All 6 tasks of the course PSY3312 Psychopharmacology followed at Maastricht University, FPN. This course I followed during the minor Advanced Psychology, as part of the bachelor Gezondheidswetenschappen at FHML. The tasks are extensive and got me an 8.5 for the final exam! :)
TASK 1: ARREST OF SANDRA JONES // BASIC PRINCIPLES OF PSYCHOPHARMACOLOGY
Pharmacology: the scientific study of the actions of drugs and their effects on a living organism.
- The rapid introduction of many new drugs by the pharmaceutical industry has forced the
development of several specialized areas of pharmacology
o Neuropharmacology: concerned with drug-induced changes in the functioning of
cells in the nervous system
o Psychopharmacology: emphasizes drug-induced changes in mood, thinking, and
behaviour
o Neuropsychopharmacology: identifies chemical substances that act on the nervous
system to alter behaviour that’s disturbed because of injury, disease, or
environmental factors
Drug action: the specific molecular changes produced by a drug when it binds to a particular target
site or receptor.
- These molecular changes lead to drug effects: more widespread alterations in physiological
or psychological functions
- The site of drug action may be very different from the site of drug effect (e.g., morphine)
- Because drugs act at a variety of target sites, they always have multiple effects
o Therapeutic effects: the drug-receptor interaction produces desired physical or
behavioural changes
o Side effects: all other effects produced, varying in severity
- Therapeutic and side effects can change, depending on the desired outcome
- Specific drug effects: those based on the physical and biochemical interactions of a drug with
a target site in living tissue
- Nonspecific drug effects: those based not on the chemical activity of a drug-receptor
interaction, but on certain unique characteristics of the individual
o An individual’s background (e.g., drug-taking experience), present mood,
expectations of drug effect, perceptions of the drug-taking situation, attitude toward
the person administering the drug, and other factors influence the outcome of drugs
o Nonspecific drug effects help to explain why the same individual self-administering
the same amount of alcohol may experience a sense of being light-hearted on one
occasion, and depressed on another
o Common example: the placebo. Belief in a drug may produce real physiological
effects despite the lack of chemical activity
▪ Essential in experiments because it eliminates the influence of expectation
on the part of the subject
Psychoactive drugs: have an effect on thinking, mood, and behaviour.
- CNS stimulants: produce increased activity in the brain, behavioural arousal, alertness, and a
sense of well-being
o Amphetamine, cocaine, methylphenidate, caffeine, nicotine
- CNS depressants: depress CNS function & behaviour to cause relaxation and drowsiness
o Barbiturates, benzodiazepines, alcohol
- Analgesics: reduction of pain, frequently have CNS-depressant qualities
o Narcotics, or opiates, such as morphine or codeine, but also aspirin, ibuprofen
- Hallucinogens: often called psychedelics, alter one’s perceptions (visual illusions or
distortions)
o LSD, MDMA, ketamine, psilocybin
- Psychotherapeutics: used almost entirely to treat clinical disorders of mood or behaviour
,LEARNING GOALS:
1. Pharmacodynamics
Pharmacodynamics: the study of the physiological and biochemical interaction of drug molecules
with target issue that’s responsible for the ultimate effects of a drug; the study of the mechanism of
drug action
- Knowing which receptors a drug acts on and where these receptors are located is crucial for
understanding what actions and side effects will be produced; drug-receptor interactions
Receptors: large protein molecules located on the surface of or within cells, are the initial sites of
action of biologically active agents such as NT, hormones, and drugs (all referred to as ligands)
- Ligands: any molecule that binds to a receptor with some selectivity
- Principal types of receptors:
o Extracellular receptors (A)
▪ Receptors on exterior cell surface
▪ Most drugs and NT
o Intracellular receptors (B)
▪ Enter cell => act on receptor
▪ Many hormones
- Receptors recognize specific molecular shapes
o Receptor agonists: molecules that can
bind to a particular receptor protein to
initiate a cellular response
▪ Molecules with the highest
affinity attach most readily to the
receptor
o Receptor antagonists: produce no
cellular effect after binding, and prevent
an “active” ligand from binding by
“blocking” the receptor
o Partial agonists: less efficacious than
agonists
o Inverse agonists: initiate a biological
action when bound that’s opposite to
that produced by an agonist
- Hence, drugs can vary in efficacy along a
continuum, ranging from full agonists (max
efficacy) to inverse agonists
(inverse efficacy)
- More generally, drugs are…
o Agonists, if they enhance
synaptic function by
increasing NT synthesis or
release, or by prolonging
the action of the NT
o Antagonists, if they
reduce NT synthesis or
release, or by terminating
