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PHRM2101 > WEEK 12: Mental Health > Flashcards

WEEK 12: Mental Health Flashcards

(109 cards)

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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
Side effects of TCAs include...
a dry mouth, blurred vision, constipation, difficulty urinating, sedation, sexual problems and weight gain.
26
Tricyclic antidepressants (TCAs) block the reuptake of ... and ... in presynaptic terminals
serotonin (5-HT) noradrenaline (NA)
27
Tricyclic antidepressants act as competitive antagonists on post-synaptic ..., ... and ... receptors.
post-synaptic cholinergic, muscarinic, and histaminergic receptors (H1).
28
T or F The adverse effects of tricyclic antidepressants are largely due to the interactions with non-monoamine associated receptors.
T
29
Due to tricyclic antidepressants blockade of ...., these drugs can lead to blurred vision, constipation, xerostomia, confusion, urinary retention, and tachycardia.
cholinergic receptors
30
TCAs may cause cardiovascular complications, including sudden cardiac death in patients with pre-existing ....
ischemic heart disease.
31
Due to the blockade of ...., TCAs can cause orthostatic hypotension and dizziness.
alpha-1 adrenergic receptors
32
Due to the blockade of ...., TCAs can cause sedation, increased appetite, weight gain, and confusion.
histamine (H1) receptors
33
TCAs are the second-line treatment for ... after the failure of other treatments.
fibromyalgia
34
What conditions (other than depression) can TCAs be used to treat?
migraine prophylaxis, obsessive-compulsive disorder (OCD), insomnia, anxiety, and chronic pain, especially neuropathic pain conditions such as myofascial pain, diabetic neuropathy, and postherpetic neuralgia.
35
What does SNRIs stand for?
Serotonin and Noradrenaline Reuptake Inhibitors
36
What is the major difference between TCAs and SNRIs?
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.
37
T or F TCAs have minimal affinity for H1 histaminergic and muscarinic receptors.
F SNRIs do
38
SNRIs increase the concentrations of ... and ... in the synaptic cleft.
noradrenaline and serotonin
39
T or F SNRIs are more specific than TCAs in their antagonism of targets.
T
40
The first line treatment in most patients diagnosed with depression involves ...
selective serotoninergic reuptake inhibitors (SSRIs).
41
In normal functioning, ... detect the presence of serotonin that is released into the synaptic gap following an action potential by the serotonergic neuron itself.
autoreceptors
42
T or F Activation of the autoreceptor leads to gradual reduction in serotonin release – a negative feedback process.
T
43
T or F Deactivation of the post-synaptic 5-HT1A receptors are key for anti-depressant effects
F Activation
44
Hypothalamic 5-HT 1A receptors are involved in ...regulation and ... control.
thermoregulation and neuroendocrine control.
45
T or F The activation of 5-HT 1A receptors is implicated in delay of therapeutic onset of antidepressants.
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
T or F .../... receptors control ACh release and aspects of memory function.
Septum/hippocampal
47
T or F SSRI treatment is thought to desensitize and downregulate autoreceptors over time.
T
48
What is "downregulation" in the context of SSRI treatment?
As a response to serotonin stimulation, the serotonergic neuron reduces the number of 5HT1A receptors, this phenomenon is known as downregulation.
49
T or F The downregulation of 5HT1A receptors, when exposed to SSRIs, is immediate.
F It takes weeks.
50
What is the oldest drug class of antidepressants?
Irreversible Monoamine Oxidase Inhibitors (MAOIs)
51
The MAO enzyme is responsible for...
the degradation of monoamines in their respective pre-synaptic neurons.
52
Why are MAOIs thought to help patients with depression?
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
There are 2 different types of monoamine oxidase enzymes, namely...
MAO-A and MAO-B
54
What does MAO-A do?
Enzymatically degrades serotonin and norepinephrine.
55
What does MAO-B do?
Primarily degrades dopamine but also degrades serotonin and norepinephrine at high concentrations.
56
T or F MAO-A is only present in the brain.
F It is also present within the digestive tract.
57
MAO-A It is also present within the digestive tract where it serves an important role in metabolising dietary ...
tyramine.
58
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?
Tyramine is then absorbed into the blood supply, making its way to the blood brain barrier, which it readily crosses.
59
Tyramine can pass through the reuptake transporters for ... and subsequently displace ... from its synapses, leading to its unregulated release into synapses.
noradrenaline noradrenaline
60
Tyramine metabolism by MAOA is ...% and MAOB is ...% in the small intestine.
80% 20%
61
Tyramine metabolism by MAOA is ...% and MAOB is ...% in the liver.
50% 50%
62
Tyramine reuptake when taking MAOIs can lead to a ... crisis.
hypotensive
63
What strategies can be implemented to work around a hypotensive reaction caused by MAOIs?
Going on a tyramine-restricted diet and consideration of administration of MAOI's via a transdermal patch.
64
What does "STS" stand for?
