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Gargi's & Emma's notes - Anxiety Disorders Flashcards

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1
Q

Define acute stress reaction

A
  • A transient disorder of significant severity which develops in an individual without any other mental disorder, in response to a severe stressor
  • Also described as an understandable ‘state of shock’ after traumatic events
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2
Q

What is the aetiology of acute stress reaction?

A
  • Occurs in response to a traumatic stressor e.g. physical or sexual assault, RTA, war
  • Individual vulnerability and coping capacity play a role in the occurrence and severity
    • May be higher incidence in anxious patients
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3
Q

What is the epidemiology of acute stress reaction?

A
  • Up to 50% adults experience a traumatic event in their lives
  • Prevalence of acute stress reaction after a traumatic event is 5-20%
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4
Q

What is important to ascertain when formulating a differntial to incl acute stress reaction?

A

Must be a clear relationship between the stressor and symptoms, onset of symptoms is within mins

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5
Q

What are the signs and symptoms of acute stress reaction?

A
  • Symptom onset is within minutes of the event
  • Intense anxiety, autonomic symptoms of anxiety
    • e.g. tachycardia, hypertension, sweating, anxious, restless, may wander aimlessly or be hyperactive
  • State of ‘daze’: narrowing of attention, inability to comprehend stimuli, depersonalisation, derealisation, disorientation, confusion
  • May be irritable, hyperactive, aggressive, hopeless
  • Later, there may be partial or complete amnesia of the event
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6
Q

What are the investigations for ?acute stress reaction?

A
  • Thorough history, collateral history, MSE
    • Determine nature and severity of the stressor (psychosocial vs traumatic stressor)
    • Exclude other neuroses, psychoses or organic disorders producing delirium
  • Basic examination à exclude injury
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7
Q

What are the complications of acute stress reaction?

A
  • May progress to PTSD
  • If transient stressor, symptoms must resolve after 8h, if exposure to stressor continues then symptoms must continue to diminish after 48h, if they persist – suggest patient at risk of developing PTSD
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8
Q

What must be excluded with ?acute stress reaction?

A

Exclude other neuroses, psychoses or organic disorders producing delirium

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9
Q

What is the management of acute stress disorder?

A
  • Remove stressor if possible
  • Psychological interventions:
    • Support and reassurance –> usually sufficient
  • Pharmacological treatment:
    • Benzodiazepines
      • Short-term relief of symptoms, aid sleep
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10
Q

What is the prognosis of acute stress reaction?

A

Usually subsides within hrs-days

May progress to PTSD

  • Benzodiazepines do not prevent progression
  • Formal, immediate, psychological ‘debriefing’ (describing trauma and emotional response) increases risk
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11
Q

Define adjustment disorder

A

Distress and emotional disturbance, usually interfering with social functioning and performance, arising in response to a significant life change or stressful life event

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12
Q

What is the timescale involved in adjustment disorder?

A
  • Prolonged abnormal response to stress beginning within 1 month of a stressful life event,
  • lasting no more than 6 months
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13
Q

What is the aetiology of adjustment disorder?

A
  • Maladaptive psychological responses to stressful life events – divorce, unemployment
  • Any age of onset, up to 20% of patients attending a psych outpatient clinic could be diagnosed with adjustment disorder
  • Life changes/psychosocial stressors require ability to cope with new situations
    • It is normal to have fleeting anxiety, low mood, irritability or sleep disturbance
    • In adjustment disorder, the person’s reaction is out of proportion to the original stressor, or causes disturbance of functioning
      • Symptoms are not severe enough to diagnose a depressive disorder
      • The individual’s personality and vulnerability to stress contribute
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14
Q

What are the 5 stages of grief?

A
  • 5 stages of grief (not rigid):
    1. Denial
    2. Anger
    3. Bargaining
    4. Depression
    5. Acceptance
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15
Q

What is the length of a normal grief reaction?

A
  • Length of a normal bereavement reaction is variable –> commonly 1 year (after all anniversaries) can last up to 2 years
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16
Q

What should the patient be assessed for if the grief reaction is abnormal?

A
  • If a bereavement reaction is abnormal, assess for depression
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17
Q

What are some signs suggesting depression rather than grief reaction?

