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Psych Flashcards

1
Q

What is the most common cause of psychosis?

A

Schizophrenia

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2
Q

What is psychosis?

A

Delusions, hallucinations and/or a thought disorder without insight

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3
Q

What is schizophrenia?

A

Common chronic relapsing condition often presenting in early adulthood with psychotic symptoms, disorganisation symptoms, negative symptoms and sometimes cognitive impairment.

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4
Q

Risk factors for schizophrenia?

A
  • FH (if both parents have it, child has 50% chance)
  • Premature birth
  • Abnormal development
  • Social isolation/migrant
  • Illicit drugs (cannabis, cocaine, amphetamines)
  • More common in temporal lobe epilepsy and huntingtons
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5
Q

3 phases of schizophrenia?

A

1) Prodrome: Withdrawn, anxious, suspicious, irritable
2) Active: sx like delusions and hallucinations
3) Residual: Cognitive symptoms

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6
Q

Criteria for diagnosis of schizophrenia?

A

1 first rank sx or 2 or more secondary symptoms.

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7
Q

What are schneiders first rank symptoms?

A

1) Auditory hallucinations
- 3rd person
- Running commentary
- Thought echo
2) Passivity phenomena
- Somatic passivity
- Thought withdrawal, insertion and broadcast
- Passivity of affect
3) Delusional perception

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8
Q

What are the secondary symptoms?

A
  • 2nd person auditory hallucinations
  • Other sensory hallucinations
  • Thought disorder
  • Catatonic behaviour
  • Negative symptoms
  • Delusions
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9
Q

What are positive symptoms?

A

Add to normal experience. eg. hallucinations, delusions, passivity phenomena, thought alienation, change in mood (lack of insight)

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10
Q

What are negative symptoms?

A

Take away from normal experience eg blunting of affect, amotivation, poverty of speech/thought, reduced verbal/non-verbal communications.

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11
Q

Classic MSE in schizophrenia?

A 
A: Withdrawn, suspicious
S: Thought blocking, loosening of association
E: Flattened/incongrous/odd mood
P: Delusions
T: Thought control and passivity
I: No insight 
C: Cognition subtly different
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12
Q

Investigations in schizophrenia?

A
  • Bloods: LFTs, FBC,
  • Serology for syphilis
  • Urine toxicology
  • Brain imaging and EEG
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13
Q

Types of schizophrenia?

A
  • Paranoid schizophrenia: Paronoid delusions, auditory hallucinations, perceptual disturbances
  • Catatonic schizophrenia: Hyperkinesis or negativism
  • Hebephrenic schizophrenia: Fluctuating affect
  • Residual schizophrenia: Long term negative symptoms
  • Simple schizophrenia: Negative sx without psychotic symptoms
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14
Q

Management of schizophrenia?

A

First line: Risperidone or olanzapine

Second line: Clozapine

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15
Q

Common s/e of antipsychotics?

A
  • Hyperprolactinaemia
  • Sexual dysfunction
  • Weight gain
  • DM
  • CV effects
  • Drowsiness
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16
Q

What is Schizoaffective disorder?

A

When a patient experiences both symptoms of a mood disorder (mania or depression) and schizophrenia at the same time (within days) and of the same intensity without another medical disorder or substance misuse cause.
Treatment is with antipsychotic and mood stabiliser to manage both condition.

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17
Q

What are the affective mood disorders?

A
  • Depression
  • Bipolar
  • Cyclothymia
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18
Q

What is depression?

A

Pervasive lowering of mood associated with biological and psychosocial symptoms

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19
Q

Risk factors for depression?

A
  • Chronic illness (RA, IBD, cancer, parkinsons)
  • Divorce
  • Unemployed
  • Lack of confiding relationship
  • Low self esteem
  • Poor social support
  • Low social class
  • Comorbidity w/ other psych problems eg substance misuse, anxiety disorders
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20
Q

How is depression diagnosed?

A

At least 2 core symptoms AND 3/4 other symptoms.

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21
Q

The core symptoms of depression are?

A
  • Low mood
  • Loss of energy (inergia)
  • Loss of pleasure (anhedonia)
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22
Q

Other symptoms of depression?

A 
Biological:
- Change in sleep
- Change in appetite
- Change in libido
Psychological:
- Loss of confidence
- Loss of concentration
- Guilt and hopelessness
- Suicidal ideation
- Diurnal mood variation
- Agitation
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23
Q

What is the mneumonic to remember depression symptoms?

A 
D Depressed mood
E Energy levels reduced
A Anhedonia
D Disturbed sleep
S Suicidal ideation
W Worthlessness
A Appetite reduced
M Mentation decreased (concentration)
P Psychomotor retardation
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24
Q

How is depression classified?

A

Mild: 2 core sx + 2 other
Moderate: 2 core sx + 3 other
Severe: 3 core sx + 4 other
Severe w/ psychotic sx: Mood congruent, nihilistic, guilty, delusions, hallucinations and stupor.

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25
Q

Typical MSE of depressed patient?

A

Appearance: Signs of neglect eg. unkempt, w loss
Behaviour: Poor eye contact, down cast eyes, tearful
Speech: Slow, non-spontaneous, quiet
Mood: Low. suicidal ideation
Thought: Pessimistic, guilt, worthlessness, nihilistic delusions
Perception: 2nd person auditory hallucinations (often derogatory)
Cognition: Poor concentration
Insight: Usually good

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26
Q

Investiagations to rule out a medical cause of depression?

A

Bloods: TFT, LFT, FBC, U+E, calcium, glucose

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27
Q

Management of depression?

A

1) Low intensity psychosocial intervention eg CBT
2) Antidepressant:
a) SSRI: Sertraline, citalopram, fluoexetine
b) TCA: Lofepramine
3) High intensity psychsocial intervention

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28
Q

What is serotonin syndrome?

A

Serotonin toxicity from serotenergic agents. Consequence of excessive stimulation of the CNS and peripheral serotonin receptors.
Leads to rhabdomyolysis > coma > death.

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29
Q

Sx of Serotonin syndrome?

A

Fever (autonomic hyperactivity)
Agitation (altered mental state)
Tremor, Hyperreflexia, Clonus (neuromuscular excitation)

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30
Q

What is bipolar affective disorder?

A

Two or more episodes in which the patients mood and activity levels are significantly disturbed

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31
Q

What is bipolar 1?

A

One or more manic episodes with or without a history of depressive episodes (mania and depression)

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32
Q

What is bipolar 2?

A

One or more depressive episodes with at least one hypomanic episode. Often diagnosed as recurrent depression, creating tx issues.

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33
Q

What is hypomania?

A

Not full mania. Has no psychotic symptoms and less dysfunction.

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34
Q

What are the sx of hypomania?

A
  • 4+ days
  • Elevated mood
  • Increased energy
  • Increased talkativeness
  • Poor concentration
  • Mild reckless behaviour eg. overspeeding
  • Increased libido / sexual disinhibition
  • Decreased sleep
  • WITHOUT PSYCHOTIC SYMPTOMS
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35
Q

What are the sx of mania?

