Block 33 Week 1 Flashcards

Anxiety and Depression

1
Q

performance vs arousal curve

A
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2
Q

physical symptoms of anxiety - muscle tension?

A

headaches, pain, fatigue

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3
Q

physical Sx of anxiety - hyperventilation?

A

dizziness, tingling fingers + toes (¯pCO2 ® Ca2+ changes)

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4
Q

physical symptoms of anxiety - sympathetic overactivity?

A

(­HR +BP, ectopic beats, sweating, pale skin (cf shock), dry mouth, ‘butterflies’, nausea, loose motions, frequent urination)

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5
Q

psychological symptoms of anxiety?

A
  • CNS: poor conc., memory, feeling unreal
  • Mood: fear, panic, worry, on edge, irritable
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6
Q

thoughts in anxiety?

A
  • future danger: “something bad will happen and I won’t be able to cope” (v. depression: past loss)
  • Fear of dying/losing control
  • Worry about worry: I will go mad/die just by worrying
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7
Q

Anxiety: unhelpful behaviours?

A
  • attempts at coping: (caffeine, smoking, alcohol, illegal or prescribed drugs)
  • avoiding fear provoking situations
  • safety behaviours
  • asking for reassurance (visiting GP, ­somatic complaints, checking body)
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8
Q

prevalence of anxiety disorders?

A
  • anxiety disorders affect at least 1 in 10 ppl
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9
Q

Anxiety screening tool?

A
  • GAD-2
  • anxiety disorder is likely if a person answers 2 or 3 to one or both Qs (ie anxiety present > 50% time)
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10
Q

History taking for anxiety?

A
  • triggers and situations
  • thoughts - worst fears
  • emotions
  • physical reactions
  • behaviours - before/ during/ after
  • coping - avoiding, substance use, safety seeking behaviours
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11
Q

free floating anxiety classifications?

A
  • If free floating, present from time to time (panic) or all the time (generalised anxiety)
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12
Q

anxiety: the worry tree

A
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13
Q

investigations for anxiety?

A
  • TFTs - hypothyroidism
  • MCV/GGT - alcohol misuse
  • glucose - hypoglycaemia
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14
Q

other investigations that can be done for anxiety?

A
  • urine - illicit drug use
  • ECGs (SVT/ MVP)
  • MRI head (SOL)
  • EEG (TEL)
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15
Q

psychological Ix for anxiety?

A
  • GAD-7 for anxiety
  • PHQ-9 for depression
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16
Q

Tx fir anxiety?

A
  • education
  • relaxation
  • advice on sleep and exercise
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17
Q

what is CBT?

A
  • psychological treatment that teaches us how to feel better by changing the way we feel think and behave = change behaviour (eg graded exposure) and/ or change thinking (eg anxiety is unpleasant but not dangerous)
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18
Q

Pharmacological Tx of anxiety (3)

A
  • SSRI antidepressants eg sertraline, citalopram
  • Benzodiazepines eg diazepam (max 2-4wks)
  • Beta-blockers eg propranolol
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19
Q

what is a phobia?

A
  • A marked and persistent fear
  • Triggered by a specific object/situation
  • Leads to avoidance of that situation
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20
Q

agoraphobia?

A

(public places, crowds, shops) 6% 1 yr prevalence in population

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21
Q

social phobia?

A

(eating, speaking, performing) 4%

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22
Q

specific phobias?

A

(animals, heights, needles) 9%

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23
Q

maintenance of a phobia?

A
  • phobic stimulus -> anxiety -> avoidance -> anxiety reduced
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24
Q

Tx of phobias - graded exposure?

A

graded exposure (systematic desensitisation) = the deliberate confrontation of a feared object or situation until the anxiety evoked reduces (habituates)

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25
Q

Graded exposure needs to be:

A
  • clearly planned - SMART targets
  • prolonged
  • repeated freq
  • graded e.g. ladder or steps
  • w/o dissociation
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26
Q

how can graded exposure be done?

A
  • Done in CBT session, then as homework
  • Self-directed, or accompanied by therapist, friend or relative
  • In reality or imagination (eg PTSD/trauma)
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27
Q

graded exposure can be gradual or?

A

one-off prolonged (‘flooding’)

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28
Q

what is systematic desensitisation?

A

graded exposure plus relaxation

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29
Q

CBT for generalised exposure - behavioural?

A
  • behavioural: anx management
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30
Q

CBT for generalised exposure - cognitive?

A
  • cognitive: tackle worry about worry
  • Test out unhelpful beliefs about worry eg ‘worry helps me solve problems’
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31
Q

CBT for generalised exposure - mindfulness?

A
  • Mindfulness: awareness plus acceptance
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32
Q

mindfulness -

A
  • Purposeful and non-judgemental attentiveness to one’s own experience, thoughts and feelings
  • letting it be
  • focusing on present moment > distressing thoughts
  • notice
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33
Q

CBT for panic: summary

A
  • Education: anxiety is normal, fight or flight
  • Draw a vicious circle (diagram with arrows)
  • Exposure to own body sensation
  • Experiments: test out fears to disprove them
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34
Q

Clark’s CBT model for panic attacks?

