Clinical Pharmacology of Stable Coronary Artery Disease Flashcards

1
Q

Describe stable angina.

A

Stable angina is a clinical syndrome characterized by predictable chest pain triggered by exercise or emotional stress, leading to increased myocardial oxygen demand.

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2
Q

Define atypical angina.

A

Atypical angina is similar to stable angina but presents with symptoms that are not clearly identifiable as ischemic chest pain.

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3
Q

How is stable angina differentiated from ACS?

A

Stable angina is not usually a medical emergency and does not require immediate medical attention, unlike Acute Coronary Syndrome (ACS).

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4
Q

Do beta blockers help in treating stable angina?

A

Yes, beta blockers are used to relieve symptoms, reduce workload, improve coronary blood flow, slow/halt the disease process, prevent myocardial infarction, and prevent premature death in stable angina patients.

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5
Q

Describe the mechanism of action of beta blockers.

A

Beta blockers work by blocking the beta1 and beta 2 receptors, inhibiting the sympathetic system, and reducing heart rate, contractility, and systolic wall tension.

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6
Q

How do calcium channel blockers function in stable angina treatment?

A

Calcium channel blockers can act as rate-limiting agents or vasodilators, helping to reduce myocardial oxygen demand and improve coronary blood flow in stable angina patients.

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7
Q

Describe the mechanism of action of calcium channel blockers.

A

They prevent calcium influx into myocytes and smooth muscle arteries/arterioles by blocking L-type Ca channels.

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8
Q

What are the main differences between dihydropyridine and non-dihydropyridine calcium channel blockers?

A

Dihydropyridines mostly relax smooth muscle, while non-dihydropyridines mostly reduce heart rate.

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9
Q

Define the role of nitrates as vasodilators.

A

Nitrates release Nitric Oxide, which mediates smooth muscle relaxation, reducing preload and afterload.

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10
Q

How does Nicorandil function as a vasodilator?

A

It activates ATP sensitive potassium channels, causing potassium influx and inhibiting calcium influx, leading to smooth muscle relaxation.

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11
Q

Do Ivabradine act as a rate-limiting medication? If so, how?

A

Yes, Ivabradine is a rate-limiting medication that inhibits the ‘funny’ channels located in the SA node.

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12
Q

Describe the mechanism of action of Ranolazine.

A

Inhibits late sodium current in myocardial cells and inhibits rapid phase of delayed potassium rectifier current, reducing intracellular calcium.

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13
Q

What are the benefits of using Ranolazine?

A

Reduced O2 demand, potential antiarrhythmic effects, and slowing disease progression.

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14
Q

Define HMG-CoA Reductase inhibitors and provide examples.

A

They reduce cholesterol production. Examples include Atorvastatin, Simvastatin, and Rosuvastatin.

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15
Q

How does Ezetimibe work in reducing cholesterol levels?

A

It inhibits cholesterol uptake in the gut, forcing the liver to increase uptake from the bloodstream, thus lowering LDL levels.

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16
Q

Describe the LDL targets for different risk categories.

A

Low risk: 3.0, Moderate risk: 2.5, High risk (recent MI): 1.8.

17
Q

What is the mechanism of action of Aspirin as an antiplatelet?

A

It inhibits platelet activation via the TXA2 pathway.

18
Q

Do P2Y12 inhibitors like Clopidogrel work in inhibiting platelet activation?

A

Yes, they inhibit platelet activation via the ADP-mediated pathway.

19
Q

Define the role of Fibrates in reducing cardiovascular risk.

A

They reduce the rate of MI, stabilize plaques, and help reduce LDL while increasing HDL levels.

20
Q

How is aspirin used in the context of prophylaxis and why is it no longer recommended?

A

It was previously used but is now avoided due to the associated risk of GI bleeding. A proton pump inhibitor is often used for protection.