topic 4: stimulants and alcohol Flashcards

1
Q

what is meant by a half life

A

how long it takes for it to leave the system.

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2
Q

define cocaine (intake, peak etc.)

A

typically snorted in powder or smoked, reaches its peak in blood (30-60 minutes).

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3
Q

what is the biological half life of cocaine

A

30-90 minutes.

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4
Q

what are the short term effects of cocaine?

A

It is a stimulant which increases euphoria, energy, confident, alertness and talkative.

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5
Q

cocaine can occur at what type of synapse?

A

mono-aminergic synapses.

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6
Q

the role of reuptake channels for cocaine

A

presynaptic terminal can recycle NTs differnt to the autoreceptors which signal the terminal to reduce release of NTs.

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7
Q

what are the long term effects of cocaine?

A

lack of reuptake means depletion of monoamines, so they crash and which they remedy with cocaine.

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8
Q

regular users of cocaine may experience:

A

destruction of nasal septum, schizophrenia like symptoms, sexual dysfunction, tolerance and sensitisation for others.

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9
Q

what leads to the addictiveness of cocaine?

A

direct effect on dopamine released in the NA and PFC. Activate seeking or reward pathway- its strong psychologically and not physically addictive.

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10
Q

how do amphetamines work?

A

work on mono-aminergic synapses, they tend to reverse the uptake channels- push NTs out and dont need action potentials.

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11
Q

how does ritalin act?

A

act similar to cocaine and block it, gradual release but without the immediate effects of cocaine.

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12
Q

caffeine (peak and halflife)

A

concentration peaks after 40 mins, passes through blood brain barrier. biological half life is 3.5-5hrs.

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13
Q

what are the short term efects of caffeine?

A

increases alertness and wakelfulness, difficulty with fine movements, increase cardia contractions and constricts blood vessels.

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14
Q
A
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15
Q

what is the psychological action that occurs when we have caffeine

A

blocks adenosine receptors and stimulates adrenaline release from adrenal medulla.

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16
Q

what does adenosine do

A

is a NT that induces sleep and vasolidation.

17
Q

what are the long term effects of caffeine

A

mostly sleep deprivation, cna counter effects by using more caffeine.

18
Q

the addictiveness, withdrawal and psychological dependence of caffeine.

A

withdrawal- headaches, sleepiness, irritability and difficulty concentrating. Dependence- increases dopamine release in the NA.

19
Q

nicotine: intake, peak and half life.

A

tobacco leaf, smoked and chewed. Within 7sec puff 25% of nicotine has crossed the blood-brain barrier. The half life is 2 hours for a chronic smoker.

20
Q

what are the short term effects of nicotine?

A

vomiting, reduces muscle tone, reduces weight gain, increase heart rate and blood pressure.

21
Q

what is the physiological action behind nicotine?

A

binds to nicotinic acetylcholine receptors, involved in stimulation of SNS- release of adrenaline. The receptors are also found in the brain.

22
Q

what are the long term effects of nicotine

A

easy tolerance, wears heart out quicker, causes cancer.

23
Q

addictiveness, withdrawal of nicotine.

A

physical dependence; withdrawal of craving, irritability, increased appetite and insomnia. most addictive drug psychologically. Nicotine and dopamine release in nucleus accumbens.

24
Q

alcohol: intake, peak…

A

usually ingested, reaches peak in 30-90 minutes, easily crosses blood brain barrier, mostly eliminated through the liver.

25
short term effects of alcohol
low dose; mild euphoria and anxiolytic effect. Higher dose; intoxication.
26
alcohol is the agonist of...
GABA-A receptors: increase inhibitory processes.
27
alcohol is the antagonist of...
NDMA receptors- suppresses excitatory processes. The NDMA is involved in memory formation in the hippocampus.
28
what are the long term effects of alcohol
cirrhosis of liver, liver failure, brain damage especially in the hippocampus.
29
withdrawal symptoms of alcohol
hangover for mild drinking. After chronic use there are very strong withdrawal (delirium tremens)- can be fatal. not enough inhibition which overactivates the system.