Amphetamines (speed) & Cocaine Flashcards
What type of neurotransmitters do they mimic/release?
What does cocaine do at synapses?
What does MDMA/amphetamines/heroin do at synapses?
What type of receptors do they affect & what do they do?
What is psychological dependence?
How is cocaine/MDMA relevant to the dopamine reward pathway?
How do opioids, alcohol & cannabis play into the dopamine reward pathway?
monoamines - 5-HT, DA & NA
Blocks the re-uptake of dopamine by binding to the transporter
Causes release of neurotransmitters (dopamine)
Activate mu & cb1 receptors - inhibitory action
Drugs triggering reward / reinforcement mechanisms
Preventing re-uptake or release of dopamine leads to reward
Inhibit GABA-A receptors (inhibitory) - decreased inhibitory response so dopamine released from VTA
What are the symptom differences between amphetamines & cocaine? Why is this?
What are the low dose effects of stimulants? 6
What are the high dose effects of stimulants? 8
What do amphetamines & cocaines have in structure which is similar to something else?
What does this allow them to do?
What is the limitation with cocaine?
Amphetamines = slower onset & longer lasting
Cocaine = rapid onset & short duration action
Pharmacokinetics
Mood amplification, increased energy, talkativeness, insomnia, mild anorexia & increased sexual interest
Irritability, hostility, motor stereotypes (chewing), extreme energy, rambling thoughts, total anorexia, decreased sexual interest, total insomnia
2 rings - mimic monoamines like 5-HT, dopamine, noradrenaline
Interact with transporters & alter synaptic levels of these monoamines
Because cocaine is not identical - can only bind to transporter (not taken up into the presynaptic terminal) so only blocks re-uptake
What does a NT binding to its autoreceptor result in?
If you take a drug that alters the synaptic level of a NT, what does this depend on?
Why do the drugs have a wide effect?
How can cocaine be used as an anaesthetic?
Inhibits further NT release
Baseline release of transmitter
Diffuse systems - widespread action on nervous system
Blocks Na+ channels - blocks pain dentistry (not stimulant/monoamine effects)
What is cocaine made of?
What is crack made of?
How is it taken?
What is the difference between doses between cocaine & crack?
Purity?
Onset?
Duration?
Therefore which one is used more often?
Why is crack more likely to be re-taken?
Powder extract (cocaine) from coca plant
Powder extract (cocaine) from coca plant, add HCl & sodium bicarbonate + heat -> free base (crystal form) + sodium chloride (salt)
Smoke - combusts better & more rapid entry to brain
Cocaine 25-30mg line but crack 80mg
Cocaine 40-70% pure & crack 90%
Cocaine 1-4 mins, crack seconds
Cocaine 30 mins & crack 10 mins
Crack
High is higher & low is lower - shorter duration & rebound low is more profound
Why does cocaine have cardiovascular effects?
What are cocaine effects on brain? 6
How can cocaine cause heart failure?
What else can it cause?
How does cocaine cause destroyed septum?
Noradrenaline transmitter in sympathetic nervous system outside of brain - cocaine causes increased DA & NA levels
Mood increases, alertness, confidence, dry mouth, palpitations (heart rate increases & secretions decrease), anxiety/panic
Increase NA in autonomic nervous system increase blood pressure & heart rate - causing failure
Cerebral haemorrhage - rise in blood pressure causing rupture of vessels & brain bleed
Vasoconstriction in the nose leading to death of cells of septum
How is amphetamine different to cocaine origin wise?
What is it used to treat?
What form is it prescribed in?
Which is the predominant form of the drug used and why?
What is khat?
What was amphetamines used to treat in 1920s?
When was it made prescription only?
Amphetamine is synthetic
ADHD
Salt form/soluble form - amphetamine sulfate
D-amphetamine sulphate - interacts with monoamine transmission
plant grows in yemen - ingredients similar to amphetamines
Low bp + asthma - dilates the airways
1956
What is dexedrine?
What was the problem & how was this treated?
How does amphetamine act on pre synaptic terminals?
What are the effects? 3
What does too much amphetamine do?
How does this occur?
What other problem does amphetamine give rise to?
What are 2 other effects similar to cocaine?
Stimulant for pilots in the RAF WWII (hostility) (go pill)
No go pill - benzodiazepines
Enter terminal through uptake transporter (mimic dopamine/monoamine) & increased amount amphetamine pushes out dopamine - stimulates release by physical movement of NT out
Alert, awake, confident
Amphetamine psychosis like scz - paranoid, irritability, withdrawal
Dopamine malfunction - amphetamines releasing too much dopamine
Motor function like chewing due to dopamine
Insomnia & anorexia
What is crystal meth?
How are they taken?
What is the onset/duration?
What is MDMA?
When did it come about?
How does MDMA work?
What does the 5HT1B autoreceptor do however?
Where is the 5HT1A autoreceptor & what does this do?
How can you try to overcome this come-down caused?
Amphetamine in crystal form (not salt form)
Smoked but eaten, snorted or injected - pill form
Quick onset like crack but has much longer duration than crack 2-12 hours
3,4,methylene-dioxy-metamphetamine (ecstasy)
Synthesised 1912 - for depression, scz, anxiety in 1950s & 1980s dance scene
Enters nerve terminal through uptake mechanism & pushes 5-HT out into the synaptic cleft
5-HT on release it’s activated & binds & inhibits further 5-HT release
Cell body of neurone - activation by 5-HT reduces firing of presynaptic neurones
5-HTP (precursor of 5-HT)
What is MDMA’s signalling involved in?
How many days of comedown?
What are the long term effects?
Where are the 5-HT neurones?
Stop-go signalling due to release of both 5-HT & dopamine - causing empathy, energy, calmness & enhanced sense of surroundings
3-4 days - for 5-HT reduction
Damaging serotonin receptors, decrease in serotonin release/production, serotonin deprivation lead to depressive symptoms/depression, memory loss, aggression, poor judgement
Mid-brain & brain stem - but project over brain
Where do 5-HT neurones extend to?
What is it involved in?
What would happen in the 80s?
What are the withdrawal symptoms of stimulants?
Hypothalamus
Emotional & autonomic response & body temperature
MDMA caused dehydration & increased body temp - caused death from dehydration or consuming too much water
Mainly psychological (not physical) - paranoia, depression, dysphoria, maybe difficulty breathing (maybe physical due to lack of dilation of airways), gastric fluctuations/pain (less 5-HT neurones in gastrointestinal tract), lethargia
What is 2CB used for & how is it taken?
What effects does it cause?
What happens at high doses?
What is BZP?
What are the effects?
What is GHB?
Effects?
Used at peak of ecstasy trip to keep E going long as possible - tablet or powder
Low dose - mildly trippy/speedy, increased senses, more psychedelic than E
Bad trip last 4-8 hours, more hallucinations
acts as an agonist for dopamine & 5-ht receptors
Tingling, alert, cheerful, anorexic & insomnia
Related to GABA - used to be sleep aid but produces stimulant effects
Loss of inhibitions, euphoria, increased confidence & libido - like ecstasy but similar to being drunk
