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Systems: Cardiovascualar AB > SIHD and Angina- Therapy > Flashcards

SIHD and Angina- Therapy Flashcards

1
Q

What is included under the umbrella ischaemic heart disease?

A
  • ACS

- Chronic or stable ischaemia

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2
Q

What is included in chronic or stable ischaemia?

A
  • Angina pectoris

- Silent ischaemia

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3
Q

What are the risk factors for ischaemic heart disease?

A
  • Hypertension
  • Smoking
  • Hyperlipidaemia
  • Hyperglycaemia
  • Male
  • Post-menopausal females
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4
Q

What is the purpose of drug treatment for ischaemic heart disease?

A
  • Relieve symptoms
  • Halt the disease process
  • Regression of the disease process
  • Prevent MI
  • Prevent death
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5
Q

What marks the start of hyperlipidaemia?

A

Atherosclerosis

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6
Q

What is hyperlipidaemia?

A
  • Disease of the muscular arteries

- Progressive deposition of cholesterol esters

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7
Q

What vessels are affected by hyperlipidaemia?

A
  • Coronary arteries

- Cerebral arteries

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8
Q

How do atherosclerotic lesions start?

A
  • As fatty streaks

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

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9
Q

What are fibrous plaques?

A
  • More advanced than fatty streaks and the cause of disease
  • Develop from fatty streaks
  • Projects into arterial lumen
  • Reduce blood flow
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10
Q

Where do most atherosclerotic changes occur?

A
  • In the intimal layer

- Accumulation of monocytes. lymphocytes, foam cells and connective tissue

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11
Q

What is the origin of most foam cells?

A

Smooth muscle

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12
Q

What is the main structure of an atheroma?

A
  • Necrotic core

- Fibrous cap

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13
Q

What does stable IHD arise as a result of?

A

Mismatch between myocardial blood/oxygen supply and demand

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14
Q

What may precipitate an angina attack?

A
  • Any stress which increases cardiac work and myocardial oxygen demand
  • Anything which increases heart rate, stroke volume or blood pressure
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15
Q

What is demand ischemia?

A

Ischaemia during stress (physical/emotional)

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16
Q

What are the determinants of demand ischaemia?

A
  • Heart rate
  • Systolic blood pressure
  • Myocardial wall stress
  • Myocardial contractility
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17
Q

What is supply ischaemia?

A

Ischaemia at rest

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18
Q

What are the determinants of supply ischaemia?

A
  • Coronary artery diameter and tone
  • Collateral blood flow
  • Perfusion pressure
  • Heart rate (duration of diastole)
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19
Q

What is the common pathology of ischaemic heart disease?

A

-Atherosclerosis

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20
Q

Type III atherosclerotic lesion

A

Preatheroma

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21
Q

Type IV atherosclerotic lesion

A

Atheroma

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22
Q

Type V atherosclerotic lesion

A

Fibroatheroma

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23
Q

Type VI atherosclerotic lesion

A

Complicated lesion

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24
Q

How can drugs help in IHD?

A
  • Decreasing myocardial oxygen demand by reducing cardiac workload
  • Increasing the supply of oxygen to ischaemic myocardium
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25
Q

How can cardiac workload be reduced?

A
  • Reduce heart rate
  • Reduce myocardial contractility
  • Reduce afterload
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26
Q

What is the drug therapy for IHD?

A
  • B-blockers
  • Ivabridine
  • Calcium channel blockers
  • Nitrates
  • Potassium channel openers
  • Aspirin/clopidogrel/ticagrelor
  • Cholesterol lowering agents
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27
Q

What drugs are rate limiting?

A
  • B-blockers
  • Ivabridine
  • Calcium channel blockers
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28
Q

What drugs are vasodilators?

A
  • Calcium channel blockers

- Nitrates

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29
Q

What drugs are cholesterol lowering agents?

