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Lernmaterialien für Geist - Pxsxyxcxh an der Fachhochschule der Diakonie

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How do we diagnose depression?

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  • Core symptoms (min.2)
    1. Depressed mood
    2. Anhedonia – lack of pleasure
    3. Anergia - lack of energy
  • Additional symptoms ( 2 or more)
    1. increased/decreased appetite
    2. poor concentration
    3. guilt
    4. worthlessness
    5. hopelessness
    6. disturbed sleep
    7. slowing of movements
  • > 2 weeks
  • associated occupational and social impairment
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What are the main hypotheses of the aetiology of depression? (6)

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  1. Monoamine deficiency
  2. Circadian Rhythms
  3. HPA axis disturbance 
  4. Cortical abnormalities
  5. Genetic vulnerability (Kindling hypothesis)
  6. Reduced GABAergic activity 
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TESTE DEIN WISSEN

Explain the important facts about the monoamine deficiency (depression)?

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  • deficiency in neuroamines
  • this leads to receptor upregulation on post-synaptic membrane
  • drugs that increase neuroamine levels can reduce depressive symptoms
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Explain the important facts about the circadian rhythms theory (depression)?

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  • no deep sleep
  • problems falling asleep
  • early waking up
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Explain the important facts the HPA axis hypothesis (depression)?

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  • Overreactive HPA circuit in depressed patients 
  • lack of neg. feedback exerted by cortisol on hypothalamus/pituitary
  • increased cortisol: increased stress
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Explain the important facts about the cortical abnormality hypothesis (depression)?

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  • changes in thickness 
  • reduced neurogenesis and neuroplasticity in hippocmapus
  • less remodelling
  • shrinking of hippocampus
  • reduction of intracellular growth promotors
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Explain the genetic vulnerability hypothesis (depression)?

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  • Kindling hypothesis
  • genetic predisposition interact with environmental factors
  • this leads to alerted neurochemistry and neurobiology
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What are pharmacological treatment options for depression?

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  • SSRIs - Selective Serotonin reuptake inhibitors
  • SNRIs - Serotonin - noradrenaline reuptake inhibitors
  • TCAs - Tricyclic antidepressants
  • MAOI - Nonoamine oxidase inhibitors
  • Atypical:bupropion, stimulants, lithium, mirtazapine
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What are SSRIs and what are their main features?

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  • Selective serotonin reuptake inhibitors
  • M:  inhibits the reuptake of serotonin from the synaptic cleft by Serotonin transporter SERT in pre-synaptic neurone
  • S/E: sexual dysfunction
  • Safe in overdose 
  • e.g. fluoxetine, sertraline, paroxetine
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What are SNRIs and what are their main features?

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TESTE DEIN WISSEN
  • SNRIs = Serotonin-noradrenaline Reuptake Inhibitors
  • inhibits the reuptake from the synaptic cleft of 
    1. NA (by the norepinephrine transporter NET)
    2. Serotonin (by 5-HT)
    3. Dopamine (?) (by dopamine transporter DAT) 
  • S/E: increased blood pressure
  • Dangerous in overdose, higher suicide risk, less well tolerated, but a bit more effective
  • e.g. venlafaxine, duloxetine
Lösung ausblenden
TESTE DEIN WISSEN

What are TCAs and what are their main features?

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  • = Tricyclic Antidepressants
  • M: inhibits the reuptake of NA (by NET) and serotonin (by SERT) from the synaptic cleft + block other post-synaptic receptors (e.g. muscarinic, H1, a-1)
  • S/Es: weight gain, cardiotoxicity (large doses), muscarinic S/E (e.g. dry mouth, constipation), postural hypotension, sedation
  • suicidal behaviour may increase within first weeks
  • e.g. amitriptyline, imipramine
Lösung ausblenden
TESTE DEIN WISSEN

How common is depression?