A
  • The trigger can be external (eg crowds) or internal (eg heartbeat) – ‘selective attention’/ ‘hypervigilence’
  • The person misinterprets normal body sensations as meaning that a physical or mental disaster is imminent – ‘catastrophic misinterpretation’
  • The ‘fight or flight’ survival response produces more symptoms - which fuel the ‘vicious cycle’ of panic
  • attempts by the person to manage panic bring short term relief but make it worse in the long term (avoidance + safety behaviours)
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35
Q

panic diaries include?

A
  • situation
  • worst symptoms
  • worst dears
  • safety behaviours
  • alt explanation
  • behavioural experiment - nexttime it occurs
  • predictons
  • outcome
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36
Q

what are anxiety disorders?

A
  • excessive anxiety - exaggeration of the normal anxiety response
  • out of proportion to stimulus
  • anxiety is prolonged after stimulus removed and does not assist in dealing w the situation
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37
Q

Classification of anxiety disorders?

A
  • GAD
  • Panic disorder
  • Phobic anxiety disorders: social phobia, simple phobia, agoraphobia
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38
Q

GAD =

A
  • anx symptoms persistent but may fluctuate in intensity, not situation specific
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39
Q

GAD symptoms?

A
  • sleep disturbance
  • worrying
  • feeling on edge
  • irritability
  • poor conc
  • autonomic symptoms - palpations, sweating, dry mouth
  • inc muscular tension giving rise to head, neck and backaches
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40
Q

epidemiology of GAD?

A
  • 1 year prev - 3%
  • F >M
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41
Q

DDs for GAD

A
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42
Q

RF for GAD?

A
  • Genetic
  • biological mechanisms - breakdown of the mechanisms
  • personality traits - neuroticism
  • childhood adversity - especially when lack of secure attachments
  • stressful life events
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43
Q

Panic disorder?

A
  • panic attacks often occur w other disorders e.g. GAD, agarophobia, depressive disorders
  • the anxiety is unrelated to any paticular circumstances so is unpredictable
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44
Q

what are panic attacks?

A
  • characterised by sudden onset of symptoms, reaching a peak within 10 mins
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45
Q

panic attacks - depersonalisation vs derealisation?

A
  • depersonalisation = patient feels detached from their surroundings, feel unable to feel emotions - out of body experiences
  • derealisation = surrounds don’t seem real
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46
Q

symptoms of a panic attack?

A
  • sweating, hot flushes
  • SOB
  • paraesthesia
  • dizziness
  • choking
  • chest pain, palpations
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47
Q

prevalence of panic attacks?

A
  • 1.4% 1 year prevalence
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48
Q

phobic anxiety disorders?

A
  • intermittent episodes of anxiety occuring in spec circumstances
  • anxiety out of prop to threat
  • can lead to anticipatory anxiety and habitual avoidance of the circumstances
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49
Q

Specific/ simple phobias?

A
  • fear of spiders e.g.
  • onset in childhood usually
  • 1 yr prev ~4%
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50
Q

social phobias?

A
  • fear of performance failure and negative evaluation in social situations
  • onset in teenage years usually
  • 1 yr prev 7% which reduces in adults
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51
Q

agoraphobias?

A
  • symptoms provoked by being away from home, in situations which can’t be left easily such as crowded or confined spaces e.g. supermarkets, cinemas
  • in severe cases ppt may be housebound
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52
Q

agoraphobias - onset is usually before?

A

35

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53
Q

agoraphobia - 1 yr prev is double in?

A

females

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54
Q

aetiology of agoraphobia?

A
  • ppts often constitutionally vulnerable to anxiety symptoms which they may exp and misinterpret in certain situations
  • conditioning and avoidance maintain the symptoms as can the response of family members
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55
Q

RF for agoraphobias?

A
  • Genetics
  • personality traits e.g. dependent personality traits
  • learning theories - conditioning and avoidance
  • family influences e.g. overprotective
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56
Q

OCD prevalence?

A
  • 1 yr prev = 2%
  • F =M
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57
Q

OCD - mechanism?

A
  • Obsession can be a thought, impulse or action
  • there is a sense of complusion associated with it
  • it is resisted leading to anxiety
  • it’s recognised as nonsensical and is recognised as coming from within the patient
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58
Q

Types of obsessional phenomena - thoughts and impulses?

A
  • thoughts - e.g. single words, usually unpleasant
  • impulses - or urges to perform violent or embarassing acts
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59
Q

types of obsessional phenomena - ruminations and rituals?

A
  • ruminations - endless internal debates abt trivial problems
  • rituals - counting or cleaning, checking
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60
Q

brain disorders linked to OCD?

A

encephalitis lethargica, Gille de la Tourette syndrome

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61
Q

PTSD?

A
  • severe reaction to extremely stressful circumstances
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62
Q

core features of PTSD?

A
  • hyper-arousal
  • re-experiencing aspects of the stress e.g. flashbacks, dreams, thoughts
  • avoidance of reminders
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63
Q

What are adjustment disorders?

