Antianginal Drugs Flashcards

1
Q

Organic nitrites and nitrates

A

Amyl nitrite
Nitroglycerin
Isosorbide dinitrate
Isosorbide mononitrate

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2
Q

Organic nitrites and nitrates - MoA

A

Act by releasing nitric oxide in vascular smooth muscle cells. Nitric oxide activates guanylyl cyclase forming cGMP, cGMP activates cGMP dependent kinases that appear to cause relaxation of vascular smooth muscle by phosphorylating proteins that decrease intracellular calcium mobilization and decrease myosin light chain-phosphatase. They relax venous smooth muscle, with small effect on arteriolar. This leads to venous pooling of blood, a decrease in venous blood return to the heart and a decrease in ventricular volume, pressure, and wall tension. The nitrites reduce cardiac preload and output, which leads to reduction in BP

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3
Q

Organic nitrites and nitrates - Adverse effects

A
Hypotension
Reflex tachycardia (to prevent this, can give B-blocker)
Headache
Dizziness
Euphoria
Increased libido

Methemoglobinemia (Only nitrites, not nitrates)

Pharmacodynamics tolerance to their vasodilate effects (transdermal patches should be removed for at least 10h every day, while drugs should be adm no more than two times per day)

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4
Q

Organic nitrites and nitrates - Interactions

A

Phosphodiesterase-V inhibitors (sildenafil)- potentiate the hypotensive effect

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5
Q

Amyl nitrite - Clincal use

A

Treatment of acute angina attacks

Initial management of cyanide poisoning (given iv, thiosulfate is also given to convert cyanide to inactive thiocyanate)

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6
Q

Nitroglycerin - Clinical use

A

Prevent and treat angina attacks

Reduce preload and afterload in pat who have acute heart failure associated with MI or other(iv)

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7
Q

Isosorbide dinitrate and Isosorbide mononitrate - Clinical use

A

Prevent and treat angina attacks

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8
Q

Calcium Channel Blockers

A
Amlodipine
Felodipine
Isradipine
Nicardipine
Nifedipine
Nimodipine
Diltiazem
Verapamil
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9
Q

Calcium Channel Blockers - MoA

A

By blocking calcium ion channels in the plasma membranes of smooth muscle, the CCBs relax vascular smooth muscle and causes vasodilation. They have greater effect on arteriolar smooth muscle then venous, effect on BP is mainly because a reduction in PVR.

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10
Q

Calcium Channel Blockers - Adverse effects

A
Fatigue
Headache
Dizziness
Flushing
Peripheral edema
Gingival hyperplasia (not diltiazem and verapamil)
Constipation
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11
Q

Amlodipine, Felodipine and Nicardipine - Clinical use

A

Hypertension

Treatment of angina pectoris

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12
Q

Isradipine - Clinical use

A

Hypertension

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13
Q

Nimodipine - MoA

A

Dilates small cerebral vessels and increases collateral circulation to the affected areas of the brain.

It also reduces neuronal damage caused by the excessive release of calcium that is evoked by cerebral ischemia

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14
Q

Nimodipine - Clinical use

A

Reducing neurologic complications of Subarachnoid hemorrhage

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15
Q

Nimodipine - Contraindications

A

IV administration causes severe hypotension, cardiac arrest and fatalities

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16
Q

Diltiazem and Verapamil - MoA

A

Decrease SA node automaticity, cardiac contractility and AV node conduction velocity to a greater degree then other CCBs

17
Q

Diltiazem and Verapamil - Clinical use

A

Cardiac arrhythmias
Management of angina pectoris
Typical and variant angina

18
Q

Diltiazem and Verapamil - Contraindications

A

Patients with heart failure because it suppress cardiac contractility

19
Q

Diltiazem and Verapamil - Adverse effects

A

Reduce peristalsis

20
Q

Diltiazem and Verapamil - Interactions

A

Reduce the clearance of digoxin and can thereby increase serum digoxin levels and precipitate digoxin toxicity.

21
Q

Beta blockers

A

Atenolol
Metoprolol
Nadolol
Propanolol

22
Q

Beta blockers - MoA

A

Prevent ischemic episodes due to their ability to prevent exercise induced tachycardia and increased myocardial oxygen demand. They also can prevent reflex tachycardia induced by either organ nitirates or dihydropyridine CCBs

23
Q

Beta blockers - Clinical use

A

Typical angina pectoris

Acute MI

24
Q

Beta blockers - Interactions

A

Avoid verapamil, due to reduction in cardiac output.

25
Q

Heart rate-lowering drug

A

Ivabradine

26
Q

Ivabradine - MoA

A

Reduces heart rate by blocking the If current (funny current) in the SA node, which is mixed Na+-K+ inward current activated by hyperpolarization, modulated by the autonomic nervous system, and responsible for diastolic depolarization and cardiac impulse initiation

27
Q

Ivabradine - Clinical use

A

Chronic angina

Heart failure

28
Q

Ivabradine - Adverse effects

A
Headache 
Visual disturbances
Bradycardia
Atrial fibrillation
AV block
29
Q

Drugs that modify myocardial metabolism

A

Ranolazine

Trimetazidine

30
Q

Ranolazine - MoA

A

Block the pathologic activation or prolongation of the late inward sodium current (INa-L) in myocardial cells. This abnormal current leads to increased sodium-calcium exchange, intracellular calcium accumulation, and increased left ventricular wall tension. By blocking INa-L, ranolazine decreases diastolic wall tension, improves diastolic subendocardial perfusion, and reduces oxygen consumption. It has no effect on heart rate or blood pressure

31
Q

Ranolazine - Clinical use

A

First line - Chronic stable angina

32
Q

Ranolazine - Adverse effects

A

Dizziness
Headache
Nausea
constipation

33
Q

Ranolazine - Contraindications

A

Contraindication: Persons with QT prolongation and in those taking QT-prolonging drugs or this with hepatic impairment (because the drug is metabolized in the liver)

34
Q

Trimetazidine - MoA

A

Inhibits ketoacyl coenzyme A thiolase, a key enzyme in B-oxidation pathway of fatty acid metabolism. The resulting decrease in fatty acid oxidation evokes a compensatory increase in glucose metabolism and reduces oxygen consumption by about 20%.

35
Q

Trimetazidine - Clinical use

A

Angina, decreases number of episodes

Increase ejection fraction in persons with left ventricular dysfunction

36
Q

Nifedipine - Contraindication

A

Coronary heart disease because of increased risk of mortality