Psychopharmacology
EXAM: Monday 27th January, 2020
INDEX
1. Introduction and neurons 2
2. Neurotransmission 7
3. Neurotransmitter transport, agonists/antagonists, ion channels, enzymes 12
4. Genetics and heritability 15
5. Psychosis and schizophrenia 16
6. Mood disorders 22
7. Anxiety and OCD 27
8. Addiction 31
This summary includes (almost) everything from the lectures and info from the book.
DISCLAIMER
This summary was made by a student!
Studying from it and relying on it for 100% is your own responsibility.
THANKS & GOOD LUCK!!! J
J YOU CAN DO IT!!! CA
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Introduction and neurons
Stahl Ch. 1, 2, 3
Introducing terms
o Pharmacology – knowledge about drugs or medicine; the art of preparing medication
§ studying the reciprocal actions, or interactions, between pharmacological substances and
physiological processes
§ pharmakon = medicine = drug = pharmaceutical product
o Drug – pharmacologically active substance. 2 ways of ‘interpreting’ this term:
§ Medication or other substance with a physiological effect
§ Psychoactive substance for abuse, narcotic or stimulating
Classification – different grounds
o Based on working mechanism
§ Would be ideal, but we know too little about working mechanisms of drugs
o Based on chemical structure
§ Interesting, but chemicals with the same structure can have different effects and vice versa
§ Also: we would have to be very very specific, because there are substances (often agonists vs
antagonists) that differ on only a few molecules, but still have entirely different (opposite!)
functions
o Based on behavioral effects
§ This is easiest and thus what we do
§ We can see the effects of a drug
Classification based on behavioral effects
CNS suppressors Anti-anxiolytics Anti-epileptics
- Barbiturates (tranquilizers) - Benzodiazepines (Valium/Librium)1 - Benzodiazepines
- Ethyl alcohol - Non-benzodiazepines - Clonazepam
- Anesthetics (Zolpidem/Buspiron)2 - Clorazepate
Stimulants Antidepressants5 Mood stabilizers
- Cocaine, caffeine, nicotine - Tricyclic (imipramine) - Lithium
- Amphetamine (speed)3 - SSRI’s
- Methylphenidate4 - Monoamine Oxidase Inhibitors
(MAOI)
Narcotic pain killers Psychedelics and hallucinogens Antipsychotics
- Opioids - LSD(= Mescaline) - Chlorpromazine
- Morphine - Marijuana - Risperidone
- Codeine - Hashish - Haloperidol
- Heroin - Mescaline
1. Benzodiazepines have a wide array of effects, meaning they also have a lot of side-effects.
2. Always try non-benzo before trying benzo.
3. Stimulates inhibitory systems
4. When you do not have ADHD, methylphenidate is addictive.
5. In general, they inhibit the reuptake and degradation of serotonin.
Administration
- 4 stages
o Absorption (from site of administration à blood)
o Distribution (throughout the body)
o Metabolism (conversion by body)
o Excretion (elimination from body)
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Absorption
- Mucosal
o Oral: safe & commonly used
§ Part of drug is already degraded in stomach
§ Drawback = takes long for effect
o Rectal – 2/3 is absorbed straight away
o Via oral mucosa
- Parenteral – not via digestive tract. Sensitive to allergic response. Important to know of your patients!!
o Intravenous
o Intramuscular
o Subcutaneously
- Inhalation
Distribution
- In blood (albumin)
- Can be…
o Extracellular (via blood plasma)
o Intracellular (water in body cells)
o Usually both at the same time
- Speed of distribution depends on lipid solubility
o Lipid solubility – the capability of a substance to dissolve in lipids or fats.
§ When dissolving into lipids, substances can more easily pass through membranes via passive
diffusion that follows concentration gradient
o Higher lipid solubility à better/faster distribution because it goes through the membranes more
easily
Metabolism & excretion
- Pharmacokinetics – the study of how the body acts upon drugs,
especially to absorb, distribute, metabolize and excrete them
o Includes also absorption and distribution
o Interaction with receptor (= metabolism)
o Elimination
o Change over time in terms of serum concentration of
medication and metabolites
§ How does the body process the medication?
o Entire blood circulation in +- 1 minute
§ There are 10 billion capillaries
§ Every cell < 10-20 microns from capillary
§ 2 full circulation systems in our body (don’t have to know
these)
- Pharmacodynamics – the therapeutic effects and side effects of the drug
o The medication-receptor interaction
o Determine the pharmacological, therapeutic and toxic effect
o Time-concentration relation
§ T0 (time 0)
1. Large peak in medication concentration in plasma
2. Then straight after à large decrease medication concentration, because straight away the
drug starts spreading through the body, leaves bloodstream, enters body
§ Half-lifes
1. Distribution half-life (𝜶 phase) – the time it takes for the concentration at T0 to get to 50%
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2. Elimination half-life (𝜷 phase) – the time it takes for the concentration of a drug in the full
body to be reduced to 50% by degradation (liver) and excretion (kidneys)
3. 6 half-lives = 98% elimination
§ Example graph half-lives
1. The dotted, steep line is the concentration at
the T0 point in the body à we look at the y-
axis to see the concentration.
o Example of where the concentration is
“halved” is when you go from 1 to 0.5.
o Then looking at the x-axis, this shows us
that this went over a time period of
o 7.9 minutes. Thus, distribution half-life is
T# % elimination % present
7.9 minutes.
0 0 100
2. The straight, full line is the concentration of the
1 50 50
drug in the entire body.
o Looking at where this is halved (also 2 75 25
going from 1 to 0.5), we find that the 3 87.5 12.5
elimination half-life is 44.6 minutes. 4 93.75 6.25
3. Statistically, we can never have 0 of the drug in 5 96.875 3.125
the body 6 98.4375 1.5625
4. After 6 half-lives we can say there is no longer a pharmacological drug active in the body
Anatomy of neurotransmission
- Neurons
o Cell body = soma
o Dendrites (with & without spines)
o Axons
- Connections between neurons are called synapses
o Synapses are axonal endings that form a connection with
postsynaptic neurons
§ Mitochondria provide energy for synapses
§ Neurotransmitters (NT) are transported in vesicles
1. Because inside the neurons it’s very busy and you do not
want the NT to get damaged/degrade while traveling
§ Receptors are on both sides of the synaptic cleft! On the
presynaptic membrane we call them autoreceptors. They also
keep an eye out for how much of a NT is actually in the cleft
and whether it should reuptake etc.
1. Synaptic cleft = space between two pre- and postsynaptic
neurons
o Types of synapses
§ Axodendritic synapses (axon of presynaptic neuron à dendrite
of postsynaptic neuron)
§ Axosomatic synapses (axon of presynaptic neuron à soma of
postsynaptic neuron)
§ Axoaxonic synapses (axon of presynaptic neuron à axon of postsynaptic neuron)
o SO a neuron can receive information on the spines of dendrites; the soma; the axon.
- Neurons
o Subcellular organelles
o Take part in protein synthesis
o Internal transport
