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Psychiatry Flashcards

1
Q

What is Section 2 of the Mental Health Act 2007?

A
  • Admission for assessment
  • Maximum duration = 28 days
  • Application = AMHP
  • 2 doctors (at least 1 has to be section 12 approved)
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2
Q

What is Section 3 of the Mental Health Act 2007?

A
  • Admission for treatment
  • Maximum duration = 6 months
  • Application = AMHP
  • 2 doctors ( at least 1 has to be section 12 approved)
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3
Q

What is Section 5 (2) of the Mental Health Act 2007?

A
  • Holding order for a patient already on the ward (NOT A&E)
  • Maximum duration = 72 hours
  • Requires 1 doctor
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4
Q

What is Section 136 of the Mental Health Act 2007?

A
  • Police order to remove a person appearing to suffer from a mental health disorder from a public place to a place of safety
  • Maximum duration = 72 hours
  • Enforced by a police office
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5
Q

What is capacity?

A
  • The ability to make decisions and is presumed to be intact unless proven otherwise
  • It is related to specific decisions and should be assessed separately for each decision

NOTE: unwise decisions doesn’t mean the patient lacks capacity

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6
Q

To have capacity, one must be able to:

A
  • Understand the information relevant to the decision
  • Retain that information
  • Use or weigh that information as part of the process of making the decision
  • Communicate that information
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7
Q

What should happen if someone lacks capacity?

A
  • Steps should be taken in the person’s best interests
  • These steps should be least restrictive of their rights and freedoms, should allow them to participate as much as possible in the decision-making process and should take into account their personal beliefs
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8
Q

What are affective disorders?

A
  • Illnesses where the main feature is is excessively high or low mood
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9
Q

What is the lifetime risk of depression?

A
  • 16.6%
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10
Q

What is the lifetime risk of bipolar affective disorder?

A
  • 3.9%
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11
Q

What is the role of genetics in affective disorders?

A
  • A combination of genes increase the risk of mood disorders
  • Can run in families
  • Specific genes associated with an increased risk of depression (e.g. serotonin transporter genes)
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12
Q

How do childhood and life experiences influence affective disorders?

A
  • Impact on confidence, trust and self-esteem
  • Examples include early childhood abuse, relentless criticism, parental loss and perceived loss of affection
  • In adults, vulnerability factors increase the risk of depression (e.g. unemployment, lack of a confiding relationship, lower socio-economic status, social isolation)
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13
Q

What is the Holmes-Rahe Social Adjustment Scale?

A
  • Death of a spouse
  • Divorce
  • Marital separation
  • Jail term
  • Death of a close relative
  • Depression increases 6-fold in the 6 months following these life events
  • Losses are important precipitants e.g. loss of role (retirement) or loss of autonomy (physical illness)
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14
Q

What are some physical and other causes of affective disorders?

A
  • Chronic pain can precipitate depression (associated with increased suicide risk)
  • Physical illnesses that directly cause depression:
    • Cushing’s syndrome
    • Hypothyroidism
    • Parkinson’s disease
    • Stroke
    • Multiple sclerosis
    • Hyperparathyroidism
  • Some medications (e.g. beta-blockers, antihypertensives, cocaine)
  • Can also trigger mania
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15
Q

What is the monoamine hypothesis?

A
  • Suggests that depression is due to a deficiency in brain monoamine neurotransmitters
    • Noradrenaline (affects mood and energy)
    • Serotonin (affects sleep, appetite, memory and mood)
    • Dopamine (affects psychomotor activity)
  • Supported by the fact that drugs that deplete monoamines can cause depression and most antidepressants aim to increase the levels of neurotransmitters
  • Drugs that increase monoamine levels can precipitate mania
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16
Q

How do endocrine abnormalities affect affective disorders?

A
  • Cortisol is a stress hormone and may be the link between stressful life events and depression
  • May damage hippocampal neurones
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17
Q

What are the core symptoms of depression?

A
  • Low mood
  • Anergia
  • Anhedonia
  • Diagnosis requires at least 2 core symptoms
  • Diagnosis requires at least 2 weeks of symptoms
  • Diurnal variation of mood can occur which is classically worse in the mornings
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18
Q

What are the cognitive symptoms of depression?

A
  • Worthless
  • Hopeless
  • Helpless
  • They may also feel:
    • Guilty about past misdeeds
    • Pessimistic about the future
    • Poor concentration
    • Memory impairment (mainly in the elderly)
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19
Q

What are the biological symptoms of depression?

A
  • Altered sleep
    • Initial insomnia
    • Early morning wakening (waking at least 2 hours earlier than normal)
    • Hypersomnia is possible (may coexist with hyperphagia)
  • Reduced appetite
  • Reduced libido
  • Constipation, aches and pains and dysmenorrhoea
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20
Q

What are psychotic symptoms in depression?

A
  • Occur in SEVERE depression
  • Auditory hallucinations are usually of unpleasant derogatory voices
  • Visual hallucinations may be of scenes of destruction
  • Delusions are often nihilistic and persecutory
    • Persecutory delusions may be linked to a deep feeling of guilt (that they should be punished)
  • Depression can be classified as mild, moderate, severe or severe with psychotic features
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21
Q

What are the subtypes of depression?

A
  • Seasonal Affective Disorder: presents predictably with low mood in the winter. Usually reversed biological symptoms of overeating and oversleeping
  • Atypical Depression: no seasonal variation but shows reversed biological symptoms and may retain mood reactivity
  • Agitated Depression: depression with psychomotor agitation (instead of retardation) such as restlessness and pacing
  • Depressive Stupor: when psychomotor retardation is so profound that the person grinds to a halt, they become mute and stop eating, drinking or moving
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22
Q

What are differential diagnoses of depression?

A
  • Physical causes (e.g. hypothyroidism)
  • Adjustment disorder (unpleasant but mild affective symptoms follow a life event, but do not reach the severity needed to diagnose depression)
  • Normal sadness
  • Bereavement
  • BPAD/schizoaffective disorder/schizophrenia
  • Substance misuse
  • Postnatal depression/puerperal illness
  • Dementia
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23
Q

What is Grief?

A

Normal stages:
- Numbness

  • Pining
  • Depression
  • Recovery
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24
Q

When is Grief abnormal?

A
  • Extremely intense (reaching the level of depression)
  • Prolonged (>6 months) with no relief
  • Delayed (no sign of an emotional response)
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25
Q

What are investigations for depression?

A
  • Collateral history
  • Physical examination
    • Blood tests
    • TFT
    • FBC (anaemia causes fatigue)
    • Glucose and HbA1c (DM can cause fatigue)
  • Rating scales to monitor severity and treatment response (e.g. PHQ-9)
  • Rarely, CT or MRI if suspecting cerebral pathology
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26
Q

What is the management of depression?

A
  • Mild depression often resolves spontaneously
  • Psychological treatment
  • Pharmacological treatment
  • ECT
    • Can be life-saving in severe or psychotic depression
    • Electrodes are used to produce generalised tonic-clonic seizures whilst the patient is anaesthetised
    • Some people experience a degree of memory loss afterwards
  • Light therapy (Can be used in seasonal affective disorder (compensates for fewer hours of daylight in winter)
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27
Q

How else is mild depression managed?

A
  • May refer to supportive counselling or problem-solving therapy
  • Community mental health teams can provide support at home (e.g. through home treatment teams)
  • Advice on:
    • Sleep hygiene
    • Exercise
    • Self-help
    • Access to CBT and counselling
  • Social stressors may need intervention (e.g. time off work, respite for carers, refuge from abusers, debt advice, support groups)
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28
Q

What are some types of psychological treatment for affective disorders?

A
  • CBT
  • Psychodynamic psychotherapy
  • Interpersonal therapy
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29
Q

What is CBT?

A
  • Focuses on the here and now and vies psychological problems as a result of the patient’s distorted perceptions of themselves, the world or the future
  • The therapist helps the patient identify negative automatic thoughts (NATs) that result in unhelpful moods and behaviours
  • Mood, thought and behaviour all interact and are dependent on each other
  • CBT aims to influence thought and behaviour with the hope that it will improve mood
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30
Q

How is CBT used in depression?

A
  • Depressed people often feel they are worthless and life is hopeless - this leads to lowered mood and unhelpful behaviour
  • CBT aims to challenge negative beliefs and increase the patient’s exposure to positive stimulating activities
  • Patients are encouraged to challenge their NATs
  • They are taught about common thinking errors:
  • Generalisation - ‘I always mess everything up’
  • Minimisation - ‘I only passed the exam by chance. I’m not good enough.’
  • Distorted beliefs are tested through:
  • Discussion during sessions - ‘how do you know for sure that no one cares about you?’
  • Behavioural experiments - e.g. inviting a friend to dinner to test out the idea that nobody wants to spend time with them
  • The therapist helps build a set of more realistic beliefs about themselves
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31
Q

What is psychodynamic psychotherapy?

