Pharmacology: Test 2 Stimulants

Front 1

Caffeine

Back 1

found in coffee and tea is a trimethylated xanthine (1,3,7 trimethylxanthine).

Front 2

theophylline

Back 2

found in tea, 1,3 dimethylxanthine. Less able to cross into CNS. Used to be used for asthma tx.

Front 3

theobromine

Back 3

found in chocolate, 3,7 dimethylxanthine.

Front 4

Caffeine properties

Back 4

CNS stimulant, delay onset of drowsiness and fatique, promote concentration, produce keener appreciation for sensory stimuli.//

Constricts cerebral vasculature, antagonist to vasodilatory effects of adenosine.//

Front 5

Peripheral effects of caffeine

Back 5

increase HR, increase GFR, acid secretion, and lower bowl irritability.

Front 6

Caffeine Mech of action

Back 6

During periods of wakefulness, ATP and cAMP is generated, and upon their breakdown, adenosine is released. Adenosine activates receptors resulting in drowsiness and sleep. Caffeine antagonizes the effects of adenosine.

Front 7

Adenosine receptors

Back 7

A1, A2a, A2b, A3.//

Front 8

Caffeine effects on A1-R

Back 8

A1: brain, presynaptic, inhibit AC, decrease cAMP, especially in arousal areas. //

Front 9

Caffeine effects on A2a-R

Back 9

A2a-R: basal ganglia, postsynaptic. They activate AC and increase cAMP which enhances tonic inhibitory action of basal ganglia. Caffeine release this tonic inhibition resulting in psychomotor stimulation.

Front 10

Caffeine Toxicity and OD:

Back 10

rare, overconsumptions may cause headaches (excessive vasocontriction), insomina, anxiety and panic attack.

Front 11

Caffeine withdrawal and Tolerance.

Back 11

little tolerance; headache, depression and inablity to concentrate 24-48 hrs after last dose. Headache due to excessive vasodilation.

Front 12

Xanthine action on Phosphodiesterase (PDE)

Back 12

PDE removes cAMP, and things like caffeine inhibit it causing increased cellular cAMP. Not seen with typical coffee consumption dose.

Front 13

Theophylline and muscle

Back 13

used to be for asthma treatment. At high dose would inhibit PDE, resulting in SM relaxation. NO longer drug of choice for asthma.

Front 14

Nicotine

Back 14

agonist at the nAchRn. Peripheral effects include vasocontriction, and bradycardia (ganglionic) and increased perspiration (aortic chemoreceptors). CNS effects involve cortical arousal.//

Front 15

CNS sympathomimetics

Back 15

involves global neuromodulation by monoaminergic neurons located in midbrain and the brainstem.

Front 16

Cocaine

Back 16

obtained from leaves of Erythroxylon coca.//

Front 17

Cocain CNS effects

Back 17

tachycardia, systolic and distolic BP rise, euphoria.... after 40-80 min, followed by depression, dysphoria, and intense craving for more cocaine.

Front 18

Cocaine effects depending on route of administration

Back 18

injected, smoked and intranasal result in greater risk of binge use.//

Oral risks of delayed OD and heart attack.//

Front 19

Cocaine Mech of action

Back 19

CNS: blockade of reuptake for NE, DA, and serotonin (5HT). >> increased activation of their receptors.//

DA activation: cause reinforcing effects at mesolimbic 'reward' pathways in Nucleus accumbens.

Front 20

Difference btwn cocaine action and amphetamines?

Back 20

effects are similar but cocaine has shorter duration and its actions are activity-dependant.

Front 21

Cocaine's Medical use?

Back 21

local anesthetic in upper resp. tract.

Front 22

Cocaine addiction

Back 22

seems to cause permanent changes in brain, causing less DA release to same stimulus >>> drug craving, depression

Front 23

Cocaine toxicity

Back 23

High acute dose: arrhythmias, heartblock, cardiac arrest.

Higher dose: termor, tonic-clonic convulsion, vomiting... followed by depression and respiratory failure.

