adrenergic modulators Flashcards
what sort of receptor mediates vasoconstriction
Alpha 1
what is the indication of Doxazosin, and how does it work
its used to reduce mild to moderate HTN, not usually as a monotherapy however
it is a vascular alpha 1 blocker, so it blocks SNS tone on the alpha 1 receptors thereby causing relaxation of the vascular smooth muscle, reducing TPR.
why is DOxazosin good
it is less likely to cause reflex tachycardia than non-selective alpha blockers. also less likely to block the presynaptic alpha 2 receptors
whats the suffix for alpha receptor blockers,
-zosin
what is the suffix of beta blockers
-olol
how do the beta blockers work
these drug bind to and reversibly antagonise the binding of NA and Adrenaline to the beta adrenoreceptors. thereby less cAMP so less channel phosphorylation so less Ca2+ hence weaker contractions and slower contractions - slower as there is less PLN phosphorylation so slower Ca2+ uptake from the SERCA.
whats the difference between carvedilol and metoprolol
the metoprolol is more selective for the Beta-1 receptors. whereas the carvedilol will bind to the B1, B2 and alpha 1
there is the blocking of beta 1 on the heart causing the lower HTN effects, what does blocking beta 1 on the kidney do
this will inhibt the release of renin which would otherwise be stimulated by SNS on the beta ones. hence less RAAS activity, thereby lowering BP even more so.
whats the pharmacological value of a beta blocker
rate control (-ve chronotrope)
decreased work of the heart
increased rate of cardiac relaxation
decreased conduction through the AV node.
what are the best uses for metoprolol
rate control in atrial fibrillation, use in angina and MI due to the decreased cardiac work, heart failure. not really indicated for HTN anymore
when is a beta blocker absolutely contra indicated
when the patient has asthma. as we can induce a bronchospasm, but also block the beta receptors that would be agonised by salbutamol. therefore we cannot bronchodilate when we need to
what are the adverse effects of beta blockers
bronchospasm due to B2 interaction, reduced exercise tolerance, peripheral vasoconstriction, decreased cardiac output which can promote heart failure, worsening of lipid profiles
pharmacokinetics of metoprolol and carvedilol
these have lipophilic side chains and can thus cross the blood brain barrier and cause CNS effects like nightmares.
high oral absorption, extensively first pass metabolised by CYP2D6
pharmacokinetics of atenolol
hydrophilic side chain so cannot cross the blood brain barrier very well hence less CNS effects.
has a longer T1/2 and is mostly excreted unchanged via the kidneys.
difference between metoprolol tartrate and succinate
tartrate is immediate release
succinate is slow release
