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Case 4 > Management of Stable Angina with Drugs > Flashcards

Management of Stable Angina with Drugs Flashcards

1
Q

When is the myocardium perfused with oxygenated blood

A

During diastole (as the coronary vessels are squished during systole)

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2
Q

What is myocardial oxygen demand a function of

A

How hard the heart is having to work (heart rate increases) and ventricular wall tension (determined by the pressure, chamber volume and wall thickness)

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3
Q

Describe the vasculature of the heart

A

Aorta, anterior surface: left coronary artery (LCA) initially branches to yield the left anterior descending (LAD) or anterior interventricular artery, the LCA then progresses to become he left marginal artery (LMA) and left circumflex artery (Cx- left posterior surface). Right coronary artery (RCA) comes from the aorta and branches to form the right marginal artery (RMA) anf the posterior interventricular artery (Plc) posteriorly (right posterior surface)

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4
Q

What is coronary blood flow determined by

A

Myocardial oxygen demand

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5
Q

What is resting coronary blood flow

A

c.224 ml/min

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6
Q

What can vigorous exercise flow be

A

c.800+ ml/min

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7
Q

Why is there a factor 4 increase in coronary blood flow during vigorous exercise

A

The heart requires a lot of oxygen

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8
Q

What does compromised coronary artery flow have major implications for

A

The myocardium

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9
Q

What are risk factors for coronary artery disease

A

Obesity, hypercholesterolaemia, family history of CAD, hypertension, smoking, diabetes, kidney disease (>men, >65 women), physical inactivity and psychosocial stress

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10
Q

What does the fact that many of the risk factors for coronary artery are lifestyle related mean

A

There is need for primary intervention and empowering patients to take care of their own health

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11
Q

What does normal blood flow rely on

A

Vessels elastically expanding after pulsatile ejections

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12
Q

What can make artery walls less elastic and more rigid and what impact does this have

A

Age and risk factors make artery walls less elastic and more rigid, increasing cardiac inotropy to compensate

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13
Q

What can increasing cardiac inotropy lead to

A

Ventricle hypertrophy and increased myocardial oxygen demand

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14
Q

What does the fact that you have a pulse wave mean

A

That vessels dilate after each heart beat which males the job of the heart less hard which reduces afterload

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15
Q

What happens if the vessels are stiffer and more rigid

A

They can’t accommodate meaning that the heart has to work harder which increases the amount of muscle resulting in left ventricular hypertrophy which is pathological

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16
Q

What are the main features of atherosclerosis

A

The growth of LDL-cholesterol laden plaques in the sub-endothelium

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17
Q

Describe the process of atherosclerosis and what it leads to

A

The process is multi-factorial and leads to tissue ischaemia

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18
Q

What effects do the plauques have on the vessel

A

The plaques narrow the bore of the vessel resulting in a lack of oxygenated blood that can pass as the vessels are partially occluded

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19
Q

When is ischaemia inevitable

A

If oxygenated blood cannot meet the myocardial demand

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20
Q

What happens in myocardial anaerobic glycolysis

A

Large quantities of lactate are generated from pyruvate

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21
Q

When does myocardial ischaemia occur

A

When the vessel bore id reduced

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22
Q

Why is it formed and what does lactate trigger

A

Lactate is produced during ischaemia as there is a lack of oxygenated blood and this can trigger pain

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23
Q

What are the signs and symptoms of angina

A

Crushing, burning or ‘tight’ chest pain often accompanied by shortness of breath, nausea and sweating

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24
Q

What determines the nature/ severity of angina symptoms

A

Which coronary arteries and how narrowed they are

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25
Q

What are angina symptoms precipitated by

A

Physical exertion or emotional stress

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26
Q

What are angina symptoms relieved by

A

By rest (relieved within minutes)

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27
Q

What are examples of physical exertion that can bring on angina pain

A

Gardening, walking for the bus and lifting shopping

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28
Q

When is transient ischaemia resolved

A

When you stop exertion and rest

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29
Q

What do angina symptoms warrant

A

Further investigation and conformation that it is stable angina

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30
Q

When do acute coronary symptoms appear

A

At rest, although may be due to vasospasm

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31
Q

What does ACS usually indicate

A

Unstable (vulnerable) plaque ruture (whcih coronary arteries and how long determine the nature of the nature of the symptoms and severity) with thrombus fragments adding to the narrowing of the coronary vessels

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32
Q

What did acute coronary syndrome used to be called

A

Unstable angina

33
Q

What does a thrombus do

A

Further occlude a blood vessel resulting in transient narrowing of a vessel

34
Q

What does the fact that acute coronary syndrome is acute mean

A

It can lead to a full on MI depending on the nature of plaque rupture

35
Q

What ECG changes are seen during exertion with someone with angina

A

Characteristic ‘ST depression’ seen on a 12-lead ECG in a patient taking an exercise stress (treadmill) test. People tend to display a relatively normal ECG at rest with normal P, Q, R, S, T waves at rest. Atfer 7 minutes of walking on a treadmill people with angina display characteristic ST depression. When the treadmill is stopped the ECG returns back to normal. People are also asymptomatic at rest

