Psych Flashcards

1
Q

differentiate between suicide and deliberate self harm

A
suicide = intentional self-inflicted death
DSH = intention, non-fatal self-inflicted harm
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2
Q

what factors make someone more likely to attempt suicide?

A
mental illness, in particular: 
depression
bipolar disorder
schizophrenia
alcohol/substance misuse
emotionally unstable personality disorder
anorexia nervosa

also:
chronic pain/disease
availability of means (ligature points, firearms, paracetamol pack size reductions)
family history of suicide
lack of social support or recent adverse event (bereavement, loss of job/relationship)

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3
Q

give some suicide prevention strategies

A
  • detect and treat mental illness
  • be alert to risk and respond to it - lots of people see GP in the weeks preceding suicide
  • safer prescribing - avoid prescribing drugs with high overdose toxicity to patients with suicide risk
  • urgent hospitalisation/detention for people with suicide intent
  • careful management of DSH - high risk of future completed suicide
  • tackle population factors like unemployment, access to means
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4
Q

describe epidemiological differences between who self harms and who completes suicide (e.g. by age, sex etc)
also give some of the common methods for each

A

suicide - M > F, older single men big risk. hanging most common method in UK, others incl jumping in front of train/car, poisoning
DSH - F > M, more common in women, under 35s, lower social classes and single/divorced
means - mostly drug overdose or physical self-injury e.g. cutting or stabbing

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5
Q

give four different categories that motives behind DSH can broadly be categorised into

A
  • desire to interrupt a sequence of events seen as inevitable or undesirable
  • need for attention
  • attempt to communicate
  • true wish to die
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6
Q

what are indicators of high risk in a suicide/DSH history

A

leaving a note, making a will, continued determination to die, marked feelings of hopelessness, precautions taken against discovery, high lethality risk (either objective, or patient believes! i.e. 3 paracetamol is high risk if patient believed that’s lethal dose)

also if older, male, unemployed, socially isolated
hx of previous attempts/DSH - biggest indicator of future completed suicide

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7
Q

list the different options for management of DSH

A
MEDIATE
Medically stabilise
Establish rapport
Diagnose and treat mental illness
Iatrogenic risk - prescribe safely (e.g. SSRIs rather than tricyclics)
Assess likelihood of recurrence:
Thoughts might return? = make a plan
Evaluate social problems

basically want to reduce risk of them doing it again, ensure treatment of underlying mental illness is either started or continued, address any social problems and make sure they know what to do if they feel like they might do it again - e.g. come to A&E, contact crisis team - do they need admission?
DBT good for repeated DSH in EUPD

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8
Q

what are the main areas to consider in a psychiatric risk assessment?

A

risk to self
risk to others
risk of self neglect/accidental harm
vulnerability to abuse

risk should be regularly reviewed as it fluctuates
remember past behaviour biggest predictor of future risk!!

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9
Q

what would you document when assessing risk to self?

A
  • current suicidal thoughts, plans and intent
  • anything that prevents patient acting on these thoughts eg. family, religion (protective factors)
  • prev eps of DSH - circumstances, methods, management
  • factors predisposing to DSH/suicide (FHx, social isolation, substance misuse etc)
  • hx of disengagement from support services, whether they’re currently willing to engage

in MSE look for thoughts of hopelessness/worthlessness, command hallucinations inciting self-harm

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10
Q

what would you document when assessing risk to other?

A
  • acts or threats of violence - to whom, frequency, severity, methods used, any serious harm resulting
  • deliberate arson
  • sexually inappropriate behaviour
  • episodes of containment (compulsory detention, treatment in hospital, secure unit, locked ward, prison, police station)
  • compliance with prev and current treatment - note past disengagement

Factors increasing risk:

  • recent stopping prescribed drugs
  • change in use of recreational drugs
  • alcohol/substance misuse
  • impulsive or unpredictable behaviour
  • recent stressful life events, change in personal circumstances, lack/loss of social support

in MSE:

  • expressed violent intention or threats
  • irritability, disinhibition, suspiciousness
  • persecutory delusions
  • delusions of control/passivity phenomena
  • command hallucinations
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11
Q

give examples of self-neglect/accidental injury someone with mental illness could be at risk of

A
  • malnutrition - forgetting to eat, eating out of date foods
  • failure to access healthcare
  • living in squalid conditions
  • falls - physical frailty, drug/alcohol intoxication
  • failure to take safeguards against fire/explosion e.g. cigarette burned bed sheets, leaving gas on)
  • wandering, poor road safety
  • accidental overdose/not taking meds
  • vulnerability to crime due to leaving door open, persistently losing key or inviting strangers in
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12
Q

give examples of abuse someone with mental illness could be at risk of

A

abuse = single or repeated lack of appropriate action occurring within any relationship where there is an expectation of trust and which causes harm or distress to a vulnerable person
may be verbal, physical, financial or sexual, or neglect
- people in institutions are at risk
- also occurs in private homes
make sure carers aren’t having to deal with verbal/physical abuse from patient

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13
Q

what acronym can you use to remember factors affection risks to vulnerable adults?

A

HOW SAFE?
HOme safety e.g. leaving gas on
Wandering

Self neglect e.g. poor self care
Abuse, neglect, crime vulnerability
Falls
Eating - malnutrition

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14
Q

describe steps that should be taken in immediate management of a violent patient

A
  • consider if admission necessary, need for MHA assessment - PICU, secure ward?
  • staff will be trained in breakaway techniques (to exit situation) and also in respectful restraint (talking down always first)
  • medication e.g. benzodiazepines and/or antipsychotics e.g. midazolam (short acting), lorazepam (intermediate acting)
  • seclusion if needed
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15
Q

what acronym can you use to remember immediate management of violence?

A

BE CAREFUL
Breakaway
Evaluate and talk down

Control and restraint
Assess need for medication to sedate and/or treat disorder
RE-evaluate setting - higher security?
FULly review care plan

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16
Q

what steps can be taken to prevent future violence after a violent incident?

A
WARN
Write risk incidents in notes
Assess in safe environment
Read documentation before assessing
Notifying professionals involved of risks

communication between agencies, good use of care plans, monitoring level specific to that patient’s needs

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17
Q

in the context of a risky patient, when is it appropriate to break confidentiality?

A
  • if aware of specific threat to named individual - must inform that person (and probably also the police)
  • rarely, can justify breaking in name of public interest e.g. to assist in prevention, detection or prosecution of serious crime
  • also must report significant abuse causing harm to children and vulnerable adults - to social services or police if severe
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18
Q

explain the mechanism of action of ECT

A

induction of a modified cerebral seizure - patient undergoes a series of these (e.g. twice a week for 4-12 sessions)
effects include (nobody really knows):
neurotransmitter release - serotonin, noradrenaline, dopamine
transient increase in blood-brain-barrier permeability
modulation of neurotransmitter receptors
synaptogenesis and neurogenesis
hypothalamic and pituitary hormone secretion

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19
Q

explain the legal aspects of ECT

A

if a patient with capacity refuses it, it cannot be given - not even if under section.
patient must give informed consent before each session
or can be given if:
pt lacks capacity and it doesn’t conflict with advanced decision
AND it’s an emergency and independent consultant has not yet assessed
OR
independent consulted appointed by mental health act commission agrees

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20
Q

what are some indications for use of ECT?

A
  • severe depression (this is the main one)
  • prolonged or severe episode of mania that doesn’t respond to treatment
  • catatonia
  • moderate depression not responsive to multiple drug and psychological therapies

must only be used to induce fast and short-term improvements of severe symps after all other options failed
patients usually need subsequent treatment to prevent relapse

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21
Q

what are some relative contra-indications to ECT?

A

raised ICP
recent stroke
recent MI
unstable angina

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22
Q

how is ECT given?

A

patient fasts for 4 hours
anaesthetist gives short-acting anaesthetic + muscle relaxant + preoxygenation
psychiatrist then runs electric current through electrodes on head
induces seizure - lasts 20-60s, monitor EEG and movement
monitor during recovery

typically twice a week for 4-12 sessions depending on response

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23
Q

give some side effects of ECT

A
  • cognitive impairment is the biggie - cognition should be assessed before, during and after a course of treatment
  • if significant impairment - consider switching electrode placement, reducing stimulant dose or stopping treatment
    also:
  • anaesthetic complications
  • dysrhythmias due to vagal stimulation
  • post-ictal headache
  • confusion
  • retrograde and anterograde amnesia - difficulties in registration and recall may persist for several weeks
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24
Q

explain a bit about the newer methods of brain stimulation

A

transcranial magnetic stimulation (TMS) - prefrontal cortex stimulation by application of strong magnetic field - shows promise for depression
vagal nerve stimulation - used in epilepsy and refractory depression - generator implanted under skin used to electrically stimulate the nerve
deep brain stimulation - thin electrode inserted directly into brain - used in Parkinsons, research into its role in OCD

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25
Q

what are the first and second rank symptoms for schizophrenia? (ICD 10)

A

ICD 10 says need these for >1 month

first rank (any one = schizophrenia):

  • Thought echo/insertion/withdrawal/broadcast
  • Delusions of control, influence, ot passivity or phenomenon
  • third person auditory hallucinations (discussing them/running commentary)
  • Bizarre persistent delusions

second rank (any two)

  • any persistent hallucination
  • neologisms (made-up words) or other forms of disorganised speech/thought disorder
  • ‘negative’ symptoms e.g. apathy, poverty of speech, blunted affect & catatonic Sx
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26
Q

what is ‘psychosis’? give some examples of psychotic disorders

A

losing touch with reality - misperception of thoughts/ perceptions arising in the patient’s own mind as reality - includes delusions and hallucinations - symptom rather than a diagnosis

e.g. schizophrenia, delusional disorder, schizoaffective disorder, psychotic depression and bipolar affective disorder

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27
Q

what are the positive symptoms of schizophrenia?

A

delusions - persecutory, or delusions of reference
hallucinations
formal thought disorder (disorganised sepech) e.g. neologisms

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28
Q

what are the negative symptoms of schizophrenia?

A
poverty of speech
flat affect
poor motivation
social withdrawal
lack of concern for social conventions
poor attention and memory (cognitive symptoms)
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29
Q

what are the DSM 5 criteria for schizophrenia?

A

at least two of following, including 1 positive symp (1-3), for at least 6 months (incl 1 month of symptoms):

1) delusions
2) hallucinations
3) disorganised speech
4) disorganised or catatonic behaviour
5) negative symptoms

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30
Q

what are the different subtypes of schizophrenia according to ICD 10 (DSM 5 doesn’t have subtypes)?

A
  • paranoid schizophrenia - most common, delusional and auditory hallucinations
  • catatonic - psychomotor disturbances e.g. rigidity, posturing, echolalia, echopraxia
  • hebephrenic aka disorganised - early onset, poor prognosis, irresponsible behaviour, mood inappropriate, affect incongruous e.g. lots of giggling etc, fleeting delusions and hallucinatiosn
  • residual - history of one of the ones above, but currently it’s mostly just negative symptoms
  • simple schizophrenia - negative symps without preceding overt psychotic symptoms - rare
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31
Q

what features might suggest someone is at risk of an acute psychotic illness?

A
  • prodromal period - symptoms of anxiety, depression, ideas of reference (feelings of being watched)
  • person that’s distressed, with declining social functioning and transient psychosis - at risk
  • consider CBT and treatment of comorbid conditions, but antipsychotics not appropriate
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32
Q

aetiology/risk factors of schizophrenia?

A
  • genetics - definite familial element
  • advancing paternal age - to do with germ line mutation in dad
  • neurodevelopmental hypothesis - factors interfering with early brain development increase risk e.g. obstetric complications
  • social factors - SE deprivation, urbanity, excess of life events in 3 weeks before symptoms (e.g. bereavement, loss of job etc)
  • early cannabis use
  • ethnicity - afro-caribbean/black african at higher risk
  • those in families with high expressed emotion
  • neurochemical changes- possible final pathway involving dopamine excess
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33
Q

what are the key components of management of acute schizophrenia?

A

early intervention is key
antipsychotics - normally kick in within 2-3 weeks, gradually becoming more effective - benzodiazepine used to sedate/keep calm in mean time.
psychology - self-help, psychoeducation (education of family helps!)
social - support, focus on engagement, hope, reduce stigma.

early intervention team support people in first few years of illness. aim for community treatment but may require admission/detention - for assessment and treatment.

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34
Q

describe management options for schizophrenia in terms of reducing risk of relapse and promote long-term recovery after controlling an acute psychotic episode

A

maintenance treatment on antipsychotics
psychology - family therapy to reduce expressed emotion if present, also CBT for schizophrenia. art therapy.
support to reduce substance misuse, gain employment/study and find accommodation

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35
Q

describe the role of medication in treatment of schizophrenia

A

after single acute episode - antipsychotics started and should be continued for 12-24 months before tailing off if they remain well - don’t stop earlier as massive risk of relapse, but if well don’t keep on forever either due to risk of tardive dyskinesia etc.
typical and atypical effective but different side effects.

trial a drug for 4-6 weeks before deciding whether to up it or switch. IM/depot used if non-compliance or patient preference.

clozapine is saved for if failed to respond to 2 other drugs - requires regular bloods.

antipsychotic/benzodiazepine sedation if agitated/violent.
negative symptoms not improved by clozapine or other antipsychotics!

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36
Q

describe the role of psychological treatment for schizophrenia

A

should all be offered individual CBT for schizophrenia - alleviates distress and disability, doesn’t focus on eliminating voices etc, more on strategies to cope with them e.g. playing music, how to respond to them.
family therapy to reduced excessive expressed emotion.
art therapy - particularly for negative symptoms.
self-help groups e.g. Hearing Voices group.

