PSU BBH 143 Exam 2 Study Guide with
Complete Solutions
Amphetamines and ADHD Treatment: ADHD Treatment - ANSWER-a. reuptake
inhibitor of dopamine and norepinephrine
b. hypothesized ADHD is caused by deficiencies in dopamine and norepinephrine
c. unclear if short term benefits translate into long term benefits
Amphetamines and ADHD Treatment: Early Uses - ANSWER-a. related to ephedrine, a
plant derivative. Isolated in 1887, amphetamine discovered as a related compound.
b. Benzedrine (1933) - recreationally used amphetamine
c. made schedule II in 1970 under Controlled Substances Act
Amphetamines and ADHD Treatment: Forms - ANSWER-a. d-amphetamine is more
potent. Same chemical formula, but atoms arranged differently.
Amphetamines and ADHD Treatment: Pharmacodynamics - ANSWER-a. blocks
reuptake
Amphetamines and ADHD Treatment: Pharmacokinetics - ANSWER-a. oral (therapeutic
use), intranasal, intravenous, inhalation (not common)
b. Half life of 9-11 hours for d-amphetamine
Anti-anxiety drugs: Benzodiazepines - ANSWER-a. Pharmacokinetics: generally oral,
half life ranges from 2.5 to 50 hours
b. Pharmacodynamics: Bind to GABA receptor and act as an allosteric modulator (more
inhibition), causes increased GABA signaling, neural inhibition
Anti-anxiety drugs: Beta blockers - ANSWER-a. Typically used to treat high blood
pressure; Antagonist at receptors of sympathetic nervous system (for norepinephrine &
epinephrine)
Anti-anxiety drugs: History - ANSWER-a. shortcomings of barbiturates was high risk of
overdose
b. Chlordiazepoxide (Librium) released in 1960l was first benzodiazepine to be
developed
Anti-anxiety drugs: Nonbenzodiazepine BZRAs (zolpidem, zaleplon, eszopiclone) -
ANSWER-Zolpidem (Ambien), half-life of 2-2.5 hours
Zaleplon (Sonata), short half-life of <1 hours
Eszopiclone (Lunesta), half life of 5-7 hours
, Anti-anxiety drugs: Tolerance & Dependence - ANSWER-a. Tolerance to anxiolytic
effects develops more slowly than to the sedative effects
Antidepressants: First Generation Drugs - ANSWER-a. First generation antidepressants
were monoamine oxidase inhibitors (MAO-Is) and tricyclic antidepressants (TCAs). Both
increase levels of norepinephrine and serotonin.
b. TCAs caused drowsiness & confusion, and could be toxic at high doses. Serious side
effects occurred when MAO-Is were mixed with certain drugs or foods
Antidepressants: Other Antidepressants - ANSWER-a. Buproprion - inhibits dopamine
and norepinephrine reuptake
b. Ketamine - may reduce symptoms in ppl. w/ treatment-resistant depression,
sustained benefit for several weeks, rapid onset
Antidepressants: Serotonin Hypothesis - ANSWER-a. treatment that don't target
serotonin specifically work just as well as those that do; experimentally depleting
serotonin levels doesn't result in depression
Antipsychotics: Phenothiazines and other first generation drugs - ANSWER-a.
Pharmacodynamics: block dopamine receptors
b. Tardive dyskinesia: causes involuntary abnormal movements, i.e., ticks. Potentially
irreversible, effects may stay even after no longer taking drug; Parkinsonian symptoms;
both due to the blockade of dopamine receptors which has widespread effects
Antipsychotics: Schizophrenia mechanism - ANSWER-a. dopamine explains the
positive effects, but not the negative
Antipsychotics: Second generation drugs - ANSWER-a. side effects - weight gain,
diabetes (independent from weight gain), cardiac problems
Caffeine: Addiction & Withdrawal - ANSWER-a. not problematically addictive, because it
doesn't cause significant life disruption
b. withdrawals caused by up-regulation of adenosine receptors during caffeine intake
Caffeine: Health Benefits - ANSWER-a. associated with lower risk of coronary heart
disease and stroke; can provide relief from headaches; decreased risk of some cancers;
etc.
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