A
  • > 7 days
  • Extreme elation (uncontrollable)
  • Overactivity
  • Pressure of speech
  • Impaired judgement
  • Extreme risk behaviour
  • Inflated self esteem
  • Flight of ideas
  • With psychotic symptoms
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36
Q

Classic MSE of bipolar patient?

A

Appearance: Dressed inappropirately/bright/outlandish. Neglect personal hygeine
Behaviour: Overfamiliar. Flirtatious. Increased psychomotor activity. Restless
Speech: Loud, uninterruptable, flight of ideas, pressure of speech, puns/rhyme
Mood: Elated, but can quickly turn to irritability and anger
Thought: grandiose or persecutory delusions
Perception: Auditory hallucinations, often mood congruent
Cognition: Attention and concentration often impaired
Insight: Poor

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37
Q

Investigations for bipolar disorder?

A

Exclude other causes for manic episode: Substance misuse, SoL, hyperthyroidism, corticosteroids, anabolic adrenergic steroids.
Bloods: FBC, U+E, LFT, calcium, TFTS, glucose
Urine drug screen

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38
Q

Management of bipolar disorder?

A 
Non-pharmacological:
- Education support groups
- CBT
Pharmacological:
- Lithium: Prevents relapse, used as prohylaxis and acute
- Sodium valproate
- Olanzapine
Rapid tranquilisation -> Benzodiazapine
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39
Q

Why does Lithium need monitoring?

A 
Must be within 0.5-1mmol/L. If over 1.5 you get lithium toxicity.
- Nausea, vomiting, diarrhoea
- Confusion
- Excessive sleeping
- Seizures
- Tremors
Management: 
- STOP lithium
- Rehydrate
- Haemodialysis

Lithium is teratogenic.

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40
Q

Causes of bipolar affective disorder/

A

Medication: Steroids, illicit drug (amphet, cocaine), antidepressants
Physical: Infection, stroke, neoplasm, epilepsy, MS, hyperthyroid and other metabolic disturbances.

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41
Q

What is catatonia?

A

Increased resting muscle tone which is not present on active or passive movement.
> a motor symptom of schizophrenia (contrasts rigidity assoc with Parkinson’s + EPSE)

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42
Q

What are the characteristic signs of catatonia?

A 
Mutism
Posturing
Negativism
Staring
Rigidity
Echopraxia/echolalia
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43
Q

What are the typical forms of catatonia?

A

Stuporous/retarded

Excited/delirious

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44
Q

What are the common causes of catatonia?

A

General medical disorder

  • metabolic disturbances
  • drug-related
  • endocrine disorders
  • autoimmune disorder
  • heat stroke
  • typhoid fever
  • viral infections (HIV)

Neurological disorders

  • general paresis
  • lesions of thalamus or parietal lobes
  • frontal lobe disease
  • bilateral globus pallidus disease
  • seizures
  • parkinsonism
  • post encephalitic states

Mood disorder
- most commonly mania

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45
Q

DD of catatonia

A

Elective mutism: usually assoc with pre-existing personality disorder and clear stressor
Stroke: mutism assoc with focal neurological signs (locked-in syndrome)
Stiff-person syndrome: painful spasms brought on by touch/noise/emotional stimuli
Malignant hyperthermia: post anaesthetic + muscle relaxant in predisposed individuals
Akinetic parkinsonism

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46
Q

What are the catatonia-like subtypes?

A
  • malignant catatonia
  • neuroleptic malignant syndrome
  • serotonin syndrome
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47
Q

How do you treat catatonia?

A

Give benzodiazepines

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48
Q

How is CAMHS different to adult psych?

A

Less pharmacological treatment
Wider range of therapies (esp creative ones)
More emphasis on involving family + school

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49
Q

Questions to ask in a developmental history:

Pre + post-natal

A
  • pregnancy: was mum okay or ill
  • birth: normal or traumatic
  • milestones: e.g. smiling at 6 weeks
  • what kind of baby? easy, cuddly, anxious?
  • who was looking after them? parent have mental illness?
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50
Q

Questions to ask in a developmental history:

Toddler

A
  • who was main care?
  • did carer’s change? when did mum go to work?
  • how did they find separating?
  • what was language development like?
  • was there any ‘obsessive’ special interest?
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51
Q

Questions to ask in a developmental history:

School years

A
  • what was it like separating from parent?
  • friends + bullying
  • academic achievement
  • how was it moving up to secondary school?
  • how did they cope with changes?
  • were there important life events?
  • what was home environment like?
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52
Q

Questions to ask in a developmental history:

Teenage years

A
  • what was socialising like?
  • drugs and alcohol use
  • how were boundaries implemented a home?
  • any risky behaviour?
  • changes in academic level
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53
Q

What is childhood physical abuse significantly assoc with?

A
  • 15% increase in medical diagnosis
  • increased risk of heart disease in women
  • increased risk of cancer in both men and women
  • increased risk of COPD
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54
Q

What is the attachment theory?

A

An infant needs to develop a relationship with at least 1 primary caregiver for the child’s successful social and emotional development, and in particular for learning how to effectively regulate their feelings.
0-3months: indiscriminate attachment
3-6months: preference for main caregivers
6-12 months: only main caregiver
12-24 months: increasingly able to separate from main caregiver

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55
Q

What is OCD?

A

Obsessive-compulsive disorder
- an anxiety disorder which the patient suffers from time-consuming obsessions and compulsions that interfere with normal every day life.

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56
Q

What are RF for OCD?

A
  • genetics (35% of 1st degree relatives have it)
  • serotonin dysfunction
  • frontal cortex + basal ganglia abnormalities
  • anankastic premorbid personality traits (70%)
  • 15% of patients have schizophrenia
  • 30% of patients have comorbid depression
  • Tourette’s syndrome
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57
Q

How is OCD diagnosed?

A

Obsession and compulsion present on most days for 2 weeks, and not accounted for by the presence of another mental illness.
Features:
- acknowledged as originating in the mind
- persistent, repetitive and intrusive
- patient tries to resist them
- not intrinsically pleasurable
- cause distress and interfere with functioning

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58
Q

What are obsessions?

A 
Unwanted, persistent, intrusive thoughts, images, doubts or impulses which reoccur in the mind. 
Common content:
- contamination
- bodily fears (?)
- aggression
- orderliness/symmetry
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59
Q

What are compulsions?

A 
Repetitive, stereotyped acts of behaviour/mental acts that are recognised as excessive, unreasonable or exaggerated. If resisted they cause tension leading to compulsion.
Commonly involve:
- cleaning
- checking (doors locked)
- counting
- hoarding
- repeating a phrase
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60
Q

What do you find O/E for an OCD pt?

A
  • poor concentration if distracted by unwanted thoughts
  • increasing anxiety if prevented from yielding compulsions
  • patient recognises thoughts are their own + excessive
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61
Q

Mx for OCD?

A

1st line: psych intervention e.g. CBT, ERP (exposure response prevention)

2nd line: SSRI

3rd line: antipsychotic

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62
Q

What is personality?

A

The combination of characteristics/qualities that form an individual’s distinctive character.

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63
Q

What is a personality disorder?

A

A severe disturbance in the characterological condition and behavioural tendencies of the individual, usually involving several areas of the personality and nearly always associated with considerable personal and social disruption.

