Pharmacological treatment of Angina Flashcards Preview

Medicine MD3001 cardiovascular system > Pharmacological treatment of Angina > Flashcards

Flashcards in Pharmacological treatment of Angina Deck (35):

what drugs are given to reduce chest pain symptoms?

-beta blockers, nitrates, calcium channel antagonists, nirocandil, ivabradine, ranolazine


what 4 drugs are given to prolong survival?

beta blockers, aspirin, statins , ACE


what 3 factors shorten the window for coronary flow?

-shorten diastole increase HR
-increased ventricular end diastolic pressure aortic stenosis
-reduced diastolic arterial pressure mitral or aortic valve incompetence


what is the common cause of coronary ischaemia?

atherosclerosis causing a lack of blood flow to areas which require it


what is ischaemia?

ischemia is a restriction of blood supply to tissues causing shortage of glucose and oxygen needed for cellular metabolism


what is angina? what feelings are experienced as a result?

chest pain due to inadequate supply of oxygen to the heart
-crushing or severe pain
-feeling of suffocation and pressure behind the sternum


what is the usual distribution of pain from angina?

chest, arm, neck and jaw


what factors bring on pain due to angina?

exertion, cold, excitement


what are the 3 different categories of angina?

-Printzmetals variant angina
-chronic stable angina
-unstable angina


what is the difference between supply and demand ischaemia?

supply- even at rest you can't get a supply of blood to that area
demand- exercise stresses the heart muscle then demand for oxygen goes up to area of the heart and the heart can't meet the demand


describe the features of stable angina. what is the principle of treating stable?

-predictable chest pain on exertion
-fixed narrowing of coronary arteries

-treat by decreasing workload of heart so as to decrease O2 demand, prolong survival


describe the features of unstable angina. what is it usually associated with?

-occurs at rest with less exertion than stable angina
-associated with thrombus from ruptured plaque


what is the cause of Printzmetals variant angina?

-caused by coronary artery spasm


what are the 2 broad classes of drugs used to treat angina? what are their objectives?

-work by reducing the metabolic demand of the muscle
-vasodilators- decrease preload and afterload
-beta blockers-slow down the heart


what is the mechanism of action of vasodilators?

-decrease preload decreasing volume of blood returning to the heart, heart heart doesn't need to cope with pumping high volume of blood
-afterload decreased means pressure heart is working against is less therefore less demand on heart


what is the mechanism of action of beta blockers?

act on beta 1 receptors which are intrinsically related with rate of the heart
decrease cardiac oxygen consumption by slowing the rate of the heart


what are 2 examples of beta blockers?



what class of drug are calcium antagonists?



what is the mechanism of action of calcium antagonists on smooth muscle?

calcium regulates activity of smooth muscle constriction, constriction of the vasculature. hence decreasing constriction of smooth muscle decreases total peripheral resistance
=drop in afterload and dilates coronary vessels


how can calcium antagonists also affect the rate of the heart?

-calcium channels present in conduction pathways of the heart
-calcium influx drives action potential generated in nodal tissue of heart
-hence altering influx of calcium in nodal tissue means you can control heart rate
-prevent opening of L-type DHP calcium channels


what are examples of DHP derivative calcium antagonists? what do they affect?

amlodipine, lercanidipine
-these affect vasculature only


give examples of rate limiting calcium antagonists. What do they affect?

-affect both heart rate and afterload


what are the side affects of calcium antagonists?

headache, constipation, ankle oedema because of increased dilation of vessels q


what type of angina is treated with DHP derivative calcium antagonists?

printzmetals variant angina


what class of drugs are organic nitrates?

powerful vasodilators


when are organic nitrates taken?

prior to exertion and at early onset of angina


what is the mechanism of action of organic nitrates?

-metabolised to nitric oxide
-relax smooth muscle by diffusing across the short distances between endothelial cells and smooth muscle


how do nitrates help treat angina?

-decreases preload, predominately absorbed in the venous system
-decreases cardiac workload by causing dilation of collateral coronary vessels this allows alternative routes for blood to get to ischaemic vessels


what are 2 examples of organic nitrates?

-glyceryl trinitrate
-isosorbide mononitrate


what types of angina can organic nitrates be used to treat?

stable angina- glyceryl trinitrate shortly before exercise
unstable angina- IV glyceryl trinitrate


what are the side effects of organic nitrates?

-postural hypotension due to altering the dilation of veins


what is the mechanism of action of potassium channel activators?

-have a nitric oxide dilating effect+ decrease preload
-activates potassium ATP channels hyperpolarises vascular smooth muscle means smooth muscle less likely to depolarise increasing dilation and decreasing total peripheral resistance


what is an example of potassium channel activator?



what are side effects of potassium channel activators?



how does Ivabradine operate?

inhibits f-type channels in the heart decreasing the slope of the pacemaker potential causing a decrease in heart rate

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