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Drugs and Behaviour > Last Test > Flashcards

Last Test Flashcards

1
Q

By which year does WHO predict that depression will be the leading cause of premature mortality and disability?

A

2030

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2
Q

How much of the population will experience depression at some point in their lives?

A

approximately 13-17%

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3
Q

Which gender is more likely to suffer from depression?

A

Women (twice as likely)

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4
Q

Major depressive disorder is also called:

A

Mood disorder

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5
Q

What was previously thought to be an apparent cause of depression?

A

Bereavement

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6
Q

Anhedonia

A

loss of interest in normally pleasurable activities.

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7
Q

Which gender is more likely to turn to substances when they are depressed?

A

Males

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8
Q

Mild depression can also be termed:

A

dysthymic disorder

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9
Q

Depression is the most common psychiatric condition of people with which disease?

A

Parkinson’s

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10
Q

Which monoamine is depleted in Parkinson’s patients?

A

Dopamine

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11
Q

What are the two main theories of depression?

A
  1. The Monoamine Theory of Depression

2. The Glucocorticoid Theory of Depression

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12
Q

Mood is related to the funtioning of which monoamines?

A

NE, DA, and 5-HT

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13
Q

Which system is involved with the Monoamine Theory of Depression?

A

The mesocorticolimbic system

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14
Q

What does the Monoamine Theory of Depression suggest?

A

that depression was a result of reduced levels of activity in these monoamine systems.

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15
Q

Why may it be wrong?

A

The effect of antidepressants should be immediate on the monoamine receptors, but they take up to 12 weeks to reach full effectiveness.

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16
Q

Treatments that have been shown to be effective in relieving depression ultimately increase transmission at which synapses?

A

Serotonin synapses.

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17
Q

NE fibres come from:

A

the locus coeruleus in the midbrain.

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18
Q

Serotonergic fibres come from:

A

areas of the raphe system.

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19
Q

Dopaminergic fibres come from:

A

Ventral tegmental area

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20
Q

The monoamine neurotransmitters send projections to various parts of the limbic system and the forebrain through:

A

the medial forebrain bundle

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21
Q

SPECT imaging data indicate that depressed individuals exhibit decreased numbers of:

A

5-HT reuptake transporter proteins in the brainstem.

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22
Q

5-HT1A receptors are mostly:

A

autoreceptors located on the presynaptic neuron

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23
Q

Stimulation of 5-HT1A receptors causes:

A

inhibition of cell firing and reduction of 5-HT activity.

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24
Q

Changes in the sensitivity or number of the 5-HT1A receptors could:

A

make the individual more vulnerable to depression.

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25
Q

Individuals diagnosed with major depressive disorder have:

A

low cerebrospinal-fluid levels of 5-HT, it’s amino acid precurson tryptophan, and its major metabolite 5-H1AA.

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26
Q

Below-normal levels of 5-H1AA could result in

A

a nearly fivefold increase in suicide risk.

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27
Q

5-HT1A receptors can:

A

change their binding potential.

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28
Q

antidepressants significantly reduce the amount of:

A

5-HT transporter protein mRNA in the raphe nuclei.

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29
Q

In stress response, the hypothalamus’ neurons secrete:

A

corticotropin-releasing hormone (CRH)

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30
Q

the release of CRH initiates the release of:

A

adrenocorticotropic hormone (ACTH) from the anterior pituitary

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31
Q

the ACTH stimulates the secretion of:

A

glucocorticoids (cortisol in humans) from the cortex of the adrenal glands, which sit above the kidneys.

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32
Q

Point of the Glucocorticoid Theory of Depression:

A

Once a stressful experience ends, the HPA-axis response must be terminated. So, over-activity of the HPA-axis, indicated by high levels of CRH and cortisol, is a frequent finding in patients with major depressive disorder and in suicide victims.

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33
Q

What are the first-generation antidepressants?

A 
monoamine oxidase inhibitors (MAOIs) -1950s
tricyclic antidepressants (TCAs) -1950s
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34
Q

What was wrong with MAOIs?

A

Could cause liver damage at high doses

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35
Q

What was the first MAOI?

A

iproniazid- first used in the treatment of TB

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36
Q

What was the first TCA?

A

imipramine -discovered accidentally during research on antipsychotics.

37
Q

What are the second-generation antidepressants?

A

selective serotonin reuptake inhibitors(SSRIs)

38
Q

What was the first SSRI?

A

fluoxetine (Prozac)

39
Q

Why were second gen. better?

A

They appeared safer with fewer side effects and could be used to treat a variety of psychiatric conditions, such as anxiety.

40
Q

What are the third-generation antidepressants?

A

Atypicals.

serotonin and norepinephrine reuptake inhibitors (SNRIs)

41
Q

Why are 3rd gen. better?

A

They don’t alter the functioning of muscarinic acetylcholine receptors and therefore don’t produce some of the side effects associated with older antidepressants.