36
Q

What causes ST depression

A

Ventricular tissue becoming ischaemic

37
Q

What can coronary angiography be used to diagnose

A

Angina

38
Q

Describe angiography

A

It is an x-ray based imaging technique that can identify narrowing or partial occlusion of coronary arteries. A radio-opaque contrast dye is injected into the coronaries via a catheter. The catheter goes through the femoral artery and terminates at the start of the coronary vessels. Any narrowing= cardiac ischaemia

39
Q

Describe echocardiography

A

A non-invasive ultrasound imaging technique that can identify chamber wall motion abnormalities that may indicate coronary artery disease. Can identify problems in walls or valves. Ischaemic conditions give rise to wall motion abnormalities

40
Q

What are drugs being used for symptomatic relief of angina used for

A

Can be used to reduce/ relieve angina symptoms associated with an episode of ischaemic stress which is symptomatic relief

41
Q

What are prophylactic angina drugs used for

A

To reduce incidence of angina episodes which is preventative

42
Q

What drug provides symptomatic relief of angina

A

Glyceryl trinitrate

43
Q

What forms does glyceryl trinitrate come in

A

IV, sub-lingual spray (goes under the tongue because there are lots of blood vessels which means it quickly dilates coronary vessels) and patch

44
Q

What drug provides preventative relief of angina

A

Bisoprolol

45
Q

What form does Bisoprolol come in

A

Tablets

46
Q

What are organic nitrate drugs like isiosorbide mononitrate and glyceryl trinitrate reduced to in the body

A

Nitric oxide (NO)

47
Q

What is NO

A

A potent vasodilator

48
Q

Describe the MOA of NO

A
  1. NO activated guanylyl cyclase (GC) in vascualr smooth muscle cells. 2. cGMP increases which activates protein kinase G (PKG). 3. PKG activity prevents Ca2+ entry into smooth muscle cells. 4. Coronary vessels dilate (reducing angina symptoms)
49
Q

What does the fact that calcium can’t enter the muscle mean

A

The muscle can’t contract as forcefully

50
Q

What is nitrate tachpylaxis

A

The body gets used to NO which means that it doesn’t work because you become desensitised to NO

51
Q

What are common ADRs of NO

A

Postural hypotension, tachycardia, throbbing headache

52
Q

What are uncommon ADRs of NO

A

Flushing, heartburn, nausea, rash, syncope, temporary hypoxaemia, vomiting

53
Q

What are very rare ADRs of NO

A

Angle-closure glaucoma

54
Q

What are contraindications of NO

A

Aortic stensosis, cardiac tamponade, constrictive pericarditis, hypertrophic cardiomyopathy, hypotensive conditions, hypovolaemia, marked anaemia, mitral stenosis, raises intracranial pressure due to cerebral haemorrhage, raised intracranial pressure due to head trauma, toxic pulmonary oedema

55
Q

What is the MOA of β1-adrenoreceptor antagonists

A

Effective means of reducing onset of angina episodes/ attacks. β1-adrenoreceptor antagonists competitively inhibit β1-adrenoreceptors in cardiac tissue, preventing binding of agonists noradrenaline and adrenaline. This has a negative chronotropic an negative ionotropic effect that reduces cardiac output

56
Q

What are ADRS of β1-adrenoreceptor antagonists

A

Dry eyes, rashes

57
Q

What are contraindications of β1-adrenoreceptor antagonists

A

Asthma; cardiogenic shock; hypotension; marked bradycardia; metabolic acidosis; phaeochromocytoma (apart from specific use with alpha-blockers); Prinzmetal’s angina; second-degree AV block; severe peripheral arterial disease; sick sinus syndrome; third-degree AV block; uncontrolled heart failure

58
Q

What is the method of action of calcium channel blockers

A

Impede Ca2+ traffic through L-type voltage-gated channels. The CCB crosses the membrane, binds to the channel and induces a conformational change which forces the channel to remain inactive stopping Ca2+ traffic. Electrical conduction through the heart is dependent on calcium cations. CCB block intracellular Ca2+ channels meaning that Ca2+ is inactive resulting in the tissue being kept in the refractory period and Ca2+ can’t get into the contractile myocytes

59
Q

If CCB don’t fix the problem what do they do

A

They stop the problem from happening/ keep a patient stable/ CCB therapeutically keep a patient stable meaning that they stay healthier for longer

60
Q

What is an example of a CCB

A

Verapamil

61
Q

What do CCB do

A

Cause vasodilation by preventing smooth muscle cell contraction plus they reduce the force of ventricle contraction and rate-limit the heart reducing cardiac output

