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1.1.3 The Human Body > 4. Drugs > Flashcards

4. Drugs Flashcards

1
Q

4 Methods of Administration

A

Ingestion
Absorption
Inhalation
Injection

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2
Q

Ingestion

A
  1. Goes through the digestive system into the intestines, where they are absorbed into the blood
  2. Relatively safe & easy but unpredictable (food intake and other factors affect rate)
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3
Q

Absorption

A

Through mucus membranes

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4
Q

Inhalation

A
  1. e.g. smoking
  2. Cannot regulate dose
  3. Damage to lungs if done incorrectly
    1. Absorbed into the blood from the lungs
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5
Q

Injection

A
  1. Into muscles, fatty tissue or veins
  2. Intravenous - blood stream takes them straight to the brain
    1. Little to no opportunity to counteract an overdose or allergic reaction
    2. Scar tissue, collapsed veins and infections are also a risk
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6
Q

Drug penetration of the CNS

A
  • Travel through the bloodstream to blood vessels of the CNS
  • Blood-brain barrier makes it difficult for drugs to get past into the “extracellular” space surrounding the neurons and glia of the CNS
  • Drugs like alcohol & many general anesthetics diffuse across neural membranes (nerve cells)
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7
Q

Drug metabolism

A

Enzymes in the liver convert active drugs to non-active forms
Most cases: inhibits the drugs ability to pass through lipid membranes, meaning it can no longer get past the blood-brain barrier

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8
Q

Agonists

A

Drugs that facilitate the effects of a specific neurotransmitter e.g. a dopamine agonist
Activate certain receptors

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9
Q

Antagonists

A

Drugs that inhibit the effects of a specific neurotransmitter e.g. a dopamine antagonist
Block certain receptors

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10
Q

Affinity & Efficacy

A

Affinity - tendency to bind to a receptor
Efficacy - tendency to activate a receptor

A drug that binds easily but does not stimulate would be high in affinity and low in efficacy
This would also be an antagonistic effect

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11
Q

Mesocorticolimbic System

A

a component of the mesotelencephalic dopamine system which play an important part in mediating ICSS (Intracranial self-stimulation)

  1. Self-stimulation occurs at many brain sites that are part of the mesocorticolimbic system
  2. ICSS is associated with spikes in dopamine release in the mesocorticolimbic system
  3. Dopamine agonists increase ICSS and dopamine antagonists decrease ICSS
  4. ICSS is disrupted when there are lesions (abnormal tissue growth) in the mesocorticolimbic system
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12
Q

Intracranial self-stimulation

A

self-administration of weak electrical stimulation to the brain
- Think rats and levers

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13
Q

Ventral Tegmental Area (VTA)

A

The cell bodies of the neurons composing the MDS (Mesotelencephalic Dopamine System) are contained here and in the substantia nigra
- Axons of the neurons in the VTA mostly project into many cortical and limbic sites
- This section of the MDS is called the Mesocorticolimbic system

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14
Q

Nucleus Accumbens

A

‘Reward centre’
Motivation (anticipation of reward) and reward
‘Dopaminergic’ input is sent from the VTA to the nucleus accumbens - strongest, clearest relation to reward and pleasure
- Lesions in this area stopped rats administering drugs to themselves

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15
Q

Subcutaneous Injection

A

Into fatty tissue

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16
Q

Intramuscular Injection

A

Into large muscles

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17
Q

Intravenous Injection

A

Into veins

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18
Q

Amphetamine

A

Blocks reuptake of dopamine & several other transmitters

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19
Q

Cocaine

A

Blocks reuptake of dopamine + others
Stimulant

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20
Q

Methylphenidate (Ritalin)

A

Blocks reuptake of dopamine + others, gradually

21
Q

MDMA (Ecstasy)

A

Releases dopamine & serotonin

22
Q

Nicotine

A

Stimulates nicotinin-type acetylcholine receptor, increasing dopamine release in the nucleus accumbens

23
Q

Opiates (e.g. heroine, morphine)

A

Stimulates endorphin receptors

24
Q

Cannabinoids (marijuana)