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37
Q

describe the role of social support/interventions in treatment of schizophrenia

A

schizophrenic patients often struggle with day to day life so social support/rehab really important.

  • need to help them get back to work/study and appropriate accommodation to give them a good QoL.
  • if work not poss - volunteering or day centres to provide structure
  • often require supported living requirement and/or extensive rehab focussed on maximising independence
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38
Q

list some good prognostic factors for a person with schizophrenia

A
FINDING PLANS:
Female
In relationship, good social support
No negative symptoms
aDheres to medication
Intelligence (more educated)
No stress
Good premorbid personality
Paranoid subtype
Late onset
Acute onset
No substance misuse
Scan (CT/MRI brain) normal
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39
Q

give some differential diagnoses for a patient presenting with schizophrenia vibes

A
delusional disorders
psychotic depression
manic episode
schizoaffective disorder
schizotypal disorder
puerperal psychosis

organic disorders - substance misuse, drug-induced psychosis, iatrogenic (levodopa, methyldopa, steroids, antimalarials), complex partial epilepsy, delirium, dementia, Huntington’s disease, SLE, syphilis

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40
Q

what drugs can cause a patient to become psychotic?

A

steroids, levodopa, methyldopa, antimalarials, isoniazid

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41
Q

what is “high expressed emotion” and what does it mean in relation to schizophrenia?

A

families with high expressed emotion = more at risk of schizophrenia, much more at risk of relapsing as well.
expressed emotion is intensity and amount of emotional involvement of the family with the patient - e.g. overbearing, lots of critical comments etc.

theory is that family therapy focussed on reducing this can reduce relapses.
note that if expressed emotion too low, this exacerbates negative symptoms of apathy and withdrawal.

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42
Q

list some factors associated with poor prognosis of schizophrenia

A

demographics:

  • young age at onset (<25 yrs)
  • male
  • isolated, unmarried
  • poor work record
  • premorbid personality disorder
  • substance misuse

illness characteristics:

  • insidious onset
  • prolonged untreated psychosis (early intervention is key!!!)
  • disorganized subtype
  • no mood disturbance
  • early negative symptoms
  • non-compliance with medication
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43
Q

list some biological vs psychological risk factors for schizophrenia

A

biological:

  • FHx
  • obstetric complications
  • season of birth
  • advancing paternal age
  • early cannabis - may be precipitating, also psychoactive substance use in general is a maintaining factor

psychological:

  • life stressors (precipitating and/or maintaining)
  • high expressed emotion in family (maintaining)
  • social
  • poverty
  • urban birth/upbringing
  • migration
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44
Q

briefly outline the dopamine hypothesis of schizophrenia

A

excess of dopamine transmission (hyperdopaminergia) in schizophrenia (unclear if due to excess dopamine, excess receptors or what)
they think this cos:
- antipsychotic drugs are all dopamine D2 receptor antagonists
- dopamine agonists (e.g. levodopa, amphetamines) can produce paranoid psychosis
- some CSF and brain studies have shown abnormal levels of dopamine/metabolites/enzymes/receptors

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45
Q

what is schizoaffective disorder?

A

affective and schizophrenic symptoms occur together with equal prominence
used for patients who satisfy criteria for schizophrenia AND mood disorder during the same episode - otherwise diagnosis predominant syndrome (or neither!)
i.e. one first-rank symptom in mania doesn’t mean schizoaffective disorder, neither does a bit of a labile mood in schizophrenia

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46
Q

what is the management and prognosis of schizoaffective disorder?

A

use a combo of mood stabilisers (e.g. lithium) and antipsychotics to treat the mood and psychosis problems.
prognosis - somewhere between those for schizophrenia and mood disorder - better in those whose mood problem is mania rather than depression

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47
Q

what are delusional disorders? what kind of delusions is it normally?

A

fixed delusion or delusional system (associated delusions) with other areas of thinking and functioning well preserved.
so basically have delusions but not hitting criteria for schizophrenia and also don’t have organic cause.

usually persecutory delusions - hallucinations rare.

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48
Q

what is acute delusional disorder? what are the clinical features?

A

acute onset of delusions, not schizophrenia though, usually rapidly resolving.
features - multiple, transient, persecutory delusions, suspicious, labile mood.
can be caused by drugs (in which case not actually delusional disorder!) or follow extreme stresses.

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49
Q

what is persistent delusional disorder? what are the features of this?

A

lasting 3+ months - systematised delusions (stable and combined into a complex system) often focussed on alleged injustices.
but rest of mental state is normal.
onset usually middle age - social isolation, deafness, paranoid personality traits are risk factors.

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50
Q

what are the specific (mostly eponymous) types of delusional disorder?

A
Othello's syndrome aka morbid jealousy
somatic delusional disorder
de Clerambault's syndrome aka erotomania
folie a deux
Capgras delusion
Fregoli's delusion
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51
Q

what is Othello’s syndrome?

A

type of delusional disorder where patient (normally male) has delusional belief of partner being unfaithful.
can be dangerous - they often threaten/attack partner or supposed lover.
usually symptom of psychotic depression of schizophrenia but can be isolated delusional disorder.
considered risky enough to overrule confidentiality - must do full risk assessment.

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52
Q

what is somatic delusional disorder?

A

delusional belief that the personal has an illness/deformity - aka monosymptomatic hypochondriacal psychosis - generally fixed on one specific illness - distinguishes from hypochondriasis.

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53
Q

what is de Clerambault’s syndrome?

A

aka erotomania - patient, usually female, has delusion that man of high standing (e.g. pop star, or their doctor) is in love with her.
seen in some stalkers.

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54
Q

what is folie a deux?

A

when two people, often isolate sisters, share a delusion - one is truly psychotic while other is ‘induced’ to become so and will normally recover spontaneously when they’re separated.

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55
Q

what is Capgras’ delusion?

A

aka illusion des soisies

belief that someone close by has been replaced by imposter/double

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56
Q

what is Fregoli’s delusion?

A

belief that someone close to them is impersonating other people.

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57
Q

what is schizotypal disorder? what are the key features?

A
like a chronic, attenuated schizophrenia - beliefs stop short of being delusion, sensory experiences not quite hallucinatory.
features:
- aloof and suspicious manner
- eccentric behaviour
- avoidance of social contact
- odd beliefs, magical thinking
- vague, rambling or metaphorical speech
- tendency to odd ideas and sensory experiences
- 3+ of the above for >2 years
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58
Q

what are the core symptoms of depression?

A

ICD-10 states should have at least two of these, every day for at least two weeks:

1) low mood
2) anhedonia - loss of enjoyment in formerly pleasurable activities
3) decreased energy (or increased fatiguability)

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59
Q

list some of the non “core” symptoms of depression

A
  • reduced concentration and attention - cognitive features
  • reduced self-esteem and self-confidence
  • ideas of guilt and worthlessness
  • feelings of hopelessness for the future
  • thoughts of self-harm
  • decreased sleep and/or appetite

severity of depression (mild/moderate/severe) depends on:

  • no. symptoms present
  • severity of symptoms
  • degree of associated distress
  • interference w/ daily activities

any psychotic features = severe.

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60
Q

what is Beck’s cognitive triad?

A

the three main areas focussed on by negative/pessimistic thoughts in depression:

1) the self (low self esteem)
2) the world
3) the future

other areas incl. guilt/worthlessness, death/suicide

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61
Q

give some biological symptoms of depression

A

reduced sleep - classically early waking >2hrs earlier than normal - mood is lowest in morning as well (diurnal variation)
reduced appetite - leading to weight loss (some people experience overeating and weight gain)
reduced libido
psychomotor agitation/retardation/both - of speech and/or movement

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62
Q

what kinds of delusions/hallucinations are typically experienced in severe depression?

A

usually nihilistic - believe that they/a body part is dead/rotting
also hypocondriacal - concerning illness or death

hallucinations - usually auditory, in second person and derogatory or urging suicide.

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63
Q

give some differentials for depression

A
  • normal sadness, esp in context of bereavement or severe physical illness
  • if psychotic symps - differentiate from schizophrenia
  • alcohol or drug withdrawal
  • if recurrent depressive episodes = unipolar depressive disorder (consider bipolar dx even when no mania if really strong FHx, v early onset and marked agitation)
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64
Q

describe the aetiology of depression

A
  • genetic contribution, particularly if bipolar.
  • current theory is genetic predisposition that will be triggered if exposed to adverse life events
  • monoamine neurotransmitter availability in synaptic cleft reduced (noradrenaline and serotonin) - this is where antidepressants act
  • psychosocial factors - adverse life events, unemployment, lack of confiding relationship, parental loss, major childhood stress/abuse
  • physical illnesses (most endocrine things, cancers) and medications (incl steroids, isotretinoin)
  • structural features - limbic system and prefrontal cortex play a role
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65
Q

when would you refer a depressed patient for management beyond GP land

A

if:

  • pt not responding to treatment
  • substantial risk of harm to self or others
  • second opinion on diagnosis/treatment needed
  • combo of drugs or rarely used drugs being considered
  • to access specialised psychology, OT etc
  • pt is severely unwell and admission or ECT needed
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66
Q

describe management of depression

A

mild = self-help groups, structured physical activity, guided self-help, computerised CBT
next step = individual CBT or IPT
moderate/severe = combine CBT and antidepressants - technically shouldn’t just be on meds!
always keep on antidepressants for at least 6 months after episode to reduce relapse - if recurrent depression, keep on for at least a couple of years

if treatment resistant - consider augmenting with antipsychotic or lithium or another antidepressant (E.g. mirtazipine)
still not working - consider ECT

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67
Q

what psychological treatment options are recommended by NICE for moderate-severe depression / persistent mild depression?

A

individual CBT/IPT/behavioural activation - 16-20 sessions over 3-4 months
behavioural couples therapy (where relevant) - 15-20 sessions over 5-6 months

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68
Q

what is ‘somatic syndrome’ in relation to depression?

A

physical/biological manifestations of depression - psychomotor retardation (slow movements and thinking), agitation, loss of libido, constipation, amenorrhoea

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69
Q

what is dysthmia?

A

long standing mild/subthreshold depressive symptoms

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70
Q

what is Cotard’s syndrome?

A

nihilistic delusions where patient believes they, or a part of them, is dead - common in psychotic depression.

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71
Q

what are the symptoms of psychotic depression?

A

Cotard’s syndrome/nihilistic delusions
auditory hallucinations - derogatory or encouraging DSH/suicide
severe psychomotor retardation - to point of ‘depressive stupor’ - sitting mute and still (?indication for ECT)

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72
Q

list some factors that might affect choice of management options in depression, and what each one implies

A
  • serious suicide risk = consider admission, drug rx w/SSRI not TCA as less toxic in overdose
  • psychotic symps? = add antipsychotic, consider ECT
  • what are the main symptoms? = can affect drug choice e.g. sedative antidepressant (mitrtazapine) if insomnia
  • past hx of response? = use what worked last time
  • past hx of mania? = caution with antidepressants, consider mood stabiliser
  • any comorbid medical problems? = avoid TCAs after recent MI
  • what does patient want? = might have preference for drug vs psychology
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73
Q

give some options for managing someone with depression that has not responded to first line drug treatment

A
  • switch class e.g. from SSRI to SNRI, or try another drug within the same class
  • add psychological therapies if haven’t already
  • trial mirtazapine
  • augment - add mirtazapine to an SSRI - useful for insomnia/agitation; add lithium; add second-gen antipsychotic e.g. olanzapine or quetiapine esp. if psychotic symptoms, agitation or insomnia
  • switch to an MAOI, esp if atypical depression
  • psychiatric referral
  • consider ECT for severe and intractable
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74
Q

what is bipolar affective disorder?

A

characterised by recurrent episodes of altered mood and activity - episodes of depression and mania

episodes are either - depressive, manic, hypomanic, mixed

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75
Q

define hypomania

A

less severe than mania and without psychotic symptoms.
lasts >4 days (mania tends to be >7 days)
core features are mild or moderate
dysfunction only mild or moderate
partial insight preserved
no psychotic features

they basically have excess ‘zest for life’ and energy, but are just about holding it together
people who’s mood never exceeds hypomania are said to have bipolar II disorder (DSM)

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76
Q

define mania

A

mood that is predominantly elevated, expansive or irritable and definitely abnormal for the individual.
plus 3 of the following:
- increased activity or physical restlessness
- pressure of speech
- flight of ideas
- socially disinhibited/inappropriate behaviour
- decreased need for sleep
- inflated self-esteem/grandiosity
- distractibility/constant changes in activity or plans
- risky/reckless behaviour
- marked sexual energy/inappropriate sexual behaviour

can have psychotic features - mood congruent, grandiose e.g. blessed with special powers, might hear voices supporting this

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77
Q

what is cyclothymia?

A

mild, chronic bipolar variation of mood - cycle between the two states, but only mildly

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78
Q

give some organic causes of depressive mood disorders

A
Cushing's 
Addison's 
hypothyroidism
hypercalcaemia
DM
beta blockers
carcinomas
digoxin
chronic amphetamine use
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79
Q

give some organic causes of manic mood disorders

A
hyperthyroidism
steroids
acute amphetamine use
levodopa
antidepressants
bromocriptine
isoniazid
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80
Q

give some organic causes of either manic or depressive mood disorders

A
MS
cerebrovascular disease
SLE
epilepsy
brain tumours
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81
Q

explain aetiology of bipolar affective disorder

A
  • genetic link really strong
  • no childhood risk factors known
  • some structural abnormalities implicated e.g. in limbic system
  • always consider drug-induced mania
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82
Q

how do you manage a manic patient?

