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CP2 > PSYCH > Flashcards

PSYCH Flashcards

1
Q

What is psychosis?

A

= a syndrome characterised by a loss of contact with reality.

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2
Q

What are the key symptoms of psychosis?

A

Delusions = fixed, false, unshakeable beliefs

Hallucinations = perception of something in the absence of external stimuli
=> Auditory (most common), visual, smell, taste

Formal thought disorder = pattern of disordered language reflecting disordered thoughts.

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3
Q

What kind of delusions are common in psychosis?

A

Persecutory – being stalked/spied-on, etc.

Grandiose – elevated self-importance

Somatic – think something is physically wrong with themselves.

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4
Q

DDx of Psychosis

A

Organic cause - delirium, endocrine, medication-induced, epilepsy

Other Psychiatric Disorder -
=> Schizophrenia, Depression, Schizotypal disorder, Schizoaffective disorder, Delusional disorder

Substance-induce - e.g. cannabis, hallucinogens, caffeine, alcohol

Systemic - e.g. MS, SLE, HIV, hypoglycaemia, etc.

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5
Q

What medications can induce psychosis?

A

Dopamine agonists,
Corticosteroids,
Stimulants

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6
Q

Schizotypal disorder

A

disordered thoughts but hallucinations/delusions not prominent

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7
Q

Schizoaffective disorder

A

Prominent mood disorder alongside 1st rank schizophrenia symptoms

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8
Q

Delusional disorder

A

delusions not so bizarre and no hallucinations

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9
Q

Acute Transient Psychosis

A

= Sudden onset psychotic symptoms lasting <28 days, with no identifiable organic cause

Linked to stress

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10
Q

What is schizophrenia?

How common is it?

A

= a psychotic disorder characterised by the presence of first rank symptoms for >28 days with no organic cause.

  • 1 in 1000
  • M=F
  • Peak = 23-26 years (then 30-40 years)
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11
Q

What are considered the 1st rank symptoms of schizophrenia?

A

Hallucinations (auditory):
=> 3rd person/being talked about
=> Thought echo / Running commentary

Delusional perception – attribute false meaning to an external stimulus.

Delusions of thought interference – insertion/withdrawal/broadcasting.

Passivity Phenomena:
=> Control of impulses/actions/feelings/sensations by an “external force”

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12
Q

Other symptoms of schizophrenia (i.e. not 1st rank)

A

Positive – delusions, hallucinations, formal thought disorder

Negative – blunted/flat affect, social withdrawal, poverty of speech, anhedonia, decreased motivation

Cognitive – poor attention, learning, problem solving

Motor – catatonic movements, waxy flexibility.

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13
Q

Schizophrenia - cause / risk factors

A

A mixture of genetics (80%) and environment.

RFs:

  • FHx
  • Obstetric complications, maternal illness in pregnancy, low birth weight
  • Urban living, migration, adverse life events, poor pre-morbid personality, abnormal family dynamics
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14
Q

Schizophrenia - Prodrome

A

period of symptoms development but not yet at diagnostic criteria.

  • Non-specific negative symptoms
  • Distress/agitation
  • Transient psychotic symptoms
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15
Q

Schizophrenia - Acute phase

A

relapsing and remitting positive and negative symptoms

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16
Q

Schizophrenia - outcomes

A

20% only have 1 episode
50% recover but relapse in future
30% develop chronic schizophrenia
10-15% commit suicide

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17
Q

Good Prognostic Factors for schizophrenia

A 
Female
Married
Acute Onset
Prominent mood symptoms
Good premorbid personality
Early Tx with good response
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18
Q

Poor Prognostic Factors for schizophrenia

A 
Male and Unmarried
FHx of schizophrenia
Early onset or insidious onset
Prominent negative symptoms
Substance abuse
Lack of insight/non-compliance
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19
Q

What are the aims of investigation in ?schizophrenia

A
  1. Establish if there is any organic cause

2. Prepare for Tx with antipsychotics

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20
Q

Schizophrenia - investigations

A

History (+ collateral Hx) and MSE

Physical examination
=> BMI, neurological

Bloods
=> FBC, U&E, LFT, TFT, glucose, lipids, cholesterol

Urine drug screen = most important

ECG

+/- brain scan, EEG

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21
Q

What is the most important investigation in diagnosis of schizophrenia?

A

Urine drug screen to rule out substance misuse as cause of Sx

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22
Q

Schizophrenia - management

A
  1. Biological:
    => Antipsychotics
    => Annual physical health review – smoking, alcohol, BP, BMI, bloods, ECG
  2. Psychological:
    => CBT
    => Psychoeducation – signs of relapse, prevent relapse, crisis plans
    => Education and support for carers
  3. Social:
    => OT assessment of functioning – ADLs, occupation, hobbies
    => Social assessment for housing, benefits, finances, education/career
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23
Q

Aims of management of schizophrenia

A

Recovery isn’t necessarily about completely stopping hallucinations/delusions, BUT rather:

  • How to deal/cope with them
  • Providing social support
  • Reducing stigma
  • Reducing risk to self and others
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24
Q

Treatment Resistant Schizophrenia

A

= no response to TWO different antipsychotics

  1. Check Dx, check compliance and check for substance misuse
  2. Mx = CLOZAPINE:
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25
Q

What are the most important side effects of the antipsychotic clozapine?

A

SEs – agranulocytosis, neutropaenia, cardiomyopathies

Patient will need weekly FBCs

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26
Q

Non-compliance in schizophrenia Tx

A

Can be due to:

  • Side effects
  • Lack of insight
  • Delusions about medications/prescriber
  • Gains remission and thinks medication no longer needed
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27
Q

Antipsychotics - mechanism of action

A

Block post-synaptic receptors in dopaminergic pathways.
=> Decreases psychotic symptoms
=> Can cause hyperprolactinaemia
=> Can cause extra-pyramidal side effects

The aim is to reduce positive and negative symptoms, with minimal side effects.

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28
Q

Typical/first generation antipsychotics

A

e.g. chlorpromazine, haloperidol, sulpiride, flupentixol, trifluperazine.

= D2 receptor antagonists

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29
Q

Side effects of Typical/first generation antipsychotics

A

Extrapyramidal SEs
Decreased seizure threshold
Sedation
Neuroleptic malignant syndrome (NMS) = EMERGENCY

Apathy, confusion, depression

Dry mouth, blurred vision, constipation, urine retention

Arrythmias, hyperprolactinaemia, hypotension, weight gain

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30
Q

Extrapyramidal SEs

A
  • Akathisia – uncontrollable urge to fidget (e.g. pacing, crossing and uncrossing legs) => Increased risk of suicide
  • Acute dystonia – involuntary muscle spasms, causing abnormal movement/posture (fatal if laryngeal mm.)
  • Parkinsonism – tremor, rigidity, bradykinesia
  • Tardive Dyskinesia – involuntary hyperkinetic movements
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31
Q

Features of neuroleptic malignant syndrome (NMS)

A

= EMERGENCY

  • Hyperthermia
  • Muscle rigidity
  • Tremor
  • Acidosis
  • Tachycardia
  • Confusion
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32
Q

Atypicals/Second Generation antispychotics

A

e.g. aripiprazole, onlanzapine, risperidone, clozapine

= D2 receptor antagonists +/- 5-HT receptor antagonists.

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33
Q

Side effects of Atypicals/Second Generation antispychotics

A 
General – nausea, constipation, dizziness (postural hypotension) 
Weight gain
Sedation
Metabolic syndrome
\+/- insomnia, hyperprolactinaemia

(Risperidone has EPSEs)

(Clozapine – agranulocytosis, neutropaenia, cardiomyopathy)

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34
Q

What is the 1st line class of antipsychotic and why?

A

Generally, atypicals are 1st line as they have the same efficacy but fewer EPSEs than 1st-generation antipsychotics.

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35
Q

Eating Disorders - Risk factors

A
  • Adolescence (peak onset)
  • Female (F:M = 10:1)
  • Perfectionism
  • Low self-esteem
  • Early sexual development
  • Hx of abuse
  • Personality disorder
  • Hx of eating disorder
  • Exposure to “diet culture”
  • Middle/upper class
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36
Q

Definition of anorexia nervosa

A

BMI <17.5
Persistent restriction of energy intake
Often excessive exercise
Intense fear of gaining weight/becoming fat
Lack of insight into seriousness of low BMI

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37
Q

DDx of anorexia

A
  • Hyperthyroidism
  • Depression, OCD, psychosis
  • Body dysmorphic disorder
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38
Q

Anorexia nervosa - psychiatric Sx

A 
Inflexible thinking, 
obsessions/habits, 
poor concentration, 
irritable/flattened mood, 
interests centred around food
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39
Q

Anorexia nervosa - cardiac Sx

A

Low BP and pulse

Increased risk of arrythmias/heart failure

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40
Q

Anorexia nervosa - reproductive Sx

A

Reduced libido,
Amenorrhoea/low testosterone,
Reproductive dysfunction

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41
Q

Anorexia nervosa - MSK Sx

A

Muscle wasting/cramp

IRREVERSIBLE osteopenia/osteoporosis

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42
Q

Anorexia nervosa - hair/skin Sx

A

Broken skin
Dry, brittle hair
Hair growth on face/body for warmth (Lanugo hair)

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43
Q

Anorexia nervosa - Other Sx

A

Cold extremities/hypothermia
Infections
Metabolic disturbances
Iron deficiency anaemia, leucopaenia, thrombocytopaenia

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44
Q

Anorexia Nervosa - Biological Management

A

Weight restoration

Regular monitoring
=> Weight, FBC, U&Es, LFT, glucose, (magnesium, Ca, CK, B12)

+/- DEXA scan

+/- ECG

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45
Q

What is there a risk of in weight restoration in anorexia?