A
  • A good relationship between the therapist and the patient is essential
  • The patient applies unconscious templates of relationships, derived from past experiences, to the new situation with the therapy (e.g. ‘I will be rejected’)
  • These distorted perceptions are known as transferences
  • Putting words to these feelings allows the patient to recognise their hidden beliefs and re-evaluate them in the light of current reality
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32
Q

What is interpersonal therapy?

A
  • Focuses on the main themes of unresolved loss, psychosocial transitions, relationship conflict and social skills deficit
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33
Q

How does pharmacological treatment work in depression?

A
  • Increase the overall level of monoamines at the synapse
  • This leads to downregulation of serotonin and central beta-adrenergic receptors (may account for 4-6 week delay in antidepressant effects)
  • Usually indicated for moderate to severe depression (ideally given with psychotherapy)
  • SSRIs are usually the first choice because of relatively mild side-effects
  • Treatment should continue until the patient is no longer depressed
  • It should then be continued for 6 more months to prevent relapse
  • In recurrent depression, treatment may continue for much longer
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34
Q

What is some general advice regarding pharmacological treatment in depression?

A
  • Can cause hyponatraemia
  • Can cause reduced libido/sexual dysfunction
  • Lower seizure threshold (careful in epilepsy)
  • Avoid in mania or hypomania
  • Do not drink alcohol (increased sedation)
  • Never drive if feeling drowsy on antidepressants
  • Explain that the onset of action is delayed
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35
Q

What are some examples and side-effects of SSRIs?

A
  • Fluoxetine, sertraline, paroxetine, citalopram, escitalopram
  • Side-effects:
    • Nausea and vomiting
    • Appetite/weight change
    • Blurred vision
    • Anxiety and agitation
    • Insomnia, tremor, dizziness
    • Headache
    • Sweating
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36
Q

What are some examples and side-effects of SNRIs?

A
  • Venlafaxine, duloxetine
  • Side-effects: Same as SSRIs but also
    • Constipation
    • Hypertension
    • Raised cholesterol
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37
Q

What are some examples and side-effects of TCAs?

A
  • Amitriptyline, clomipramine, imipramine, lofepramine, dosulepin
  • Side-effects:
    • Tachycardia, arrhythmias
    • Dry mouth
    • Blurred vision
    • Constipation
    • Urinary retention
    • Postural hypotension
    • Sedation
    • Nausea
    • Weight gain
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38
Q

What is stopping and swapping?

A
  • If suddenly stopped, antidepressants can cause discontinuation symptoms (e.g. flu-like symptoms, electric shock sensations, headaches, vertigo)
  • Antidepressants should be withdrawn over a few weeks
  • Antidepressants of different classes can have dangerous interactions so check carefully before changing
  • Some can be cross-tapered and others need a drug-free washout period
  • Serotonin syndrome is caused by excess serotonin (from giving 2 antidepressants at once)
    • Can be life-threatening
    • Causes restlessness, sweating, myoclonus, confusion and fits
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39
Q

What is treatment resistance in antidepressants?

A
  • Failure to respond to 2 adequate trials of different classes of antidepressants at adequate doses and for a period of 6-8 weeks
  • Make sure you reconsider the diagnosis and check that the patient is taking medication properly
  • Specialist augmentation strategies
    • Lithium
    • Thyroxine
    • Buspirone (anxiolytic that has no antidepressant effect alone, but has a synergistic effect with SSRIs)
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40
Q

What is the prognosis of depression?

A
  • About 50% will have at least one more episode
  • Each episode lasts on average 8-9 months
  • Treatment can reduce this to 2-3 months
  • Psychotic depression has a poorer prognosis but has a better response to ECT
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41
Q

What is the clinical presentation of mania?

A
  • To diagnose a manic episode, symptoms should last at least a week and prevent work and ordinary social activities
  • Less severe symptoms that do NOT entirely disrupt the patient’s ability to function leads to a diagnosis of hypomania

NOTE: hypomanic periods be quite productive

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42
Q

What are the core symptoms of mania?

A
  • Mood, energy and enjoyment are elevated
  • Raised mood can range from cheerfulness to elation and uncontrollable excitement, through irritability and aggression
  • Mood can be labile
  • People describe boundless and are overactive
  • Increased enjoyment and interest may prompt the patient to indulge in many new activities
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43
Q

What are the cognitive symptoms of mania?

A
  • Inflated self-esteem and confidence
  • They may believe that they are gifted, attractive, creative, intelligent and extremely special
  • They feel hopeful and the world seems full of opportunity
  • Thoughts race
  • Concentration dissolves
  • Despite being very distractible, the patient may feel that they can think more clearly than ever
  • Speech becomes pressured and topics change rapidly (flight of ideas)
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44
Q

What are the biological symptoms of mania?

A
  • Sleep is reduced and people may be up all night without feeling tired
  • Voracious appetites for food and sex
  • Behaviour may become reckless, disinhibited and inappropriate with increased libido and risky sexual liaisons can take place
  • Patients may spend excessively, drive recklessly or gamble their money
  • Drugs or alcohol become new interests and make the patient more disinhibited
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45
Q

What are psychotic symptons in mania?

A
  • Optimism can develop in grandiose delusions (e.g. an important mission, fame, special powers)
  • Persecutory delusions may arise if the patient believes that others are jealous of them
  • Auditory hallucinations may reflex the elevated mood
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46
Q

What is bipolar affective disorder?

A
  • When a patient has suffered a manic episode and any other affective episode (e.g. depressed, hypomanic, manic or mixed)
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47
Q

What are the BPAD subtypes?

A
  • Type I
    • Manic episodes interspersed with depressive episodes
  • Type II
    • Mainly recurrent depressive episodes, with less prominent hypomanic episodes
  • Rapid Cycling BPAD
    • Four or more affective episodes in a year
    • More common in women
    • May respond better to sodium valproate
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48
Q

What are differential diagnoses of mania?

A
  • Organic causes should be excluded:
    • Drug-induced states (e.g. amphetamines, cocaine)
    • Dementia
    • Frontal lobe disease
    • Delirium
    • Cerebral HIV
    • Myxoedema madness (hypothyroidism causing frenzied activity)
  • Schizophrenia/schizoaffective disorder
    • Psychotic symptoms preceded and outweigh the affective symptoms
  • Cyclothymia
    • Persistent mood instability with many episodes of mild low mood and mild elation
    • None of them are severe or prolonged enough to meet the criteria for mild depression or hypomania
  • Puerperal disorders
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49
Q

What are some investigations for mania?

A
  • Collateral history
  • Physical examination
  • Blood tests:
    • FBC
    • TFTs
    • CRP (exclude infection)
  • Urine drug screen
  • CT/MRI brain to exclude organic causes (if indicated)
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50
Q

What is the pharmacological treatment for mania?

A
  • Mood stabilisers
  • Even out the extreme highs of mania and profound lows of depression
  • More effective against mania
  • THREE main drugs:
    • Lithium
    • Sodium valproate
    • Carbamazepine
  • Mechanism of action is uncertain (may have something to do with sodium channels or GABA)
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51
Q

Describe lithium use in mania

A
  • Therapeutic range: 0.6-1.0 mmol/L
  • Becomes toxic from 1.2 mmol/L
  • Lithium levels should be checked 1 week after starting or changing dose and monitored weekly until a steady therapeutic level is achieved
  • It should be monitored every 3 months from then on
  • U&E and TFTs should be monitored ever 3-6 months (can cause renal impairment and hypothyroidism)
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52
Q

What is lithium toxicity and its presentation?

A
  • Level > 1.2 mmol/L
  • Life-threatening
  • Presentation:
    • GI disturbance
    • Sluggishness
    • Giddiness
    • Ataxia
    • Gross tremor
    • Fits
    • Renal failure
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53
Q

What are triggers for lithium toxicity?

A
  • Salt balance changes (e.g. dehydration, D&V)
  • Drugs interfering with lithium excretion (e.g. diuretics)
  • Accidental or deliberate overdose
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54
Q

What is the management of lithium toxicity?

A
  • Stop lithium

- Transfer for medical care (rehydration, osmotic diuresis)

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55
Q

Describe valproate use in mania

A
  • Anticonvulsant
  • Treats acute mania
  • Prophylaxis in BPAD
  • Given as sodium valproate because of reduced side-effects
  • Plasma levels do not need monitoring
  • NO widely accepted therapeutic range
  • Dose-related toxicity is NOT usually an issue
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56
Q

Describe carbamaezepine use in mania

A
  • Anticonvulsant
  • Can cause toxicity at high doses
  • Induces liver enzymes
  • Close monitoring of carbamazepine levels is essential
  • Check for drug interactions before prescribing
  • 2nd line for BPAD prophylaxis
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57
Q

How do mood stabilisers affect pregnancy?

