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Drugs and Behavior 345A > midterm #1 > Flashcards

midterm #1 Flashcards

1
Q

median effective dose ED50

A

dose that’s effective in 50% of individuals tested

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2
Q

median lethal dose LD50

A

dose that’s lethal in 50% of individuals tested

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3
Q

ionized molecules (3 + what percentage depends on (3))

A
  • when drug dissolved in a liquid, some of its molecules become ionized
  • ions not lipid-soluble, cannot cross membranes
  • percentage of ionized molecules depends on: drug acid/base, liquid acid/base, drug pKa (pH at which half its molecules are ionized)
  • faster absorption with lower percentage of ionized molecules!
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4
Q

first-pass metabolism

A

metabolism of drugs in the liver before the drug is distributed throughout the body

  • ingested drugs reach liver before arriving at the heart
  • only applies to drugs absorbed by the intestines
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5
Q

rates of elimination

A

first-order elimination:

  • half-life, asymptotic elimination rate
  • low toxicity

zero-order elimination:

  • constant elimination rate
  • as soon as toxicity is hit (e.g. alcohol, overdose response)
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6
Q

kidneys

A
  • maintain balance of water and salt
  • excrete unwanted molecules (e.g. liver metabolites)
  • filter out everything, then allow re-absorption of all that’s required
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7
Q

oral administration

A

stomach: impermeable, no distribution

intestines: permeable, distribution
- much easier absorption for lipid-soluble drugs

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8
Q

combination of absorption and elimination

A

rate of elimination (half-life) for any drug stayconstant, but absorption differs depending on administration route

-> resultant curve depends on administration

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9
Q

upregulation vs downregulation

A

upregulation:

  • increase in receptors/sensitivity/transmitter production
  • response to drugs blocking receptors

downregulation:

  • decrease in receptors/sensitivity/transmitter production
  • response to drugs activating receptors
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10
Q

blood-brain barrier: active vs passive diffusion

A

active:

  • transport, also against concentration gradients
  • requires energy

passive:

  • diffusion through channel protein
  • attaching to carrier protein
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11
Q

urinalysis and blood sampling

+ problems (3)

A

urinalysis: looks for metabolites
blood sampling: looks for drug itself

problems:

  • elimination time > detection time (cannot say when drug’s been taken)
  • length of drug use (metabolic deposits)
  • individual differences
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12
Q

tempering with drug tests

A

substitution: put in someone else’s urine
adulteration: change molecules, e.g. attach to fat
dilution: decrease concentration

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13
Q

potency
efficacy
effectiveness

A

potency: amount required to produce a given effect
efficacy: maximum response achievable for a given dose
effectiveness: ability to produce the therapeutic effect, taking into account secondary and side effects

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14
Q

therapeutic index

A

LD50/ED50 -> safety ratio, how safe a drug is

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15
Q

protective index

A

TD50/ED50 -> safety ratio
TD50: dose at which 50% of people have complaints
- reserved for humans

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16
Q

certain safety factor

A

LD1/ED99 -> where 99% have effect and 1% dies

- pertains to instant and not long-term use

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17
Q

pharmacological antagonism (2)

A

reduced effect due to presence of another drug

(1) competitive:
- at site of action
- need more drug to achieve max result (curve shifted to right)

(2) non-competitive:
- drug B binds to receptor or allosteric site, reduces receptor activity
- reduces max achievable result (decreased efficacy)

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18
Q

physiological antagonism

A

when substances produce different effects counteracting each other, via different binding sites and mechanisms

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19
Q

additive effects (2)

A

combined drug effects

(1) synergistic: combined effects are greater than their sum
(2) potentiation: ineffective drug becomes (more) effective in presence of another drug

20
Q

pharmacodynamic tolerance (2)

A

tolerance in CNS (number of receptors/neurotransmitters)

(1) protracted:
- after several exposures
- need more drug for same psychological effect (graded)

(2) acute / tachyphylaxis:
- after only one exposure
- psychological effects during intake, not elimination
- reduced subjective effect (threshold)

21
Q

pharmacokinetic tolerance

A

changes in metabolism resulting from constant concentrations in body

increases in rates of:

  • enzymes (enzyme induction)
  • elimination from body
22
Q

cross-tolerance + factors (2)

A

tolerance that extends to another drug

factors:

  • enzymes
  • CNS: site of action (downregulation), similar reward-feedback mechanism (upper limit for DA release)
23
Q

behavioural tolerance + factors (2)

A

adjustment and compensation as a result of experience

factors:

  • self-awareness
  • determination
24
Q

homeostasis

allostasis

A

homeostasis: internal equilibrium condition

allostasis: physiological changes to obtain homeostasis to adapt to severe environmental demands
- more permanent state with chronic illness or stress

