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CHAPTER 7: PSYCHOMOTOR STIMULANTS PowerPoint PPT Presentation


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CHAPTER 7: PSYCHOMOTOR STIMULANTS. Brought to you by: Stephanie Andrus, Kimberly Bernosky and Steve Marshall. General Effects of Psychomotor Stimulants:. Increase in behavioral and motor activity Increase in alertness and disruption of sleep

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CHAPTER 7: PSYCHOMOTOR STIMULANTS

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Chapter 7 psychomotor stimulants l.jpg

CHAPTER 7:PSYCHOMOTOR STIMULANTS

Brought to you by:

Stephanie Andrus,

Kimberly Bernosky

and Steve Marshall


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General Effects of Psychomotor Stimulants:

  • Increase in behavioral and motor activity

  • Increase in alertness and disruption of sleep

  • Pupil dilation, shift in blood flow from skin and organs to muscle, increased body temp.

  • Increase in blood pressure and heart rate

  • Increased O2 and glucose levels in the blood

  • Side effects of anxiety, insomnia and irritability

  • Effects synaptic action of dopamine, serotonin & norepinephrine


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Cocaine:Forms of Cocaine

  • Coca leaves contain 0.5-1% active ingredient of cocaine (benzomethylecognone)

  • Coca paste contains 60-80% cocaine, then is treated with HCl to produce H2O soluble salt. One line of cocaine = 25 mg

  • This salt is injectable, but decomposes with heat

  • Freebase (crack cocaine) is not H2O soluble, but it is soluble in alcohol, acetone & ether.

  • Freebase is relatively heat tolerant, so it can be smoked. One dose of crack = 250–1000 mg


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CocainePharmacokinetics of Cocaine: Absorption

  • Absorption through mucous membranes (snorting): Cocaine’s vasoconstrictive property limits its own absorption (20-30% absorbed).

    Peak reached in 30-60 minutes

  • Inhalation of freebase smoke:

    Onset of effect in 8-10 seconds.

    6-32% reaching plasma.

    Peak plasma levels reached at 5 minutes, persisting for 30 minutes.

  • Intravenous Administration:

    Onset of effect in 30-60 sec


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CocainePharmacokinetics of Cocaine: Distribution & Metabolism

  • Penetrates BBB rapidly, initial brain concentration far exceeds plasma concentration

  • Removed slowly from brain

  • Half-life in plasma = 30-90 minutes

  • Rapid enzymatic breakdown

  • Detectable for 12+ hrs after use (metabolites detectable up to 2 weeks after use)

  • Freely crosses placental barrier


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Cocaine:Neurotransmitter Actions of Cocaine

  • Potentiates synaptic action due to actively blocking the reuptake of DA, NE & serotonin

  • Exerts inhibitory effect on postsynaptic dopamine receptors

  • Blocks the presynaptic transporter protein for DA

  • Increases levels of DA at the synaptic cleft, creating a euphoric sensation

  • Serotonin binding provides additional reinforcement


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Cocaine: Physiological Effects of Short-term Low-Dose Cocaine Use

  • Low dose is hard to maintain due to increasing tolerance (progressively higher doses needed)

  • Appetite repression

  • See Slide 2: General effects of psychomotor stimulants (increased BP, HR, body temp etc.)


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Cocaine: Psychological Effects of Short-term Low-dose Cocaine Use

  • Euphoria, giddiness, boastfulness, self-consciousness (lasting 30 minutes) then mild euphoria, anxiousness (lasting 60-90 minutes)

  • Then cocaine craving & rebound depression

  • Eventually, loss of coordination, tremors & seizures

  • Increased interest in sex & increased sexual dysfunction


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Cocaine: Effects of Long-term High Dose Cocaine Use

  • Toxic Paranoid Psychosis – anxiety, sleep deprivation, hypervigilance, paranoia, suspiciousness

  • Hyperreactivity, impulsiveness, aggression, homicidal tendencies

  • Withdrawal can result in hallucinations


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Cocaine:Treatment of Cocaine Addiction

  • Obstacles – rewarding nature of cocaine, tendency towards relapse, presence of other disorders/addictions

  • Areas of Need – antiwithdrawal agents, anticraving agents (blocking dopamine receptors), treatment of comorbid disorders