A

Risk of refeeding syndrome

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46
Q

What might be identified on an ECG in anorexia?

A

Prolonged QTc,
HR <50,
arrythmias

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47
Q

Anorexia Nervosa - Psychological/social Management

A

Psychotherapies – CBT, motivational interviewing, mindfulness

Family therapy if <18 years old

SOCIAL - Involve family and friends for support, carer support.

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48
Q

Indications for hospitalisation in anorexia nervosa

A

BMI <13.5
Very deranged bloods
Syncope/arrythmias

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49
Q

Anorexia Nervosa - 10-year Prognosis

A

50% recovered
40% chronic problem
10% mortality (1/3 suicide)

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50
Q

Anorexia Nervosa - Poor prognostic factors

A
  • Low body weight
  • Bulimic features
  • Family difficulties
  • Personality problems
  • Longer illness duration
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51
Q

Features of Bulimia Nervosa

A

Features = once a week (or more) of the following, for 3 months:

  • Recurrent binge eating
  • Recurrent compensatory behaviour (vomiting, laxatives, diuretics, fasting, exercise)
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52
Q

Bulimia Nervosa - Sx

A

Poor concentration, irritable

Tooth decay/erosion, hoarse voice, bleeding, swollen parotid glands (=> “chipmunk face”)

Callouses, scars, abrasions on backs of fingers due to self-induced vomiting.

Electrolyte imbalances:
=> Seizure, muscle paralysis, arrythmias

Swollen/painful stomach, constipation, delayed gastric emptying, oesophagitis, rectal prolapse, renal failure.

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53
Q

Bulimia Nervosa - Biological Mx

A

Anti-depressant – SSRI, usually fluoxetine.

Advise laxative and alcohol cessation

Regular monitoring
=> Weight, FBC, U&Es, LFT, glucose

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54
Q

Bulimia Nervosa - Psychological/social Mx

A

Psychoeducation – coping mechanisms

Psychotherapies – CBT, compassion-focussed, mindfulness

Social:

  • Involve family/friends for support
  • Carer support
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55
Q

Bulimia Nervosa - prognosis

A

10-year prognosis:

  • 70% recovered
  • 1% mortality

Poor prognostic factors:

  • Low body weight
  • Comorbid depression
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56
Q

Prevalence of depression

A

10-20%

Late 20s = peak onset
F:M = 2:1

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57
Q

Prognosis of depression

A

50% recover within 1 year
25% go on to have chronic depression (>2 years)
5-15% commit suicide

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58
Q

Core symptoms of depression

A
  1. Low Mood (worse in the morning)
  2. Anhedonia
  3. Fatigue
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59
Q

Other symptoms of depression

A 
Guilt/hopelessness
Appetite changes (weight loss/gain)
Poor memory, pessimism, psychosis
Sleep disturbances
Self-harm/suicidal thoughts
Self-esteem = low
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60
Q

ICD-10 criteria for depression

A

symptoms for 2+ weeks:

  • Mild – 2 core and 2 other
  • Moderate – 2/3 core and 3/4 other
  • Severe – 3 core and 5 other
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61
Q

What are the 3 biggest risk factors for depression?

A

Life events
FHx
Substance misuse

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62
Q

Risk Factors for depression

A

Social – life events, isolation, loss, childhood abuse

Biological – FHx, hormonal changes, chronic/severe illness

Psychological – negative thoughts, high expressed emotion, criticism, personality disorder

Medications – steroids, antipsychotics, substance misuse

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63
Q

Depression - differentials

A

Psychiatric – dementia, schizophrenia, anxiety disorder, SAD, bipolar

Neurological – PD, MS, head injury, cerebral tumour

Endocrine – hypothyroidism, hyperparathyroidism, Cushing’s, Addison’s

Infections – HIV/AIDs, glandular fever, STIs

Systemic – malignancies, SLE, RA, renal failure

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64
Q

Management of depression - biological

A

Biological Interventions:

  • Antidepressants
  • Atypical antipsychotics (if psychosis)
  • Augmentation with Lithium (Tx resistant)
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65
Q

Management of depression - psychological

A 
Psychoeducation
CBT
Mindfulness
Sleep hygiene
Self-help (e.g. apps)
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66
Q

Management of depression - social

A

Support for education, training, employment
Support for housing/benefits
Carer support – info, support groups, assessment
CPN (monitor Sx, mood, mental state) if severe

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67
Q

Mild/ moderate depression - management

A

Manage in Primary care

Low-intensity psychological interventions
Consider 1st line medication (SSRI)

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68
Q

When is an SSRI not indicated in depression

A

SSRI is not indicated if only mild/subthreshold symptoms for <2 years and no Hx of depression.

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69
Q

Moderate/severe Depression or Tx-resistant - management

A

Manage in primary care (may consider referral to 2o)

1st line medication (SSRI) or alternative
High-intensity psychological interventions

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70
Q

Severe depression - Management

A

Inpatient or Crisis Resolution and Home treatment

1st line medication or alternatives/adjuncts
High intensity psychological interventions
?ECT

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71
Q

Counselling newly diagnosed depression patients

A

Make sure you have a good Hx and risk assessment

Be aware of stigma
Explain different courses, outcomes, treatments
Remain positive and highlight the benefits of Tx

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72
Q

What is important to do before starting anti-depressant Tx?

A

Rule out bipolar before starting antidepressant monotherapy!

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73
Q

Starting anti-depressants

A
  1. Consider SEs, cautions, CIs
  2. Start an effective but tolerated dose
    => Trial for 3-4 weeks before deciding if it is working
    => 70% will respond to 1st Tx
  3. Review regularly
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74
Q

Anti-depressant withdrawal

A

DO NOT STOP ABRUPTLY – taper dose over 4 weeks

Withdrawal symptoms particularly noticeable with paroxetine and venlafaxine.

  • Dizzy, numb/tingling
  • Nausea/vomiting
  • Headache
  • Sweating, shaking
  • Anxiety
  • Sleep disturbances
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75
Q

How long should anti-depressants be used for?

A

Continue for at least 6 months after resolution of Sx.

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76
Q

SSRIs - mechanism of action

How long does it take to take effect?

A

Inhibit pre-synaptic 5-HT reuptake.

Take up to 6 weeks for effect.
Sx may worsen before improving.

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77
Q

SSRIs - side effects, cautions, CIs

A

SEs – nausea, headaches, drowsiness, insomnia, diarrhoea, dizziness, SEXUAL DYSFUNCTION, restlessness

Cautions – Long QTc, bleeding disorders (especially citalopram)

CIs – poorly controlled epilepsy.
=> Paroxetine = teratogenic

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78
Q

Which medication is 1st line for depression

A

SSRIs (due to fewer SEs)

Although TCAs are 1st line in pregnancy

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79
Q

SNRIs - mechanism of action

A

Inhibit 5-HT and NA reuptake

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80
Q

Which medication is 2nd line for depression?

A

SNRIs (venlafaxine, duloxetine)

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81
Q

SNRIs - side effects, cautions, CIs

A

SEs – more prominent sedation and sexual dysfunction, and same as SSRIs.

Cautions – diabetes, uncontrolled HTN, bleeding disorders, epilepsy

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82
Q

TCAs - mechanism of action

A

Inhibit 5-HT and NA reuptake

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83
Q

TCAs - side effects, cautions, CIs

A

SEs – sedation, weight gain, dizziness, HTN, delirium, antimuscarinic SEs

Cautions – bipolar, diabetes, epilepsy, high suicide risk (dangerous in overdose)

CIs – arrythmias, heart block, post-MI

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84
Q

MAOIs - mechanism of action and use

A

Irreversible MAO A & B inhibition

Tx resistant/atypical depression

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85
Q

MAOIs - side effects, cautions, CIs

A

SEs – nausea, diarrhoea, constipation, dry mouth, sleep disturbance, postural hypotension, headache

Cautions – bleeding disorders, diabetes, elderly

Interact with many drugs/tyramine containing foods (hypertensive crisis) => so not often used

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86
Q

NaSSA (mirtazapine) - mechanism of action and use

A

Alpha2-receptor antagonist – increases NA and 5-HT

Adjunct in Tx-resistant depression

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87
Q

NaSSA (mirtazapine) - side effects, cautions

A

SEs – increased appetite and weight gain, sedation

Cautions – diabetes, seizures, urinary retention, elderly

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88
Q

Alcohol and antidepressants

A

With SSRIs and SNRIs advise against alcohol as this will have additive sedation effects.

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89
Q

St John’s Wort

A

= an unlicenced herbal remedy for treating depression => some evidence of efficacy but difficult to guide on dosing.

