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Disease in the brain > Depression & bipolar (done) > Flashcards

Depression & bipolar (done) Flashcards

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1
Q

What is depression?

A
  • More than simply feeling unhappy or fed up for a few days
  • Patients persistently feel sad for weeks or months
  • Real illness w underlying neurobiology
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2
Q

What is bipolar disorder?

A

A mental health condition that affects moods, which can swing from one extreme to another

Used to be known as manci depression

Symptoms depend on which mood patient is currently experiencing - each extreme can last for several weeks

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3
Q

What are the episodes that ppl with bipolar disorder suffer from?

A
  • Depression
  • Mania - feeling very high & overactive
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4
Q

What are the 2 symtoms that must be expereinced in depression?

A

At least 1 of these 2 to be diagnosed:

  • Depressed mood
  • Loss of interest of pleasure
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5
Q

What are the 9 symptoms of depression in the DSM-V?

A
  • Depressed mood
  • Loss of interest or pleasure
  • Change in weight or appetite
  • Insomnia or hypersomnia
  • Psychomotor retardation or agitation
  • Loss of energy or fatigue
  • Feeling of worthlessness or guilt
  • Impaired concentration or indecisiveness
  • Suicidal ideation / suicide attempt
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6
Q

How many of the 9 symptoms of depression listed int he DSM-V are required for depression diagnosis?

A

At least 5 of 9

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7
Q

What is the main requirement to be diagnosed with bipolar disorder?

A

Subgroups all include manic episode:

Abnormally & persistently elevated/irritable mood lasting at least a week & present most of the day nearly every day

& at least 3 of the 7 symptoms listed in DSM-V

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8
Q

What are the 7 symptoms for bipolar disorder listed in the DSM-V?

A
  • Inflated self esteem & grandiosity
  • More talkative than usual or pressure to keep tlaking
  • Dec need for sleep
  • Flight of ideas or subjective experience that thoughts are racing
  • Distractability
  • Increase in goal-directed activity
  • Excessive involvement in activities w high potential for painful concequences
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9
Q

Who made the monoamine hypothesis of depression?

A

Schildkraut - 1965

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10
Q

What were the 2 main parts of the monamine hypothesis?

A

1 –> Depression due to functional DEFICIT of MOA tranmitters & mania due to funtional EXCESS

2 –>
Drugs that ince MOA neurotransmission inc mood

Drugs that dec MOA neurotransmission dec mood

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11
Q

What are the drugs that inc MOA neurotransmission to inc mood in the MOA hypothesis?

A
  • Tricyclic antidepressants (TCAs) that blcok reuptake
  • MOA oxidase inhibitors (MAOI) that inhibit metabolism
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12
Q

What are the drugs that dec MOA neurotransmission to dec mood in the MOA hypothesis?

A
  • Reserpine, alpha-methyltyrosine & methyldopa that inhibit synthesis or storage
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13
Q

What are the shortcoming sof the MOA hypothesis of depression?

A
  • Doesn’t clarify pathophysiology of depression
  • Doesn’t explain delayed theraputic onset or treatment-resistance
  • Drugs like cocaine & amphetamine enhance MOA neurotransmission, but aren’t antidepressant
  • Some clinically effective antidepressants don’t affect MOAs
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14
Q

Give examples of delayed theraputic onset or treamtent resistance (a shortcoming) in the MOA hypothesis?

A
  • SSRIs elevate synpatic 5-HT within hours (& side effects appear)
  • Antidepressant effects take ~3 weeks & don’t occur in 30% of cases
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15
Q

What are the 3 other explanations for depression other than MOAs?

A
  • HPA axis
  • Neuroplasticity & neurogenesis
  • Inflammation
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16
Q

What is the HPA axis like in depressed patients?

A

They display HPA hyperactivation

This means they have impaired -ive feedback

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17
Q

What symptoms does HPA hyperactivity in depressed patients cause?

A
  • Inc cortisol in saliva, plasma & urine
  • Inc CRH in CSF & limbic brain regions
  • Inc size & activity of the pituitary & adrenal glands
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18
Q

How do antidepressants work on the HPA axis?

A

They enhance negative feedback to dec HPA axis hyperactivity

(Correct the overactivity in HPA - not so much cortisol being produced)

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19
Q

How does hippocampal volume change in depression patients?

