Beta Blockers Flashcards
What are beta-adrenoceptor blocking drugs and calcium channel blockers used to treat?
Angina
Hypertension
Cardiac arrhythmia
Describe hypertension.
- when long-term force of blood against artery walls is high enough to cause damage.
- bp determined by amount of blood the heart pumps and the resistance to blood flow in arteries.
- build up of plaque in artery walls are going to narrow the lumen of arteries = more resistance to blood flow.
- narrower arteries = higher bp - leads to enlarged heart, blocks and blood clots.
Describe angina.
- angina is discomfort or pain in the chest when not enough oxygen-rich blood reaches the muscle cells of the heart.
- CAD = main cause of angina.
- CAD is caused by atherosclerosis - condition where fatty deposits called plaque is deposited along inside of blood vessels.
- angina occurs when blood vessels become blocked due to plaque.
Describe cardiac arrhythmia.
- these are heart rhythm problems which occur when electrical impulses that coordinate the heartbeats don’t wok properly, causing heart to beat too fast/too slow/irregularly.
- sometimes harmless sometimes fatal.
What are adrenoceptors?
These are receptors which mediate the central and peripheral actions of the NT noradrenaline and adrenaline. The receptors are important in regulation of the autonomic nervous system (SNS and PNS).
Where are adrenoceptors found?
In nearly all peripheral tissues.
What does noradrenaline and adrenaline do?
They have important roles in the control of bp, myocardial contractile rate and force, airway reactivity and many metabolic and CNS functions.
What types of adrenoceptors are there?
Alpha and Beta
subtypes = a1 and a2, B1, B2 and B3.
What does activating alpha adrenoceptors result in?
Contracts smooth muscle except in the gut
What does activating B2 adrenoceptors result in?
Relaxes smooth muscle
What does activating B1 adrenoceptors result in?
Contracts cardiac muscle
Which adrenoceptor predominates the airways?
B2
Which adrenoceptor predominated the heart?
B1
What are noradrenaline and adrenaline?
Both are catecholamines
NA and A are neurotransmitters. A is a hormone as well.
What is the difference in structure of A and NA?
A contains a methyl group.
What are the 7 drug targets for preventing the activation of adrenoceptors?
- Enzymes in the biosynthesis of noradrenaline.
- Vesicles carrying noradrenaline.
- Exocytosis of vesicles with cell membrane.
- Adrenergic receptor.
- Transport protein for noradrenaline.
- Metabolic enzymes.
- Presynaptic receptors.
What is the most effective drug target?
Blocking adrenoceptor/adrenergic receptors - to prevent NA/A from interacting with the receptor.
How do beta blockers work (briefly)?
They prevent catecholamine, NA and A from accessing the beta adrenergic receptor sites in the heart, bronchi and other organs.
Do the Beta and Alpha adrenoceptors have hydrophobic pockets?
Beta does alpha does not.
How can selectivity to the B-adrenoceptor be achieved?
By having bulky groups on the amide of NA or A.
How can you differentiate between 1st, 2nd and 3rd generation B blockers?
1st = double aromatic rings 2nd = para substituted aromatic ring 3rd = chain extension
How do beta blockers treat hypertension?
Beta blockers decrease arterial bp by reducing cardiac output as bp is caused by increased blood volume and cardiac output.
Chronic treatment required to treat hypertension. Acute treatment not effective in reducing arterial pressure due to compensatory increase in systemic vascular resistance.
How do beta blockers treat angina and prevent myocardial infarction?
Anti-anginal effects of beta blockers are attributed to their cardio-depressant and hypotensive actions.
By reducing heart rate, contractility and arterial pressure, beta-blockers reduce the work and oxygen demand of the heart.
Reducing oxygen demand improves oxygen supply/demand ratio - relieves patient of anginal pain caused by reduction in oxygen supply/demand ratio due to CAD.
How do beta blockers treat arrhythmias?
Anti-arrhythmic properties of beta blockers - related to their ability to inhibit sympathetic signals on cardiac electrical activity.
Sympathetic nerves increase sinoatrial node automaticity by increasing the pacemaker currents which increase sinus rate. Sympathetic activation also increases conduction velocity and stimulates aberrant pacemaker activity.