Selegiline transdermal system
65
The most common side effects of MAOIs include...
dry mouth, nausea, diarrhoea or constipation, headache, insomnia, drowsiness, dizziness or light-headedness, and possible skin reactions at the patch site.
66
What are some less common side effects of MAOIs?
hypotension, reduced sexual desire or difficulty achieving orgasm, weight gain, muscle cramps.
67
What does "NASSAs" stand for?
Noradrenergic and specific serotonergic antidepressants
68
T or F MAOIs are classified as "mixed-action"antidepressants.
NASSAs are
69
NASSAs have an affinity for and antagonist effects against the .... receptors.
noradrenaline alpha2 autoreceptors.
70
NASSAs can lead to downregulation and desensitization in the long term of .... receptors.
noradrenaline alpha2 autoreceptors
71
How long should we try an antidepressant treatment before we know whether it is working or not?
Depending on the agent 4 weeks to 3 months.
72
What does euthymia mean?
A normal, tranquil mental state or mood.
73
T or F Most antidepressant medications are equal in their efficacy.
T Although individual patient response may vary markedly.
74
Approximately ... of adults with moderate to severe depression respond to antidepressant treatment.
half
75
T or F Depression relapse is relatively uncommon.
F It is relatively common.
76
T or F SSRIs can be regarded as first-line drugs for adults due to their generally favourable risk-benefit ratio.
T
77
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.
4-6
78
Why is it important for patients to be eased off antidepressants slowly?
When treatment ceases, easing concentrations gradually is vital to maintain basic equilibrium across many synaptic levels and hopefully avoid reoccurrence.
79
T or F All antidepressants directly increase the activity of serotonin in the brain.
F Some indirectly do this.
80
Elevated serotonin levels can lead to what syndrome?
serotonin syndrome
81
In addition to antidepressant medications, what other substances can increase serotonin levels in the body and brain?
St John’s Wort, some cough medications, MDMA, migraine medications.
82
What are some mild symptoms of serotonin syndrome?
Sweating, fever, agitation, confusion, akathisia, anxiety, tacahycardia, diarrhea, tremors and poor coordination.
83
What are some moderate symptoms of serotonin syndrome?
Hyperthermia, shivering, diaphoresis, hypomania, hyper-vigilance, hypertension, hyperflexia, clonus and myoclonus.
84
What are some severe symptoms of serotonin syndrome?
Rigidity, seizures, coma, hyperthermia >40 degrees celsius and death
85
T or F Antidepressant pharmacology can cure depression.
F
86
It is estimated that only about ...% of patients are effectively managed long-term for depression.
30
87
What is the most effective treatment for severe depression?
Electroconvulsive therapy (ECT)
88
T or F ECT can be used to treat mania
T
89
T or F ECT can be used to treat anxiety
F
90
T or F ECT can be used to treat schizophrenia
T
91
What are some possible short-term side effects of ECT?
Tiredness and confusion after waking up from the procedure, Nausea or headache, muscle soreness or jaw stiffness, temporary short-term memory loss.
92
Why can ECT help with depression?
ECT treatment causes molecular changes which enhance communication between neurons in key areas of the brain affected by antidepressant medications.
93
T or F The effects of ECT are short-lived.
T
94
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.
T
95
Why do antidepressants not work for everyone?
Because depression is a multifactorial disease, deficiency of monoamines is likely not the only contributing factor leading to a patient's depression.
96
The ‘cheese reaction’ is characterised by .... when taking oral antidepressants.
flushing of the skin, sweating, and tachycardia
97
T or F The word "anxiety" medically covers a range of conditions.
T
98
T or F Agoraphobia is an anxiety disorder.
T
99
What are some conditions that are classified as anxiety disorders?
Agoraphobia, selective mutism, panic disorder, separation anxiety disorder, generalised anxiety disorder and phobias
100
What are the 4 main neurotransmitters thought to be involved in anxiety disorders?
Dopamine, serotonin, noradrenaline and gamma-aminobutyric acid (GABA)
101
The ... within the brain may respond with heightened outputs to triggers linked to anxiety
amygdala
102
due to effects of alcohol on GABAA receptors, combining ... and alcohol is potentially lethal
barbiturates
103
T or F Agomelatine has no influence on extracellular serotonin levels.
T
104
T or F Aglomelatine has some effect on monoamine uptake.
F It has no effect
105
T or F Other than the melatonin receptors MT1 and MT2 agomelatine has negligible affinity for receptors.
T
106
Agomelatine is thought to provide antidepressant effects via interactions in which brain regions?
the hippocampus and frontal cortex
107
Why is agomelatine thought to provide antidepressant effects?
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
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.
neurogenesis hippocampus monoamine frontal cortex
109
Agomelatine is an antagonist on ... receptors.
5-HT2C

PHRM2101 (12 decks)

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