Opiates Flashcards

1
Q

Opiates

A

Narcotic - pain relief

Analgesics - make you sleepy

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2
Q

Active Ingredient of Opiates

A

10% morphine, 0.5% codeine

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3
Q

Heroin - Form

A

Black tar - IV injections can cause venous sclerosis

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4
Q

Routes of administration (opiates)

A

Snort
Inject
Orally
Inhalation

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5
Q

Elimination (opiates)

A

Kidneys

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6
Q

Exposure during pregnancy (opiates)

A

pass through placental barrier

Newborns enter withdrawals w/in a few hours of birth

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7
Q

Pharmacological Effects - CNS

A
drowsiness
decreased sensitivity to stimuli
loss of anxiety/inhibitions
muscle relaxant
pain reliever (analgesic)
decreased ability to concentrate
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8
Q

Pharmacological Effects - ANS

A

CV and respiratory depression
constriction of pupils (pin-point pupils”
Nausea (area postrema)

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9
Q

Pharmacological Effects - Increasing dose/Overdose

A

Increasing dose, more euphoria/elation “rush” and nausea worsens (“good sick” based on learning/conditioning)

Overdose - drowsiness deepens to loss of consciousness, and respiratory depression (loose CO2 trigger response)

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10
Q

Pharmacological Effects - GI Tract

A
decreases tonus and motility of muscles of stomach and intestines
slower passage of contents through tract
increased absorption of water
increased solidity of feces
constipation
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11
Q

Mu receptors

A

Most widely distributed - found in all GRCReceptors

Analgesia (medial thalamus,Peri Aqueductal Gray (PAG), median raphe nucleus, spinal cord)

Reinforcement (NAc, limbic system)

Autonomic functions (brain stem, medulla, area postrema)

Mu and delta exist in overlapping neuronal populations

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12
Q

Delta Receptors

A

More restricted distribution

Olfaction

Motor Integration (neocortex, striatum, substantia nigra)

Reinforcement (NAc)

Analgesica (brain stem, spinal cord)

Mu and delta exist in overlapping neuronal populations

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13
Q

Kappa Receptors

A

Most restricted distribution

Analgesia - PAG, Raphe Nuclei, Spinal Cord, Locus Coeruleus

Hormonal Control - temperature, H2O balance, food intake (hypothalamus, pituitary)

Dysphoria - amygdala, NAc

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14
Q

Heroin - Form

A

Black tar - IV injections can cause venous sclerosis

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15
Q

Routes of administration (opiates)

A

Snort
Inject
Orally
Inhalation

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16
Q

Elimination (opiates)

A

Kidneys

17
Q

Exposure during pregnancy (opiates)

A

pass through placental barrier

Newborns enter withdrawals w/in a few hours of birth

18
Q

Pharmacological Effects - CNS

A
drowsiness
decreased sensitivity to stimuli
loss of anxiety/inhibitions
muscle relaxant
pain reliever (analgesic)
decreased ability to concentrate
19
Q

Endogenous Opiates: Prodynorphin

A

Kappa receptors

Alpha-neoendorphin, beta-neoendorphin, DYNORPHIN

20
Q

Pharmacological Effects - Increasing dose/Overdose

A

Increasing dose, more euphoria/elation “rush” and nausea worsens (“good sick” based on learning/conditioning)

Overdose - drowsiness deepens to loss of consciousness, and respiratory depression (loose CO2 trigger response)

21
Q

Pharmacological Effects - GI Tract

A
decreases tonus and motility of muscles of stomach and intestines
slower passage of contents through tract
increased absorption of water
increased solidity of feces
constipation
22
Q

Mu receptors

A

Most widely distributed - found in all GRCReceptors

Analgesia (medial thalamus,Peri Aqueductal Gray (PAG), median raphe nucleus, spinal cord)

Reinforcement (NAc, limbic system)

Autonomic functions (brain stem, medulla, area postrema)

Mu and delta exist in overlapping neuronal populations

23
Q

Delta Receptors

A

More restricted distribution

Olfaction

Motor Integration (neocortex, striatum, substantia nigra)

Reinforcement (NAc)

Analgesica (brain stem, spinal cord)

Mu and delta exist in overlapping neuronal populations

24
Q

Kappa Receptors

A

Most restricted distribution

Analgesia - PAG, Raphe Nuclei, Spinal Cord, Locus Coeruleus

Hormonal Control - temperature, H2O balance, food intake (hypothalamus, pituitary)

Dysphoria - amygdala, NAc

25
Q

Cellular Mechanisms: Postsynaptic Inhibition

A

Open K+ channels to hyperpolarize

Found in Mu and delta receptors

26
Q

Cellular Mechanisms: Axoaxonic inhibition

A

Close Ca++ channels - decreases Ca conductance –> decreased NT release
Found in mu, delta, and kappa receptors

27
Q

Cellular Mechanisms: Autoreceptors

A

Inhibits NT release
seen in mu and delta receptors

**Disinhibition - when you inhibit an inhibitory neuron –> excitatory

28
Q

Endogenous Opiates: Pro-opiomelanocortin

A

Mu and delta

Beta-endorophin

29
Q

Endogenous Opiates: Proenkephalin

A

Mu and delta

Met-ENK AND Leu-ENK

30
Q

Endogenous Opiates: Prodynorphin

A

Kappa receptors

Alpha-neoendorphin, beta-neoendorphin, DYNORPHIN

31
Q

Tolerance

A
  • After several months of heavy use, some addicts administer 40-50 times the normal lethal dose for a naive individual
  • euphoria and analgesia show rapid tolerance
  • constipation and pupil constriction show little tolerance
  • cross tolerance appears to be receptor dependent
  • predominant mechanism is pharmacodynamic
32
Q

Physical Dependence/Withdrawal Symptoms

A
  • Opposite of acute symptoms
  • unpleasant, flu-like (strong motivator for continued use)
  • onset: 3-4 hrs
  • peaks: 36-48 hrs
  • lasts 7-10 days
  • cross dependence
  • intensity of symptoms varies with intensity of drug use and health of individual
33
Q

Mechanisms of Tolerance and Dependence

A

1) downregulation of opioid synthesis (KO CREB –> decreased enkephalin)
2) downregulation of opioid receptors (less R’s) –> not a lot of evidence
3) Receptor desensitization by G-P uncoupling –> Less FUNCTIONAL receptors –> lots of evidence

34
Q

Treatment

A

No current treatment is curative
Basic goals are to reduce withdrawal symptoms, cravings, block effects of drug, improve functional living

Agonist maintenance approach - treat with long-acting agoinst like Methadone (mu receptor agonist 1/2 life~20 hrs) or buprenorphone (mu agonist/K antagonist 1/2 life~37 hrs)