62
Q

ADRs of CCB

A

Common- constipation. Uncommon-ankle oedema, dizziness, fatigue, flushing, headache, nausea, vomiting. Rare- Allergic reactions; angioedema; arthralgia; asystole; bradycardia; erythema; erythromelalgia;gingival hyperplasia after long-term treatment; gynaecomastia after long-term treatment ;heart block; heart failure; hypotension; increased prolactin concentration; myalgia; paraesthesia; pruritus; Stevens-Johnson syndrome; urticaria

63
Q

Contraindications of CCB

A

Acute porphyrias; atrial flutter or fibrillation associated with accessory conducting pathways (e.g. Wolff-Parkinson-White-syndrome); bradycardia; cardiogenic shock; history of heart failure (even if controlled by therapy); history of significantly impaired left ventricular function (even if controlled by therapy); hypotension; second- and third-degree AV block; sick sinus syndrome; sino-atrial block

64
Q

Describe the MOA of nicorandil

A

It is a vasodilator. 1. stimulates guanylyl cyclase to increase cGMP this reduce Ca2+ entry into vascualr smooth muscle cells. 2 Activates K+ATP channel effluxer, hyperopolarising cells thus preventing coltage-gated Ca2+ channel activity (cell us hyperpolarised and therefore can’t depolarise and switch on voltage-gated Ca2+ channels)

65
Q

What are ADRs of nicorandil

A

Common or very common- Cutaneous vasodilation with flushing; dizziness; headache (especially on initiation, usually transitory); increase in heart rate (at high doses); nausea; rectal bleeding; vomiting; weakness. Uncommon- angioedema; hypotension; myalgia; oral ulceration. Rare- Abdominal pain; anal ulceration; cholestasis; gastrointestinal ulceration; hepatitis; jaundice;pruritus; rash; skin ulceration. Very rare- eye ulceration.

66
Q

What are contraindications of nicorandil

A

Acute pulmonary oedema; cardiogenic shock; hypovolaemia; left ventricular failure with low filling pressures; severe hypotension

67
Q

What is the MOA of ivabradine

A

Rate limiter. : Dose-dependently inhibits the mixed Na+/K+ inward ion current that constitutes the ‘funny current’ in the SA node, reducing pacemaker automaticity. The ‘funny current’ is phase 4 so a rate limiter decreases the frequency of impulse firing in the SA node and therefore decreases pacemaker activity

68
Q

ADRs of ivabradine

A

Common or very common- Atrial fibrillation; blurred vision; bradycardia; dizziness; first-degree heart block; headache; phosphenes; ventricular extrasystoles; visual disturbances. Uncommon- angioedema; constipation; diarrhoea; dyspnoea; eosinophilia; hyperuricaemia; muscle cramps; raised plasma-creatinine concentration; rash; supreventricular extrasystoles; vertigo. Very rare- second and third-degree heart block; sick sinus syndrome.

69
Q

Contraindications of ivabradine

A

Acute myocardial infarction; cardiogenic shock; congenital QT syndrome; do not initiate for angina if heart rate below 70 beats per minute; do not initiate for chronic heart failure if heart rate below 75 beats per minute; immediately after cerebrovascular accident; patients dependent on pacemaker; second- and third-degree heart block; severe hypotension; sick-sinus syndrome; sino-atrial block; unstable angina; unstable or acute heart failure

70
Q

What is the MOA of statins

A

Inhibit hydroxymethyl glutaryl (HMG) CoA reductase (required for cholesterol synthesis), therefore statins limit how much cholesterol we produce.

71
Q

What is one of the best pharmacologicalmeans of reducing CAD risk

A

Lowering serum LDL cholesterol if >5.2 mmol/L with statins

72
Q

Why are statins not a treatment for angina

A

Reduce the risk from hypercholesterolaemia. Statins are preventative

73
Q

What are the ADRs of statins

A

Rare- hepatitis; jaundice. Very rare- hepatic failure; interstitial lung disease; lupus erythematosus-like reactions; pancreatitis

74
Q

What are the contraindications of statins

A

Elderly; high alcohol intake; history of liver disease; hypothyroidism; patients at increased risk of muscle toxicity, including myopathy or rhabdomyolysis (e.g. those with a personal or family history of muscular disorders, previous history of muscular toxicity and a high alcohol intake)

75
Q

What is the best way to avoid developing coronary artery disease

A

A healthy lifestyle

76
Q

What type of drugs are nitrates

A

Symptomatic relief

77
Q

What type of drugs are β1-adrenoreceptor blockers and CCBs

A

Prophylactic

78
Q

What best describes how Glyceryl trinitrate (GTN) spray relieves angina symptoms

A

De-nitration of GTN yields nitric oxide (NO) a potent vasodilator in the coronary arteries, relieving ischaemia-induces symptoms

79
Q

What is a voltage-gated calcium channel blocker suitable for treating angina

A

Nicorandil- both increases cGMP and efflux K+ATP channel activity

Case 4 (7 decks)

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