A
  • Signs suggesting depression: excess guilt, suicidal ideation, worthlessness, psychomotor retardation, prolonged/marked functional impairment, hallucinations (other than transiently seeing/hearing deceased)
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18
Q

Which criteria must not be met for adjustment disorder to be diagnosed?

A
  • If criteria for depression are not met, adjustment disorder is diagnosed
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19
Q

What is a prolonged grief reaction?

A
  • Prolonged grief reaction is when the intensity and duration of grief is beyond what would be expected à may have difficulties accepting death, functioning, avoiding reminders, persistent preoccupation with deceased
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20
Q

What are the signs and symptoms of adjustment disorder?

A
  • Precipitated by a psychosocial stressor
    • Symptoms start within 1 month (ICD-10) / 3 months (DSM-5); resolve within 6 months
  • Symptoms of anxiety/depression not severe enough to diagnose anxiety/depressive disorder
    • No biological features of depression
  • Functional impairment à difficulty with day-to-day activities
  • Occasionally disturbances of conduct (e.g. aggression) –> esp in adolescents
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21
Q

What are the investigations for ?adjustment disorder?

A
  • Thorough history, collateral history, MSE, risk assessment
    • Identify stressor
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22
Q

What is the Mx of adjustment disorder?

A

1)Remove stressor if possible

2) Psychological interventions:

  • Support and reassurance
  • Counselling and problem-solving counselling (usually sufficient)
    • To assist in removing the stressor, or teach coping techniques to deal with it
  • CBT

3) Pharmacological management (not usually needed):

  • Benzodiazepines for symptomatic treatment
  • Antidepressants (but not usually needed because criteria for depression have not been reached)
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23
Q

What are the 2 types of anxiety disorders? Describe them

A
  • Generalised (free-floating) anxiety
    • Generalised anxiety disorder
    • Does not occur in discrete episodes; lasts for hours/days/longer
    • Mild-moderate severity
    • Not associated with a specific external threat but is rather excessive worry/apprehension about many life events
  • Paroxysmal anxiety
    • Abrupt onset, occurs in discrete episodes and tends to be severe
      • In its severest form, paroxysmal anxiety occurs as panic attacks (panic disorder)
    • May occur spontaneously (panic disorder) or in response to a specific imagined or external threat (phobia)
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24
Q

What are the signs and symptoms seen in all anxiety disorders?

A

The experience of anxiety consists of 2 interrelated components:

  1. Thoughts of being apprehensive/nervous/frightened
  2. The awareness of a physical reaction to anxiety (autonomic or peripheral anxiety)
    • The physical signs of anxiety are:
      • Tachycardia, palpitations, chest pain, HTN
      • Shortness of breath/rapid breathing
      • Choking sensation
      • Tremors, shaking, muscle tension
      • Sweating, cold skin, facial flushing
      • Paraesthesias – tingling/numbness
      • Nausea or vomiting, diarrhoea
      • Abdominal discomfort (‘butterflies’)
      • Dizziness, lightheadedness, syncope
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25
Q

Which investigations must be conducted for all anxiety disorders?

A
  • Thorough history, collateral history, MSE
    • Rating scales: Beck anxiety inventory, Hospital Anxiety and Depression Scale (HADS))
    • Assess severity or provide baseline scores to measure treatment response
    • Assess functioning and effect on QoL
  • Exclude organic causes
    • FBC, U&Es, LFTs, Ca (hypocalcaemia  arrhythmias), TFTs
    • Glucose
    • ECG/24hr ECG (for tachycardia/palpitations)
    • 24hr urine for catecholamines (phaeochromocytoma)
    • UDS/history for substance misuse
      • Intoxication: alcohol, caffeine, cocaine
      • Withdrawal: alcohol, benzodiazepines, caffeine, nicotine, opiates, cocaine
      • SEs of prescribed drugs: SSRIs/TCAs, corticosteroids, thyroid hormones
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26
Q

Define GAD

A

Generalised and persistent anxiety, that is not restricted to or predominating in any particular circumstances

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27
Q

What are the GAD-specific symptoms?