A

if severe, can require admission (usually compulsory)
antipsychotics (risperidone, olanzapine) or valproate and lithium are all effective anti-manics.
benzodiazepines for sedation
if on antidepressant already - MUST stop
if on lithium already - check levels to assess adherence
ECT if intractable

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83
Q

how do you manage a bipolar patient in a depressive episode?

A

quetiapine (atypical antipsychotic) can be highly effective - sedation and weight gain limits long term acceptability
antidepressants typically less effective - must be used with mood stabiliser/antimanic agent or else they can destablise and precipitate mania
lamotrigine can help
if severe - antipsychotics, ECT and admission could all be needed

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84
Q

what longer-term drug management options are there for bipolar affective disorder?

A

mood stabilisers - lithium first-line

valproate second-line

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85
Q

what needs to be done when starting someone on lithium?

A
  • advise the person that poor adherence or rapid discontinuation may increase the risk of relapse
  • measure BMI and do for U&Es incl calcium, eGFR, TFTs, FBC
  • ECG for people with CVD or risk factors for it
  • give leaflets etc on taking lithium safely
  • establish a shared-care arrangement with GP for prescribing lithium and monitoring adverse effects
  • measure plasma lithium 1 week after starting, and 1 week after every dose change until they stabilise

tell patient to:

  • seek medical attention if they develop D&V or become acutely ill for any reason
  • ensure they maintain their fluid intake, particularly after sweating (for example, after exercise, in hot climates or if they have a fever), if they are immobile for long periods or if they develop a chest infection or pneumonia
  • talk to their doctor ASAP if they become pregnant or are planning a pregnancy.
  • don’t take OTC NSAIDs - avoid prescribing them too
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86
Q

what monitoring is required for a patient on lithium (after stable levels)?

A

measure plasma levels every 3 months for first year
after first year measure every 6 months, or every 3 months for people in the following groups:
- older people
- people taking drugs that interact with lithium
- people who are at risk of impaired renal or thyroid
- function, raised calcium levels or other complications
- people who have poor symptom control
- people with poor adherence
- people whose last plasma lithium level was 0.8 mmol per litre or higher

monitor BMI, U&Es (specifically calcium), eGFR, TFTs every 6 months
at each appt, ask about symptoms of neurotoxicity, including paraesthesia, ataxia, tremor and cognitive impairment, which can occur at therapeutic levels of lithium

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87
Q

what is puerperal psychosis? treatment? risk factors?

A

occurs in 1-2 in 1000 births - psychosis in postpartum period.
usually onset in second postnatal week.
baby at risk either of direct harm due to mum’s delusions, or of neglect due to mum’s preoccupation with her own symptoms.
almost always requires admission - MBUs!
Rx = antipsychotics, antidepressants, low threshold for ECT
usually full recovery, big increase in risk after next delivery/in lifetime.
RFs - past or family Hx of puerperal psychosis, diagnosis of bipolar affective disorder, being primigravida

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88
Q

what are baby blues?

A

tearful, labile, irritable mood typically on 3rd/4th postnatal day
symps resolve within days without treatment - explanation and reassurance helpful though.
no association with other mood disorders.
thought to be due to fall in sex steroids after delivery.

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89
Q

what is PND? tool to screen for it? treatment?

A

starts within a month of delivery - negative thoughts focussed on perceived failings of mother or baby’s wellbeing.
use edinburgh PND score.
Rx - explain and reassure. consider interventions for mother-baby relationship. mother’s groups, midwife, health visitor.
consider antidepressants or psychology if moderate/severe - otherwise should resolve on its own within a few weeks.
if admission - MBU.
it’s more common in women with hx of psychiatric disorder - change in sensitivity of dopaminergic system implicated.

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90
Q

what are the characteristic features of ‘normal’ grief?

A

5 classic stages:
Denial: this may include a feeling of numbness and also pseudohallucinations of the deceased, both auditory and visual. Occasionally people may focus on physical objects that remind them of their loved one or even prepare meals for them
Anger: this is commonly directed against other family members and medical professionals
Bargaining
Depression
Acceptance

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91
Q

how do you manage the normal grief reaction? when is it an ‘abnormal’ grief reaction?

A

bereavement counselling and support - often voluntary sector has a role here.

abnormal grief:

1) absent/delayed - either no outward signs of grief, or grieving doesn’t begin for a few weeks
2) prolonged - if prominent symptoms after 6-12 months - begin to consider whether this is depression
3) excessive - more intense than would be expected - although who are we to define this? - be vigilant for depression

all of this is a bit of a grey area!!

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92
Q

when is a substance regarding as being ‘misused’?

A

if it produces physical, psychological or social harm

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93
Q

what are the different categories of substance misuse?

A

“at-risk consumption” - (alcohol) intake at a level associated with increased risk of harm
“harmful use” - misuse associated with health and social consequences but without dependence
“dependence” - prolonged, regular use of substances e.g. alcohol, opioids, amphetamines can lead to dependence (addiction) and withdrawal syndromes
“intoxication” - acute effect of the substance e.g. being drunk or high

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94
Q

list commonly misused substances by ‘type’

A

alcohol
legal/prescribed drugs - benzodiazepines, nicotine, caffeine, cannabis
opioids - heroin, morphine, methadone
stimulants - amphetamines, cocaine, ecstasy
hallucinogens - LSD, phencyclidine (PCP), solvents

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95
Q

what are the main principles of managing substance misuse?

A
  • identify at-risk consumption and harmful use early and give accurate info and advice
  • in dependency, facilitate withdrawal (detox) and abstinence
  • help maintain abstinence
  • if abstinence not possible, minimise harm with continuing use
  • treat complications e.g. drug induced psychosis
  • prevention - population-level interventions e.g. pricing policies
  • advise on risks and legalities of driving under influence
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96
Q

give some aetiological/risk factors for substance abuse

A
  • genetic - inherited vulnerability/predisposition
  • neurobiological - abnormalities in dopamine, GABA, endogenous opioid systems, trait EEG patterns
  • psychological - personality factors, learned behaviours, positive reinforcement (drugs lead to behaviours that increase their use)
  • socioeconomic - price and availability, cultural norms/acceptability
  • legal - restrictions on sale, penalties for possession/dealing
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97
Q

what are the definitions of different levels of drinking in UK?

A

hazardous = above recommended limits (14 units per week)
harmful = >50 units p/w men, >35 units p/w women
dependent drinking = people with features of dependence/addiction

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98
Q

what are the clinical features of alcohol dependence/alcoholism?

A
  • feeling compelled to drink
  • primacy of drinking over other activities e.g. work, family
  • increased tolerance
  • relief drinking - drinking to stop/prevent withdrawal symptoms
  • stereotyped pattern of drinking
  • reinstatement after abstinence aka unable to give up alcohol for long
  • drinking despite awareness of harmful consequences
  • withdrawal symptoms
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99
Q

what are the clinical features of alcohol withdrawal?

A

onset 6-12 hours after stop drinking

  • tremors (the shakes)
  • agitation
  • nausea and retching
  • sweating
  • overwhelming desire to drink (craving)
  • withdrawal symps relieved by alcohol
  • might experience withdrawal symptoms on waking

if severe, can progress to delirium tremens and/or seizures
seizures peak onset = 36 hours
DT at 48-72 hours

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100
Q

what are the clinical features of delirium tremens?

A

onset at 48-72 hours

  • delirium
  • visual hallucinations (classically lilliputian aka little animals in corners etc)
  • delusions - usually persecutory and transient
  • fear and agitation, sometimes aggression
  • coarse tremor
  • seizures
  • autonomic disturbance (sweating, fever, tachycardia, hypertension)
  • insomnia
  • dehydration and electrolyte disturbance
  • lasts 3-4 days, then exhaustion and patchy amnesia

POTENTIALLY FATAL

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101
Q

what is Wernicke’s encephalopathy?

A

triad of ophthalmoplegia/nystagmus, ataxia and confusion is classic.
caused by thiamine deficiency - petechial haemorrhages occur in a variety of structures in the brain including the mamillary bodies and ventricle walls

Features:
nystagmus (the most common ocular sign)
ophthalmoplegia
ataxia
confusion, altered GCS
peripheral sensory neuropathy

urgently treat with thiamine replacement

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102
Q

what is Korsakoff’s syndrome?

A

occurs if Wernicke’s encephalopathy goes untreated. called Wernicke-Korsakoff syndrome - characterised by the addition of antero- and retrograde amnesia and confabulation in addition to Wernicke’s encephalopathy symptoms.

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103
Q

how can GPs screen for hazardous alcohol consumption?

A
  • ask about alcohol intake during all consultations
  • use any of FAST, CAGE or AUDIT questionnaires
  • follow up on any comments suggesting patient thinks they drink too much
  • brief motivational interviewing has a role
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104
Q

describe the use of screening tools/questionnaires in alcohol misuse

A

CAGE - 4 screening qus (cut down, annoyed, guilty, eye opener)
FAST - 4 qus, if above certain threshold it’s an indication for doing AUDIT
AUDIT - 10 qu questionnaire
SADQ - assesses severity of dependence

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105
Q

list some harmful medical effects of alcohol

A

liver damage - fatty liver, hepatitis, cirrhosis
cardio - cardiomyopathy, HTN
GI - peptic ulcer, oesophageal varices, pancreatitis
neoplasms - liver, oesophagus
blood - anaemia, haemochromatosis

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106
Q

list some harmful neurological/organic psychiatric effects of alcohol

A
blackouts
epilepsy
neuropathy
DT
Wernicke's syndrome
Korsakoff's syndrome
cerebellar degeneration
central pontine myelinosis
head injury (from falls)
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107
Q

list some harmful psychiatric effects of alcohol

A
alcoholic hallucinations
morbid jealousy
alcoholic dementia
depressive disorders
anxiety disorders
sexual dysfunction
suicide
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108
Q

list some harmful social effects of alcohol

A
accidents
problems with relationships
domestic violence
employment difficulties
crime
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109
Q

what management should be done for someone with hazardous/harmful drinking?

A

usually brief interventions in primary care e.g. FRAMES advice

  • structured Feedback on risk/harm
  • emphasis patient’s Responsibility for change
  • clear Advice on changing drinking
  • discuss Menu of options for making change
  • express Empathy and be non-judgement
  • reinforce patient’s Self-efficacy

principles - accurately assess consumption, nature/extent of harm (e.g. do LFTs), give brief advice on hazards of excess, book in to review

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110
Q

what is involved in managing an alcohol dependent patient through detox?

A

initial step = detox - controlled withdrawal, using reducing course of benzodiazepine (often chlordiazepioxide)

if mild - withdraw at home ± chlordiazepoxide

if moderate - at home, chlordiazepoxide over 5 days, thiamine supplementation (oral, IV if high Wernicke’s risk)

if severe/hx of DTs/seizures - higher doses of chlordiazepoxide and probs want them in hospital so you can manage seizures. IV thiamine.

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111
Q

how do you manage a patient to maintain abstinence from alcohol after detox period?

A
  • complete abstinence needed really - controlled drinking rarely works
  • regular LFTs and breath alcohol tests to monitor progress
  • encourage attending AA or other local groups
  • medications - disulfram (antabuse), acamprosate or opioid antagonists
  • disulfram = negative reinforcement - basically massively exaggerates hangover after hardly any alcohol
  • acamprosate = reduces craving for alcohol
  • opioid antagonists act on autonomic nervous system
  • psychology - offer CBT, social skills training, problem solving and motivational interviewing
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112
Q

how does cannabis act on the brain?

A

derived from hemp plant
THC = main psychoactive ingredient (tetrahydrocannabinol)
acts on endogenous cannabinoid receptors in brain

cannabis also contains cannabidiol - slightly antagonises effects of THC
THC content varies - increasing in UK over time

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113
Q

list the effects of cannabis

A

dose-related impairment in reaction time, info processing, coordination, motor performance, attention
exaggeration of pre-existing mood
mellowness and increased enjoyment of aesthetic experience
distortion of sense of space and time
reddening of eyes

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114
Q

give some adverse health effects of cannabis

A
  • anxiety and panic, esp in first time users
  • paranoid ideation, occasionally delirium - also in first time users typically
  • increased risk of road traffic accidents
  • risk of using other, more harmful drugs
  • possible increased risk of respiratory disease
  • can provoke angina in people with CVD
  • mild long-term cognitive impairment if heavy/regular use
  • doesn’t cause dependence/withdrawal - some tolerance can occur, also ‘psychological dependence’
  • early and heavy use = risk of schizophrenia
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115
Q

what options are there to treat cannabis use?

A

CBT can reduce use but high rates of reuse within 6-12 months
don’t think anybody really gets treated for cannabis use unless it’s insanely bad/they get drug-induced psychosis

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116
Q

explain the pharmacology of opioids / what ones are used recreationally and how?

A

mimic endogenous endorphins and enkephalins - activate opioid receptors
e.g. morphine, codeine, heroin, methadone
highly addictive
heroin causes intense euphoria - most commonly misused
modes of use:
- IV injection - risk of infections, thrombosis and phlebitis, also hep B and C, HIV
- inhalation
- snorting

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117
Q

list the effects of opioids

A
euphoria
analgesia
drowsiness
respiratory depression
cough reflex suppression
N&V
bradycardia and hypotension
lowering of body temp
pupillary constriction
constipation
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118
Q

list some adverse of opioid misuse

A
  • high levels of morbidity/mortality
  • IV injecting = infections, VTE, phlebitis, hep B/C, HIV
  • different routes have big influence on bioavailability, speed of onset, severity of dependence etc - makes it easy to accidentally OD!
  • suicide rate increased x14
  • psych comorbidity, incl misuse of other substances
  • major negative social effects
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119
Q

what features indicate dependence on opioids?