Cytochrome P450 inducer, causing metabolism and therapy failure of OCP, digoxin, warfarin, phenytoin, carbamazepine.

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90
Q

Acute Stress Reaction

A

= a brief response (<1 month) to a severely stressful event

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91
Q

What is the link between acute stress reaction and PTSD?

A

~80% formally diagnosed with acute stress reaction develop PTSD.

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92
Q

Acute Stress Reaction - Sx

A

(overlap with anxiety/depression Sx)

  • Numbness, detachment, decreased concentration, derealisation.
  • Insomnia, restlessness, anger
  • Autonomic Symptoms
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93
Q

Acute Stress Reaction - Coping strategies

A
  • Avoid thinking/speaking of event
  • Denial/cannot remember event
  • Alcohol
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94
Q

Acute Stress Reaction - Mx

A
  • Taking to friends/family/professionals to relieve anxiety
  • Encourage recall
  • Learning effective coping strategies

Anxiolytics (if severe anxiety)
Hypnotics (if insomnia)

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95
Q

Adjustment Disorder

A

= physiological reaction to adapting to a new set of circumstances (e.g. new job/home, divorce, bereavement).

Starts within 3 months (more gradual than acute stress reaction)

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96
Q

Adjustment Disorder - Sx

A

(overlap with anxiety/depression Sx)

  • Autonomic symptoms
  • Irritability/aggressive outbursts
  • Social functioning impaired
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97
Q

Adjustment Disorder - Coping strategies

A

Alcohol/drug abuse

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98
Q

Adjustment Disorder - Mx

A

Talking to friends/family/professionals to relieve anxiety

Help natural process of adjustment – avoid denial/avoidance, encourage problem solving behaviour

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99
Q

What is the normal bereavement process?

A
  1. Alarm/panic
  2. Numbness
  3. Pining
  4. Depression
  5. Recover/reorganisation
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100
Q

Abnormal grief

A

Symptoms of normal grief, persisting >6 months
=> Low mood, guilt, worthlessness, disturbed sleep and appetite, suicidal thoughts

Significant psychomotor retardation

Prolonged, serious functional impairment

Hallucinatory experiences other than those relating to the deceased person

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101
Q

What is abnormal grief, which does not meet the depression criteria?

A

this is considered to be an adjustment reaction

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102
Q

What is PTSD?

A

= delayed (often a few months) response to a stressful event of an exceptionally threatening/catastrophic nature (an event which would distress anyone).

Symptoms persists >6 months after the event.

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103
Q

Symptoms of PTSD

A
  1. HYPERAROUSAL – persistent anxiety, irritability, insomnia, poor concentration.
  2. RE-EXPERIENCING – “flashbacks”, recurrent dreams, cannot recall event at own will
  3. AVOIDANCE – of reminders, detachment, numbness, anhedonia
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104
Q

Complex PTSD

A

Complex PTSD has an added emotional element – often resulting from ongoing/multiple experiences of “trauma” (e.g. abuse)

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105
Q

PTSD - coping strategies

A

Alcohol/drug abuse

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106
Q

PTSD - prognosis

A

50% recover in 1st year

Poor prognosis if comorbid mental illness, long duration, poor support

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107
Q

PTSD - Mx

A
  1. Psychological – psychoeducation, CBT, eye movement desensitisation reprocessing.
  2. Biological – antidepressants (SSRI) +/- antipsychotic
  3. Social – educate family, social reintegration, alcohol avoidance
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108
Q

Indications for ECT

A
  • Treatment-resistant depression
  • Life-threatening severe depression
  • Treatment-resistant mania
  • Catatonia
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109
Q

What is catatonia?

What forms can this come in?

A

Catatonia is a psychomotor syndrome occurring in acute psychiatric illness.

RETARDED – immobility, staring, mutism, rigidity, withdrawal and refusal to eat, posturing, grimacing, negativism, waxy flexibility, echolalia, automatic obedience

EXCITED – severe psychomotor agitation, potentially leading to life-threatening complications such as hyperthermia, altered consciousness, and autonomic dysfunction.

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110
Q

What is the most common indication for ECT?

A

depression

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111
Q

How often do ECT sessions occur?

A

A patient will typically receive between 4 and 12 sessions in a course of ECT.

The sessions usually occur twice per week.

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112
Q

How does ECT work?

A

The exact mechanism of action of ECT is unknown.

The mechanism of action is likely to be a combination of:

  • Modulation of neurotransmitter functioning
  • Changes in regional blood/activity
  • Modulation of neuronal connectivity
  • Alterations of neuronal structures, including hippocampal neurogenesis
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113
Q

Why is the use of ECT falling?

A

ECT remains to be quite an effective treatment, especially for depression.

Decreased usage is likely to be due to:

  1. increasingly available treatments,
  2. concerns over side-effects
  3. public/clinicians’ perceptions.
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114
Q

What is an absolute contraindication for ECT?

A

cochlear implant

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115
Q

What are relative contraindications for ECT?

A
  • Raised intracranial pressure
  • Intracranial aneurysm
  • History of cerebral haemorrhage
  • Recent myocardial infarction (less than 3 months)
  • Aortic aneurysm
  • Uncontrolled cardiac arrhythmias
  • Decompensated cardiac failure (ECHO may be helpful)
  • Acute respiratory infection
  • Deep vein thrombosis
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116
Q

Common side effects of ECT

A
  • Headache
  • Confusion
  • Impaired cognitive function
  • Temporary retrograde and anterograde amnesia
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117
Q

Longer-term side-effects of ECT

A

a specific component of retrograde memories before ECT may be affected longer term, this usually related to autobiographical memories

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118
Q

What is an important side effect to mention to patients when explaining/gaining consent for ECT?

A

Though the evidence for this is somewhat inconsistent, patients should ALWAYS be advised that their memory of some events in the previous years could potentially be affected.

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119
Q

What are the two different types of ECT?

Which is more effective?

A

BILATERAL ECT – one pad on each side.
UNILATERAL ECT – both pads on one side.

=> Bilateral placement is probably more effective but may well give rise to more cognitive side-effects.

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120
Q

Give a brief explanation of the ECT process

A

ECT is given in a hospital setting, under anaesthetic with muscle relaxant. A mouth guard is used to protect the tongue/teeth

Two electrical pads are placed on the patient’s head.

The ECT machine delivers a series of brief electrical pulses, for three to eight seconds, to induce a seizure

The patient’s body will stiffen and then there will be twitching, but the muscle relaxant reduces the amount of movement involved.
=> This usually lasts for less than 90 seconds.

The muscle relaxant wears off within a couple of minutes. The mouth guard will then be removed, and the patient will recover from the anaesthesia

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121
Q

How is the dose of ECT decided?

A

During the first session of ECT, a dose titration is carried out to establish the seizure threshold.

The effective treatment dose can then be calculated.

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122
Q

what is echolalia?

A

repetition of another person’s speech

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123
Q

what is echopraxia?

A

mimicry of another person’s movements

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124
Q

Acute Intoxication

A

= transient physical and mental abnormalities shortly after administration.

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125
Q

Harmful substance use

A

= continued use despite evidence of damage to physical/mental health or social wellbeing.

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126
Q

Substance withdrawal

A

= physical dependence causes symptoms on abrupt cessation

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127
Q

Substance tolerance

A

= need to take more of the drug to have the same effect.

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128
Q

ICD-10 criteria for substance dependence syndrome

A

5/6 in the past year of:

  • Tolerance
  • Control loss
  • Primacy (i.e. priority in life)
  • Tremor (withdrawal Sx)
  • Compulsion
  • Persistence despite harm
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129
Q

What is the trend of drinking in the younger/older populations?

A

Younger people drink more heavily, older people drink more frequently.

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130
Q

Risk Factors for alcohol misuse

A

Genetics and gender – M>F

Mental illness

Stress, low self-esteem, social anxiety/isolation

Significant life events – bereavement, trauma

Lower socio-economic status

Occupation – bartenders, farmers, healthcare professionals

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131
Q

Medical complications of alcohol misuse

A

CNS – cognitive/memory impairment, reduced brain volume, Wernicke-Korsakoff Syndrome

PNS – peripheral neuropathy, optic atrophy

Hepatic – fatty liver, hepatitis, cirrhosis, malignancy, pancreatitis

Gastric – gastritis/ulcer, malignancy, varices, Barret’s, Mallory-Weiss tear

Renal – CKD, hepato-renal syndrome

CVS – cardiomyopathy, arrythmias, HF, cerebrovascular events

Reproductive – sexual dysfunction, infertility, foetal alcohol syndrome

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132
Q

Psychiatric complications of alcohol misuse

A

Alcoholic Hallucinosis

Pathological jealousy

Alcohol-related Brain Damage (cognitive/memory impairment and dementia)

Anxiety & Depression

Suicide (10-15% risk)

Schizophrenia (increases risk of relapse and violence)

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133
Q

Alcoholic hallucinosis

A

hallucinations while sober (usually auditory)

=> Responds well to anti-psychotics

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134
Q

Pathological jealousy

A

Primary delusion that partner is unfaithful

Associated with violence.

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135
Q

Social complications of alcohol misuse

A 
Relationship problems
Domestic violence
Risky sexual activity
Missed work/poor performance
Financial and legal problems
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136
Q

Wernicke-Korsakoff Syndrome - why does it occur and what are the features?

