antianginal drugs Flashcards

1
Q

what is the most common cause of mortality

A

CAD,IHD or as known as Artherosclerotic diseases

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2
Q

what are the characteristic of typical angina

A

sudden,severe,crushing chest pain that may radiate to the neck,jaw,back and arms

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3
Q

does stable angina (Transient, self-limited episodes of myocardial ischemia) result in cellular death or MI

A

no

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4
Q

what can acute coronary syndrome (MIor unstable angina) and chronic ischemia lead to

A

deterioration of cardiac function, HF, arrhythmias, and sudden death.

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5
Q

what should IHD patients receive

A

guideline-directed medical therapy with lifestyle modifications (smoking cessation, physical activity, weight management) and management of risk factors (HTN, diabetes, dyslipidemia) to reduce CV morbidity and mortality

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6
Q

what are the following for stable angina
characteristics
causes
and treatment

A

1) a short-lasting burning, heavy, or squeezing
feeling in the chest.

2)the reduction of coronary perfusion due to a fixed
obstruction produced by atherosclerosis.(ischemia)

The heart becomes vulnerable to ischemia whenever there is increased demand, such as that produced by physical activity, emotional excitement, or any other cause of increased cardiac workload.

3)Typical angina pectoris is promptly relieved by rest or nitroglycerin

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7
Q

what is unstable angina and what are the following
characteristics
is it relieved by nitroglycerin

A

a stage between stable angina and MI

1)Chest pains occur with increased frequency, duration and intensity and are precipitated by progressively less effort.
Any episode of rest angina longer than 20 minutes, any new-onset of angina, any increasing (crescendo) angina, and even sudden development of shortness of breath, is suggestive of unstable angina.

2) no, It requires hospital admission and more aggressive therapy to prevent progression to MI and death.

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8
Q

what is Prinzmetal angina

A

variant, vasospastic, or rest angina

Prinzmetal angina is an uncommon pattern of episodic angina that occurs at rest and is due to coronary artery spasm.

Symptoms are caused by decreased blood flow to the heart muscle from the spasm of the coronary artery.

The angina attacks are unrelated to physical activity, HR, or BP.

Prinzmetal angina generally responds promptly to coronary vasodilators, such as nitroglycerin and CCBs.

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9
Q

what is acute coronary syndrome

A

is an emergency that commonly results from rupture of an atherosclerotic plaque and partial or complete thrombosis of a coronary artery.

Most cases occur from disruption of an atherosclerotic lesion, followed by platelet activation of the coagulation cascade and vasoconstriction.

This process culminates in thrombosis and vascular occlusion.

If the thrombus occludes most of the blood vessel, and, if the occlusion is untreated, necrosis of the cardiac muscle may ensue.

The acute coronary syndrome may present either as
ST-segment elevation MI,Non–ST-segment elevation MI, or as unstable angina, where no increases of biomarkers of myocardial necrosis are present.

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10
Q

how can we typify MI

A

by the increase in the serum level of biomarkers such as creatine kinase

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11
Q

what drugs do we use for angina in the following cases if the patient had

no concomitant disease

MI

asthma, copd

hypertension

diabetes

chronic renal diseases

A

1) long acting nitrates (LAN), beta blockers, ca+2 blockers

2) LAN, B-blocker

3) LAN, Ca+2 blocker

4) LAN (less effective), B-blocker, Ca+ blocker

5) LAN, Ca+ blocker

6) LAN , B-blocker(less effective), Ca+ blocker

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12
Q

how useful are beta blockers for angina

A

recommended as initial therapy in all patients
unless contraindicated.

Agents with ISA (pindolol) are less effective and should be avoided in angina.

useful in the treatment ofpatients with MI and have been shown to prolong survival.

The β-blockers can be used to increase exercise duration.

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13
Q

what do CCBs cause

A

decrease in smooth muscle tone and vascular
resistance.

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14
Q

how do dihydropyridine CCBs help in angina

A

◼ Amlodipine functions mainly as an arteriolar
vasodilator.

◼ The vasodilation effect is useful in the treatment
of variant angina caused by spontaneous coronary
spasm.

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15
Q

how do nondihydropyridine CCBs help in angina

A

Verapamil slows cardiac AV conduction directly, and
decreases HR, contractility, BP, and O2 demand.

Verapamil is contraindicated in patients with preexisting
depressed cardiac function or AV conduction abnormalities.

Diltiazem can relieve coronary artery spasm and is
particularly useful in patients with variant angina.

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16
Q

what are organic nitrates MOA

A

◼ These cause dilation of the large veins, resulting in
pooling of blood in the veins. This diminishes
preload and reduces the work of the heart.
◼ Also dilate the coronary vasculature, providing an
increased blood supply to the heart muscle

they release nitric oxide—-increases cGMP—- causes dephosphorylation of myosin therefore muscle relaxation

17
Q

what are the pharmacokinetics of nitrates

A

nitrates differ in their onset of action and rate of elimination.

For prompt relief of an angina attack precipitated by exercise or emotional stress, sublingual nitroglycerin is the drug of choice.

Significant first-pass metabolism of nitroglycerin occurs in the liver.

Isosorbide mononitrate owes its improved bioavailability and long duration of action to its stability against hepatic breakdown.

Oral isosorbide dinitrate undergoes denitration to 2 mononitrates, both of which possess antianginal activity.

18
Q

what are the side effects of nitrates

A
  1. headaches

2.High doses of nitrates can also cause postural
hypotension, facial flushing, and tachycardia.

3.Phosphodiesterase V inhibitors such as sildenafil
potentiates the action of the nitrates. To preclude the
dangerous hypotension that may occur, this combination is contraindicated

4)Tolerance to the actions of nitrates develops rapidly as the blood vessels become desensitized to vasodilation.

Tolerance can be overcome by providing a daily “nitrate free interval” to restore sensitivity to the drug.

This interval is 10 to 12 hours, usually at night.