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Drugs and the Brain > Mood Disorders > Flashcards

Mood Disorders Flashcards

1
Q

What are two examples of affective disorders?

A
  • Major depressive disorder
  • Bipolar disorder
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2
Q

What percentage of the world popultation suffers from major depressive disorder?

A

2-7

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3
Q

What percentage of the world suffers from bipolar disorder?

A

1

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4
Q

Which gender is MDD more common in and by how much?

A

2X more common in women than men

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5
Q

What is the main peak age for MDD?

A

30-40 (but is decreasing)

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6
Q

What age is the onset of bipolar disorder?

A

15-19 (rarely after 40)

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7
Q

Which sex is more likely to have bipolar disorder?

A

They are equal!

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8
Q

What are the three largest economic burdens of depression?

A
  • Direct healthcare costs
  • Suicide costs
  • Workplace costs (largest)
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9
Q

What are the three main medical costs of depression?

A
  • Treatment costs of major depressive disorder
  • Other depressive disorders
  • Comorbidities such as heart disease or other psychiatric illnesses
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10
Q

What are the two psychiatric diagnostic manuals used?

A
  • DSM-5 (american psychiatric society)
  • ICD-11 (World health organisation)
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11
Q

What are the two categories of mood disorders?

A
  • Low mood
  • Elevated mood and low mood
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12
Q

What are two examples of mood disorders that fall under ‘low mood’?

A
  • Major depressive diorder
  • Dysthymia
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13
Q

What is an example of a disorder that fall under ‘elevated mood and low mood’ category of mood disorders?

A

Bipolar disorder

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14
Q

What are the two necessary DSM-5 symptoms in order to be diagnosed with MDD?

A
  • Depressed mood
  • Diminished interest or loss of pleasure in almost all activities (anhedonia)
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15
Q

Give some examples of other diagnostic points for MDD

A
  • Significant weight change or appetite disurbance
  • Sleep disturbance
  • Psychomotor agitation or retardation
  • Fatigue or loss of energy
  • Feelings of worthlessness
  • Diminished ability to concentrate
  • Recurrent thoughts of death
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16
Q

What is the diagnostic criteria for MDD

A

In a two week period, must have 5 of the symptoms which must cause distress or impairment and do not have another cause.

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17
Q

What do diagnostic specifiers aim to acheive?

A

They make the diagnostic more precise

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18
Q

What are some examples of diagnostic specifiers?

A

MDD with

  • Anxious distress
  • Atypical features
  • Post-partum onset
  • Seasonal pattern
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19
Q

What are some diagnostic specifiers to do with the severity/course of the MDD?

A
  • Mild
  • Moderate
  • Severe
  • With Psychosis
  • In partial remission
  • In full remission
  • Single/recurrent
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20
Q

How does NICE diagnose MDD?

A
  • Uses the DSM-5
  • Based on the Patient Health Questionnaire 9 further stratifies depression as:
  • Less severe (PHQ-9<16)
  • More severe (PHQ-9>16)
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21
Q

What is another name for bipolar disorder?

A

Manic depression

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22
Q

What two periods of mood does bipolar consist of?

A

Depressive episodes

and

Manic episodes

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23
Q

How are the depressive episodes of bipolar disorder diagnosed?

A

Using the same criteria as MDD

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24
Q

What percentage of people with bipolar disorder attempt suicide?

A

35%

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25
Q

What is the key diagnostic criteria for bipolar disorder manic episodes?

A
  • Abnormally elevated, expansive or irritable mood and persistently increased activity or energy, present most of the time for at least a week
  • Need three or four (if irritable mood) of the other critereon
  • Episode causes marked impaiment to functioning or has psychotic features
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26
Q

List some diagnostic criteria for manic episodes

A
  • Inflated self esteem, grandiosity
  • Decreased need for sleep
  • More talkative than usual
  • Flights of ideas, racing thoughts
  • Distractibility
  • Increase in goal directed activity or psychomotor agitation
  • Excessive involvement in damaging activities
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27
Q

What are two mania subtypes?

A
  • Hypomania
  • Mixed episode
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28
Q

What is Hypomania?