A

Due to thiamine (vit B1) deficiency – due to poor diet and decreased absorption/hepatic storage.

Wernicke’s Encephalopathy:

  1. Acute confusion
  2. Ophthalmoplegia/nystagmus
  3. Ataxic gait

Progresses to Korsakoff Syndrome:

  1. Antero/retrograde amnesia
  2. Confabulation (false memories)
  3. Apathy (indifference/decreased interest)

15% mortality if left untreated

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137
Q

Treatment of Wernicke-Korsakoff Syndrome

A

IV Pabrinex (Vit B&C) and alcohol withdrawal Tx

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138
Q

Alcohol misuse History

A
  • Lifetime pattern of consumption
  • Current pattern of consumption
  • Signs of dependence:
    Withdrawal Sx in morning/after not drinking
    Having to drink more for the same effect
    Episodes of memory loss/blackouts
  • Social/Occupational problems
  • Any previous services or Tx ?
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139
Q

What are 4 screening questions to detect alcohol misuse?

A

= CAGE

  1. CUT DOWN – have you ever felt you should cut down your drinking?
  2. ANNOYED – have you ever been annoyed with others criticising your drinking?
  3. GUILTY – have you ever felt bad/guilty about your drinking?
  4. EYE OPENER – have you ever drunk first thing in the morning?
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140
Q

Alcohol Withdrawal Sx

A

Last 2-5 days.

Tremor, restless, sweating, tachycardia, insomnia, N&V
Anxiety, confusion, visual hallucinations

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141
Q

Delirium Tremens

A

Can occur during alcohol withdrawal
= EMERGENCY ADMISSION

Decreased consciousness, amnesia, hallucinations
Tremor, fever

Mx = lorazepam PO, thiamine, hydration and investigations to r/o other causes of delirium.

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142
Q

Alcohol abuse - investigations

A
  • MCV – remains raised 3-6 months after abstinence
  • GGT – alcohol-related liver inflammation
  • Liver USS – if indicated
143
Q

In what setting is alcohol misuse managed?

A

Manage in the community unless severe/high risk of delirium tremens/liver failure.

144
Q

Psychological management of alcohol misuse

A
  • Drug and alcohol services (e.g. alcoholics anonymous)

- Motivational interviewing, CBT, counselling, self-help resources.

145
Q

What are the aims of biological management of alcohol misuse?

A

Detoxification/Withdrawal Management

Maintaining Abstinence

146
Q

Detoxification/Withdrawal Management for alcohol

A

A reducing regimen over 7-10 days.

Chlordiazepoxide – a BZD to treat withdrawal Sx.

Thiamine (B1) – avoid/treat Wernicke-Korsakoff Syndrome

147
Q

Medications to help maintain Abstinence from alcohol

A

Disulfiram – irreversible inhibition of ALDH, causing acetaldehyde to build up, causing unpleasant Sx of flushing, headache, and nausea to deter further alcohol consumption

Acamprosate – enhances GABA transmission to reduce alcohol cravings.

148
Q

Opiates - mechanism and effects

A

mu-opioid receptor agonist = GABA inhibition = reduced inhibition of dopamine release.

Effects = euphoria, sedation, strong analgesia

149
Q

Opiates - side effects

A

N&V, constipation, respiratory depression, decreased consciousness, pinpoint pupils

150
Q

Opiates - withdrawal

A 
irritable/anxious, 
sweating, shaking, restlessness, insomnia, 
fever/chills, 
diarrhoea, 
arthralgia/myalgia, 
blown pupils

=> Very unpleasant but rarely serious

151
Q

Which drugs are depressants?

A

Alcohol, cannabis, barbiturates, BZDs

152
Q

Effects of depressants

What are the side effects?

A

Suppressed CNS activity, anxiolytic.

SEs – sedation, dizziness, impaired concentration/coordination, depression.

153
Q

Withdrawal from BZDs

A

Agitation, anxiety, insomnia, seizures, delirium, psychosis.

=> Can be fatal

154
Q

Which drugs are stimulants?

A

Cocaine (snorted), crack cocaine (smoked), amphetamines, MDMA

155
Q

Mechanism of cocaine

A

monoamine reuptake inhibition (increased DA, NA, serotonin)

156
Q

effects of stimulant drugs

A

euphoria, feelings of extreme well-being,

increased mental & motor activity, alertness, energy and confidence,
=> leading to risky/aggressive behaviour.

157
Q

Side effects of cocaine

A

tachycardia, arrythmias, septal necrosis, panic disorder/paranoia, psychosis.

158
Q

Side effects of MDMA

A

nausea, blurred vision, dehydration, depression/anxiety

159
Q

Withdrawal from stimulant drugs

A

Dysphoria/anxiety, fatigue, muscle aches/tremors, craving.

=> Unpleasant but rarely serious.

160
Q

Which drugs are Hallucinogens?

A

Cannabis, LSD, PCP (phencyclidine), ketamine, psilocybin (magic mushrooms).

161
Q

Mechanism of cannabis

A

THC = active chemical, binds CB1 receptors to cause effects.

162
Q

Mechanism of LSD

A

5HT receptor agonist.

163
Q

Effects of hallucinogens

A

altered sensory/perceptual experiences (delusions/hallucinations), detachment.

164
Q

Side effects of hallucinogens

A 
Dizziness, 
Dilated pupils, 
Tachycardia, 
HTN, 
Increased appetite, 
Anxiety/panic attacks.
165
Q

How can you assist with detoxification/withdrawal from drugs

A 
Symptom reduction:
•	Lofexidine – alpha-blocker for autonomic Sx
•	Loperamide – diarrhoea
•	Metoclopramide – nausea
•	Z-drugs – insomnia
•	Analgesia
166
Q

Methadone in drug detoxification

A

long-acting opioid, causes constant receptor occupation so taking illicit opioid on top has no effect.

167
Q

Buprenorphine in drug detoxification

A

opiate replacement

168
Q

Psychosocial management of drug misuse

A
  • Drug and alcohol services
  • Motivational interviewing, CBT, counselling, self-help resources.
  • Housing, financial, child-care support.
  • Harm reduction – promote use of sterile needles/don’t reuse or share needles.
169
Q

What is an anxiety disorder?

A

= pathological responses to minimal environmental triggers, resulting in persistent symptoms that impair function and/or cause disabling behaviours (e.g. avoidance).

170
Q

Psychological symptoms of anxiety

A 
Worrying thoughts
Irritable
Sensitive to noise
Fearful anticipation
Poor concentration
171
Q

Physical symptoms of anxiety

A

Sleep disturbance (insomnia, night terrors)

Muscle tension (aches, tremors)

Hyperventilation (causing dizziness and tingling numbness)

Autonomic arousal (dry mouth, sweaty, SOB, hot/cold, chest pain, palpitations, diarrhoea, urgent micturition) feels like MI

172
Q

Which anxiety disorders have episodic symptoms?

A

Phobias, PTSD, OCD, Panic disorders

173
Q

Which anxiety disorders have constant symptoms?

A

Generalised anxiety disorder

174
Q

ICD-10 criteria for generalised anxiety disorder

A

Generalised and persistent somatic and psychological symptoms.

  • Apprehension/fear of the future
  • Motor tension
  • Autonomic overactivity
  • Over-cautious behaviour.

Present most days for at least several weeks at a time.

175
Q

ICD-10 criteria for Panic Disorder

A

Recurrent attacks of severe anxiety (lasting <10 minutes)

  • Sudden onset of threatening body sensations (e.g. dizziness, choking, palpitations).
  • Loss of touch with reality/catastrophic thoughts (e.g. losing control, going mad, dying).

Comparative freedom from symptoms between attacks.

In circumstances of no objective danger.
- Not restricted to particular situations, so unpredictable.

176
Q

Agoraphobia

A

Marked fear and avoidance of at least 2 of:

  • Crowds/public places
  • Travelling alone
  • Travelling away from home
177
Q

Social Phobia

A

Marked fear and avoidance of being the focus of attention and scrutiny/humiliation.

  • Blushing/shaking
  • Fear of vomiting
  • Urgency of micturition.
178
Q

Specific (Isolated) Phobia

A

Marked fear and avoidance of a specific object/situation:

=> Animals, birds, insects, heights, thunder, flying, small spaces, blood, injections, dentists, hospitals.

179
Q

Obsessive Compulsive Disorder

A

Obsessions (thoughts, impulses, images) AND/OR compulsive acts/rituals (physical behaviours).

=> Originate in the mind of the patient, acknowledged as excessive/unreasonable.

Present most days for at least 2 weeks.

Cause distress and interference with activities.

180
Q

OCD in children

A

Obsessions and compulsions are common in kids (average onset = 9 years) and considered normal at this age.