A

Hippocampal volume dec by ~10% in depression

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20
Q

What are the 2 explanations of dec hippocampal volume in depression patients?

A
  • Neuroplasticity hypothesis
  • Neurogenesis hypothesis
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21
Q

What is the neuroplasticity hypothesis?

A

Atrophy of mature neurons (shortened dendrites, dec spine density)

Neuronal connectivity decreases

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22
Q

What is the neurogenesis hypothesis?

A

Dec adult neurogenesis leads to dec new neurons & neural precursors

(No atrophy, formation of new neurons inhibited)

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23
Q

What supports the neuroplasticity & neurogenesis hypotheses?

A

Both are supported by pharmacological evidence:

Ketamine (rapid onset antidepressant)
–> inc no. & fucntion of spines in PFC
–> Many antidepressants inc adult neurogenesis

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24
Q

Why are ketmaine studies good support fromt eh neurplasticity & neurogenesis hypothesis?

A

Ketmaine acts on glutamate receptors - not MAOs

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25
Q

What are examples inflammatory markers?

A

Cytokines, chemokines & acute-phase proteinsW

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26
Q

What are inflammatory marker levels like in depression?

A

Patients w depression have inc inflammatory markers

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27
Q

What have preclinical studies about inflammatory markers shown?

A

That these markers induce depressive symptoms

28
Q

How has cancer & hepatitis treatment shown evidence for inflammation in depression?

A

Inflammation can precipitate depression in hepatitis or cancer patients treated with IFNɑ or IL-2

29
Q

Which systemic diseases w inflammatory component are proof for inflammation in depression?

A
  • Rheumatoid arthiritis
  • Inflammatory bowl synrome (IBS)
30
Q

What is the 3 points of supporting evidence for inflammation causing depression?

A
  • Preclinical studies show inflammatory markers induce depressive symptoms
  • Inflammation causing depression in pateints being treated for cancer or hepatitis
  • Systmeic diseases with inflammatory component inc risk of depression
31
Q

What is the non-pharmacoloigcal treatment of depression?

A

Cognitive Behavioural Therapy (CBT)

32
Q

What is the aim of CBT?

A

Aims to stop negative cycle that influences emotion & behaviour

33
Q

What are the 4 components in the CBT cycle?

A
  • Thoughts
  • Moods
  • Physical functioning
  • Behaviours
34
Q

What are the 2 main modes of pharmacological treament for depression?

A
  • Inhibit reuptake of MOA NTs, to inc synaptic levels
  • Block presynaptic receptors that inhibit MOA release, to inc synaptic levels
35
Q

What mode were old pharmacological treatments of depression based on & why are these not used anymore?

A

Monoamine oxidase inhibitors (MOAI) e.g. phenelzine & tranylcypromine inhibit MOA metabolism (Inhibit the breakdown of MOA)

They can have serious side effects, including interactions with food so they aren’t used mucha anymore

36
Q

How do drugs that inhibit the reuptake of MOA NTs work?

A

More MOA levels in synapse = more bind on postsynaptic recpetors

Increases synaptic levels

37
Q

How do drugs that block presynaptic receptors that inhibit MOA release work?

A

They block presynaptic receptors that bind to MOAs & detect levels in the synsapse

When there are enought MOAs in synapse these receptors inhibit release of any more

These drugs block these receptors to inc synaptic levels of MOA

38
Q

What are the 5 pahmacological treatments for depression?

A
  • Selective serotonin reuptake inhibitors (SSRIs)
  • Tricyclic antidepressants (TCAs)
  • Serotonin-noradrenaline reptake inhibitors (SNRIs)
  • Noradrenaline reuptkae inhibitor
  • Mirtazapine
39
Q

What is the action of SSRIs & why are they used?

A
  • Inc synaptic 5-HT levles by inhibiting reuptake
  • First line option, favourale side-effect profile, less toxic in overdose
40
Q

Give some examples of SSRIs:

A
  • Citalopram
  • Fluoxetine
  • Paroxetine
  • Sertraline
41
Q

Why aren’t SSRIs always the best treatment option for those who need instant treatment?

A

Effects aren’t instant - have to be taken dialy for 3 weeks b4 we know if they’ll work

42
Q

Why is it thought that SSRIs take 3 weeks to work?

