CNS Stimulants Flashcards
What are the 3 classes of CNS Stimulants with examples?
Convulsants and respiratory stimulants (eg. doxapram)
Psychotomimetic drugs:
- hallucinogens (eg. LSD, psilocybin, mescaline, MDMA)
- dissociative anaesthetics (eg. ketamine, PCP)
- cannabis
Psychomotor stimulants:
- amphetamines (eg. khat, cocaine, nicotine)
- methylxanthines (eg. caffeine, theophylline)
What is doxopram and its clinical use?
Short acting respiratory stimulant (increases depth and rate of breathing) used in respiratory failure:
- post-operative respiratory depression
- acute respiratory failure
- neonatal apnoea
Describe the mechanism of action of hallucingoens
- upregulate the serotonin pathway altering serotonin signalling
- drugs act on 5-HT receptors and transporters
- affects the locus coeruleus affecting sensory signals of the brain
- affects the raphe nuclei affecting sleep, wakefulness and mood
Tolerance, dependence and risks associated with hallucinogens
Tolerance: develops quickly (and cross-talk)
Dependence: no physical withdrawal, psychologically results in flashbacks and psychosis
Risks:
- injury or accidental death
- poisoning
- adrenergic effects with LSD
- GI effects with psilocybin
Describe the mechanism of action of dissociative anaesthetics and the effects that it causes
NMDA receptor antagonists
Effects:
- analgesic
- stereotyped motor behaviour
- ‘bad trip’
Tolerance, dependence and risks associated with dissociative anaesthetics
Tolerance: rapid over regular, repeated doses
Dependence: physical and psychological withdrawal with PCP
Risks:
- accidents/loss of control/automatic behaviour
- PCP: hyperthermia, convulsions
- ketamine: overdose with heart attack/respiratory failure
What are the effects of psychomotor stimulants?
- locomotor stimulation
- euphoria and excitement
- insomnia
- anorexia (diminishes with continued use)
- stereotypic behaviour
Describe the mechanism of action of amphetamines
- causes NET to work in reverse so instead of it taking NTs (noradrenaline and dopamine) released from the synaptic vesicles and packaging them, they release them into the synapse
- also inhibits MAO which further increases the release of NTs (noradrenaline and dopamine) into the synapse
Dopamine signalling affected:
- motor control (nigrostriatal)
- behavioural effects (mesolimbic and mesocortical)
- endocrine control (tuberohypophyseal)
Noradrenaline signalling affected:
- LC (wakefulness, alertness)
- medulla/hypothalamus (BP regulation)
Tolerance, dependence and risks of amphetamines
Tolerance: rapid to euphoric and anorexic effects, slow to other effects
Dependence: moderate potential due to euphoric effects
Risks:
- vascular accidents (eg. tachycardias, arrhythmias, increased BP)
- cerebral convulsions and coma
- excitation syndrome
- anorexia
- chronic paranoid psychosis
- cognitive impairment
What are the clinical uses of amphetamines?
- lisdexamfetamine mesylate: ADHD
* phentermine and diethylpropion: weight loss
Tolerance, dependence and risks of cocaine
Tolerance: rapid
Dependence: physically mild, psychologically strong
Risks (acute):
- CV (hypertension, tachycardia, ventricular fibrillation, MI, resp arrest, stroke)
- muscle spasms, tremors
- hyperthermia
- seizures, headache, excited delirium
Risks (chronic):
- MI
- malnutrition and weight loss
- decreased libido and impotence
- personality/mood
- ‘toxic syndrome’ - like paranoid schizophrenia
What are the effects of methylxanthines?
- stimulate CNS
- diuretics
- cardiac muscle stimulants
- smooth muscle relaxants
- reduces fatigue and improves mental performance
What is the mechanism of action of methylxanthines?
- inhibit cAMP/cGMP phosphodiesterases
- block purine receptors (adenosine A1 and 2 receptors)
- diuresis (due to vasodilation of afferent glomerular arterioles causing increased GFR)