A

Excites negative-feedback receptors on presynaptic cells; ordinarily responding to anandamine & 2AG

Inhibits GABA & glutamate, leading to dopamine release
Psychoactive effects due to TCH
Antagonist

25
Q

Hallucinogens

A

Stimulate serotonin type 2A receptors

26
Q

Burgers’ Disease

A

Blood vessels (particularly in the legs) become constricted, possibly leading to amputation

27
Q

Alcohol

A

Depressor
GABA agonist - facilitates response at receptors
Glutamate antagonist - blocks activity at receptors, leading to decreased brain activity

28
Q

Drug tolerance

A

Decreased sensitivity to a drug due to exposure to it

There is no 1 mechanism that leads to this

29
Q

Dose-response curve

A

A graph demonstrating the effect sizes of different doses of a drug

30
Q

Cross tolerance

A

Tolerance to one drug can lead to tolerance to other drugs of the same type (that work by the same mechanisms)

31
Q

Drug sensitization

A

we become increasingly sensitive to certain effects of a drug, often as we gain tolerance in others

32
Q

2 categories of changes facilitating drug tolderance

A

Metabolic tolerance
Functional tolerance

33
Q

Metabolic tolerance

A

Changes that reduce the amount of the drug reaching sites of action
Amount

34
Q

Functional tolerance

A
  1. Changes that reduce the reactivity to the drug at the sites of action
  2. Mostly with psychoactive
    Reactivity
35
Q

Conditioned Drug Tolerance

A

Situations where tolerance effects are expressed only when the drug is administered in the same situation as before

36
Q

Seigel’s Hypothesis

A

We are more vulnerable to an overdose in new contexts
We build tolerance and start administering more of the drug - when the environment is changed, the tolerance is no longer present and overdose is more likely

37
Q

Conditioned stimuli

A

Environmental stimuli predicting regular use of the drug

38
Q

Exteroceptive stimuli

A

External stimuli e.g. the environment

39
Q

Interceptive stimuli

A

Internal stimuli e.g. thoughts (have been shown to evoke a conditioned response)

40
Q

Unconditional stimuli

A

The effects of the drug

41
Q

Conditioned compensatory responses

A

Conditional stimuli leads to opposite responses to the drug that would normally be seen (due to tolerance)

Conditional stimuli predict greater ‘conditioned compensatory responses’ which counteract the natural (unconditioned) effects of the drug in the same situation, thus building situationally specific tolerance

42
Q

Conditioned Compensatory Responses vs Withdrawal

A
  • Both produce almost identical, opposite effects to the unconditioned effect of the drug
  • Withdrawal - caused by not receiving the drug
  • CCR - caused by the body predicting the drug is coming through context cues?
42
Q

Conditioned Compensatory Responses vs Withdrawal

A
  • Both produce almost identical, opposite effects to the unconditioned effect of the drug
  • Withdrawal - caused by not receiving the drug
  • CCR - caused by the body predicting the drug is coming through context cues?
43
Q

Theories about Addiction

A

Genetic influences
Positive incentivisation theory

44
Q

Contingent Drug Tolerance

A

Tolerance develops only to drug effects that are actually experienced

45
Q

Genetic Influences (Gene for Acetaldehyde Dehydrogenase production)

A

Enzyme that controls alcohol metabolism
Gene for less AD production = acetaldehyde is metabolized slower, effects like nausea, headaches, increased heart rate, flushed face etc. are more common
- Less likely to develop alcoholism

46
Q

Incentive sensitization theory

A
  • Dopamine release in the nucleus accumbens happens from craving the drug, not necessarily doing it
  • Incentive value goes up, hedonic value goes down
  • Pleasure goes down due to tolerance
47
Q

Positive incentive theory

A

Taking drugs to not feel the withdrawal effects

48
Q

3 Major Causes of Relapse

A

Stress: major factor in relapse e.g. nicotine
Priming: a single exposure to a formerly abused drug (just once)
Exposure to environmental cues: people, time, places or objects associated with drug taking

1.1.3 The Human Body (8 decks)

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