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Biology of Psychological Disorders > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What is referred to as drug action

A

pharmacokinetics

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2
Q

first pass metabolism

A
  • before the blood goes to the rest of the body from the gastrointestinal tract, it passes through the liver
  • the liver is the major organ that breaks down drugs. therefore, a certain amount of the drug will be inactivated or metabolized as it goes through the liver.
  • other routes may not be subject to this “first pass” effect
  • the breakdown of drugs as they are transported through the liver before they reach the rest of the body through the circulatory system
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3
Q

therapeutic effects due to depot binding

A

slower onset and reduced effects
varying effects
high binding means less free drug so some people seem to need higher doses
low binding means more free drug so they seem more sensitive
higher than expected blood levels of the displaced drug possibly causing greater side effects
drug remains in the body for prolonged action
rapid termination of drug action

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4
Q

side effects

A

drug-induced effect that accompanies the primary effect for which the drug is administered.

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5
Q

bioavailability

A

the portion of original drug dose that reaches its site of action.

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6
Q

biotransformation

A
  • drug metabolism
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7
Q

depot binding

A
  • drug binding to inactive sites where no biological effect is initiated (plasma proteins, muscles, fat, bone)
  • drug molecules cannot reach active sites or be metabolized by the liver, but binding is reversible
  • affects magnitude and duration of drug action
  • reduces the concentration of drug at its site of action and delays effects
  • individuals vary in the amount of depot binding.
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8
Q

depot binding and its affects on drug action

A

affects the magnitude and duration of drug action

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9
Q

routes of drug administration

A
  • oral
  • intravenous
  • intramuscular
  • subcutaneous
  • topical
  • transdermal
  • epidural
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10
Q

drug metabolism

A

bioinformatics

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11
Q

CYP450 families

A
  • CYP1, 2, and 3 = most common for drug metabolism .

- CYP2D6 and CYP3A (especially 3A4) metabolize over 50% of drugs.

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12
Q

first-order elimination

A
  • elimination of a constant fraction of drug, per time unit, of the amount present in the organism. the elimination is proportional to the drug concentration.
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13
Q

half-life

A
  • time it takes for a half of the amount of drug in the circulation to be eliminated
    •Mostly in hours; some measured in days.
    •First-order elimination.
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14
Q

how many half-lives it usually takes for drugs to be elevated from the system

A

the ability of a drug to produce its intended effect.

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15
Q

enzyme induction

A

increased production of drug-metabolizing enzymes in the liver, stimulated but certain drugs (inducers). as a result of induction, drugs that are metabolized by the induced enzyme will degraded more rapidly. it is one mechanism by which pharmacological tolerance is produced.

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16
Q

enzyme inhibition

A
  • some drugs inhibit CYP enzymes and increase their own levels, as well as levels of any drug metabolized by that enzyme.
  • can produce much more intense/prolonged drug effects and high levels of drug toxicity
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17
Q

pharmacokinetics

A
  • study of drug molecules into through and out of the body
  • science that studies routes of administration absorption and distribution bioavailability biotransformation and excretion of drugs
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18
Q

pharmacodynamics

A

study of interactions of a drug with the structure with which it interacts to produce its effects

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19
Q

ligands

A
  • neurotransmitters
  • can be specific to certain receptors but a drug may be more specific than the endogenous neurotransmitter
  • bind to receptors
  • any molecule that binds to a receptor with some selectivity.
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20
Q

receptors

A
  • fairly large molecules (usually protein)
  • located in sites where naturally occurring compounds (transmitters or modulators) produce biological effect
  • neurotransmitters (ligand) can be specific to certain receptors, but a drug may be more specific than the endogenous neurotransmitter.
  • drugs form reversible ionic bonds with specific receptors. they do not create unique effects: merely modulate normal neural functioning.
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21
Q

antagonist

A
  • by itself produces no response
  • It is possible to determine if a drug has an antagonistic action by seeing if it reduces the effect of the agonist.
  • Irreversible or noncompetitive antagonists cause a downward
    shift of the maximum, with no shift of the curve on the dose axis.
  • drugs that attach to receptors and blocks the action of either an endogenous transmitter or an agonistic drug
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22
Q

agonist

A

drug that attaches to a receptor and produces actions that mimic or potentiate those of endogenous transmitter.

