Lesson C1 - Drugs for the Treatment of Angina Pectoris & Congestive Heart Failure Flashcards Preview

Pharmacology > Lesson C1 - Drugs for the Treatment of Angina Pectoris & Congestive Heart Failure > Flashcards

Flashcards in Lesson C1 - Drugs for the Treatment of Angina Pectoris & Congestive Heart Failure Deck (20):

what are the 3 major classes of antianginal drugs?

1) the organic nitrates which include the
short-acting nitroglycerin, and the long-acting isosorbide dinitrate; (2) the β-adrenergic
antagonists of which propranolol is a prototype drug; and (3) the calcium channel blockers of
which nifedipine is a prototype drug


Angina pectoris was first described by the English physician

William Heberden in 1768


Angina pectoris (a choking pain in the chest) is usually due to

lipid deposits in the coronary
arteries hindering blood flow (atherosclerosis).


The pain arises from

diminished blood flow and a diminished oxygen supply to an area of
the heart muscle.


To reduce the pain, one must

decrease the oxygen requirement of the heart
and/or increase the oxygen supply to oxygen deficient areas of the heart muscle


Angina pectoris is precipitated by the four “E’s”, namely

Eating, Exercise, Excitement, Exposure
to cold.


organic nitrates relax the smooth muscle of blood vessels and exert their
therapeutic effect by

Relaxation of large veins, leading to vasodilation and by Dilating large coronary arteries


Nitroglycerin enters blood vessels and is converted in blood vessels into nitric oxide.
Nitroglycerin therefore owes its effectiveness to its conversion into a normal body constituent,

nitric oxide.


In endothelial cells lining blood vessels, the enzyme nitric oxide synthase catalyses the
conversion of arginine into

citrulline and nitric oxide.


Nitric oxide passes from endothelial cells
into smooth muscle cells where it activates the enzyme guanylyl cyclase and leads through a
series of steps to

relaxation of the blood vessel


Therapeutic Uses of GTN

For termination of an individual attack, Prevention of individual attack and Chronic prophylaxis


An alternative drug used for chronic prophylaxis of angina pectoris is a

β-adrenergic blocking
agent. In order to understand the mechanism of action of β-adrenergic blocking drugs, such as
propranolol, in angina it is necessary to understand that angina is precipitated by factors that
increase sympathetic nervous system (SNS) activity, e.g. stress and exercise.


Increased SNS activity results in an increase in heart rate and an increase in myocardial (heart
muscle) contractility. This in turn leads to an increase in

cardiac output and an increase in
myocardial oxygen requirement resulting in the pain of angina.


A β-adrenergic blocking drug such as propranolol will block β receptors in the heart, thereby
decreasing heart rate and myocardial contractility. As a result, cardiac output and myocardial
oxygen requirements will

decrease and therefore the pain of angina will be alleviated.


Newer drugs or drugs in development, modify cardiac work load by

either slowing the heart
by altering electrical conduction or alter the metabolism of the heart to require less oxygen.


Calcium enters the vascular smooth muscle cell through a

Calcium enters the vascular smooth muscle cell through a


Calcium enters the vascular smooth muscle cell through a

a calcium-calmodulin complex.


Cardiac glycosides (digitalis) have a specific and powerful action on the myocardium (heart
muscle). Digitalis binds specifically to an enzyme sodium, potassium-ATPase, and i

inhibits the
extrusion of sodium from cardiac cells. This leads to an increase of calcium in cardiac cells and
to a greater force of contraction of the heart.


Therapeutic Uses of Digitalis

Congestive heart failure, Treatment of disordered electrical rhythms of the heart


Adverse Effects of digitalis

Nausea and vomiting, Disordered rhythms in the heart (arrhythmia), Disturbances of vision – often blurred and neurological effects