Drugs of Abuse - CNS pharmacology Flashcards
what are the main classes of abused drugs
sedatives
opioids
stimulants
hallucinogens
cannabinoids
what is the mode of action for the most addictive substances
increase dopamine levels in the limbic system (can lead to psychosis)
drug tolerance vs dependence
tolerance = reduced drug effect resulted from repeated use
dependence = the need to keep taking the drug because of adaptations your body has made
types of drug tolerance
behavioural: compensate for drug effect
functional: changes in drug action
metabolic: increased drug metabolism
types of drug dependence
psychological: drug seeking behaviour - associated with addiction
physiological: discontinued use of drug produces symptoms often opposite to effects sought out by user - withdrawal
theraputic approach to drug abuse
- treat overdose: symptoms, antagonists
- management of withdrawl symptoms: administration of drug to suppress acute withdrawal followed by gradual reduction in dose
- long-term rehabilitation
Sedatives as a drug of abuse
- e.g. benzo, barbituates, ethanol
- users seek escape or alternating patterns
- used as date rape drugs
- enhance GABA response
- combinations of sedatives can be fatal
drugs to treat sedative dependence (withdrawal)
- clonidine: helps with autonomic symptoms of withdrawal
- benzodiazepines: can be used to treat ethanol withdrawal (sedative to treat another sedative)
symptoms of sedative withdrawal
tremor
irritability
anxiety
hypertension
nausea
vomiting
sweating
perceptual distortion
tolerance to sedatives
to sedative itself but not respiratory depressant effects
metabolic tolerance to ethanol
- MEOS usually has minor role in ethanol metabolism
- MEOS is induced in chronic alcoholism therefore individuals addicted to alcohol may have enhanced rate of ethanol metabolism
opioids as a drug of abuse
- e.g. morphine, heroin
- users seek initial rush followed by euphoria, tranquility and sleepiness
- presynaptically: decrease Ca+, decrease neurotransmitters
- postsynaptically: increase K+ efflux, inhibition of postsynaptic neurons
- probably wont become addicted if actually taking them for pain
Heroin addiction
- doses vary in potency so risk of overdose
- effects last 3-5 house, several doses a dat to prevent withdrawal
- administered via inhilation, SQ or IV - increased risk of spreadinf diseases with shared needles
heroin acute toxicity (overdose)
- symptoms = respiratory depression, coma and death
- treatment = naloxone (opioid receptor antagonist)
drugs for heroin detoxification - manage withdrawal
methadone: take orally, longer-acting opioid receptor agonist
clonidine: for autonimic symptoms of withdrawal
stimulants as drugs of abuse
- e.g. amphetamine and cocaine
- highly addictive
- main routes of administration = inhilation, IV, oral
- increase NE, dopamine and seretonin levels
tolerance and dependence of stimulants
- involves changes in sensitivity of dopamine transporters and receptors
- desired effects = alertness and euphoria
- adverse effects = psychosis and delusions, excess sympathomimetic activity
stimulant overdose
- cocaine - intracranial hemorrhage, stroke, seizure, arrythmias, heart attack, hyperthermia, coma, death
- amphetamines less commonloy fatal but halflife may be more harmful to CNS
hallucinogens as a drug of abuse
- LSD: agonist at 5-HT receptor
- PCP: NMDA receptor antagonists
- desired effects = visual illusions and preceptual distortion
tolerance of hallucinogens
- develops short-term, likely involving receptors
- dependence is rare
adverse effects of hallucinogens
- panic reactions, psychosis, flash-backs, SNS symptoms
- LSD is partially harmful in pregnancy
- PCP overdose can be fatal
cannabinoids as drugs of abuse
- e.g marijuana, hashish
- THC = psychoactive component
- CB1 receptor in CNS and CB2 receptor in PNS
- inhibits GABA or glutamate release
- main route of administration = inhilation, oral
- tolerance and mild physiological dependence
mechanism of endocannabinoids
- increased Ca2+ at post synaptic neuron increases endocannabinoid production
- binds presynaptic CB1 receptor
- decreases glutamate (or GABA) release
mechanism of THC
- activates the CB1 receptor on presynpatic neuron
- decreases glutamate (or GABA) release
effects of cannabinoids
initial = euphoria, laughter, altered sense of time
secondary = relaxation, introspecton, sleepiness
- impaired cognition and perception
- decreased reaction time
- paranoia, anxiety, hallucinations
chronic use of cannabis
leads to bronchitis and lung cancer
theraputic uses of cannabinoids
cancer: decrease pain, nausea and vomitting
AIDS: appetite stimulation
Glaucoma: decreased intraoccular pressure