A
  • Often seen as a personality trait rather than a disorder
  • Mildly elevated mood and energy levels
  • Must produce definite change in functioning that is noticeable by others
  • Impairment not so great: individuals can be highly productive whilst hypomanic
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29
Q

What is mixed episode as a mania subtype?

A
  • Patient has elevated energy levels, psychosis but is simultaneously depressed
  • Even higher risk of suicide
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30
Q

What are the 3 Bipolar disorder subtypes?

A
  • BP type 1
  • BP type 2
  • Cyclothymia
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31
Q

What are the characteristics of BP type 1?

A
  • ‘Classic manic depression’
  • Also a possibility of rapid cycling (>4 episodes in a year)
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32
Q

What are the characteristics of BP type 2?

A
  • Depressive episodes and hypomania
  • Can also get rapid cycling (>4 episodes in a year)
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33
Q

What are the characteristics of Cyclothymia?

A
  • Mild depression and hypomania for more than 2 years
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34
Q

What does BP disorder being labelled the ‘mad genius’ condition mean?

A

There is a link between BP disorder to creativity

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35
Q

Which areas of the brain atrophy during MDD?

A
  • Prefrontal cortex
  • Hippoampus
  • Anterior Cingulate Cortex
  • Amygdala
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36
Q

What happens to hippocampal volume in MDD when people are not treated?

A

Hippocampus decreases by about 30%

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37
Q

What occurs to glucose metabolism in the prefrontal cortex during MDD and why is this linked to MDD?

A

There is lower glucose metabolism due to the reduction of cell numbers in that region

Prefrontal cortex exerts inhibitory control of the hypothalamus (regulates cortisol) and emotion- therefore it is less regulated when less metabolism

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38
Q

What happens to brain activity of the PFC in the different phases of bipolar disorder?

A
  • Activity is decreased during a depressive phase
  • Activity is increased during a manic episode
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39
Q

What can happen to MDD if the Ventral PFC is lesioned?

A

Can illeviate the depression

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40
Q

How is the Amygdala functionally different in depression?

A

Volume is reduced in major depressive disorder

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41
Q

How is Amygdala activity different in major depressive disorder?

A

The amygdala is overactive to sad stimuli and underactive to happy stimuli

Due to endocrine ties, the amygdala when overactive influences the production of cortisol

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42
Q

What is the monoamine hypothesis?

A

MDD is the dysfunction of serotonerfic and noradrenergic transmission

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43
Q

What is chronic stress as a mechanism of depression?

A
  • Dysfunction of the HPA axis
  • Errors witht the prefrontal cortex and hippocampus
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44
Q

What is Iproniazid?

A
  • Developed to treat TB
  • Patients seemed innapropriately happy
  • Approved as an anti depressant in 1958
  • Is an irreversible MAO inhibiter
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45
Q

What is Reserpine?

A
  • Early antihypertensive and antipsychotic
  • Blocks vesicular monoamine transporter (VMAT) and depletes MA
  • Suggested to cause depression
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46
Q

What occurs when there is a depletion of tryptophan?

A
  • Lowers mood
  • Induces relapse
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47
Q

What are two bits of supporting evidence for the monoamine hypothesis?

A
  • Almost all antidepressant drugs act by altering serotonergic or noradrenergic transmission
  • Effects on transmission are very quick
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48
Q

What is the main problem with the monoamine hypothesis?

A
  • Antidepressant effects are delayed by 2-4 weeks
  • The hypothesis tries to explain this by changes in receptor expression and desensitizatoin
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49
Q

What does HPA stand for?

A

Hypothalamic Pituitary Adrenal Axis

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50
Q

What hormone does the hypothalamus produce in the HPA axis and what does it target?

A
  • CRF (Cortisol releasing factor)
  • Targets the anterior pituitary gland
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51
Q

What hormone does the pituitary gland produce in the HPA axis and what does it target?

A
  • ACTH (adrenocorticotrophic hormone)
  • Targets the adrenal cortex
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52
Q

What hormone does the adrenal cortex produce in the HPA axis and where does it act?

A
  • Cortisol
  • Acts as a negative feedback loop to glucocorticoid receptors in the hypothalamus and pituitary gland
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53
Q

How can we increase cortisol production via the HPA axis?

A
  • Increase stress
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54
Q

What percentage of depressed patients have hyperactivity of the HPA axis?

