Depression Flashcards

(57 cards)

1
Q

What is the prevalence of depression/anxiety in the UK?

A

1 in 4

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2
Q

What is the difference between anxiety and depression?

A

Anxiety is a fear of what might happen in the future where depression is past/present

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3
Q

Describe the hypothalamic-pituitary-adrenal (HPA) axis in depression

A

HPA hyperactivation. Increased CRH, ACTH and cortisol, along with enlarged pituitary and adrenal glands. Impaired negative feedback

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4
Q

What is the target for the HPA axis with antidepressants?

A

Enhance negative feedback and reduce HPA axis hyperactivity

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5
Q

What is BDNF?

A

Brain derived neurotrophic factor - regulates neurogenesis and development

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6
Q

Explain the neurotrophic hypothesis of depression?

A

Proposes that depression is associated with reduced brain BDNF levels. Antidepressants aim to increase BDNF levels

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7
Q

What is the first line option of pharmacological treatment of depression?

A

Selective serotonin reuptake inhibitors (SSRIs) - citalopram, fluoxetine…

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8
Q

How do SSRIs work?

A

Block the serotonin reuptake in he presynaptic nerve terminal, maintains a high level of serotonin levels in the synaptic cleft

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9
Q

Why do SSRIs take 4-6 weeks to work?

A

Because SSRIs change the genetic code that codes for serotonin reuptake transporters. It takes a while to phase out the old transporter molecules

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10
Q

What antidepressant would be used to treat under 18s?

A

Fluoxetine if needed

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11
Q

What are SNRIs and how do they work?

A

Serotonin-noradrenaline reuptake inhibitors. Block the serotonin/noradrenaline reuptake transporter in the presynaptic membrane

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12
Q

What are TCAs and how do they work?

A

Tricyclic antidepressants. Inhibit serotonin and noradrenaline reuptake (e.g. amitryptyline)

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13
Q

What are MAOIs and how do they work?

A

Monoamine oxidase inhibitors (e.g. phenelzine). Monoamine oxidases are enzymes which usually inactivate excess neurotransmitters. Inhibitors work by binding with the enzyme to cause irreversible inactivation

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14
Q

What is the MAOI ‘cheese reaction’?

A

Tyramine (found in food such as aged cheeses) usually degraded by MAOs in the gut. Inhibition of MAOIs mean increased tyrosine which causes the release of stored catecholamines, leading to a hypertensive crisis.

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15
Q

What pharmacological treatment would you use to treat symptoms of anxiety?

A

β-adrenoceptor antagonists (propranolol) to manage autonomic symptoms

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16
Q

What is GABA?

A

γ-aminobutyric acid. Major inhibitory neurotransmitter in the CNS

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17
Q

How do benzodiazepines work?

A

Positive allosteric modulators on GABAa receptor complex. Bind between α and γ subunits leading to a conformational change allowing GABA to bind. GABA binding = conformational change and a greater flow of Cl- into neurone leading to hyperpolarisation and inhibition

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18
Q

What is the structure of the GABAa receptor?

A

Ligand gated chloride selective channel. 2 α and β subunits and 1 γ subunit

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19
Q

Give some examples of benzodiazepines

A

Lorazepam, diazepam, chloridazepoxide

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20
Q

Why are benzodiazepines short term use only?

A

Because they change the functioning of the brain and lead to drug dependence

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21
Q

What is bipolar disorder?

A

Cycle between depressed mood and mania

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22
Q

How would you treat bipolar disorder?

A

Mania phase - antipsychotics
Depression phase - antidepressants

Long term treatment includes use of lithium

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23
Q

What is the limbic system?

A

A transitional position between subcritical nuclei and neo-cortex

24
Q

What are the two types of declarative memory?