the action of the NT more
quickly
- Binding or attachment of the
specific ligand is temporary. Once the ligand dissociates from the receptor, it has
opportunities to attach again. Receptor proteins have a normal life cycle
, o How much intracellular activity occurs depends on:
▪ # of interactions with the receptor
▪ Ability of ligand to alter the shape of the receptor, which reflects its efficacy
- Receptors are modified both in:
o # (long-term regulation)
▪ Up-regulation: increase receptor #
• Reflects compensatory changes after prolonged absence of receptor
agonists or chronic use of receptor antagonists
▪ Down-regulation: reduction receptor #
• Reflects compensation after chronic receptor activation
o Sensitivity (more rapid regulation via 2nd messengers
- Receptor subtypes: the varied receptor proteins of a given drug which have different
characteristics in different target issues
- Receptor antagonism: receptor antagonists compete with agonists for binding sites
o Competitive antagonists: drugs that compete with agonists to bind to receptors but
fail to initiate an intracellular effect, thereby reducing the effects of the agonists
▪ Can be displaced from those sites by an excess of the agonist; increased
concentration of
drug can compete
more effectively
for # of receptors
o Non-competitive
antagonists: drugs that
reduce the effects of
agonists in ways other than
competing for the receptor
▪ E.g., disturbing the
cell membrane
▪ Causes distorted
dose-response
curve & disrupts
maximum effect
o Physiological antagonism:
2 drugs that act in distinct
ways but interact in a way
that they reduce each
other’s effectiveness
▪ E.g., contradicting
drug effects
▪ Additive effects:
when the outcome
equals the sum of
the 2 individual
affects of 2 agents
▪ Potentiation: the
combi of 2 drugs
produces effects
greater than the
sum of their
individual effects
2. Pharmacokinetics and the difference with respect to pharmacodynamics
, Pharmacokinetics: the dynamic, interacting factors that determine bioavailability. How the drug
concentration changes over time as the drug is moved through your body
- Bioavailability: the amount of drug in the blood that is free to bind at specific target sites
- Pharmacokinetics is the journey of a drug from the outside world to the brain and elsewhere
o The study of the absorption, distribution, and biotransformation of a drug
o Important part of most forensic alcohol analyses
o The psychoactive effects of a drug fall under the more specific field of
neuropharmacology (or psychopharmacology), directly related to the
pharmacodynamics of drug action
The pharmacokinetic factors determining drug action
1. Routes of administration: how & where a drug is administered determines how quickly and
how completely the drug is absorbed into the blood
• Major categories of administration methods:
o Enteral methods: use the gastrointestinal tract (gut)
▪ Generally slow in onset & produce high variable blood levels of drug
▪ Oral and rectal routes
o Parenteral methods: all other routes of administration
▪ Example: injection, pulmonary, topical
• Oral administration is the most popular route for taking drugs because it’s safe, self-
administered, economical and avoids injection
o To be effective, the drug must dissolve in stomach fluids, pass through the
stomach wall to reach blood capillaries, and must be resistant to destruction
by stomach acid and enzymes that play a role in normal digestion
• Absorption: movement of the drug into the blood circulation
o Most drugs are not fully absorbed until they reach the small intestine
o Factors that influence how quickly a drug reaches the small intestine, and
hence determine the ultimate rate of absorption:
▪ Food in the stomach, particularly if it’s fatty => delays absorption
▪ The amount of food consumed
▪ The level of physical activity
▪ Many others
o First-pass metabolism: an evolutionarily beneficial function because
potentially harmful chemicals and toxins that are ingested become altered by
enzymes before passing to the circulation throughout the body
▪ Reduces the bioavailability of drugs
▪ Drugs with extensive first-pass effect must be administered at higher
doses or in an alternative manner (e.g., injection)
o Because of these factors, oral administration produces drug plasma levels that
are irregular, unpredictable and rise more slowly
• Rectal administration: the placement of a drug in the rectum, where it dissolves
o May avoid some first-pass metabolism
o Absorption is irregular, because it depends on how deep the drug is placed
• Intravenous injection: the most rapid & accurate method, because a precise quantity
is placed directly into the blood
o Eliminates passage through cell membranes such as the stomach wall
o Cons: little time for correction of an overdose or allergic reaction, and the drug
cannot be removed from the body (by stomach pumping)
o Intramuscular injection: slower, more even absorption
o Subcutaneous administration: injected just below the skin; absorption rate
dependent on blood flow to the site, usually fairly slow and steady
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