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64
Q

What maladaptations may manifest in personality disorders?

A
  • cognition
  • affectivity
  • control over impulses and gratification of needs
  • manner of relating to others
  • handling of interpersonal situations
  • manner of handling stress
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65
Q

What are the different clusters that you can split personality disorders into?

A

Cluster A: weird, odd + eccentric (more likely to have schizophrenia)

1) paranoid (accusatory)
2) schizoid (aloof)
3) schizotypal (awkward)

Cluster B: wild, dramatic, emotional + erratic (genetic relationship with mood disorders + subtonic abuse disorders)

1) Antisocial/dissocial
2) Borderline/Emotionally unstable
3) Histrionic
4) Narcissistic

Cluster C: worried, anxious, fearful (link with anxiety disorders)

1) Avoidant (cowardly)
2) Obsessive-compulsive (compulsive)
3) Dependent (clingy)

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66
Q

Describe borderline personality disorder / emotionally unstable

A

Cluster B

  • unstable moods (intense joy to rage)
  • relationship issues
  • impulsive + unpredictable
  • self-harm
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67
Q

Describe histrionic PD

A

Cluster B

  • over-dramatic events, attention-seeking
  • excessive emotionality
  • superficial relationships, views as shallow, egocentric
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68
Q

Describe narcissistic PD

A

Cluster B

  • grandiose self-image
  • dreams of unlimited success, power + intellectual brilliance
  • craves attention
  • lack empathy
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69
Q

Describe narcissistic PD

A

Cluster B

  • grandiose self-image
  • dreams of unlimited success, power + intellectual brilliance
  • craves attention
  • lack empathy
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70
Q

Describe avoidant PD

A

Cluster C - cowardly
(aka anxious personality disorder)
- very anxious + tense (worry a lot)
- feel insecure + inferior
- extremely sensitive to criticism; have to be liked
- timid, shy, socially inhibited
- exaggerate potential dangers + risks = avoid everyday activities

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71
Q

Describe obsessive-compulsive PD

A

Cluster C - compulsive
(aka anankastic PD)
- perfectionist: rigid routines, cautious, detail
- worry about doing wrong thing
- find it hard to adapt to new situations
- high moral standards
Different from OCD because this is ego-syntonic (patient is happy with how they are) but in OCD, the patient wants to stop (ego-dystonic)

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72
Q

Describe dependent PD

A

Cluster C- clingy

  • intense fear of separation + Rejection (cling to relationships)
  • lack self-confidence
  • difficulty making simple decisions (e.g. what to eat)
  • excessive reliance on others
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73
Q

Describe dependent PD

A

Cluster C- clingy

  • intense fear of separation + Rejection (cling to relationships)
  • lack self-confidence
  • difficulty making simple decisions (e.g. what to eat)
  • excessive reliance on others
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74
Q

Risk factors for personality disorders

A

Upbringing:

  • physical or sexual abuse in childhood
  • violence in family
  • alcoholic parents

Childhood problems:

  • severe aggression
  • disobedience
  • repeated temper tantrums

Brain problems
Triggers

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75
Q

How do you Ix personality disorders?

A
  • collateral, thorough Hx
  • MRI
  • Psychometric assessment (Eg. million clinical multiraxial inventory)
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76
Q

What are some psychosocial management options for PD?

A 
DBT: dialectal behavioural theory
MBT: mensualisation based therapy
CBT
Schema focused therapy
Transference focused therapy
Dynamic psychotherapy
Cognitive analytical therapy
Tx in a therapeutic community
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77
Q

Medication for PD?

A

Low-dose antipsychotics
Antidepressants for unstable pD
Carbamazepine for episodic behavioural dyscontrol and aggression

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78
Q

Medication for PD?

A

Low-dose antipsychotics
Antidepressants for unstable PD
Carbamazepine for episodic behavioural dyscontrol and aggression

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79
Q

What is anorexia nervosa?

A

Marked distortion of body image, pathologically low-weight, and weight-loss behaviours/

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80
Q

Who is often affected by anorexia nervosa?

A
  • women
  • mean age of onset: 16-17 yrs (rare>30)
  • upper/middle class
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81
Q

What can cause anorexia nervosa?

A
  • genetics
  • adverse life events (childhood trauma)
  • psychodynamic: family pathology (over protective, weak boundaries), indin (disturbed body image due to dietary issues in early life)
  • biological (hypothalamic dysfunction, neuropsychological deficits, personality trait, high achievers, psuedo atrophy or unilateral temporal lobe hypo perfusion)
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82
Q

DD of anorexia nervosa

A
  • chronic debilitating physical disease
  • brain tumours
  • GI disorders (crohns, malabsoprtion syndrome)
  • loss of appetite (secondary to drugs like SSRI)
  • depression/OCD
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83
Q

What is the diagnostic criteria for anorexia nervosa?

A

1) Low body weight (15%+ below expected, BMI<17.5)
2) Self-induced weight loss
- avoidance of fatty foods
- vomiting/purging
- excessive exercise
- using appetite supresion
3) Body image distortion
- ‘dread of fattness’
- overevaulated idea
- imposed low weight threshold
4) Endocrine disorders
- amenorrhoea
- decreased sexual interest/impotence
- increased GH levels
- increased cortisol
- altered TFTs
- abnormal insulin secretion
5) Delayed/arrested puberty (if onset pre-pubertal)

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84
Q

What are some psych sx of anorexia nervosa?

A 
Irritability
Conc/memory/decision-making problems
Low self-estee
Depression
Loss of appetite
Obsessiveness regarding food
Loss of libido
Insomnia
Social withdrawal
Reduced energy
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85
Q

What are some systemic sx of anorexia nervosa?

A 
Amenorrhoea
Cold hands and feet
Weight loss
Dry skin
Lethargy
Dizziness/fainting
Headaches
Hair loss
Constipation
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86
Q

What is bulimia nervosa?

A

Recurrent episodes of binge eating, with compensatory behaviours and over-valued ideas about ‘ideal’ body shape + weight

  • often past hx of anorexia nervosa
  • body weight may be normal
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87
Q

Aetiology of bulimia nervosa?

A

similar to anorexia but also:

  • personal/family hx of obesity
  • fam hx of affective disorder
  • fam hx of substance misuse
  • dysregulation of eating, related to serotnergic mechanism
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88
Q

What is the diagnostic criteria for bulimia nervosa?

A
  • persistent preoccupation with eating
  • irresistible craving for food
  • binges (episodes of overeating)
  • attempts to counter ‘fattening’ effects of food (self-induced vomiting, starvation)
  • morbid dread of fatness, with imposed ‘low-weight threshold’
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89
Q

What are some specific problems due to ‘purging’?

A 
Cardiac failure (sudden death)
Arrhythmias
Electrolyte disturbance (Decreased K+, Na+ and Cl-) --> met acidosis (laxatives) // met alkalosis (vomiting)
Leucopaenia/lymphocytosis
Dental erosion
Constipation/steatorrhea
Pancreatitis
Gastric/duodenal ulcers
Oesophageal/gastric perforation
Oesophageal erosions
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90
Q

What are some specific problems due to ‘purging’?