181
Q

Differentials of Anxiety Sx

A

Endocrine - Thyroid dysfunction, Phaeochromocytoma

Cardiac/Hypoxia - Arrythmias, CCF/angina, COPD

Metabolic - Acidosis, Hyper/hypothermia

Drug Withdrawal/Intoxication - Alcohol, Opiates, Amphetamine/cocaine

Psychiatric - Depression, Personality disorders

182
Q

Steps of management of anxiety disorders

A 
Step 1:
Psychoeducation
Active monitoring
¯
Step 2:
Guided self-help
Low-intensity psychological interventions 
¯
Step 3:
High intensity psychological interventions (e.g. CBT, psychodynamic psychotherapy)
OR drug treatment
¯
Step 4:
Refer to 2o care (MDT)
Complex therapies
Complex drug regimens
183
Q

Psychological Interventions in anxiety disorders

A

For mild-moderate anxiety.

  1. Psychoeducation – improve patient and carer understanding of illness.
    => E.g. process, causes, treatment, prognosis.
  2. Guided self-help/ low-intensity psychotherapy
  3. CBT:
    - Phobias – systematic desensitisation/graded exposure
    - OCD – exposure and response prevention
    - PTSD – eye-movement desensitisation reprocessing
  4. Others:
    => Counselling, relaxation techniques, social skills training (for social phobia)
184
Q

Pharmacological Interventions in anxiety disorders

A

For severe anxiety/psychological treatment failed.

  1. Antidepressants (SSRI) – proven efficacy long-term (especially combined with psychological treatments)
    => Do cause a short-term increase in anxiety.
  2. Beta-blockers – symptom control (reduce HR and autonomic arousal).
  3. BZDs – acute management only (max 4 weeks)
    => Dependence
    => SEs – drowsiness, ataxia, reduced concentration
    => Lorazepam = short half-life, Diazepam = long half-life
185
Q

What is health anxiety?

A

= an umbrella term encompassing:

  • Excessive/unrealistic health-related concerns
  • Somatic perceptions – preoccupied with bodily sensations
  • Behaviours – reassurance-seeking, repeated symptom checking, avoid medications/doctors
186
Q

Possible pre-disposing factors to health anxiety?

A
  • Personal experience of previous illness
  • Significant illness of a loved one
  • Early life trauma
  • Family members with health anxiety
187
Q

What disorders come under health anxiety?

A

Hypochondrial Disorder
Factitious Disorder/Munchausen’s
Malingering
Dissociative (conversion) Disorder

188
Q

Hypochondrial Disorder - definition

A

At least 6 months of:

Belief of 1 or 2 serious physical diseases (specifically named by patient)
OR
Preoccupation with presumed deformity/disfigurement

189
Q

Factitious Disorder

A

The patient feigns/exaggerates symptoms for no obvious reason (internal motivation to adopt the sick role).

May inflict self-harm to produce signs/symptoms.

190
Q

Malingering

A

the patient feigns/exaggerates symptoms for secondary gain (e.g. benefits).

191
Q

Dissociative (conversion) Disorder

A

A traumatic event disrupts consciousness, memory, identity or perception.
=> Patient converts anxiety into more tolerable symptoms to attract benefits of the sick role.

Variable presentation – amnesia, stupor, trance, motor disorders, anaesthesia, convulsions.

192
Q

Differentials of Health Anxiety/Somatisation

A
  • Depression/anxiety
  • Personality disorder
  • Schizophrenia/psychosis (hypochondrial delusions)
  • Organic causes with vague symptoms (MS, lupus, porphyrias).
193
Q

Somatisation Disorder

A

At least 2 years of complaints of multiple and variable physical symptoms from at least 2 body systems.

Complaint may change frequently

Symptoms are real but cannot be explained by a detectable physical disorder.

Causes persistent distress, significant functional impairment (especially relationships) and refusal to accept medical reassurance.

194
Q

Somatisation Disorder - management

A

General – build rapport (acknowledge suffering, regular appointments), minimise investigations (although ensure suitable investigations are done).

Psychological therapy – CBT, psychoeducation, self-help

Social – encourage normal functioning, normal ADLs/hobbies, involve social network/support.

Biological – anti-depressants (evidence of long-term efficacy is weak)

195
Q

What HCPs are required for a MHA section 2/3?

A
  1. At least 1 “section 12” approved doctor.
  2. Another doctor (ideally one who knows the patient (e.g. GP))
  3. Approved mental health practitioner (AMHP)
196
Q

MHA section 2

A
  • Type – assessment
  • Length – up to 28 days
  • Staff – 2 doctors and AMHP

Used when diagnosis is unclear.

Allows detention for a period of assessment (and Tx if needed).

After 28 days, must decide on section 3 or informal Tx (cannot implement back-to-back sections).

197
Q

MHA section 3

A
  • Type – treatment
  • Length – up to 6 months
  • Staff – 2 doctors and an AMHP

Used when diagnosis is certain.

Allows detention and Tx against the patient’s will.

Can be renewed after 6 months.

198
Q

MHA section 4

A
  • Type – emergency
  • Length – up to 72 hours
  • Staff – 1 doctor and AMHP

Allows emergency detention if only 1 qualified mental health doctor present. Can convert to section 2/3 after 2nd doctor assessment.

199
Q

MHA Section 5(2)

A
  • Type – emergency (“doctor’s holding power”)
  • Length – up to 72 hours
  • Staff – 1 doctor (NOT F1, ideally most senior doctor available)

Allows detention by any ward doctor until a formal assessment can be done. This only applies to inpatients (excludes A&E).

AHMP or psychiatrist needs to be informed that this in place ASAP.

Cannot treat under this section and cannot implement back-to-back sections.

200
Q

MHA Section 5(4)

A
  • Type – emergency (“nurse’s holding power”)
  • Length – up to 6 hours
  • Staff – 1 registered mental health nurse

Allows detention until an appropriate doctor can assess.

201
Q

MHA Section 135

A
  • Type – power of entry
  • Length – up to 72 hours
  • Staff – magistrate

Allows police to enter a home and remove a person believed to be suffering from a mental health disorder to a place of safety for assessment

202
Q

MHA Section 136

A
  • Type – place of safety
  • Length – up to 72 hours
  • Staff – Police Officer

Allows police to remove a person to a place of safety where they can be formally assessed (e.g. police station, A&E, 136 suite).

203
Q

MHA Section 17A

A
  • Type – community treatment order
  • Length – as needed/indefinitely
  • Staff – AMHP

Allows Tx under MHA while living in community or on leave from hospital.

This only relates to psychiatric care (not physical health).

Non-compliance can result in recall to hospital/detainment.

204
Q

What components do you need to cover in a full psychiatric assessment

A 
PC + HPC
PMHx
DHx
FHx
SHx
Past Psych Hx
Forensic Hx
Pre-morbid personality
MSE
Risk Assessment
205
Q

How should you undertake a past psych history?

A

What age did they first present to the mental health services?

Give a chronological account of events and list the known diagnoses:

  • When diagnosis made
  • Treatment and progress in the community
  • Psychiatric admissions
206
Q

Important aspects of a social Hx in psychiatry

A

• Birth complications, developmental milestones

• Childhood
=> Parents, siblings, attachment/separation problems; growing up in care

• School:
=> Friends, bullying, academics; further education; qualifications

  • Occupation history
  • Relationships, marital history and children
  • Any traumatic experiences, including abuse

• Social history (current)
=> Living circumstances (type of accommodation; household members; additional care they receive)
=> Income and any financial difficulties
=> Activities of daily living; level of functioning
=> Social activities, hobbies

• Substance use/misuse

207
Q

Forensic History

A

Ask the patient about any “trouble” with the police

Specifically looking for offences, charges, convictions, community orders, prison sentences (dates)

208
Q

How do you identify a person’s pre-morbid personality?

A

Ask:

  • How they would describe their personality;
  • How others close to them would describe them;
  • Temperament and interpersonal relationships.

Identify their reaction to stressful times in their life and coping mechanisms.

Try to screen for personality disorders.

209
Q

Components of a mental state examination

A

A – Appearance and Behaviour

S – Speech

E – Emotion (mood and affect)

P – Perception

T – Thought

I – Insight

C – Cognition

210
Q

MSE - Appearance/behaviour

A
  • Gender, race, age, build, clothing, cleanliness/kempt

- General disposition, rapport, eye contact, mannerisms

211
Q

MSE - speech

A
  • Rate, Tone, Volume
212
Q

MSE - emotion

A

Identify patient’s mood and affect:

  • Subjectively – according to the patient;
  • Objectively – as per your observation

Dysphoric (depression, anxiety, guilt),
Euthymic (normal),
Euphoric (implying a pathologically elevated sense of well-being)

213
Q

Mood vs Affect

A

Affect = the patient’s immediate expression of emotion
=> affect is inappropriate when there is no congruence between what the patient is experiencing/describing and the emotion he is showing at the same time

Mood = more sustained emotional makeup of the patient’s personality

214
Q

MSE - perception

A
  • Visual/auditory/tactile hallucinations – Ask if they are experiencing these, further details if present
  • If not reported, do they seem to be responding to unseen stimuli?
215
Q

MSE - thought

A
  1. FORM
    - Any evidence of formal thought disorder?
  2. CONTENT
    - Delusional content?
    - Thoughts of self-harm, suicide, homicide?
216
Q

MSE - Insight

A

1) recognition of the disease itself (awareness)
2) the ability to recognise symptoms (attribution)
3) compliance with treatment (acceptance)

217
Q

MSE - Cognition

A

Mention scores of tests or summarise findings of cognitive assessments

If formal cognitive assessment was not done, can comment on:
• Attention and Orientation to time, place and person
• General impression short and long term memory as observed during the consultation

218
Q

Presenting a full psychiatric assessment

A

State your impression of the patient’s problem(s) or diagnosis

Mention the relevant factors contributing to this:
=> 3 P’s – predisposing, precipitating and perpetuating factors

219
Q

What is personality?

