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PHRM2101 > WEEK 12: Mental Health > Flashcards

WEEK 12: Mental Health Flashcards

1
Q

What are the diagnostic indicators for depression?

A

Having five of the following symptoms may inform a diagnosis of depression: depressed mood for 2+ weeks, loss of interest in things normally enjoyed, changes in appetite, changes in sleep patterns, restlessness or slowness, poor concentration, feelings of worthlessness or guilt, suicidal ideation or thoughts.

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2
Q

How does depression compare to general feelings of sadness?

A

General sadness is a mood that comes and goes in most individuals. It is a natural part of life but is usually not as long lasting or as impactful as depression.

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3
Q

Which neurotransmitters are of key interest in the physiology of depression?

A

Certain monoamine neurotransmitters such as dopamine, norepinephrine and serotonin

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4
Q

Which brain structures are of key interest in the physiology of depression?

A

The frontal lobes and the hippocampus.

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5
Q

T or F
The physiology of depression can include hormonal abnormalities.

A

T

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6
Q

T or F
Blunted circadian rhythms and sleep patterns can be indicators of depression.

A

T

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7
Q

T or F
Depression can increase hippocampal volumes in the brain.

A

F
Depression can decrease hippocampal volumes in the brain.

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8
Q

As well as causing a decrease in hippocampal volumes, depression can also decrease the size of the brains ….

A

frontal lobes.

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9
Q

Approximately…% of adults will struggle with depression in their lifetime.

A

10%

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10
Q

Serotonin is also known as …

A

5-hydroxytryptamine, or 5-HT in short.

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11
Q

Serotonin is synthesised from …

A

tryptophan (an α-amino acid)

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12
Q

Serotonin is loaded into vesicles via the ….

A

vesicular monoamine transporter (VMAT).

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13
Q

Serotonin undergoes …-mediated exocytosis

A

calcium

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14
Q

Once serotonin is released into the synaptic cleft it binds to …

A

5-hydroxytryptamine receptors (5-HTr)

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15
Q

When 5-hydroxytryptamine binds to 5-hydroxytryptamine receptors it produces a … effect.

A

serotonergic

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16
Q

Once serotonin has acted on 5-hydroxytryptamine receptors in the synaptic cleft it is reabsorbed into the presynaptic cell via the …

A

serotonin transporter (SERT)

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17
Q

Once serotonin has acted on 5-hydroxytryptamine receptors in the synaptic cleft it is reabsorbed into the presynaptic cell via the … and is reloaded into …

A

serotonin transporter (SERT)
vesicles

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18
Q

What does the monoamine theory of depression state?

A

there is a deficiency of monoamine neurotransmitters within the brain. Deficiencies of ley monoamines including serotonin (5-HT) and noradrenaline lead to symptoms of depression.

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19
Q

T or F
Most of the mechanisms of action of the drugs used to treat patients with depression are effective in increasing synaptic concentrations of monoamines.

A

T

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20
Q

T or F
All patients with depression experience a decrease in symptoms when exposed to monoamine-increasing drugs.

A

F

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21
Q

Tricyclic antidepressants block what 2 receptors and 2 transporters?

A
  1. serotonin transporter (SERT)
  2. norepinephrine transporter (NET)
  3. histamine H3 receptor (H3r)
  4. Muscarinic acetylcholine receptors (MAChr)
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22
Q

Acetylcholine reuptake into presynaptic neurons occurs via…

A

diffusion after degradation from acetylcholinesterase (ACE)

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23
Q

Adrenaline reuptake into presynaptic neurons occurs via…

A

the norepinephrine transporter (NET)

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24
Q

Why is it not recommended to drink alcohol when depressed?

A

It tends to worsen the depression. It also interacts with TCAs, increasing sedation.

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25
Q

Side effects of TCAs include…

A

a dry mouth, blurred vision, constipation, difficulty urinating, sedation, sexual problems and weight gain.