A

50

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55
Q

What percentage of severely depressed patients have HPA axis hyperactivity?

A

80

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56
Q

What is the Dexamethasone suppression test?

A
  • Dexamethosome is a potent syntheic glucocorticoid which acts on receptors in the pituitary and hypothalamus
  • It acts to reduce the cortisol
  • In a control it will reduce their cortisol by 85%
  • In a depressed individual it will decrease cortisol byb 45% (negative feedback loop isn’t working correctly)
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57
Q

How does chronic stress reduce the feedback loop?

A

Elevated levles of hydro cortisol over a long period of time compromises the feedback loop and dramatically increases cortisol and CRF

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58
Q

What two areas important for emotion regulation have receptors for cortisol and what does increased cortisol cause in these areas?

A
  • Hippocampus
  • Prefrontal cortex
  • Both have increased apoptosis
  • Both have decreased neurogenesis
  • Causing atrophy and depression
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59
Q

What is Cushing’s syndrome?

A
  • Increased cortisol, with long term glucocorticoid treatment
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60
Q

What is a common co-morbidity with cushing’s disease?

A

Depression

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61
Q

What areas act to regulate the HPA axis and no longer do this in depressed individuals?

A
  • Prefrontal cortex
  • Hippocampus
  • Amygdala
  • Loss of regulation into the hypothalamus
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62
Q

What is the main genetic factor associated with the HPA axis problem?

A

Polymorphisms in HPA genes

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63
Q

What causes epigenetic factors in the HPA axis problem?

A
  • Childhood trauma and deprivation
  • These cause hyperactivity of the HPA which can persist into adulthood
  • Can even predict later depression based on these early origins
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64
Q

How do antidepressant drugs work to regulate the HPA axis?

A
  • Act via monoamine transmission, infleuncing the rate of apoptosis and neurogenesis
  • These then restore structures of the brain
  • When these are bacl working, the HPA axis may come under control and will further promote neurogesis and decrease apoptosis
  • This decreases the cortisol and CRF levels
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65
Q

What is concordance in terms of twin studies?

A

The percentage chance that one twin will develop a disorder if the other twin already has it

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66
Q

What can be assumed if concordance rate is 100%?

A

A concordance of 100% prodives strong evidence for the involvement of genetic factors

67
Q

What can be assumed if the concordance rate is less than 100%?

A

If the prevalence is greater than the disease in the general population suggests that there may be genetic factors at play

68
Q

What is an issue with twin studies?

A

They are prone to confounding factors, especially as identical twins often have very similar environements in early life

69
Q

What are the benefits of Genome Wide Association studies?

A

Can use a larger study population than twin studies

70
Q

What is an issue of genome wide association studies?

A

Has confounding studies that make interpretation of the data difficult

71
Q

What are the overall results of genetic identification factors?

A

Around 40% of the risk of major depressive disorder is genetic

There is no single depression gene but a large number of genetic differences

72
Q

By how much does a polymorphism in SERT increase the risk of depression?

A

20%

73
Q

What type of polymorphisms are linked to depression in the dopiminergic pathway?

A
  • Dopamine transporter (DAT)
  • Dopamine D4 receptor
74
Q

What gene polymorphisms affect the HPA axis?

A
  • Mineralocorticoid receptor
  • Corticotrophin releasing hormone receptor
  • FKBP5
75
Q

What does the FKBP5 protein do?

A

Modulates the sensitivity of the glucocorticoid receptor

76
Q

What part of the G protein has associations with depression when there is a polymorphism?

A

Subunit beta 3

77
Q

How is Methylenetrahydrofolate reductase linked to depression?

A
  • Mutations to this have been linked to depression and other psychiatric problems
  • The exact mechanism is unclear but it could be that this impacts on the ability to metabolise folate and might compound environmental factors such as childhood neglect.
78
Q

What percentage of bipolar disorder is heritable according to twin studies?

A

80%

79
Q

What are 3 major genes involved in the development of major depressive disorder found by gene wide association studies?

A
  • ANK3
  • CACNA1C
  • TRANK1
80
Q

What does ANK3 do?

A

Codes for ankyrin B which is a protein involved in neuronal myelination

81
Q

What does CACNA1C do?

