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Drugs And The Brain > anxiety > Flashcards

anxiety Flashcards

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1
Q

physiological anxiety

A

anticipation of a stressful event
acts as a stimulus to prepare for that event
increased alertness
focus on ‘threat’

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2
Q

pathological anxiety

A

anxiety is out of proportion to threat

in some cases anxiety can exist without threat

it interferes with day to day activities, and can be very disabling

can be diverse

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3
Q

disorders related to pathological anxiety

A

generalised anxiety disorder

panic attacks

post traumatic stress disorder

phobias

OCD

Social anxiety

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4
Q

psychological symptoms of anxiety

A

fearful anticipation

cognitive disturbance

minor depressive symptoms

irritability

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5
Q

physical symptoms of anxiety

A

sympathetic arousal
-sped up heart rate
-faster breathing and hyperventilation
-sweating

hyperventilation

increase muscle tension

sleep disturbance

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6
Q

epidemiology of anxiety

A

10-20% of adults have an anxiety disorder in a year

lifetime prevalence of 20-30%

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7
Q

treatments for anxiety

A

anxiolytic drugs and psychological therapy

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8
Q

types of anxiolytic drugs

A

beta blockers
anti depressants
pregabalin
buspirone
benzodiazepines

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9
Q

how many people does generalised anxiety disorder affect

A

5% of the UK,
huge problem from health and economic perspective

2-4% of population in a year

2x as common in women

higher in middle ages, median onset of 30

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10
Q

criterion for diagnosing anxiety

A

ICD11 and DSM5

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11
Q

DSM 5 criteria

A

excessive worry and anxiety most of the time for > 6 months

worry is about a number of different things

cannot control worry

at least three of: restlessness, fatigue, poor concentration, irritable, sleep problems

symptoms result in poor functioning, cannot be managed by patient and are not due to drugs or other psychiatric conditions

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12
Q

aetiology of GAD

A

Twin studies show heritability of about 30%
-No “GAD gene” but links to serotonin and monoamine transmission genes

Risk factors
-childhood trauma
other health conditions e.g. heart attack or stroke

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13
Q

neurobiology of GAD

A

possibly due to dysfunction of the amygdala, medial prefrontal cortex and insular

involved in memory, decision making, emotional reaction, fear and threat perception

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14
Q

4 step approach to treatment of generalised anxiety disorder from NICE

A

education: may in itself improve symptoms

individual or group self CBT

drug therapy or high intensity CBT

combinations of drugs or drugs + psychological interventions
-SSRIs, SNRIs, pregabalin (BDZ only for short term use)

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15
Q

Buspirone mechanism

A

partial agonist at 5H21A receptors

5HT1A receptors found pre and post synaptically
-presynaptic: acts as inhibitory autoreceptors un serotonergic synapses, and as heteroreceptors in other synapse types

Buspirone will modulate the release of 5HT and other neurotransmitters

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16
Q

advantage of buspirone

A

doesn’t produce pronounced sedation and has relatively mild side effects

Some sources suggest there are no withdrawal effects, others suggest discontinuation syndrome

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17
Q

what is buspirone used for

A

licenced for GAD and occasionally used in other anxiety disorders

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18
Q

Compulsions

A

driven by obsessions

Repetitive, involuntary activities that are undertaken to provide temporary relief from these obsessions

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19
Q

types of intrusive/ disturbing thoughts

A

sexual thoughts
violent thoughts
thoughts of hurting themselves or other people
hygiene or contamination obsessions
obsessions around symmetry or order

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20
Q

types of compulsion

A

checking

counting

touching

arranging

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21
Q

pure obsession OCD

A

this is where most problems arise from the intrusive and disturbing thoughts

may still have some compulsions, but they are a minor part of the condition or hidden somehow

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22
Q

causes of OCD

A

Neurobiology largely unknown

Genetic (50% ish) and epigenetic (childhood trauma)

Can be triggered by atypical antipsychotics
-produce OCD in people who didn’t have it prior to taking the antipsychotic

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23
Q

trichotillomania

A

Compulsive pulling out of hair

Is sometimes combined with the eating of hair

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24
Q

dermatillomania

A

compulsive picking of the skin

25
Q

body focused repetitive behaviours

A

have a distinct diagnostic category in the DSM

trichotillomania
dermatillomania

very commonly linked with OCD , people with OCD often display these as part of their compulsions
-seems to be common in people who have contamination obsessions
-possible to have these conditions without actually having obsessions

26
Q

treatment of OCD for mild impairment

A

Low intensity psychological interventions (<10 h)
CBT inc. ERP (Exposure Response Prevention)

27
Q

moderate impairment OCD treatment

A

SSRIs or more intense CBT inc. ERP

28
Q

severe impairment OCD treatment

A

SSRIs and more intense CBT inc. ERP

29
Q

ERP

A

exposure response prevention

30
Q

exposure response prevention

A

You expose the person to what they are fearful of in a controlled way, and you gradually help them to overcome their fear

Can form a part of therapy for PTSD, phobias

31
Q

neurobiology of OCD

A

Neuroimaging has mostly implicated the OFC and basal ganglia.

