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PHAR 100 > PHAR 100 - Module 2 > Flashcards

PHAR 100 - Module 2 Flashcards

1
Q

functions of the nervous system

A
  • recognize
  • process and integrate
  • react
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2
Q

CNS

A
  • brain → receives and processes info

- the spinal cord - carries sensory info

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3
Q

forebrain

A
  • cerebral cortex (cerebrum) → sensory and motor coordination, intelligence, memory, vision, speech
  • thalamus → relay centre from which impulses are transmitted to the cerebral cortex; coordinates and filters incoming signals
  • hypothalamus → controls involuntary functions, feeding, sexual responses
  • limbic system → integrates memory, emotion and reward
  • pituitary → secretes hormones
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4
Q

midbrain

A

relay centre for visual (eye) and auditory (ear) stimuli or signals

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5
Q

the hindbrain

A
  • pons → conducting signals from the cerebral cortex down to the medulla and cerebellum
  • medulla → regulation of respiration, HR, BP
  • cerebellum → coordination and posture
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6
Q

neuron

A
  • cell body → contains the nucleus
  • dendrites → receive incoming info
  • axon → carries incoming info away from dendrites and cell body
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7
Q

glutamate

A

primary excitatory neurotransmitter in the CNS

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8
Q

gamma-aminobutyric acid (GABA)

A

primary inhibitory neurotransmitter in the CNS

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9
Q

acetylcholine

A

produces an excitatory response in the CNS

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10
Q

types of cholinergic receptors

A
  • nicotinic receptors → can be stimulated by acetylcholine/nicotine
  • muscarinic receptors → can be stimulated by acetylcholine/muscarine
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11
Q

dopamine

A

a catecholamine

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12
Q

norepinephrine

A

can bind to a large number of receptor types, but the 2 main classes are alpha and beta

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13
Q

serotonin

A

hyperactivity of the serotonergic system is involved in anxiety, and hypo-activity has been implicated in depression

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14
Q

opioid peptides

A

3 main classes of opioid peptides: enkephalins, endorphins and dynorphins

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15
Q

substance use disorder

A

when a person’s use of a drug or other substance leads to health issues of problems at work, school or home

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16
Q

factors influencing substance use disorder

A
  • genetic factors
  • co-existing disorders
  • environmental risk factors
  • developmental aspect
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17
Q

the dopamine hypothesis

A

explains addiction; suggests that drugs of abuse increase dopamine in the reward systems of the brain

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18
Q

characteristics of addictive drugs

A
  • increase dopamine (CNS stimulants, alcohol, cannabis)
  • produce novelty (LSD, ecstasy)
  • reduce anxiety (benzodiazepines, barbiturates)
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19
Q

substance abuse

A

a pattern of substance use manifested by recurrent and significant adverse consequences

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20
Q

abuse potential of a drug

A
  • dependence liability → nature of the drug; route of administration; amount and frequency of use
  • availability
  • inherent harmfulness
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21
Q

dependence liability

A
  • tendency of a drug to cause dependence and addiction
  • determined by 3 factors:
    → nature of the drug - most drugs are natural reinforcers (like food)
    → route of administration - drugs that can be administered by routes that give rapid absorption and hence rapid effects have a greater potential for abuse
    → amount and frequency of use - the greater the dose and the frequency of use, the greater the potential for dependence
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22
Q

inherent harmfulness

A
  • potential of the drug to cause harm
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23
Q

substance dependence

A

a complex disease process of the CNS that regulates repeated consumption, or chronic use, of the substance

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24
Q

drug tolerance

A
  • repeated administration of a given dose of a drug has progressively less pharmacological effects, or a state in which the dose of a drug must be increased to obtain the same magnitude of pharmacological effect as was produced by the original drug dose
  • usually expressed by a shortened duration of action and a decreased magnitude of effect
25
Q

drug dependence and withdrawl

A
  • an abnormal physiological state produced by repeated administration of a drug that leads to the appearance of a withdrawal syndrome when drug administration is discontinued or dose is decreased
26
Q

drug addiction

A

a state in which stopping or abruptly reducing the dose of a given drug produces non-physiological symptoms

27
Q

substance abuse example

A

Becky binge drinks once a month so she blacks out

28
Q

substance dependence example

A

Amanda has been drinking 4 black coffees since starting undergrad; if she doesn’t drink it she gets headaches and is irritable

