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Psychopharmacology > Opiates > Flashcards

Opiates Flashcards

1
Q

opium origin

A
  • somniferum: somni = sleep
  • poppy plant, papaver
  • morphine, morpheus: god of dreams
  • dreamy euphoria
  • pain relief
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2
Q

natural opiates

A
  • codeine

- morphine

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3
Q

semi-synthetic opiates

A
  • heroin

- slightly altered in lab

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4
Q

synthetic opiates

A
  • fentanyl
  • very powerful: used for anaesthesia
  • “china white”: illegal version
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5
Q

history of opiates and opium

A
  • ancient times: joy plant
  • sumarians and assyrians
  • ancient egypt, greece, rome (medical use)
  • islam: arab traders (substitute for alcohol)
  • india and china: from arab traders (can’t tolerate alcohol, introduced smoking opiates)
  • europe: war, trade, exploration
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6
Q

drug use in the 1800’s

A
  • widespread through europe and usa
  • few restrictions on sale and supply
  • no prescription needed
  • cure many aliments: panacea
  • high degree of addiction
  • new methods of administration: smoking (chinese), injections (civil war, soldiers disease)
  • opium wars (britain vs. china)
  • opium did not produce aggression or violence: no urge to ban
  • kept the poor quiescent
  • late 1800’s: heroin = 2x potent in brain
  • Harrison Narcotics act 1914
  • controlled drugs act 1970
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7
Q

modern medical use

A
  • pain relief / analgesia: main medical use
  • diarrhea: loperamide (oral rehydration therapy is more common)
  • cough suppression: codeine linctus (suppresses coughing center in the brain: dry cough)
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8
Q

abuse of prescription opiates

A
  • oxytocin

- when doc stops prescribing, already addicted patients turn to illegal opioids

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9
Q

Morphine standart

A
  • standard by which others are measured
  • analgesia value of 1
  • more potent: heroin (2), oxycodone (1.5)
  • equipotent: hydrocodone
  • less potent: codeine (10x weaker)
  • fentanyl: 100x more potent
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10
Q

pain and pain relief

A
  • important warning / survival mechanism

- stimilus (nociceptors) > pain pathways > spinal cord > perceived in the brain (cortex)

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11
Q

brains response to pain

A
  • release endorphins: endogenous opioid peptides (small protein)
  • natural pain-killers
  • analgesia and well-being
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12
Q

endorphins

A
  • natural pain-killers
  • inhibitory neurotransmitters
  • bind to post-synaptic opiate receptos via signal transdoction pathway
  • open potassium channels, K+ exit the cell
    = hyperpolarization (very negative charge inside the cell, very unlikely to reach threshold)
    = post-synaptic inhibition
    = inhibit pain signal
    = inhibit the perception of pain in the cortex
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13
Q

opiates and endorphines

A
  • morphine and other opiates: structurally similar to endorphins (mimic natural endorphins)
  • are agonists at the endorphin (opiate) receptor
  • opiates inhibit pain transmission
  • CNS depressants
  • analgesia and sleepiness
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14
Q

opiate receptors

A
  • 3 main receptors: µ, κ, δ
  • morphine and heroine: µ receptor
  • µ- receptor associated with euphoria
  • κ-receptor: dysphoric effects, thought to balance out euphoric effects of endorphins in vivo (otherwise one would become addicted to pain)
  • κ-receptors: new target for pain-relief therapies, that are not addictive
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15
Q

pharmacokinetics: absorption

A
  • oral
  • inhalation
  • intranasal: not so much
  • subcutaneous injection:
  • intramuscular injection: slower than IV, but constant release, painful
  • intravenous: veins get damaged over time (collapsed veins)
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16
Q

Addicts: progression in injection

A
  1. inject right under the skin: subcutaneous
  2. intramuscular
  3. IV: problem with sharing needles
    - life expectancy for IV addict: 1 year
17
Q

chasing the dragon

A

don’t want to heat heroin up too much: slang term for right heating

18
Q

distribution

A
  • body organs, including brain
  • morphine poorly penetrated BBB
  • heroin (diacetylmorphine): more lipidic = penetrates BBB more easily, once in brain it is converted to morphine
19
Q

metabolism and excretion

A
  • liver metabolism
  • urine excretion
  • 90% excreted within 1 day
  • traces detectable for 2-4 days
  • more or less 4 h action and 8 h to be removed
20
Q

opiates addictive

A
  • euphoria, rush, well-being, dopamine release: limbic system
  • GABA: inhibitory effect on dopamine release in parts of the mesolumbic system (opening of gaba receptors: Cl- flows in: hyperpolarization)
  • opiates inhibit GABA release
  • inhibit an inhibitory NT: enhance dopamine release
  • morphine prevents release of GABA, therefore GABA can’t prevent dopamine release anymore
  • µ- receptor associated with euphoria
  • addictive effect because of euphoria from dopamine release
21
Q

