Drugs of Dependence, Addiction and Overdose Flashcards

1
Q

define physical dependence

A

occurs when pharmacological adaptation leads to tolerance in which more drug is needed to achieve same effect

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2
Q

define psychological dependence

A

emotional-motivational withdrawal symptoms, many daily drug users show both dependences

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3
Q

What variables work simultaneously to influence probability that user will develop physical/psychological dependence and/or addiction

A

agent, host and environment in which use occurs

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4
Q

Describe the physical reward pathway in the brain

A

natural systems reward actions that promote propagation of species producing slight mood elevation

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5
Q

what brain structures are involved in the reward pathways

A

VTA, nucleus accumbens and frontal cortex

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6
Q

describe the connection between the brain structures in the reward pathways and DA

A

DA is released in the VTA and is sent to many structures including the nucleus accumbens and frontal cortex

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7
Q

How does the brain cope with change?

A

CNS has plasticity where it can modify its hardware to best function in changing environments specifically change in receptor numbers

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8
Q

describe the reasons for an increase and decrease in receptor numbers on post-synaptic membranes

A

increase caused by up regulation due to the presence of an antagonist drug/molecule for a long period of time which significantly reduces the amount of NT released by the pre-synaptic membrane as well as blocking the post-synaptic receptors = more receptors present to try and collect as much of the NT as possible
decrease caused by presence of agonist for a long period of time resulting in down-regulation which blocks the reuptake of NTs causing too many available to post-synaptic membrane = less receptors present

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9
Q

What factors affect likelihood for drug abuse?

A

availability, cost, purity and potency, mode of administration, time of onset, level of addictiveness

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10
Q

What host factors affect likelihood for abuse?

A

heredity, metabolism, psychiatric symptoms, prior experiences, propensity for risk taking behaviour

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11
Q

Describe the relationship between morphine and heroin

A

morphine is synthetically acetylated to produce heroin, once heroin is injected it crosses the BBB and converts to morphine

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12
Q

Describe heroins effect on DA in the brain

A

heroin binds to the mu opioid receptor inhibiting the release of GABA from the nerve terminal. This reduces GABAs inhibitory effect on DA neurons causing an increase in DA release in the nucleus accumbens. This causes sustained activation of the post-synaptic membrane lasting around 3-5 hours

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13
Q

List the effects of heroin

A

dry mouth, slurred speech, droopy eyelids, bradycardia, respiratory depression

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14
Q

Why is OD more common in long term drug users?

A

long term use of the drug causes down regulation of receptors when users tolerance increases and they can’t be sure which concentration they are receiving until its too late

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15
Q

describe cocaine’s effect on DA in the brain

A

cocaine binds to and blocks DA reuptake transporters on pre-synaptic membranes inhibiting clearance of DA from the synaptic cleft and degradation by the MAO in the nerve terminal, the DA then remains in the synaptic cleft and is free to bind to its receptors on post-synaptic membrane

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15
Q

why do cocaine and heroin together produce an even more intense DA activation?

A

because they work on different mechanisms on DA neurons of the reward pathway

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16
Q

List the effects of cocaine

A

talkativeness, physical energy, short term euphoria, tachycardia, HTN

16
Q

What are the medical uses for amphetamines?

A

ADHD, obesity and narcolepsy

17
Q

describe the effect of amphetamines on DA in the brain

A

amphetamines have a similar structure to DA and competitively inhibit DA transport, once inside the neuron amphetamines interfere with vesicular monoamine transporter (VMAT) and impede the filling of synaptic vesicles and cytoplasmic DA concentration increases causing the reversal of DAT direction (into synapse instead of into neuron) and increased non-vesicular release of DA

17
Q

what is the MOA of nicotine?

A

nicotine activates the nAChRs, stimulates sympathetic and parasympathetic ganglia, skeletal muscles and CNS followed by depression, this leads to enhanced NT release and increased excitation

17
Q

what do vapes contain

A

nicotine, flavouring and humectant

17
Q

what is the most dangerous dependence producing drug

A

nicotine

18
Q

describe the absorption of ethanol

A

ethanol is rapidly absorbed in the GIT, first pass metabolism occurs in most cases but saturation of enzymes occurs quickly causing increased absorption into the bloodstream

18
Q

what enzyme is induced by long term alcohol use and what does it relate to

A

CYP2E1, relates to tolerance

19
Q

What nerve does methanol damage when ingested?

A

optic nerve

20
Q

what is the antidote for methanol toxicity?

A

ethanol prevent the conversion of methanol into formate

21
Q

What effects does ethanol have on the brain?

A

chronic exposure of ethanol in the brain alters GABA receptors expressed components (decrease alpha1 and increase alpha 4 subunits) resulting in positive allosteric effect reduction, down regulation of GABA a receptors, disinhibition of reward pathways in DA in nucleus accumbens

22
Q

What cross tolerance occurs with chronic ethanol use?

A

produces tolerance to alcohol and cross tolerance to benzodiazepines and other sedatives

23
Q

Where is cannabis stored in body, how long until it reaches peak concentration here and how long does it take to clear?

A

cannabis is stored in body fats reaching peak concentration after 4-5 days, slowly released back into body and cleared after 30 days

24
Q

what are some effects of cannabis

A

psychomimetic (hallucigen), depressant, relaxation, euphoria, increased appetite, anxiety, paranoia

25
Q

describe the cannabinoid receptors

A

CB1Rs: abundant in hippocampus, cerebellum, activation of these Rs inhibits NT release (GABA, Glu)
CB2Rs: exist in immune tissue, modulate pain, explain why cannabis can act as pain relief

26
Q

What effects can chronic cannabis use have on reproductive system?

A

can decrease testosterone and sperm count

27
Q

List the medicinal uses of cannabis

A

nausea and vomiting, appetite stimulation, glaucoma treatment, treatment resistant epilepsy

28
Q

Describe what happens in death by resp failure and the most common drugs that cause this

A

resp depression occurs after decrease in excitatory effect of Glu resulting in px passing out and having reduced breaths, px may inhale own vomit, most commonly caused by opioids and alcohol

29
Q

Describe most common causes of death by stimulants and name the most common stimulants involved

A

burst blood vessels in brain, CV heart attack, hyperthermia, most commonly involves cocaine and amphetamines

30
Q

Why does withdrawal often cause opposite effects of drug?

A

due to re-sensitisation and re-regulation of receptors in CNS and PNS

31
Q

List some strategies used in detox and rehab

A

substitution therapy combined with symptomatic relief then weaning off, counselling, making drug experience unpleasant eg disulfiram for chronic alcohol abuse

32
Q

What is the best opioid to prescribe in substitution therapy?

A

long acting opioid, avoids lows whilst maintaining “hit”

33
Q

What is the most effective nicotine withdrawal treatment?

A

combining a nicotine patch with a self-administered form of nicotine replacement

34
Q

What are the three phases involved in psychostimulant withdrawal?

A

crash, withdrawal, extinction