A

tolerance! develops rapidly - means OD is common, often fatal due to respiratory depression

  • makes pain management in opioid user difficult
  • high risk of OD after detox e.g. released prisoners
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120
Q

list features of opioid withdrawal

A
onset within 8-12 hours of last dose, peaking 24-48h later and subsiding over 10 days (process longer for methadone)
features (severe, but rarely life threatening):
- craving
- restlessness, insomnia
- myalgia
- sweating
- abdo pain, D&V
- dilated pupils, running nose and eyes
- tachycardia
- yawning
- 'goose bumps'
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121
Q

list some features suggesting opioid misuse

A
rhinorrhoea
needle track marks
pinpoint pupils
drowsiness
watering eyes
yawning
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122
Q

list some complications of opioid misuse

A

viral infection secondary to sharing needles: HIV, hepatitis B & C
bacterial infection secondary to injection: infective endocarditis, septic arthritis, septicaemia, necrotising fasciitis
venous thromboembolism
overdose may lead to respiratory depression and death
psychological problems: craving
social problems: crime, prostitution, homelessness

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123
Q

what is the emergency management of opioid overdose?

A

ABCDEs

IV or IM naloxone: has a rapid onset and relatively short duration of action

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124
Q

what are some harm reduction interventions for opioid misuse?

A

needle exchange

offering testing for HIV, hepatitis B & C

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125
Q

give a general overview of management of opioid misuse

A

usually managed by specialist drug dependence clinics although some GPwSIs offer similar services
offered maintenance therapy or detoxification
NICE recommend methadone or buprenorphine as first-line in opioid detoxification
compliance is monitored using urinalysis
detoxification should normally last up to 4 weeks in an inpatient/residential setting and up to 12 weeks in the community

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126
Q

how should detoxification and abstinence be managed for opioid misuse?

A

inpatient detox more effective than outpatients - avoids the chaotic environment that’s usual in opioid misusers
substitute drug e.g. methadone linctus, clonidine, naltrexone prescribed in reducing doses.
ideally then discharge into an abstinence programme e.g. residential houses of recovered addicts etc
relapse rate very high sadly

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127
Q

describe harm reduction/maintenance or substitution treatment as used for opioid dependence?

A

abstinence is so unrealistic for a lot of opioid dependent people - focus on harm reduction (e.g. reduce injecting, needle exchanges, screening for BBVs) ± substitute prescribing
substitute prescribing = oral methadone (or sometimes buprenorphine) used as alternative to injected street opiates.
usually ends up being long term use, rather than using this to detox.

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128
Q

how do you manage suspected opioid overdose?

A

recognising opioid OD - unconscious, pinpoint pupils, bradycardia, hypotension, shallow breathing/snoring, even respiratory arrest
naloxone (opioid antagonist) used to restore adequate spontaneous ventilation

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129
Q

what stimulant drugs are commonly misused?

A

amphetamines - speed, methamphetamine
cocaine
MDMA

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130
Q

give some info on amphetamine misuse/dependence/withdrawal

A
  • taken orally, snorted or injected
  • produce symps like hypomania - elevated mood, over-talking, increased energy, insomnia
  • pulse and BP raised, pupils dilate, mucous membranes dry
  • dependence - leads to depression and mood swings
  • withdrawal = ‘crash’ - depression, agitation, lethargy, suicidal thoughts, cravings
  • intoxication/psychosis - treat w/benzodiazepines and antipsychotics
  • prolonged use –> paranoid psychosis
  • potent dopamine enhances - inhibit its reuptake and stimulate its release - also enhances noradrenaline and serotonin
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131
Q

give some info on cocaine misuse

A
  • similar effects to amphetamines, but more dramatic
  • snorted or smoked as crack/freebase
  • cocaine misuse is often accompanied by alcohol/opioid misuse
  • intoxication can mimic psychosis/mania
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132
Q

give some info on MDMA misuse

A
  • tolerance really common
  • adverse reactions - hyperpyrexia, acute renal failure due to dehydration - also water intoxication in users who overcompensate
  • can cause acute psychosis
  • neurotoxic to serotonin fibres so chronic users can have low central serotonin levels and some cognitive deficits
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133
Q

what are hallucinogens? what’s the main one used widely? give some info

A

drugs altering perception, producing psychadelic experiences
LSD most common, also magic mushrooms
LSD - ‘trip’ starts 2 hours after consumption, lasts 8-12 hours - distorted sensory perception, alteration of sense of time and scale, changes in body image (E.g. out of body experience)
- rarely cause dependence or withdrawal
- might get acutely referred to psych due to panic/anxiety of ‘bad trip’ - sedate with benzodiazepines

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134
Q

define ‘personality’

A

characteristic behavioural, emotional and cognitive attributes of an individual - we all have particular traits that emerge mid-adolescence and once established remain stable - but when these are extreme this can be a personality disorder

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135
Q

define personality disorder

A

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

“an enduring pattern of inner experience and behaviour that deviates markedly from the expectations of the individuals culture, is pervasive and inflexible, has onset in adolescence/early adulthood, and leads to distress or impairment”

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136
Q

what core features required for diagnosis of a personality disorder?

A
  • personality attributes cause distress of dysfunction for individual or those around them
  • dysfunction occurs across a range of situations
  • characteristics are pervasive, stable and recognisable since late adolescence
    specific PDs are then diagnosed according to domains of personality that are most affected
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137
Q

what are the three clusters of personality disorder?

A
cluster A (eccentric) - 'mad' - paranoid/schizoid
cluster B (dramatic) - 'bad' - antisocial, emotionally unstable, histrionic, narcissistic
cluster C (anxious) - 'sad' - anankastic (obsessive), anxious (avoidant), dependent
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138
Q

what are the characteristics of paranoid PD?

A

suspicion and distrust of others
sensitivity to criticism
bears grudges
self-importance

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139
Q

what are the characteristics of schizoid PD?

A

emotionally cold and detached
introspective
social isolation
lack of joie de vivre

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140
Q

what are the characteristics of antisocial PD?

A
callous
unstable, transient relationships
low frustration threshold
irritable and impulsive
failure to learn from experience
failure to accept responsibility
lack of guilt
tend to be young men
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141
Q

what are the characteristics of emotionally unstable PD?

A
multiple, turbulent relationships
impulsivity
recurrent emotional crises
variable, intense mood
stress-related psychotic-like symptoms
tend to be young women
history of frequent DSH
classically got a history of childhood sexual abuse
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142
Q

what are the characteristics of histrionic PD?

A
exaggerated, theatrical displays of emotion
attention seeking
vain
suggestible (easily swayed)
shallow, labile mood
crushes and fads
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143
Q

what are the characteristics of narcissistic PD?

A
gradiose self-importance
exaggerates achievements and abilities
exploits others
arrogant
expects special praise and restraint
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144
Q

what are the characteristics of anankastic/obsessive PD?

A

excessive orderliness
preoccupation with detail
inflexible and dogmatic
humourless

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145
Q

what are the characteristics of anxious/avoidant PD?

A

persistent tens and apprehensive feelings
avoid personal contact
fear of criticism and rejection

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146
Q

what are the characteristics of dependent PD?

A

encourage others to make decisions for them

excessive need to be taken care of

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147
Q

what is known about aetiology of personality disorders?

A

not loads!
evidence that early childhood experiences, plus general upbringing and childhood traumas etc have a role
some genetic element

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148
Q

how do eccentric (paranoid or schizoid) PDs tend to present?

A

they avoid services and usually present when suspiciousness or persecutory beliefs lead them to start accusing people or promising retribution.

challenging to distinguish from delusions, and to establish the level of risk.
difficult to treat - low dose antipsychotics are an option, but compliance poor. social interventions offered but they don’t view their isolation as a problem. psychotherapy can actually be harmful so is CI’ed.

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149
Q

how do patients with emotionally unstable personality disorder tend to present?

A

frequent A&E attendance with repeated OD or DSH.
they have turbulent relationships - e.g. threaten OD every time boyf tries to leave.
may present with dramatic plea/demand for help (‘section me’).
often a history of childhood sexual abuse.
some association with eating disorders (more bulimia than anorexia)

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150
Q

how do patients with antisocial PD tend to present?

A

rarely treated because there’s no interventions that are effective.
admission often avoided - disruptive to other patients.
forensic psych deal with them usually, and they’re often detained in secure units from court or prison.
basically presents with loads of crime! rates high in prisoners.
problems worsened by drugs/alcohol.

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151
Q

how do anxious personality disorders tend to present?

A

doesn’t normally present clinically, sometimes diagnosed in people with depression/anxiety (and is a risk factor for both)

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152
Q

what are the broad principles of managing personality disorders?

A

difficult to treat - apart from ‘dramatic’ cluster B types.

  • help them to avoid situations that cause problems (e.g. confrontation, intoxication)
  • have a clear and consistent crisis management plan
  • carefully differentiating any mood disorders/psychosis and treating them
  • written care plans, good CMHT
  • for EUPD - dialectical behavioural therapy helps decrease self-harm, cognitive analytical therapy may be helpful, as may therapeutic communities
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153
Q

explain what is meant by ‘phobic anxiety’

A

situational anxiety - restricted to a specific experience or anticipation of particular situation
can be very specific e.g. spiders or more general e.g. agoraphobia.
person tends to avoid the situations - this gives them relief but ultimately reinforces the fear so is BAD - overcoming this avoidance is key.

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154
Q

give some general symptoms of anxiety

A
  • anxious/irritable mood
  • exaggerated worries and fears
  • avoidance of feared situations
  • checking
  • seeking reassurance
  • somatic symptoms - chest tightness, shortness of breath, palpitations, ‘butterflies’, tremor, tingling of fingers (hyperventilation), aches and pains, poor sleep
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155
Q

how are phobic anxiety disorders treated?

A

key is exposure therapy - either in reality or in imagination.
CBT can help with this.
antidepressants and anxiolytics have a role.

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156
Q

what is agoraphobia?

A

most common fear - intense anxiety provoked by open/large spaces that are crowded and difficult to escape from e.g. supermarket queues
often associated with panic attacks - “panic disorder with agoraphobia”
- cognitions focus on fainting/dying or other catastrophe rather than on the actual shop/space
- can end up housebound if severe
- more common in young women, on average takes 2 yrs before help sought

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157
Q

list some symptoms of agoraphobia

A
  • situational anxiety - in shops, crowded large places
  • cognitions = thoughts of collapsing and being left helpless in public
  • avoidance of panic-provoking situations
  • panic attack symptoms
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158
Q

what is social phobia?

A

fear of other people - anticipation of a negative evaluation by them - distinguish from normal shyness, or social withdrawal due to depression/other condition.

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159
Q

what are the symptoms of social phobia? how is it managed?

A
  • situational anxiety in social gatherings
  • cognitions = being judged negatively by others
  • avoidance of social occasions
  • blushing/trembling classic
  • associated with secondary alcohol misuse (self medicating)

Rx - CBT, SSRIs can be helpful.

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160
Q

what are the symptoms of a panic attack?

A
  • severe incapacitating anxiety
  • cognitions = of dying, going mad, losing control
  • sense of impending doom
  • chest tightness
  • palpitations
  • tremor
  • tingling fingers (hyperventilation)
  • nausea
  • shortness of breath

attacks must be recurrent over at least 1 month for panic disorder diagnosis - differentiate from physical causes and from panic as part of phobia etc

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161
Q

how is panic disorder managed?

A

CBT usually very effective - helps pt understand symptoms as result of anxiety.
antidepressants might help, but initial increase in anxiety often puts patients off.

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162
Q

what is generalised anxiety disorder?

A

persistent anxiety associated with chronic uncontrollable and excessive worry - occurring more days than not for >6 months.
associated with 3+ of following on more days than not for >6 months: restlessness or feeling keyed up or on edge; being easily fatigued; difficulty concentrating or mind going blank; irritability; muscle tension; sleep disturbance.

PLUS at least 4 of:
Autonomic arousal symptoms:
- Palpitations or pounding heart.
- Accelerated heart rate.
- Sweating.
- Trembling or shaking.
- Dry mouth (not due to medication or dehydration).
Symptoms involving chest and abdomen:
- Difficulty breathing.
- Feeling of choking.
- Chest pain or discomfort.
- Nausea or abdominal distress (such as churning in stomach).
Symptoms involving mental state:
- Feeling dizzy, unsteady, faint, or light-headed.
- Feeling that objects are unreal (derealisation) or that the self is ‘not really here’ (depersonalisation).
- Feeling of losing control, ‘going crazy’, or passing out.
- Fear of dying.
General symptoms:
- Hot flushes or cold chills.
- Numbness or tingling sensations.
- Muscle tension or aches and pains.
- Restlessness and inability to relax.
- Feeling keyed up, on edge, or mentally tense.
- A sensation of a lump in the throat or difficulty in swallowing.
Other nonspecific symptoms:
- Exaggerated response to minor surprises or to being startled.
- Difficulty in concentrating or mind ‘going blank’ because -of worrying or anxiety.
- Persistent irritability.
- Difficulty in getting to sleep because of worrying.

often associated with depression.
it’s NOT - paroxysmal (panic disorder), situational (phobic), or lifelong (PD)

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163
Q

what are some risk/protective factors for GAD?