A
  • Symptoms should be present on most days for at least several weeks; can fluctuate in intensity
  • Symptoms should involve elements of:
    • Apprehension
      • Worries about future misfortunes, feeling on edge, difficulty concentrating
    • Motor tension
      • Restlessness, fidgeting, tension headaches, trembling
    • Autonomic overactivity (physical symptoms)

If severe, patients may have panic attacks

28
Q

What is the Mx of GAD?

A

Psychological intervention:

  • Psychoeducation and reassurance
    • May be enough to prevent early/mild problems worsening
  • Teach relaxation techniques/breathing exercises
  • Lifestyle advice, e.g. sleep hygiene, exercise
  • Counselling and problem-solving counselling
    • To address worries and deal with stressors
  • CBT – joint 1st line with SSRIs (esp if children/pregnant/don’t want medication)
    • Self-help material, computer-based CBT, individual CBT
    • Aims to reduce the patient’s expectation of threat and behaviours that maintain threat-related beliefs
    • Behavioural responses to anxiety/worry include avoidance and reassurance-seeking  CBT tests predictions of worry with behavioural experiments and looking at errors of thinking

Pharmacological therapy:

  • SSRIs/SNRIs – joint 1st line with CBT
    • TCAs are 2nd line
  • Benzodiazepines
    • Short-term treatment (e.g. while waiting for SSRIs to work) – max 2-4wks
  • Beta-blockers
    • To treat physical adrenergic symptoms
29
Q

What is panic disorder?

A

Presence of panic attacks that occur unpredictably and are not related to any particular situation or objective danger

  • For diagnosis, there must be recurrent panic attacks (usually several within a month)
  • Between episodes, the patient is relatively free of anxiety.
30
Q

What are the panic disorder-specific signs and symptoms?

A
  • Rapid onset, rapidly builds up to peak level of anxiety, lasts up to 30mins (self-limiting)
  • Strong autonomic (physical) symptoms, feelings of depersonalisation/derealisation
    • Secondary fear of dying/losing control/going mad → further panic (vicious cycle) until reassurance/safety behaviours
  • Little anxiety between attacks
    • There may be anticipatory anxiety  fear of further panic attacks
31
Q

What is the Mx of panic disorder?

A

Psychological interventions:

  • Psychoeducation and reassurance
  • Teach relaxation techniques/breathing exercises
  • Counselling and problem-solving counselling
  • CBT – 1st line
    • Educates patient on the meaning of symptoms (panic, not signs of major catastrophe) → helps to terminate panic attack
    • Exposure therapy (to relevant uncomfortable physical sensations, e.g. hyperventilation, tachycardia by over-breathing/exercising in a hot room)  to show that these are not harmful

Pharmacological therapy:

  • SSRIs/SNRIs – joint 1st line with CBT
    • TCAs are 2nd line
  • Benzodiazepines
    • Short-term treatment (e.g. while waiting for SSRIs to work) – max 2-4wks
    • Or if intolerance/poor response to antidepressants
  • Beta-blockers
    • To treat physical adrenergic symptoms

Management of acute panic attack:

  • Reassurance
    • That symptoms are not dangerous and attack will subside soon
    • Encourage slowing of breathing, quiet room
  • Benzodiazepines (if available/necessary)
32
Q

What are phobic disorders? Name some and define them

A

Group of disorders in which anxiety is evoked only, or predominantly, in certain well-defined situations that are not currently dangerous

  • Agoraphobia: anxiety associated with places/situations from which escape may be difficult, e.g. crowds, public places
  • Social phobia: persistent fear of social situations that may lead to scrutiny/criticism/embarrassment
  • Specific phobia: persistent fear of a specific object or situation, out of proportion to the threat
33
Q

What is the aetiology of phobic disorders?

A
  • Genetic factors
  • Classical conditioning and negative reinforcement
    • Often follows a precipitating event, e.g. panic attack in agoraphobia, negative experience with object/situation in specific phobias
  • Modelling may contribute (i.e. watching parents)

Social phobia may be secondary to a depressive illness, when performance declines

34
Q

What is the epidemiology of:

  • agoraphobia
  • social phobia
  • specific phobia
A

Agoraphobia:

  • Onset late 20s
  • F>M

Social phobia:

  • Onset gradual from adolescence
  • F>M

Specific phobia:

  • Onset usually in childhood (varies)
  • F>M
35
Q

What are the specific symptoms seen in phobic disorders?