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26
Q

Tricyclic antidepressants (TCAs) block the reuptake of … and … in presynaptic terminals

A

serotonin (5-HT)
noradrenaline (NA)

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27
Q

Tricyclic antidepressants act as competitive antagonists on post-synaptic …, … and … receptors.

A

post-synaptic cholinergic, muscarinic, and histaminergic receptors (H1).

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28
Q

T or F
The adverse effects of tricyclic antidepressants are largely due to the interactions with non-monoamine associated receptors.

A

T

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29
Q

Due to tricyclic antidepressants blockade of …., these drugs can lead to blurred vision, constipation, xerostomia, confusion, urinary retention, and tachycardia.

A

cholinergic receptors

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30
Q

TCAs may cause cardiovascular complications, including sudden cardiac death in patients with pre-existing ….

A

ischemic heart disease.

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31
Q

Due to the blockade of …., TCAs can cause orthostatic hypotension and dizziness.

A

alpha-1 adrenergic receptors

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32
Q

Due to the blockade of …., TCAs can cause sedation, increased appetite, weight gain, and confusion.

A

histamine (H1) receptors

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33
Q

TCAs are the second-line treatment for … after the failure of other treatments.

A

fibromyalgia

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34
Q

What conditions (other than depression) can TCAs be used to treat?

A

migraine prophylaxis, obsessive-compulsive disorder (OCD), insomnia, anxiety, and chronic pain, especially neuropathic pain conditions such as myofascial pain, diabetic neuropathy, and postherpetic neuralgia.

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35
Q

What does SNRIs stand for?

A

Serotonin and Noradrenaline Reuptake Inhibitors

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36
Q

What is the major difference between TCAs and SNRIs?

A

Reduced side effects. SNRIs have minimal affinity and therefore minimal antagonism for the H1 histaminergic and muscarinic receptors. This means there are reduced sedation and cardiovascular effects.

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37
Q

T or F
TCAs have minimal affinity for H1 histaminergic and muscarinic receptors.

A

F
SNRIs do

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38
Q

SNRIs increase the concentrations of … and … in the synaptic cleft.

A

noradrenaline and serotonin

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39
Q

T or F
SNRIs are more specific than TCAs in their antagonism of targets.

A

T

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40
Q

The first line treatment in most patients diagnosed with depression involves …

A

selective serotoninergic reuptake inhibitors (SSRIs).

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41
Q

In normal functioning, … detect the presence of serotonin that is released into the synaptic gap following an action potential by the serotonergic neuron itself.

A

autoreceptors

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42
Q

T or F
Activation of the autoreceptor leads to gradual reduction in serotonin release – a negative feedback process.

A

T

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43
Q

T or F
Deactivation of the post-synaptic 5-HT1A receptors are key for anti-depressant effects

A

F
Activation

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44
Q

Hypothalamic 5-HT 1A receptors are involved in …regulation and … control.

A

thermoregulation and neuroendocrine control.

45
Q

T or F
The activation of 5-HT 1A receptors is implicated in delay of therapeutic onset of antidepressants.

A

F
The activation of 5-HT 1A receptors mediates the therapeutic properties of antidepressants. The activation of raphe autoreceptors is implicated in the delay of therapeutic onset.

46
Q

T or F
…/… receptors control ACh release and aspects of memory function.

A

Septum/hippocampal

47
Q

T or F
SSRI treatment is thought to desensitize and downregulate autoreceptors over time.

A

T

48
Q

What is “downregulation” in the context of SSRI treatment?

A

As a response to serotonin stimulation, the serotonergic neuron reduces the number of 5HT1A receptors, this phenomenon is known as downregulation.

49
Q

T or F
The downregulation of 5HT1A receptors, when exposed to SSRIs, is immediate.

A

F
It takes weeks.

50
Q

What is the oldest drug class of antidepressants?

A

Irreversible Monoamine Oxidase Inhibitors (MAOIs)

51
Q

The MAO enzyme is responsible for…

A

the degradation of monoamines in their respective pre-synaptic neurons.

