CNS Stimulants Flashcards
Caffeine MOA:
- Blocks adenosine receptors (post-synaptic receptors produce IPSPs, pre-synaptic receptors inhibit glutamate release – blocks both of those inhibitor effects).
- At higher doses, blocks PDE – results in an increase in cAMP, beneficial for asthma.
Caffeine effects:
CNS: increased alertness, decreased fatigue.
Peripheral: -positive chronotropic, inotropic effects.
-Dilates coronary and general systemic blood vessels but constricts cerebral blood vessels.
Caffeine SEs:
- Nervousness, tremors.
- High doses can stimulate medullary respiratory, vasomotor and vagal centers.
- Tolerance, withdrawal.
Methylphenidate MOA:
Releases NE, DA, 5HT, blocks transmitter uptake into presynaptic terminals, direct partial agonist of alpha-adrenergic receptors, MAO inhibition (at high doses).
Methylphenidate use:
ADHD
Cocaine MOA:
- Potent inhibitor of the reuptake of NE, DA, 5HT.
- -Increasing DA produces feelings of euphoria, feelings of elation.
- Increasing NE causes vasoconstriction, tachycardia, increased alertness.
Cocaine SEs:
- Neurotoxic effects due to damage to DA systems. OD can cause seizures and/or CV effects.
- Fetal effects – low birth weight, learning and emotional problems, attachment disorder, addiction.
Amphetamine MOA:
-Releases NE, DA, 5HT, blocks transmitter uptake into presynaptic terminals, direct partial agonist of alpha-adrenergic receptors, MAO inhibition (at high doses).
-Metabolized and excreted unchanged.
Produces wakefulness, alertness, decreased fatigue, increased intellectual performance. Peripheral sympathomimetic effects.
Amphetamine uses:
Narcolepsy, ADHD
Amphetamine SEs:
- Insomnia, abdominal pain, anorexia.
- Toxicity: sympathomimetic effects, restlessness, dizziness, tremor.
- Abuse liability.
Methamphetamine MOA:
Same as amphetamines, but better CNS bioavailability.
Nicotine MOA:
- Agonist of nicotinic cholinergic receptors.
- Sympathetic ganglia activation results in release of epinephrine.
- Parasympathetic effects result in GI motility.
- CNS effects: increased alertness, activates DA signaling.
- Is reinforcing: activates neuronal symptoms designed to maintain behaviors that are important for survival. Each puff of a cigarette is reinforcing – reason why it is so addicting.
Bupropion MOA:
Seems to enhance noradrenergic and dopaminergic signaling.
Bupropion uses:
Reduces craving and nicotine withdrawal symptoms.
Verenicline MOA:
Partial agonist of CNS nicotinic receptors. Effect is twofold: activates nicotinic receptors enough to reduce craving and withdrawal, reduces the effects of the full agonist (nicotine).