A

= combination of consistent thoughts, feelings and behaviours shown over time and in a variety of settings.

Thought to develop during childhood and adolescence.

220
Q

What is a personality disorder?

A

= when unhelpful personality traits cause functional difficulties/distress.

  1. Pervasive – occur in most/all areas of life.
  2. Persistent – evident from adolescence and into adulthood, enduring rather than discrete episodes
  3. Pathological – cause distress to self/others and impair function (occupation, relationships, etc.)
221
Q

Causes of personality disorder

A

= multifactorial

  • Genetics/neurochemical imbalance
  • Childhood temperament – innate/biological disposition to an emotional response
  • Childhood experience – neglect, trauma, abuse
  • Attachment problems with primary caregiver
222
Q

What conditions are commonly co-morbid to personality disorder?

A
  • Anxiety disorder
  • PTSD, OCD
  • Depression
  • Adjustment disorder/stress reaction
  • Substance misuse/alcoholism (can often cause delayed diagnosis of PD)
223
Q

DSM-5 Clusters of Personality Disorders

A

Cluster A = “mad”

  • Paranoid
  • Schizoid
  • Schizotypal

Cluster B = “bad”

  • Antisocial
  • Histrionic
  • Borderline
  • Narcissistic

Cluster C = “sad”

  • Obsessive compulsive (not OCD)
  • Anxious/avoidant
  • Dependent
224
Q

Which cluster of personality disorders is most linked with higher rate of suicide?

A

cluster B

but all PDs are associated with increased risk of suicide

225
Q

ICD-10 classification of personality disorders

A 
Paranoid
Schizoid
Dissocial
Emotionally Unstable
Histrionic
Anankastic
Anxious/Avoidant
Dependent
226
Q

Paranoid personality disorder

A

Suspicious, Unforgiving, Sensitive, Possessive/jealous, Excessive self-importance, Conspiracy theories, Tenacious sense of self-rights

227
Q

Schizoid personality disorder

A

Anhedonic, lack relationships, only small emotional range, Normal conventions ignored, Excess fantasy world

228
Q

Dissocial personality disorder

A

Guiltless/heartless, no concerns for others, irresponsible, easily loses temper, Blames others

229
Q

Emotionally Unstable personality disorder

A
  1. Borderline – Self-image unclear, Chronic emptiness, abandonment fear, Relationships unstable/intense, Self-harm/suicide, Labile emotions, Impulsive, Emotions very intense
  2. Impulsive – lacks impulse control, aggressive outbursts, inability to plan, thoughtless of consequences
230
Q

Histrionic personality disorder

A

Attention-seeking, Concerned about self, Theatrical, Open to suggestion, Racy/seductive, shallow

231
Q

Anankastic personality disorder

A

Perfectionist, excessive detail, doubtful, inflexible, intrusive thoughts, excludes pleasure/others

232
Q

Anxious/avoidant personality disorder

A

Avoids social contact, fears rejection/criticism, restricts lifestyle, apprehensive, desires acceptance

233
Q

Dependent personality disorder

A

Subordinate, relies on others to make decisions, seeks reassurance, abandonment fears

234
Q

Personality Disorder - management

A

LONG-TERM MANAGEMENT:

  • Psychoeducation
  • Self-help – mood diary, coping behaviours, maintain physical health, sleep hygiene
  • !!!Talking therapies !!! – CBT, DBT, MBT, CAT
  • Social support

MEDICATION ( little evidence in treating PDs - all meds are currently “off licence” for PD Tx and only indicated for comorbidities)

  • Antipsychotics – for transient psychosis, reducing impulsivity/agitation
  • Antidepressants – for comorbid anxiety/depression
  • Mood stabilisers
  • Short-term sedative/minor tranquilisers – in crisis situations, max 1 week.
235
Q

Splitting

A

The individual tends to think in extremes (i.e., an individual’s actions and motivations are all good or all bad with no middle ground).

236
Q

Transference

A

the feelings a person has are unconsciously redirected or transferred to the present situation

(e.g. people transferring feelings about their parents to their partners or children)

237
Q

Why is there commonly treatment failure in personality disorders?

A

Usually due to poor engagement/insight

238
Q

Dysthymia vs depression

A

Dysthymia = chronically low mood but no episode justifying a diagnosis of depression

239
Q

What is acute mania?

A

= 1 episode of mania

240
Q

What is mania?

A

Mania is a syndrome characterised by abnormally elevated arousal, affect and energy level.

241
Q

what is Cyclothymia?

A

= persistent mood instability with numerous subthreshold manic and depressive periods.

242
Q

Symptoms of hypomania

A

= symptoms for 4 days

Mildly elevated or unstable mood
Increased energy
Mild over-spending and risk-taking
Increased sociability and overfamiliarity 
Distractibility
Increased sexual energy
Decreased need for sleep
243
Q

Symptoms of mania

A

= symptoms for 1 week

Elevated, expansive or irritable mood
Increased activity (often goal-directed)
Reckless behaviour (overspending, sexual)
Disinhibition
Marked distractibility
Marked increased sexual activity
Flight of ideas and pressured speech
Grandiose/persecutory delusions
Auditory hallucinations
244
Q

What is bipolar disorder?

What are the types?

A

= periods of profound depression alternating with periods of mania.

Type 1 = at least one episode of major depression and one episode of mania.

Type 2 = at least one episode of major depression and at least one episode of hypomania

245
Q

when is the peak age of onset of bipolar disorder?

A

early 20s

246
Q

Risk factors for bipolar disorder?

A

Genetics – FHx of bipolar

Life events – prolonged stress, childbirth

Substance misuse – amphetamines, cocaine, steroids

247
Q

Bipolar disorder - prognosis

A

Average episode = 6 months
Recurrence = 90%

10% commit suicide

248
Q

Reasons for relapse in bipolar disorder

A 
Non-compliance with medication 
Life events/stress
Substance misuse
Childbirth
Disrupted circadian rhythm
249
Q

Bipolar disorder - differentials

A 
Substance misuse
Hyperthyroidism, Cushing’s
Metabolic disturbance
Space-occupying lesion
Epilepsy
250
Q

Pharmacological management of acute mania

A
  1. Antipsychotic (haloperidol, risperidone, quetiapine, olanzapine)
    • 2nd antipsychotic
    • lithium or valproate
  4. May consider BZDs

STOP routine anti-depressants

251
Q

Pharmacological management of bipolar disorder

A
  1. Antipsychotic (2nd gen)
    • routine antidepressant
    • Lamotrigine/other mood stabiliser

Only prescribe routine antidepressants alongside anti-manic agents.

LONG-TERM: Lithium OR Valproate/Olanzapine (if lithium not tolerated)

252
Q

Psychosocial management of bipolar disorder

A

Psychological:

  • Psychoeducation – recognising relapses
  • CBT
  • CPN visits – monitor mood, mental state, symptoms

Social:

  • Support for education, training, employment
  • Support for carers/family
253
Q

Which drugs are mood stabilisers?

A

Lithium, valproate, lamotrigine, carbamazepine

254
Q

Indications for use of lithium

A

acute hypomania/mania,
bipolar disorder,
Tx-resistant depression.

255
Q

Cautions/CIs of lithium

A

Cautions = cardiac disease, epilepsy, elderly

Contraindications = pregnancy (teratogen => cardiac defects), arrythmias, long QT

256
Q

Monitoring of lithium

A

Narrow Therapeutic Window – measure lithium levels at day 5 and then 3-monthly.

Monitor U&Es and TFTs 6 monthly

Monitor Calcium

257
Q

Lithium toxicity - Sx and Mx

A

Diarrhoea, dehydration, coarse tremor, ataxia, muscle weakness, fasciculations, nystagmus, decreased consciousness, confusion, seizures, coma, renal failure, death.

Mx – Stop lithium immediately, rehydration, diuresis/haemodialysis if severe

258
Q

Indications for valproate (in psychiatry)

A

acute hypomania/mania,

bipolar disorder

259
Q

Indications for Lamotrigine (in psychiatry)

A

bipolar depression,
treatment resistant depression,
bipolar affective disorder.

260
Q

Which is the least teratogenic mood stabiliser?

A

Lamotrigine

261
Q

Indications for Carbamazepine

A

acute hypomania/mania,
bipolar disorder,
bipolar depression

262
Q

Screening for risk of postnatal mental disorder

A
  1. All women should be screened at antenatal clinic for previous/current/FHx of psychiatric disorder
  2. Refer necessary cases for psychiatric assessment and referral
    => Pregnant/postpartum women should have priority in psychiatric service pathways.
  3. Regularly monitor mental state of all peri/postnatal women, regardless of whether they’ve been referred.
263
Q

Which pregnant women should be referred to psychiatric services for assessment?