A

Codes for a voltage sensitive calcium channel that is known to be expressed in the brain and which may have roles in both development and signalling

82
Q

What does TRANK1 do?

A

Expression of its produt is increased by mood stabalizers such as sodium valproate, perhaps offering clues to the mechanism of action of these drugs in bipolar disorder

TRANK1 is also associated with schizophrenia

83
Q

What is learned helplessness?

A

The idea that when it is not possible to immediately overcome a stressor, it is better to conserve energy in order to survive

84
Q

How is learned helplessness an evolutionary advantage?

A

In our ancestral societies food supplies were frequently precarious so withdrawing from day to day activities may have helped to conserve energy

85
Q

What is sickness behaviour?

A

People with depression have similar behavioural patterns to people suffering from physical illness

In primitive societies,the best strategy if you were ill would have been to stay put and not expose yourself to dangers from predators

86
Q

How does sickness behaviour help to explain high levels of anxiety in depression?

A

Anxiety is a state of hypervigilance and that would have an evolutionary advantage if you were sick and sheltering from danger

87
Q

What is the animal model of acceptance of subservient position?

A

Place young rats in a cage with a dominant male rat

The best way for someone in a position like this is to be subservient and accept their position

Sadly, ,this is a facet of ancient behaviour that still permeates many parts of modern society

88
Q

How can depression serve as a benefit?

A
  • It has been shown in some studies that people who are depressed are actually better at solving certain kinds of problems than non-depressed individuals
  • By shutting down other behaviours, depression may allow us to focus on certain types of problems and find a solution
  • This may be particularly important in solving social dilemmas e.g. whether to stay in a relationship
89
Q

What type of diagnostic techniques are the DSM-5 and the ICD-11?

A

Symptom counts

90
Q

What is a common UK questionnaire based depression rating scale?

A
  • The Patient Health Questionnair 9
  • It breaks down the DSM-5 symptom list which breaks each symptom into how frequently a patient experiences it
91
Q

What is a new NICE questionnaire based depression rating scale?

A

The Hamilton Depression Rating Scale (HDRS or HAM-D)

92
Q

Where are four potential monoamine drug sites for MDD?

A
  • MAOA (outer MT membrane)
  • Re-Uptake (SERT, NET)
  • Post-synaptic receptor
  • Autoreceptor
93
Q

What are two potential monoamine drug sites for bipolar disorder?

A
  • Intracellular signalling
  • Presynaptic ion channels
94
Q

What are two types of monoamine oxidase?

A

A and B

95
Q

Where does monoamine oxidase A act?

A
  • CNS: 5HT, NA, dopamine
  • Periphery: dietary monoamines
96
Q

Where does monoamine oxidase B act

A
  • CNS: primarily dopamine
  • Periphery: dietary monoamines located on outer mitochondrial membrane
97
Q

What is the effect of inhibiting Monoamine oxidase?

A
  • Increases presynaptic monoamine
  • The effect in monoamine is immediate but take 2 weeks for a clinical effect
98
Q

What are some examples of non selective (A vs B) irreversible inhibitors?

A
  • Phenelzine
  • Tranylcypromine
  • Isocarboxazid
99
Q

What disorders are non selective irreversible inhibitors very effective at treating?

A
  • MDD
  • Bipolar (+ mood stabalizer)
  • Anxiety disorders
100
Q

Why are doctors reluctant to prescribe non selective irreverisble inhibitors?

A

Due to the large number of interactions, especially dietary

101
Q

What is Tyramine?

A

A dietary monoamine found in high concentrations in mature cheeses

102
Q

What normally breaks down Tyramine?

A

Normally broken down in the liver by MAO

103
Q

What happens to tyramine when MAO-A is inhibited?

A

Tyramine from the diet can cause big problems

104
Q

What is the cheese reaction?

A
  • Tyramine when not broken down acts as a false substrate for NET and is taken into the presynaptic nerve terminals as sympathetic neruons
  • It is then taken into vesicles and displaces noradrenaline from the vesicles
  • Noradrenaline is then released non vesicularly and can result in stroke and even death
105
Q

What causes serotonin syndrome?

A

When an SSRI or tricyclic antidepressant is saken alongside a MAOI

There is a massive increase in synaptic serotonin

106
Q

What are the symptoms of serotonin syndrome?

