Psychopharmacology Flashcards

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1
Q

Psychoactive drugs

A
  • An exogenous chemical, not required by an organism for normal function, which significantly alters cellular function at relatively low doses
  • Measurable physiological changes to an organism’s processes ⇒ observable behaviour changes
  • In order for a psychoactive drug to have an effect, it must get to the brain – it must pass through the blood-brain barrier, it then gets broken down by enzymes (pharmacokinetics)
  • Drugs can affect all stages of a NT’s life cycle with resultant effects on neurochemistry and behaviour (pharmacodynamics)
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2
Q

Pharmacokinetics

A
  • The movement of drug in the body in terms of its absorption, distribution, metabolism, and excretion
  • The study of how the organism affects the drug
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3
Q

Pharmacodynamics

A
  • The effects of a drug on the body, and behaviour
  • Pharmacodynamics is the study of how a drug affects an organism
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4
Q

Cocaine phamacokinetics

A
  • Absorption
    • Cocaine (and amphetamines) penetrate BBB easily
    • Routes of administration: Insufflated (snorted), IV (mainlined), Inhaled (freebased), Oral
  • Clearance
    • Half-life: ~5-10 hours
  • Modulates dopamine
    • Dopamine is removed from the synapse by a transporter molecule (DAT)
    • DAT causes reuptake by pumping dopamine out of the synaptic cleft back into the presynaptic neuron
    • Cocaine blocks DAT and is therefore a dopamine reuptake inhibitor
    • Cocaine binds tightly to DAT and inhibits its function ⇒ Dopamine remains longer in the synaptic cleft, increasing the amount of dopamine in synapse
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5
Q

Amphetamine (speed) pharmacokinetics

A
  • Absorption
    • Cocaine (and amphetamines) penetrate BBB easily
    • Routes of administration: Insufflated (snorted), IV (mainlined), Inhaled (freebased), Oral
  • Clearance
    • Half-life: ~5-10 hours
  • Mimics dopamine and enters the presynaptic terminal via the DAT:
  1. Competes with DA for reuptake ⇒ more DA in the synaptic cleft
  2. Facilitates the movement of DA out of vesicles and into the cytoplasm ⇒ release of DA independent of action potential
  3. Promotes DAT-mediated reverse-transport of DA into the synaptic cleft ⇒ Reverses the reuptake process
  • Compared to cocaine:
    • amphetamine has a longer course of action (pharmacokinetics)
    • is less euphoric but more stimulating, due to different binding characteristics (pharmacodynamics)
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6
Q

Cocaine pharmacodynamics

A
  • Increased dopamine signaling in the mesolimbic pathway (the brain’s reward circuit) ⇒pleasurable and addictive
  • As addiction develops dopamine receptors become desensitized ⇒Higher doses needed for same effect
  • Increased dopamine signaling in the nigrostriatal pathway leads to enhanced basal ganglia and thalamic activity ⇒ increased motor activity (hyperlocomotion)
  • Effects are not limited to dopamine → Cocaine produces reward through simultaneous actions on transporters for other NTs
    • It inhibits the action of SERT (serotonin tranporter) and NET (norepinephrine transporter)
    • Cocaine can also directly bind to serotonin (5-HT) receptors, 5-HT3 in particular
    • Local anaesthetic effects due to deactivation of sodium channels
  • At low doses, cocaine causes:
    • Increased energy, reduced appetite
    • Mental alertness (but also irritability, restlessness)
  • At high doses, cocaine causes:
    • Addiction
    • Paranoia and hallucinations (psychosis)
    • impaired cognitive function and muscle breakdown
    • risk of seizure, stroke, coma, heart attack
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7
Q

Amphetamine (speed) pharmacodynamics

A
  • Increased dopamine signaling in the mesolimbic pathway (the brain’s reward circuit) ⇒pleasurable and addictive
  • As addiction develops dopamine receptors become desensitized ⇒Higher doses needed for same effect
  • Increased dopamine signaling in the nigrostriatal pathway leads to enhanced basal ganglia and thalamic activity ⇒ increased motor activity (hyperlocomotion)
  • At low doses, amphetamine causes:
    • Mood improvement, reduced appetite
    • improvements in cognition, including working memory
    • increased wakefulness (but also anxiety, irritability, restlessness)
    • physical effects such as improved reaction time, fatigue resistance, and increased muscle strength
  • At higher/repeated doses both can cause:
    • Addiction
    • Paranoia and hallucinations (psychosis)
    • impaired cognitive function and muscle breakdown
    • risk of seizure, stroke, coma, heart attack
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8
Q