A

Risk factors
Being aged between 35 and 54.
Being divorced or separated.
Living alone or as a lone parent.

Protective factors
Being aged between 16 and 24.
Being married or cohabiting.

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164
Q

describe NICE stepped care for GAD

A

Step 1 (for all new GAD) - assessment, education, monitoring
Step 2 (no change on education and lifestyle changes) - IAPT/low intensity psychology, guided self-help, psychoeducational groups
Step 3 - CBT/applied relaxation or drug treatment (SSRI or venfalaxine)
Step 4 - psych referral if still refractory

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165
Q

what tool can be used to screen for GAD?

A

GAD 7 - like PHQ 9 but for GAD

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166
Q

what is OCD?

A

anxiety disorder in which obsessions and compulsions are prominent and persistent (can be either/or)

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167
Q

what are the diagnostic criteria for OCD?

A
  • obsessions or compulsions (or both) must be present on most days for > 2 weeks.
  • acknowledged as originating in the mind of the patient and imposed by outside persons or influences.
  • they’re repetitive and unpleasant and at least one obsession or compulsion must be present that is acknowledged as excessive or unreasonable.
  • subject tries to resist them (but if very long-standing, resistance to some obsessions or compulsions may be minimal). At least one obsession or compulsion must be present which is unsuccessfully resisted.
  • carrying out the obsessive thought or compulsive act is not in itself pleasurable.
  • the obsessions or compulsions cause distress or interfere with the subject’s social or individual functioning, usually by wasting time.
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168
Q

what aetiological factors are there for OCD?

A

Genetic predisposition
Developmental factors - abuse or neglect, social isolation, teasing or bullying may predispose.
Psychological factors - Personality characteristics maintain OCD (e.g. anankastic PD predisposes)
Stressors/triggers - common stressor is pregnancy or the postnatal period.

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169
Q

how is OCD treated?

A

mild functional impairment = IAPT for CBT ± “exposure and response prevention” (ERP) - these can be individual, group or telephone/internet based
moderate = patient choice between high intensity (>10h) CBT and ERP or SSRI. chlormipramine (TCA) alternative to SSRI.
severe = high intensity CBT/ERP and SSRI.

170
Q

what are conversion/dissociative disorders?

A

when there’s a loss of function, often a neurological deficit e.g. paralysis, that isn’t explained by organic disease, and is often connected to a clear stressor/event
e.g. athlete loses function of right leg day before a big race - patient isn’t making it up or aware that it’s psychological though

171
Q

differentiate between dissociative/conversion disorders, factitious disorder and malingering?

A

in conversion - patient not consciously putting on symptoms
factitious - patient is consciously feigning symptoms to obtain medical care
malingering - putting on symptoms for personal gain
hard to distinguish if someone is faking it! - look out for inconsistencies e.g. limps into consultation room but runs for bus

172
Q

how are conversion/dissociative disorders best managed?

A

nobody really knows but:

  • accept the reality of symps but explain they could be reversible
  • encourage gradual return to normal function
  • treat coexisting depression if present
  • refer for psychotherapy if nothing else working
173
Q

give some different types of ‘stress reaction’ or stress-related disorders

A

acute stress reaction - begins and ends within hours-days of stressor
adjustment disorder - begins less acutely, lasts several months
PTSD - delayed response to an extreme stress, key feature being re-experiencing of trauma in dreams/imagination

174
Q

what are acute stress reactions? how are they managed?

A

transient, but severe, emotional reactions following an exceptional stressor.
patient is dazed, may have amnesia/denial of event, be overactive or conversely withdrawn
Rx = remove stressor, reassure and support. short course of benzos if needed. early ‘debriefing’ (telling therapist about event asap) is now shown to be unhelpful.

175
Q

what are adjustment disorders? how are they managed?

A

reactions to a stress that are more prolonged than the acute stress reaction.
symps are 1 month post stressor, lasting for <6 months.
features = depression, anxiety, poor concentration, preoccupied with event, angry outbursts etc.
Rx - CBT/counselling, treat depression/anxiety as needed

176
Q

what is PTSD?

A

delayed response to exceptional stressors - key feature is intensely realistic, involuntary flashbacks/dreams reliving event - often triggered by reminders of trauma (even if pt is unaware of triggers)
onset can be months or years after trauma.

177
Q

what are the main symptoms/features of PTSD?

A

re-experiencing- hyperreal flashbacks/nightmares etc
avoidance/ruminating
hyperarousal or emotional numbing e.g. exaggerated startle response, irritability, sleep problems etc

178
Q

how is PTSD managed?

A

eye movement desensitisation and reprocessing (EMDR) - pt recalls event while moving eyes rapidly from side to side - unclear how it works!
trauma-focused CBT
antidepressants might help (e.g. paroxetine, mirtazapine)
manage substance abuse

179
Q

what is hypochondriacal disorder?

A

somatoform disorder in which pt is preoccupied with idea that they have a serious medical condition that they don’t have.
persistently seeks medical reassurance and investigation - but not reassured by either.
presentation usually with repeated requests for investigations to exclude disorder.

180
Q

how do you manage hypochondriacal disorder?

A

CBT and antidepressants can help - but have to be careful not to be seen as dismissing them as psychiatric

181
Q

what are somatization disorders?

A
somatic symptoms (e.g. fatigue, pain) not adequately explained by medical disease
similar to what medicine calls functional disorders.
182
Q

what are the symptoms of somatization disorder, as a psych diagnosis? how is is managed?

A

patient, nearly always woman, presents with multiple different medially unexplained symptoms that have occurred for years - ‘illness as a way of life’.
Rx - long follow up, treat associated depression/anxiety - poor prognosis

183
Q

what is factitious disorder?

A

patient consciously elaborates or makes up symptoms to gain medical care - unclear exactly how ‘conscious’ it is though.
aka Munchausen’s syndrome
also - Munchausen’s syndrome by proxy = when someone makes someone else appear to be physically/psychiatrically unwell for attention - often carer and child

184
Q

what is malingering?

A

patient elaborating/making up symptoms for fraudulent purposes (e.g. to avoid court or military conscription) - factitious disorder is a psychiatric disorder, malingering is not.

185
Q

generally speaking, what the difference between anorexia nervosa and bulimia nervosa?

A
  • people with anorexia nervosa restrict what they eat and may compulsively overexercise to maintain an excessively low body weight
  • people with bulimia nervosa have intense cravings, secretively overeat, and then try to ‘purge’ prevent weight gain (e.g. vomiting)
  • some people with mixed symptoms are diagnosed with ‘eating disorder not otherwise specified’
186
Q

give some aetiological/risk factors for eating disorders

A
  • genetic element
  • altered brain serotonin function
  • personality - anxious, obsessive, depressive traits all more common
  • childhood environment - abuse, overprotecting/controlling environment in which food/appearance overvalued, bullying related to weight
  • culture - societal values regarding weight
187
Q

list some physical symptoms of anorexia nervosa

A
cold sensitivity
GI symps - constipation, bloating
amenorrhoea
dizziness
poor sleep
188
Q

list some physical signs of anorexia nervosa

A

emaciation
cold extremities
dry skin, might be orange (hypercarotinaemia)
downy lanugo hair on back, forearms and cheeks
poorly developed/atrophic secondary sexual characteristics
bradycardia, postural hypotension, arrhythmias
peripheral oedema
proximal myopathy

189
Q

list some investigation abnormalities you might see in anorexia nervosa

A
low LH, FSH, oestradiol, T3
raised cortisol, growth hormone
hypoglycaemia
hypokalaemia, hyponatraemia, metabolic alkalosis
ECG - prolonged QT interval
hypercholesterolaemia
osteopaenia and osteoporosis
low WBC and platelets
delayed gastric emptying
acute gastric dilatation (if over-rapid refeeding)
190
Q

list clinical/presenting features of anorexia nervosa

A
  • refusal to maintain a normal body weight for age and height.
  • weight below 85% of predicted (adults = BMI < 17.5, under 18 = use BMI centile charts)
  • dieting or restrictive eating practices. Friends or family may report a change in eating behaviour.
  • rapid weight loss.
  • having a dread of gaining weight.
  • disturbance in the way weight or shape is experienced, resulting in over-evaluation of size/disproportionate worry about weight or shape.
  • denial of the problem.
  • lack of desire for intervention, or resistance to it.
  • social withdrawal; few interests.
  • enhanced weight loss by over-exercise, diuretics, laxatives and self-induced vomiting.
  • problems managing pre-existing chronic diseases which involve dietary control, such as diabetes or coeliac disease
191
Q

list some general risk factors for eating disorders

A

female - although not uncommon in men!!
adolescence/early adulthood - pubertal changes often trigger
living in Western society

192
Q

list some family history risk factors for eating disorders

A

eating disorder
depression
substance misuse / obesity - for bulimia specifically

193
Q

list some ‘premorbid experiences’ that are risk factors for eating disorders

A

adverse parenting - low contact, high expectations, arguments
sexual abuse
family dieting
critical comments about eating, weight or shape - esp familial, but also bullying from peers
pressure to be slim - familial/societal/peers

194
Q

list some premorbid characteristics that are risk factors for eating disorders

A

low self-esteem
anxiety
specific to anorexia - perfectionism
specific to bulimia - impulsivity, obesity, early menarche

195
Q

list some specific groups that are at risk of eating disorders

A

ballet dancers
models
jockeys
gymnasts

196
Q

what are the objectives of treatment in anorexia nervosa?

A
  • alter attitude to weight and body shape via psychological treatments
  • help them gain weight
  • detect and treat medical complications
197
Q

what are the principles of management in anorexia?

A
  • maintain a good therapeutic relationship - important for helping them recognise need for help
  • encourage weight gain early - breaks cycle, and overcomes problem that starvation interferes with psychological treatments
  • therapy - family therapy is first line also CBT
  • drugs - no clear role, can be used if comorbid depression
  • monitor physical condition, consider multivitamins/supplements
198
Q

in adults, what features indicate severe/high risk anorexia and should prompt you to consider urgent referral/admission?

A
  • BMI of 13-15 conveys medium risk; a BMI <13 is high risk.
  • weight loss > 0.5 kg per week
  • pulse rate: < 40bpm
  • systolic BP < 90, diastolic BP <70, postural drop >10
  • squat test: unable to get up from squatting or lying down without using arms for balance or leverage.
  • core temperature < 35°C.
  • blood tests: low potassium, sodium, magnesium or phosphate. raised urea, creatinine or transaminases. low albumin or glucose.
  • ECG: prolonged QT interval, T-wave changes, bradycardia.
199
Q

what guidelines should be used in deciding how to manage anorexia?

A

MARSIPAN guidelines

200
Q

give some general info on management of anorexia nervosa?

A

need to address weight first to allow brain to focus on psychology later - use behavioural techniques and dietician to agree an achievable rate of weight gain and meal plan.
then - for adolescents - family therapy, for everyone - CBT.
compulsory admission ± NG feeding may be required.

201
Q

what must you be aware of when initiating weight gain plan for an anorexic patient? how do you manage/avoid this?

A

refeeding syndrome - results from depletion of cardiac muscle secondary to starvation.
can lead to electrolyte imbalances (serum phosphorous, magnesium and potassium) occurring with insulin release in response to eating food - can lead to heart failure.

measure all serum electrolytes every 507 days
use a gradual refeeding programme e.g. 1200kcal/day then increase every 5 days.
monitor for tachycardia and oedema.
also use diet rich in phosphate (milk) and lower in carbs - use of high calorie supplement drinks useful here.

202
Q

list some factors associated with poor outcome in anorexia

A

long duration prior to presentation
onset in adulthood
severe weight loss
vomiting

203
Q

list some possible complications of anorexia nervosa

A
  • hypokalaemia: common, may cause fatal arrhythmias.
  • hypotension.
  • other cardiac problems including arrhythmias, mitral valve prolapse, peripheral oedema, sudden death.
  • anaemia and thrombocytopenia.
  • hypoglycaemia.
  • osteoporosis: restoring weight is the best treatment, but may never fully recover
  • constipation.
  • lack of growth in teenagers, and lack of development of secondary sexual characteristics.
  • infertility.
  • infections.
  • renal calculi
  • acute kidney injury or chronic kidney disease.
  • alcohol dependency in some patients.
  • anxiety and mood disorders.
  • social difficulties.
204
Q

what is bulimia nervosa?

A

characterised by uncontrolled eating binges - these are excessive, repetitive and often associated with self-induced vomiting or other purging behaviour.

typically, first binge was triggered by diet-induced hunger and then compensatory purges - over time this generalises to become a way to deal with emotional stress.

205
Q

what are the features in a history indicating bulimia nervosa?

A
  • regular binge eating, loss of control of eating during binges - once/twice a week for a few months
  • attempts to counteract the binges - 80% will purge (vomiting, laxatives, diuretics etc), 20% compensatory (dietary restriction and excessive exercise)
  • BMI maintained > 17.5
  • preoccupation with weight, body shape and body image. Self-evaluation is unduly based on body weight and shape.
  • preoccupation with food and diet. This is often rigid or ritualistic and deviations from a planned eating programme cause distress. The affected person therefore starts to avoid eating with others and becomes isolated.
  • regret/shame after binges
  • doesn’t meet criteria for anorexia nervosa
206
Q

what physical symptoms/signs are seen in bulimia?

A

if BMI normal, these are often rarer - but if low then similar to anorexia ones.