A
  • HMG CoA reductase inhibitors

- Fibrates

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30
Q

Give 2 examples of B blockers.

A
  • Bisoprolol

- Atenolol

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31
Q

What are B blockers?

A
  • Reversible antagonists of the B1 and B2 receptors
  • Newer drugs are cardioselective acting primarily on the B1 receptors
  • These agents block the physiological responses to adrenaline and noradrenaline
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32
Q

What are the 3 major determinant of myocardial oxygen demand that B blockers decrease?

A
  • Heart rate
  • Contractility
  • Systolic wall tension
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33
Q

What do B blockers allow?

A

Improved perfusion of the subendocardium by increasing diastolic perfusion time

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34
Q

What affect for B blockers have on the heart?

A
  • Decrease heart rate
  • Decrease the force of myocardial contraction
  • Decrease cardiac output
  • Decrease the velocity of contraction
  • Decrease blood pressure
  • Protect cardiomyocytes from oxygen free radicals formed during ischaemic episodes
35
Q

What do B blockers do by reducing HR, force of contraction and BP?

A

Increase the exercise threshold at which angina occurs and so move the balance point at which the demand for oxygen outstrips the supply of oxygenated blood

36
Q

What is rebound phenomena?

A

Sudden cessation of B blocker therapy may precipitate MI

37
Q

Who is at risk of rebound phenomena?

A

Patients with angina and men over 50 receiving B blockers for other reasons

38
Q

What are the contraindications for B blockers?

A
  • Asthma
  • Peripheral vascular disease
  • Raynauds syndrome
  • Heart failure
  • Bradycardia/ heart block
39
Q

What adverse drug reactions can occur with B blockers?

A
  • Tiredness/fatigue
  • Lethargy
  • Impotence
  • Bradycardia
  • Bronchospasm
  • Rebound
40
Q

What drug-drug interactions can occur with B blockers?

A
  • Primary pharmacodynamics
  • Hypotension: hypotensive agents
  • Bradycardia: verapamil, diltiazem
  • Cardiac failure: negatively inotropic agents
  • Exaggerate and mask hypoglycaemic actions of insulin
41
Q

Give 3 examples of calcium channel blockers.

A
  • Diltiazem
  • Verapamil
  • Amlodipine
42
Q

What do calcium channel blockers do?

A

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

43
Q

What CCBs are rate limiting?

A

Diltiazem and verapamil reduce heart rate and force of contraction

44
Q

What CCBs are vasodilating?

A

Nifedipine or amlodipine may produce a reflex tachycardia

45
Q

How do CCBs reduce myocardial work load?

A

Reduce vascular tone and so produce vasodilation and reduce afterload

46
Q

How do CCBs reduce myocardial oxygen requirements?

A

Rate limiting CCBs reduce the heart rate and force of myocardial contraction

47
Q

What affect can CCBs have on coronary vessels?

A

May produce coronary vasodilation

48
Q

What should you never use CCB wise?

A

NEVER USE NIFEDIPINE IMMEDIATE RELEASE

49
Q

What are the contraindications for CCBs?

A
  • Post MI

- Unstable angina

50
Q

What may rapidly acting vasodilating CCBs do?

A

Precipitate acute MI or stroke

51
Q

Why should CCBs not be given post MI?

A

May increase the morbidity and mortality in patients with impaired LV function

52
Q

Why should CCBs not be given to those with unstable angina?

A

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

53
Q

What adverse drug reactions can occur with CCBs?

A
  • Ankle oedema
  • Headache
  • Flushing
  • Palpitation
54
Q

Give 3 examples of nitrovasodilators.

A
  • Glyceryl trinitrate
  • Isosorbide mononitrate
  • Isosorbide dinitrate
55
Q

How can glyceryl trinitrate (GTN) be administered?

A
  • Sublingual
  • Buccal
  • Transdermal
56
Q

How can Isosorbide mononitrate be administered?

