Lecture 6: Psychopharmacology Flashcards

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1
Q

non-medicinal drug

A

can be defined as something, often an illegal substance, that causes addiction

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2
Q

medicinal drugs

A

substances that can be recognized by an official pharmacopeia
- intended for the treatment of diseases

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3
Q

psychoactive drugs

A

chemical substances that pass through the blood-brain barrier and reach the central nervous system to change something there

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4
Q

pharmaceutical drugs

A

substances used to diagnose/treat/prevent diseases or affect the structure/function of the body

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5
Q

psychopharmacology

A

the study that deals with the effect of drugs

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6
Q

class A

A

these drugs are considered the most harmful
- includes heroin, methadone, crack, ecstasy, magic mushrooms, and crystal meth

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7
Q

class B

A

these drugs are considered less harmful than class A drugs
- include amphetamines, barbiturates, and dihydrocodeine
- some class B are reclassified to class A when prepared for injection (amphetamines, dihydrocodeine, and codeine)

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8
Q

class C

A

these drugs are considered the least harmful of the controlled drugs
- bezodiazepines and steroids

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9
Q

pharmacokinetics

A

deals with the factors that influence a drug
- what the body does with the drug
- route of administration, rate of absorption, termination of drug action, and elimination of the drug are important

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10
Q

pharmacodynamics

A

what the drug does to the body

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11
Q

oral (PO) route of administration

A

through the mouth
- the drug must be lipid-soluble
- rate of absorption influenced by the contents of the stomach

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12
Q

rectal (PR) route of administration

A

administered into the rectum
- route is irregular, unpredictable, and incomplete

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13
Q

aerosol route of administration

A

inhaled through the lungs
- allow for rapid delivery of the drug molecules to the brain

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14
Q

transdermal (TD) route of administration

A

through the skin

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15
Q

transmucosal (TM) route of administration

A

administration through the mucous membranes
- intranasally (nose)
- sublingually (under tongue)

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16
Q

parenteral route of administration

A

does not go through the gastrointestinal system

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17
Q

intravenous route of administration

A

when a drug is delivered directly to the bloodstream and therefore reaches the brain very quickly

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18
Q

subcutaneous (SC) route of administration

A

when the drug is delivered just under the skin
- slow and depends on the blood supply to the area of injection

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19
Q

intreperitoneal (IP) route of administration

A

the drug is delivered through the abdominal wall into the abdominal cavity (peritoneal cavity)

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20
Q

intramuscular (IM) route of administration

A

the drug is administered into the muscle

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21
Q

intrathecal route of administration

A

the drug is injected into the subarachnoid space in the spinal canal, reaching the cerebrospinal fluid

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22
Q

intracerebroventricular (ICV) route of administration

A

the drug is delivered to the ventricles of the brain
- performed in animals

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23
Q

epidural route of administration

A

the drug is delivered to the epidural space

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24
Q

distribution of ingested drugs

A

the stomach and intestines must actively absorb it
- first passes through the blood vessels to the liver
- there is a separate blood vessel system that first passes through the liver and only then to the rest of the body
- the liver can transform the drug and therefore a smaller percentage can be measured in the blood than was initially taken

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25
Q

cell membrane

A

the drug must pass through the phospholipid cell membrane to enter the cell
- fat-soluble drugs can easily pass through the cell membrane, but many drugs are not fat-soluble

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26
Q

walls of the capillaries

A

to enter the cell, the drug must leave the capillaries
- thin and formed by a single layer of cells
- between the cells are small holes that allow the exchange of small molecules

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27
Q

blood-brain barrier

A

has 2 major components, capillaries and glial cells
- in the brain, capillaries are tightly packed together and covered by a glial sheath made by astrocytes
- all psychoactive drugs can cross the blood-brain barrier

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28
Q

placental barrier

A

the placenta connects the mother to the fetus
- the point where drugs that the mother has taken can be passed on to the unborn child
- drugs crossing this barrier can have devastating effects on the development of the fetus

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29
Q

exit routes of drugs

A
  • kidneys (most common)
  • lungs
  • bile
  • skin
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30
Q

two phases of biotransformation (hepatic metabolism)

A

phase 1: involves the oxidation of the drug
- the liver converts it into a compound that is less fat-soluble and also less active
phase 2: involves the combination (conjugation) of the drug and a small molecule by the liver
- small molecules, such as glucuronide that are important in inactivating the drug, produce a metabolite that is highly ionized (slow/passive)