A
  • reaction to stressful experience which is understandanle and in prop e.g. divorce
  • symptoms can be v variable but can include many anxiety symptoms
  • worries usually focused on the stressor
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64
Q

Mixed anxiety and depressive disorder ?

A
  • symptoms of both equally present
  • neither dominates
  • neither symptoms severe enough to meet criteria for an anxiety or a depressive disorder
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65
Q

Tx of anxiety?

A
  • psychological treatments are the treatment of choice
  • include counselling, CBT
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66
Q

specific psychological technique for phobias?

A

exposure therapy

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67
Q

spec technique for obsessional phenomena?

A

thought stopping

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68
Q

pharmacological management of anxiety?

A
  • antidepressants - anxiolytic affects used for GAD and panic attacks
  • BBs useful for palpations and tremor from anxiety
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69
Q

precipitating factors in GAD?

A

Stressful life events eg relationship problems, physical illness, threatened loss of employment (contrast losses - which tend to provoke depression)

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70
Q

Maintaining factors in GAD?

A
  • CBT theory states that in GAD worrying abour worry maintains anxiety and leads to unsuccessful attempts to control it
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71
Q

mechanism of phobias - natural selection?

A
  • phobias are acquired not innate
  • Evolutionary theory suggests that increased likelihood of fear towards certain objects (snakes, spiders, being alone, the dark) conferred a survival advantage to our ancestors, leading to natural selection
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72
Q

the double learning theory suggests a 2 stage acquisition of fears:

A

1 - pavlovian conditioning
2 - maintained by operant conditioning

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73
Q

pavlovian conditioning?

A
  • initial acquisition of a phobia
  • (association of a conditioned with unconditioned response) eg lost and anxious when out walking as a child and see a cat leading to cat phobia
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74
Q

operant conditoning?

A
  • maintains the phobia
  • Contact with cats causes anxiety (punishment) leading to less contact, plus avoidance of all cats brings reward of no anxiety (= negative reinforcement).
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75
Q

step 1 of the CBT model of panic disorders?

A
  • catastrophic misinterpretation of body systems
  • panic occurs and is maintained by an inappropriately learned response to normal physiological symptoms (eg palpitations)
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76
Q

step 2 in the CBT model of panic disorders?

A

Selective attention to body symptoms and avoidance of anxiety provoking situations also reinforces behaviour.

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77
Q

OCD presentation in males?

A
  • earlier onset
  • clinical themes: exactness, sexual, odd rituals, symmetry
  • asosicated with increased rates of bipolar disorder
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78
Q

OCD presentation in females?

A
  • later onset
  • more aggressive obsessions and cleaning compulsions
  • associated with increased rates of panic disorder
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79
Q

biochemistry behind OCD

A
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80
Q

psychodynamic theory of OCD - Freud?

A
  • OCD represents defensive regression to anal stage
  • (defensive triad of orderliness, obstinacy and parsimony ie stinginess).
  • utilisation of defence mechanisms
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81
Q

defence mechanisms in OCD - reaction formation?

A
  • Reaction formation = feeling or behaving in a way which is opposite of unconscious unacceptable impulses (eg excessive prudery if increased sex drive)
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82
Q

defence mechanisms in OCD - undoing?

A

attempting to cause past thoughts not to have occurred

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83
Q

defence mechanisms in OCD - isolation?

A

separation of an idea from its associated affect

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84
Q

precipitating factors in OCD?

A

environmental stress especially life events indicating increased responsibility

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85
Q

maintaining factors of OCD - behavioural theory?

A
  • rituals (checking, cleaning etc),
  • avoidance and reassurance seeking produce short-term relief from anxiety symptoms but cause long-term worsening of problems (negative reinforcement of behaviour, operant conditioning)
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86
Q

maintenance of OCD - cognitive theory?

A
  • states that OCD kept going by exaggerated appraisal of threat, assuming excessive responsibility for consequences, and attempts to suppress recurrent worrying thoughts
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87
Q

Managament of OCD?

A
  • Offer info, education, self help and support groups
  • involve family/carers (drop reassurance/safety seeking), involve religious or community leaders (if OCD/culture boundary unclear)
  • involves a stepped care model
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88
Q

secondary/ specialist care for OCD?

A
  • only gets involved if comorbitidy. severe or treatment resistant cases
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89
Q

mild OCD (functional impairment)?

A

CBT (under 10 therapist hrs) using individual, phone, structured self help or group approach

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90
Q

moderate OCD Tx?

A

1) Offer either any SSRI or CBT (over 10 therapist hrs): both equally effective
2) Increase dose after 4-6 weeks if no response

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91
Q

moderate OCD - review for?

A
  • 12 months and then discharge back to PC if well
  • Teach individual to adapt techniques learned to new symptoms
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92
Q

severe OCD first line?

A

1) Offer SSRI and CBT in combination

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93
Q

severe OCD - if no response after 12 weeks offer?

A

2) No response after 12 wks (or patient not engaged): different SSRI, and then/or
3) Clomipramine up to BNF max (+ECG+BP if significant CVS disease)

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94
Q

step 4 in the management of severe OCD?