A
  • Mood stabilisers are teratogenic
  • Risk of harm should be weighed against harm of manic relapse
  • Lithium - Ebstein’s anomaly
  • Valproate + carbamazepine - spina bifida
  • Women of childbearing age should be given contraceptive advice and prescribed a folate supplement if using valproate
  • Closely monitor the foetus if medications are used in pregnancy
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58
Q

What other drugs are used for mania?

A
  • Antipsychotics (e.g. olanzapine)
    • Usually atypical (e.g. olanzapine, risperidone, quetiapine) because of fewer side-effects
  • Anticonvulsants
    • Lamotrigine is good for prophylaxis in BPAD type II
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59
Q

What is the acute treatment of mania or hypomania?

A
  • Stop all medications that may include symptoms (e.g. anti-depressants, drugs of abuse, steroids and dopamine agonists)
  • Monitor food and fluid intake to prevent dehydration
  • If treatment free
    • Give an antipsychotic OR mood stabiliser (can be given together if not responding)
    • A short course of benzodiazepines is often added for sedation (sleep deprivation can exacerbate mania)
  • If already on treatment
    • Optimise the medication
    • Check compliance
    • Adjust doses
    • Consider adding another agent (e.g. antipsychotic as well as mood stabiliser)
    • Short-term benzodiazapines may help
  • ECT may be used if patients are unresponsive to medication
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60
Q

What is the long term treatment for mania?

A
  • Mood stabilisers are the mainstay
  • Other drugs may be added when symptoms arise or when facing stress that could precipitate relapse (e.g. antipsychotics or benzodiazepines)
  • Depression in BPAD is DIFFICULT because antidepressants can cause a switch to mania
  • To reduce this risk, antidepressants should only be given with a mood stabiliser or antipsychotic
  • Monitor closely for signs of mania and immediately stop antidepressants if signs are present
  • Medication can be cautiously withdrawn if the patient is symptom-free for a sustained period
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61
Q

How is psychological treatment used in mania?

A

CBT
- Identify relapse indicators

  • Relapse prevention strategies:
    • Developing routine
    • Ensuring good-quality sleep
    • Promoting a healthy lifestyle
    • Avoiding excessive stimulation/stress
    • Addressing substance misuse
    • Ensuring drug compliance
  • Helps patients to test out their excessively positive thoughts to gain a sense of perspective

Psychodynamic psychotherapy
- Useful if mood is stabilised

Social Interventions

  • Family support and therapy
  • Aiding return to education or work
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62
Q

What is the prognosis of mania?

A
  • Manic episodes begin abruptly and are often shorter than depressive episodes (usually 2 weeks - 5 months)
  • Recovery is usually complete between episodes
  • Remissions become shorter with age and depressions become more frequency
  • 15% of people with BPAD will commit suicide
  • Lithium reduces this to the same levels as the general population
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63
Q

Describe the genetics of schizophrenia

A
  • Lifetime risk increases from 1% to 10% if you have a first-degree relative with schizophrenia
  • Likely to be multiple susceptibility genes
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64
Q

What obstetric complications are associated with schizophrenia?

A
  • Maternal prenatal malnutrition
  • Viral infections
  • Pre-eclampsia
  • Low birth weight
  • Emergency C-section
  • These may reflect genetic abnormalities or may be linked to hypoxic brain damage
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65
Q

What substances can cause schizophrenia?

A
  • Cannabis, amphetamines, cocaine and LSD
  • Cannabis, in particular, increases risk of developing schizophrenia
    • The Val-Val mutation in the COMT gene causes the highest risk of developing schizophrenia in cannabis users
    • Skunk is a particularly dangerous form of cannabis for those vulnerable to schizophrenia
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66
Q

How is social disadvantage associated with schizophrenia?

A
  • Higher rates in lower socioeconomic classes
  • This is not linked to the socioeconomic class at birth (the downward drift is due to illness causing social isolation and unemployment)
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67
Q

How are urban life & birth and migration/ethnicity associated with schizophrenia?

A
  • Twice as high in urban areas
  • 1st and 2nd generation immigrants are at increased risk compared to indigenous populations
  • Afro-Caribbean populations show the highest rates
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68
Q

What else is associated with schizophrenia?

A
  • Expressed emotion: Close contact with highly critical or over-involved relatives double risk of relapse
  • Premorbid personality: Premorbid schizoid personality precedes schizophrenia in 25% of cases
    • Schizotypal disorder is associated with schizophrenia
  • Adverse life experience
    • Sexual or physical abuse in childhood or adulthood increases risk
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69
Q

What are some of the theories for schizophrenia?

A
  • Neurodevelopmental theories
  • Neurotransmitter theories
  • Psychological theories
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70
Q

What are the neurodevelopmental theories of schizophrenia?

A
  • Initial brain abnormalities (either genetic in origin or due to early brain damage) may lead to schizophrenia
  • Maturation of the brain, along with other risk factors can lead to functional and connectivity abnormalities
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71
Q

What are the neurotransmitter theories of schizophrenia?

A
  • Dopamine Hypothesis: schizophrenia is result of dopamine overactivity in certain areas of the brain
  • Positive symptoms (hallucinations and delusions) = excess dopamine in the mesolimbic tracts
  • Negative symptoms (apathy and social withdrawal) = deficient dopamine in the mesocortical tracts
  • Evidence: All known antipsychotics are dopamine antagonists
    • Antipsychotics work better against positive symptoms
    • Dopaminergic agents (e.g. amphetamine, cocaine, L-dopa can all induce psychosis)
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72
Q

What are the psychological theories associated with schizophrenia?

A
  • Subtle defects in thinking (e.g. tendency to jump to conclusions without adequate evidence) predisposes to delusions
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73
Q

What are the different phases of schizophrenia?

A
  • Prodrome: at-risk mental state before onset of schizophrenia
  • Acute Phase: positive symptoms (hallucinations and delusions)
  • Chronic Phase: negative symptoms reflecting things that are lost in schizophrenia e.g. motivation
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74
Q

What is the prodrome stage of schizophrenia?

A
  • Consists of low grade symptoms such as
    • Social withdrawal
    • Loss of interest in work, study and relationships
    • NO frank psychotic symptoms
  • Patients are usually in their late teens or early 20s
  • They may have dropped out of college or work after a period of increasing absences
  • They may seem distant with no reason for isolating themselves
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75
Q

What is the acute phase of schizophrenia?

A
  • Delusions: a fixed, false belief, held despite rational argument or evidence to the contrary. It cannot be explained by the patent’s cultural, religious or educational background
  • Hallucinations: a perception in the absence of a stimulus
  • Thinking is disturbed resulting in muddled speech and withdrawn, overactive or bizarre behaviour
  • Negative symptoms may also be present
  • Thought interference
  • Formal thought disorder
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76
Q

What are different types of auditory hallucinations?

A
  • Voices discussing or arguing about the patient
    • No-one likes her
    • Yeah, it’s because she’s ugly
  • Voices giving a running commentary on the patient’s action
    • Now he’s falling a sleep, and he’s calling a cab, whilst he’s having a smoke, and he’s taking a drag
  • Thought echo: the voice says that patient’s thoughts out loud
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77
Q

What are different types of delusions?

A
  • Delusional perception: A real perception is interrupted in a delusional way
    • E.g. the traffic lights changed to green and I knew I was the king of Sri Lanka
  • Passivity
    • Belief that movement, sensation, emotion or impulse are controlled by an outside form
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78
Q

What is thought interference?

A
  • The patient believes their thoughts are under the control of something else
  • Thought Withdrawal: thoughts are removed from the patient’s mind
  • Thought Insertion: thoughts are placed directly into the patient’s mind
  • Thought broadcasting: thoughts are broadcast to others so that people can know what they are thinking
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79
Q

What is formal thought disorder?

A
  • When thoughts become disconnected (loosening of associations)
  • May produce disjointed speech that is hard to follow
  • Poverty of thought and thought blocking may occur
  • Word salad is when the words are so disconnected that sentences don’t make any sense
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80
Q

What is the chronic phase of schizophrenia?

A
  • Mainly negative symptoms
    • Apathy - loss of motivation
    • Blunted affect - decreased reactivity to mood
    • Anhedonia - inability to enjoy interests/activities
    • Social withdrawal
    • Poverty of thought and speech
  • May manifest as a lack of attention to personal hygiene/care, reduced repertoire of activities and social isolation
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81
Q

What are the subtypes of schizophrenia?

A
  • Paranoid
  • Catatonic
  • Hebephrenic
  • Simple
  • Residual
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82
Q

What is paranoid schizophrenia?

A
  • MOST COMMON type

- Main symptoms are prominent delusions and hallucinations

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83
Q

What is catatonic schizophrenia?

