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NSB Lectures > Anxiety Disorders - Neurobiology, Neurochemistry & Treatment > Flashcards

Anxiety Disorders - Neurobiology, Neurochemistry & Treatment Flashcards

1
Q

What are the three divisions of anxiety disorders?

A

Continuous anxiety

Episodic anxiety

OCD

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2
Q

Which part of the brain generates the fear response?

A

Amygdala

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3
Q

What happens if you remove the amygdala?

A

Ps stop fearing things (such as spiders) that they were pathologically scared of before the surgery

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4
Q

What are the three key sensory inputs to the amygdala in the brain?

A

Sensory thalamus
Somatosensory cortex
Anterior cingulate gyrus

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5
Q

What role does the hippocampus provide to the amygdala?

A

Relays fearful memories to present contexts

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6
Q

Which three main areas of the brain does the amygdala excite in response to a fear stimulus?

A

Lateral hypothalamus

Locus coeruleus

Periventricular hypothalamus

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7
Q

What does the lateral hypothalamus do in response to fear stimulus (via the amygdala)?

A

Activates the SS

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8
Q

What does the locus coeruleus do in response to fear stimulus (via the amygdala)?

A

Fight or flight response

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9
Q

What does the periventricular hypothalamus do in response to fear stimulus (via the amygdala)?

A

Activates the HPA Axis

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10
Q

Which part of the brain is responsible for the autonomic part of the acute stress response?

A

Lateral hypothalamus

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11
Q

Which part of the brain is responsible for the behavioural part of the acute stress response?

A

Locus coeruleus

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12
Q

Which part of the brain is responsible for the endocrine part of the acute stress response?

A

Periventricular hypothalamus

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13
Q

How does the HPA Axis work?

A

Fear stimulus tiggers the amygdala

Amygdala activates the hypothalmus

Hypothalamus releases CRH (corticotrophin releasing hormone) –> pituitary gland

Pituitary gland releases ACTH –> adrenal glands

Adrenal cortex releases cortisol = stress hormone = inhibits the Hypothalamus and Pituitary gland

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14
Q

Which two parts of the brain regulate the input to the Hypothalamus as part of the HPA axis? How do they both influence it?

A

Amygdala - stimulates the hypothalamus to release CRH.

Hippocampus - inhibits the hypothalamus from releasing more CRH.

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15
Q

When will the hippocampus send inhibitory messages to the hypothalamus?

A

Hippocampus - has lots of glucocorticoid receptors - these are stimulated by release of cortisol from the adrenal cortex - stimulates the hippocampus to send inhibitory messages to the hypothalamus.

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16
Q

Which part of the brain is responsible for the behavioural (fight or flight) response to stress?

What is it activated by?

What does it release?

A

Locus Coeruelus

Activated by the amygdala

Releases noradrenaline

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17
Q

Where is the origin of the noradrenergic system? What is it responsible for?

A

Locus coeruleus

Increases arousal and anxiety. When fearful stimuli are received - locus coeruleus releases NOR throughout the brain.

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18
Q

Where is the origin of the serotonergic system?

What can decreased levels of 5-HT cause?

A

Raphe nuclei

Decreased levels of 5HT can cause inappropriate fear and anxiety

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19
Q

What role does GABA play in anxiety? How do benzodiazepines affect anxiety?

A

GABA reduces anxiety (inhibitory). Benzos modulate GABA receptors and also work to reduce anxiety

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20
Q

Which three NTs in the brain are involved in fear and anxiety?

A

Noradrenaline
Serotonin
GABA

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21
Q

What is increased amounts of noradrenaline in the prefrontal cortex associated with?

A

Impaired cognitive function

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22
Q

Pharmacologically, what can we use to improve stress-induced cognitive impairment?

A

Adrenergic receptor antagonists - reduces the amount of noradrenaline binding in the PFC = improved cognitive function

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23
Q

Where are the Raphe nuclei found?

A

In the brainstem

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24
Q

Which drugs increase serotonin levels in the brain?

What are they used to treat?

A

Selective serotonin reuptake inhibitors (SSRIs)

Treat anxiety and depression

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25
Q

How do noradrenaline and serotonin interplay in the brain? How can this be related to anxiety disorders in patient?

What can be used to treat this?

A

Both NOR and 5HT have opposing effects in the brain and are often involved in fine balance for normal behaviour.

If this balance is upset - e.g. too little 5HT - can cause fear response to inappropriate stimuli.

SSRIs can push the balance back to normal levels.

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26
Q

What is the noradrenergic paradox?

A

The fact that some antidepressants which work increase reuptake of 5HT AND Nor = by increasing NOR amounts in brain it is thought that it should make Ps more anxious - HOWEVER this does not happen. Complicated reasons why, not not fully understood.

27
Q

How do drugs that increase GABA affect anxiety?

A

They decrease anxiety

28
Q

What is a partial agonist of GABA receptors?

29
Q

What is an indirect agonist of GABA receptors?

A

Benzodiazepines
Barbituates

30
Q

In what was is it thought that GABA receptors can play a role in anxiety?

A

Thought that Ps with anxiety could have

  1. Fewer GABA A receptors = less inhibition
  2. There is an endogenous neuromodulator which blocks the benzodiazepines site on GABA A = means less inhibition occurs
31
Q

What is the difference between using a benzodiazepine antagonist and a GABA antagonist?