A

Semantic - the Eiffel Tower is in Paris

Episodic - I kissed my love under the Eiffel

25
What part of the limbic system is key to episodic memory?
Hippocampus
26
What is long term potentiation?
Synaptic plasticity is the basis of long-term memory. Long lasting change in synaptic funtion
27
What would be a common effect if hippocampus disorder?
Memory impairment
28
What is the amygdala?
Collection of subnuclei that receive multiple sensory and limbic inputs and coordinate an emotional response. Special role in fear
29
What is Kluver-Bucky syndrome?
Bilateral temporal lobe resection removing amygdala. Effects include: Docile behaviour Hypersexuality Lost ability to discriminate between edible and inedible
30
How do we measure sleep?
Using an electro-encephalogram (EEG) to record electrical activity
31
Describe the different stages of a sleep cycle
Stage 1 - theta waves prominent Stage 2 - mixed EEG activity Stage 3 and 4 - slow-wave with more delta waves REM sleep - low-voltage, high frequency waves
32
How does REM duration change during sleep period?
Progressively longer duration through each cycle
33
What are the results of sleep deprivation?
``` Increased sleep time Decreased glucose metabolism in brain Mood changes Higher level cognitive functioning disrupted Perceptual changes ```
34
What are the contributing factors to insomnia?
Distress Organic cause (e.g. depression) Poor sleep management Pain
35
What is the target for treating insomnia?
Treat cause not symptom. Primary target is non pharmacological
36
What are the P’s for good sleep hygiene?
``` Psychological - decrease stress Physiological - increase relaxation Pharmacological - decrease caffeine, alcohol, nicotine Psychiatric - anxiety/depression Physical - decrease pain ```
37
What is the physiological difference between REM and non-REM sleep?
REM sleep - fluctuating HR, BP and resp rate. Skeletal muscles relaxed but some movements may occur Non-REM sleep - steady HR, BP and resp rate. Muscles relaxed
38
How is sleep induced in the brain?
Ventrolateral preoptic nucleus (VLPO) neurons activated and induce sleep. Inhibit arousal centres
39
How is wakefulness induced in the brain?
Ventrolateral preoptic nucleus (VLPO) neurons inhibited and cerebral cortex activated
40
How is adenosine related to sleep?
Levels increase during sleep and decreased during wakefulness. Caffeine is an adenosine receptor antagonist and reduces sleepiness
41
Where in the brain is circadian drive regulated (body’s ‘master clock’)?
Hypothalamic suprachiasmatic nucleus (SCN)
42
How is REM sleep induced?
Pons increases firing and ACh release
43
How is non-REM sleep induced?
Raphe nucleus and locus coeruleus release 5HT and NA and decrease firing of pons cells
44
What are the advantages and disadvantages of using benzodiazepines to treat sleep disorders?
Lethal dose very high Small effect in sleep pattern Few side effects Hang-over Dependence and withdrawal
45
What drugs would you use to treat sleep disorders?
Benzodiazepines or Z-drugs (zopiclone) | Barbiturates (no longer used)
46
What are Z-drugs?
Not benzodiazepines but bind to same site on GABAa receptor
47
How does the mini-mental state exam assess mental state?
Points awarded for certain responses to questions and then total score used to discriminate
48
What is operant conditioning?
A to B to C where: A = stimulus B = behaviour C = consequence
49
What is systematic desensitisation (counter-conditioning)?
Training patients to associate alternative response to stressful stimulus (e.g. deep muscle relaxation)
50
What is Beck’s negative triad of depression?
Negative thoughts about: Oneself The world The future
51
What is the basis of cognitive behaviour therapy (CBT)?
Behaviour is learnt and can therefore be re-learnt or reconditioned
52
What are the advantages of cognitive behavioral therapy?
Focus on ‘here and now’ Short term structure Collaborative approach
53
What are the drawbacks to cognitive behavioural therapy?
May not be suitable for people with more complex mental health problems. Doesn’t address problems from the past
54
What are the 6 basic emotions?
``` Happiness Sadness Fear Anger Disgust Surprise ```
55
What is the James-Lange theory of emotion processing?
We feel emotions based on feedback of physiological response (e.g. we feel sad because we cry)
56
What is the Lazarus theory of emotion processing?
Primary appraisal - ‘Am I in trouble?’ Secondary appraisal - ‘What can be down about it?’ Coping mechanism, either positive or negative
57
What is the Canon-Bard theory of emotion?
Physiological changes and emotional response to a stimulus are separate and independent