A
  1. PHx +/- FHx of:
    • Schizophrenia/psychosis
    • Bipolar disorder
    • Puerperal psychosis
    • Severe depression – i.e. required secondary care input (depression treated by GP doesn’t need referral)
  2. On mood stabilisers
264
Q

Normal Post-partum Psychiatric Symptoms

A

‘The Pinks’ - within 48 hours postpartum
Excitement, euphoria, overtalkative, overactive, insomnia.

‘The Blues’ - Day 3-10 postpartum
Emotional lability, tearful, anxious, irritable.

Both should have spontaneous Resolution

265
Q

Onset of post-partum depressive illness

A

Bi-peak onset = 2-4 weeks and 3 months postpartum.

Prevalence = 10%

Risk Factors:

  • Previous postpartum depression
  • Serious depressive illness
266
Q

Symptoms of post-partum depressive illness

A

Symptoms = similar to normal depressive illness:

  • Guilt and concerns over parental ability = common
  • Anxious preoccupation with baby’s health
  • Reduced affection for baby/impaired bonding
  • Obsessional phenomena (may involve harming baby)
267
Q

Prognosis of post-partum depressive illness

A

With treatment – 2/3 resolve within 2-3 months

Without treatment – can take >6 months to recover

268
Q

Management of post-partum depressive illness

A

RISK ASSESS

CBT

Sertraline/Paroxetine – if severe
=> Small amounts are transferred in breast milk but can still breast feed.

Admission to mother-baby unit/ECT – if very severe/high risk to self or baby

269
Q

Onset of Puerperal/Postpartum Psychosis

A

Onset normally within 2-3 weeks postpartum.

Prevalence = 0.2%

Risk Factors:

  • Previous postpartum psychosis
  • Bipolar disorder
  • Primiparity, obstetric complications, unmarried.
270
Q

Prognosis of Puerperal/Postpartum Psychosis

A

Good short-term progress if treated early

  • Most severe symptoms last 2-12 weeks
  • Most make a full recovery within 12 months

BUT associated with significant morbidity and mortality

271
Q

Management of Puerperal/Postpartum Psychosis

A

Treat has high risk

Admission to mother and baby unit – may need MHA

High intensity physical and psychological care

Support services – support groups, help with childcare/housework, etc.

272
Q

What are considered psychiatric emergencies?

A 
Suicidal Patients
Agitated/Violent patients
Grief reaction
Rape
Panic attacks
Neuroleptic Malignant Syndrome & Serotonin Syndrome
Delirium
Overdose/withdrawal
273
Q

Causes of acute behavioural disturbance

A

Psychiatric symptoms,
Non-psychiatric symptoms,
Substance misuse.

274
Q

Assessment of acute behavioural disturbance

A

HISTORY:
• Establish any diagnoses and medication
• Any previous similar episodes and cause/Tx
• Consider medication compliance or SEs
• Use of alcohol/illicit drugs
• Recent changes in social life (e.g. employment, relationships)
• History of self-harm/suicide/violence – risk assessment

Factors to Consider – deciding the need for urgent Tx/admission:
•	Severity of illness
•	Level of insight
•	Risk of harm to self/others
•	Other support available
275
Q

Acute behavioural disturbance - de-escalation

A
  • Encourage patient to move area away from others
  • Speak confidently, slowly, clearly
  • Non-threatening body language
  • Explore concerns with patient – try to build rapport

Pharmacological Management/Physical Restraint
= LAST RESORT
=> Rapid Tranquillisation – calm patient without full sedation
=> BZDs, antipsychotics, promethazine – minimum dose, PO if possible.

276
Q

what is Neuroleptic Malignancy Syndrome ?

A

A rare (<1%) adverse reaction to antipsychotics (dopamine blockade causes hyperactivity of SNS).

277
Q

Symptoms of neuroleptic malignancy syndrome?

A
  • Fever, sweating
  • Rigidity
  • Confusion, fluctuating consciousness
  • Autonomic instability (fluctuating BP, HR, salivation, incontinence).
278
Q

Neuroleptic malignancy syndrome - risk factors

A
  • Hx – previous NMS, brain damage, alcoholism
  • Mental state – agitation, hyperactivity, catatonia
  • Physical – dehydration
  • Treatment – recent increase/decrease in dose, high dose, IM injections.
279
Q

Neuroleptic malignancy syndrome - investigations

A
  • Raised CK (may be >1000 units/L)
  • Raised leucocytes
  • Deranged LFTs
280
Q

Neuroleptic malignancy syndrome - Treatment

A

WITHDRAW ANTIPSYCHOTIC MEDICATION

  • Rehydration
  • Monitor temperature, BP, pulse
  • Consider BZDs for sedation
281
Q

What is serotonin syndrome?

A

= increased serotonin due to increased synthesis, decreased uptake/metabolism, or direct receptor activation.

282
Q

Common causes of serotonin syndrome?

A
  • Switching antidepressant

- Combining antidepressants (with other ADs or supplements)

283
Q

Symptoms of serotonin syndrome

A
  • Psychiatric – restlessness, confusion, agitation
  • Autonomic – hyperthermia, diarrhoea, tachycardia, hypo/hypertension, mydriasis
  • Neuromuscular – myoclonus, rigidity, tremors, hyperreflexia, ataxia, convulsions.
284
Q

Serotonin syndrome - treatment

A

STOP precipitating medication

  • Rehydration
  • BZDs if agitated
  • If severe, transfer to ED.
285
Q

How do NMS and serotonin syndrome differ in onset?

A 
NMS = Slow (days-weeks)
SS = Rapid
286
Q

How do NMS and serotonin syndrome differ in progression?

A 
NMS = Slow (24-72 hours)
SS = Rapid
287
Q

How does muscle rigidity differ in NMS and serotonin syndrome ?

A 
NMS = Severe
SS = Less severe
288
Q

How do blood results differ in NMS and serotonin syndrome ?

A 
NMS = Raised CK, raised WCC	
SS = Normal
289
Q

Who is most at risk of self-harm?

A
  • F>M
  • 2/3rd are <35 years old
  • Divorced > Single > Widowed > Married
290
Q

Risk factors for self-harm

A

BIOLOGICAL – genetics, age (teens/young adults), personality disorder

PSYCHOLOGICAL – Abuse (sexual, physical, emotional), bullying, bereavement, relationship breakdown, endings/changes

SOCIAL – substance misuse, friends who self-harm, financial/living conditions, work/school pressures, isolation/loneliness.

291
Q

Self-harm - Management

A
  1. Assessment:
    • Physical and mental health
    • Safeguarding concerns
    • Further self-harm and suicide risk
  2. Treatment:
    • Of physical injuries
    • Specialist psychosocial assessment
    • Monitor in a healthcare setting to reduce risk of recurrence.
292
Q

Factors predicting repetition of self-harm

A 
Number of previous episodes
Personality disorder
History of violence
Alcohol misuse
Unmarried
293
Q

Factors indicating suicidal intent

A

Risk of suicide is 66x greater if self-harmed

Trying to avoid intervention
Planning suicide
Leaving a note
Anticipatory acts (e.g. leaving a will, settling debts)
Use of violent methods
294
Q

Who is most at risk of suicide?

A

M>F

Second leading cause of death in 15-29 year olds.

Hanging/strangulation is most common method

Vulnerable groups – prisoners, asylum seekers, LGBTQ backgrounds, veterans.

295
Q

Screening questions for depression

A

During the past month, have you often been bothered by feeling down, depressed or hopeless?

During the past month, have you often been bothered by having little interest or pleasure in doing things?

296
Q

Assessment of post-natal depression

A
  1. Edinburgh Postnatal Depression Scale (EPDS) or the Patient Health Questionnaire (PHQ-9)for screening
  2. Assess severity of depression
  3. RISK ASSESSMENT – risk of self-neglect/self-harm/suicide, and any risk to the infant.
297
Q

What is a formal thought disorder?

A

= a disruption of the form/structure of thought presenting as disorganised speech.

298
Q

Poverty of speech

A

= loss of speech production, either in amount or content.

299
Q

Thought blocking

A

= an abrupt stop in the middle of a train of thought which may or not be able to be continued

300
Q

Circumstantial thinking

A

= an inability to answer a question without giving excessive, unnecessary detail
(but the person DOES eventually return to the initial point)

301
Q

Clanging

A

a severe form of flight of ideas whereby ideas are related only by similar or rhyming sounds rather than actual meaning

302
Q

In which disorders is clanging most often seen?

A

Most commonly seen in bipolar disorder (manic phase),

Often also observed in patients with primary psychoses.

303
Q

Derailment/Loose Association/Knight’s Thinking

A

= thought frequently moves from one idea to another which is obliquely related or unrelated.

304
Q

Distractible Speech

A

= during mid-speech, the subject is changed in response to a nearby stimulus

305
Q

Echolalia

A

= echoing of another’s speech

306
Q

Flight of Ideas

A

= abrupt leaps from one topic to another, possibly with discernible links between successive ideas.

307
Q

In which disorders is flight of ideas most often seen?

A

Most characteristic of the manic phase of bipolar illness.

308
Q

Incoherence/Word Salad

A

= speech that is unintelligible because, though the individual words are real words, the manner in which they are strung together results in incoherent gibberish.

