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SL - 1 - Cardiovascular Disease > Pharmacology of Angina > Flashcards

Pharmacology of Angina Flashcards

1
Q

What are the three common places for atherosclerosis to build up?

What pathologies do they cause?

A

Coronary arteries - causes MI.

Renal arteries - causes Chronic Kidney Disease.

Carotid arteries - causes Stroke.

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2
Q

Different mechanism between stable and unstable angina

A

Stable angina:

  • Atherosclerosis has a thick fibrous cap and so does not rupture.
  • Angina is caused by the loss of coronary blood flow (coronary flow reserve).

Unstable angina:

  • Atherosclerosis has a thin fibrous cap and so has a higher chance to rupture.
  • Acute coronary syndrome where there is a sudden decrease in coronary blood flow.
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3
Q

Angina of Effort:

A
  • From a stable atherosclerosis.
    • Effort brings on the symptoms.
  • Symptoms:
    • tightness, squeezing, crushing sensation in the chest.
  • Most common form of angina;
    • due to exertion/emotion, stops with rest or GTN.
  • ↑O2 demand with restricted blood flow.
  • ↓O2 in cardiac tissue…
  • Vasodilation does not work as it is already fully dilated!
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4
Q

Vasoplastic Angina:

A
  • “Prinzmetal’s”
  • Due to spasm of coronary artery.
    • So no fixed plaque.
    • most likely due to endothelial damage to the coronary artery.
  • Occurs at rest, often at night.
  • Rare form.
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5
Q

What are the aims (and mechanisms behind them) to treat angina?

A

To limit the number, severity and sequellae of anginal attacks, thereby improving the quality of life.

  • The main mechanism for the pharmacological treatment of ‘angina of effort’ is to decrease cardiac O2 demand.
  • A secondary mechanism is to increase the O2 supply to the ischaemic zone by decreasing the heart rate and increasing the blood flow in coronary arteries.
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6
Q

What is the mechanism of action of Nicorandil and Ranolazine

A
  • Ivabradine;
    • (inhibits If (funny current) channels, lowers HR)
  • Nicorandil;
    • (activates K channels, induces vasodilation of arterioles)
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7
Q

How do organic nitrates slow the heart?

A
  • dilates veins,
  • decrease CVP,
  • decreases heart wall tension,
  • decreases CO.
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8
Q

How to b-blockers increase cardiac muscle perfusion?

A
  • Reduces cardiac contractility,
  • Reduces HR,
  • LV wall has more time to reperfuse with O2 during diastole.

drug - ivabradine.

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9
Q

How does Ranolazine reduce cardiac wall tension?

A
  • Opens Na channels in LV,
  • Relaxes LV wall,
  • Decreases wall tension.
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10
Q

Two modes that NO regulates smooth muscle tone.

A

Nitric Oxide:

  • Activates Ca pumps which pump Ca extracellularly.
  • Less Ca in the cell to cause contraction.
  • Causes vasodilation.
  • Opens K channels,
  • Hyperpolarises cell.
  • Prevents cell depolarisation.
  • Less ability to contract = vasodilation.
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11
Q

Cellular mechanism of organic nitrates?

A

Nitric Oxide (NO) donor

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12
Q

Haemodynamic mechanism of organic nitrates?

A
  • decreases CVP, therefore preload,
    • decreases cardiac work.
  • increases coronary blood flow.
    • (lower HR so during diastole).
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13
Q

How is glyceryl trinitrate (GTN) taken?

Why?

A

Taken sublingually has a very rapid effect (1min).

  • Used for cutting short an angina attack or preventing an anticipated attack.

if taken orally, GTN will be digested before an effect is given.

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14
Q

How do you avoid GTN tolerace?

(after use of around 12hrs)

A

Daily 8-hour drug-free period (typically at night)

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15
Q

Side effects of GTN?

Mechanism behind this?

A

Headache and facial flushing.

Caused by:

  • Decrease in BP,
    • Reflex increases HR (tachycardia). Due to vasodilatation
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16
Q

What are coronary collaterals?

A

Ischemia in the heart activates angiogenesis.

Growth of new blood vessels distal to the stenosis. Bypasses the stenosis.

Slows down the progression of angina.

17
Q

What is the mechanism of action behind GTN?

A

Metabolised to give NO by an enzyme in the mitochondria.

  • Activates guanylate cyclase,
  • Increases cyclic GMP,
  • Vasodilation.
18
Q

How do b-blockers work?

And what receptor do they work on?

And what is the most widely used b-blocker?

A

b-blockers inhibit sympathetic stimulation of the heart.

  • b1-selective-adrenergic antagonist.
    • (so has fewer effects on the lungs)

e.g. Bisoprolol.

19
Q

What is the main contraindication of b-blockers?

A

Vasospastic angina.

  • because b-blockers tend to make vaso-spasm worse.
20
Q

What is the mechanism of action of B-blockers that decreases O2 demand to the heart?

A

Heart rate decreases (antagonistic B1)

  • Decreases O2 demand.

Decreases release of renin from kidneys (also has B1 receptors).

  • decreases BP,
  • decreases afterload.
21
Q

What is the mechanism of action of B-blockers that increases O2 supply to the heart?

A

HR is decreased.

  • Coronary flow increases due to longer diastole.
  • Increases O2 supply.
22
Q

How to Ca channel blockers slow the heart?

What is the most commonly used CCB?

A

Block the L-type Ca channels that initiates constriction.

Common drug = amlodipine

  • (which is a dihydropyridine, DHP)
23
Q

Main KATP channel activator drug?

A

Nicorandil.

24
Q

What is the dual action of KATP channel activators?

A
  • Opens ATP-sensitive K+ channels in vascular smooth muscle cells.
    • Hyperpolarises the muscle.
    • Less chance of depolarising, therefore contracting.
  • Stimulates guanylate cyclase;
    • Increase in intracellular cGMP.
    • This has many affects that causes relaxation.
25
Q

How does Ivabradine affect the heart

A

Blocks If (the ‘funny’ current) which is involved in SAN pace-making.

  • Therefore decreases HR.
26
Q

What does ‘use-dependent’ mean?

What makes ivabradine‘use-dependent’?

A

‘Use-dependency’ means that it tends to block more when the HR goes up.

  • Ivabradine is one of these drugs.

Ivabradine blocks If by entering the open channel from inside the cell, gets trapped when the channel shuts.

  • This means that the binding of ivabradine in the channel builds up when the channel is opening more frequently.
27
Q

How do statins work?

Give an example of a statin.

A

Blocks the rate-limiting enzyme which produces cholesterol.

(Also increases the uptake of LDL into the liver)

Example of a statin = Atorvastatin

28
Q

What is Percutaneous Coronary Intervention (PCI)?

A

Placing a stent into a coronary artery, allowing reperfusion.

29
Q

What procedure is used in preference to PCI in patients with more serious/advanced coronary artery disease?

A

Coronary artery bypass grafting (CAPG).

SL - 1 - Cardiovascular Disease (6 decks)

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