A

They inhibit SERT(?) transporter = more 5-HT binds to postsynaptic

This also means more availble to bind to presynaptic receptors, reduces 5-HT in synpase due to feedback

Over the 3 week the presynaptci receptors desensitise - then beneficial effects seen

43
Q

Give examples of tricyclic antidepressants:

A
  • Amitryptyline
  • Imipramine
44
Q

What action do tricyclic antidepressants have?

A

Inc synaptic 5-HT & NA levels by inhibiting reuptake

(Not selective so block both 5-HT NA)

45
Q

What are the side effects of tricyclic antidepressants like?

A
  • Sedative side effects (H1 antagonism)
  • Anticholinergic side effects (dry mouth & blurred vision)
  • Cardiovascular effects can be fatal in overdose
46
Q

Give examples of SNRIs:

A
  • Venlafaxine
  • Duloxetine
47
Q

What is the action of SNRIs?

A

Inc synaptic 5-HT & NA levels by inhibiting reuptake - so cna be more effective than SSRIs

48
Q

What are the side effects of SNRIs?

A

Targetting NA can inc BP

49
Q

Give an example of a noradrenaline reuptake inhibitor:

A

Reboxetine

50
Q

What is the action of mirtazapine?

A

Enhances NA & 5-HT release by blocking presynaptic ɑ2 & 5-HT2 receptors that inhibit NA & 5-HT release

51
Q

What are the sedative side effects of mirtazapine?

A

They have sedative side effects –> can help with sleeping difficulties

Although can cause excessive sleepiness & weight gain too

Many pateints will stop taking these due to the side effects

52
Q

What are the 3 next generation treatments for depression?

A
  • Ketamine (glutamate NMDA receptor antagonist)
  • Vagal nerve stimulations for treatment-resistant depression
  • Pscyhedelics (5-HT2A receptor agonist)
53
Q

How is ketamine being used as a next generation treatment?

A
  • Low dose infusions thru IV have rapid-onset effects that last weeks–>months
  • Mechanisms may invovle mTOR signalling & BDNF
54
Q

What are the drawbacks of using ketamine as a treatment for depression?

A
  • Will the treatment given last and can it be repeated on the same patient for a long term solution? We are unsure
  • Patient must come to hospital to receive transfusion
55
Q

When is vagal nerve stimulation used to treat depression patients?

A

Used for ppls who don’t react to drugs etc

56
Q

Give an example of psychidelics used to treat depression:

A

Psilocybin –> COMP360 currently in phase III clinical trials

57
Q

How promising is psychedelic treatment?

A

Good effects found & promising results in small scale trials in depression patients

Ppl are supported thru the treatment & experience –> is it the drug that helps them or the therapy in the psychidelic state

Either way it seems to work

58
Q

What are the 3 types of drugs used to treat mania in bipolar disorder?

A
  • Lithium
  • Antipsychotics
  • Anticonvulsants
59
Q

What action does lithium have for treating mania in bipolar disorder?

A

Reduces excitatory DA & glutamate neurotransmission, inc inhibitory GABA neurotransmission

It has a narrow theraputic window so careful monitoring is essential

60
Q

What is the theraputic window for lithium treatment for mania?

A

Between 0.5mmol/L & 1mmol/L

61
Q

What happens if too much/too little lithum given to bipolar patient?

A

Too little = ineffective

Too much = toxic & can lead to death

62
Q

Give examples of antipsychotica used to treat mania in bipolar disorder:

A
  • Olanzapine
  • Quetiapine
  • Risperidone
  • Cariprazine
63
Q

What action do antipsychotics have in treating mania in bipolar patients?

A

Reudce MOA activity –> D2 & 5-HT2A receptor antagonists

64
Q

What are the side effects of antipsychotics in treating mania in bipolar patients?

A

Side effectsinclude weight gain

65
Q

Give examples of anticonvulsants to treat mania in bipolar patients?

A
  • Valproate
  • Carbamazepine
  • Lamotrigine
66
Q

What are the negatives of anticonvulsants to treat mania in bipolar patients?

A

Valproate cannot be taken when pregnant –> causes birth defects & developmental disorders

Those who do take it need at anti-pregnancy plan when on the drug

Disease in the brain (22 decks)

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