psychopharmacology - week 6 part 3 Flashcards

1
Q

alcohol

A

injested

behavioural stimulation or depression depending on dose
usually categorised as a depressant

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2
Q

alcohol - effects on brain

A

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

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3
Q

alcohol - long term effects

A

general health issues
- liver cirrhosis
- cancer
- fetal alcohol syndrome

brain effects
- korsoloff’s syndrome
- brain adapts
—> rebound hyper-excitability
—> anxiety, tremor, seizures

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4
Q

cocaine

A

stimulant drug
routes of administration
- nasal
- inhaled

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5
Q

cocaine - effects on brain

A

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)

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6
Q

cocaine - physical and psychological effects

A

cardiovascular damage

smoking ; lung congestion

snorting ; damaged nasal membranes

psychosis

formication - sensations of insects crawling under skin

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7
Q

amphetamines

A

synthetic stimulants
- d- amphetamine
- meth amphetamine

swallowed, snorted, injected, smoked

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8
Q

amphetamines - absorption

A

methamphetamine more lipid soluble than d-amph
- crosses membrane more easily
- enters brain more quickly
- may explain why its used more

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9
Q

amphetamines - physical effects

A

inital:
euphoria, feeling of well being, decreased tiredness

followed by:
irritability, paranoia, tremor, long term use –> psychosis

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10
Q

amphetamines - effects on brain

A

blocks dopamine + noradrenaline re uptake

also stimulates the release of dopamine and noradrenaline

doubly increases dopamine (+ noradrenaline) transmission

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11
Q

nicotine

A

tobacco products

gum and patch replacement products

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12
Q

nicotine - mechanisms of action

A

direct agonist
stimulant
nicotinic acetylcholine receptors –> enhance dopamine neurotransmission
activation increases release of neurotransmitters including dopamine

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13
Q

opiates

A

opioid drugs

natural; morphine and codine

synthetic; heroine, fentanyl, oxycodone

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14
Q

opiates - metabolism

A

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

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15
Q

opiates - types of receptor

A

5 types

Mu

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16
Q

opiates - how do opioids effect dopamine

A

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

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17
Q

coffee (caffeine)

A

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

18
Q

caffeine - long term use

A

brain responds by making more adenosine
- more caffeine needed for same response

also may feel withdrawals (feeling more tired)

19
Q

caffeine - effects

A

stimulates the production of adrenaline
- increased HR
- open airways

prevents dopamine reabsorption into the brain
- this is what makes coffee moderately addictive

20
Q

marijuana

A

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

21
Q

marijuana - cannabinoids

A

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

22
Q

marijuana - dopamine

A

effects levels of dopamine and norepinephrine in brain
- euphoria
- relaxation
- pain modulation
- enhancement of experience

and anxiety

23
Q

marijuana - cannabinoid receptors

A

in areas of brain controlling short term memory, learning, coordination, movement control, higher cognitive function

24
Q

factors contributing to drug differences

A

kinetic differences
pharmacodynamics
hypersensitivity, hypo, allergic reactions, idiosyncratic response
- might reflect genetics / prior experience to viruses or toxins

25
Q

factors contributing to drug differences
- between people

A

body size
age
health
sex
ethnicity / race

26
Q

factors contributing to drug differences
body size

A

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

27
Q

factors contributing to drug differences
age

A

metabolism
excretion
drug-disease and drug-drug interactions
compliance

28
Q

factors contributing to drug differences
age - metabolism

A

liver mass reduced
decreased in liver function
liver less able to metabolize many drugs

29
Q

factors contributing to drug differences
age - excretion

A

kindneys less able to excrete drugs into urine

30
Q

factors contributing to drug differences
age - drug disease and drug-drug interactions

A

chronic disease status
use of multiple medications

31
Q

factors contributing to drug differences
age - compliance

A

40% of older people do not take drugs as directed

32
Q

factors contributing to drug differences
sex

A

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

33
Q

factors contributing to drug differences
bio transformation of alcohol

A

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)

34
Q

factors contributing to drug differences
bio transformation of alcohol - factors effecting

A

presence of food in stomach
- full stomach retains alcohol for longer so that more is metabolised by the gastric enzyme

35
Q

factors contributing to drug differences
sex

A

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

36
Q

factors contributing to drug differences
genetic

A

map onto racial and ethnic (not a perfect marker for these differences) group and effect drug response

37
Q

factors contributing to drug differences
ethnic

A

genetic
social

38
Q

factors contributing to drug differences
tolerance

A

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

39
Q

factors contributing to drug differences
sensitisation

A

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>

40
Q

factors contributing to drug differences
expectancies

A

what we expect infliences the way we may respond
placebo effects (pharamacologically inert)
both behavioural and physiological