A

Refer to “Specialist multidisciplinary team with expertise in OCD/BDD” whose roles are to: advise, assess, treat, educate + increase skills of other professionals

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95
Q

OCD in children and younger ppl?

A
  • more emphasis on age approproate family, indiv and group interventions
  • recommends CBT first line 12 weeks for all OCD even if severe
  • then consider adding SSRI
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96
Q

body dysmorphic disorder Tx pathway?

A
  • same as OCD (CBT/SSRI, stepped care, specialist teams) but
  • fluoxetine is the first choice drug 1)
  • then other SSRIs then try adding in buspirone.
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97
Q

Acute stress reaction includes?

A
  • Includes crisis reaction
  • e.g.s accident, battle, criminal assult, domestic fire
  • onset - immediate or within minutes vs within 6 months for PTSD usually
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98
Q

duration of acute stress reactions?

A
  • duration 0-72 hrs, PTSD is over 1 month - lifelong
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99
Q

symptom clusters in PTSD?

A

Traumatic event + the RAHR symptom clusters

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100
Q

RAH + Reaction mneumonic?

A
  • Re-experiencing
  • Avoidance
  • Hyperarousal
  • Reaction - altered cognitions and mood
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101
Q

PTSD - re-experiencing?

A
  • thoughts, dreams, flashbacks
  • dissociative reactions - derealisation, depersonalisation, losing conciousness
  • distress or reactivity when exposed to traumatic reminders
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Not at all
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3
4
5
Perfectly
102
Q

PTSD - avoidance?

A
  • of thoughts, feelings, people, places, conversations, activities, objects or situations associated with the trauma or that evoke memories of it
103
Q

PTSD - hyperarousal?

A
  • Irritable, aggressive, self destructive or reckless behaviour
  • Hypervigilance (scanning for danger)
  • Exaggerated startle response (eg jumps to loud noise)
  • Sleep disturbance. Difficulty concentrating.
104
Q

PTSD - reaction?

A
  • altered cognitions and mood
  • began/ worse after trauma
  • negative emotions and beliefs
105
Q

PTSD - reaction: dissociation

A

Inability to recall an important aspect of the trauma (amnesia)

106
Q

PTSD reaction - diminished…

A

interest/participation in normal activities

107
Q

For PTSD diagnosis, symptoms need to be present for?

A

one month and clinically sig distress or functional impairment

108
Q

complex PTSD?

A
  • An event or series of events of an extremely prolonged or repetitive nature, most commonly where escape is difficult or impossible
  • Symptoms of PTSD - RAHR plus BAR
109
Q

BAR mneumonic for complex PTSD?

A

Beliefs - persistent beliefs as self as dimished, defeated or worthless
Affect - problems in affect regulation
Relationships - difficulties in sustaining relationships

110
Q

PTSD aetiology - predisposing factors?

A

pre-morbid personality

111
Q

PTSD aetiology - precepitiating?

A

stressor event

112
Q

PTSD aetiology - maintaining?

A

victim’s enviornment

113
Q

pre-morbid personality in PTSD?

A
  • genetics
  • personality
  • childhood abuse, adult trauma, drug and alcohol abuse
  • neurotic disorder
114
Q

what happens in PTSD?

A
  • Extreme, prolonged or repeated stress -> overactivity of normal defence mechanisms, involving 3 catacholamine systems
115
Q

PTSD - NA system?

A

locus coeruleus/noradrenaline system -> ­ activity of amygdala, hippocampus, hypothalamus and cerebral cortex

116
Q

PTSD - dopamine system?

A

prefrontal cortex activity

117
Q

PTSD - sensory nervous system?

A

physiological arousal + NA + A secretion

118
Q

therapies treating PTSD?

A
  • CBT
  • psychoeducation
  • EDMR
119
Q

Psychoeducation for PTSD?

A
  • Psychoeducation about reactions to trauma, strategies for managing arousal and flashbacks
  • processing trauma related memories
  • overcoming avoudance
  • improving function (work/ social relationships)
120
Q

EDMR?

A
  • eye movement desensitisation reprocessing
  • should use repeated in- session bilateral stimulation for specific target memories (often visual images) until memories no longer distressing, plus teaching of self-calming/techniques to manage flashbacks within and between sessions,
121
Q

drug therapies for PTSD?

A
  • not first line, usually added onto CBT/ EMDR
  • venlafaxine or any SSRI e.g. sertraline or paroxetine
122
Q

which drugs can be added to antidepressants to manage hyperarousal?

A
  • antipsychotics like risperidone can be added for disabling symptoms like hyperarousal, or if not responding to other symptoms
123
Q

exposure therapy for PTSD?

A
  • Role of therapist in exposure work = to encourage patient to describetrauma as if they were in the situation now
  • Therapist first presents rationale for exposure
  • ppt rates fear/distress at the beginning, middle and end
124
Q

exposure therapy - rewind and hold technique?

A
  • rewind and hold technique - encourage ppt to stop and go back over the hot stop to allow habitation to occur
125
Q

Cognitive therapy aims to change the way people feel by:

A

a) challenging their automatic negative thoughts and underlying assumptions eg using a diary of situation, thoughts, evidence for/against thought being true
b) getting patient to suggest more rational ,alternative, balanced explanations.