A 
Cardiac failure (sudden death)
Arrhythmias
Electrolyte disturbance (Decreased K+, Na+ and Cl-) --> met acidosis (laxatives) // met alkalosis (vomiting)
Leucopaenia/lymphocytosis
Dental erosion
Constipation/steatorrhea
Pancreatitis
Gastric/duodenal ulcers
Oesophageal/gastric perforation
Oesophageal erosions
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91
Q

DD of bulimia nervosa

A 
Upper GI disorders (assoc with vomiting)
Brain tumours
Personality disorder
Depressive disorder
OCD
Drug-related increased appetite
Menstrual-related syndromes
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92
Q

What comorbidites often accompany bulimia?

A 
Anxiety/mood disorder
Multiple dyscontrol behaviour
- cutting/buring
- overdose
- alcohol/drug misuse
- promiscuity 
- other impulse disorders
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93
Q

Tx for bulimia

A

Usually manages as an outpatient unless: suicidal, physical problems, extreme refectory cases, pregnant (increased risk of spontaneous abortion)

Meds: SSRI (fluoxetine 60mg)
Psych: CBT, IPT, guided self-help

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94
Q

What screening tool is used for eating disorders?

A

SCOFF (>2 answered yes = detailed Hx before referral)
S: do you make yourself sick because you feel uncomfortably full?
C: do you worry you have lost control over how much you eat?
O: have you recently lost >1 stone in a 3-month period?
F: do you believe yourself to be fat when others say you are too thin?
F: would you say that food dominates your life?

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95
Q

What are neuroses?

A

A relatively mild mental illness that is not caused by organic disease, involving symptoms of stress but not a radical loss of touch with reality.

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96
Q

Define generalised anxiety disorder?

A

Anxiety that is generalised and persistent but not restricted to, or even strongly predominating in, any particular environmental circumstances.

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97
Q

RF for GAD?

A
  • female
  • 35-54 years
  • divorced
  • living alone
  • genetic predisposition
  • current stress
  • life events
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98
Q

Sx of GAD?

A 
Excessive anxiety + worrying (apprehensive expectation) for most days for >/6months about wide range of events (work or school performance)
Difficult to control worry.
3 or more of:
- restlessness
- on edge
- easily fatigued
- muscle tension
- difficulty concentrating
- mind block
- irritability 
- sleep disturbance
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99
Q

What is found O/E of GAD?

What Ix should you do?

A

Tachycardia
Tachypnoea

Ix: FBC, U+E, LFTs, Ca, TFTs

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100
Q

How do you mange GAD?

A

1) educate/monitor
2) low-intensity psychological therapy (guided self-help)
3) CBT or drugs
- SRRI: escitalopram or paroxetine
- SNRI: venlafaxine

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101
Q

What is a panic disorder?

A

Recurrent attacks of severe anxiety which are not restricted to any particular situation or set of circumstances and are therefore unpredictable.
Due to GABA receptor dysfunction.

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102
Q

How do you diagnose a panic disorder?

A

Panic attacks must be associated with >1months duration of subsequent persisting anxiety about recurrence of the attacks; the consequences of the attacks or significant behavioural changes associated with them.

4 panic attacks in 4 weeks for diagnosis

103
Q

What is a panic attack?

A

Discrete episode of intense subjective fear where at least 4 of the characteristic Sx arise rapidly and peak within 10mins of the onset of panic.

104
Q

What are the characteristic Sx of panic attacks?

A

Autonomic arousal

  • palpitations
  • tachycardia
  • sweating
  • dry mouth
  • shaking

Physical

  • SOB
  • choking sensation
  • chest pain
  • nausea
  • dizzy

Mental state

  • depersonalisation/derealisation
  • fear of losing control/dying
  • concentration difficulties

General

  • hot flushes/chills
  • numbness
  • tingling

Sx of tension

  • muscle ache/pains
  • restlessness/inability to relax

Tends to last 20-30mins

105
Q

What is agoraphobia?

A

Avoidance of exposed situations for fear of panic or inability to escape
- not a stand alone diagnosis (v rarely occurs without panic disorder)

106
Q

What is ECT?

A

Electro-compulsive therapy
Under GA, electrodes on pt head deliver mild electrical pulses that cause lots of neurone to fire simultaneously and create a controlled seizure. A muscle relaxant keeps spasms spreading to rest of body.
- used achieve rapid and short-term improvement of severe symptoms after an adequate trial of other treatment options have proven ineffective.
- not recommended as maintenance therapy in depressive illness

107
Q

When is ECT indicated?

A
  • Severe depression: suicidal, failure to eat/drink, failure of drug treatment
  • Treatment-resistant psychosis + mania
  • Schizo-affective disorder
  • Catatonia
  • NMS
108
Q

Which patients should ECT be limited for?

A
  • cerebral aneurysm
  • recent MI
  • cardiac arrhymthias
  • intercerebral haemorrhage
109
Q

What are the limitations + SE of ECT?

A

Limitations: time-limited action (dissipates after few weeks)

SE:
Short term/early
- loss of short term memory
- headache
- confusion
- N/V
- clumsiness
- muscle aches

Late
- loss of long term memory

Mortality - rare (2:100,000)

110
Q

What is a typical course of ECT?

A 
Initially 3x/week (reduced to 2 then 1)
Cycle is 1min
Catatonia: 3-5 tx
Depression: 6-12 tx
Psychosis/mania: 20 tx
111
Q

Which drugs raise seizure threshold in ECT?

A

Benzodiazpines

Anticonvulsants

112
Q

Which drugs lower seizure threshold in ECT?

A

Antipsychotics (clozapine should be suspended 24hrs before ECT)
Antidepressants
Lithium

113
Q

What is a mental disorder?

A

Any disorder or disability of the mind (excluding alcohol or drug use) of nature or degree which warrants detention in hospital assessment or treatment.

114
Q

What are the minimum requirements for section under MHA?

A
  • Pt must have a mental disorder which must require hospital detention for assessment or treatment
  • The detention must be necessary in the interests of the patient’s health or safety o with a view to protect others.
115
Q

What are the application requirements for section 2 + 3 of MHA?

A
  • AMHP (approved mental health practitioner, usually social worker)
  • Nearest relative
116
Q

What do you need to enforce section 2 or 3 of MHA?

A

1) AMHP - final decision
2) 1 specialist knowledge (section 12 approved)
3) 1 with prior knowledge of patient (GP) - F2 onwards

117
Q

What is section 2 of the MHA?

A

Compulsory admission for assessment (+/- treatment) of a suspected mental disorder
- 28 days max
- power to treat without consent
- right to appeal by patient
- converted to section 3
Have some symptoms of illness but unsure what’s going on. Need to be in hosp bc they are at risk to themselves or someone else.
- diagnosis unneeded, just a mental disorder
- for their safety or others

118
Q

What is section 3 of the MHA?

A

Long term power to detain for treatment of an established mental disorder

  • 6 months, renewable after 6 months then yearly
  • can treat without consent (after 3 months not consenting or incapable - SOAD)
  • ECT: consent or SOAD (2nd opinion dr)
  • pt has mental disorder needing hospital prescription
  • in patient or public’s interest
119
Q

What is section 4 of the MHA?