A
  • Sustained release formulation

- Tablets

57
Q

How can isosorbide dinitrate be released?

A
  • Sustained release formulation

- Tablets

58
Q

What is the pharmacology behind nitrovasodilators?

A

-They relax almost all smooth muscle by releasing NO which then stimulated the release of cGMP which produces smooth muscle relaxation

59
Q

How do nitrovasodilators reduce myocardial oxygen consumption?

A

Reduce preload and afterload

60
Q

How do nitrates relieve angina?

A
  • Arteriolar dilatation and so reduced cardiac afterload and thus myocardial work and oxygen demand
  • Peripheral venodilation and so reduces venous return, cardiac preload and thus myocardial work load
  • Relieves coronary vasospasm
  • Redistributes myocardial blood flow to ischaemic areas of the myocardium
61
Q

Why is GTN used?

A
  • Rapid treatment of angina pain
  • To avoid first pass metabolism
  • May be used frequently and prophylactically
62
Q

Why are oral nitrates used?

A
  • Can be give as a once a day sustained release formulation

- Prophylaxis

63
Q

Why are IV nitrates used?

A

Main stay treatment of unstable angina where they are used combination with heparin

64
Q

How is tolerance to the effects of nitrate therapy overcome?

A
  • Giving asymmetric doses of nitrate 8am and 2pm

- Using a sustained release preparation which incorporates a nitrate free period

65
Q

What are the adverse drug reactions with nitrates?

A
  • Headaches (increase dose slowly)

- Hypotension producing GTN syncope

66
Q

Give an example of a potassium channel opener

A

Nicorandil

67
Q

What do potassium channel openers do?

A
  • Active silent potassium channels

- The entry of potassium into cardiac myocytes inhibits the calcium influx and so has a negative inotropic action

68
Q

Why are potassium channel openers now third line treatment?

A

Can result in Crohns like bowel ulcerations

69
Q

What is ivbradine?

A

A selective sinud node I channel inhibitor

70
Q

What does ivabridine do?

A
  • Slows the diastolic depolarisation slope of the SA node
  • Results in a reduction in heart rate
  • Reduces heart rate and myocardial oxygen demand
71
Q

Give an example of an anti-platelet agent.

A

Low dose aspirin (75-150mg)

72
Q

What is aspirin

A

A potent inhibitor of platelet thromboxane production

73
Q

What does thromboxane stimulate?

A

Platelet aggregation and vasoconstriction

74
Q

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

A

Low dose aspirin

75
Q

What does clopidogrel do?

A

Inhibits ADP receptor activated platelet aggregation

76
Q

When is clopidogrel used?

A
  • Prevention of atherosclerotic events in PVD

- ACS

77
Q

How does clopidogrel differ in its incidenc of bleeding to aspirin?

A

Same incidence of bleeding but possibly lower GI bleeding

78
Q

Give 3 examples of cholesterol lowering agents.

A
  • Simvastatin
  • Pravastatin
  • Atorvastatin
79
Q

What are simvastatin, pravastatin and atorvastatin examples of?

A

HMG CoA reductase inhibitors

80
Q

What is the treatment regime for IHD?

A
  • B blocker
  • Rate limiting CCB
  • Dihydropirinde CCB
  • Ivabridine/ranolazine
  • Nicorandil
  • Aspirin
  • Statin
  • Long acting nitrate
  • Refer to cardiology for work up and possible stenting
81
Q

What are the indications for ivabridine?

A
  • In adults unable to tolerate or with contr-indications to B blockers
  • In combination with B blockers in patients inadequately controlled with an optimal B blocker dose
82
Q

What is ivabradine used for?

A

Symptomatic treatment of chronic stable angina in adults with normal sinus rhythm and heart rate >70bpm

83
Q

Ivabridine is only effective in reducing the incidence of coronary artery disease in who?

A

Patients with heart rate of 70 bpm or over

Systems: Cardiovascualar AB (42 decks)

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