A

(psychomotor disturbance)

  • Stupor - state of being immobile, mute and unresponsive, despite appearing to be conscious (eyes are open and will follow people around the room)
  • Excitement - periods of extreme and apparently purposeless motor hyperactivity
  • Posturing - assuming and maintaining inappropriate or bizarre positions
  • Rigidity - holding a rigid posture against efforts to be moved
  • Waxy Flexibility - patient’s limbs offer minimal resistance to being placed in odd positions which are maintained for unusually length periods (cataplexy)
  • Automatic Obedience - to any instructions
  • Perseveration- in appropriate repetition of words or movements
    • What’s your name?
      Nik Ubhi
    • Where were you born?
      Nik Ubhi
    • What’s your job?
      Nik Ubhi
  • Catatonia can be seen in organic conditions (e.g. encephalitis)
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84
Q

What is hebephrenic schizophrenia?

A
  • Usually between 15-25 years
  • Characterised by a disorganised and chaotic mood, behaviour and speech
  • Affect is often shallow and inappropriate
  • Sometimes described as ‘child-like’ behaviour
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85
Q

What is simple schizophrenia?

A
  • NEGATIVE features only
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86
Q

What is residual schizophrenia?

A
  • Prominent negative symptoms are all that remains after delusions and hallucinations subside
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87
Q

What are Schneider’s First Rank Symptoms?

A
  • Delusional perception
  • Passivity
  • Delusions of thought interference
    • Thought insertion
    • Thought withdrawal
    • Thought broadcasting
  • Auditory hallucinations
    • Thought echo
    • Third person voices
    • Running commentary
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88
Q

What are differential diagnoses of schizophrenia?

A
  • Organic
  • Acute and Transient Psychotic Episode
  • Mood disorder
  • Schizoaffective Disorder
  • Persistent Delusional Disorder
  • Schizotypal Disorder
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89
Q

What are organic differential diagnoses of schizophrenia?

A
  • Substance misuse
    • Common drugs: amphetamine, cocaine, LSD, ecstasy,
  • Dementia
  • Delirium (especially elderly)
  • Epilepsy (especially temporal lobe epilepsy)
  • Medication side-effect (e.g. steroids, dopamine agonist)
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90
Q

What is an acute and transient psychotic episode?

A
  • Resolves completely within a few months but can look identical to schizophrenia
  • Can be stress-related
91
Q

What is Mood Disorder?

A
  • Severe depression or mania can produce psychotic symptoms
  • Schizophrenia should NOT be diagnosed in the presence of striking mood disturbance unless the schizophrenic symptoms came first
92
Q

What is Schizoaffective Disorder?

A
  • Both schizophrenic and affective symptoms develop together and are roughly evenly balanced
93
Q

What is Persistent Delusional Disorder?

A
  • Delusions with few or no hallucinations
94
Q

What is Schizotypal Disorder?

A
  • Lifelong state of eccentricity with abnormal thoughts and affect which is regarded as a personality disorder
  • Patients may be suspicious, cold or aloof with odd ideas without showing definite symptoms of schizophrenia
95
Q

What are some investigations for schizophrenia?

A
  • Full physical examination and investigations to exclude an organic cause
  • Also important to establish baseline physical health before starting medical treatment
  • Blood tests (FBC, TFTs, U&E, LFTs, CRP, fasting blood glucose)
    • Consider HIV, VDRL
    • Lipids should be checked before starting antipsychotics
  • MSU
  • Urine drug screen
  • CT scan (rule out organic pathology if suspected)
  • EEG (if epilepsy or other organic cause suspected)
  • Symptoms rating scales
  • OT assessment of ADLs
  • Social work assessment of housing, finances and carers’ needs
  • Collateral history
96
Q

What is the management of schizophrenia?

A
  • Biopsychosocial model
  • Early Intervention Service
  • Antipsychotics
  • Psychological Management
97
Q

What is the biopsychosocial model in terms of schizophrenia?

A
  • Biological therapies (mainly antipsychotics)
  • Psychological therapies
  • Social interventions
98
Q

What is Early Intervention Service?

A
  • Psychosis is toxic, the longer a patient is psychotic, the more it will affect their cognitive abilities, insight and social situation
  • The sooner effective treatment can be started the better the prognosis
  • The Early Intervention Service aims to engage patients with very early symptoms
  • Patients are offered antipsychotics and psychosocial interventions with the aim of keeping the duration of untreated psychosis (DUP) under 3 months
99
Q

What are typical antipsychotics?

A
  • Dopamine antagonists (block D2 receptors)
  • Extrapyramidal side-effects (EPSEs) can occur at higher concentrations of ALL antipsychotics (but less common with atypicals)
  • Chlorpromazine
  • Haloperidol
  • Flupentixol decanoate
  • Cause EPSEs at normal doses
  • Effective, cheap and provide depot options
100
Q

What are atypical antipsychotics?

A
  • In addition to dopamine receptors, these also block serotonin 5-HT2 receptors
  • Examples:
    • Olanzapine
    • Risperidone (available as depot)
    • Quetiapine
    • Aripiprazole
    • Clozapine
    • Amisulpride
  • Consider starting an atypical antipsychotic when:
    • Choosing 1st-line treatment in newly diagnosed schizophrenia
    • There are unacceptable side-effects from typical antipsychotics
    • Relapse occurs on a typical antipsychotic
101
Q

What are some EPSEs of antipsychotics?

A
  • Dystonia
  • Akathisia
  • Parkinsonism
  • Tardive dyskinesia
102
Q

What are some side effects of antipsychotics?

A
  • Hyperprolactinaemia
    • Galactorrhoea, amenorrhoea, gynaecomastia and hypogonadism
    • Sexual dysfunction
    • Increased risk of osteoporosis
  • Weight gain (especially olanzapine and clozapine)
  • Sedation
  • Increased risk of diabetes
  • Dyslipidaemia
  • Anticholinergic side-effects (dry mouth, blurred vision, constipation, urinary retention, tachycardia)
  • Arrhythmias
  • Seizures (reduces seizure threshold)
  • Neuroleptic malignant syndrome
103
Q

What is neuroleptic malignant syndrome?

A
  • Rare but life-threatening side-effect of antipsychotics
  • Usually triggered by a new antipsychotic or dose increase
  • Thought to be idiosyncratic response to dopamine antagonism
  • Symptoms
    • Muscle stiffness and rigidity
    • Altered consciousness
    • Disturbance of autonomic nervous system (fever, tachycardia and labile BP)
  • Raised CK and WCC
  • Treatment
    • Stop antipsychotics immediately
    • Get urgent medical treatment (usually ITU)
  • Death may occur due to several causes (e.g. rhabdomyolysis leading to renal failure)
104
Q

How do you monitor those on anti-psychotics?

A
  • Anyone on an antipsychotic long-term needs regular monitoring and review
  • BMI and waist circumference
  • Blood pressure
  • FBC, LFTs, U&Es, glucose tolerance test (or fasting glucose/HbA1c) and lipids
  • Some may need:
    • Prolactin levels (if hyperprolactinaemia suspected)
    • ECGs (monitor QTc interval)
105
Q

What is the first-line drug treatment for treatment resistance schizophrenia?

A
  • Treatment Resistance: failure to respond to two or more antipsychotics, at least one of which is atypical, each given at a therapeutic dose for at least 6 weeks
  • WARNING: there is a small but significant risk of agranulocytosis (0.7%)
  • Requires weekly blood tests to detect early signs of neuropaenia
  • NOTE: the sooner effective treatment is started, the better the patient’s prognosis, so if other treatments fail, a trial of clozapine should follow promptly
106
Q

How is CBT used in schizophrenia?

A
  • Should be offered to ALL patients
  • Particular emphasis on reality testing
  • The therapist aims to gently challenge the patient’s beliefs, aiding awareness of illogical thinking
    • E.g. ‘I’m a bit confused by that, if the Prime Minister is stalking you all day, how does he find time to run the country and appear on TV?’
  • The patient is encouraged to think about the evidence and consider alternative explanations
  • CBT can also help patients cope with troublesome hallucinations and delusions
107
Q

How is family therapy used in schizophrenia?

A
  • Can reduce relapse rates
  • Effects of high expressed emotion (discussed earlier) can be ameliorated through communication skills, education about schizophrenia, problem-solving and helping patients expand their social network
  • Can offer respite for the families
108
Q

What is concordance therapy in schizophrenia?

A
  • Collaborative approach where the patient is encouraged to consider the pros and cons of the management
109
Q

What social measures should be used in schizophrenia?

A
  • May include admission to hospital for observation, treatment or refuge
  • Provide help with practical needs like benefits, housing, training and education
  • Social skills training can help improve interpersonal skills
  • Needs to address
    • Education, training and employment
    • Skills (e.g. budgeting, cooking)
    • Housing (e.g. supported accommodation, independent flats)
    • Accessing social activities
  • Developing personal skills (e.g. creative writing)
110
Q

What is a risk assessment for schizophrenia?