29
Q

amphetamines chemistry

A
  • synthetic organic compounds

- structurally similar to dopamine and norepinephrine

30
Q

amphetamines pharmacology

A
  • increase excitation by increasing amount of dopamine or norepinephrine in the synaptic cleft
  • amphetamines are substrates for the dopamine transporter → compete with dopamine for the dopamine transporter
  • once in the nerve they block the VMAT (transporter that brings dopamine into vesicles to be released)
  • increase in dopamine in the synaptic cleft = increase in CNS excitation
31
Q

amphetamines CNS effects

A
  • decreased threshold for transmitting sensory input to the cerebral cortex, leading to excitation
  • feeling of euphoria and reward
  • temp-regulation and feeding centre modifications, leading to appetite suppression
  • increase in aggressive behaviour and mood swings
32
Q

amphetamines effects of short-term use

A
  • heart attack, heart pain
  • cardiovascular collapse
  • increased respiratory rate
33
Q

amphetamines effects of long-term use

A
  • chronic sleeping problems
  • poor appetite
  • anxiety
  • elevated BP
34
Q

amphetamines therapeutic uses

A
  • narcolepsy → a chronic sleep disorder

- ADHD → drug increases attention/concentration

35
Q

amphetamines abuse potential

A
  • abuse liability of amphetamines is very high (euphoria)
  • produce a rapid and intense response
  • inherent harmfulness is due to its long-term toxicities
36
Q

amphetamines dependence

A
  • tolerance → develops to euphoria and mood-elevating effects
  • dependence → cessation results in mood depression, prolonged sleep, huge appetite
  • addiction → euphoria and “rush” will act as rewards
37
Q

cocaine pharmacology

A
  • causes generalized CNS stimulation
  • inhibits the active re-uptake of dopamine and serotonin into the presynaptic nerve terminal
  • increases the concentration of these transmitters in the synaptic cleft, and in turn increases activation of the post-synaptic receptors
38
Q

cocaine effects in the CNS

A
  • almost indistinguishable from amphetamine in it’s acute effects and pattern of toxicity
  • main difference is that cocaine has a shorter duration of action
39
Q

cocaine therapeutic uses

A
  • local anesthetic for the mouth and throat
40
Q

cocaine effects of long-term use

A
  • toxic psychosis
  • hallucinations
  • permanent brain damage
41
Q

cocaine abuse potential

A
  • has one of the highest abuse liabilities
42
Q

cocaine dependence

A
  • tolerance → develops to the mood-elevating effect, but not the psychotic effect
  • dependence → withdrawal symptoms are similar to those from amphetamines
  • addiction → can occur
43
Q

nicotine pharmacology

A
  • nicotine exists in cigarette smoke in small particles, and when inhaled these particles are rapidly absorbed
  • stimulates nicotinic receptors at synapses
  • activation of nicotinic receptors increases psychomotor activity, attention
44
Q

nicotine therapeutic uses

A

only therapeutic use is in smoking cessation programs

45
Q

nicotine short-term effects of smoking

A
  • dizziness, nausea, headache

- mild euphoria, increased ability to concentrate

46
Q

nicotine long-term effects of smoking

A
  • respiratory and carcinogenic effects

- lung disease risk is increased

47
Q

nicotine abuse potential

A
  • is a powerful reinforcer and has a high degree of abuse liability
48
Q

nicotine dependence

A
  • tolerance → doesn’t really occur

- dependence → withdrawal from smoking results in irritability, restlessness, anxiety, insomnia

49
Q

caffeine pharmacology

A
  • in the brain, activation of receptors termed adenosine receptors stimulates GABAergic neurons that then inhibit dopamine release
  • actions of caffeine are exerted by competitively blocking adenosine receptors in the brain
  • when caffeine blocks these receptors, the neurons are released from the adenosine inhibition, causing an increase in dopamine release
50
Q

short-term effects of caffeine

A
  • mild mood-elevation, reduce fatigue

- constriction of cerebral blood vessels, rapid HR

51
Q

long-term effects of caffeine

A

restlessness, nervousness, insomnia, increased urinary output

52
Q

caffeine abuse potential

A
  • abuse liability of caffeine is low
  • it does act as a mild reinforcer
  • inherent harmfulness is low
53
Q

caffeine dependence

A
  • tolerance → can develop
  • dependence → abrupt cessation = headache, fatigue
  • addiction → mild addiction can occur
54
Q

amphetamines in sport

A
  • CNS stimulants that work by increasing the release of the neurotransmitters dopamine and norepinephrine
  • increased alertness, feeling of power, reduction of fatigue, increased aggression
55
Q

anabolic steroids in sport

A
  • increase muscle mass
  • produce an anti-catabolic response
  • anabolic effects of the drug result in protein production
  • produce aggressive behaviours
  • usually has greater effects on females
56
Q

benzodiazepines in sport

A
  • drugs like Valium are used to reduce anxiety during competition
  • taken by ski jumpers to calm nerves
57
Q

growth hormone in sport

A
  • HGH will increase muscle mass and strength

- not as easily detected

58
Q

blood doping and erythrotopien in sport

A
  • both techniques result in an increase in the number of red blood cells, and hence increases oxygen carrying capacity of the blood
59
Q

diaretics in sport

A
  • drugs that enhance the excretion of salt and water through kidneys
  • used to reduce body water to allow the athlete to compete at a lower weight class

PHAR 100 (6 decks)

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