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31
Q

the renal system

A

processes hydrophilic drugs and those that have undergone hepatic biotransformation

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32
Q

half-life of drugs

A

the time it takes for the drug concentration to drop by 50% and then by 50% again
- first half-life, then second half-life

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33
Q

shape and charge of binding protein

A

determine which ligands will bind

34
Q

ligand

A

is a molecule that binds to a receptor

35
Q

high-affinity binding site

A

the ligand binds to this site more easily because the protein has both the right shape and charge

36
Q

intermediate-affinity binding site

A

the ligand matches the receptor in shape, but not in charge (e.g. both negatively charged)

37
Q

low-affinity binding site

A

the ligand cannot bind to the receptor because they do not match in shape and charge

38
Q

saturation

A

occurs at the time when 2 receptors can bind to the same ligand

39
Q

non-competitive drug

A

does not bind to the same site as the neurotransmitter, so they can both bind

40
Q

competitive drug

A

wants to bind to the same site as the neurotransmitter, so there is competition

41
Q

efficacy

A

the property of a ligand that changes the target cell after binding
- subject to interpretation by cells and it is the interaction of drug and cell that result in the observed drug/receptor activity

42
Q

agonists

A

full agonists facilitate action at the synapse
- produces the full maximal response capacity of the cell

43
Q

antagonists (blockers)

A

inhibit the activity of a neurotransmitter at the synapse
- can block receptors by binding to the same site as the endogenous agonist (orthosteric), or by binding to a separate site and changing the conformation of the receptor (allosteric)

44
Q

orthosteric antagonism

A

where the drug completely blocks the agonist effect without any degree of the antagonism (all or nothing)
- competitive

45
Q

allosteric antagonist

A

can modulate drug effects without resorting to all or nothing principles
- non-competitive

46
Q

partial agonists

A

function somewehere between full agonist and a full antagonist
- binds to the receptor, preventing other ligands from binding, but only has reduced efficacy at the receptor to produce a functional and biochemical change
- cause agonism at low doses when no other agonist is present
- cause antagonism when a full agonist is present

47
Q

inverse agonists

A

produce a response opposite to that of an agonist
- antagonists inhibit a response (produce no response)
- inverse agonists produce an opposite (negative) effect

48
Q

precursur-preloading drugs

A

these drugs improve the synthesis and increase the turnover of a neurotransmitter by acting as a precursor in the synthesis of the neurotransmitter
- provide some of the ingredients for a neurotransmitter, such as a percursor to dopamine
- one of the main therapies used in patients with Parkinson’s disease

49
Q

synthesis inhibition

A

drugs can interrupt and inhibit synthesis, preventing a neurotransmitter from being made

50
Q

storage prevention

A

once synthesized, drugs can prevent the neurotransmitter from being stored in the vesicle

51
Q

enhance neurotransmitter release

A

drugs can enhance the release of neurotransmitters from presynaptic terminals

52
Q

postsynaptic stimulation

A

drugs can act on the postsynaptic receptor and mimic endogenous neurotransmitters

53
Q

postsynaptic antagonism

A

a drug can act on the postsynaptic receptor to block the action of endogenous neurotransmitters (an antagonist)

54
Q

stimulation and antagonism of the autoreceptor

A

drugs can act at the autoreceptor to provide false feedback on synaptic activity

55
Q

drugs that block reuptake

A

the level of neurotransmitters can be increased by drugs, which act at the reuptake transporter
- prevents the neurotransmitter from being removed from the synapse (blocking the metabolic escape route)

56
Q

inhibition of metabolism

A

drugs can prevent the neurotransmitter from being metabolized

57
Q

multiple sites of drug action

A

drugs often act in multiple locations, which may lead to increased therapeutic efficacy, but may also contribute to neurotoxicity and adverse effects

58
Q

stimulants
- psychostimulants

A

include cocaine, amphetamines, nicotine, and caffeine

59
Q

cocaine

A

a dopamine transporter (DAT) agonist and requires an action potential to release dopamine before it can be effective
- blocks the DAT, preventing the reuptake of dopamine into the synapse
- if it cannot be reabsorbed, it remains in the synapse and remains available to stimulate receptors

