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4/ BAB > Anxiety and Depression > Flashcards

Anxiety and Depression Flashcards

1
Q

What is anxiety disorder? What is it characterised by>

A

“an inappropriate or excessive, anticipatory manifestation of the fear response, often to a stressor’
- defensive behaviours
- autonomic reflexes
- corticosteroid secretions
- negative emotions
= pathology if interferences with normal life

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2
Q

What are the types of anxiety disorder?

A
  • general anxiety disorder –> somatic and autonomic effects e.g. restlessness, agitation, tachycardia, sweating, sleep disturbance
  • phobic anxiety
  • panic disorder
  • post-traumatic stress disorder
  • obsessive compulsive disorder
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3
Q

Draw the hypothalamic-pituitary-adrenocortical axis and describe how it might be altered in anxiety disorders

A

see lecture

  • may be overactive in anxiety
  • presence of the stressor may not be necessary to activate it
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4
Q

what are the 3 options for treatment of anxiety disorders?

A
  • self-help
  • psychological e.g. CBT
  • pharmacological
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5
Q

What are the 3 classes of anxiolytic drugs?

A
  1. B blockers
  2. Benzodiazipines
  3. Antidepressants
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6
Q

How do beta blockers reduce anxiety?

A
  • reduce somatic symptoms by blocking affects of released adrenaline and NA
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7
Q

What are the useful effects of benzodiazepines?

A
  • reduce anxiety

- induce sleep

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8
Q

What is the mechanism of action of benzodiazepines?

What areas of the brain to they act on?

A
  • increases affinity for GABA at the GABAa receptor –> increase Cl –> hyperpolarisation
  • these act in amygdala and prefrontal cortex
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9
Q

What are the short and long term problems with benzidiazipine use?

A 
Short term 
- sedation 
- acute overdose, esp. with alcohol 
Long term 
- tissue tolerance 
- dependence and withdrawal
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10
Q

Which class of antidepressants can be used in anxiety?

A

SSRIs

serotonin selective reuptake inhibitors

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11
Q

What are the symptoms of unipolar depression?

A
  • misery, despair, loss of motivation, appetite, suicidal throughts, move less
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12
Q

What are the two types of causes of depression

A

reactive (75%)

endogenous (25%)

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13
Q

What are the 4 classes of antidepressants?

A
  1. SSRIs
  2. TCAs
  3. MAOIs
  4. atypical
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14
Q

What is the monoamine theory of depression?

Which Its are monoamines?

A
  • depression is due to hypoactivity at monoaminergic (NA and 5-HT) synapses in the brain
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15
Q

What is the evidence for and against the monoamine theory of depression?

A

Evidence for:
- ADs increase MA in brain rapidly
Evidence against:
- ADs take >1-3 weeks to work

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16
Q

How do you choose which antidpressant to use?

A
  • efficacy

- side effect profiles

17
Q

Describe the action of MAOIs using the biochemistry of the central monoaminergic synapse

A

MAO inhibitor prevents breakdown of NA and 5-HT and so increases intraterminal MA and intrasynaptic MA

18
Q

What are the immediate effects of MAOIs?

When does the antidepressant action start?

A
  • euphoria

- 4 weeks in

19
Q

Give an example of a MAOI

A
  • moclobemide

- reversible binding, MAO-A selectivity

20
Q

What are some unwanted effects of MAOIs?

A
  • the cheese reaction, unmetabolised tyramine from diet displaces NA and increases BP
  • antimuscarinic effects
  • alpha1 antagonism
21
Q

Give examples of SSRIs

A

fluoxetine

22
Q

What is the mechanism of action of SSRIs?

A
  • block re-uptake 5-HT
23
Q

How long do SSRIs take to have an AD effect?

What are their unwanted effects?

A
  • 2-4 weeks delay to clinical effect
  • serotonin syndrome –> suicidal thoughts
  • GI and N+V
24
Q

Give an example of a TCA?

What are their mechanism of action?

A

amitriptyline

5-HT/NA reuptake inhibition

25
Q

What are the unwanted effects of TCAs?

A
  • anti-muscarininc
  • sedation (H1 antagonism)
  • overdose
26
Q

Newer drugs proposed MoA

A

NEW = melatonin receptor antagonists

  • various uptake/receptor mediated effects for 5-HT, NA, dopamine
  • better adverse effect profile
27
Q

Do AD drugs work?:

  • How many patients may not respond?
  • Why is it difficult to evaluate efficacy
A 
- 30% of patients may not respond 
Difficult to evaluate efficacy 
- trial and error required so studies are difficult to conduct 
- slow onset of action 
- mood is variable 
- high placebo effect
28
Q

Describe the new theory - the network hypothesis

A
  • depression leads to an increase in CRF (from hypothalamus) and cortisol in the CSF
  • this is reversed by ADs
  • hyperactivity/sensitivation of the neuroendocrine stress reponse –> depression
    Mechanism
  • chronic stress
  • decrease glucocorticoid receptors and BDNF
  • decrease neurogenesis and neuroplasticity
    AD –> increase MA –> increase neurogenesis –> restore neuronal network
  • this is the reason for the delay
29
Q

What is BDNF?

A
  • a neurotrophic factor that helps to maintain healthy synapses

4/ BAB (25 decks)

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