interactions of beta blockers?

A

Hypotentsion when used with other hypotensive agents

Bradycardia when used with other rate limiting drugs such as verapamil or diltiazem

Cardiac failure when used with negatively inotropic agents such as verapamil, disopyramide or diltiazem

NSAIDS antagonise antihypertensive actions

Exaggerate and mask hypoglycaemic actions of insulin or oral hypoglycaemics

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21
Q

How do calcium channels work?

A

Prevent calcium influx into myocytes and smooth muscle lining arteries and arterioles by blocking the L-Type calcium channel.

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22
Q

Give examples of rate limiting CCB’s and what they do

A

Diltiazem and verapamil - reduce heart rate and force of contraction - reducing myocardial oxygen requirements

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23
Q

Give an example of a vasodilating CCB and what it does

A

Amlodipine - (may produce a reflex tachycardia)

Vasodilitation, reducing afterload

Reduces myocardial work load

24
Q

Do CCB’s cause coronary vasodilatation?

A

Yesm but of little importance

25
Q

What is the effect of a rapidly acting vasodilatory CCB? (nifedipine)

A

May precipitate acute MI or stroke

26
Q

What are the common adverse drug reactions associated with calcium channel blockers?

A

Ankle oedema (–Affects 15-20% of patients and does not respond to diuretics)

Headache

Flushing

Palpitation

27
Q

Give examples of nitrovasodilators

A

•GLYCERYL TRINITRATE (GTN)

–Sublingual, buccal, transdermal

•ISOSORBIDE MONONITRATE

–Sustained release formulation, tablets

•ISOSORBIDE DINITRATE

–Sustained release formulation, tablets

28
Q

How do nitrovasodilators work?

A

Relax almost all smooth muscle by releasing NO

Stimulates the production of cGMP which causes smooth muscle relaxation

Reduces preload and afterload so reduces myocardial oxygen consumption

29
Q

What are the uses of GTN and oral nitrates?

A

GTN - rapid treatment of angina pain

Oral nitrates -

–Commonly given as a once a day sustained release formulation

–Used for prophylaxis

30
Q

When are intravenous nitrates used?

A

Treatment of unstable angina used in combination with heparin

31
Q

How do you overcome the development of tolerance to nitrate therapy?

A

–Giving asymmetric doses of nitrate 8am and 2pm

–Using a sustained release preparation which incorporates a “nitrate free period”

32
Q

What are the adverse drug reactions for GTN?

A

Headache

Hypotension (GTN syncope)

33
Q

Summary Table

A
34
Q

Why is nicorandil said to have a negative ionotropic action?

A

It activates ATP sensitive potassium channels, •The entry of potassium into cardiac myocytes inhibits calcium influx and so has a negative inotropic action.

35
Q

How does nicorandil cause a decrease in preload and afterload?

A

Activates Cyclic GMP, causing the dilation of capacitance vessels, decereases preload

Opens ATP sensitive potassium channels, these channels are involved in dilation of coronary resistance arterioles, these decrease afterload and are also thought to mimic ischaemic preconditioning - a potential cardioprotective effect

36
Q

How does the activation of ATP sensitive potassium channels result in the relaxation of vascular smooth muscle and the dilitation of systemic and coronary arterioles?

A

ATP sensitive potassium channels cause potassium efflux, causing voltage gated calcium channels to close, intracellular levels of calcium decrease - relaxation of vascular smooth muscle

37
Q

How does Ivabradine reduce heart rate?

A

Selective sinus node channel inhibitor, slows the diastolic depolarisation slope of the SA node

38
Q

Which patients can ivabridine used for?

A

Those who have a heart rate of 70 and over.

Not effective at reducing the incidence of coronary artery disease outcomes in patients with heart rate less than 70 bpm

Symptomatic treatment of stable angina only effective if sinus rhythm and heart rate is greater than 70 beats per minute

39
Q

What are the indications for ivabradine?

A

Patients who cannot use beta blockers

Patients who are inadequately controlled with optimal beta blocker dose

40
Q

What is the action of thromboxane?

A

Stimulates platelet aggregation and vasoconstriction

41
Q

How does aspirin inhibit platelet thromboxane production?

A

Aspirin acts by inhibiting the ability of the COX enzyme to synthesize the precursors of thromboxane within platelets

42
Q
A
43
Q

What is the effect of aspirin on acute MI and unstable angina?

A

Acute MI: Reduces mortality, in conjunction with streptokinase it can also reduce reinfarction

Unstable MI: Reduces MI and death

44
Q

What is the most common cause of admission with GI bleed?

A

Aspirin

45
Q

What is the effect of clopidogrel?

A

Inhibits ADP receptor activated platelet aggregation

46
Q

What are the most effective cholesterol lowering agents?

A

HMG CoA reductase inhibitors - SIMVASTATIN, PRAVASTATIN, ATORVASTATIN

47
Q

What is the point in cholesterol lowering agents post MI?

A

Can reduce cardiovascular mortality and total mortality

48
Q

Treatment regimen

A
49
Q

What is the NICE guidance for treatment for the relief of symptoms of stable angina?

A

Beta blockers first line therapy

Calcium channel blocker should be added if adequate control of symptoms is not achieved

•If the person’s symptoms are not satisfactorily controlled consider either switching to the other option or using a combination of the two

50
Q

Which SIHD patients are offered •long term standard aspirin and statin therapy?

A

All patients with stable angina due to atherosclerotic disease

51
Q

Who is offerec ACEi?

A

•All patients with stable angina should be considered for treatment with ACEi.

52
Q

What drugs are given for the secondary prevention of cardiovascular disease?

A
  • Aspirin 75 mg daily taking into account the risk of bleeding and comorbidities.
  • ACE inhibitors for people with stable angina and diabetes.
  • Statin treatment
  • Treatment for high blood pressure
53
Q

Overview

A
54
Q

Overview for angina relief

A
55
Q

Overview for event protection

A

Semester 2 (150 decks)

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