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Summary PSY3312 Psychopharmacology

Name: PSY3312 Psychopharmacology
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Author: vvanbeek

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Maastricht University (UM)

Complete and elaborate summary of all resources of the course Psychopharmacology at FPN Maastricht (PSY3312, minor course). Summary contains a lot of figures and schemas from articles and Stahl (100 figures).

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psy3312
pharmacology
psychopharmacology
pharmacokinetics
pharmacodynamics
ssri
snri
benzodiazepine
phenothiazines
antipsychotics
ketamine
psilocybin
psychedelics
schizophrenia
depression
fpn
maastrich

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PSY3312 Psychopharmacology vvanbeek

TASK 1 – PHARMACOLOGY

BASIC PRINCIPLES OF PHARMACOLOGY

Source: Meyer & Quenzer (2013)

PHARMACOKINETICS

Although it is safe to assume that the chemical structure of a drug determines its action, it is
clear that additional factors are also powerful contributors. The dose of drug administered is
important, but more important is the amount of drug in the blood that is free to bind
(bioavailability). Collectively, all dynamic factors that contribute to bioavailability are called
pharmacokinetics. In other words, pharmacokinetics is ‘what the body does to the drug’.

(1) Routes of administration; how and where a drug is administered determines how
quickly and how completely the drug is absorbed into the blood.
(2) Absorption and distribution; a drug rarely acts where it is administered, so it must pass
through a variety of cell membranes and enter the blood plasma.
(3) Binding; once in the blood plasma, some drug molecules move to tissues to bind to
active receptors. While in the blood, a drug may also bind (depot binding) to plasma
proteins or may be stored temporarily in bone or fat.
(4) Inactivation; drug inactivation, or biotransformation, occurs primarily as a result of
metabolic processes in the liver. Drug-concentration depends on the dynamic balance
between absorption and inactivation.
(5) Excretion; the liver metabolites are eliminated from the body with the urine or feces.
Some drugs are excreted in an unaltered form by the kidneys.

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,PSY3312 Psychopharmacology vvanbeek

Route of
administration Advantages Disadvantages
Oral (PO) Safe; self-administered; Slow and highly variable absorption;
economical; no needle-related subject to first-pass metabolism;
complications. less-predictable blood levels.
Intravenous Most rapid; most accurate blood- Overdose danger; cannot be readily
(IV) concentration. reversed; requires sterile needles and
medical technique.
Intramuscular Slow and even absorption. Localized irritation at site of the
(IM) injection; needs sterile equipment.
Subcutaneous Slow and prolonged absorption. Variable absorption depending on
(SC) blood flow.
Inhalation Large absorption surface; very Irritation of nasal passages; inhaled
rapid onset; no injection small particles may damage lungs.
equipment needed.
Topical Localized action and effects; easy May be absorbed into general
to self-administer. circulation.
Transdermal Controlled and prolonged Local irritation; useful only for lipid-
absorption. soluble drugs.
Epidural Bypasses blood-brain barrier; Not reversible; needs trained
very rapid effect on CNS. anaesthesiologist; possible nerve
damage.

Drug distribution and the blood-brain barrier

The principle component of the blood-brain barrier is the distinct morphology of brain
capillaries. The walls of typical capillaries are made up of endothelial cells that have both
small gaps (intercellular clefts) and larger openings (fenestrations) through which
molecules can pass. In addition, they have pinocytotic vesicles that envelop and transport
larger molecules through the capillary wall. In contrast, in brain capillaries, the intercellular
clefts are closed because adjoining edges of the endothelial cells are fused, forming tight
junctions. Also, fenestrations are absent and pinocytotic vesicles are rare.

The blood-brain barrier is selectively permeable, not impermeable. It does reduce diffusion
of water-soluble molecules, but does not impede lipid-soluble molecules. The blood-brain
barrier is not complete. One area, area postrema (chemical trigger zone, CTZ), is located in
the medulla of the brainstem and causes vomiting when toxic substances are detected in the
blood. Typically, less than 1% of the total oral dose passes the blood brain barrier.
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,PSY3312 Psychopharmacology vvanbeek

Depot-binding

In addition to active binding-sites, drug binding occurs at inactive sites, where no measurable
biological effect is initiated. Such sites, called drug depots, include plasma protein, muscle
and fat. Any drug molecules in these drug depots cannot bind to active sites or be metabolized
by the liver. The drug binding is reversible, so the drug remains bound until blood levels drop.

Depot-binding characteristics Therapeutic outcome
Rapid binding to depots before Slow onset and reduced effects.
reaching target tissue.
Individual differences in amount of Varying effects; high binding means less free drugs,
binding. so some people seem to need higher doses. Low
binding means more free drug, these people seem
more sensitive.
Competition among drugs for Higher-than-expected blood levels of the displaced
depot-binding sites drug, possibly causing greater side effects, even
toxicity.
Bound drug is not metabolized. Drug remains in the body for prolonged action.
Binding to depots follows the rapid Rapid termination of drug action.
action at targets (redistribution).

Drug-clearance from the blood usually occurs
exponentially and is referred to as first-order
kinetics. Exponential elimination means that a
constant fraction (50%) of free drug in the blood is
removed during each time interval. The amount of
time required for removal of 50% of the drug in
blood is called the half-life. Half-live is important
because it determines the time interval between
doses.

Although most drugs are cleared from the blood by first-order kinetics, under certain
conditions some drugs are eliminated according to the zero-order model. Zero-order kinetics
means that drug molecules are cleared at a constant rate regardless of drug concentration. It
happens when drug levels are high and routes of metabolism or elimination are saturated.

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, PSY3312 Psychopharmacology vvanbeek

The steady state plasma level is the desired
blood concentration of a drug achieved when
the absorption/distribution phase is equal to the
metabolism/excretion phase. The steady state
plasma level is approached after a period of
time equal to five half-lives.

Drug metabolism occurs in two
steps. Phase I consists of oxidation,
reduction, or hydrolysis and produces
an ionized metabolite that may be
inactive, equally active or more active
than the original drug. Phase II
metabolism involves conjugation of
the drug with a simple molecule
provided by the body, such as
sulphate. Products of phase II
metabolism are always inactive and
more water-soluble.

Dose-response curve

The dose-response curve describes the amount of
biological or behavioral effect (response) for a given
drug concentration (dose). The threshold is the
smallest dose that produces a measurable effect. The
ED50 (50% effective dose) is the dose that produces
half the maximal effect, and the maximum response
occurs at a dose at which we assume the receptors are
fully occupied (the ED100).

The figure depicts three pharmacological effects of
drug A, which is prescribed for anxiety. Comparing
the ED50 for relieving anxiety and the TD50 (50%
toxic dose) for respiratory depression, you can see
that for most individuals the toxic dose is much
higher than the dose producing the desired effect.
Therefore, pharmacologists would say the drug has a
relatively favourable therapeutic index (TI = TD50 /
ED50).

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