A
  • Anxiety symptoms (may cause panic attack) when exposed to the phobic situation (not at other times)
    • Anticipatory anxiety when contemplating entry to the phobic situation
  • Avoidance of these situations (or endurance with dread)
    • Overall anxiety/impact on QoL may be low if patient successfully avoids the situation
  • Agoraphobia:
    • Fear of crowds, public places, travelling alone, being away from home → overwhelming urge to return home to safety
    • May feel better if accompanied by someone else
    • If severe: housebound, dependent on small circle of family/friends
  • Social phobia:
    • Situational anxiety in social groups parties, meetings, classrooms
      • Can usually tolerate 1-1 or anonymous crowd
    • Fear of scrutiny/humiliation/embarrassment
    • May have specific worries, e.g. eating in public
  • Specific phobia:
    • Fear of specific objects/situations e.g. animals, blood, heights
36
Q

What is the Mx of phobic disorders?

A

Psychological interventions:

  • Psychoeducation and reassurance
  • Teach relaxation techniques/breathing exercises
  • Counselling and problem-solving counselling
  • CBT with graduated exposure therapy
    • 1st line
    • Explores the actual likelihood and impact of the anticipated catastrophe
    • E.g. CBT in social phobia  explores predictions such as “I will embarrass myself”; behavioural experiments set up to challenge them  increases confidence with situation
      • Focuses on removing ‘safety behaviours’ e.g. excessive self-monitoring
    • Exposure therapy:
      • Used when there are strong elements of avoidance and escape
      • Uses a gradual approach (desensitisation)
        • A goal is set (something that would make patient more functional); steps to reach the goal are made
        • Patient tackles each step in turn with ‘homework’
        • Mission is to stay in situation until anxiety has resides (habituation)  with repeated attempts habituation occurs more quickly each time
      • E.g. agoraphobia tasks may include small shop, then big supermarket

Pharmacological therapy:

  • SSRIs/SNRIs
    • 1st line in social phobia (joint with CBT)
  • Benzodiazepines
    • Considered short-term if phobia needs to be endured (e.g. needle phobias interfering with chemotherapy, claustrophobia interfering with MRIs, travel phobia interfering with work)
  • Beta-blockers
    • To treat physical adrenergic symptoms
37
Q

What is OCD?

A

An anxiety disorder in which the patient suffers from obsessions and compulsions that interfere with day-to-day life

Obsession: involuntary thoughts/images/impulses, which:

  • Are recurrent and intrusive, and experiences as unpleasant/distressing
  • Enter the mind against conscious resistance
  • Originate in the patient’s own mind (different to auditory hallucinations)

Compulsion: repetitive mental or physical acts, which:

  • Patients feel compelled to perform
  • Are unpleasant and have no realistically useful purpose
38
Q

What is the aetiology of OCD?

A

Biological factors:

  • Genetics
    • 35% of 1st degree relatives also have OCD; up to 80% concordance in monozygotic twins
  • Neurobiology:
    • Neurotransmitter theories related to 5-HT dysfunction
    • Basal ganglia abnormalities  risk of OCD increased in illnesses which affect basal ganglia (Sydenham’s chorea, Tourette’s syndrome, PANDAS)
    • Deficit in frontal lobe inhibition  intrusive thoughts harder to suppress

Psychological factors:

  • Many have premorbid anankastic personality traits (rigidity, orderliness)
  • Comorbid depression in 30% OCD patients
  • 15% patients with schizophrenia have OCD

Social factors:

  • Stress may precipitate symptoms
39
Q

What are the diagnostic criteria for OCD?

A
  • Criteria for diagnosis (ICD-10)
    • Obsessions or compulsions present on most days for >2wks (and not accounted for by presence of another mental illness, e.g. schizophrenia)
    • Acknowledged as originating from the patient’s own mind
      • Insight that the thoughts are irrational is often retained
    • Persistent, repetitive and intrusive
    • Patient tries to resist them
      • Resistance causes anxiety until they are carried out
    • Not intrinsically pleasurable (except for relief of anxiety)
    • Cause distress and interfere with functioning
40
Q

Name some common obsessions/compulsions seen in OCD

A
  • Fear of contamination → excessive washing/cleaning
  • Pathological doubt (e.g. have I turned the oven off) → exhaustive checking
  • Violent/unpleasant thoughts/impulses (e.g. impulse to murder) → act of redemption
  • Need for symmetry/precision → repeatedly arranging objects
41
Q

What are the Ix for OCD?