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TESTE DEIN WISSEN
  • very common
  • 2 week prevelance ~ 2.5%
Lösung ausblenden
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  • 40 Studierende
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Q:

How do we diagnose depression?

A:
  • Core symptoms (min.2)
    1. Depressed mood
    2. Anhedonia – lack of pleasure
    3. Anergia - lack of energy
  • Additional symptoms ( 2 or more)
    1. increased/decreased appetite
    2. poor concentration
    3. guilt
    4. worthlessness
    5. hopelessness
    6. disturbed sleep
    7. slowing of movements
  • > 2 weeks
  • associated occupational and social impairment
Q:

What are the main hypotheses of the aetiology of depression? (6)

A:
  1. Monoamine deficiency
  2. Circadian Rhythms
  3. HPA axis disturbance 
  4. Cortical abnormalities
  5. Genetic vulnerability (Kindling hypothesis)
  6. Reduced GABAergic activity 
Q:

Explain the important facts about the monoamine deficiency (depression)?

A:
  • deficiency in neuroamines
  • this leads to receptor upregulation on post-synaptic membrane
  • drugs that increase neuroamine levels can reduce depressive symptoms
Q:

Explain the important facts about the circadian rhythms theory (depression)?

A:
  • no deep sleep
  • problems falling asleep
  • early waking up
Q:

Explain the important facts the HPA axis hypothesis (depression)?

A:
  • Overreactive HPA circuit in depressed patients 
  • lack of neg. feedback exerted by cortisol on hypothalamus/pituitary
  • increased cortisol: increased stress
Mehr Karteikarten anzeigen
Q:

Explain the important facts about the cortical abnormality hypothesis (depression)?

A:
  • changes in thickness 
  • reduced neurogenesis and neuroplasticity in hippocmapus
  • less remodelling
  • shrinking of hippocampus
  • reduction of intracellular growth promotors
Q:

Explain the genetic vulnerability hypothesis (depression)?

A:
  • Kindling hypothesis
  • genetic predisposition interact with environmental factors
  • this leads to alerted neurochemistry and neurobiology
Q:

What are pharmacological treatment options for depression?

A:
  • SSRIs - Selective Serotonin reuptake inhibitors
  • SNRIs - Serotonin - noradrenaline reuptake inhibitors
  • TCAs - Tricyclic antidepressants
  • MAOI - Nonoamine oxidase inhibitors
  • Atypical:bupropion, stimulants, lithium, mirtazapine
Q:

What are SSRIs and what are their main features?

A:
  • Selective serotonin reuptake inhibitors
  • M:  inhibits the reuptake of serotonin from the synaptic cleft by Serotonin transporter SERT in pre-synaptic neurone
  • S/E: sexual dysfunction
  • Safe in overdose 
  • e.g. fluoxetine, sertraline, paroxetine
Q:

What are SNRIs and what are their main features?

A:
  • SNRIs = Serotonin-noradrenaline Reuptake Inhibitors
  • inhibits the reuptake from the synaptic cleft of 
    1. NA (by the norepinephrine transporter NET)
    2. Serotonin (by 5-HT)
    3. Dopamine (?) (by dopamine transporter DAT) 
  • S/E: increased blood pressure
  • Dangerous in overdose, higher suicide risk, less well tolerated, but a bit more effective
  • e.g. venlafaxine, duloxetine
Q:

What are TCAs and what are their main features?

A:


  • = Tricyclic Antidepressants
  • M: inhibits the reuptake of NA (by NET) and serotonin (by SERT) from the synaptic cleft + block other post-synaptic receptors (e.g. muscarinic, H1, a-1)
  • S/Es: weight gain, cardiotoxicity (large doses), muscarinic S/E (e.g. dry mouth, constipation), postural hypotension, sedation
  • suicidal behaviour may increase within first weeks
  • e.g. amitriptyline, imipramine
Q:

How common is depression?

A:
  • very common
  • 2 week prevelance ~ 2.5%
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