A

Benzo antagonists - only work to negate the modulatory effect of the benzo - so GABA levels return to normal baseline.

GABA antagonists inhibit the GABA receptors completely - therefore much reduce the GABA levels to below the baseline.

32
Q

What did PET studies on benzodiazepine binding sites show?

A

That some Ps with panic disorder had fewer of the benzo binding site = does this mean that they had less inhibitory control via GABA?

33
Q

How does neuroanatomy feature in anxious Ps?

A

Often seen with changes to their neuroanatomy - e.g. reduced volume & hyperactivity of amygdala, thalamus & hippocampus, anterior cingulate cortex & PFC

Overactivity of insula cortex

34
Q

How does chronic stress affect the hippocampus?

A

Chronic stress = chronic activation of the hippocamus

This increase amount of calcium in the neurons = excitotoxicity & cell death = damage to hippocampus, loss of volume & loss of ability to limit cortisol production.

35
Q

How has the hippocampus been viewed in Ps with PTSD?

A

Reduced in volume

36
Q

Name 5 things seen in the neurobiology of PTSD?

A
  • Dysregulation of HPA axis
  • Increased NOR
  • Decreased 5HT
  • Decreased GABA
  • Increased glutamate
37
Q

What does dysregulation of the HPA axis mean for a patient with PTSD?

A

There will be abnormal stress and fear processing.

Can cause hippocampus atrophy

38
Q

What does increased noradrenaline mean for a P with PTSD?

A

Increased alertness, startle response, encoding of fear memories, inc pulse & BP

39
Q

What does decreased 5HT mean for a P with PTSD?

A

Disturbs dynamic between amygdala and hippocampus - inc levels of NOR.

Increases vigilance, startle, impulsive & memory intrusions

40
Q

What does decreased GABA mean for Ps with PTSD?

A

Compromised inhibition of other systems

41
Q

What does increased glutamate mean for Ps with PTSD?

A

Linked to derealisation and depersonalisation

42
Q

What neuroanatomical changes are seen in a P with PTSD?

A

Reduced hippocampal vol (& activity)

Increased activity of amygdala (hypervigilance & impaired discrimination of threat)

Reduced volume of PFC (impairing executive function)

Reduced anterior cingulate volume (inc fear responses)

43
Q

Which area of the brain is seen to be hyperactive in Ps with fear phobia?

44
Q

Anticipation of a phobic stimulus activates which part of the brain?

A

Anterior cingulate cortx

45
Q

What role does the cortex play in phobia?

A

Failure to activate the cortical regions that regulate the limbic system (e.e ventromedial PFC) - means there is no rationality to the phobic response

46
Q

What is seen functionally in Ps with OCD?

A

Functional changes in neural networks (cortico-striatal-thalmo-cortical path) and hyperactivity in caudate nucleus.

47
Q

What conditions is OCD associated with?

A

Conditions which affect the basal ganglia (e.g. Tourettes, encephalitis lethargic & Sydenham’s chorea)

48
Q

What treatments are given to Ps at risk of anxiety or with mild anxiety?

A

Social prescribing

Psychoeducation, problem-solving techniques, self-help & CBT

49
Q

What treatments are given to Ps with moderate anxiety?

A

CBT or pharmocotherapy or both

50
Q

What treatments are given to Ps with severe anxiety / unresponsive anxiety?

A

CBT + pharmocotherapy

51
Q

What does CBT focus on and try to change/

A

Maladaptive thinking and behaviour

52
Q

Which is the first line antidepressant used?

53
Q

What is the minimum period of time that SSRIs should be used for?

54
Q

Why is use of benzos avoided where possible?

A

High risk of dependance and tolerance

55
Q

How long do symptoms have to be present in order to be diagnosed for generalised anxiety disorder? What does this mean?

A

6 months
Symptoms are chronic by time of diagnosis

56
Q

What are outcomes for generalised anxiety treatment like?

A

Relatively poor - 25% remission from secondary care. Tends to be chronic and fluctuating course.

57
Q

How are panic disorders treated?

A

Same principles as anxiety disorders +

Psychoeducation for hyperventilation

CBT for panic attacks

58
Q

How are specific phobias treated?

A

No real medication for these (poss benzos for immediate situation - e.g. flying).

CBT inc graded exposure

59
Q

What is graded exposure in CBT?

A

Gradual introduction of the feared stimulus - thinking about etc to actual introduction of the stimulus

60
Q

How are social anxiety disorders treated?

A

Specialist CBT
Psychodynamic psychotherapy
SSRIs may be effective

61
Q

How is OCD treated?

A

CBT - focussing on the O & Cs.

Medication - SSRIs & poss Clomipramine

If no response - may add antipsychotic

62
Q

What is PTSD not treated before 4 weeks?

A

P may be suffering from acute stress reaction that may recover spontaneously.

63
Q

What is the treatment for PTSD?

A

1st - Specialist psychological therapy - CBT & EMDR (eye movement desensitisation therapy).

2nd - Antidepressants

Specialist = combination of drugs inc antipsychotics

64
Q

What is the first line treatment for most anxiety disorders?

A

Psychological therapy

NSB Lectures (48 decks)

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