A
  • Risk to Self
    • Suicide (10% lifetime risk)
      • High risk in the early years after diagnosis, following first admission or where there are depressive symptoms
    • Self-neglect
    • Social decline
    • Victimisation
  • Risk to Others
    • Very small subgroup of people with schizophrenia
    • Factors increasing the risk of violence:
      • Past history
      • Substance misuse
      • Acute psychotic symptoms
      • Non-concordance with treatment
      • Access to weapons
      • Specific threats to a victim
      • Comorbid personality disorder (dissocial, emotionally unstable, paranoid)
  • Risk from others
    • Increased risk of being victims of crime
111
Q

What is the prognosis of schizophrenia?

A
  • 1/4 of patients recover and will experience no further difficulties after a single episode
  • 2/3 remain liable to relapse or continue to have symptoms
  • 1/10 will be seriously and continuously disabled
  • Mortality in patients with schizophrenia is 2 x general population
  • NOTE: poor physical health contributes to the high mortality
112
Q

What is personality?

A
  • Set of consistent thoughts, feelings and behaviours shown across time in a variety of settings
113
Q

What are the Big Five personality traits? (OCEAN)

A
  • Openness to experience (curiosity, imagination, appreciation of art, adventure and emotion)
  • Conscientiousness (ability to plan and be self-disciplined to achieve goals)
  • Extraversion (predisposition to experience positive social events)
  • Agreeableness (tendency to be cooperative, trusting and kind)
  • Neuroticism (predisposition to negative emotions (e.g. anxiety, anger, depression))
114
Q

What 3 Ps help differentiate a personality DISORDER from a personality TRAIT?

A
  • Pervasive - occurs in all/most areas of life
  • Persistent - evident in adolescence and continues through adulthood
  • Pathological - causes distress to self or others, impairs function
115
Q

What is the ICD-10 criteria for diagnosis of a personality disorder? (REPORT)

A
  • Relationships affected
  • Enduring
  • Pervasive
  • Onset in childhood/adolescence
  • Result in distress
  • Trouble in occupational/social performance
  • NOTE: the behaviour must NOT be attributable to brain damage or disease
116
Q

What is Cluster A personality disorder?

A

Odd or Eccentric

  • Paranoid
  • Schizoid
117
Q

What is Cluster B personality disorder?

A

Dramatic, erratic or emotional

  • Histrionic
  • Emotionally unstable
  • Dissocial
118
Q

What is Cluster C personality disorder?

A

Anxious and fearful

  • Anankastic
  • Anxious (avoidant)
  • Dependent
119
Q

What is the aetiology of personality disorder?

A
  • Genetics (50%)
  • Childhood temperament
  • Childhood experience
  • Personality disorder theories
120
Q

How does childhood temperament affect personality disorders?

A
  • Temperament = infant’s pattern of activity, attention span, response to new situation and intensity of emotional responses
  • Children with ‘difficult’ temperament are more likely to have issues coping as adults
121
Q

How does childhood experience affect personality disorders?

A
  • Personality disorder is associated with insecure attachment and traumatic/neglectful/chaotic upbringing
122
Q

What are theories of personality disorder?

A
  • The quality of early relationships and the environment in which someone is raised influences their expectations about themselves and the world (e.g. people feel lovable because they were first loved)
  • Personality disorders may occur as a form of psychological defence to manage uncomfortable feelings
    • Acting out - impulses are expressed through actions without conscious awareness of the underlying emotion (e.g. self-harm)
    • Splitting - other people are thought of in polarised terms (either idealized or denigrated)
    • Projection - uncomfortable feelings are put onto someone else and experienced as belonging to them
  • Neurotransmitter theories - lower serotonin levels in dissocial personality disorder have been demonstrated
123
Q

What are features of Paranoid personality disorder?

A

SUSPECT

  • Sensitive
  • Unforgiving
  • Suspicious
  • Possessive and jealous of partners
  • Excessive self-importance
  • Conspiracy theories
  • Tenacious sense of rights
124
Q

What are the differential diagnoses for Paranoid personality disorder?

A
  • Schizophrenia

- Persistent delusional disorder

125
Q

What are the features of Schizoid personality disorder?

A

ALL ALONE

  • Anhedonic
  • Limited emotional range
  • Little sexual interest
  • Apparent indifference to praise/criticism
  • Lacks close relationships
  • One-player activities
  • Normal social conventions are ignored
  • Excessive fantasy world
126
Q

What are the differential diagnoses for schizoid personality disorder?

A
  • Asperger’s syndrome
  • Agoraphobia
  • Social phobia
  • Psychosis
  • Depression
127
Q

What are the features of Histrionic personality disorder?

A

ACTORS

  • Attention seeking
  • Concerned with own appearance
  • Theatrical
  • Open to suggestion
  • Racy and seductive
  • Shallow affect
128
Q

What are the differential diagnoses of Histrionic personality disorder?

A
  • Hypomanic/manic episode

- Substance misuse

129
Q

What are the features of emotionally unstable personality disorder?

A

AEIOU

  • Affective instability
  • Explosive behaviour
  • Impulsive
  • Outburst of anger
  • Unable to plan or consider consequences
130
Q

What are the features of Borderline personality disorder?

A

SCARS

  • Self-image unclear
  • Chronic empty feelings
  • Abandonment fears
  • Relationships are intense and unstable
  • Suicide attempts and self-harm
131
Q

What are differential diagnoses of borderline personality disorder?

A
  • Adjustment disorder
  • Depression
  • Psychosis
132
Q

What are the features of Impulsive type personality disorder?

A

LOSE IT

  • Lacks impulse control
  • Outbursts or threats of violence
  • Sensitivity to being thwarted or criticised
  • Emotional instability
  • Inability to plan ahead
  • Thoughtless of consequences
133
Q

What are the differential diagnoses to Impulsive type personality disorder

A
  • Affective disorder
  • Adjustment disorder
  • Adult ADHD
134
Q

What are the features of dissocial personality disorder?

A

FIGHTS

  • Forms but cannot maintain relationships
  • Irresponsible
  • Guiltless
  • Heartless
  • Temper easily lost
  • Someone else’s fault
135
Q

What are the differential diagnoses of dissocial personality disorder?

A
  • Acute psychotic episode

- Manic episode

136
Q

What are the features of anankastic personality disorder?

A

DETAILED

  • Doubtful
  • Excessive detail
  • Tasks not completed
  • Adheres to the rules
  • Inflexible
  • Likes own way
  • Excludes pleasure and relationships
  • Dominated by intrusive thoughts
137
Q

What are the differential diagnoses for anakastic personality disorder?

A
  • OCD

- Autism spectrum disorder

138
Q

What are the features of anxious (avoidant) personality disorder?

A

AFRAID

  • Avoids social contact
  • Fears rejection/criticism
  • Restricted lifestyle
  • Apprehensive
  • Inferiority
  • Doesn’t get involved unless sure of acceptance
139
Q

What are differential diagnoses for anxious (avoidant) personality disorder?

A
  • Social phobia
  • Autism spectrum disorder
  • Schizophrenia
140
Q

What are the features of dependent personality disorder?

A

SUFFER

  • Subordinate
  • Undemanding
  • Feels helpless when alone
  • Fears abandonment
  • Encourages others to make decisions
  • Reassurance needed
141
Q

What are the differential diagnoses of dependent personality disorder?

A
  • Reliance because of cognitive impairment

- Anxiety disorder

142
Q

What are the investigations for personality disorders?

A
  • Second interview and collateral history (confirm whether the traits amount to a disorder)
  • Psychology/psychotherapy assessment
143
Q

What is the management of personality disorders?

A
  • They are TREATABLE
  • Encourage the individual to take responsibility for their actions
  • Boundaries are essential
  • Psychotherapy
  • Medication
  • Treat Comorbid problems: Substance misuse, affective and anxiety disorders require management
144
Q

What psychotherapies are used for personality disorders?

A
  • CBT
  • Dialectical behaviour therapy (DBT)
    • Type of CBT that has been adapted for people who experience emotions very intensely
    • Used to treat emotionally unstable (borderline) personality disorder
    • Focuses on changing unhelpful behaviours AND accepting who you are at the same time
  • Cognitive analytical therapy (CAT)
  • Mentalisation
    • Integrative form of psychotherapy that brings together aspects of psychodynamic, CBT and systemic approaches
  • Therapeutic communities
    • Group-based approach to long-term mental illness
  • Psychodynamic and psychoanalytical psychotherapy
145
Q

What medications are used for personality disorders?

A
  • Antipsychotics - may reduce impulsivity and aggression (e.g. risperidone)
  • Antidepressants - may reduce impulsivity and anxiety
  • Mood stabilisers - may be used for labile affect (effects aren’t evidence-based)
146
Q

What is the prognosis for personality disorders?