A

Emergency admission with 1 doctor and 1 AMHP

  • lasts 72 hours
  • usually used in A+E
  • when not enough time to wait for 2 doctors for a section 2
  • no power to treat
  • assess and concert to 2 and 3 or discharge
120
Q

What is section 5(2)?

A

2,3,4 in community or hospital
5 (2): patient is already in hospital but wanting to leave
- does NOT cover A+E or OP (must already be voluntary inpatient)
- dr’s holding power (RC or delegate)
- max 72hrs to decide what to do or they can go
- no right to medicate (unless emergency- common law), except normal medication)
- no leave
- pt needs to be seen by RC/MHA team within 72hrs: informal/section 2/3 recommended

121
Q

What is section 5(4)?

A

Must already be an inpatient

  • Nurses’ holding power (registered MH or lD)
  • Max 6hrs
  • Ends when pt seen by Dr assessing for section 5(2), irrespective of the outcome of dr’s assessment
  • cannot treat coercively
122
Q

What is section 136?

A

A compulsory detention by police of someone with suspected mental disorder, from PUBLIC place (not home) to a place of safety
- up to 72hrs (MHA assessment)

123
Q

What is section 135?

A

Police can force entry into someone’s house who needs assessing under the MHA
Police removing someone from their home with court approval to a place of safety (eg police cell/psychiatric unit)

124
Q

What is psychosocial treatment?

A

Recovery model based on social inclusion and mental state

  • money, housing, education, employment
  • family work, psych therapy and counselling
125
Q

What is psychoeducation?

A

Working with people to teach them about their mind and their condition and what may affect it.

126
Q

What is a formulation in psych?

A

Constructing a meaningful narrative of the person’s symptoms and problems as part of a life story.
The BioPsychoSocial model helps to create formulation.

127
Q

What are the 4P’s in a BioPsychoSocial model?

A

Predisposing
Precipitating
Prolonging
Protective

128
Q

What is IAPT?

A

Improving Access to Psychological Therapy

  • primary care psychotherapy service
  • either self-referral or GP referral
  • mainly CBT + self-guided help
129
Q

What is psychotherapy?

A

Commonly involves talking to people, often 1:1 to make unconscious feelings become conscious and become aware of potential causes.

130
Q

What is transference?

A

Behaviour of patient towards therapist relating to past experiences.

131
Q

What is psychoynamic/psychoanalytic?

A

Freud’s original model focussed on therapy as a proves of uncovering past trauma to resolve present day symptoms

  • making connections between past and present
  • give meaning to symptoms
  • hoping pt become more aware of the unconscious processes which are giving rise to sx
  • weekly sessions for a year
  • therapeutic relationship in safe environment
132
Q

What is CBT?

A

Cognitive behavioural therapy
- thoughts, behaviours, emotions
1st wave: behaviour therapy (what we do influences how we feel)
2nd wave: cognitive (behavioural) therapy
3rd wave: mindfulness + acceptance and DBT
- generally structured and brief, focus on here and now and problems in day to day life
- 6-20 sessions

133
Q

What is counselling?

A

A primary care service which is fairly short. The aim is to help the patient be clearer about their problems and come up with their own answers; not aimed to help you change as a person.
Often used to hep someone cope with RECENT events they have found difficult/

134
Q

What is cognitive analytical therapy?

A

Integrates cognitive and psychoanalytic approaches (patient describes how problems have developed from events in their life and their personal experiences)

  • focus on their ways of coping and how to improve
  • letters, diagrams
  • brief 16-24 sessions, 50 mins
135
Q

What is interpersonal therapy?

A

Aims to help patient understand how problems may be connected to the way their relationships works. Helps identify how to strengthen relationships and find better ways of coping

  • depression (main use)
  • anxiety
  • buliia
136
Q

What is DBT?

A

Dialectic Behavioural Therapy
- aimed at BPD, goal is to help pt manage difficult emotions by letting them experience, recognise + accept them
Dialectics: trying to balance seemingly contradictory positions (e.g. balancing acceptance of yourself as person and change - positive in life)
Combines behavioural and 3rd wave CBT
Intense (year to 18months)
1:1 sessions weekly and group sessions weekly

137
Q

What is family therapy?

A

Family attend together

  • often used in CAMHS
  • sometimes observed by other therapists/recorded to help therapists and family reflect
  • help family members think about different ways of behaving with each other
138
Q

What is marital therapy?

A

Work without couples

Problems between partners or stresses they are both facing (e.g. los of a child)

139
Q

To assess suicide (content vs reaction) what questions are good to ask?

A

Before

  • precipitant
  • planned/impulsive
  • final acts
  • precautions against discovery?
  • use of alcohol?

During

  • method
  • alone?
  • where?
  • thoughts?
  • did they think it would kill them?
  • what did they do straight after?

After

  • call anyone? how did they get to hosp? who found them?
  • feelings when help arrived?
  • feelings about the attempt now?
  • current mood?
  • still feeling suicidal?
  • if they went home, what would they do for next few days?
  • if felt same again, what would they do differently?
  • protective factors?
  • accepting of treatment?
140
Q

What are the RF for suicide?

A
  • male
  • middle-aged
  • unemployed
  • recently bereaved
  • single
  • known mood disorder
141
Q

What is the bidirectional relationship of physical and mental illness in old-age psychiatry?

A
  • Physical illness increases RF of mental illness
  • Consequences of physical illness (e.g. stroke, PD)
  • Consequences of mental illness of physical health (e.g. secondary to self-neglect; lithium causing renal failure.
142
Q

What are the main conditions of old-age psychiatry?

A

1) depression
2) dementia
3) delirium

143
Q

What is dementia?

A

A progressive neurological disorder impacting cognition (memory, communication + thinking) which causes functional impairment.
- affects 850,000 in UK

144
Q

What are the different types of dementia?

A

Alzheimer’s disease
Vascular dementia
Lewy body dementia
Mixed (usually Alzheimer’s and vascular)

145
Q

How is dementia diagnosed?

A
  • *Collateral history- ask about onset, progression, fluctuations
  • MMSE
  • Tests of exclusion: FBC, B12, folate, LFTs
  • Imaging: structural (MRI, CT), functional (DaT, SPECT)
  • Objective assessments: MOCA or ACEIII
146
Q

What are the 5 domains of ACE III assessment?

A

1) attention
2) memory
3) fluency
4) language
5) visuospatial
82/100 is normal

147
Q

What are some reversible causes of dementia?

A 
Substance misuse - MCV, Folate, B12
Hypothyroidism - TSH, T4
SOL - CT/MRI
Normal pressure hydrocecphalus
Syphylis - serology
Vit b12/folate/b3 deficiency
148
Q

Describe Lewy body dementia?

A

Memory problems first
Or
Memory + movement problems within 12 months

149
Q

Describe Parkinson disease dementia

A

Movement problems first

Memory problems >12 months later

150
Q

Describe mild cognition impairment (MCI)

A

Decreased cognitive function (greater than expected for age) but no functional impairment present. Often a pre-dementia state/

151
Q

What is pseudo dementia?

