psychopharmacology - week 6 part 3 Flashcards
alcohol
injested
behavioural stimulation or depression depending on dose
usually categorised as a depressant
alcohol - effects on brain
enhances GABA transmission by binding to GABAA receptor
- allosteric modulation
- increases flow of Cl- ions through ion channels
inhibits NMDA (glutamate) receptor
indirectly effects neurotransmssion in seretonin, opioid and dopmaine systems
- alcohol can increase mesolimbic dopamine transmission via action at cannabinoid receptors
alcohol - long term effects
general health issues
- liver cirrhosis
- cancer
- fetal alcohol syndrome
brain effects
- korsoloff’s syndrome
- brain adapts
—> rebound hyper-excitability
—> anxiety, tremor, seizures
cocaine
stimulant drug
routes of administration
- nasal
- inhaled
cocaine - effects on brain
blocks dopamine transporter
- reduces reuptake of dopaine into neuron
- prolongs the duration that dopamine remains in synapse
- indirect agonist
acts in ventral tegmental area (lots more dopamine)
cocaine - physical and psychological effects
cardiovascular damage
smoking ; lung congestion
snorting ; damaged nasal membranes
psychosis
formication - sensations of insects crawling under skin
amphetamines
synthetic stimulants
- d- amphetamine
- meth amphetamine
swallowed, snorted, injected, smoked
amphetamines - absorption
methamphetamine more lipid soluble than d-amph
- crosses membrane more easily
- enters brain more quickly
- may explain why its used more
amphetamines - physical effects
inital:
euphoria, feeling of well being, decreased tiredness
followed by:
irritability, paranoia, tremor, long term use –> psychosis
amphetamines - effects on brain
blocks dopamine + noradrenaline re uptake
also stimulates the release of dopamine and noradrenaline
doubly increases dopamine (+ noradrenaline) transmission
nicotine
tobacco products
gum and patch replacement products
nicotine - mechanisms of action
direct agonist
stimulant
nicotinic acetylcholine receptors –> enhance dopamine neurotransmission
activation increases release of neurotransmitters including dopamine
opiates
opioid drugs
natural; morphine and codine
synthetic; heroine, fentanyl, oxycodone
opiates - metabolism
heroine crosses the blood-brain barrier more easily than morphine (distribution)
in the brain heroine in metabolised into morphine
morphine has psychological affect on brain
opiates - types of receptor
5 types
Mu
opiates - how do opioids effect dopamine
mesolimbic dopamine pathway
cell bodies of dopamine neurons in ventral tegmental area
these project into nucleus accumbens
stimulation of nucleus accumbens result of release of dopamine
in the ventral tegmental area also inhibitory influences on these dopamine neurons via GABA
interneurons
-> keep dopamine in check
-> opioids inhibit this
therefore more dopamine released in nucleus accumbens
coffee (caffeine)
when awake adenosine slowly accumulates in brain
this binds to adenosine receptors which slow down brain activity
–> more adenosine = more tired
when asleep conc. declines
caffeine similar to adenosine in structure
- works way through bloodstream into brain
- competes for and binds with adenosine receptors
- because not adenosine not sleepy
caffeine - long term use
brain responds by making more adenosine
- more caffeine needed for same response
also may feel withdrawals (feeling more tired)
caffeine - effects
stimulates the production of adrenaline
- increased HR
- open airways
prevents dopamine reabsorption into the brain
- this is what makes coffee moderately addictive
marijuana
contains molecules that resemble those produced in our brains
- cannabinoids
naturally these circulate in much lower quanities compared to large influx imposed my smoking
specifically the chemical THC (tetrahydrocannabinol) resembles anandamide
marijuana - cannabinoids
are specialised neurotransmitters released by neurons having just fired
- neurons temporarily become unresponsive after firing to prevent them overreaching or being too dominant
- cannabinoids interrupt this (in some points of brain)
- they remove refactory period of neurons that are already active
- causing thoughts, imagination and perception to utterly magnify itself
marijuana - dopamine
effects levels of dopamine and norepinephrine in brain
- euphoria
- relaxation
- pain modulation
- enhancement of experience
and anxiety
marijuana - cannabinoid receptors
in areas of brain controlling short term memory, learning, coordination, movement control, higher cognitive function
factors contributing to drug differences
kinetic differences
pharmacodynamics
hypersensitivity, hypo, allergic reactions, idiosyncratic response
- might reflect genetics / prior experience to viruses or toxins
factors contributing to drug differences
- between people
body size
age
health
sex
ethnicity / race
factors contributing to drug differences
body size
same dose produces smaller response in a larger person
-> drug is distributed in greater blood volume
large person generally need more of a drug for same effect
factors contributing to drug differences
age
metabolism
excretion
drug-disease and drug-drug interactions
compliance
factors contributing to drug differences
age - metabolism
liver mass reduced
decreased in liver function
liver less able to metabolize many drugs
factors contributing to drug differences
age - excretion
kindneys less able to excrete drugs into urine
factors contributing to drug differences
age - drug disease and drug-drug interactions
chronic disease status
use of multiple medications
factors contributing to drug differences
age - compliance
40% of older people do not take drugs as directed
factors contributing to drug differences
sex
compared with men women have:
- lower plasma volume
- higher proportion of body fat
- differences in drug response according to stage of menstrual cycle
- metabolise some drugs differently
factors contributing to drug differences
bio transformation of alcohol
1st metab. by alcohol dehydrogenase (liver+stomach)
coverts into metabolite acetaldehyde
a steady amount of a[[rox. 10ml of 100% ethanal per hour (rate limiting step)
factors contributing to drug differences
bio transformation of alcohol - factors effecting
presence of food in stomach
- full stomach retains alcohol for longer so that more is metabolised by the gastric enzyme
factors contributing to drug differences
sex
on average, equivilent amounts of alcohol greater effect on women
men have a greater vascular capacity
men have more gastric alcohol dehydronase
–> less into blood
factors contributing to drug differences
genetic
map onto racial and ethnic (not a perfect marker for these differences) group and effect drug response
factors contributing to drug differences
ethnic
genetic
social
factors contributing to drug differences
tolerance
need more over time for same effect
metabolic
- usually metabolised faster with repeated use “induce enzymes”
cellular
- target cells adjust their functioning to compensate for action of drug on cells
factors contributing to drug differences
sensitisation
need less over time for same effect
response to drug increases over time
opposite of tolerance
common for stimulant drugs
underlying theory for substance dependence>
factors contributing to drug differences
expectancies
what we expect infliences the way we may respond
placebo effects (pharamacologically inert)
both behavioural and physiological