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23
Q

drug potency

A

measure of drug activity expressed in terms of the amount required to produce an effect of given intensity. potency varies inversely with the amount of drug required to produce this effect- the more potent the drug, the lower the amount required to produce the effect.

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24
Q

drug efficacy

A

maximum effect obtainable, with additional doses producing no effect. Some drugs may be
potent but might never be able to produce a peak response no matter how much is given.

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25
Q

drug competition

A

•Some drugs compete for the same metabolic system: elevated level on drug 1 will
reduce metabolic rate of drug 2.
•This is the case for alcohol and sedatives like barbiturates or Valium

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26
Q

what information can we derived from dose-response relationships

A

•Used to evaluate receptor activity.
•Describes the amount of response for a given drug dose
A. Curve obtained by plotting the dose of drug against the percentage of subjects showing a given
response at any given dose.
B. Curve obtained by plotting the dose of drug against the intensity of response observed in any single
person at a given dose.

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27
Q

sensitization

A

the opposite of tolerance. sometimes call reversed tolerance. the enhancement of drug effects following repeated administration of same drug dose.

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28
Q

drug tolerance

A
  • state of progressively decreasing responsiveness to a drug.
  • a diminished response to the same dose of drug. a larger dose is eventually needed to have the same response as before.
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29
Q

metabolic

A

More water soluble and less active (or inactive) than parent drug.

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30
Q

steady state

A

the point of balance at which the rate of drug administration approximates the rate of excretion. steady stay concentrations can be reached in about six times the drug’s elimination half-life and is independent of the actual dosage.

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31
Q

therapeutic index

A
  • the ratio of the toxic dose and the therapeutic dose of a drug, which provides a measure of drug safety.
  • LD50/ED50
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32
Q

behavioral supersensitive

A

upregulation

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33
Q

how to achieve receptor upregulation

A
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34
Q

potential consequences of receptor upregulation

A
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35
Q

how do you achieve receptor downregulation

A

downregulation

- given over longer periods of time

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36
Q

inotropic

A
  • work very fast; important role in fast neurotransmission
  • has several subunits
  • at the center of receptors is a channel or pore to allow the flow of ions
  • at rest- channels are closed
  • when neurotransmitters bind - channels immediately open
  • when ligand leaves binding site - channel quickly closes.
37
Q

metabotropic

A
  • works more slowly than ionotropic receptors
  • takes longer for a postsynaptic cell to respond, the response is somewhat longer-lasting
  • comprise a single protein subunit, winding back-and-forth through the cell membrane seven times
  • they do not possess a channel or pore
38
Q

partial agonist

A

drug that binds to a receptor, contributing only part of the action exerted by endogenous neurotransmitter or producing a submaximal receptor response.

39
Q

non-competitive drug interactions

A
40
Q

therapeutic window

A
  • drugs should be given in such a way that the blood concentration stays between a level that is too high and too low.
  • the range of drug dose, or blood concentration, that maintains a safe therapeutic effect.
41
Q

behavioral tolerance

A
  • context-specific tolerance
  • tolerance and occur in the same environment in which the drug was administered
  • involves different forms of learning: habituation, classical conditioning, and operant conditioning
42
Q

cross-tolerance

A

condition in which tolerance of one drug results in a lessened response to another drug.