The cingulate cortex (red) has also been suggested a role, with the ACC of showing hyperactivity

32
Q

bilateral cingulotomy

A

Psychosurgical technique as a practice of last resort for OCD
-and a few other conditions- intractable pain, depression

Involves severing connections to the cingulate cortex

Is done with the aid of fMRI scans therefore is precise

Is done using electrodes of gamma knife

Recover is generally very quick (a few days), with relatively few people experiencing serious side effects

~40% of those who undergo this procedure to treat OCD are benefitted

33
Q

side effect of panic attacks

A

physical symptoms

high level of sympathetic activation, parasthesias

psychological symptoms

depersonalisation, derealisation, fear of loosing control or dying

34
Q

what are panic attacks

A

Intense anxiety with a sudden onset

Usually symptoms come on over a period of a few minutes

35
Q

physical symptoms of panic attacks

A

heart pounding, accelerated heart rate, palpitations

trembling

sweating

chest pain?

36
Q

what is parasthesias?

A

pins and needles feeling

37
Q

what disorders can panic attacks occur as a part of?

A

other anxiety disorders, e.g., phobias

as part of a physical condition., hyperthyroidism or pheochromocytoma can sometimes provoke panic attacks

38
Q

what is needed to be diagnosed as having a panic attack

A

to be diagnosed as having a panic attack you need to experience 4/13 symptoms listed on the DSM

39
Q

what is needed to be diagnosed as having a panic attack

A

to be diagnosed as having a panic attack you need to experience 4/13 symptoms listed on the DSM

40
Q

what is panic disorder

A

Recurrent panic attacks and

A period of at least a month in which there is persistent anxiety about having a panic attack and/or
Changed behaviour aimed at avoiding panic attacks e.g. avoiding social situations

41
Q

treating mild to moderate panic disorder

A

low intensity psychological interventions

e.g. self help, support groups

42
Q

moderate to severe panic disorder treatments

A

CBT o

if CBT not effective

SSRI or SNRI

If SSRI or SNRI not effective

a tricyclic antidepressant

not mentioned in NICDE guidelines: beta-blockers are sometimes used for treating anxiety and panic disorders

43
Q

main example of a beta blocker

A

propranolol

44
Q

what is the mechanism of beta blockers

A

B1 adrenoreceptor antagonists

45
Q

what is the effect of beta blockers

A

Mask symptoms of sympathetic activation

Reduce physical effects of panic attacks

Will not directly treat the psychological symptoms, however may break cycle of physical symptoms making psychological symptoms worse.

More useful in the short term

46
Q

what is social anxiety disorder?

A

a fear of social situations

47
Q

what is the most common anxiety disorder? What is its prevalence?

A

social anxiety disorder, 12%

48
Q

criteria for social anxiety disorder

A

Marked fear or anxiety about one or more social situations in which the individual is exposed to possible scrutiny by others. Examples include social interactions, being observed, and performing in front of others

The individual fears that he or she will act in a way or show anxiety symptoms that will be negatively evaluated

The social situations almost always provoke fear or anxiety.

The social situations are avoided or endured with intense fear or anxiety

The fear or anxiety is out of proportion to the actual threat posed by the social situation and to the sociocultural context

The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.

The fear, anxiety, or avoidance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.

must have lasted 6+ months, cannot be explained by another condition

49
Q

what is first recommended treatment for social anxiety?

A

specialised CBT

recommendation for individual therapy, not group therapy

50
Q

what treatment for social anxiety if CBT is ineffective

A

further CBT, SSRIs

SNRIs or MAO inhibitors as a potential further treatment

51
Q

what is PTSD

A

condition someone can develop following any kind of trauma

52
Q

people who get PTSD

A

those who have been in combat experiences (military service)

sexual assault

being in a terrorist attack or involved in an incident

53
Q

symptoms of PTSD

A

hypervigilance, aggression, flashbacks to the trauma, cognitive problems, intrusive thoughts and memories, and nightmares

Many people find that episodes of PTSD are provoked by specific triggers that are connected (perhaps only loosely) with original trauma.

54
Q

suicide and PTSD

A

These can be extremely distressing and debilitating, which is reflected in a much higher suicide rate (9.8x general population) in people with PTSD

55
Q

neurobiology of PTSD

A

Seems to involve reductions in the volume of the hippocampus and prefrontal cortex

The amygdala also shows abnormalities in PTSD
-key structure for emotional processing and the acquisition of fear behaviours
-becomes hyper-responsive and seems to result in an excessive threat responses to non-threatening stimuli

changes in HPA axis
-often have lower plasma cortisol levels and have a greater response to the dexamethasone suppression test than control subjects (surprise as you would expect stress to increase cortisol levels)
-has been hypothesised that a low level of cortisol following a traumatic event may result in increased noradrenergic signalling both in the CNS and in the periphery
-Increased release of noradrenaline by neurons originating in the locus coeruleus may result in “over-consolidation” of fearful memories about the trauma.

56
Q

prevention of PTSD

A

Most people who experience a trauma will have an ‘acute stress reaction’ in the immediate aftermath

However, there is often a delay before PTSD ‘properly’ establishes itself

If people who experience acute stress reaction are given specialised CBT for a month following the trauma, it can:
-reduce the rate at which people go on to develop PTSD
-lessen symptoms of those who develop PTSD

57
Q

treatment of PTSD

A

NICE does not recommend treating established PTSD with drugs

Recommends treating established PTSD using specialised CBT and for non-combat trauma EMDR can be offered

If patients prefer they can be offered SSRIs or SNRIs instead of CBT

If PTSD has psychotic symptoms, then atypical antipsychotic drug such as risperidone might be considered

58
Q

EDMR

A

Eye Movement Desensitisation and Reprocessing

controversial therapy that seems to work, but no-one knows why

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