A
  • Personality disorders disrupt relationships, education and employment
  • Although they are persistent, they may change in severity over time
147
Q

What are psychological symptoms of anxiety?

A
  • Fear
  • Worry
  • Irritability
  • Poor concentration
148
Q

What are motor symptoms of anxiety?

A
  • Fidgeting

- Feeling “on edge”

149
Q

What are neuromuscular symptoms of anxiety?

A
  • Tremor
  • Headache
  • Muscle aches
  • Tinnitus
150
Q

What are gastrointestinal symptoms of anxiety?

A
  • Dry mouth
  • Difficulty swallowing
  • “Butterflies” in stomach
  • Nausea
  • Flatulence
151
Q

What are cardiovascular symptoms of anxiety?

A
  • Chest discomfort

- Palpitations

152
Q

What are respiratory symptoms of anxiety?

A
  • Difficulty inhaling

- Tight chest

153
Q

What are genitourinary symptoms of anxiety?

A
  • Erectile dysfunction
  • Urinary frequency
  • Amenorrhoea
154
Q

What is the aetiology of anxiety?

A
  • Some genetic link
  • More common in people showing the personality trait of neuroticism
  • Childhood adversity
  • Derangement of neurotransmitters (serotonin, noradrenaline and GABA) contribute to anxiety disorders
  • Cognitive and behavioural theories
155
Q

What are the behavioural and cognitive theories of anxiety?

A
  • Classical Conditioning: repeated pairing of a neutral stimulus with a frightening one results in a fear reaction to a neutral stimulus
  • Negative Reinforcement: behaviours that relieve anxiety (e.g. running away) are repeated. This prevents habituation.
  • Cognitive Theories: worrying thoughts are repeated in an automatic way which induces and maintains the anxiety response
  • Attachment Theory: quality of attachment between children and their parents affects their confidence as adults
156
Q

What is generalised anxiety disorder?

A
  • Anxiety that is not triggered by a specific stimulus, but instead is continuous and generalised
  • Life is a worry - past mistakes and future imagined catastrophes occupy the mind ceaselessly
  • Diagnosing GAD requires symptoms to be present for at least 6 months
157
Q

What is the differential diagnosis of GAD?

A
  • Hyperthyroidism
  • Substance misuse
    • Intoxication (e.g. amphetamines)
    • Withdrawal (e.g. benzodiazepines, alcohol)
  • Excess caffeine
  • Depression
    • Mixed anxiety and depressive disorder is when low-level depressive and anxiety symptoms are present equally together
  • Anxious (avoidant) personality disorder
    • Patients describe themselves as anxious people with no recent major increase in anxiety levels
    • Usually present from late adolescence
  • Dementia
  • Schizophrenia
158
Q

What are the phobia anxiety disorders?

A
  • Intermittent anxiety occurs in specific but quite ordinary circumstances
  • Seriousness depends on the resultant disability
    • E.g. a fear of slugs in someone living in a flat in London is not a huge disability
    • E.g. a pilot with a fear of flying is a severe disorder
159
Q

What is Agoraphobia?

A
  • Fear of being unable to easily escape to a safe place (usually home)
  • Includes fear of open places and fear of situations that are confined and difficult to leave without attracting attention
  • Common issues: travelling on trains, planes or buses, queuing, supermarkets and large crowds
  • Onset is usually 20s-30s
  • May be gradual or precipitated by a sudden panic attack
  • They experience an overwhelming urge to return to safety
  • The prospect of leaving home generated anxiety
  • Presence of a dependable companion can increase their range
  • Depression is common
160
Q

What is the differential diagnoses of agoraphobia?

A
  • Depression (can cause social withdrawal)
  • Social phobia (fear of scrutiny or humiliation)
  • OCD (time-consuming rituals can confine people to their homes)
  • Schizophrenia (patients may stay at home due to social withdrawal or as a way of avoiding perceived prosecutors)
161
Q

What is Social Phobia?

A
  • Onset normally in late teens
  • Core fear is being scrutinised or criticised by other people
  • Patients often worry about embarrassing themselves
  • They can tolerate anonymous crowds (unlike agoraphobia) but small groups (e.g. dinner, parties) are very intimidating
  • There may be specific worries (e.g. eating in public)
  • May self-medicate with alcohol and drugs
  • Patients may complain about embarrassing symptoms (e.g. blushing, sweating)
162
Q

What are the differential diagnoses of Social Phobia?

A
  • Shyness: some people are naturally shy. In social phobia there is overt fear
  • Agoraphobia: need to get somewhere safe is more important than fear of scrutiny
  • Anxious (avoidant) Personality Disorder: lifelong history of disabling shyness and anxiety
  • Poor social skills/autistic spectrum disorders
  • Benign essential tremor: this is a familial tremor that is worse in social situations. It responds to benzodiazepines and alcohol. There are no other features of anxiety.
  • Schizophrenia/Psychosis: patients may avoid social situations because of paranoia or because they have delusions of being watched. People with social phobia, on the other hand, know that their fears are exaggerated
163
Q

What are specific phobias?

A
  • Phobias are restricted to a single, specific situation (e.g. slugs = molluscophobia)
  • Develop in childhood
  • Usually occur after a frightening experience (e.g. stepping on a slug barefoot)
  • Always exclude comorbid depression
164
Q

What is Panic Disorder?

A
  • Aka episodic paroxysmal anxiety
  • Anxiety is intermittent and does NOT have an obvious trigger
  • Patients experience alarming thoughts (e.g. losing control, dying) and this causes further panic until the patient gains reassurance or engaged in safety behaviours
  • Safety behaviours are actions to avert catastrophe (e.g. calling an ambulance, taking aspirin)
  • Panic attacks are self-limiting and last < 30 mins
  • A diagnosis of panic disorder, requires recurrent panic attacks (several within month)
  • In between episodes, the patient is relatively free of anxiety
165
Q

What is a panic attack?

A
  • A panic attack is a sudden attack of extreme anxiety with accompanying physical symptoms such as:
    • Breathing difficulties/choking feeling
    • Chest tightness
    • Palpitations
    • Tingling or numbness in the hands, feet or around the mouth (caused by hypocalcaemia due to increased respiratory rate)
    • Depersonalisation/derealisation
    • Shaking
    • Dizziness
    • Sweating
166
Q

What are the differential diagnoses of panic disorder?

A
  • Other anxiety disorder (e.g. GAD, agoraphobia)
  • Depression
  • Alcohol or drug withdrawal (can cause severe anxiety which mimics panic attacks)
  • Organic causes (e.g. cardiovascular/respiratory disease, phaeochromocytoma)
167
Q

How do you investigate anxiety disorders?

A
  • Thorough history and physical examination
  • Rating scales of anxiety
    • GAD7 questionnaire
    • Beck anxiety inventory
    • Hospital anxiety and depression scale
    • These can provide a baseline score to measure treatment response
  • Social and occupational assessments for effect on quality of life
  • Collateral history
168
Q

What is the management of anxiety disorders?

A
  • Advice and reassurance (may be enough for mild problems)
  • Basic counselling (to address worries)
  • Problem-solving (help deal with stressors)
  • Self-help material
    • CBT-based books
    • Encourage reliance on supportive contacts (e.g. friends, family)
  • Relaxation techniques and breathing exercises
  • CBT
  • Exposure Therapy
169
Q

How does CBT work in anxiety?

A
  • Aims to reduce patient’s expectation of threat, and the behaviours that maintain threat-related beliefs
  • Often begins with teaching techniques for managing arousal (relaxation and controlled breathing)
  • Explore the actual likelihood and impact of the anticipated catastrophe
  • Test the feared situation and their belief in a catastrophic outcome using behavioural experiments
  • This gradually increases the patient’s confidence in their capacity to cope with the feared situation
170
Q

How does CBT affect GAD?

A
  • Main feature is worry

- Therapy involves testing predictions of worry with behavioural experiments and looking at errors in thinking

171
Q

How does CBT affect panic disorder?

A
  • Panic may be triggered by misinterpretation of physical anxiety symptoms as signs of major catastrophe
  • Safety behaviours may be adopted which reinforce beliefs (e.g. avoiding situations)
  • CBT educates the patient on the true meaning of the symptoms (i.e. panic not perish)
  • Helps them test whether their behaviours keep them safe and whether their beliefs are true or misinterpretations
172
Q

What is Exposure Therapy?

A
  • Used as part of the CBT approach when there are strong elements of avoidance and escape
  • In the absence of actual harm, the body can only remain extremely anxious for a short time (usually < 45 mins) before habituation occurs and anxiety levels drop
  • Habituation is characterised by a decrease in anxiety until fear dies out (extinction)

Exposure is usually through a gradual (or graded) approach called desensitisation

  • The patient identifies a goal (e.g. being able to hold a slug) and constructs a hierarchy of feared situations
  • The patient tackles it from least frightening to most frightening
  • The aim is to stay in the situation until the anxiety has subsided to induce learning and challenge existing thoughts
  • Agoraphobia can be treated using this strategy
173
Q

What is the pharmacological management of anxiety disorders?