42
Q

Who discovered Cannabis sativa?

A

Carolus Linnaeus 1753

43
Q

Who classified Cannabis indica?

A

Jean-Baptiste Lamarck 1785

44
Q

What are the three species of cannabis?

A

Cannabis sativa, cannabis indica, and cannabis rude ralis

45
Q

What is the origin of the word cannabis?

A

Scythian

46
Q

How long has cannabis been known to China?

A

6000 years. The Chinese word for hemp “ma”, has been used for at least 3000

47
Q

What is the word for cannabis in Africa?

A

bangi or dagga

48
Q

W.B. O’Shaughnessy

A

1839- he reported that hemp was an effective anticonvulsant and an appetite stimulant.

49
Q

Sir Walter Raleigh

A

he was ordered to grow hemp in his Virginia colony

a crop was grown alongside tobacco in 1611

50
Q

When id marijuana start to attract attention universally?

A

1920s

51
Q

Marijuana Tax Act

A

1937-imposed prohibitive taxes on possession and use, effectively eliminating the legitimate medical use of marijuana and driving recreational users underground.

52
Q

Controlled Substances Act

A

1970- ignored the previous century of accumulating medical evidence and declared that marijuana had no potential use but had the potential for abuse.

53
Q

When did marijuana reach its peak?

A

1970s

54
Q

What is the primary active ingredient in cannabis?

A

delta-9-hydrocannibinol

55
Q

What chemical class do cannabinoids belong to?

A

terpenophenolics, of which 85 have been identified in cannabis.

56
Q

Which cannabinoid may have anxiolytic and/or antipsychotic properties?

A

CBD (cannabidiol)

57
Q

Is THC a base or an acid?

A

a weak acid

58
Q

What is the pKa of THC

A

10.6

59
Q

Are cannabinoids lipid soluble or not?

A

They are extremely lipid soluble.

60
Q

When do the peak effects of oral administration of THC occur?

A

1-3 hours following ingestion and may last 5 hours or longer.

61
Q

When do blood levels of THC peak?

A

within 15 minutes.

62
Q

When do the effects of THC peak?

A

after 30-60 minutes

63
Q

What is delta-9-THC converted to in the liver?

A

11-hydroxy-delta-9-THC

believed to be more active than delta-9-THC

64
Q

When was a receptor for cannabinoids identified?

A

1990

65
Q

Where is the CB1 receptor located?

A

primarily in the CNS

66
Q

Where is the CB2 receptor located?

A

Mainly outside of the nervous system

67
Q

Where are CB1 cannabinoid receptors concentrated?

A

cortex, hippocampus, cerebellum, and substantia nigra, but also occur in the hypothalamus, brainstem, and spinal cord.

68
Q

Where are the CB2 receptors concentrated?

A

in the spleen and immune system.

69
Q

Gene CNRI is located where?

A

chromosome 6

70
Q

Who discovered the first endocannabinoid?

A

William Devane and Raphael Mechoulam

71
Q

What was the first endocannabinoid called?

A

anandamide

72
Q

What is the second endocannabinoid called?

A

2-AG

73
Q

DSE

A

depolarization-induced suppression of excitation

74
Q

DSI

A

depolarization-induced suppression of inhibition

75
Q

DSI and DSE operate on neurons that use many different neurotransmitters, such as:

A

NE, DA, 5-HT, ACh, histamine, opioid peptides, GABA, and prostaglandins

76
Q

Where are cannabinoid receptors found?

A

in the nucleus accumbens

also in the cerebellum and basal ganglia, other parts of the extrapyrimidal motor system, and the hippocampus.

77
Q

THC increases DA activity in which system?

A

the mesolimbic dopamine reward system.

78
Q

How long do the physiological effects of marijuana last?

A

2-3 hours

79
Q

antiemetic

A

a drug that stops nausea and vomiting.

80
Q

Cannabis disrupts the ability to:

A

recall words or narrative material.

81
Q

temporal disintegration

A

loss of ability to retain and coordinate information for a purpose.

82
Q

gaze nystagmus

A

involuntary eye movements as someone sights a moving object.

83
Q

THC has a ______ effect on spontaneous motor activity.

A

biphasic.

84
Q

ataxia

A

decrease in motion

85
Q

Cannabinoid discrimination can be blocked by the cannabinoid receptor antagonist:

A

SR-414716A

86
Q

Withdrawal symptoms of marijuana:

A

appetite changes, restlessness, and thoughts of and cravings for cannabis.

87
Q

The average daily user of cannabis in the USA consumes how much THC per day?

A

50g

88
Q

Amotivational syndrome

A

apathy, loss of effectiveness, and a diminished capacity or willingness to carry out complex long-term plans, endure frustration, concentrate for long periods, follow routines, or successfully master new material.

Drugs and Behaviour (3 decks)

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