126
Q

dissociative disorder (hysteria)?

A
  • production of symptoms and signs of illness in absence of physical pathology
  • involuntary
  • not automatic
  • usually involves signs of CNS
127
Q

hysteria epidemiology?

A
  • F>M 6:1
  • commoner in developing countries
  • usually presents before 40
128
Q

main features of hysteria?

A
  • partial or complete loss of normal integration between memories of the past, awareness of identity + immediate sensations + bodily movements
129
Q

dissociative states =

A

traditionally mental symptoms + signs in absence of organic brain disease.

130
Q

what can be seen in hysteria?

A
  • Narrowing of field of consciousness (restricted awareness) which may be limited to one area of experience eg amnesia, stupor, fugue, trance, Ganser’s syndrome, multiple personality
131
Q

coversion disorder?

A
  • Conversion disorder = traditionally physical symptoms + signs occurring in organs under voluntary (not autonomic) control (usually nervous system)
  • eg paralysis, weakness, bizarre gait, abnormal movements, dysphonia, blindness, pseudoseizures, numbness.
132
Q

RF for anxiety?

A
  • Female sex
  • Family history
  • Childhood abuse and neglect
  • Environmental stress(e.g. redundancy, divorce)
  • Emotional trauma
  • Substance abuse
133
Q

diagnostic criteria for anxiety?

A
134
Q

step 1 of anxiety management?

A
  • address environmental stressors and substance abuse issues
  • assess severity, duration and impact on normal life
  • evaluate for co-existing depression
135
Q

step 2 of anxiety management?

A
  • low intensity psychological interventions
  • includes individual non-facilitated self-help, individual guided self-help and psychoeducational groups.
136
Q

Step 3 - GAD with marked functional impairment or that has not improved after step 2 interventions?

A
  • high intensity psych intervention
  • pharmacological treatment - SSRI or SNRI (ventafaxine)
137
Q

step 4 of anxiety management?

A
  • referral to specialist care
  • if steps 1-3 didn’t work
  • or if risk of SH/ suicide, significant co-morbitiries or self neglect
138
Q

interaction between cognitive, behavioural, emotional and physiological factors in anxiety?

A
  • thoughts affect behaviour, emotions and physiological state
  • behaviours affect thoughts, emotions and physiological state
  • CBT addresses these domains
139
Q

CBT - challening the cognitive domain of anxiety?

A
  • Identifying and re-evaluating negative thoughts, beliefs and patterns of thinking
  • Learning more effective problem-solving and decision-making strategies
140
Q

CBT - cognitive - mindfulness?

A
  • Using mindfulness to deal with “uncontrollable” and racing thoughts, allowing you to let go of unnecessary thoughts without getting caught up in them
141
Q

CBT - challenging the behavioural domain of anxiety?

A
  • Changing unhelpful behaviours such as social isolation, avoiding situations, procrastination and inactivity
  • Learning to be more assertive and communicate more effectively
  • Pursuing pleasurable activities and interests that promote happiness and make life more meaningful and fulfilling
142
Q

CBT - challenging emotional domain of anxiety?

A
  • Learning how to experience and accept negative emotions without becoming overwhelmed
  • Techniques to transform painful emotions into more manageable feelings
  • Strategies to help tolerate emotional distress and manage extreme emotional reactions such as intense anger, anxiety or sadness
143
Q

CBT - challenging physiological domain of anxiety?

A
  • Breathing exercises and relaxation techniques to calm physiological responses and reduce stress levels
  • Mindfulness practices to cope with stress and physical discomfort or pain
  • Improving sleep, diet and exercise habits to improve physical well-being
144
Q

Stress response in anxiety?

A
  • activation of SNS
  • body’s fight or flight response activates -> adrenaline, NA and ACTH release
  • allows us to peform well in a short term situation
145
Q

personality and anxiety?

A
  • individuals with high neuroticism scores were more likely to feel anxious
  • correlation between anxiety, introversion and neuroticism
146
Q

coping strategies in anxiety?

A
  • limiting alcohol and caffiene
  • sleeping well
  • deep breathing
  • exercising and setting small daily goals
  • distracting yourself - e.g. music, books, podcasts
147
Q

resilience factors =

A
  • Resilience factors (RFs) are psychological resources that buffer the potentially negative effects of stress on mental health.
148
Q

examples of resilience factors?

A
  • the ways in which individuals view and engage with the world
  • the availability and quality of social resources
  • specific coping strategies
149
Q

problem solving and anxiety?

A
  • anxiety (especially chronic) can hinder our ability to filter things that we think of as a threat in order for our brains to accurately concentrate on the retrieval of info necessary for problem solving
150
Q

members of community MH teams?

A
  • nurses
  • occupational therapists
  • psychologists
  • MH support workers
  • consultant psychiatrists
151
Q

Community mental health teams work as part of an MDT to:

A
  • provide medical support
  • putting patients in touch with other agencies
  • short term work for a specific mental health diagnosis which requires short term support
  • physical health monitoring
152
Q

CMHTs work as part of an MDT and can provide support with (3)?