  • New types of treatment – ritalin & tricyclic antidepressants


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Amphetamines: Mechanism of Action

CNS effects are caused by release of NE and DA from presynaptic storage sites in the nerve terminals, increasing the amounts available at the postsynaptic receptor (see attached Figure 7.2, page 186 in the text)


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Amphetamines: Pharmacological Effects

  • Response intensity and duration varies w/type of drug, dose & route of administration

  • Low dose: typical psychomotor stimulation

  • Moderate dose: tremors, insomnia, agitation, increased respiration

  • Continuous high doses: repetitive activity, aggression, delusions, anorexia

  • Detectable in urine for 48 hours


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Amphetamines:ICE

  • Analogous to crack cocaine

  • Highly abused illicit substance

  • Easily synthesized from obtainable chemical

  • Methamphetamine HCl is used orally, IV & by snorting, but breaks down at the temperatures needed for smoking

  • ICE does not break down at these temperatures, so it is smoked.

  • Absorption through lungs & mucous membranes can be faster than IV administration of Meth. HCl


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AmphetaminesICE: Pharmacokinetics

  • Near immediate absorption into plasma with additional absorption over the next four hours

  • Half-life ≈ 12 hours (intense, persistent drug action)

  • 60% slowly metabolized in the liver

  • Metabolized & unmetabolized ICE excreted through kidneys


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AmphetaminesICE: Effects & Toxicity

  • Effects are nearly indistinguishable from those of cocaine

  • Repeated high doses result in long-lasting, irreversible decreases in DA and serotonin in the brain

  • Change in sleep patterns, depression, movement disorders, sexual dysfunction & schizophrenic psychoses can result from these chemical changes

  • Fatalities occur in cases of high cardiac toxicity, resulting in pulmonary edema or heart failure


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Non-Amphetamine Behavioral Stimulants

  • Differ from amphetamines in that they lack the basic amphetamine nucleus

  • Have similar effects to amphetamines

  • Include ephedrine (ma-huang) which is used among athletes as a stimulant and is found in some OTC weight loss treatments


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Non-Amphetamine Behavioral Stimulants: Used in Weight Loss

  • Sibutramine (Meridia)

  • Serotonin and norepinephrine reuptake inhibitor

  • Does not appear to have properties lending it to compulsive misuse

  • Causes significant increases in heart rate and blood pressure, limiting its use

  • Orlistal (Xenical) can be used as an alternative


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Treatment of ADHD:Non-Amphetamine Behavioral Stimulants

  • Methylphenidate (Ritalin)

  • Used in treatment of ADHD to calm hyperactivity and improve attention (prescribed in 90% of cases)

  • Half-life ≈ 2-4 hours

  • Variable absorption rates, but generally a rapid onset with short duration (multiple administrations needed over the course of a day)


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Treatment of ADHD:Non-Amphetamine Behavioral Stimulants

  • Methylphenidate (continued)

  • No currently available susatained-release preparation

  • Low-abuse potential

  • Increases syn. conc. of DA by blocking the presyn. DA transporter (like cocaine) and increases the release of DA (like amphetamine)


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Treatment of ADHD:Non-Amphetamine Behavioral Stimulants

  • Pemoline (Cylert)

  • Structurally dissimilar to amphetamine & methylphenidate

  • Decreases ADHD symptoms by potentiating dopaminergic transmission

  • May cause hepatitis-like liver damage

  • Modafinil

  • Potentiates glutamate neurotransmission, and inhibits activity of GABA neurons in the nucleus accumbens and cerebral cortex

  • Used in treatment of ADHD, narcolepsy and causes cognitive improvement in Alzheimer’s patients


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Treatment of ADHD: Amphetamines

  • Dextroamphetamine (Dexedrine) and an amphetamine mixture (Adderall)

  • A one-time dose of Adderall is similar in effect to the typical two daily doses of methylphenidate


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Treatment of ADHD

  • Stimulants improve behavior and learning in 60-80% of correctly diagnosed children

  • 10-30% of ADHD individuals are treatment resistant (little to no response to treatment)

  • Alternatives: antidepressants like fluoxetine (Prozac), buproprion (Welbutrin) and buspirone (Buspar)

  • With antidepressants, rare cases of high cardiac toxicity have been found


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