60
Q

amphetamine

A

currently used in the treatment of narcolepsy and ADHD, but is also used by the military to keep personnel awake and alert
- works by increasing dopamine release from the presynaptic neuron

61
Q

nicotine

A

acts on ACh receptors called nicotine receptors
- the activation of these receptors underlie the addictive nature of smoking
- stimulation of nicotinic receptors at the ventral temental area means that nicotine facilitates the release of dopamine in a similar manner to that of amphetamine

62
Q

caffeine

A

has multiple effects, including the blockage of benzodiazepines at GABA-A receptors, the stimulation of calcium release, and the blockade of adenosine receptors

63
Q

depressants

A

opioids, alcohol, anxiolytics

64
Q

opioids

A

drugs that interact with endogenous neuropeptides (pain-relieving)
- opiates are CNS depressants and produce postsynaptic, axoaxonic and presynaptic inhibition
- heroin (diacetylmorphine) crosses the blood-brain barrier quickly (makes more morphine in the brain)

65
Q

alcohol

A

a complex molecule with a broad spectrum of action, but the net effect is CNS depression
- the effects of alcohol are also dose-dependent with disinhibition and euphoria as characteristics at low doses
- deterioration of numerous cognitive and motor functions is characteristics at higher doses

66
Q

anxiolytics

A

drugs used to treat anxiety include CNS depressants
- the action of these drugs targets the GABA receptor
- it is the GABA-A receptor that mediates the anxiolytic effects of the drugs
- Diazepam (Valium): a benzodiazepine agonist

67
Q

mind-altering drugs

A

hallucinogens, cannabinoids

68
Q

hallucinogens

A

mind-altering drugs that cause perceptual and cognitive changes
- LSD: symptoms include dizziness, restlessness, optical distortions, dreamlike state, feelings similar to intoxcation, a kaleidoscope of colors, and exaggerated imagination (higher doses cause dissociation and hallucinations)
- mescaline: has serotonergic effects
- psilocybin (magic mushrooms): has serotonergic effects
- ketamine and phencyclidine (PCP): psychedelic drugs that target glutamate as their site of action

69
Q

cannabinoids

A

main active component of cannabis is the cannabinoid delta9-tetrahydrocannabinol (THC)
- THC is the common denominator in male forms of cannabis and its behavioral effects are well documented
- we have a endocannabinoid system: a widespread distribution of cannabis receptors with cortical and subcortical regions

70
Q

tricyclic antidepressants (TCA)

A

a type of structure-based antidepressant
- affects more substances than just serotonin

71
Q

monoamine oxidase inhibitors (MAOIs)

A

an antidepressant that blocks the enzymatic breakdown of catecholamines and indoleamine by monoamine oxidase

72
Q

selective serotonin reuptake inhibitors (SSRIs)

A

a medication that blocks the reuptake of released 5-HT
- used as an inhibitor of an antidepressant

73
Q

selective noradrenergic reuptake inhibitors (SNRIs)

A

a medication that blocks the reuptake of released norepinephrine
- used as an inhibitor and antidepressant

74
Q

reuptake inhibitors

A

inhibit the reuptake of monoamines into the synaptic cleft
- are antagonists

75
Q

antipsychotics

A

are used to treat schizophrenia and have been essential in developing a better understanding of the disorder
- the prevailing view is that all of these drugs cause a blockade of dopamine receptors

76
Q

Nuremberg Code

A

focuses on the human rights of research subjects

77
Q

declaration of Helsinki

A

adopted the original point of the Nuremberg Code as a guide to medical ethics
- focuses on the obligations of physician-investigators for research subjects

78
Q

phases of clinical trials

A

phase I: takes place in a small number of human volunteers
- small amounts of the new drug given
- compared to placebos
phase II: studies involving administering the new drug to a small number of the target population
- highly controlled
phase III: includes many patients randomly assigned to treatment groups
- within the context of how the drug is marketed in terms of efficacy and safety
phase IV: takes place after a product has been licensed and marketed
- information obtained from such large studies allows for a clearer picture of a drug or intervention

79
Q

randomized controlled trial (RCT)

A

applied to avoid contamination of experimentation effects of allocation supply

80
Q

single-blind experiment

A

the individual participants do not know which group they are in

81
Q

double-blind experiment

A

neither the experimenter nor the participant knows which group they are in

82
Q

meta-analysis

A

can be usesd to convert a large amount of research work into one sensible account