A
  • SSRIs
    • Treat many anxiety disorders
    • May be combined with CBT
    • Therapeutic doses for anxiety disorder are generally higher than for depression and responses take longer (6-8 weeks)
  • TCAs
    • E.g. clomipramine, imipramine
    • May be useful if not responding or not tolerating SSRIs
  • Buspirone
    • Serotonin partial agonist
    • Has a delayed action and dysphoric effects
  • Benzodiazepines
    • Useful for short-term anxiety treatments (e.g. whilst waiting for SSRIs to work)
    • Tolerance builds rapidly and dependence is an issue
    • Must NOT be used for > 2-4 weeks
    • Side-Effects: amnesia, ataxia, respiratory depression
  • Beta-blockers
    • E.g. propranolol
    • Sometimes used to treat adrenergic symptoms (e.g. tremor, palpitations)
    • IMPORTANT: consider contraindications
174
Q

What is the prognosis of anxiety disorders?

A
  • Rule of thirds
    • 1/3 recover completely
    • 1/3 improve partially
    • 1/3 fare poorly and suffer considerable disability
  • Early diagnosis and treatment are essential
  • The shorter the duration of symptoms the better the prognosis
175
Q

What is OCD?

A
  • OCD affects 1% of the population
  • Some genetic component
  • 1/4 patients with OCD have anankastic personality traits (rigidity, orderliness)
  • Stress may precipitate OCD symptoms
  • Diseases associated with OCD: Sydenham’s chorea, encephalitis lethargica and Tourette’s syndrome
176
Q

What is the clinical picture of OCD?

A
  • Obsessions: recurrent unwanted intrusive thoughts, images or impulses that enter the patient’s mind despite attempts to resist them
  • The thoughts are unpleasant but the patient recognises them as irrational and their own (unlike delusions and thought insertion)
  • Common themes of obsessions:
    • Contamination
    • Aggression (thoughts of harming self or others)
    • Infection
    • Morality (sex and religion)
  • Obsessions make the patient feel acutely uncomfortable or anxious
  • They may feel responsible for the damage that their thought might do (e.g. a violent thought might really harm someone)
  • This tension is neutralised by a compulsion
  • Compulsions: repeated, stereotyped and seemingly purposeful rituals that the patient feels compelled to carry out, even though they are irrational and may lack any obvious link to the obsession
  • Examples: cleaning, counting, checking and ordering objects
  • Compulsions can be very time-consuming and decrease quality of life
  • Resistance to obsessions and compulsions may decrease in chronic disease
177
Q

What is the differential diagnoses of OCD?

A
  • Anxiety disorders
  • Depression
    • 50% of patients with OCD experience depressive symptoms
    • If the patient meets the criteria for depression, this diagnosis takes priority
  • Anankastic personality disorder
    • Lifelong personality of rigidity with high standards of orderliness/hygiene
  • Schizophrenia
    • Beliefs are delusions not obsessional
  • Organic causes (e.g. Sydenham’s chorea)
178
Q

What is the management of OCD?

A
  • Education and self-help
  • CBT: Exposure and Response Prevention
    • Compulsions are analogous to escape in phobias
    • CBT aims to prevent compulsive behaviour, allowing the tolerated anxiety to habituate
    • E.g. someone with obsessions about contamination is supported to touch something dirty and instead of immediately washing their hands, they are encouraged to experience anxiety and discuss it with the therapist
    • A hierarchy of feared situations is used
    • Effective in well-motivated patients
  • SSRIs
    • Effective in OCD
    • Clomipramine (TCA) is also effective
179
Q

What is the prognosis of OCD?

A
  • OCD has a chronic course with symptoms worsening at times of stress
  • Often disabling
  • Comorbid depression is common
180
Q

What is Acute Stress Reaction?

A
  • Transient state starting within minutes of trauma and resolving spontaneously within hours (1-3 days maximum)
  • Person is usually anxious but my appear dazed
  • May experience amnesia and depersonalisation/derealisation
  • Often disorientated and agitated
  • Sometimes irritable and panicky
181
Q

What is the management of acute stress reaction?

A
  • Exclude injury
  • Support and reassurance
  • Benzodiazepines may alleviate short-term distress (does NOT prevent later PTSD)
182
Q

What is PTSD?

A
  • Follows a traumatic event of an exceptionally threatening or catastrophic nature likely to cause pervasive distress in anyone
  • Examples: natural disasters, war, accidents, rape, terrorism
  • Lifetime prevalence: 6.8%
183
Q

What is the aetiology of PTSD?

A
  • 10% of those experiencing extreme trauma develop PTSH
  • Some genetic component
  • Risk factors: neurotic traits, personal or family history of psychiatric problems, childhood abuse, poor early attachment
184
Q

What is the clinical picture of PTSD?

A
  • There is often a latency period
  • PTSD usually begins within 6 months of trauma
  • Re-Experiencing
    • Flashbacks: vividly reliving the trauma, feeling as if it’s happening all over again
    • Nightmares
    • Intrusive memories: being unable to keep the mind clear of memories of what happened
  • Avoidance
    • Avoiding reminders of the event (as it often triggers flashbacks and increased anxiety)
  • Hyperarousal
    • Persistent inability to relax
    • Hypervigilance (patient always feels on red alert)
    • Enhanced startle reflex
    • Insomnia
    • Poor concentration
    • Irritability
  • NOTE: there is an overlap with depression and other anxiety disorders
185
Q

Apart from the main triad, what other changes are seen in PTSD?

A
  • Emotional detachment (numbness)
  • Decreased interest in activities
  • Powerful emotion including anger, loss of control, shame and uncontrollable crying
186
Q

What is the differential diagnoses of PTSD?

A
  • Depression or anxiety disorder

- Adjustment disorder

187
Q

What is the management of PTSD?

A
  • Trauma-Focused CBT
    • A traumatic event can shatter previous belief systems (e.g. the world is an unsafe place, I am vulnerable)
    • These thoughts can be examined and tested
    • Exposure therapy is important (support the patient to work through their memories)
    • WARNING: talking about the experience can make the patient feel re-traumatised
  • Eye Movement Desensitisation and Reprocessing (EMDR)
    • Original trauma is deliberated re-experienced in as much detail as possible (e.g. making the patient narrate every step of it)
    • Whilst doing this, they fix their eyes on the therapist’s finger as it quickly passes from side to side in front of them
    • Eye movements can be replaced by any alternating left-right stimulus (e.g. tapping hands)
    • This aids memory processing
  • Pharmacological Treatment
    • SSRIs
      • First-line
      • Preferably in combination with psychological therapies
188
Q

What is the prognosis of PTSD?

A
  • Most patients recover
  • Some suffer for many years
  • Chronicity can lead to personality change
189
Q

What is Adjustment Disorder?

A
  • Person’s reaction to life changes that require adaptation to cope (e.g. moving to university) is greater than usually expected
  • It is NOT severe enough to diagnose anxiety or depressive disorder
  • Symptoms start within 1 month of the stressor and resolve within 6 months
  • Support, reassurance and problem-solving are often all that are needed
190
Q

What is the epidemiology of autism?

A
  • Affects 1 in 4000 children

- Male to female ratio: 4:1

191
Q

What are risk factors for autism?

A
  • Obstetric complications
  • Perinatal infections
  • Genetic disorders e.g. Down’s syndrome
192
Q

What is the clinical presentation of autism?

A
  • Reciprocal Social Interaction
    • Not interested in people
    • Tend to play alone
    • Lack the ability to read the emotional states of others
    • Attachments are impoverished
    • Do not tend to turn to parents for comfort
    • Eye contact may be odd (avoidant or looking ‘through’ you)
  • Communication Abnormalities
    • Expressive speech and comprehension are delayed or minimal
    • Ideas are taken literally (concrete thinking)
    • Gestures are usually absent (e.g. pointing, waving goodbye)
    • Speech may consist of monologue, interminable questions and echolalia (repeating what has been said)
    • ‘I’ and ‘me’ may be confused with ‘you’ and ‘he/she’
  • Restricted Behaviours and Routine
    • Characterised by repetitive, stereotypes behaviours and restricted interests (rather than imaginative play)
    • Small changes in routine (e.g. using the wrong spoon) can result in intense tantrums
  • 75% have significant learning disabilities
  • 25% suffer from seizures
193
Q

What is the differential diagnoses of autism?

A
  • Deafness (causing poor language acquisition)
  • Asperger’s syndrome
  • Specific language disorder (delayed speech with normal IQ and social ability)
  • Learning disability (IQ problems but relatively intact social skills)
  • Rare disorders (e.g. childhood schizophrenia, Rett’s syndrome)
  • Neglect (can lead to language delay and poor socialisation)
194
Q

What are investigations for autism?

