Final exam - Psychopharmacology Flashcards

1
Q

Routes of Drug Administration

A
  • Oral administration is the safest, easiest, most common route
  • Oral administration is also most complex (more barriers that drug must cross to have desired effect) goes through gut & digestive track, takes brain longer to have drug
  • Other methods (inhalation or injection) produce much faster effects because fewer barriers for drug to pass
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2
Q

Blood-Brain Barrier (BBB)

A
  • Helps prevent most substances (including drugs) from entering brain via the bloodstream
  • Endothelial cells in brain tightly joined and presence of astrocytes help keep most substances out
  • To enter brain drugs need to cross BBB, astrocytes (glial cells) which is a shield for most substances
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3
Q

BBB - Part 2 (molecules)

A
  • Small, uncharged molecules (ex. oxygen & carbon dioxide) are fat soluble and can freely cross the BBB (nicotine)
  • Larger, charged molecules (ex. glucose, amino acids, fats) must be actively transported across the BBB
  • Difficulty developing drugs for brain (must be small and uncharged or structurally similar to substance that already has an active transporter that allows it to pass the BBB)
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4
Q

Barrier-Free Brain Sites

A
  • Pineal gland (hormones) : Allows entry of chemicals that affect day-night cycles
  • Pituitary (hormones) : Allows entry of chemicals that influence pituitary hormones
  • Area postrema (in brain stem) : Allows entry of toxic substances that induce vomiting (if you have too much alcohol, throw up because of this area, senses are in trouble)
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5
Q

Drug Action at Synapses

A
  • Most psychoactive drugs exert their effects by influencing chemical reactions at synapses (cocaine, leaves drug for long time, allows dopamine to bind postsynaptically)
  • Agonist : substance that ENHANCES the function of a synapse
  • Antagonist : substance that BLOCKS the function of a synpase
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6
Q

Seven major stages of synaptic transmission

A
  • Drugs can alter chemical processes at any of these stages
  • Synthesis, Storage, Release, Receptor Interaction, Inactivation, Reuptake, Degradation
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7
Q

Antianxiety Agents and Sedative Hypnotics

A
  • Benzodiazepines : minor tranquilizers, antianxiety agents (drugs that reduce anxiety ex. valium & xanax, often used for temporary purposes ex. coping with stress due to a death)
  • Benzodiazepines : high level of dependance, usually given when going through event, 4 potential uses, can be used anti-compulsion, muscle relaxant, all 3 work on GABA receptors
  • Alcohol
  • GABA agonists
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8
Q

GABA Receptors

A
  • Excitation produces an influx of chloride (CI-) ions, which hyperpolarizes the neuron
  • The GABA Receptor has 3 sites : Sedative-Hypnotic Site - Alcohol (directly influences CI-influx), Antianxiety Site - Benzodiazepines (enhances binding effects of GABA, effect is dependant upon amount of GABA present harder to overdose, benzodiazepine binds but only works if GABA is around if it combines with alcohol there’s a very high chance overdosing)
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9
Q

Images of binding

A
  • Binding of sedative-hypnotic drugs (such as alcohol or barbiturates) acts like GABA, causing increased chloride conductance
  • Binding of antianxiety drugs (benzodiazepines) enhances binding effects of GABA
  • Because of their different actions, these drugs should never be taken together, combined doses can cause coma or death
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10
Q

Antipsychotic Agents

A
  • Major Tranquilizer blocks dopamine (Neuroleptic) : drug that blocks the D2 dopamine receptor, used mainly for treating schizophrenia, mechanism of therapeutic action is still not understood *immediate effect of reducing motor activity, after short period of use reduction in symptoms of schizophrenia, negative side effect = dyskinesia (impaired control of movement), if blocking dopamine receptor you can get diskinesia
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11
Q

Three Classes of Antidepressants

A
  1. Monoamine Oxidase (MAO) Inhibitors : block MAO from degrading neurotransmitters such as DA, NA, 5-HT (very limiting, given restrictions on drugs can use & dietary protocol)
  2. Tricyclic Antidepressants : first-generation antidepressants - block 5-HT reuptake transporter proteins
  3. Second-Generation Antidepressants : similar to #2 but more selective in its action on the serotonin reuptake transporter proteins ex. zoloft & prozac, *selective serotonin reuptake inhibitors (SSRIs - serotonin in synapse for longer period, many people don’t feel anything for long time *treatment resistance)
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12
Q

Narcotic Analgesics

A
  • Endorphin : peptide hormone that acts as neurotransmitter and may be associated with feelings of pain or pleasure, mimicked by opiate drugs such as morphine, heroin, opium & codeine (natural pain killer, flood of endorphines when hurt yourself)
  • Morphine acts on 3 opioid-receptor classes : mu delta & kappa, mu receptor is critical for morphine’s effect on pain and for its addictive properties (binds at same receptor than endorphine but much stronger, typically mu receptor pain killing & addictive part of narcotic)
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13
Q

Behavioural Stimulants

A
  • Increase motor behaviour and elevate a person’s mood and level of alertness
  • Cocaine : blocks dopamine reuptake, leaving dopamine in synapse for longer
  • Amphetamine : dopamine agonist, releases dopamine into the synapse and blocks the reuptake of dopamine as well
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14
Q

Psychomotor Activation

A
  • Increased behavioural and cognitive activity
  • At certain levels of consumption, the drug user feels energetic and in control
  • Occurs with many drugs
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15
Q

Tolerance

A
  • Lessening of response to a drug over time
  • Larger dose is require to maintain the drug’s initial effect
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16
Q

Disinhibition Theory

A
  • Alcohol has a selective depressant effect on the cortex (the region of the brain that controls judgement), while sparing subcortical structures (those areas of the brain responsible for more-primitive instincts, such as desire)
  • Limitation : behaviour under the influence of alcohol often differs depending upon the context