A
  • support w employment support
  • psychological approaches
  • support with day to day activities and functioning
153
Q

organisiation of MH services?

A
  • Primary care - GP
  • community - MH teams
  • hospitals and in specialist services
  • this is primary, secondary and tertiary care
154
Q

NHS LTP?

A

is going to create intergrated community mental health servcies

155
Q

primary MH services?

A

GP - refer to secondary services but these can also be accessed through the single point of access

156
Q

secondary MH services?

A

specialised, include teams like community MH teams, crisis resolution and home treatment teams and hospital care

157
Q

voluntary MH services?

A
  • Running alongside primary and secondary services are voluntary services: support provided in the community, usually by charities and other non-profits.
  • You can often access these services without a referral
158
Q

tertiary MH services?

A

highly specialised treatment like forensic MH services or specialist psychotherapy services

159
Q

intergrated care systems =

A
  • removing traditional divisions between different tiers of care
  • so that people get less disjointed care
160
Q

what do ICS aim to do?

A
  • aims to remove divisions such as those between hospials and GPs, physical and mental health and the NHS & local authority
161
Q

ICS are new partnerships between?

A

between the NHS and other health and care organisations. Such as the local authority, voluntary sector and social enterprise sector

162
Q

depression epidemiology?

A
  • 4th leading casue of disability worldwide
  • point prevalence 2-5%
163
Q

one depressive episode =

A

F32 Depressive Episode

164
Q

if there is more than one depressive episode it’s either:

A
  • F31 Bipolar Affective Disorder
  • F33 Recurrent (Unipolar) Depressive Disorder
165
Q

RF for depression?

A
  • genetics
  • Gender – twice as common in women
  • Childhood experience – e.g. loss of parent, lack of parental care, abuse
  • Personality – especially neuroticism
  • Social environment – life stresses, lack of social network etc
  • Physical illness
166
Q

ICD-10 criteria for depression

A
167
Q

Tx of depression - non pharm?

A
  • Education
  • Lifestyle changes - diet, alcohol, sleep hygiene
  • Physical health problems improved
  • Problem- solving - helping resolve trigger factors like unemployment or marital problems
168
Q

Psychological treatment (psychotherapy) for depression?

A
  • attempt at relieving a person’s psychological distress using psychological means
  • different methods of counselling - CBT, CAT, psychodynamic
169
Q

what does psychotherapy involve?

A
  • Confiding relationship for listening and talking
  • Release of emotion
  • Giving information
  • Provision of rationale to make problems understandable
  • Restoration of morale
170
Q

levels of CBT - self help materials?

A
  • Self-help materials – This is not a form of psychotherapy and no CBT skills or training are required by the individual reading the self-help material (e.g. books/ websites).
171
Q

levels of CBT - assisted self help?

A
  • Assisted self-help - computerized CBT, self-help material presented to a support group or individuals by a health worker, such as a graduate mental health worker or assistant psychologist
172
Q

levels of CBT - CBT approaches?

A
  • CBT approaches - Specific CBT interventions for specific problem areas, e.g. anxiety management, coping with voices etc.
173
Q

levels of CBT - formulation driven CBT?

A
  • Formulation driven CBT– This is a form of psychotherapy, the patients are not fully able to help themselves and have sought help from a trained professional.
174
Q

what are the levels of CBT?

A

1) Self help materials
2) assisted self help
3) CBT approaches
4) formulation driven CBT

175
Q

what do the therapist and patient agree on during CBT?

A
  • Patient and therapist agree problem list and goals. Treatment is a collaborative partnership
  • Focuses on ‘here and now’
176
Q

Which type of questioning is used in CBT?

A
  • socratic questioning used by the therapist
  • open therapeutic process
  • homework used
177
Q

what is the CBT model of depression?

A
  • Underlying beliefs centre around being helpless or unloveable
  • Trigger events typically involve loss or ‘failure’
  • This produces negative cognitions about self/ future/ world which reinforce underlying beliefs, and affect mood and behaviour
178
Q

CBT model of depression - how are negative thoughts maintained?

A
  • These negative thoughts are maintained by distorted information processing (e.g. overgeneralization, personalization, selective abstraction)
179
Q

techniques used in CBT?

A
  • Activity monitoring and scheduling (mastery and pleasure)
  • Distraction
  • Systematic desensitization
180
Q

techniques used in CBT - anxiety management?

A

progressive muscular relaxation, imagery, breathing control etc

181
Q

cognitive techniques used in CBT?

A
  • identifying and challenging negative thoughts using thought records -replacing with balanced thoughts
  • identifying cognitive biases
  • working on deeper levels of cognition like behavioural experiments to challenge dysfunctional assumptions
182
Q

social factors in depression ?

A
  • Social problems
  • Past history of depression
  • Chronic disease e.g. diabetes, heart disease, chronic obstructive pulmonary disease, cancer
  • Alcoholism
  • Bereavement
  • Old age
183
Q

red flags in depression?

A
  • Risk of suicide
  • Feeling of hopelessness
  • Chronic pain
  • Disabling symptoms
  • Severe and prolonged symptoms
184
Q

How do young adults tend to present with depression?