309
Q

Neologisms

A

= the person forms completely new words or phrases whose origins and meanings are usually unrecognizable.

310
Q

Perseveration

A

= persistent repetition of words or ideas even when another person attempts to change the topic.

This may also involve repeatedly giving the same answer to different questions.

311
Q

Pressured speech

A

= rapid speech without pauses, difficult to interrupt.

312
Q

Referential Thinking

A

= patients’ tendency to view innocuous stimuli as having a specific meaning for the self.

313
Q

Semantic Paraphasia

A

= substitution of inappropriate word

314
Q

Stilted Speech

A

= sentences may be stilted or vague; speech characterized by the use of words or phrases that are flowery, excessive, and pompous.

315
Q

Tangential Speech

A

= wandering from the topic and never returning to it or providing the information requested.

316
Q

Child/adolescent psychiatry - when is pharmacological management considered?

A

Usually less common/little evidence as first-line treatment

Consider in ADHD/depression.

317
Q

Child/adolescent psychiatry - pharmacological management options

A

Antidepressants are only prescribed by specialist (child psychiatrist), due to – concerns of suicidal behaviour in teens taking SSRI

Use FLUOXETINE ONLY.

318
Q

Child/adolescent psychiatry - psychosocial management

A
  • Psychological – most commonly used are CBT and family therapy.
  • Social – very important, especially regarding education and social services
319
Q

Definition of Intellectual Disability

A

= significantly sub-average intellectual functioning (IQ <70)

Onset before 18 years

320
Q

Mild intellectual Disability

A

IQ - 50-69

Prevalence - 1.5-3%

Functioning - Only need help if problems arise (often not recognised as ID)

321
Q

Moderate intellectual Disability

A

IQ - 35-49

Prevalence -0.5%

Functioning - May need supervision in some elements of daily living/work

322
Q

Severe intellectual Disability

A

IQ - 20-34

Prevalence - 0.5%

Functioning - Need help with many ADLs (often physical disability, limited communication)

323
Q

Profound intellectual Disability

A

IQ - <20

Prevalence - 0.05%

Functioning - Extensive/total help with ADLs, minimal communication.

324
Q

Cause of intellectual Disability

A

30% have no identifiable cause

  1. Genetic/Chromosomal (most common = Down’s Syndrome)
  2. Pre-natal, peri-natal, post-natal Factors
325
Q

Prenatal factors causing intellectual disability

A
  • Congenital hypothyroidism
  • Foetal alcohol syndrome
  • Pre-eclampsia
  • Placental insufficiency
  • TORCH infections
326
Q

Peri-natal factors causing intellectual disability

A
  • Birth trauma/hypoxia
  • Intraventricular haemorrhage
  • Hyperbilirubinaemia
327
Q

Post-natal factors causing intellectual disability

A
  • Brain infection / tumour
  • Head injury
  • Chronic lead poisoning
  • Neglect/ abuse / malnutrition
328
Q

Mental illness and intellectual disability

A

The risk of mental illness is 3 times higher in those with ID.

Mental illness may present differently, or the patient may have difficulty describing symptoms.

329
Q

What is the basic premise of CBT?

A

= that you feel the way you think and changing negative cognitions can change behaviours and feelings

330
Q

Indications for CBT?

A

Stand-alone Treatment:

  • Depression
  • Anxiety disorders (e.g. generalised anxiety disorder, Obsessive Compulsive Disorder, Post-traumatic Stress Disorder and Phobias)

Adjunct to Treatment:

  • Schizophrenia
  • Bipolar Disorder
331
Q

CBT - initial sessions

A
  • Spent building a therapeutic relationship.
  • The therapist explains the model and its rationale to ensure that the patient has a good understanding of the way thoughts, behaviours and feelings are connected.
332
Q

CBT - ongoing sessions

A
  • Sessions tend to take place weekly or fortnightly.
  • Sessions tend to last 50-60 minutes
  • Patients are expected to complete homework between sessions
  • The focus is on challenging and correcting cognitive errors, and replacing maladaptive with more adaptive coping mechanisms.
333
Q

what is the basis of psychodynamic psychotherapy?

A

that our feelings and behaviours are influenced by unconscious motives that are the result of early childhood experiences

334
Q

Psychodynamic psychotherapy - how do you assess the unconscious?

A

Dream analysis

Free association
=> Speaking whatever comes to the mind

“Slips of the tongue”
=> Freud suggested that these are not “accidents” – but the unconscious mind trying to make itself heard.

Transference and counter-transference
=> i.e. being aware of the feelings generated in oneself during therapy (and in the patient) can be useful clinical information.

335
Q

Counter-transference

A

= the process of the therapist transposing his/her feelings that they may have held for significant others in their childhood to the patient

336
Q

The process of psychodynamic psychotherapy

A

establish a therapeutic relationship with the patient that helps draw links between a triad of the patient’s:

  1. Early childhood experiences (including early trauma),
  2. Defence mechanisms
  3. Current symptoms
337
Q

Psychoanalysis vs. Psychodynamic Therapy

A

PSYCHOANALYSIS
Quite rigorous
3-5 times/week
50-60 mins/session

Patients need to be able to tolerate intensive self-reflection and not become dependent or impulsive

PSYCHODYNAMIC THERAPY
Also called insight-oriented psychotherapy
1-2 sessions/week
50-60 mins/session
Can last 1-2 years but brief psychodynamic therapy only 14-20 sessions

338
Q

When is psychoanalysis indicated?

A

Indicated for long-term personality difficulties

339
Q

when is psychodynamic psychotherapy indicated?

A

Indicated in the treatment of personality disorders, certain cases of mood and anxiety disorders especially when co-morbid personality difficulties present

340
Q

When is dialectical behavioural therapy indicated?

A

for the treatment of emotionally unstable personality disorder

341
Q

What is the aim of DBT?

A

to help people manage difficult emotions by letting them experience, recognise and accept them.

This model says that, with acceptance, people become more able to change damaging behaviours

342
Q

What are the 4 typical elements of DBT?

A
  1. Individual therapy – weekly 1-1 therapy with a DBT therapist lasting about an hour
  2. Skills training in groups – focussing on developing practical skills (tolerating distress, managing personal relationship issues, mindfulness)
  3. Telephone crisis coaching – gives service receivers telephone contact with their therapist outside of therapy sessions
  4. Therapists’ consultation groups – members of the team of people providing DBT may meet together weekly to discuss issues that have come up in treatment sessions
343
Q

How long does a course of DBT usually last?

A

about a year

344
Q

DBT vs. CBT

A
  • DBT better meets the needs of people who experience particularly intense emotional responses.
  • DBT focuses on changing unhelpful behaviours, while allowing acceptance of the whole person – including unhelpful thoughts (rather than challenging thoughts like in CBT)
  • In DBT, the relationship between the service user and the DBT therapist is key. This relationship is used to actively motivate change.
345
Q

Forms of psychotherapy

A 
CBT
DBT
Family therapy
Inter-personal therapy
Problem-solving therapy
346
Q

Why does risk need to be reviewed regularly?

A

Risk is MULTIFACTORIAL and DYNAMIC

=> changes with time, people, place, mental state, etc.

Therefore, needs to be considered in the short-term and long-term, and reviewed regularly

347
Q

Types of risk to assess

A 
1.	Self:
•	Self-harm
•	Accidental harm
•	Suicide
•	Self-neglect
•	Deterioration of mental health
•	Deterioration of physical health
•	Risk of vulnerability/exploitation
  1. To Others
    • Risk of physical aggression/violence
    • Risk to vulnerable others (including children)
    • Gun licence
  2. Property
    • Risk to their/others property
    • Do they drive?
348
Q

Suicide Hx - before the incident

A
  • Any trigger/precipitant?
  • Planned/impulsive?
  • Final acts? (leaving notes, settling debts, leaving a will)
  • Precautions against discovery? (closing curtains, locking doors, going somewhere remote, etc.)
  • Was alcohol used?
349
Q

Suicide Hx - during the incident

A
  • What method? (e.g. overdose, cutting, hanging, etc.)
  • Specific details of the method – e.g. what medication/how much, etc.
  • Were you alone?
  • Where?
  • What was going through your mind at the time?
350
Q

Suicide Hx - after the incident

A
  • Who found them/did they present themselves?
  • How did they feel when help arrived?
  • How do you feel about the attempt now? Regret?
  • Current mood? Still feel suicidal?
  • If you were to go home today, what would you do?
  • Do you feel you have anything to live for?
351
Q

Risk assessment - identifying risk to others

A

Historical – previous violence, past mental illness, stability of relationships

Current – ongoing symptoms, response to treatment, insight, hallucinations.

Compliance to medication

Plans

Access to Weapons

Any Children/dependants?

352
Q

What is considered prolonged QTc?

A

> 440ms in men

> 460ms in women

353
Q

Which psychiatric drugs can cause prolonged QTc?

A

Antipsychotics - e.g. Chlorpromazine, Haloperidol, Quetiapine, Olanzapine

TCAs - e.g. Amitriptyline, Nortriptyline, Imipramine

Other antidepressants - e.g. citalopram, Escitalopram, Venlafaxine, Bupropion

354
Q

How is acute dystonia secondary to antipsychotics/metoclopramide usually managed?

A

Procyclidine

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