A

Cognitive impairment secondary to mental illness (e.g. depression) not due to underlying dementia.
- won’t guess answers if unknown but a proper dementia patient would.

152
Q

What is the Mx for alzheimer’s/LBD?

A

1) Acetylcholinesterase inhibitors
1st line for Alz: Donepezil
1st line for LBD: Rivastigimine (2nd line for Alz)
- increase level of choline

2) NMDA antagonist
> memantine
- decrease level of glutamate in brain

3) Cognitive stimulation therapy

153
Q

What are the SE and CI of Acetylcholinesterase inhibitors in dementia Mx?

A

SE: Nausea, constipation
CI: heart block, stomach ulcer, COPD/asthma

154
Q

What is delirium?

A

An acute confusional state with changes in level of consciousness and cognitive impairment

  • medical emergency
  • reversible
155
Q

What are some causes of delirium?

A

CVS: congestive heart failure, TIA/Stroke
Endocrine: hypoglycaemic, DKA, Cushing’s, thyroid dysfunction
Metabolic: hypoxia, electrolyte imbalance, dehydration, liver failure
Infection: UTIs, meningitis
Trauma: post-concussion, subdural haematoma
Drugs: anaesthetic, opiates, corticosteroids

156
Q

What are the hyperactive Sx of delirium?

A
  • agitated + aggressive
  • incoherent
  • disorganised thoughts
  • delusions + hallucinations
  • disorientation
157
Q

What are the hypoactive Sx of delirium?

A
  • sluggish
  • drowsy
  • less reactive
  • looks withdrawn
158
Q

What is the Mx for delirium?

A

Treat underlying cause
Maintain adequate fluid/electrolye balance
Good lighting
Avoid changes in staff + location

159
Q

Ix for delirium?

A

Urine dipstick
Bloods
EEG

160
Q

What are some differences in depression in older-age psych?

A
  • hypochondriacal Sx
  • agitation + anxiety
  • focus on physical complaints
  • lack of appetite
161
Q

What is vascular depression?

A

Caused by structural changes to blood vessels in the brain.

162
Q

Who might late-onset schizophrenia affect?

A
  • females >60yrs
  • sensory deficits
  • social isolation
  • secondary to delirium of primary mental illness
163
Q

What is psychotic depression?

A

Depression with delusions
Commonly have:
- nihilistic delusions
- somatic delusions (unable to swallow, pain)

164
Q

What is Charles Bonnet Syndrome?

A

Patient with visual impairment has complex visual hallucinations
- no role for anti-psychotics

165
Q

What is a delusional disorder?

A

No hallucinations, but delusions

166
Q

What is erotonmania?

A

Somebody you have never met is in love with you.

167
Q

What are the key neurotransmitters that psych medications target?

A

Dopamine (DA)
Serotonin (SHT)
Acetylcholine (ACh)
Glutamate (Glu)

168
Q

How does schizophrenic medication work?

A

It is based on blocking D2 receptors because in schizophrenia there are overactive dopamine receptors (D1 + D2)

169
Q

Which dopamine receptor is more abundant?

170
Q

What are the different mechanisms of action for blocking dopamine receptors?

A

1) mesolimbic/mesocortical (blocking this causes most antipsychotic effect)
2) nigrostriatal
3) hypothalamus (pituitary gland)

There are also D2 receptors in the chemoreceptor trigger zone.

171
Q

What do the different pathways do?

A

Mesolimbic: hyperactive + positive Sx
- blocking this is good bc it stops positive sx

Mesocortical: underachieve + negative Sx
- blocking this is bad bc enhances neg Sx

Nigrostriatal (extrapyramidal nervous system): controls motor function and movement.
Decrease: Parkinsonism movements + dystonia
Increase: hyperreflexia
- blocking this can lead to extrapyramidal Sx

Tuberofundibular: prolactin
- blocking this can increase prolactin

172
Q

What do the typical/1st generation anti-psychotics do?

A

They are not specific so block all the pathways (variety of SE)

173
Q

What are the 1st generation anti-psychotics?

A 
High potency
- haloperidol
- prochlorperazine 
- pipothiazine
- fluphenazine
> stronger effect at low doses but more SE

Low potency
- chlorpromazine
> Doesn’t bind to receptor as tight but also binds to adrenergic, cholinergic + histamine receptors and blocks them

174
Q

What are some SE of chlorpromazine?

A 
Restlessness
Constipation
Sedation
Hypotension
Tardive dyskinesia

High BP (adrenergic), dry mouth (cholinergic), sedation, weight gain (histamine)

175
Q

How do the atypical/2nd generation anti-psychotics work?

A

Block D2 and serotonin receptors

Looser D2 binding, better for resistant forms of Schizophrenia.

176
Q

What are some 2nd gen anti-psychotics?

A

Clozapine
Risperidone
Olanzapine
Quetiapine

177
Q

What are some SE of 2nd gen anti-psychotics?

A

Metabolic: weight gain, increase glucose + lipids
Sedation
Postural hypotension
Nausea
Hyperprolactinaemia (risperidone esp)
Long QT arrhythmias (aripiprazole doesn’t have as much affect on QT)

Less EPSE

178
Q

What is a main caution with clozapine?

A

Agranulocytosis

- bone marrow doesn’t produce granulocytes (WBC)

179
Q

What are the EPSE?

A

SE from blocking nigrostriatal pathway (1st gen, typical anti-psychotics)

1) Movement abnormalities
- acute dystonic reaction (hours)
- muscle spasm
- acute torticolis
- ocular gyrate crisis

2) Akasthisia (days-weeks)
- inner restlessness
- pacing + agitated
- intolerable

3) Parkinsonism (days)
- tremor
- bradykinesia

4) Tardive dyskinesia (months-years)
- pointless involuntary reparative movements (e.g. lip smacking, tongue protrusion, grimacing)

OTHER

  • drowsiness
  • hypotension
  • QT prolongation (arrhythmias)
  • erectile dysfunction
  • hyperprolactinaemia (due to tuberohypophyseal blockage)
180
Q

What is the danger of using 1st gen drugs in dementia patients?

A

Increased risk of stroke and death

181
Q

What is the relationship between prolactin and dopamine?

A

Prolactin is produced in lactotroph cells of anterior pituitary gland under inhibitory control by dopamine. Decreased dopamine = increased prolactin.

182
Q

What are the effects of increased prolactin?

A

Females:

  • inhibits FSH + LH secretion = menstrual dysfunction.
  • galactorrhea

Males:
- direct reversible effect on hypothalamus, causing secondary hypogonadism = decreased libido + erectile dysfunction.

183
Q

What are some typical uses of 1st gen anti-psychotics?

A

Psychomotor agitation
Schizophrenia
Bipolar disorder (acute)
N+V control (palliative)

184
Q

Why does dopamine increase BP?

A

It is a catecholamine drug which acts by inotropic effect on the heart muscle. It causes more intense contractions which increases BP.

185
Q

What drug classes are used for depression?

A

Selective Serotonin Reuptake inhibitors (SSRI)
Selective Noradrenaline Reuptake inhibitors (SNRI)
Tricyclic Anti-Depressants (TCAs)

186
Q

How do SSRIs work?

