heart medications Flashcards

1
Q

Management
of angina
Aim of treatment

A

is to control
symptoms and halt the
progression of underlying
coronary disease.

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2
Q

Antianginals control symptoms

and

A

work by restoring the
balance between myocardial
oxygen demand and supply

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3
Q

Management

of angina

A
Beta adrenergic receptor blockers
Calcium channel blockers
Nitrates / vasodilators
COX inhibitors
Lipid lowering agents
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4
Q

Beta adrenergic receptor blockers

Mechanism of action

A

Mechanism of action
•  Blockers decrease cardiac O2 demand by causing a fall in the resting and
exercising heart rate and decreasing myocardial contractility and wall stress
• There are cardio-selective (1 ) and non-selective 1/2 beta adrenergic blockers
• Examples

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5
Q

• Examples

Beta adrenergic receptor blockers effects

A

• 1 – Atenolol, Metoprolol
• B1/2 – Propranolol, Sotalol
•Adverse effects – fatigue, reduced LV function, bradycardia, impotence in men, can
precipitate asthma and can worsen insulin induced hypoglycaemia in people with
diabetes

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6
Q

Calcium channel blockers
Mechanism of action

A

Block the calcium channels that allow depolarisation-mediated influx of calcium
into smooth muscle cells and cardiac myocytes
• Prevent angina mainly by causing systemic arteriolar vasodilation and decreasing
afterload. They prevent coronary vasospasm
• Dihydropyridine calcium channel blockers act on vascular smooth muscle channels.
Non-dihydropyridines block these channels in cardiac myocytes as well (reduce HR)

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7
Q

Calcium channel blockers
examples
adverse effects

A

• Examples
• Amlodipine, Nifedipine (dihydropyridine CCB)
• Verapamil, Diltiazem (Non-dihydropyridine CCB)
• Adverse effects – headache, dizziness, N&V, abdominal pain, AV block, palpitations,
tachycardia, hypotension

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8
Q

Nitrates / vasodilators

Mechanism of action

A
  • Dilate the veins (reducing venous return and preload) and dilate coronary arteries and open up collateral circulation
  • GTN is converted into NO in the body (NO is a potent vasodilator)
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9
Q

Nitrates / vasodilators
Examples
adverse effects

A

•Glyceryl trinitrate (GTN), isosorbide mononitrate
•Nicorandil
Adverse effects
•Headache, reflex tachycardia and orthostatic hypotension

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10
Q

COX inhibitors

Mechanism of action

A

Cyclooxygenase is an enzyme that promotes platelet activation. Therefore COX inhibitors, inhibit this enzyme and the platelet activator
(thromboxane A2 is inhibited)

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11
Q

COX inhibitors
example adverse effects
drug reaction

A

Example
•Aspirin
Adverse effects
•GI complaints, dizziness, tinnitus, vertigo
Drug interaction
•anti-coagulants, hypoglycaemic agents, alcohol, corticosteroids, all increase risk of gastric ulceration
•Enteric coated aspirin should not be given with antacids (affect stomach pH)

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12
Q
Lipid lowering agents
mechanism of action
Examples
•Simvistatin, atorvastatin (Statins)
•Gemfibrozil (Fibrate)
•Colestyramine (Blie acid sequestrants)
•Adverse effects
•GI disturbance (Statins, Fibrates, Bile acid sequestrants) myositis (Statins, Fibrates), Increased liver enzymes, insomnia (Statins)
A

•Mechanism of action
•HMG-CoA reductase inhibitors (Statins) work by reducing hepatic synthesis of cholesterol, causing upregulation of hepatic receptors and B and E
proteins. (Increases the clearance of LDL from the plasma, they also modestly increase HDL)
•Fibrates stimulate lipoprotein lipase, increasing the hydrolysis of triglycerides in VLDL. Free fatty acids are sent for storage in muscle (burned off)
•Bile acid sequestrants bind and trap bile acids in the intestine, increasing their excretion

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13
Q

Lipid lowering agents
Examples
adverse effects

A
  • Simvistatin, atorvastatin (Statins)
  • Gemfibrozil (Fibrate)
  • Colestyramine (Blie acid sequestrants)
  • Adverse effects
  • GI disturbance (Statins, Fibrates, Bile acid sequestrants) myositis (Statins, Fibrates), Increased liver enzymes, insomnia (Statins)
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