52
Q

Why are MAOIs thought to help patients with depression?

A

It is thought proposed that “protection” of 5-HT or noradrenaline from degradation means that they are packaged more quickly into synaptic vesicles for re-release. This enhances the speed with which the pre-synaptic neuron can respond to an action potential and therefore alleviates the presumed deficiency of monoamines in depression.

53
Q

There are 2 different types of monoamine oxidase enzymes, namely…

A

MAO-A and MAO-B

54
Q

What does MAO-A do?

A

Enzymatically degrades serotonin and norepinephrine.

55
Q

What does MAO-B do?

A

Primarily degrades dopamine but also degrades serotonin and norepinephrine at high concentrations.

56
Q

T or F
MAO-A is only present in the brain.

A

F
It is also present within the digestive tract.

57
Q

MAO-A It is also present within the digestive tract where it serves an important role in metabolising dietary …

A

tyramine.

58
Q

When MAO-A is inhibited by MAOI’s taken orally, and normal metabolism of tyramine is inhibited. What happens to the tyramine in the digestive tract?

A

Tyramine is then absorbed into the blood supply, making its way to the blood brain barrier, which it readily crosses.

59
Q

Tyramine can pass through the reuptake transporters for … and subsequently displace … from its synapses, leading to its unregulated release into synapses.

A

noradrenaline
noradrenaline

60
Q

Tyramine metabolism by MAOA is …% and MAOB is …% in the small intestine.

A

80%
20%

61
Q

Tyramine metabolism by MAOA is …% and MAOB is …% in the liver.

A

50%
50%

62
Q

Tyramine reuptake when taking MAOIs can lead to a … crisis.

A

hypotensive

63
Q

What strategies can be implemented to work around a hypotensive reaction caused by MAOIs?

A

Going on a tyramine-restricted diet and consideration of administration of MAOI’s via a transdermal patch.

64
Q

What does “STS” stand for?

A

Selegiline transdermal system

65
Q

The most common side effects of MAOIs include…

A

dry mouth, nausea, diarrhoea or constipation, headache, insomnia, drowsiness, dizziness or light-headedness, and possible skin reactions at the patch site.

66
Q

What are some less common side effects of MAOIs?

A

hypotension, reduced sexual desire or difficulty achieving orgasm, weight gain, muscle cramps.

67
Q

What does “NASSAs” stand for?

A

Noradrenergic and specific serotonergic antidepressants

68
Q

T or F
MAOIs are classified as “mixed-action”antidepressants.

A

NASSAs are

69
Q

NASSAs have an affinity for and antagonist effects against the …. receptors.

A

noradrenaline alpha2 autoreceptors.

70
Q

NASSAs can lead to downregulation and desensitization in the long term of …. receptors.

A

noradrenaline alpha2 autoreceptors

71
Q

How long should we try an antidepressant treatment before we know whether it is working or not?

A

Depending on the agent 4 weeks to 3 months.

72
Q

What does euthymia mean?

A

A normal, tranquil mental state or mood.

73
Q

T or F
Most antidepressant medications are equal in their efficacy.

A

T
Although individual patient response may vary markedly.

74
Q

Approximately … of adults with moderate to severe depression respond to antidepressant treatment.

A

half

75
Q

T or F
Depression relapse is relatively uncommon.

A

F
It is relatively common.

76
Q

T or F
SSRIs can be regarded as first-line drugs for adults due to their generally favourable risk-benefit ratio.

A

T

77
Q

When a patient is in remission/recovery from depression for more than one year, their medication may be reduced gradually over a … to … week period.

A

4-6

78
Q

Why is it important for patients to be eased off antidepressants slowly?

A

When treatment ceases, easing concentrations gradually is vital to maintain basic equilibrium across many synaptic levels and hopefully avoid reoccurrence.

79
Q

T or F
All antidepressants directly increase the activity of serotonin in the brain.

A

F
Some indirectly do this.

80
Q

Elevated serotonin levels can lead to what syndrome?

