(c) blocking means a neurotransmitter has actually been released, and now you want a drug that somehow blocks its activity. Taken this way, options (a) and (e) wouldn’t work, since, although they would reduce sympathetic activity, or have a “sympatholytic” action, they don’t actually block a neurotransmitter. Option (b) again is a sympatholytic action, but I don’t really think there any clinically relevant drugs that work this way. Option (d) just made up to fool you, since dentists work with local anesthetics, so you might be tempted to jump at this answer.

(e) again, why can’t they just say guanethidine reduces NE release! You might see these same options listed for several other drugs that could be substituted

(e) Trick question since we want to see if you are speed reading the options, see “false” transmitter, and jump at option (d), and not read further to see that option (e) is the correct answer. Drugs like methyldopa and clonidine are the only centrally acting antihypertensives, reducing sympathetic outflow via alpha-1 agonist action.

(d) We would be majorly surprised if they still ask questions about this drug since it hasn’t been used clinically in the last 30 yrs, but (d) is the answer, making reserpine an example of an indirect-acting sympatholytic.

(b) amphetamine is one of the many indirect-acting sympathomimetics. It acts by causing the release of neurotransmitter. Just as a review:
cocaine: reuptake inhibition and release,
TCA antidepressant: reuptake inhibition,
ephedrine: causes release but also acts at receptor itself,
MAOIs: block NT degradation.

(c) this you just gotta memorize. Option (d) is true except for the fact that the imbalance is between dopamine and too much cholinergic activity, not norepinephrine. Since levodopa has dopa in its name, you could just narrow the question down to options (b) and (c). But you still have to know, Parkinson’s is due to a deficiency in dopamine. So the treatment is to restore DA levels.

(c) – The injection of a sympathomimetic (e.g. a drug that acts like NE) stimulates both alpha and beta-receptors. Alphareceptor stimulation produces vasoconstriction, increased systolic and diastolic pressure and reflex tachycardia. Alpha and beta-receptor blockers can block these effects. the only alternative that lists both an alpha (prazosin) and beta (propranolol) blocker is (c). Atropine is a muscarinic (cholinergic ) receptor blocker that would accelerate the heart, the opposite effect that you want, thus (a) and 2 are wrong. Phenoxybenzamine is an alpha-blocker, but curare is a nicotinic receptor blocker, not beta receptor- thus (d) is wrong. As for # 5, amphetamine is an indirect acting sympathomimetic, not a blocker, thus (e) is wrong.

(c) picky memorization! They are all receptor blockers: atropine is muscarinic receptor blocker, naloxone is opioid receptor blocker, phentolamine is a non-specific alpha blocker, and hexamethonium is a ganglionic blocker. Propranolol, is the only beta-blocker listed.

a) reserpine causes depletion of NE from storage sites, thus it cannot be released by amphetamine. All of the others listed act postsynaptically. Since this drug is no longer used clinically, we would be very surprised if they asked such a question! Wait, we think we said that a few questions ago!

(ii) phentolamine is an alpha blocker, thus the epinephrine will stimulate beta receptors primarily, with the effects listed in option (ii): relaxation of bronchiolar smooth muscle (Beta-1), skeletal muscle vessel dilation (beta-2), and positiver chronotropic and inotropic action on the heart (b)

(iv) well, beta receptor stimulation means stimulation of beta-1 receptors in the cardiac muscle,which will increase systolic bP, and beta-2 stimulation which will dilate vessels going to the liver and skeletal muscle, producing a decrease in diastolic BP. Mydriasis or papillary dilation is also a beta receptor response, so c is also right. While you might be tempted by “cardiac acceleration”, none of the options including (b) work.

(b) all of the above are actions of epinephrine except bronchiolar constriction. Epinephrine would cause bronchodilation – that is why it is used to treat acute bronchospasm. So option (b) has to be the exception, because it is just obviously wrong!