43
Q

intravenous administration

A
  • directly into bloodstream

Advantages:

  • valuable for emergency use
  • permits titration of dosage
  • can administer large volumes and irritating substances when diluted

Disadvantages:

  • increased risk of adverse effects
  • must inject solutions slowly as a rule
  • not suitable for oily solutions or insoluble substances
44
Q

intramuscular administration

A
  • directly into a muscle

Advantages:
- suitable for moderate volumes, oily vehicles, and some irritating substances

Disadvantages:

  • precluded during anticoagulant medication
  • may interfere with interpretation of certain diagnostic tests
45
Q

subcutaneous administration

A

Advantages:
- suitable for some insoluble suspensions and for implantation of solid pellets

Disadvantages:

  • not suitable for large volumes
  • possible pain or necrosis from irritating substance
46
Q

Why is knowledge about the relationship between the time course of
drug action in the body and its pharmacological effects?

A
  1. Predicting optimal dosages and dose intervals needed for therapeutic effect.
  2. Maintaining therapeutic drug level for desired time period.
  3. Determining time needed to eliminate drug.
47
Q

Therapeutic Drug Monitoring (TDM)

A

•The basic principle underlying TDM is that a threshold plasma concentration of a drug
is needed at the receptor site to initiate and maintain a pharmacological response.
•Plasma concentrations of psychoactive drugs correlate well with tissue or
receptor concentrations

48
Q

Drug disposition tolerance (metabolic tolerance):

A

o more enzyme is available to metabolize a drug, and as a result, more drug must be
administered to maintain a level of drug in the body (repeated use of a drug reduces
the amount of that drug available to the target tissue).
o all drugs metabolized by the induced enzyme family will likely show diminished effect
(cross-tolerance).

49
Q

Pharmacodynamic tolerance:

A

o occurs when changes in nerve cell function compensate for the continued presence
of the drug (receptor loses sensitivity, etc.)

50
Q

Behavioral tolerance (context-specific tolerance):

A

o tolerance occurs in the same environment in which the drug was administered.
o this can involve different forms of learning: habituation, classical conditioning, and
operant conditioning.

51
Q

Sensitization:

A

The enhancement of drug effect(s)
following repeated administration of
same drug dose.

52
Q

Slope:

A

how sharply the effect changes with each change in drug dose.
• If a small change in dose produces a large change in effect, the slope is steep
• If a large change in dose produces small changes in effect, the slope is shallow

53
Q

Variability:

A

individual differences in drug responses. Some
individuals respond at very low doses and some require
much more drug genetic make-up; metabolic enzymes.

54
Q

dose-response curve

A
  • Increasing concentration produces greater analgesia.
  • Absolute amount of drug necessary to produce effect = drug potency (ED50)
  • Shape of curves indicates they work through same mechanism
  • Aspirin = different mechanism (shape of curve is different)
55
Q

therapeutic Index

A

• TI = LD50 / ED50
• The greater the TI, the safer the drug; the difference between the desired effect and the undesired or lethal effect is larger.
• If two drugs produce a therapeutic effect that is desirable, the better drug (all things being equal) would be the one with the larger TI.
•The lower the ED50, the
greater the potency; but the
lower the TI, the lower the
safety.

56
Q

Pharmacodynamic interactions:

A

two drugs with same or overlapping mechanism of

action

57
Q

Pharmacokinetic interactions:

A

one drug affects the other’s absorption, distribution,

metabolism , or excretion.

58
Q

polypharmacy,

A

medications are combined to improve therapeutic outcome.

59
Q

binding of ligand results in 1 of 3 actions:

A
  • Binding to site of norm al endogenous neurotransmitter initiates similar cellular response (agonistic action).
  • Binding to nearby site to facilitate transmitter binding (allosteric agonistic action).
  • Binding to receptor site, blocking access of transmitter to binding site (antagonistic action).
60
Q

Binding refers to Affinity:

A

• A more potent drug has greater affinity for its receptor (binds m ore tightly).
• A less potent drug has less affinity for its receptor; does not bind so tightly, can be m ore
easily knocked off the receptor. Different drugs m ay bind to the same receptor, but with
different affinities.

61
Q

Enteral routes

A 
gastrointestinal tract (GI) involvement; generally slow and 
produces variable blood levels.