  • bloating and fullness.
  • lethargy.
  • heartburn and reflux.
  • abdominal pain.
  • sore throat, hoarse voice and dental problems (e.g. pitted teeth) due to vomiting
  • Russell’s sign - callouses on back of fingers from forced vomiting
  • hypokalaemia, especially if vomiting regularly
  • swollen salivary (parotid) glands
207
Q

list some risk factors for bulimia nervosa

A
  • female sex
  • parental and childhood obesity
  • family dieting.
  • FHx of eating disorders (high heritability shown).
  • Hx of severe life stresses, sexual or physical abuse.
  • parental and premorbid psychiatric disorder or substance misuse.
  • parental problems, such as high expectations, low care and overprotection, and disruptive events in childhood such as parental death and alcohol dependency.
  • early experiences of criticism regarding eating habits or body weight.
  • perceived pressure to be thin (from cultural or family sources).
  • recreational pressure (models, jockeys, ballet dancers, athletes).
  • early menarche.
  • premorbid characteristics such as perfectionism, anxiety, obsessional traits, low self-esteem, emotionally unstable personality disorder, difficulty in resolving conflict.
208
Q

how should bulimia nervosa be managed?

A
  • there’s a bulimia specific CBT
  • IPT can work
  • self-help manuals also used, NICE recommends as first line, then do ED specific CBT if that hasn’t helped
  • fluoxetine has a role - reduces binge frequency
  • advise regular vomiters not to brush teeth for at least 1 hr after vomits, to rinse mouth with water immediately after, and to avoid acidic foods where poss - ensure regular dental reviews
209
Q

list some possible complications of bulimia nervosa

A
  • haematemesis, and metabolic complications (eg, hypokalaemia)
  • dental erosions.
  • painless enlargement of the salivary glands, tetany and seizures.
  • around 10-15% go on to develop anorexia
210
Q

list the main types of sleep disorder

A

1) insomnias - too little sleep
2) hypersomnias - too much sleep
3) parasomnias - weird sleep behaviour e.g. sleep walking

sleep problems are usually secondary to psychiatric/medical disorder but could be primary diagnosis

211
Q

what is insomnia? what causes it?

A

disturbance in normal sleep patterns - usually difficulty initiating sleep.
mostly related to anxiety/depression, but also medical disease, chronic pain, substance abuse.
<10% = primary insomnia

212
Q

how do you treat insomnia?

A

advise on sleep hygiene - sleep environment, avoid caffeine, alcohol etc
stimulus control - go to bed only when sleepy, lights out straight away, get out of bed if awake for >20 mins
relaxation therapy - before bed.
hypnotics - short-acting benzodiazepines and related drugs - effective in short term but avoid long term use due to dependance!
melatonin - can be used in short term if >55yrs old.

213
Q

what causes excessive daytime sleepiness?

A

1) insufficient sleep
2) fragmented sleep
3) primary disorder - hypersomnia

214
Q

what causes hypersomnia?

A

psychiatric - depression, chronic fatigue syndrome
medical - narcolepsy, Klein-Levin syndrome, sleep apnoea, chronic disease
also - drug use (medications or recreational)

215
Q

what is narcolepsy?

A

repeated attacks of daytime somnolence leading irresistibly to sleep.
associated with cataplexy (sudden loss of tone), hypnagogic hallucinations (on falling asleep) and sleep paralysis (pt wakes but is unable to move).
autoimmue - HLA-DR2.
stimulants - amphetamine or modafinil = main treatments.

216
Q

what are parasomnias?

A

sleepwalking, sleeptalking, nightmares etc - part of normal development in childhood, sign of emotional stress in adults.

217
Q

list some types of sexual dysfunction

A

sexual desire disorders - lack of vs. excess
failure of genital response - erectile dysfunction, vaginal dryness
orgasmic dysfunction - premature ejaculation, anorgasmia
other - vaginismus, dyspareunia

218
Q

what is erectile dysfunction?

A

inability to reach erection or to sustain it long enough for intercourse
usually secondary i.e. full erection was possible at one time - primary is rare (neuro or circulation cause)

219
Q

list some causes of erectile dysfunction

A
anxiety about sexual performance
alcohol
unwanted effects of prescription medication
diabetes
vascular disease
220
Q

how is erectile dysfunction treated?

A

ideally combine psychological and physical approach
type V phsophodiesterase inhibitors e.g. sildenafil (viagra) widespread - NHS only prescribes in specialist centres/those suffering severe distress (in theory)
treat underlying cause!

221
Q

outline psychological treatments of sexual dysfunction

A

reassurance/self-help manual
sex therapy - uses behavioural methods, treats couple together, uses graded exposure to gradually rebuild sexual relationship

222
Q

what is delirium?

A

rapid onset of a global but fluctuating dysfunction of the CNS due to an underlying infectious, toxic, vascular, epileptic or metabolic cause.

223
Q

what features are required for a diagnosis of delirium?

A

impaired consciousness and attention
PLUS
perceptual disturbance (visual illusions/hallucinations etc) OR cognitive disturbane (concentration, memory, orientation, muddle speech)
PLUS
developed over short period of time and fluctuating
PLUS
evidence it may be related to physical cause

224
Q

what are the two subtypes of delirium?

A

hypoactive - withdrawn, quiet, sleepy behaviour

hyperactive - restless, agitated and aggressive behaviour

225
Q

what are some common features of delirium?

A

mood and affect fluctuate rapidly - often worse at night (sundowning)
irritability, perplexity, apathy, depression
poorly systematised, transient delusions, often persecutory ± ideas of reference
disturbance of sleep/wake cyce

226
Q

who is at high risk of delirium and thus should be screened for it on admission to care homes/hospital?

A
  • people age >65yrs
  • people with diffuse brain disease e.g. dementia, Parkinson’s
  • people with a current hip fracture
  • severely ill

also - men, frailty/immobility, prev ep of delirium, sensory impairment

227
Q

give some causes/precipitants of delirium/acute confusional state

A

nutritional - B1, B12 or folate deficiency
intracranial - trauma, CVA, haemorrhage, epilepsy, infection
extracranial infections - UTI, pneumonia, septicaemia
- iatrogenic - sepsis secondary to chemo, sedatives, surgery (anaesthetics, analgesics, blood loss)
- alcohol - intoxication/withdrawal
- endocrine - hyper/hypothyroidism, hyper/hypoglycaemia
- metabolic - hypoxia, renal/hepatic/other system failure

228
Q

give some differentials for delirium

A
  • dementia (hard to distinguish!)
  • esp dementia with Lewy bodies
  • psychiatric conditions e.g. mania, depression, late-onset schizohrenia
  • normal response to major stress, severe pain etc
  • dissociative disorders
229
Q

how can you distinguish between delirium and dementia clinically?

A

deterioration = rapid vs slow
course = fluctuating vs slowly progressive
consciousness = clouded vs alert
thought content = vivid, complex and muddles vs impoverished
hallucinations = very common, usually visual vs in about 1/3, auditory or visual

230
Q

what investigations should be ordered for someone presenting with acute confusion?

A

bloods - FBC, ESR/CRP, U&Es, glucose, TFT, LFT, folate/B12, syphilis serology
MSU and urinalysis
CXR if poss infection
CT/MRI if poss intracranial cause

231
Q

what measures can help to prevent delirium?

A

maximising orientation - treat sensory impairment, clear signs, clocks and calendars, position near window
prevent causes of delirium - minimise polypharmacy, avoid constipation/dehydration, avoid infection (e.g. catheters)
- promote wellbeing - encourage mobilisation, good pain control, healthy diet, sleep hygiene, social interaction and visits

232
Q

how do you manage someone presenting with delirium?

A
  • TREAT CAUSE
  • lorazepam (short-acting benzo) or short term antipsychotic (haloperidol)
  • beware hypotensive and anticholinergic side effects might precipitate falls/exacerbate confusion
233
Q

list some drugs that can commonly cause delirium

A
TCAs
benzodiazepines, other sedatives
digoxin
diuretics
lithium
steroids
opiates

alcohol intoxication/withdrawal/DTs
benzodiazepine withdrawal

234
Q

list some medical conditions that can lead to delirium

A
hypoxia e.g. post-op
infection esp UTI, chest sepsis
organ failure (heart, liver, kidneys)
hypoglycaemia
dehydration
constipation
burns
major trauma
pain
epilepsy
head injury
SOL
encephalitis
235
Q

what are the organic disorders?

A

psychiatric disorders with organic/physical cause e.g.
organic brain syndromes = dementia, delirium, amnesic syndrome
organic delusional disorders = SLE
organic mood disorder = MS
organic anxiety disorders = hyperthyroidism
organic personality disorders = head injury

236
Q

what is amnesic syndrome? what are the features?

A

goes alongside dementia and delirium as an organic disorder that affects memory.
features:
- selective loss of recent memory
- confabulation (unconscious fabrication of recent events to cover gaps in memory)
- time disorientation
- attention and immediate recall intact
- long-term memory and other faculties intact

237
Q

what causes amnesic syndrome?

A
it's really rare!!
Korsakoff's - alcohol withdrawal.
herpes simplex encephalitis
severe hypoxia
head injury
238
Q

define dementia

A

acquired, progressive, usually irreversible global deterioration of higher cortical function in clear consciousness

239
Q

what are the diagnostic criteria for dementia (not type-specific)?

A
multiple cognitive deficits (e.g. memory, orientation, language, comprehension, reasoning, judgement)
PLUS
resulting impairment in ADLs
PLUS
clear consciousness
240
Q

what other symptoms, beyond those core to the diagnostic criteria, are common in dementia?

A

behavioural problems - apathy, aggression, wandering, restlessness etc
depression/anxiety
psychotic symptoms (in 1/3rd) - persecutory delusions (aggravated by forgetfulness e.g. someone is breaking into my house and moving my keys, that’s why I can’t find them), visual and auditory hallucinations
sleep problems e.g. insomnia, daytime drowsiness, confusion between day and night

241
Q

what are the different types of dementia?

A

Alzheimer’s disease
Vascular dementia (often mixed with alzheimer’s)
Lewy body
Frontotemporal

242
Q

explain the macro- and micro-scopic changes that occur in the brain in Alzheimer’s

A

macro = brain is shrunken, increased sulcal widening, enlarged ventricles
micro = neuronal loss, presence of neurofibrillary tangles and amyloid plaques - these plaques are made from A-beta, which is cleaved from the amyloid precursor protein (APP).
amyloid cascade hypothesis says Alzheimer’s is due to imbalance of too much brain A-beta production and too little A-beta clearance.

243
Q

explain what we currently know about the genetics of alzheimer’s disease

A

mutations in the APP gene and presenilin 1 and presenilin 2 increase risk of Alzheimer’s via impact on amyloid cascade - these account for most familial (early onset) Alzheimers.

late-onset Alzheimer’s is multifactorial and polygenic, but Apolipoprotein E gene has big role.

244
Q

what neurochemical changes have taken place in Alzheimer’s disease?

A

deficits in acetylcholine, noradrenaline, serotonin and somatostatin

245
Q

how does Alzheimer’s disease typically present?

A
gradual memory loss, especially short term.
dysphasia/dyspraxia
behavioural changes e.g. wandering
might get psychotic symptoms
apathy

it’s gradually progressive, 5-8yrs survival

246
Q

how does vascular dementia present?

A

more patchy cognitive impairment than Alzheimer’s
focal neurological symptoms/signs appear in ‘stepwise’ deterioration - following mini vascular events
early gait disturbance
personality changes, labile mood
early urinary symptoms
preserved insight

also - hx of vascular disease elsewhere or of vascular risk factors

247
Q

how does Lewy body dementia present?

A

fluctuating cognition and alertness
vivid hallucinations
spontaneous Parkinsonism

condition worsened by antipsychotics - do NOT prescribe!!

248
Q

how does frontotemporal dementia present?

A
younger age of onset (<70yrs)
early personality changes
relative intellectual sparing
stereotyped behaviours
early loss of insight
expressive dysphasia
early primitive reflexes
249
Q

explain the pathophysiology of vascular dementia

A

most have a mixed picture of this + Alzheimer’s
at least 1 area of cortical infarction - from past TIAs/strokes
often have vascular risk factors (although these increase risk of Alzheimer’s too!)

250
Q

explain the pathophysiology of Lewy body dementia

A

presence of Lewy bodies and neurites in basal ganglia and cerebral cortex
associated with Parkinson’s disease.

251
Q

explain the pathophysiology of frontotemporal dementia

A

degeneration focused on frontal and anterior temporal lobes.

252
Q

describe general principles of managing dementias

A
  • thorough assessment to exclude treatable causes, beware superimposed delirium.
  • comorbid depression can complication
  • careful risk and needs assessment
  • social support - home care, day centres, respite etc
  • environment - familial, calm, well lit, visible clocks/diaries/calendars
  • aromatherapy, music/art therapy etc
253
Q

what blood tests should be ordered for someone as part of the assessment of dementia? what are you looking for on each?

A

FBC - macrocytosis (B12 deficiency), anaemia, infection
U&Es + Calcium - hypercalcaemia, hyponatraemia, renal disease
LFTs - alcoholic liver disease
TFTs - hypothyroidism
B12 and folate levels - deficiencies
ESR/ANA - if suspicious of vasculitis
syphilis serology - becoming more common!!
HIV test

bloods should be done in primary care, all patients referred to memory clinic should have a CT

254
Q

what tests (not bloods) should be ordered as part of dementia assessment, what are you looking for?