A
  • Confusion, agitation
  • Muscle twitching, sweating
  • Seizures, arrhythmias, coma (death)
107
Q

What is Moclobemide?

A
  • Selective for MAO-A
  • Reversible
  • Very few adverse effects
  • Relatively fast onset
  • Useful in MDD, bipolar (plus mood stabalizer) and anxiety disorder
108
Q

What gene is the cause of the warrior gene?

A
  • In the promotor of monoamine oxidase A, there is a 30 base repeated sequence
  • The number of copies varies from 2-5
  • Alleles that result in low expression such as the 2 repeat variant (2R)
109
Q

What does SSRI stand for?

A

Selective serotonin reuptake inhibitors

110
Q

What does SNRI stand for?

A

Serotonin/Noradrenaline reuptake inhibitors

111
Q

What does NRI stand for?

A

Noradrenaline reuptake inhibitor

112
Q

What generation of drug are SSRIs?

A

2nd generation antidepressant drugs

113
Q

What are the most commonly used antidepressant drugs?

A

SSRIs

114
Q

What are 4 examples of SSRIs?

A
  • Citalopram
  • Paroxetine (Paxil)
  • Sertaline
  • Fluoxetine (Prozac)
115
Q

Give 2 examples of SNRIs

A
  • Venlafaxine
  • Duloxetine
116
Q

What are two examples of NRIs?

A
  • Reboxetine
  • Atomoxetine
117
Q

What are the SSRIs, SNRIs and NRIs useful for treating?

A
  • MDD
  • Anxiety disorders
  • Premature Ejaculation
118
Q

Why are the second generation drugs better than the first generation ones?

A

Much lower overdose suicide risk than TCA and older MAOI

Much lower side effects

119
Q

How do the 2nd/3rd generation drugs act at the synapse?

A

Block the re-uptake transporters (SERT, NET) to increase the synaptic concentrations of the neurotransmitter

120
Q

What are the side-effects of the 2nd and 3rd generation drugs?

A
  • Nausea, anorexia
  • Insomnia
  • DIscontinuation syndrome
  • Sexual side effects
  • Increased aggression, suicide ideation, self-harm in the early stages
121
Q

Which SSRI is recommended by NICE for young people?

A

Fluoxetine

122
Q

What are the Tricyclic Antidepressants?

A
  • First line treatment for MDD
  • ‘dirty drugs’ (effects at mAChR, H receptors, 5HT receptors and alpha 1 adrenergic)
  • Many side effects plus high suicide mortality in overdose
  • Now largely replaced by SSRIs and SNRIs
123
Q

What can Tricyclic antidepressants be used to treat?

A
  • Treatment resistant MDD
  • Pain
  • Migraines
124
Q

What are three examples of Tricyclic antidepressants?

A
  • Amitriptyline
  • Nortriptyline
  • Imipramine
125
Q

How do the Tricyclic antidepressants act at the synapse?

A

Inhibit SERT and NET to increase neurotransmitter concentrations

126
Q

What is the percentage of people that experience antidepressant discontinuation syndrome?

A

50

127
Q

What are the symptoms of antidepressant discontinuation syndrome?

A
  • Flu
  • Insomnia
  • Motor problems
  • Cognitive problems
  • Brain zaps
128
Q

What are brain zaps?

A

Electric shock like sensations that begin in the head and spread across the body

129
Q

How long do brain zaps usually last?

A

1-4 weeks but can be lessened by tapering the dose

130
Q

What are the worst two antidepressants for discontinuation syndrome?

A
  • Duloxetine
  • Venalafaxine
131
Q

Which two SSRIs are the worst for discontinuation syndrome?

A
  • Citalopram
  • Paroxetine
132
Q

What is the oppositional tolerance model?

A

When a drug perturbs the neurotransmitter systens, the brain will down or up regulate components of the system to try and oppose the actions of the drug

133
Q

What type of drug is Mirtazapine?

A

Noradrenergic and Specific Serotonergic Antidepressant (NaSSA)

134
Q

What does Mirtazapine do?

A

Antagonist of alpha 2 adrenoreceptors and 5HT2A and C receptors

135
Q

Why is Mirtazapine highly sedating?