– Oral administration
– Rectal administration

62
Q

Parenteral routes

A

no GI tract involvement
– Injection
– Inhalation
– Absorption through the skin (transdermal)
– Absorption through mucous membranes (topical)

63
Q

oral advantages

A

Drug must be:
– Soluble and stable in stomach fluid
– Absorbed through upper intestine through passive diffusion
– Must generally be somewhat lipid soluble
– Food in stomach may increase or decrease absorption

safe; self-administered
economical
no needle-related complications

64
Q

oral disadvantages

A

slow and highly variable absorption
subject to first-pass metabolism
less predictiable blood levels

65
Q

intravenous iv

A

most rapid

most accurate blood concentration

66
Q

intravenous disadvantage

A

overdose danger
cannot be readily reversed
requires sterile needles and medical techniques

67
Q

intramuscular im advantages

A

slow and even absorption

68
Q

intramuscular disadvantages

A

localized irritation at site of injection

needs sterile equipment

69
Q

subcutaneous sc advantages

A

slow and prolonged absorption

70
Q

subcutaneous disadvantages

A

variable absorption depending on blood flow

71
Q

inhalation

A

large absorption surface
very rapid onset
no injection equipment needed

72
Q

inhalation disadvantages

A

irritation of nasal passages

small particles inhaled may damage lungs

73
Q

topical advantages

A

localized action and effects

easy to sself-administer

74
Q

topical disadvantages

A

may be absorbed into genral circulation

75
Q

transdermal advantages

A

controlled and prolonged absorption

76
Q

transdermal disadvantages

A

local irritation

useful only for lipid soluble drugs

77
Q

epidural advantages

A

bypasses blood-brain barrier

very rapid effect on CNS

78
Q

epidural disadvantages

A

not reversible
needs trained anesthesiologist
possible nerve damage

79
Q

factors influencing drug absorption

A

– Route of administration

  • drug concentration
  • cell membrane
  • rate stomach empties
  • size and sex
  • blood brain barrier
  • solution: bbb
  • placental barrier
  • drug binding
80
Q

psychoactive drugs (termination of drug action)

A

• Usually too lipid-soluble to be passively excreted in urine.
• Must be transformed into metabolites and a rapidly excreted form by hepatocytes
(liver cells) on endoplasmic reticulum membranes.

81
Q

St. John’s Wort:

A

induces CYP450 (CYP3A), which breaks down m any other prescription drugs: Theophylline (asthma), warfarin (anti- clotting), birth control pills, antidepressants, and immunosuppressant cyclosporin. (It is recommended to consult with health care provider before using St. John’s Wort.)

82
Q

Cigarette Smoke:

A

increases certain CYP450 enzymes. Smokers may need even higher doses of drugs such as antidepressants or caffeine which are metabolized by the same CYP450 pathway.

83
Q

Grapefruit juice:

A

can induce several-fold increase of various drugs. It inhibits CYP450
(CYP3A4).

84
Q

Prozac:

A

inhibits certain CYP450 enzymes, increasing toxicity of other antidepressant
drugs and antipsychotics, as well as caffeine. Prozac and Paxil also inhibit the
conversion of codeine into morphine. Codeine not effective as pain reliever for individuals on these drugs.

85
Q

MAO inhibitors:

A

Individuals on these drugs must avoid foods rich in tyramine (found in wine, beer, cheese, and other foods) to avoid toxic high blood pressure and cardiac
arrhythmias.

86
Q

Drug Elimination:

A

• Drug clearance from blood, occurs exponentially: first-order kinetics. It can be
described in terms of half-life (t½): time taken for the body to eliminate 50% of the
drug (t½).
• Cited to describe duration of action of psychoactive drugs in the body.
• Allows comparisons between drugs with similar actions but differing half-lives.

87
Q

rectal administration

A

– Used if patient is vomiting, unconscious, or unable to swallow; infants
– Often involves irregular, unpredictable, and incomplete absorption

88
Q

Passive diffusion

A

involves the movement of drug from higher to

lower concentration.

Biology of Psychological Disorders (7 decks)

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