acute effects: opiates

A
  • euphoria (rush)
  • drowsiness, heavy limbs, vivid dream-like experiences
  • body warmth
  • intense introversion and impaired social interaction
  • choice of drug use can depend on personality type
  • CNS depressant
  • respiratory depression (less than 12 bpm, drug not administered in clinical setting)
  • cognitive impairment
  • cough suppression
  • nausea, vomiting: built tolerance to this
  • constipation: more water absorption, no tolerance to this
  • pin-point pupils: very small pupils
22
Q

toxicity

A
  • more or less 4000 † per year
  • CNS depressant: severe respiratory depression: less than 12 bpm
  • coma > death
  • clinical manifestations: coma, respiratory depression, pinpoint pupils (toxic triad for opioid use)
23
Q

chronic effects: opiates

A
  • abusers: short life span (overdose, infections)
  • 100x more likely to die
  • infection and disease: HIV (25% of IV users): virus attacks white blood cells
  • drug overdose: narrow therapeutic index, mix of CNS depressants
  • criminal activity
  • opiate abuse during pregnancy: developmental delays
  • higher risk for stroke, embolism: dirt that clogs the veins
  • hepatitis: inflammation of liver: spread through needles
  • dead skin: due to loss of blood vessels
  • neumonias: due to cough suppression
  • respiratory infection
  • endocarditis: heart infections
24
Q

opioid interactions

A
  • synergism with other CNS depressants
  • anxiolytics (benzodiazepines), alcohol
  • potentiation of CNS depression
25
Q

tolerance and withdrawal

A
  • chronic users: steadily increase the dose
  • fast tolerance to increased respiratory depression
  • fast tolerance to pain, euphoria and nausea: dose has to keep increased
  • no tolerance to constipation
  • withdrawal: motivation for drug use switches from positive to negative reinforcement to avoid withdrawal symptoms
26
Q

opiate withdrawal symptoms: phase 1

A
  • flu like symptoms
  • 8-12 h after last dose
  • runny nose and eyes
  • sweat, increased blood pressure
  • irritability, depression, anxiety, tremor
  • hypersensitivity: pain receptors were blocked for a long time that the body increased pain receptors
27
Q

opiate withdrawal symptoms: phase 2

A
  • cold turkey
  • peaks after 48-72 hours
  • more severe early symptoms
  • pupil dilation, anorexia, piloerection, spasm
  • can be so severe that patients die
  • ease through with benzodiazepines
28
Q

treating withdrawal

A
  • no treatment
  • any opiate drug
  • detoxification with methadone (another opioid, but does not produce a high)
  • high risk of relapse (90% within 6 months), especially when returning to the same environment
29
Q

abuse of opiates

A
  • prescription opioids
  • heroin
  • fentanyl: 100x more powerful than morphine, schedule II
30
Q

opioid epidemic

A
  • illegal opioids
  • prescription opiates
  • death: overdose
  • hepatitis c and bacterial endocarditis
31
Q

prescription opiates

A
  • fuelling the opioid epidemic
  • vicodin: painkiler + opioid (particulary addictive)
  • oxycontin: oxycodone: purdue pharma (market that it was a safe drug, not creating addiction and working 12h instead of 8. doctors felt safe prescribing them but al turns out to be false and a bunch of patients were addicted)
32
Q

opioid epidemic and pharma industry

A
  • slick marketing: no one should feel pain
  • lax regulations: FDA and legislators weren’t as strict with them because they were financially benefiting by licensing them
  • doctors and patients
  • over-prescription
  • turn to the black market: cheaper, easier
33
Q

response to opioid epidemic

A
  • addiction treatment: methadone
  • access to naltrexone
  • tamper-proof formulations: turn into gel when combined with water, impossible to inject
  • drug monitoring programs
  • lower prescriptions: try to only prescribe while hospitalized (3-8 days, after 8 days high risk of addiction)
34
Q

methadone

A
  • equipotent to morphine
  • orally active: avoid needle problems
  • long acting: less doses a day needed
  • acute: cope with physical withdrawal
  • maintenance: wear patients off slowly (MMT: methadone maintenance therapy)
  • addicts don’t like methadone because they don’t get the rush and euphoria, less addictive
  • used to wear addicts off of opioids
  • when not enough opioids in the body
35
Q

opioid antagonist

A
  • naltrexone
  • binds to the opioid receptors but do not activate them
  • compete with opioids for the receptors: blocking the effects
  • to reverse respiratory depression induced by opioid overdose
  • ADR’s: reversal of analgesia, increased BP, tremors, hyperventilation, rapid pulse
  • when there is too much opioids in the system

Psychopharmacology (7 decks)

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