A

Has a high affinity for H1 histamine receptors

136
Q

What effects does Mirtazapine cause?

A
  • Appetite increase
  • Discontinuation syndrome
  • Highly sedating
137
Q

What are the benefits of Mirtazapine?

A
  • Generally very effective and well tolerated
  • Faster onset of action than other AD drugs
138
Q

How does Mirtazapine act at the synapse?

A
  • On presynaptic nrve terminals there are alpha 2 adrenoreceptors which inhibit neurotransmitter release
  • In noradrenergic terminals they act as inhibitory auto-receptors
  • In serotonergic termonals, they respond to noradrenaline from neighbouring terminals
  • There is an increase in the release of monoamine
  • Also, post synaptically (involved in odd when overactive)
  • Act as an antagonist of 5HT3 receptors
  • Actions here produce anti-emetic effects (reduce nausea and vomiting)
139
Q

What is Esketamine?

A

Is the S-enantiomer of the dissociative anaesthetic ketamine (which is racaemic)

140
Q

How fast is the antidepressive effect of ketamine and esketamine?

A

4 hours after the dose is administered

141
Q

How is Ketamine administered?

A

Intravenously

142
Q

How is esketamine administered?

A

Nasal spray

143
Q

How do ketamine and esketamine act to produce an antidepressive effect?

A

Their actions as non-competative antagonists of NMDA receptors

144
Q

How long does a single dose of ketamine last?

A

At least 10 days

145
Q

What psychedelic drugs may be a viable way to treat depression?

A
  • LSD
  • Psilocybin
  • MDMA
146
Q

How do the psychedelic drugs act?

A

Through monoamines

147
Q

What is Agomelatine?

A
  • Moderately potent antagonist of the 5HT2 receptor
  • Melatonin receptor agonist
148
Q

What is Agomelatine licenced to treat?

A
  • MDD
  • Might be better tolerated than some of the other traditional drugs
149
Q

What are the NICE guidlines for less severe depression in adults?

A
  • Talking therapies
  • Drug therapies if a long waiting list
150
Q

What are NICE guidlines for more severe depression in adults?

A

Drug therapy combined with individual CBT

151
Q

What are the NICE guidlines for mild depression in children (5-18)?

A

Talking therapies only

152
Q

What are NICE guidlines for moderate to severe depression in children?

A
  • More intensive and longer courses of psychological therapies
  • Drugs but only in combination with the psychological therapies
153
Q

What drug is recommended for children with depression?

A

Fluoxetine

154
Q

What are used as mood stabalizing drugs in bipolar disorder (prophylaxis)?

A
  • Lithium
  • Anticonvulsants (lamotrigine, valproate)
  • Olanzapine (antipsychotic)
155
Q

How is mania managed when treating bipolar?

A
  • Increase mood stabalizer
  • Antipsychotic (olanzapine, quetiapine)
  • May add lithium or valproate
156
Q

How is depression managed in bipolar disorder?

A
  • Add olanzapine and fluocetine or quetiapine to existing drugs
  • Caution is advised as antidepressants can cause mania
157
Q

How does lithium act?

A
  • Inhibition of IP3 pathway
  • Neurotrophic factors
  • Inhibition of glycogen synthase kinase -3
  • Modulation cAMP signalling
158
Q

What are some issues with Lithium?

A
  • Narrow therapeutic window (need to monitor plasma levels)
  • Lots of adverse effects
159
Q

What is the aim of NHS’s Improving Access to Psychological Therapies scheme?

A

Target of seeing 90% of patients within 6 weeks

160
Q

When is Electo-convulsive therapy used?

A

For treating life threatening mental health conditions or when other treatments have failed

161
Q

How is modern Electro-convulsive therapy carried out?

A

Under the use of anaesthetics and muscle relaxants

162
Q

What are the remission rates of electro-convulsive therapy?

A
  • 52% for MDD and bipolar disorder
  • > 70% of patients see an improvement
163
Q

What side effects does electro-convulsive therapy produce?

A
  • Memory loss
  • Can be transient, or even permanent
  • Nausea
  • Loss of appetite
  • A headache
  • Confusion/drowsiness
  • Long term cognitive problems
  • Blunting of emotional responses

Drugs and the Brain (9 decks)

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