A
  • Thorough history, collateral history, MSE
    • Yale-Brown Obsessive-Compulsive Scale to measure symptom severity (useful to track progress)
  • Rule out organic causes (if necessary)
42
Q

What is the Mx of OCD?

A

Psychological interventions:

  • Psychoeducation
  • CBT – 1st line
    • Hierarchy of feared situations is used (as in exposure therapy) – allows activity to habituate
    • E.g. if obsessions about contamination  support to touch something dirty, then discuss anxiety/feelings rather than wash hands immediately

Pharmacological treatment:

  • SSRIs or clomipramine (TCA) – 1st line (at the same time as CBT if severe, or SSRI/CBT can be monotherapy)
  • TCAs (clomipramine) – 2nd line
  • Antipsychotic
    • Adjunct if insufficient response to SSRIs/clomipramine  specialist referral
43
Q

What are the complications of OCD?

A
  • Difficulty with relationships, work and social functioning
  • Comorbid depression and schizophrenia
  • Comorbid alcohol and substance misuse
  • Increased suicide risk
44
Q

What is the prognosis of OCD?

A
  • Chronic course (life-long), with worsening symptoms at times of stress
  • Poor prognostic factors: male, early onset, severe symptoms, premorbid personality disorder, life stresses
45
Q

What is PTSD?

A

An intense, delayed, prolonged reaction to an exceptionally stressful event

  • The event must be likely to cause pervasive distress to almost anyone (traumatic stressor)
46
Q

Which factors increase risk of developing PTSD:

A

Caused by a traumatic stressor (like acute stress reaction)

Factors that increase risk of developing PTSD:

  • Biological factors:
    • Genetics
    • Female gender
  • Psychological factors:
    • Borderline, paranoid or dependent personality traits
    • Past psychiatric history
  • Social factors:
    • Childhood trauma
    • Inadequate support system
    • Recent stressful life events
    • Low social class and poor education
  • Stressor factors:
    • Degree of exposure
    • Proximity
    • Human design (e.g. torture victims)
    • Survivor guilt and continual exposure to the trauma/other stressors can perpetuate symptoms
47
Q

What is the epidemiology of PTSD?

A

10-25% of those exposed to an exceptionally threatening event develop PTSD

Lifetime prevalence 1-3%

High prevalence in war veterans, asylum seekers/refugees

48
Q

What are the signs and symptoms of PTSD?

A
  • Symptoms develop 1-6 months after the event
  • There are 3 main groups of symptoms
    • Intrusions
      • Flashbacks (intrusive, vivid images), nightmares, frequent thoughts of the event
      • Distress caused by internal and external cues that resemble the stressor
      • Patients may dissociate and experience the event as if it was re-happening
    • Avoidance
      • Avoidance of stimuli associated with the stressor
      • Amnesia for aspects of the event/inability to recall aspects
      • Emotional detachment
      • Social withdrawal, anhedonia
    • Hyperarousal
      • Persistent anxiety, hypervigilance, exaggerated startle response
      • Insomnia
      • Angry outbursts, irritability, poor concentration
49
Q

What are the Ix for PTSD?

A
  • History, collateral history, MSE, risk assessment
    • Screening/assessment tools e.g. PTSD checklist, impact of event scale (IES-R)
    • Screen for co-morbid psychiatric disorders (e.g. depression)
50
Q

What is the Mx of PTSD?

A

For mild symptoms <3 months after → watchful waiting and follow-up in 1 month (intervene for severe/>3months)

  • Mild symptoms are when distress is manageable and functioning is not impaired

Psychological intervention:

  • Trauma-focused CBT (1st line)
    • Previous belief patterns have been shattered, resulting in new belief patterns, e.g. “the world is unsafe and unpredictable” “I am vulnerable”  these identified and challenged
    • Often combined with exposure therapy
  • Eye movement desensitisation and reprocessing (EMDR) (1st line)
    • The original trauma is deliberately re-experienced in as much detail as possible (e.g. by patient narrating every step that happened)
    • While doing this, they fix their eyes on the therapist’s finger as it moves side to side in front of them
    • It is thought to aid memory processing

Pharmacological treatment:

  • SSRIs/SNRI
    • Preferably in combination with psychological therapies
    • Given without psychological therapy if patient preference or failed to respond/couldn’t tolerate
51
Q

What is the prognosis of PTSD?