A

Inhibit neuronal reuptake of serotonin = increase serotonin to bind to post-synaptic receptors. Metabolised by liver.
FIRST LINE ANTIDEPRESSANT
- citalopram, fluoxetine, sertraline, escitaloram

187
Q

What are the SE of SSRIs?

A 
GI upset
Weight gain/loss
Hypersensitivity reactions (Skin rash)
Hyponatraemia (confusion)
Increased suicidal thoughts
Bleeding 
Insomnia
Increased anxiety + irritability 
Erectile dysfunction
188
Q

What are some symptoms of abrupt withdrawal of SSRIs?

A

GI upset: N+V, diarrhoea, anorexia
Flu Sx
Sleep disturbance

189
Q

How do SNRIs work?

A

Inhibit noradrenaline transporter = more serotonin and noradrenaline = bind to post synaptic receptors. Serotonin + noradrenaline are reduced in depression so if you block them it will increase.
- venlafaxine, duloxetine, desvenlafaxine, levomilnacipran

Effective in reducing pain in fibromyalgia and neuropathy

190
Q

What are the SE of SNRIs?

A 
GI upset (dry mouth, nausea)
Weight changes
CNS: headache, weird dreams, insomnia, confusion, seizures
Increase BP + HR
Loss of appetite 
Loss of sleep
191
Q

How do TCAs work?

A

Block serotonin + noradrenaline pumps but different levels of selectivity to SNRIs. Also block alpha, histamine + muscarinic receptors.
- amitriptyline, lofepramne, amoxapine, nortriptyline

192
Q

What are the SE of TCAs?

A

Antimuscarinic: dry mouth, blurred vision, urinary retention

Histamine: sedation

Alpha: hypotension

Dopamine block: hyperprolactin, parkinsonian Sx

193
Q

Should you use TCAs in patients who are suicidal?

A

No because they are toxic

194
Q

What is the 1st line Tx for bipolar?

A

LITHIUM

  • inhibits cAMPH production = inhibits monoamines
  • acute Tx of mania
  • relapse prevention
195
Q

Why should lithium be monitored?

A

It has a low therapeutic index, target is within 0.5-1mmol/L, if >1.5 it it toxic.
Checked weekly

196
Q

What are the Sx of toxicity?

A
  • N + V + Diarrhoea
  • confusion
  • excessive sleeping
  • seizures
  • tremors
197
Q

What are the SE of lithium?

A 
Movements: tremor
Nephrotoxicity
Hypothyroidism
Pregnancy problems (fetus has 10x higher chance of getting Ebsteins' anomaly - low implanted tricuspid)
N + V, polyuria, weight gain
Dampens mood
198
Q

How to manage lithium toxicity?

A

STOP lithium
Rehydrate
Haemodialysis

199
Q

How does sodium valproate work?

A

Sodium valporate

- inhibits sodium channels and increases brain GABA (sedative effect)

200
Q

What are SE of sodium valproate?

A

Hepatic necrosis

CI in pregnancy (causes spina bifida)

201
Q

How does carbamazepine work?

A

Inhibits sodium channel, increases GABA

  • used in trigeminal neuralgia, bipolar + seizures
  • risk of agranulocytosi
202
Q

How does lamotrigine work?

A

inhibits Na but doesn’t activate GABA

SE: widespread itchy rash - can progress to Steven Johnson’s disease (epidermis slips off dermis)

203
Q

What are the drugs for bipolar?

A

Lithium
Sodium valporate (TETRAOGENIC)
Carbamazepine
Lamotrigene

204
Q

What drug classes are used for anxiety?

A

Benzodiazepines
Barbiturates
Non-benzo hypnotics

205
Q

How do benzodiazepines work?

A

inhibit excitatory signals, muscle relaxant / increase frequency of ion channel opening so enhance GABA
- diazepam, lorazepam, chlordiazepoxide, clonzapem

206
Q

What are the SE of BDZ?

A

Drowsiness
Dizziness
Loss of coordination
Decreased alertness/concentration

207
Q

Explain barbiturates?

A

Enhance effect of GABA, increase ion channel opening duration + decrease activity of excretory NTS like glutamate and Act
- pentobarbital, phenobarbital

208
Q

What are some SE of barbiturates?

A

Dizziness
Light-headed
Sedation
Memory/attention impairment

209
Q

Why should BDZ be monitored?

A

Low therapeutic index

  • toxic dose is not much higher than target
  • small increase can result in coma > respiratory depression
210
Q

How do non-benzo hypnotics work?

A

Trigger chloride channel opening = hyper polarisation of membrane
- zolpidem, zaleplon, buspirone (takes while to pick in)

211
Q

What are the SE of non-benzo hypnotics?

A 
Cognitive impairment (memory loss)
Impairment of motor function
Daytime sedation
212
Q

How do you treat anxiety?

A

Benzos for acute
SSRIs for long term
BB for CVS Sx (CI in asthma)

213
Q

What are anxiolytics?

A

Drugs used to relieve anxiety. Benzodiazepines and non-benzodiazepines

214
Q

Examples of benzodiazepine anxiolytics?

A

Nitrazepam, lorazepam, alprazolam

215
Q

Examples of non- benzodiazepine anxiolytics?

216
Q

What are the risks of buspirone?

A
  • Can cause resp depression
  • Risk seizures on withdrawal
  • Gradual reduction over months
217
Q

Features of cannabis?

A
  • Anxiolytic/stimulant depending on composition. May cause/exacerbate psychosis
  • Depression, anxiety, memory problems after long term use
  • No maintenenace
  • Not dangerous on withdrawal
218
Q

Features of tobacco?

A
  • Can be anxiolytic/stimulating
  • Varying evidence for nicotine replacement, not dangerous on withdrawal
  • Buproprion (xyban) beware seizures
219
Q

How do stimulants work?

A

Potentiate euro-transmission and increase cortical excitability producing effects of increased alertness and endurance, diminished need for sleep and a subjective sense of well-being.
- caffeine
- cocaine
- amphetamines
- MDMA
Euphoria, increased energy, weight loss, can cause/exacerbate psychosis/

220
Q

Explain cocaine

A

White powder which can be inhaled, dissolved or injected. Acts as a local anaesthetic at the mucous membranes. Blocks neurotransmitter reuptake.

221
Q

What are the SE of cocaine?

A

Acute harmful effects;

  • arrhythmias
  • intense anxiety
  • htn
  • CVA
  • acute impulsivity + impaired judgment

Chronic:

  • necrosis of nasal septum
  • fetal damage
  • panic + anxiety disorders
  • persecutory delusions + psychosis
222
Q

Explain amphetamines

A

White power that can be swallowed, inhaled, dissolved or injected. Chemical similarity to noradrenaline and dopamine. Slower metabolism than cocaine but gives longer duration of action.

223
Q

SE of amphetamines

A

Acute

  • tachycardia
  • arrhythmias
  • hyperpyrexia
  • irritability
  • post-use depression
  • quasi-psychotic state with hallucinations

Chronic
- anxiety + depression

224
Q

Explain MDMA (ectasty)

A

Tablets taken orally. Causes serotonin release and blocks reuptake Hallucinogenic and stimulant properties 30 mins post-ingestion.
Increased filing of closeness to others, pleasurable agitation relieved by dancing and decreased fatigue.