A

brain CT/MRI - for any treatable cause really! any other investigations are only if specific suspicions:
CXR - infection causing delirium, lung Ca with brain mets
EEG - ?
LP - normal pressure hydrocephalus
cerebral blood flow studies
genetic testing - if early onset

255
Q

give some info on medico-legal considerations for dementia

A
  • caution about risks of driving - DVLA need to be informed
  • advanced care directives/appointing lasting power of attorney whilst still capacitous can be helpful
  • use mental capacity act as appropriate
  • consider any need for DoLS
256
Q

give some risk factors for Alzheimer’s disease

A
genetic - Apoplipoprotein E, APP/PSEN1/PSEN2 genes, Down's syndrome
female
increasing age
homocysteinaemia
obesity/diabetes in middle age
head injury
latent herpes simplex infection
hx of depression
aluminium exposure

PROTECTIVE - high educational attainment, physically and mentally active lifestyle

257
Q

explain drug treatment of alzheimer’s disease

A

cholinesterase inhibitors e.g. donepezil - for mild/moderate Alzheimer’s - acts to give a 6 month ish delay in cognitive decline.
memantine (NMDA glutamate receptor antagonist) - for moderate/severe

258
Q

what kind of treatment is helpful in vascular dementia?

A

no drug treatments but modification of vascular risk factors important - if mixed vascular/AD might benefit from donepezil.

259
Q

explain drug treatment of Lewy body dementia

A

cholinesterase inhibitors can be helpful

DON’T GIVE ANTIPSYCHOTICS

260
Q

what is separation anxiety? how is it managed?

A

excessive anxiety when faced with separation from parents/main caregivers - clings to person, avoids being separated from them, can involve sleep disturbance.
often arises at times of stress.
Rx - explain/reassure to family, remove stressors, ensure parents aren’t reinforcing by displaying anxiety when leaving.

261
Q

what is somatoform disorder in children?

A

kids easily get somatic symptoms when under stress - present with headaches/non-specific abdo pain etc - exclude medical condition, other psychiatric disorders, investigate any precipitating/perpetuating factors (unhappy at home etc)

262
Q

give some clinical features of conduct disorder at different points throughout childhood

A

pre-school - aggressive behaviour, poor concentration
mid-childhood - lying, stealing, disruptive/oppositional behaviour, bullying
adolescence - stealing, truancy, promiscuity, substance misuse, vandalism, reckless behaviour

263
Q

what is conduct disorder?

A

occurring mostly in boys, it features disturbed and antisocial conduct beyond the range of misbehaving normally observed for the age group.
not normally diagnosed till >7yo but might see features ahead of that
aka oppositional defiant disorder.

264
Q

give some factors associated with conduct disorder

A
family factors:
- parental personality disorder
- paternal alcoholism
- parental disputes and violence
- harsh, inconsistent parenting
- being in care in early life
- large family size
- social factors
- inner cities
- deprivation and overcrowding
individual factors:
- epilepsy
- brain damage
- specific reading disorder
265
Q

describe the management approach used in conduct disorder

A

no clear treatment!
family focused interventions - improve home environment, ‘parental training’ to reduce conflict
praise and reward for positive behaviour
clear rules etc
anger management
structured outlets for energy/behaviour e.g. youth clubs

266
Q

what is ADHD?

A

attention deficit hyperactivity disorder - problem must be both persistent and extreme.
often comorbid with conduct disorder, anxiety, depression, developmental disorders.

267
Q

what factors contribute to causing ADHD?

A
  • genetic contribution - FHx of ADHD, depression, learning difficulties, alcoholism, dissocial personality disorder.
  • some neurodevelopmental effect - some studies shown EEG/brain imaging anomalies
  • social deprivation
  • maternal smoking and alcohol intake
268
Q

list the core features of ADHD

A

1) hyperactivity
2) poor attention and concentration
3) impulsivity

present for >6 months
evidence of this impaired functioning in 2+ settings (i.e. complete nightmare at home but well behaved in school)
onset before 9yo, usually by 5yo.

269
Q

list some other features of ADHD beyond the core three

A
distractibility
poor at planning and organising tasks
learning difficulties
clumsiness
low self-esteem
socially disinihibited
unpopular with other children
non-localising neurological signs
50% will also have conduct disorder
270
Q

explain the management options for ADHD

A
  • support and psychoeducation for child and family
  • special needs education, especially if learning difficulties
  • firmly adhere to behavioural principles (reward the good, discourage bad behaviour)
  • drugs - stimulants e.g. methylphenidate (Ritalin), atomoxetine (SEs- liver toxicity, suicidality) - recommended as part of comprehensive treatment programme if symptoms severe
  • restriction of E numbers etc not recommended
271
Q

what is Ritalin? explain its role in ADHD management and how it works. what are the side effects?

A

methylphenidate
acts to increase dopamine in synapse
SEs - addiction, poor appetite, headaches
need to monitor growth
encourage ‘drug holiday’ e.g. don’t take Ritalin over half-term (away from school) - idea is to stop dependance

272
Q

what is ASD?

A

autism spectrum disorder - failure to develop normal communication, especially social and emotional communication.
delayed/restricted/unusual use of language.
appear oblivious to non-verbal cues and emotional expressions, difficulty interacting with others.
degree of learning disability can vary.

273
Q

give some features associated with autism, beyond the ‘core’ features

A

inappropriate attachments to unusual objects,
insistence on sameness,
a restricted range of interests and activities,
stereotyped behaviours (rocking, twirling, etc.), hyper/hyporeactivity to sensory input,
unpredictable outbursts of screaming or laughter

also associated:
learning disability
coordination difficulties
epilepsy (in 25%)
hyperactivity (40%)
anxiety
sleep disturbance
hypotonia
274
Q

what factors are associated with developing autism?

A
  • strong genetic link
  • no confirmed environmental risk factors
  • possible abnormal brain growth, or excess serotonin - unclear really
  • psychologists believe it’s failure to develop ‘theory of mind’
275
Q

how should ASD be managed?

A

intensive psychological/behavioural treatment - this focuses on breaking down various skills and teaching them to the child
psychoeducation and support for family
provision of appropriate education/accommodation

276
Q

what is asperger’s syndrome?

A

mild end of the ASD spectrum really - abnormal social communication, repetitive, isolated behaviours - but language not delayed

277
Q

what is Fragile X syndrome? what are the features?

A
strongly associated with learning disabilities.
usually male - if female, have a lot less learning/behavioural problems
X-linked dominant condition
features:
large head and ears
long face, high-arched palate
flat feet
lax joints
post puberty - large testes
poor eye contact
abnormal speech
hypersensitivity to touch/auditory/visual stimuli
hand flapping
hand biting
15-33% have autism
278
Q

define learning disability

A

IQ < 70
impairment across a wide range of functions
onset <18 yrs old

distinguish from:
lower than average intelligence but IQ >70
specific developmental disorders e.g. autism
intellectual impairment secondary to adult organic syndrome

279
Q

how are learning disabilities classified?

A

mild = IQ 69-50 (relatively independent, some basic literacy, can do semi-skilled work, normal social skills, normally no clear cause)
moderate = 49-35 (needs some help with self-care, limited communication/literacy, can work if unskilled and supervised, some impairment of social skills, cause can be found)
severe = < 35
profound = < 20
(limited self-care ability, basic/none communication, no reading/writing, few social skills, often comorbid physical problems, clear cause usually found)

280
Q

give some causes of LDs

A

genetic:
– chromosomal (e.g. Down, Klinefelter or Turner’s syn-
drome);
– X-linked: Fragile X, Lesch–Nyhan syndrome;
– autosomal dominant: tuberose sclerosis, neurofibromatosis;
– autosomal recessive: usually metabolic disorders (e.g.
phenylketonuria).
antenatal:
- infective (e.g. toxoplasma, rubella and cytomegalovirus);
- hypoxic, toxic or related to maternal disease.
perinatal: prematurity, hypoxia, intracerebral bleed
postnatal: infection, injury, malnutrition, hormonal, meta- bolic, toxic, epileptic.

281
Q

what psychiatric disorders are at increased prevalence in people with LDs? how do they present in these patients?

A

1) behavioural disturbance: increases w/ increasing severity of LD (e.g. purposeless or self-injurious behaviour, aggression or inappropriate sexual behaviour)
2) depression: diagnosis rests more on motor and behavioural changes (reduced sleep, retardation, tearfulness, etc.) than verbal expressions of distress
3) anxiety disorders (incl OCD and phobias)
4) dissociative symptoms: amnesia, episodes of unconsciousness, etc
5) schizophrenia: presents with simple and repetitive hallucinations and unelaborated, usually persecutory, delusions
6) mania: presents as overactive/irritable behaviour.

282
Q

explain principles of managing someone with a LD

A
  • most will live at home, some require supported accommodation, day centres, respite care for families
  • specific LD teams within CMHTs
  • usually a handful of inpatient beds for assessment and treatment of behavioural/psych disorders
283
Q

list some features of Down’s syndrome

A
moderate - severe LD
physical features:
- down-slanting palpebral fissures
- epicanthic folds
- small mouth w/large protruding tongue
- flat nasal bridge
- flattened occiput
- small hands with single palmar crease
- hypotonia
medical probs:
- cardiac septal defects
- GI obstruction
- atlantoaxial instability
- susceptibility to infection
284
Q

what is an illusion?

A

a misrepresentation of a real stimulus - seeing a person in the corner when in reality it’s a hat stand

285
Q

what is a hallucination?

A

sensory perceptions occurring in absence of an external physical stimulus - any sensory modality really

286
Q

what are the different types of auditory hallucination?

A

thoughts spoken aloud - either at same time, or just after
second-person hallucinations - voice talking directly to the person or giving them instructions (command hallucinations) e.g. “you are being followed; run away”
third-person hallucinations - voices heard discussing/commenting or giving a running commentary

287
Q

what are hypnagogic/hypnopompic hallucinations?

A

hallucinations occurring when going to (hypnagogic) or waking up (hypnopompic) from sleep

288
Q

what is a pseudohallucination?

A

one in which person is aware stimulus is in the mind e.g. “I can hear my late wife’s voice talking to me in my head”

289
Q

what is an overvalued idea?

A

false or exaggerated belief sustained beyond logic or reason, but with less rigidity than a delusion, also often being less patently unbelievable

290
Q

what is anhedonia?

A

inability to derive pleasure from normal activities

291
Q

what is thought withdrawal?

A

thought disorder in which patient believes thoughts are being taken out of their mind

292
Q

what is thought block?

A

thought disorder in which patient describes their thoughts suddenly stopping - not being taken out though (withdrawal)
will see them just stop speaking in the middle of a sentence

293
Q

what is thought insertion?

A

patient believes foreign thoughts are being placed into their mind

294
Q

what is thought broadcast?

A

thoughts are being transmitted to everyone around them - as though on a radio

295
Q

what is thought echo?

A

form of auditory hallucination in which patient hears own thoughts spoken aloud at same time/just after their’s

296
Q

define thought alienation

A

belief that one’s own thoughts are under the control of an outside agency - often described as thought insertion/withdrawal/echo
aka thought interference

297
Q

what is akithisia?

A

movement disorder characterized by a feeling of inner restlessness and inability to stay still, usually the legs are most prominently affected - fidget, rock back and forth, pace etc. can drive them to suicide.
usually due to typical antipsychotics

298
Q

what are delusions?

A

unshakeable false beliefs - will stand by them even in face of counter-argument - out of keeping with patient’s cultural background
may be mood congruent (depression, mania) or incongruent (schizophrenia - will tell you about horrific beliefs in very calm manner)

299
Q

what is delusional perception?

A

when patient misconstrues a real stimulus as indicating something false e.g. “the traffic light turned green and that’s when I knew I was the King of Tonga”

300
Q

what are nihilistic delusions?

A

believe that they are already dead/rotting

characteristic of psychotic depression

301
Q

what are grandiose delusions?

A

delusions of grandeur - e.g. believe they are the Queen, or they know the cure for cancer etc etc

302
Q

what are persecutory delusions?

A

most common type - theme of being followed/spied on/conspired against etc - very paranoid/suspicious

303
Q

what are ideas and delusions of reference?

A

coincidental/innocuous events interpreted to have great personal meaning e.g. TV news broadcast making direct reference to patient.
delusions of reference = bizarre and unfeasible interpretations e.g. dog’s bark carries coded message

304
Q

what is flight of ideas?

A

rapid skipping from one thought to distantly related ideas, relation often being as tentative as rhyming etc rather than actual connection between then concepts

305
Q

what is a reflex hallucination?

A

a sensation experienced in response to something e.g. when you write, I can hear your pen pressing on my heart

306
Q

what is an extracampine hallucination?

A

one in which patient says they can see/hear/whatever something beyond the actual sensory field e.g. can see behind them, can hear people talking about them in australia

307
Q

what is concrete thinking?

A

lack of abstract thinking, very literal thinking based on physical world - normal in childhood, occurs in adults with organic brain disease and schizophrenia

308
Q

what is loosening of association?

A

lack of logical association between succeeding thoughts - gives rise to incoherent speech.
it’s impossible to follow patients train of thought - knight’s move thinking/derailment.

309
Q

what is circumstantiality?

A

irrelevant wandering in conversation, talking at great length around the point but will eventually get there

310
Q

what is perseveration?

A

repetition of a word, theme or action beyond point at which is was relevant and appropriate
e.g. will answer first question correctly but then just repeat that answer

311
Q

what is confabulation?

A

giving a false account of what’s happened to fill a gap in their memory

312
Q

what is somatic passivity?

A

delusional belief that one is a passive recipient of bodily sensations from an external agency

313
Q

what is “made act/feeling/thoughts”?

A

type of passivity - person feels they are being forced to do/feel/think something or that their thoughts/feeling/actions are being imposed on them

314
Q

what is catatonia?