A

Half make a good recovery within 1yr; a minority have chronic symptoms for many years

Symptoms may resurface at anniversaries associated with the event

52
Q

Define dissociative disorder(s)

A

A physical or mental symptom (e.g. functions under voluntary motor control, loss of sensation, amnesia) that suggest neurological or medical conditions, in the absence of a physical disorder to explain them

  • NB disorders involving pain or other complex sensations mediated by the ANS are classified under somatisation disorder

Aka conversion disorders if they involve physical symptoms (conversion disorders don’t describe amnesia etc.)

53
Q

What is the aetiology of dissociative disorder(s)

A

There is loss of the normal integration between past memories, awareness of identity, awareness of immediate sensations, and control of body movements (ICD-10)

Psychodynamic theories:

  • Dissociative symptoms are caused by the repression of unconscious intrapsychic conflict and the conversion of the resulting anxiety into a physical symptom  so the symptoms are thought to be an expression of emotional conflicts/needs
  • This results in relief of emotional conflict (primary gain) and the advantages of assuming the sick role
54
Q

What are the RFs for dissociative disorder?

A

RFs are mostly social:

  • History of childhood abuse, unstable childhood
  • Traumatic events, insoluble problems
  • Disturbed relationships
  • History of trauma-related disorders, e.g. PTSD
55
Q

What are the general symptoms and signs of disassociative disorder(s)?

A
  • Symptoms appear suddenly and are often dramatic
  • Symptoms represent the patient’s concept of how a physical illness would manifest (may be odd, don’t fit with usual symptoms, doesn’t fit with dermatomes, distractible symptoms, etc.)
  • May have ‘la belle indifference’ (show less distress than would be expected with their symptoms)
    • But they usually show exaggerated emotional reactions to other things
56
Q

What are the types of dissociative disorder?

A
  • Dissociative amnesia: partial/complete memory loss, usually of recent traumatic events
  • Dissociative fugue: same features of dissociative amnesia with an apparently purposeful journey away from home
    • Self-care and social interaction are maintained
    • A new identity may be assumed
  • Dissociative pseudo-dementia: abnormality of intelligence suggesting dementia, but answers questions wrongly in a way that suggests they have the correct answer in mind
  • Dissociative stupor: motionless and mute, but aware of surroundings
  • Dissociative anaesthesia and sensory loss: cutaneous or visual sensory loss that does not correspond to dermatomes/known neurological patterns
  • Dissociative motor disorders: partial/complete paralysis of muscles, e.g. can’t move a limb
  • Dissociative convulsions (psychogenic non-epileptic seizures/pseudoseizures): presents similar to epileptic seizure but tongue-biting/serious injury/incontinence are uncommon; EEG not epileptic
  • Dissociative identity disorder (multiple personality disorder): apparent existence of 2 or more personalities in the same individual
57
Q

What are the Ix for dissociative disorder?

A
  • Thorough history, MSE
    • Rule out other psychological disorders, e.g. depression (can cause depressive stupor)
    • Rule out factitious disorder/malingering
  • Exclude physical cause → there must be no evidence of a physical cause
    • Don’t over-investigate if unlikely to have a physical cause
58
Q

What is the Mx of dissociative disorder?

A

Psychological interventions:

  • Reassurance  will resolve, no adverse effect on physical health
  • CBT, mindfulness-based CBT
    • Involves psychoeducation about symptoms, recognising automatic thoughts/triggers etc.
  • Interpersonal psychotherapy

Social interventions:

  • Support patients to address stressors
  • Encourage return to normal activities
  • Avoid reinforcing symptoms or disability (e.g. by providing a wheelchair)

Pharmacological therapy:

  • Treat comorbid depression/anxiety
59
Q

What are the complications and prognosis of dissociative disorder?

