Drug treatment of Angina Flashcards
Where do B1 Agonists act on?
B1 agonists act on the heart as B1 receptors are there
Where do B2 agonists act on?
B2 agonists act on the lungs and the skeletal muscles as B2 receptors are in the bronchioles of the lungs and the arteries of the skeletal muscles.
What are the 3 types of Angina?
Stable angina, unstable angina and variant angina.
Describe stable angina.
(most common)
- attacks predictable, e.g exercise, stress
- myocardial O2 demand not met
- involvement of atherosclerosis (use of cholesterol-lowering drugs - statins)
Describe unstable angina.
- attacks unpredictable
- coronary artery occlusion due to platelet adhesion to ruptured atherosclerotic plaque (use of anti-platelet drugs)
- like a mini heart-attack
- have a high-risk of getting a heart attack
Describe variant angina.
- attacks unpredictable
- coronary artery occlusion by vasospasm of coronary artery
- coronary artery’s lumen diameter is normal but for some unknown reason there are contractions which narrows the artery and reduces the blood supply resulting in angina.
What is the main aim of treating angina.
to reduce myocardial O2 demand
What are the drug treatments of angina.
- Beta receptor blockers
- Calcium Channel blockers
- Nitrovasodilators
- Ivabradine
What is the mechanism, side-effects and examples of beta- blockers.
used in all forms of angina
Mechanism: competitive reversible antagonist of the cardiac B1 adrenoreceptors. - decreases heart rate and force - decreases myocardial work - decreases myocardial O2 demand
Side-effects: (HIVE)
- hypoglycaemia
- exacerbate asthma
- intolerance to exercise
- vivid dreams
Examples:
- propranolol (non-selective)
- atenolol (B1 selective)
What is the mechanism, side-effects and examples of nitrovasodilators.
used in stable angina (just before exercise)
Mechanism:
enters the smooth muscle cells and mimics the action endothelial- derived NO
NO binds to haem receptors > activates sGC enzyme > converts GTP to cGMP > increases cGMP > vasodilation.
Side-effects:
- headaches
- tolerance can develop over a period of long time so need a “washout period” to restore efficacy
Examples:
- GTN
- Amyl nitrite
What is the mechanism, side-effects and examples of calcium channel blockers.
used in all forms of angina
Mechanism: - Open channel block (cork in a bottle) e.g. Verapamil and Diltiazem - Allosteric Modulation binds at allosteric site and reduces channel opening e.g. nifedipine
dilates arteries
- decreased afterload
- decrease myocardial O2 demand
- decrease heart rate and force
Side-effects: - constipation - headache - coronary steal extreme overdose: heart block or cardiac failure
What is the mechanism of Ivabradine.
- Blocks If(Na+) current that contributes to SA node depolarisation towards threshold
- Decreases heart rate but not force
- Decrease in myocardial O2 demand
used in all forms of angina
How does reducing pre-load with venous dilators bring benefit in all forms of angina.
Dilatation of veins:
- decreased pre-load (diastolic pressure that distends the relaxed left ventricle)
- decreased venous return
- decreased myocardial O2 demand
How does reducing after-load with arterial dilators bring benefit in all forms of angina.
Dilatation of arteries:
- decreased after-load (force against which left ventricle contracts)
- decreased myocardial O2 demand
What is the NICE algorithm for treating angina.
Step 1: Short acting nitrovasodilator (GTN) + Beta blocker or calcium channel blocker + drugs for secondary prevention (anti-hypertensive drugs)
Step 2: Combine beta blocker and calcium channel blocker
Step 3: Long acting nitrovasodilator or Ivabradine
Step 4: surgery (stenting or coronary artery bypass surgery)