A
  • Young adults tend to sleep a lot, overeat, withdraw and show self-neglect.
185
Q

how do older adults tend to present with depression?

A
  • Older adults often present with insomnia, anxiety, anorexia, poor self-care and exacerbation of pre-existing physical conditions like painful arthritis, constipation, head and neck and back pain
186
Q

Diagnostic criteria for depression

A
187
Q

which drugs can cause depressive symptoms?

A
  • BBS and psychoactive medications can cause depressive symptoms
188
Q

mania?

A
  • mania = period of elation - high mood
  • can be mild (hypomania) or severe (mania)
189
Q

bipolar disorder =

A
  • mania + depression = bipolar disorder/ manic depression
190
Q

depression is the ? most common reason for consulting a GP

A

3RD

191
Q

top 10 presenting symptoms of depression ?

A
  • tiredness
  • headache
  • stress
  • low mood
  • backache
  • sleep problems
  • chest pains
  • indigestion
  • dizziness
  • pain
192
Q

Normal grief reactions?

A
  • shock, denial, numbness, guilt, sadness, weeping, resolutuon
  • Emotional and practical support is normally sufficient.
193
Q

abnormal grief reactions?

A
  • if symptoms are more intense e.g. clinical depression or if they’re prolonged (beyond 6 months) or if they’re delayed in onset
  • Counselling, “guided mourning” and occasionally medication may be needed.
194
Q

socio-cultural aspects of depression - black and asian races present less ofern with?

A
  • Black and Asian races present less often to their GP with “depression”
  • Some groups are more likely to complain of physical symptoms eg Mediterranean (“nerves, headache”), China & Asia (“weak, tired”),
195
Q

what are risk factors for suicide?

A
  • migration and not speaking the local language are risk factors for suicide
  • refer to specific services e.g. Refugee council and use a professional translator
196
Q

depression acronym for symptoms

A
197
Q

for depression to be diagnosed there needs to be?

A
  • 4+ symptoms for at least 2 weeks include at least 2 of the first 3 core symptoms
198
Q

how can severe depression present?

A
  • severe depression can present with psychotic symptoms e.g. delusions or hallucinations
199
Q

somatic syndrome?

A

Depression may be more significant and respond to antidepressants if somatic (“biological”) symptoms* are present: sleep/app/wt change, anhedonia, loss of libido, constipation, amenorrhoea

200
Q

mild depression =

A
  • 4 symptoms
  • distressed but able to continue functioning
201
Q

moderate depression =

A
  • 5/6 symptoms
  • great difficulty continuing w normal functioning
202
Q

severe depression =

A
  • 7 to 10 symptoms
  • totally unable to work or function
203
Q

MSE considers?

A
  • Appearance
  • behaviour
  • speech
  • thoughts
  • perceptiuon
  • mood
  • cognition
  • insight
204
Q

drugs linked to depression?

A
  • Drugs: steroids, contraceptive pill, digoxin, beta blockers
205
Q

causes of depression - illness?

A
  • Any physical illness eg hypothyroidism, heart disease, stroke, cancer, MS
  • Other mental disorders eg psychosis, dementia, alcohol excess, illicit drug abuse
206
Q

depression is linked to?

A
  • linked to reduced levels of serotonin and noradrenaline
  • Some bipolar patients have enlarged cerebral ventricles on CT scan
207
Q

depression is an independent RF for?

A
  • Depression is an independent risk factor for osteoporosis (10% drop in bone density) & coronary heart disease (2-4 times increase in angina, MI & sudden death)
208
Q

Bipolar I disorder =

A

dep plus mania.

209
Q

bipolar II disorder =

A

dep plus hypomania

210
Q

clinical features of bipolar?

A
  • elated or irritable mood
  • high energy/ libido
  • reduced sleep and appetite
  • rash behaviour and debts are risks
  • grandiose, paranoid delusions
211
Q

advice for a bipolar patient?

A
  • avoiding alcohol and drugs
  • no over stimulation
  • ensure sleep and regular routine
212
Q

physical tx for bipolar - depression?

A
  • Antidepressants eg SSRIs
  • Anti-psychotics (if psychotic)
  • Lithium (if treatment resistant),
  • ECT (if life threatening)
    mania
213
Q

physical treatments for bipolar - mania?

A
  • Antipsychotics eg olanzapine+/-mood stabilisers eg lithium
  • ECT (if treatment resistant)
  • Lorazepam (if aggressive)
214
Q

adjustment disorder =

A

if depressive symptoms present than less than2 weeks - milder short period of low mood due to stressful life events

215
Q

mild to moderate depression Tx?

A
  • low intensity psychosocial interventions
  • guided self help based on CBT princuples, behavioural activation and problem solving techniques
216
Q

moderate to severe depression Tx?

A
  • antidepressants and CBT or interpersonal therapy
  • high intensity psychological interventions - 16-20 sessions over 3-4 months
217
Q

severe/ complex depression Tx?

A

Crisis or home treatment teams, inpatient admission, ECT

218
Q

recurrent depression Tx?