A
  • Hearing tests
  • Speech and language assessment
  • Neuropsychological testing - assess IQ and confirm diagnosis
195
Q

What is the management of autism?

A
  • Support and advice for families (National Autistic Society)
  • Behaviour therapy (reinforce positive behaviours)
  • Speech and language therapy
  • Special education
  • Treat comorbid problems (e.g. epilepsy)
  • Antipsychotic or mood stabilisers (OCCASIONALLY used for extreme aggression or hyperactivity)
196
Q

What is the prognosis of autism?

A
  • Only 1-2% of adults gain full independence

- Most need lifelong support and care

197
Q

What is Asperger’s Syndrome?

A
  • An autism spectrum disorder
  • Poor social skills and restricted interests
  • NORMAL language and IQ
  • Tendency to literal interpretation of language and difficulty in reading social cues
198
Q

What is the management of Asperger’s Syndrome?

A
  • Advice
  • Support
  • Routine
  • Social skills training
  • Better prognosis than autism
199
Q

Describe child and adolescent depression

A
  • More common in girls after puberty
  • Equal in boys and girls before puberty
  • Similar presentation to adults
  • Children are more likely to present with somatic problems (e.g. headaches, tummy-aches)
  • School performance may be deteriorating
  • IMPORTANT: you should always explore changes in functioning (e.g. schoolwork, socialising)
200
Q

What is the management of child and adolescent depression?

A
  • 1st line: CBT
  • Antidepressants are only used in severe cases
  • Good prognosis
201
Q

Describe Anxiety disorders in children and adolescence

A
  • Affect boys and girls equally
  • Similar presentation to adulthood
  • Psychological therapies are the mainstay of treatment
202
Q

What is Separation Anxiety Disorder?

A
  • Children are clingy and become distressed on separation from their parents (fearing it will be permanent)
  • Exploration of the family history may reveal threatened or unmourned loss
  • Child’s anxiety can be managed by increased periods of separation with reunion
203
Q

What is School Refusal?

A
  • Unconcealed absence from school (unlike truancy)
  • Common at times of transition (e.g. new school, new sibling)
  • May occur in families with ‘precious’ children (death of a sibling, difficulty conceiving) or vulnerable parents (life-threatening illness, agoraphobia)
  • Child will typically have a tummy ache only on week days just before school
  • Enlist the school’s support in helping deal with anxiety about performance, bullying etc.
  • Rapid return to full attendance has the best prognosis
204
Q

What is Enuresis?

A
  • Often a family history
  • Primary: toilet training was never mastered
    • Usually caused by delayed maturation of the bladder’s innervation
    • May be caused by more generalised developmental delay
    • Stress or excessively relaxed/strict toileting may contribute
  • Secondary: dryness was achieved for at least a year but has been lost
    • Usually stress-related (e.g. starting a new school)
205
Q

What is the management of enuresis?

A
  • Refer organic causes to paediatricians (e.g. epilepsy, UTI, diabetes)
  • Reassure the family and the child that the problem is common and no one’s fault
  • Address stressors and review toilet training received so far
  • Restrict fluids before bed
  • Star charts to celebrate each dry night (positive reinforcement)
  • Bell and pad (clips onto the pyjamas and wakes the child if the moisture is detected)
  • Medication (e.g. imipramine (TCA) or desmopressin (ADH))
206
Q

What is Encopresis?

A
  • DEFINITION: inappropriate defecation after age 4 when bowel control is expected
  • Most cases relate to constipation (overflow incontinence)
207
Q

What are the causes of constipation?

A
  • Dehydration
  • Painful defecation (e.g. anal fissure)
  • Fear of punishment
  • Toilet fears (e.g. monsters)
  • Hirschsprung’s disease (rare)
208
Q

What are other reasons for incontinence?

A
  • Diarrhoea
  • Learning disabilities
  • Hostility (e.g. angrily defecating in Mum’s shoe)
  • Stress
209
Q

What is the management of encopresis?

A
  • Laxatives (if constipated)
  • Reassure, address stress and review toilet training
  • Star charts
210
Q

What is Elective mutism?

A
  • Can speak but chooses not to in certain situations (e.g. at school)
  • Treatment involves reassurance, reducing stress and sometimes behavioural management
211
Q

What is the epidemiology of ADHD?

A
  • Affects 2% of children
  • 3 x more common in boys
  • Unknown cause
212
Q

What is the clinical presentation of ADHD?

A
  • Present by the age of 6 years
  • Must be persistent and pervasive across different situations
    • E.g. children who are calm at school but over-excited at school do NOT have ADHD
  • Hyperactivity
    • Boisterous with excessive energy
    • Seem to constantly be moving (running, jumping, climbing, unable to sit still for any length of time without fidgeting)
    • Usually noisy
  • Inattention
    • Distractible and unable to concentrate
    • Flits between activities and leaves tasks unfinished
  • Associated Features
    • Impulsive and reckless
    • Rarely consider the consequences of their actions
    • May engage in risky behaviour (e.g. crossing the road without looking)
    • Clumsy and accident prone
    • May be disobedient
    • Socially disinhibited and pay little attention to normal social conventions (e.g. interrupt others, cant wait until their turn)
    • Associated with learning disability and conduct disorder
213
Q

What is the differential diagnosis of ADHD?

A
  • Depression/anxiety - can cause agitation
  • Mania (RARE)
  • Conduct disorder
214
Q

What are the investigations for ADHD?

A
  • Questionnaires (e.g. Conner’s Rating Scales)
    • Completed by child, parents and teacher
  • Classroom observation of the child
  • Educational psychology assessments
  • IMPORTANT: the teachers should be involved in the assessment
215
Q

What is the management of ADHD?

A
  • Family: education about ADHD and advice on parenting
  • Behavioural management
  • Support for teachers (appropriate schooling placement)
  • Family therapy
  • Stimulant medication
    • Methylphenydate or dexamphetamine
    • Improves concentration thus allowing learning and maturation
    • Side-Effects: appetite suppression, insomnia
    • Drug holidays may be needed to limit growth retardation (usually to 1 cm)
    • NOTE: these are NOT addictive
  • NOTE: some parents report benefits from dietary changes (e.g. more oily fish and excluding certain foods)
216
Q

What is the prognosis of ADHD?

A
  • May suffer low self-esteem, peer rejection, educational under-achievement and harsh parenting
  • Symptoms improve in adolescence (but 50% have ongoing symptoms)
  • Untreated ADHD is a risk factor for later dissocial personality disorder, criminality and substance abuse
217
Q

What are the risk factors of conduct disorder?

A
  • Urban upbringing
  • Deprivation
  • Parental criminality
  • Harsh and inconsistent parenting
  • Maternal depression
  • Family history of substance misuse
  • Antisocial behaviours may be learnt from parental or societal models (may be rewarded by increased attention)
218
Q

What is the clinical presentation of conduct disorder?

A
  • Behaviour is persistently antisocial and not just rebellious
  • Examples: bullying, stealing, fighting, fire-setting, truancy and cruelty to animals or people
  • TWO types:
    • Socialised CD
      • Child has a peer group (often sharing antisocial behaviour)
    • Unsocialised CD
      • Rejected by other children making them more isolated and hostile
219
Q

What is the differential diagnosis of conduct disorder?

A
  • Oppositional defiant disorder
    • Milder form occurring in children < 10 years old
    • Provocative, angry and disobedient but NO extreme antisocial behaviour
  • ADHD
  • Depression
220
Q

What is the management of conduct disorder?

A
  • Family education
    • Make the family understand CD and how they may accidentally reinforce the behaviours
  • Parent management training
    • Teaches parents to reward good behaviour and deal constructively with negative behaviours
  • Family therapy
    • Family meets with a skilled therapist to discus current problems
    • They are helped to cooperate in problem solving
  • Educational support
  • Anger management for child
  • Treat comorbid problems (e.g. ADHD)
221
Q

What is the prognosis of conduct disorder?

A
  • 50% will develop substance misuse problems or dissocial personality disorder as adults
222
Q

What is Tic disorder?

A
  • Tic: repetitive, involuntary and purposeless movements or vocal utterances
  • Categories
    • Simple - e.g. blinding, throat-clearing
    • Complex - e.g. self-hitting, swearing
  • Transient simple tics affect 10% of children
  • OCD is commonly comorbid
  • Stress or stimulants can worsen tics
  • They recede when the sufferer is concentrating on something else
  • They can be voluntarily suppressed, but this results in internal tension (which is relieved by expression of the tic)
223
Q

What is the management of tic disorder?

A
  • Reassurance and stress management
  • Clonidine (alpha-2 agonist)
  • Haloperidol (antipsychotic)

Specialties (14 decks)

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