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CNS stims
UVa med pharmacology block 2
| Question | Answer |
|---|---|
| D-Amphetamine | Indirect sympathomimetic amine, tx hypersomnia disorders, ADHD - sim to catecholamine w/incr lipid sol crosses BBB - displaces DA/NE/5-HT from vesicles->release(DA=NE>5-HT), inhibs reuptake |
| Methylphenidate | Indirect sympathomimetic amine, tx hypersomnia disorders, ADHD - sim to catecholamine w/incr lipid sol crosses BBB - displaces DA/NE/5-HT from vesicles->release(DA=NE>5-HT), inhibs reuptake fx: growth retard, anorexia |
| Modafinil | Tx Hypersomina, cocaine dependence - amphetamine like fx: increases monoamine release No CV side fx, no cognitive behavior agitation, headaches |
| Orlistat/Sibutramine | obesity tx orlistat = non-CNS, pancreatic lipase inhibitor->decr fat absorpt sibutramine=5HT/NE reuptake inhib->satiety/thermogenesis |
| Cocaine | Stimulant - Inhibs DA, NE, 5-HT reuptake highly addicitve (incr DA), CNS fx similar to amphetamine |
| Theophylline | Methylxanthine stimulant tx asthma, apnea of prematurity low dose = competitive adenosine A1/A2 receptor inhib, High dose= PDE inhib->incr cAMP CNSfx:incr alertness, resp stim, convulsive potential |
| Caffeine | Methylxanthine stimulant tx asthma, apnea of prematurity low dose = competitive adenosine A1/A2 receptor inhib, High dose= PDE inhib->incr cAMP CNSfx:incr alertness, resp stim, convulsive potential |
| Buproprion (Wellbutrin) | Non-sedative atypical antidepress w/some amphetamine aspects (DA release) fx: decr seizure threshold, no cardiace fx, no anti-ach fx |
| Verenicline (Chantix) | Selective partial α4-β2 nicotinic receptor agonist tx nicotine addiction attenuates full agonist activity of nicotine, decr reinforcing properties, incr DA release |
| What are amphetamines CNS effects? What are the rebound effects? | alertness, delayed sleep, reduced fatigue, euphoria, increase activity rebound depression, hypersomnia |
| What is Sibutramine used for? What is its mechanism? | - Used for obesity - enhances satiety and thermogenesis by inhibiting serotonin and NE uptake |
| How does amphetamine cause tolerance? | depletion of DA, NE, and 5HT stores |
| Does DA, NE, of 5HT affect sleep in amphetamine use? | NE |
| What is Amphetamines mechanism of action? What is the end result? | - 'A' penetrates the neuronal terminals - displaces DA from synaptic vesicles by disruptic vesicular pH - DA is release into cytoplasm and then exits the terminal - Similar action on NE and 5-HT - Result is massive release of NE, DA, and 5HT |
| What is the most common treatment of nicotine addiction? | replacement therapy with gum, patches, inhalers |
| Is DA, NE, or 5HT responsible for the "high" associated with drugs that affect these? | DA |
| What is the principal medical use of methylxanthines? | - treat primary apnea of prematurity **primies respond to hypoxia by reduction is respiration due to weak chemoreflexes |
| What are the therapeutic uses of d-amphetamine and its related drug methylphendinate? | Hypersomnia ADHD |
| What are the pharmacological effects of recreational tobacco products? | nausea (goes away), increased respiration, tremor, anorexia, activation of autonomic ganglia (symp and parasymp) |
| What two drugs are used in nicotine addiction? | Burpropion and Varenicline |
| What receptors does 'A' act? What are the peripheral effects of amphetamine? | Mixed alpha and beta agonist Increase in BP Tachycardia |
| How is amphetamine administered and where is it metabolized? | Absorbed orally, metabolized in liver |
| What is the mechanism of action of Nicotine? What effects do low and high doses of nicotine have at the NMJ? | - very lipid soluble so absorbed thorugh skin and mucosa - low dose: no NMJ effect - high dose: acts on all nicotinic receptors causing depolarizing blockade leading to CV collapse, muscle weakness, respiratory failure, death |
| What is the difference between D-amphetamine and a catecholamine? | A is lipid-soluble so rapidly penetrates the CNS |
| What is Cocaine's mechanism of action? | blocks re-uptake of DA, NE, and 5HT thus increase extracellular concentration **it is a powerful local anesthetic |
| What Schedule drug is amphetamine? | Schedule II |
| How does Veranicline work? | It is a partial agonist at nicotinic receptors so it attenuates the full effect, and also helps withdrawal symptoms since it is weak agonist |
| What is the mechanism of Methylxanthine action? | - Low dose: competitive inhibition of adenosine A1 and A2 receptors - High dose: inhibit phosphodiesterase so increase cAMP - In brain, A1 receptors depress neuronal function - A2 receptors control motor function |
| What psychotic state does amphetamine overdose resemble? How do you treat an amphetamine overdose? | Resembles paranoid schizonphrenia Treat with nitroprusside, alpha blocker, sedative drugs, acidify urine to promote excretion |
| What are the three main effects of the methylxanthines? | 1) increased alertness 2) respiratory stimulation 3) convulsive @ high dose |
Created by:
sam.mrosenfeld
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