Nicotine

A
  • Pharmacokinetics:
    • Half-life ~30 minutes
    • Individual differences in elimination → smokers metabolise faster
  • Pharmacodynamics:
    • Mimics Acetylcholine
    • Binds to nicotinic ACh receptors (agonist) within the mesolimbic dopamine system
    • Triggers dopamine release in striatum
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9
Q

Caffeine

A
  • Most widely consumed CNS stimulant
  • Pharmacodynamics:
    • Main action: The caffeine molecule is structurally similar to adenosine.
    • Adenosine acts as an inhibitory neurotransmitter that suppresses activity in the CNS
    • Caffeine antagonizes adenosine receptors preventing adenosine from activating them
      • CNS stimulation
    • This promotes neurotransmitter release (dopamine, serotonin, acetylcholine, epinephrine) ⇒ stimulant effects
  • Pharmacokinetics:
    • Caffeine is absorbed within 45 minutes
    • distributed throughout all bodily tissues, crosses BBB
    • Half-life varies by liver enzyme function level but is usually between 3–7 hours
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10
Q

MDMA

A
  • Pharmacodynamics:
    • Acts primarily on serotonergic transporter activity
    • Also effects on norepinephrine, and dopamine transporters
    • Indirectly increases hormones such as oxytocin (hug effect)
    • Impairs executive function, inhibitory control, and decision making
  • Pharmacokinetics:
    • Duration of action = four to six hours, after which serotonin levels in the brain are depleted
    • Serotonin levels normalise within 24–48 hours
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11
Q

Cannabis

A
  • Main Psychoactive agent = ∆9 Tetrahydocannabinol (THC)
  • Depressant, Stimulant, mild hallucinogen
  • Pharmacodynamics
    • Binds to cannabinoid CB1 receptor- widely distributed throughout brain
    • The brain has natural cannabinoids (‘endocannabinoids’ )
    • endocannabinoids ↓ responsiveness to pain
    • endocannabinoids – role in the control in appetite and hunger
    • Binding reduces activity of intracellular enzymes, lowering neurotransmitter release
    • Causes inhibition of GABA which in turn enhances dopamine release
    • THC impairs memory due to CB1 binding in hippocampus
  • Pharmacokinetics
    • THC readily absorbed through the lungs into blood plasma
    • Metabolism in liver and fat storage, Half life of about 20- 30 hours
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12
Q

Hallucinogen

A
  • A drug that causes distortions in a person’s perceptions of reality, and can cause changes in thought, mood and consciousness
  • Large range of drugs with hallucinogenic properties (natural compounds/synthetic)
  • Often act on serotonin receptors
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13
Q

Opioids

A
  • Heroin, morphine, opium
  • Bind to the same receptors as our endogenous opioids. There are three kinds of opioid receptors widely distributed throughout the brain: mu, delta, and kappa receptors
  • By attaching to their mu receptors, these drugs reduce the amount of GABA released. Normally, GABA reduces the amount of dopamine released in the nucleus accumbens. By inhibiting this inhibitor, opiates increase the amount of dopamine produced and is thus pleasurable and rewarding
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14
Q

Alcohol

A
  • Pharmacodynamics
    • Wide spectrum of action in the body
    • Soluble in fat and water ⇒ affects all body tissues
    • Causes generalized CNS depression
    • impairs cognitive, memory, motor, and sensory processing
    • Hard to study: very low molecular weight and low potency
    • Requires very high concentrations for effects – hard to study binding on receptors
    • Operates on multiple sites:
      • Neuronal membranes
      • Ion channels
      • Enzymes
      • Receptors
  • Pharmacokinetics
    • Ethanol crosses the BBB easily by diffusion, metabolised by liver into CO2 and water, also 5-10% excreted unchanged in sweat, breath, urine
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15
Q

Addiction

A
  • Tolerance: responsiveness decreases as a consequence of continuous drug administration
  • Drug withdrawal effects: body has adapted to the drug– functions “normally” with the drug present
    • Over time, tolerance to rewarding effects, but abstinence leads to withdrawal
    • Drug use ultimately maintained by need to avoid withdrawal (negative reinforcement) – opponent process model
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