(a) epinephrine is a potent stimulator of both alpha and beta receptors. Injection of epi usually causes a rise in blood pressure due to 1) myocardial stimulation that increases ventricular contraction, 2) an increase in heart rate, and most important, 3) vasoconstriction due to alpha receptor stimulation. However, blood flow to skeletal muscles is increased due to powerful beta-2 receptor vasodilator action that is only partially counterbalanced by a vasoconstrictor action on the alpha receptors that are also present in the vascular bed. When given in the presence of an alpha blocker, beta-receptor mediated vasodilation is more pronounced, the total peripheral resistance is decreased and the mean blood pressure falls. This decrease in blood pressure is called “epinephrine reversal”. The only alpha-blocker listed is prazosin, answer (a). Atropine is a cholinergic muscarinic receptor blocker, propranolol is a betablocker, neostigmine is a cholinesterase inhibitor, and isoproterenol is a predominately beta receptor agonist.

(a)- alternatives 2-4 all increase heart rate, while NE has no effect at muscarinic receptors (e), which are specific for cholinergic drugs.

(iii) Answer is (c)- Alpha-adrenergic agonists such as epinephrine produce vasoconstriction, which would accomplish both “b” and “e”. #3 is the only alternative that includes both b and e thus you don’t have to know anything else. “a” and “c” are false. Vasoconstrictors are include in local anesthetic preparations to (1) prolong and increase the depth of anesthesia by retaining the anesthetic in the area injected, (2) reduce the toxic effect of the drug by delaying its absorption into the general circulation and (3) to render the area of injection less hemorrhagic.

(d) CPZ is a potent alpha blocker like prazosin.

(d) What is needed for bronchodilation is relaxation of bronchial smooth muscles. This is accomplished with beta2 receptor stimulation. Isoproterenol is the only drug listed with potent beta2 action. (a) stimulates alpha receptors in the CNS, (b) NE stimulates alpha and beta1 receptors more than beta2, (c) phenylephrine is an alpha receptor agonist, while (e) methoxamine is a vasoconstrictor that stimulates alpha receptors preferentially.

(iii) vasoconstriction is a result of stimulation of the smooth muscle of the peripheral vasculatire, which is an alpha-1 stimulatory action. Of the options, (a), (c) and (e) are alpha-1 agonists. Phentoalmine is a nonselective alpha blocker and thus would cause vasodilation. Propranolol is a non-specific betablocker.

(c) because that is just what it does!

(e) Guess this was true many years ago when this question was written, but we don’t know if this would still be considered to be one of the most effective treatments, but that is beside the point. You should think levodopa here, since the problem with Parkinson’s is not enough DA, so you can improve the disease by giving levodopa to increase DA levels in the brain. The problem with giving levosopa by itself is that it is rapidly metabolized in the periphery before it is able to cross the BBB, However, the levodopa gets rapidly degraded by enzymes unless you block the enzymatic degradation by giving carbidopa along with the levopdopa.

(e) levodopa apparently overstimulates DA receptors in the basal ganglia and can cause visual and auditory hallucinations (option c), dyskinesia (option (a)), mood changes, depression and anxiety. It also can stimulate the emetic center, producing the effects given in (d). That leaves you with a choice between (b) and (e). Well, apparently, one of the first things you should know about levodopa therapy is that some people think that levodopa can sensitize the beta-1 receptors in the heart and this is a contraindication to using a local anesthetic containing epinephrine. So option (e) is all that is left to be the exception. How you are supposed to remember all this stuff about levodopa is way beyond us, but good luck!

(v) Answer is (e)- Levodopa is the primary drug used to treat parkinson’s disease, which results from abnormally low levels of dopamine in the brain. Levodopa, or L-DOPA is the direct precursor of dopamine (which can’t be used because it doesn’t cross the blood brain barrier- L-DOPA does and is converted to DOPA in the brain) is used to increase dopamine in the brain. All of the effects are established side effects of L-DOPA therapy, thus the answer is (e). Abnormal involuntary movements (AIMS) are the most prevalent and troublesome “extrapyramidal” side effects, typically involving the orofacial musculature. Nausea and vomiting are seen during the first phase of therapy but tolerance develops to these effects. The psychotic effects are much less prevalent, seen in only a small percentage of patients. Increased incidence of arrhythmias is also a problem. Levodopa also sensitizes the heart to epinephrine induced arrhythmias.

(b) an asthmatic patient typically takes a drug that has bronchodilatory effects. For this action, you need a drug that is a beta-2 agonist (remember those charts?). Of the list, albuterol is the only beta-2 agonist listed. Phenylephrine is an alpha-1 agonist used for stuffy noses, pseudoephedrine might have distracted you, since it is a decongestant, prazosin and propranolol are antihypertensives.