A

serotonin syndrome

81
Q

In addition to antidepressant medications, what other substances can increase serotonin levels in the body and brain?

A

St John’s Wort, some cough medications, MDMA, migraine medications.

82
Q

What are some mild symptoms of serotonin syndrome?

A

Sweating, fever, agitation, confusion, akathisia, anxiety, tacahycardia, diarrhea, tremors and poor coordination.

83
Q

What are some moderate symptoms of serotonin syndrome?

A

Hyperthermia, shivering, diaphoresis, hypomania, hyper-vigilance, hypertension, hyperflexia, clonus and myoclonus.

84
Q

What are some severe symptoms of serotonin syndrome?

A

Rigidity, seizures, coma, hyperthermia >40 degrees celsius and death

85
Q

T or F
Antidepressant pharmacology can cure depression.

A

F

86
Q

It is estimated that only about …% of patients are effectively managed long-term for depression.

A

30

87
Q

What is the most effective treatment for severe depression?

A

Electroconvulsive therapy (ECT)

88
Q

T or F
ECT can be used to treat mania

A

T

89
Q

T or F
ECT can be used to treat anxiety

A

F

90
Q

T or F
ECT can be used to treat schizophrenia

A

T

91
Q

What are some possible short-term side effects of ECT?

A

Tiredness and confusion after waking up from the procedure, Nausea or headache, muscle soreness or jaw stiffness, temporary short-term memory loss.

92
Q

Why can ECT help with depression?

A

ECT treatment causes molecular changes which enhance communication between neurons in key areas of the brain affected by antidepressant medications.

93
Q

T or F
The effects of ECT are short-lived.

A

T

94
Q

T or F
Several factors, including stress, glutamate and its receptors, as well as brain-derived neurotrophic factor (BDNF) are thought to have contributions to depressive symptoms.

A

T

95
Q

Why do antidepressants not work for everyone?

A

Because depression is a multifactorial disease, deficiency of monoamines is likely not the only contributing factor leading to a patient’s depression.

96
Q

The ‘cheese reaction’ is characterised by …. when taking oral antidepressants.

A

flushing of the skin, sweating, and tachycardia

97
Q

T or F
The word “anxiety” medically covers a range of conditions.

A

T

98
Q

T or F
Agoraphobia is an anxiety disorder.

A

T

99
Q

What are some conditions that are classified as anxiety disorders?

A

Agoraphobia, selective mutism, panic disorder, separation anxiety disorder, generalised anxiety disorder and phobias

100
Q

What are the 4 main neurotransmitters thought to be involved in anxiety disorders?

A

Dopamine, serotonin, noradrenaline and gamma-aminobutyric acid (GABA)

101
Q

The … within the brain may respond with heightened outputs to triggers linked to anxiety

A

amygdala

102
Q

due to effects of alcohol on GABAA receptors, combining … and alcohol is potentially lethal

A

barbiturates

103
Q

T or F
Agomelatine has no influence on extracellular serotonin levels.

A

T

104
Q

T or F
Aglomelatine has some effect on monoamine uptake.

A

F
It has no effect

105
Q

T or F
Other than the melatonin receptors MT1 and MT2 agomelatine has negligible affinity for receptors.

A

T

106
Q

Agomelatine is thought to provide antidepressant effects via interactions in which brain regions?

A

the hippocampus and frontal cortex

107
Q

Why is agomelatine thought to provide antidepressant effects?

A

Circadian rhythms govern our sleep/wake cycles as well as various hormonal levels the rise and fall during the day. As sleep disruption is a symptom of depression, it is thought that activation of the MT1 and MT2 receptors by agomelatine may improve overall well-being.

108
Q

As well as promoting better sleeping patterns, agomelatine may promote … in the …, and enhance … signalling in the …., which may lead to an easing of depressive symptoms.

A

neurogenesis
hippocampus
monoamine
frontal cortex

109
Q

Agomelatine is an antagonist on … receptors.

A

5-HT2C

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