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CARD - 1 > Clinical Pharmacology of Stable Coronary Heart Disease > Flashcards

Clinical Pharmacology of Stable Coronary Heart Disease Flashcards

1
Q

Ischaemic heart disease is most common cause of death in what group of people?

A

Pre-retirement males

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2
Q

What are some acute coronary syndromes?

A

MI - STEMI or NSTEMI

Unstable angina pectoris

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3
Q

What are chronic or stable ischaemia conditions?

A

Angina pectoris

Silent ischaemia

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4
Q

What are the risk factors for developing cardiac disease?

A

Hypertension, smoking, hyperlipidaemia, hyperglycaemia, male, post-menoplausal females.

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5
Q

What are the purpose of drugs treatment in SIHD and angina?

A

Relieve symptoms
Half the disease process
Regression of the disease progress
Prevent MI and death

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6
Q

What does hyperlipidaemia lead to?

A

Atherosclerosis is the start (disease of muscular arteries) - progressive deposition of cholesterol esters.

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7
Q

How does the atherosclerosis develop to occlude arteries?

A

Lesions start as fatty streaks in 20s and can develop into fibrous plaques (which are more advanced and project into the arterial lumen) - these reduced BF.

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8
Q

What are the fatty streaks composed of?

A

Sub-endothelial accumulation of large foam cells (derived from macrophages plus SM cells) filled with lipid.

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9
Q

Most of the changes that occur in atherosclerosis are in the intimal layer, describe these changes.

A

Accumulation of monocytes, lymphocytes, foam cells and connective tissue

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10
Q

Where do most of the foam cells come from?

A

Most foam cells are of smooth muscle origin.

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11
Q

What is the core of the fibrous plaque like?

A

Necrotic and lipid filled, surrounded by fibrous cap.

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12
Q

Why does stable ischaemic heart disease arise?

A

As a result of mismatch between myocardial blood/oxygen supply and demand.

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13
Q

What may precipitate an attack of angina?

A

Any stress which increases cardiac work and myocardial oxygen demand. So, anything that increases HR, SV or BP.

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14
Q

What is demand ischaemia and what are the determinants of demand?

A

Ischaemia during stress.

HR, systolic BP, myocardial wall stress and myocardial contractility determine demand.

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15
Q

What is supply ischaemia and what are the determinants of supply?

A

Ischaemia at rest.

Coronary artery diameter and tone, collateral BP, perfusion pressure, HR (duration of diastole).

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16
Q

What is all myocardial ischaemia associated with?

A

Coronary artery stenosis.

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17
Q

What is the common pathology that causes myocardial ischaemia?

A

Atherosclerosis - disease of the muscular arteries of coronary vessels.

18
Q

What is atherosclerosis? And at what point does it cause problems?

A

Progressive deposition of cholesterol esters.

Fibrous plaque is advanced stage and cause of disease.

19
Q

What are the six types/stages of atheroma formation?

A

Coronary artery at lesion-prone location.
Type II lesion - macrophage foam cells.
Type III (preatheroma) - small pools of extracellular lipid.
Type IV (atheroma) - core of extracellular lipid.
Type V (fibroatheroma) - fibrous thickening and significant lumen narrowing.
Type VI (complicated lesion) - fissure, haemotoma - formation of thrombus.

20
Q

How can drugs correct this imbalance between demand and supply?

A

Decreasing myocardial oxygen demand by reducing cardiac workload (reduce HR, myocardial contractility, afterload).
And
Increasing supply of oxygen to ischaemia myocardium.

21
Q

What are the rate limiting drugs that can be used in SIHD treatment?

A

Beta-adrenoceptor agonists
Ivabradine
Calcium channel blockers

22
Q

What are the vasodilator drugs that can be used in SIHD treatment?

A

Calcium channel blockers

Nitrates (oral/sublingual)

23
Q

What are some other drugs that can be used in SIHD treatment?

A

Potassium channel openers
Aspirin/Clopidogrel/Tigagrelor
Cholesterol lowering agents

24
Q

Give examples of cholesterol lowering agents you might use in treating SIHD.

A

HMG CoA reductase inhibitors

Fibrates

25
Q

Name two beta blockers.

A

Bisoprolol, Atenolol.

26
Q

What are beta blockers and what are their roles in treating stable angina?

A

Reversible antagonists of the beta1 and 2 receptors.
Newer drugs are cardioselective acting primarily on beta 1 receptors.
These agents back the physiological responses to adrenaline/noradrenaline (sympathetic system).

27
Q

Beta blockers decrease three major determinants of myocardial oxygen demand, what are these?

A

Heart rate, contractility, systolic wall tension.

28
Q

In what other way are beta blockers helpful for treating stable angina?

A

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

29
Q

In summary what do beta blockers do?

A

By reducing HR, force of contraction, BP, CO, velocity of contraction beta blockers increase the exercise threshold at which angina occurs and so moves the balance point at which the demand for oxygen outstrips the supply of oxygenated blood.

30
Q

In what way do beta blockers protect cardiomyocytes?

A

Protect them from oxygen free radicals formed during episodic ischaemic episodes.

31
Q

What can sudden cessation of beta blocker therapy cause? What is this known as?

A

MI.
Rebound phenomena.
MUST wean patients off.

32
Q

Who is at risk of rebound phenomena?

A

Patients with angina and men over 50 yrs receiving beta blockers for other reasons.

33
Q

What are the contraindications for beta blocker use?

A

Asthma
Peripheral vascular disease (relative contraindication)
Raynauds Syndrome
Heart failure (those dependent on sympathetic drive)
Bradycardia/heart block

34
Q

What are some ADRs with beta blockers?

A 
Tiredness/fatigue
Lethargy 
Impotence
Bradycardia
Bronchospasm
35
Q

What are some drug-drug interactions that can happen with beta blockers?

A

Hypotension when used with other hypotensive agents.
Bradycardia when used with other rate limiting, e.g. verapamil or diltiazem.
Cardiac failure when used with negatively inotropic agents, e.g. verapamil, diltiazem or disopyramide.
NSAIDs antagonise antihypertensive actions.
Can exaggerate and mask hypoglycaemia actions of insulin or oral hypoglycaemics.

36
Q

Name three calcium channel blockers.

A

Diltiazem, verapamil, amlodipine.

37
Q

What do the calcium channels do?

A

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

38
Q

What are the rate limiting calcium channel blockers and what effect do they have?

A

Diltiazem and Verapamil.

Reduce HR, force of contraction.

39
Q

What are the vasodilating calcium channel blockers and what effect do they have?

A

Nifedipine and Amlodipine.

May produce reflex tachycardia.

40
Q

When would you use calcium channel blockers?

A

If beta blockers aren’t working or patient in tolerant. DO NOT use with beta blockers.

41
Q

What other 3 things do CCBs do?

A

Reduce vascular tone and so produce vasodilation and reduce after load (reduce myocardial work load).

Rate limiting CCBs reduce HR and force of contraction (reduce oxygen requirements).

May also produce coronary vasodilatation.

42
Q

Which drug must you never use to treat angina or hypertension?

A

Nifedipine immediate release.
Capsules some people take for Reynolds.

Evidence that use of rapidly acting vasodilatatory CCBs may precipitate acute MI or stroke.

CARD - 1 (28 decks)

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