25
Q

cellular adaptation theory

A

cells adapt by changing the number of their receptors, not their sensitivity

upregulation to avoid toxicity
downregulation to increase sensitivity

26
Q

opponent process theory:
B-processes (3)
problems (2)

A

B-processes:

  • pharmacodynamic tolerance
  • pharmacokinetic tolerance
  • environmental tolerance

problems:
- doesn’t account for drug effects: zero-order elimination, tachyphylaxis, drugs not producing withdrawal
- compensatory response is not a response but a state
(allostasis, has separate mechanisms)

27
Q

opioids (4)

dopamine (4)

A

opioids:

  • inherent
  • liking
  • subjective feeling of pleasure
  • cannot be conditioned

dopamine:

  • learned
  • wanting
  • objective homeostatic response
  • can be conditioned
28
Q

dependence

addiction

A

dependence: reliance
- physiological requirement for homeostasis

addiction: compulsion
- psychological want/need (emotional impulse)

29
Q

addictions:
physical
psychological

A

physical: continuation of use to avoid withdrawal
- negative reinforcement

psychological:

  • use motivated by craving
  • positive reinforcement
30
Q

addictive personality? Keller’s law

impulsivity and addiction?

A

traits only appear to be assoicated with addiction bc publication bias for significant results

not much evidence for impulsivity in addiction (also bc developmental pattern of impulsivity is not constant)

31
Q

addiction: interaction models

A

1) disposition (nature) x environmental stress (nurture), vulnerability x stress
2) protective factors (friends, resilience, exercise)
3) time/events (developmental trajectory, window of vulnerability)

32
Q

diathesis-stress model

A

model of risk for addiction

  • negative environmental factors
  • individual vulnerability
  • risk factors determine result
  • addictions are cause -> effect
33
Q

differential susceptibility model

A

model of risk for addiction

  • positive and negative environmental factors
  • individual susceptibility, individual plasticity
  • result is plastic based on environment
  • buffers for addiction not to develop
34
Q

drug effects

A

primary: drug - effect at targeted s.o.a.
secondary: drug - effect at site other than targeted s.o.a.

side: metabolite - effect at other than intended s.o.a.
prodrug: metabolite - metabolite of prodrug acts at intended s.o.a.

35
Q

additive/antagonistic for drugs/metabolites:

enzyme inhibition
enzyme induction

A

enzyme inhibition: drug B blocks, stops production of or decomposes enzymes for drug A

  • additive for drug
  • antagonistic for metabolites

enzyme induction: drug B activates or facilitates production of enzymes for drug B

  • additive for metabolites
  • antagonistic for drug
36
Q

role of dopamine

A

relating problem to solution

motivation: dopamine depletion causes dishínhibition, facilitates action
guidance: dopamine released for correct actions (conditioning, memory, repeating response)
reinforcement: dopamine response to obtaining reward and to restoration fo homeostasis

37
Q

hedonic homeostatic dysregulation

A

integrates physiology with psychological experience

within-system adaptation: opponent process and incentive salience -> withdrawal makes pleasure of drug use more rewarding by comparison

between-systems adaptation: allostasis -> chronic fluctuation enhances overall stress response, resulting in heightened preoccupation

=> at some point, drugs feel better because things generally feel worse

38
Q

speed of absorption from parenteral administration

A

blood vessels > intraperitoneal > intramuscular > subcutaneous

39
Q

pons: locus coeruleus and reticular formation

A

located in midbrain

locus coeruleus:
- reflexive processing of incoming sensory information

reticular formation:

  • arousal, FFFS
  • selective attention
  • wakefulness (raphe nucleus: sleep, production of pertinent neurotransmitters)
40
Q

reward circuitry: periaqueductal gray and ventral tegmental area

A

periaqueductal gray:

  • pain as a sensation
  • punishment (psychological) -> projects to PFC

ventral tegmental area:

  • reward circuitry
  • pleasure
41
Q

what she includes in midbrain (5)

A 
pons
- locus coeruleus
- reticular formation
periaqueductal gray
VTA
hippocampus
amygdala
42
Q

insula

A

consciousness, self-awareness, imagination

43
Q

Addiction in DSM-IV and DSM-5

A

DSM-IV:

  • substance abuse (affects others)
  • substance dependence (affects yourself)

DSM-5:
- substance use disorder (affects anyone)

44
Q

protein binding

A

when drug molecules bind to large proteins

  • permanent attachment, no crossing of membranes
  • temporary attachment, slow release of molecules into blood
45
Q

differences drugs and natural reinforcers (2)

A

1) natural reinforcers have satiation mechanism that terminates their reinforcing effect (drugs don’t)
2) drug reinforcement is much faster and more intense than natural reinforcers

46
Q

what she includes in forebrain (4)

A

cerebral cortex
insula
thalamus
hypothalamus

47
Q

medulla oblongata

A

autonomic:

  • breathing, heart rate etc.
  • vomiting!

Drugs and Behavior 345A (3 decks)

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