A

Complications:

  • May become chronic due to secondary gain (i.e. patient becomes excused from responsibilities)
  • Comorbid depression/anxiety/substance misuse

Usually resolves within weeks/months

Good prognostic factors: acute onset, precipitation by defined stressor, good premorbid health, no comorbidities

60
Q

What is somatisation?

A

Unconscious expression of psychological distress through physical symptoms

Somatoform disorders: group of disorders where symptoms suggest physical illness, but there are no detectable organic abnormalities  suggesting they are caused by psychological factors

Symptoms are not under voluntary control (as opposed to factitious disorders or malingering)

61
Q

What is the aetiology of somatisation?

A

Biological factors:

  • Genetics:
    • Associations with genes related to 5-HT metabolism and HPA axis

Psychological factors:

  • Personality disorder, anxiety, depression, alcohol misuse
  • Patients often have low threshold for worrying about symptoms and consulting doctors; more likely to report parental illness and have had more physical illness during childhood
  • Cognitive theories:
    • An individual’s interpretation of normal physiology can create anxiety and perpetuate somatic symptoms
    • E.g. rapid HR/palpitations when anxious  concern about MI  selective attention to the problem  increased awareness of rapid HR/palpitations when they occur

Social factors:

  • Childhood sexual abuse
  • Upbringing in environments where physical stress is more readily acknowledged than psychological distress
  • Often precipitated by life stressor
62
Q

What are the signs and symptoms of somatisation?

A
  • Multiple, recurrent, frequently changing symptoms, e.g. abdo pain, headache, pins and needles
    • Symptoms may affect any system, but usually GI, skin, sexual, menstrual → usually multiple systems involved
    • Symptoms present for >2yrs
    • No physical explanation found
    • Often history of multiple investigations/treatment  may cause iatrogenic disease, e.g. adhesions from exploratory surgery, dependence on analgesics
    • Persistent refusal to accept advice/reassurance of several doctors
    • Social or occupational function is impaired
63
Q

Name some other types of somatoform disorder and describe them

A
  • Chronic fatigue syndrome/myalgic encephalomyelitis (ME):
    • Extreme fatigue, exhaustion after mild exertion, aches and pains
    • May follow viral infection, e.g. glandular fever
  • Hypochondriacal disorder:
    • Overvalued idea that patient has a serious physical disease
      • Open to some explanation; fear can be reduced for a short time (somatic delusional disorder is diagnosed if belief is held with delusional intensity)
    • Tend to request numerous Ix and so not accept reassurance (in contrast to somatisation disorder where patients tend to seek relief from symptoms)
  • Body dysmorphic disorder:
    • Variant of hypochondriacal disorder
    • Overvalued idea  patients preoccupied by imagined/minor defect in any part of the body
    • Not due to another disorder, e.g. concerns re. weight due to eating disorder
  • Somatoform autonomic dysfunction:
    • Symptoms of autonomic arousal (objective and subjective) attributed to particular organ, e.g. CVS, resp
  • Persistent somatoform pain disorder:
    • Severe and persistent pain; usually not from multiple systems (like somatisation disorder)
64
Q

What are the Ix for somatisation?

A
  • Thorough history, MSE
    • Determine relationship of symptoms of stressful life events
  • Physical examination
  • Basic Ix to rule out physical cause, e.g. basic bloods

Careful not to over-investigate; review old notes to prevent duplication

65
Q

What is the Mx of somatisation?

A

Psychological intervention:

  • Explanation and reassurance
  • CBT, mindfulness-based CBT
    • Helps to develop alternative strategies for expressing emotions, e.g. communication, activities
  • Interpersonal psychotherapy

Social intervention:

  • Encourage normal function
  • Encourage patients to discuss difficulties with friends/family
  • Lifestyle advice, e.g. graded exercise for chronic fatigue

Pharmacological treatment:

  • Avoid unnecessary Ix, referrals or medications  these reinforce illness beliefs and increase anxiety
  • Antidepressants
    • 2nd line if psychological therapy was ineffective
    • TCAs, SNRIs, SSRIs, mirtazapine
    • May be useful even without depression
  • Treat comorbid illness, e.g. anxiety, depression

1 - Y5 Psych (23 decks)

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