Tx: symptomatic; beta blocker, diazepam and DA.

Front 24

Cocaine chronic use:

Back 24

some degree of tolerance, cardiac damage (enlarged heart), paranoia and psychotic behavior similar to amphetamines, nasal septum damage (from repeated vasoconstriction). //

Withdrawal: ahedonia, more craving, increased appetite, depression, lethargy, sexual dysfuntion.//

Front 25

What's a 'speed ball'?

Back 25

polydrug: cocain or amphetamine combined with opitates to reduce anxiety provoking effects.

Front 26

What's a DA receptor antagonist?

Back 26

haloperidol

Front 27

Amphetamines

Back 27

synthetic benzylethylamine, resembling endogenous catecholamine (NE, DA) and decongestant drugs (ephedrine, pseudoephedrine)

Front 28

Amphetamines: CNS stimulation

Back 28

increase alertness, delay fatigue, euphoria, irritability, anxiety.//

DA antagonist (haloperidol) block amphetamine actions.

depresses appetite (weight loss).

Front 29

High dose amphetamines

Back 29

stereotypical behavior of DA receptor activation: repetitive lip movement, tongue and extremities, jaw clenching, teeth grinding >>> followed by depression.

Front 30

Amphetamine Mech of action?

Back 30

indirect sympathomimetics: release NE, DA from nerve terminals both in CNS and periphery.

Front 31

compare amphetamine, methamphetamine and tyramine?

Back 31

Tyramine is the least CNS permissive. methamphetamine due to its extra methyl group enters brain more readily than amphetamine and has a longer half-life.

Front 32

Describe Amphetamine action?

Back 32

enters neurone through DA-transporter or by diffusion, inhibits MAO, enters storage vesicles and displaces DA, NE or serotonin. High monoamine result in going through plasma membrane transporter (in reverse), causing receptor activation.

Front 33

Khat

Back 33

kathionine (from katha edulis), resemple amphetamine, but less potent. used in horn of Africa and Arabian peninsula.

Front 34

Amphetamine medical use

Back 34

restricted to treatment of ADHD and narcolepsy.

Front 35

Drug for ADHD pts

Back 35

Methylphenidate (Ritalin). Inhibits NE, DA and 5HT uptake like cocaine; may also induce transmitter release similar to amphetamines. oral administration.//

amphetamine and methylphenidate have same efficacy in treating ADHD.//

Front 36

Describe Amphetamine action?

Back 36

enters neurone through DA-transporter or by diffusion, inhibits MAO, enters storage vesicles and displaces DA, NE or serotonin. High monoamine result in going through plasma membrane transporter (in reverse), causing receptor activation.

Front 37

What's a NE-selective reuptake inhibitor?

Back 37

atomoxetine, approved for ADHD. This drug is not reinforcing b/c of no DA action? compared to methylphenidate. //

many side effects; sexual dysfunction, less reliable, liver dysfunction (CYP2D6), suicidal thoughts.

Front 38

Narcolepsy treatment

Back 38

amphetamines, modanifil

Front 39

Amphetamine medical use

Back 39

restricted to treatment of ADHD and narcolepsy.

Front 40

Modanifil

Back 40

new drug for narcolepsy, shift-work sleep disorders, military. Does not activate reward pathways, no "high" or "crash" afterwards.

Front 41

Drug for ADHD pts

Back 41

Methylphenidate (Ritalin). Inhibits NE, DA and 5HT uptake like cocaine; may also induce transmitter release similar to amphetamines. oral administration.//

amphetamine and methylphenidate have same efficacy in treating ADHD.//

Front 42

ADHD

Back 42

deficiency in NE and/or DA leading to less ability to focus.

Front 43

gamma hydroxybutyrate (GHB)

Back 43

also 'date rape drug', not a stimulant but a sedative-hypnotic. Used in conjuction with modanifil, given at bedtime to enhance quality of nocturnal sleep in order to reduce daytime sleepyness in narcolepsy pts.