225
Q

SE of MDMA

A

Acute

  • sweating, nausea + vomiting
  • decreased potency despite increased libido
  • deaths due to dehydration + hyperthermia

Chronic

  • neuro-toxicity
  • hepatotoxicity
  • chronic cognitive impairment
226
Q

What are hallucinogens?

A

Ecstasy, LSD
Altered perception of reality/heightened experience
- not dangerous in withdrawal
- no maintenance

227
Q

Explain solvents

A

Similar intoxicating effect as alcohol
- no specific withdrawal syndrome

SE
Risk: laryngospasm due to cold temp, brain damage, hypoxia

228
Q

What is a common opiate?

229
Q

What are the acute effects of heroin?

A

Euphoria, drowsiness, constricted pupils, shallow breathing

230
Q

What are the withdrawal symptoms of heroin?

A

6hrs post dose

Anxiety, craving, yawning, sweating, abdo pain, dilated pupils, aches, N+V, diarrhoea

231
Q

What signs suggest heroin overdose?

A

Reduced LOC
Resp depression/arrest
Pinpoint pupils

232
Q

How do you treat heroin usage?

A

Methadone

  • long acting opiate (orally)
  • prevent withdrawal and drug seeking
  • maintenance/detox

Buprenorphine

  • partial agonist
  • wait till withdrawal sx start or can induce withdrawal

Naltrexone

  • opiate antagonist
  • prevent lapse turning into relapse

Overdose:

  • naloxone
  • opiate antagonist
233
Q

What is neuroleptic malignant syndrome?

A

Uncommon life-threatening neuroleptic (anti-psychotic)- induced disorder which requires immediate treatment.

234
Q

What are the Sx of neuroleptic malignant syndrome?

A

Fever
Muscle rigidity
Delirium
Autonomic instability

Ix: markedly raised serum creatine kinase

235
Q

How is neuroleptic malignant syndrome treated?

A

Stop causative factors
Supportive measures
Treat rhabdomyolysis + admit

236
Q

What is suicide?

A

Intentional self-inflicted death

237
Q

What is self-harm?

A

Self poisoning or injury, irrespective off the apparent purpose of the act. An expression of personal distress, not an illness.

238
Q

Why do people self harm?

A 
Communicating a message
Gaining power by escalating conflict
Emotional immaturity
inability to cope with stress
weak religious ties
availability of drugs (psychotropics + alcohol)
239
Q

RF for self harm

A 
Family Hx (witnessed)
Reduced endorphin response to emotional arousal
Abnormalities in serotonin release
Neglect in childhood
Abuse
Bullying
Substance misuse
240
Q

What factors lead to postnatal depression?

A

The risk of major depression after pregnancy is greater in those with a Hx of postpartum depression or unipolar/bipolar depression compared to those without psychiatric history.

Other factors:

  • unplanned pregnancy
  • lack of support
  • marital problems
  • social circumstances
  • sleep deprivation
  • hormonal changes
241
Q

Mx of postnatal depression?

A

CBT
Short-term antidepressants
(excreted in breast milk but TCAs and SSRIS rarely detectable but Fluoxetine shows significantly higher levels)
- observe babies for SE
- may need to stop breast feeding if large doses used

Severe: ECT (if mother not eating/drinking or strongly suicidal)

242
Q

Explain postpartum psychosis?

A

Peak onset at 2 weeks postpartum - a psychiatric episode with prominent affective symptoms (depression or mania) occurring with rapidly fluctuating symptoms, mood liability, insomnia and disorientation.

RF:

  • single parenthood
  • reduced social support
  • previous mental illness
243
Q

What scoring system is used to identify postnatal depression?

A

Edinburgh postnatal depression scale (EPDS)

244
Q

What is somatisation disorder?

A

AKA Briquet’s syndrome
Chronic, multiple, medically unexplained, difficult to treat (but sincere/genuine) symptoms, affecting any body part.
- psychological cause
- onset <30 years

245
Q

How do you treat Briquet’s syndrome?

A

Time - don’t dismiss as the ‘worried well’
Explore factors perpetuating the illness
- disordered physiology, misinformation, unfounded fears, misinterpretation of sensations, unhelpful ‘coping’ behaviour, social stressors
Agree Mx plan
Tx any depression, consider CBT

246
Q

What is the dependent syndrome?

A

The desire (often strong, sometimes overpowering) to take a substance (which may or may not have been medically prescribed.) Requires 3 or more of the following:

1) Strong desire or sense of compulsion to take the substance (craving)
2) Difficulty in controlling substance use (onset, termination, level of use)
3) A physiological withdrawal state when reducing or ceasing substance use (or using the same/similar substance to avoid withdrawal)
4) Tolerance: increased doses required to produce original effect
5) Progressive neglect of alternative pleasures or interests
6) Persisting use despite clear evidence of harmful consequences.

247
Q

How to distinguish what the cause of hallucinations and/or delusions are?

A

Either: schizophrenia, drug abuse or physical illness

  • most auditory hallucinations not assoc with falling asleep or waking up are caused by schizophrenia or depression
  • 90% of those with non-auditory hallucinations (e.g. seeing things), the cause is substance abuse, drug withdrawal or physical disease.
  • if patient recognises hallucinatory nature of the experience, then consider diagnosing substance intoxication or withdrawal.
  • if no current exposure to hallucinogens, the diagnosis may be ‘flashbacks’ (e.g. hallucinogen persisting perception disorder)
248
Q

What are phobias?

A

A group of disorders in which anxiety is expressed only, or predominantly, in certain well-defined situations that aren’t dangerous.

  • these situations are avoided or endured with dread
  • cause distress and impair function
249
Q

What are some phobias?

A

Agorophobia: a cluster of phobias: fear of travel, crowds or events away from home.

Social phobias: where we may be minutely observed (e.g. dinner parties, fear of scrutiny of others)
Sx: blushing, tremor, nausea, toilet urge

Simple phobias: numerous phobias linked to situations e.g. clowns, spiders, rodents

250
Q

Tx for phobias?

A

CBT
SSRI
TCA for panic attacks

251
Q

What is PTSD?

A

Post-traumatic stress disorder

  • develops after an exceptionally stressful, life-threatening or catastrophic event or situation.
  • more common in men
252
Q

What are common symptoms of PTSD?

A
  • re-experiencing the event in vivid nightmares or flash backs (high HR, BP, sweating)
  • anxiety + panic attacks
  • avoidance of things assoc with event
  • hypervigilance
  • sleep disturbance
  • poor concentration
253
Q

What features are assoc with PTSD?

A 
Depression
Emotional numbing
Drug/alcohol misuse 
Anger
Denial or suppression of traumatising event
254
Q

How do you treat PTSD?

A

Trauma: focused treatments

  • CBT
  • EMDR (eye movement desensitisation and reprocessing)
  • Hypnotherapy

Second line: medication
- SSRIs, TCAs, mirtazapine, SGAs

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