A

individual CBT, or mindfulness (if now well but 3 or more episodes = group mindfulness-based CBT)

219
Q

drugs for the different depression severities?

A
  • mild: not unless prolonged
  • moderate to severe: drugs and therapy
220
Q

drug pathway for depression?

A
  1. SSRIs
  2. other SSRI or mirtazepine or lofepramine,
  3. Venlafaxine / TCA/ MAOI
  4. Add lithium / antipsychotic eg quetiapine / mirtazapine
  5. ECT
221
Q

psych treatments work best in which type of depression?

A

mild to moderate

222
Q

physical treatments work best in ? depression

A
  • Physical treatments (drugs & ECT) work best in moderate to severe depression.
223
Q

the stepped approach in depression?

A
224
Q

all psychotherapies involve:

A
  • A therapeutic conversation ie talking = exchange of information + instillation of hope
  • A therapeutic relationship (alliance) between therapist and ‘client’/patient
  • A therapeutic rationale ie an explanation followed’ by therapist & patient
  • A therapeutic base ie regular meetings in time & place (eg 1 hour every week)
225
Q

ECT is used for?

A
  • used for severe/ life threatening depression requiring a rapid response (not eating or drinking, acutely suicidal, retarded, psychotic) or if other treatments are ineffective
226
Q

ECT increases synthesis of?

A
  • ECT involves giving a short acting IV general anaesthetic plus a muscle relaxant.
227
Q

what happens in ECT?

A
  • A pulsed electric current is then passed through the brain to produce a brief (15-60sec) grand mal seizure. Patients vary, but often need 6 to 12 sessions, given twice weekly
228
Q

Circle of depression and inactivity

A
229
Q

bipolar 1 vs bipolar 2?

A

Bipolar I disorder often leads to problems with day-to-day life and hospital admissions, whereas in bipolar II disorder there are no psychotic features and less impact on function.

230
Q

hypomania?

A
  • In hypomania, there is increased energy and activity with persistently elevated mood, which occurs without delusion or hallucinations.
231
Q

patterns in bipolar can be negatively influenced by?

A
  • patterns of cycles in bipolar disorder can be negatively influenced by drinking, stress, ilict drugs and other medical conditions
232
Q

PMH - which conditions can cause symptoms of mania?

A
  • PMH - HIV infection, syphilis, thyroid disease and epilepsy), which can may cause symptoms of mania through their effects on the brain.
233
Q

first line medications in mania?

A

AP

234
Q

meds for mania?

A
  • antipsychotics
  • medium to longer term: mood stabilisers
  • antidepressants and benzodiazepines
235
Q

mood stabilisers in mania?

A

valproate and lithium

236
Q

AD in mania?

A

should usually be stopped during the manic phases

237
Q

benzodiazepines in mania?

A

short term use, sometimes used for severe agitation

238
Q

systemic steroids can result in?

A

secondary mania or depression.

239
Q

speech in mania?

A
  • Speech. Pressure of speech will usually be obvious during manic phase. Slowed speech is characteristic of the depressive phase.
240
Q

thoughts in mania?

A
  • Thoughts. Thoughts may be racing and flight of ideas will be present.
  • Grandiose ideas may come up during the review.
241
Q

energy in mania?

A
  • Energy. The person will usually appear very energetic and hyperactivity is common.
242
Q

eye contact in bipolar?

A
  • Eye contact. In the depressive phase, eye contact may be reduced.
243
Q

affect in bipolar?

A
  • Affect. Patients may be tearful and apathetic during the depressive phase.
244
Q

ECT - discussions?

A
  • valid informed consent needed
  • right to withdraw at any time
  • carers/ advocates should be involeved to facilitate informed discussions
245
Q

ECT - if informed consent not possible?

A
  • if informed consent is not possible, ECT should only be given if it does not conflict with a valid advance decision, and the person’s advocate or carer should be consulted.
246
Q

ECT - monitoring?

A
  • assess clinical status after each ECT treatment and stop treatment when remission has been achieved or sooner if side effects outweight the potential benefits
  • Assess cognitive function before the first ECT treatment and monitor at least every three to four treatments, and at the end of a course of treatment.
247
Q

ECT monitoring - addenbrooke’s cognitive assessment?

A
  • addenbrooke’s cognitive assessment mainly used - measures new learning, retrograde amnesia and subjective memory impairment
248
Q

advantages of ECT?

A
  • Effective when other treatments don’t work
  • Most effective with most severe illness
249
Q

Disadvantages of ECT?

A
  • Multiple brief anaesthetics
  • Acute confusional states
  • Memory impairment: anterograde and retrograde
250
Q

Meds that interfere with ECT?

A

anticonvulsants and lithium

251
Q

short term ECT side effects?

A
  • headache
  • muscle aches
  • distressed
  • tearful
  • frightened
  • temporary memory loss
252
Q

ECT - damage to?

A
  • damage to tongue, teeth or lips because ECT causes contraction of the jaw muscles
253
Q

LT ECG side effects

A
  • memory problems
  • personality change
  • lost skills
  • ‘feel like a different person;
254
Q
A