Stimulants & Alcohol Flashcards
PSYCHOMOTOR STIMULANTS
(1) METHYLXANTHINES
(2) NICOTINE
(3) AMPHETAMINE
(4) EPHEDRINE
(5) COCAINE
METHYLXANTHINES moa
caffeine & theophylline
-inhibition of phosphodiesterases, thereby increasing cyclic AMP
-antagonist at both adenosine A1 and A2 receptors
Both of these actions result in enhanced neurotransmission by amplifying the cyclic nucleotide second-messenger cascade.
METHYLXANTHINES kinetics
- absorbed readily after oral, rectal, or parenteral administration
- metabolized in the liver by demethylation and oxidation.
NICOTINE moa
-low doses stimulate nicotinic receptors in the CNS resulting in depolarization
producing some degree of euphoria and arousal
-improves attention, learning, problem solving, and reaction time
-no therapeutic use: except for smoking cessation
NICOTINE kinetics
- highly lipid soluble
- absorption readily occurs by oral mucosa, lungs, gastrointestinal mucosa, and skin
- metabolized in the lung and liver
AMPHETAMINES
At present amphetamines are indicated for treatment of two disorders
(1) treatment of NARCOLEPSY-a disorder characterized by uncontrollable desire for sleep. –about 200,000 patients
(2) Attention-deficit hyperactivity disorder (ADHD)-hyperactivity syndrome in children
AMPHETAMINES moa
- amphetamine appears to exert most of it’s effects by causing the release of biogenic amines(norepinephrine, dopamine, and serotonin) from their storage sites in nerve terminals. There is also some evidence that suggest that amphetamine may interfere with the re-uptake of these neurotransmitters into neurons.
- the major behavior effects are probably due to the release of dopamine which leads to increased alertness, decreased fatigue, depressed appetite, and insomnia.
AMPHETAMINES kinetics
- well absorbed after oral administration
- metabolized by several catabolic pathways, however considerable amount of untransformed drug is excreted in the urine. Therefore it is possible to “ion-trap” this weak organic base.
AMPHETAMINES adverse
The acute toxic effects of amphetamine usually are extensions of its therapeutic actions.
CNS- restlessness, tenseness, irritability, weakness, insomnia, confusion, delirium, paranoid hallucinations, suicidal or homicidal tendencies.
CARDIOVASCULAR-headache, palpitation, cardiac arrhythmias, hypertension, circulatory collapse
-excessive sweating.
AMPHETAMINES agents
DEXTROAMPHETAMINE
METHAMPHETAMINE
METHYLPHENIDATE
PHENTERMINE
DEXTROAMPHETAMINE
METHAMPHETAMINE
(1) DEXTROAMPHETAMINE (DEXEDRINE) CII
(2) METHAMPHETAMINE (DESOXYN) CII-more central effects and less peripheral effects (CV) than dextroamphetamine
Amphetamines have a very high abuse potential, tolerance develops to the anorexic and euphoric effects. Psychological dependence occurs with chronic use
METHYLPHENIDATE
- used for (1) treatment of NARCOLEPSY-a disorder characterized by uncontrollable desire for sleep. (2)Attention-deficit hyperactivity disorder (ADHD)-hyperactivity syndrome in children
- has less euphoric effect and central stimulant effect
- same mechanism and profile as amphetamines
PHENTERMINE
MOA-acts on adrenergic and dopaminergic pathways, possibly like amphetamine
- short term therapy as adjunct to behavioral modification, diet, and exercise in the management of exogenous obesity ( use only for 3 weeks)
- contraindicated in patients with history of CV problems
- hypertensive crisis with monoamine oxidase inhibitors (MAOI’s)
EPHEDRINE
MOA -alpha and beta –adrenergic agonist, in addition it enhances the release of norepinephrine from sympathetic neurons.
- orally active
- not really used therapeutically, but is found in OTC asthma preps.
- biggest use for OTC “stay awake preps”
COCAINE (CII)
MOA- blocks the reuptake of dopamine by inhibiting the re-uptake transporter of neurotransmitter in the pre-synaptic neuron