A
state of excited motor activity in absence of mood disorder or neurological disease.
includes:
waxy flexibility
echolalia
echopraxia
logoclonia
negativism
palilalia
verbigeration
315
Q

what is waxy flexibility?

A

patient’s limbs feel like wax/lead pipe when moved - remain in position they are left in
found rarely in catatonic schizophrenia and structural brain disease

316
Q

what is echolalia?

A

automatic repetition of words heard

317
Q

what is echopraxia?

A

automatic repetition by the patient of movements made by examiner

318
Q

what is logoclonia?

A

repetition of last syllable of a word

319
Q

what is negativism?

A

motiveless resistance to movement

320
Q

what is palilalia?

A

repetition of a word over and over again with increasing frequency

321
Q

what is verbigeration?

A

repetition of one/several sentences or strings of fragmented words, often in a rather monotonous tone.

322
Q

what is psyhomotor retardation?

A

slowing of thoughts and/or movements, to variable degree.

occurs in depression, also seen in Parkinson’s and response to psychotropic drugs

323
Q

what is pressure of speech?

A

very rapid rate of delivery, with a wealth of unusual associations (e.g. rhymes and puns) and often wanders off point of original convo.
highly suggestive of mania.

324
Q

what is incongruity of affect?

A

emotional responses which seem grossly out of tune with situation or subject being discussed
e.g. appear really cheerful whilst saying their dog died

325
Q

what is blunting of affect?

A

objective absence of normal emotional responses, without evidence of depression or psychomotor retardation

basically they don’t seem to show any kind of emotional response to anything

326
Q

what is belle indifference?

A

lack of concern and/or feeling of indifference about a disability or symptom - often linked with conversion

327
Q

what is depersonalisation?

A

feeling of some change in the self, associated with sense of detachment from one’s own body.
feel unreal, actions seems mechanical, patient feels like apathetic spectator of his own activities

328
Q

what is derealisation?

A

sense of one’s surroundings lack reality, often appearing dull, grey and lifeless

329
Q

what is dissociation?

A

experience where a person may feel disconnected from himself and/or his surroundings - kind of umbrella term that includes depersonalisation/derealisation

330
Q

what is conversion?

A

unconscious mechanism of symptom formation - translation of a psychological conflict into somatic symptoms of motor/sensory nature

331
Q

what are ‘mannerisms’?

A

bizarre elaborations of normal activities e.g. twirling hair when speaking in public - on their own, not indicative of mental illness

332
Q

what is a stereotyped behaviour?

A

uniform, repetitive non goal-directed actions

333
Q

what is an obsession?

A

recurrent, persistent thought/image/impulse that enters consciousness unbidden, is recognised as being one’s own and often remains despite efforts to resist

334
Q

what is a compulsion?

A

repetitive, apparently purposeful behaviour performed in a stereotyped way accompanied by a subjective sense that it must be carried out, despite recognition of its senselessness and actual resistance by patient

335
Q

when may a doctor treat a patient without consent under ‘common law’?

A

in a life-threatening emergency - doctor is able to do what the public would consider reasonable in that situation, and where failing to act would be considered unreasonable.
Mental Capacity Act / Mental Health Act tend to be used instead though.

336
Q

what are the five key principles of the Mental Capacity Act (2005)?

A

1) capacity assumed until proven otherwise
2) person must be helped to make decisions before capacity is judged to be absent e.g. use of interpreters
3) pts are entitled to make unwise decisions - it’s the process by which decision is made, not the decision itself, that determines capacity
4) decisions made for people who lack capacity must be in their best interests
5) decisions must be least restrictive option in terms of human rights

337
Q

what four things must a patient be able to do in order to demonstrate capacity?

A

1) understand the information
2) retain the information
3) appropriately weigh up the information
4) communicate a decision back to you

failure on any one of the four things = lack of capacity (i.e. don’t have to fail all 4)

338
Q

what are IMCAs?

A

Independent Mental Capacity Advocates - someone who advocates for those who lack capacity

339
Q

what is “lasting power of attorney”?

A

a person may nominate someone authorised to make decisions for them if they ever lose capacity

340
Q

what are advance decisions/directives?

A

these are written statements specifying interventions a person would NOT want if they lost capacity

341
Q

what are DoLS?

A

deprivation of liberty safeguards - designed to ensure that patients lacking capacity as not subject to undue restraints of their liberties

342
Q

what are the key aspects regarding when it is appropriate to invoke the MHA 1983/2007?

A
  • behaviour must result from a known/suspected ‘mental disorder’ - disruptive behaviour, intoxication, drug abuse not themselves grounds for detention
  • person must be at acute, significant risk of self-harm, self-neglect or harming others
  • must have refused voluntary treatment
  • other options must have been considered and deemed inappropriate
  • there must be appropriate treatment available

note - only allowed to use detention to treat mental disorder, can refuse medical treatment unless direct result of mental disorder e.g. refeeding in anorexia

343
Q

who is involved in detaining a patient?

A

application made by 1 of 2 people:

1) an AMHP (e.g. senior social worker)
2) two medical recommendations - one a Responsible Clinician (RC) - usually psychiatrist, must be Section 12 approved - and the other a GP or another Section 12 doctor usually

344
Q

what is Section 2 of the MHA used for? how long does it last? who applies for it? right of appeal?

A

admission for assessment - can also give drug treatment compulsorily.
applied for by - AMHP + medical recommendation from RC and another doctor.
duration - 28 days
right of appeal - in first 14 days to Mental Health Review Tribunal (MHRT)

345
Q

what is Section 3 of the MHA used for? how long does it last? who applies for it? right of appeal?

A

admission for treatment - of established mental disorder.
applied for by - as for Section 2 - cannot proceed if nearest relative objects.
duration - 6 months, then renew/review another 6 months, then annually.
right of appeal - once per 6 months to hospital managers. at 3 months all treatment must be reviewed by a SOAD (second opinion approved doctor - usually independent psychiatrist e.g. from neighbouring region).

346
Q

what is Section 4 of the MHA used for? how long does it last? who applies for it? right of appeal?

A

for compulsory admission in emergency when second medical recommendation can’t be obtained.
applied for by - AMHP or nearest relative. recommendation by any doctor, usually GP.
duration - 72 hours in which full MHA assessment for section 2 or 3 must be completed.
right of appeal - none.

347
Q

what is Section 5(2) of the MHA used for? how long does it last? who applies for it? right of appeal?

A

used for emergency detention of an inpatient, preventing patient from leaving hospital. not allowed to enforce treatment. can’t be used to hold in A&E or OPD.
applied for by - Dr in charge of patients care or their nominee (consultant or junior dr, never FY1/2).
duration - 72hrs, in which full MHA assessment must be done.
right of appeal - none

348
Q

what is Section 5(4) of the MHA used for? how long does it last? who applies for it? right of appeal?

A

used by psych nurses to detain psych inpatient for 6 hours if no psychiatrist to hand.
equivalent of 5(2).

349
Q

what is Section 135 of the MHA used for?

A

allows police to enter private property and take person to nominated ‘place of safety’ for 72 hrs.
can only be used once.

350
Q

what is Section 136 of the MHA used for?

A

allows police to detain someone from a public health to place of safety for 72hrs.

351
Q

what are Sections 35-38, 47 and 48 of MHA used for?

A

35-37 used by a Court to send offenders to hospital for psych assessment/treatment
47 and 48 allow transfer of prisoner or other detainee to hospital.

352
Q

explain what CTOs are

A

community treatment orders - allow compulsory treatment in community if patient is currently detained under Section 3.
designed for patients who cycle between relapse and readmission, often due to stopping taking meds after discharge.
usually dictates they must reside at particular address, take meds/allow IM treatment/CMHT visits and attend appointments - if not can be recalled to hospital without new MHA assessment.

353
Q

can ECT be given compulsorily using MHA Sections?

A

generally no, unless necessary to prevent death or deterioration.
second opinion must be obtained and Section 58 completed.
in emergency it can be given using Section 62 - but this must be life-saving.

354
Q

what is psychoeducation?

A

provision of info to help patient/family understand and cope with illness - may be individual or in groups.

355
Q

what is counselling?

A

loosely defined - people are helped to overcome/cope with life’s problems.
counsellor serves as a support, facilitating emotional expression.

356
Q

what is supportive psychotherapy?

A

a formalised version of what all friends and medical professionals do for someone - listening, accepting, encouraging.
‘therapeutic relationship’

357
Q

what is problem-solving therapy?

A

structured mix of counselling and CBT - helps pt learn to deal actively with life problems.

358
Q

what is psychodynamic psychotherapy?

A

time-intensive, lengthy process (can last years) - not that widely used these days.
aims to help patient gain insight and understanding of themselves and their unconscious processes.
deals with transference and defence mechanisms etc.
mainly used for relationship difficulties and some personality disorders.

359
Q

what are the main underlying principles of psychodynamic psychotherapy?

A
  • emotional and interpersonal problems result from unconscious processes, driven by psychological mechanisms and internal representations developed early in life
  • therapist looks at patterns of prev relationships and makes interpretations about what patient says
  • pt expected to gain insight into their emotions and behaviours
360
Q

what are the underlying principles of behavioural therapies?

A

idea that adaptive behaviours can be learned/maladaptive behaviours unlearned.
involves exposure (graded or flooding) and then working on how to deal with inappropriate response, eventually desensitising them.
patient is set homework tasks etc.

361
Q

what are the underlying principles of cognitive therapies?

A

focuses on correcting unhelpful ways of thinking to improve mood/reduce anxiety.
therapist asks for detailed description of problem, focussing on the thoughts (cognitions) patient has when experiencing problem.
therapist explains role of cognitions in perpetuating problem.
patient taught to become aware of and challenge unhelpful thoughts and replace them with others.

362
Q

what is CBT?

A

combines principles of cognitive and behavioural therapy.
identifies unhelpful thoughts, uses exercises and homework to practice replacing them with positive ones.
can involve behavioural exercises confronting specific problems/situations, but will focus on cognitions during these more than straight behavioural would.

really good, can be delivered telephone/online, self-help manuals, groups, individual, intensive.
great for depression, panic disorder, phobias, OCD, there’s modified forms for eating disorders, schizophrenia, trauma.

363
Q

what is cognitive analytical therapy?

A

combines cognitive approach and psychoanalytic concepts.

used in depression.

364
Q

what is interpersonal therapy?

A

uses cognitive, behavioural and psychodynamic concepts and techniques - focuses on pt’s relationships and problems arising from them.
occasionally used in depression, bulimia

365
Q

what is dialectical behavioural therapy?

A

developed specifically for people with EUPD - combines psychoeducation with behavioural skills training, creating strong therapeutic relationship.

366
Q

what is eye movement desensitisation and reprocessing (EMDR)?

A

used in PTSD
people recall and discuss past trauma whilst doing rapid eye movements - meant to help them ‘reprocess’ and avoid flashbacks - controversia as to how it works

367
Q

what is family therapy?

A

based on ‘systemic’ theory that problem is located in family ‘system’ rather than in the (child) patient - first line in eating disorders in adolescents, but useful for all sorts in CAMHS

368
Q

list the major classes of antidepressants and examples

A
SSRIs - fluoxetine, citalopram, sertraline, paroxetine
TCAs - amitriptyline
MAOIs - phenelzine
SNRIs - venlafazine, duloxetine
Other - mirtazapine
369
Q

list some mood stabilising drugs, what are they used for?

A
lithium
valproate
lamotrigine
carbamazepine
also olanzapine and quetiapine
used for bipolar disorder
370
Q

list some major causes of non-compliance in psychiatry

A
  • reluctance to accept need for treatment
  • lack of belief in drug efficacy
  • concern about drug side effect, incl worry about becoming ‘addicted’
  • stigma
  • forgetfulness
  • expense
371
Q

give some ways you can improve compliance with medications

A
  • establish good therapeutic relationship
  • explore their views about their illness and medications, correct misunderstandings
  • share info on evidence for and against the drug, and of not taking the drug
  • consider IM preparations where appropriate
372
Q

describe the timeline of antidepressants beginning to be effective and when you should stop them

A

most will take 4-6 weeks to take full effect - don’t change meds/fiddle with doses till after this
meds should be continued for >6 months after remission to prevent relapse
should stay on for 1-2 years if recurrent depression.

373
Q

how do SSRIs work? how should they be used?

A

selectively inhibit synaptic serotonin reuptake transporters, increasing synaptic serotonin concentration

start them on full dose OD, should see effect in 7-14 days (side effects can appear first so warn patient)
always withdraw slowly

374
Q

what are the potential side effects of SSRIs? also what are the discontinuation symptoms?

A

GI upset - nausea, abdo discomfort, diarrhoea
insomnia, agitation - mostly when first started
sexual dysfunction (lack of libido/anorgasmia) common in women.
may increase risk of upper GI bleed and hyponatraemia
discontinuation - insomnia, nausea, dizziness, agitation (withdraw very gradually over a few weeks)

375
Q

what cautions/contra-indications should you consider for SSRIs?

A

may increase seizures in epilepsy

can induce serotonin syndrome if given with serotonergic drugs (e.g. MAOIs, lithium, St John’s wort)

376
Q

how do SNRIs work? how should they be used?

A

selective serotonin and noradrenaline reuptake inhibitors
venlafaxine and duloxetine.

block serotonin and noradrenaline reuptake but don’t block cholinergic receptors.

venlafaxine is slight more effective that SSRIs so can be used if SSRI non-response. given twice daily, although long acting OD version available.

377
Q

what are the potential side effects of SNRIs? anything to be aware of when using them?

A

basically the same as SSRIs but can be worse
at high dose, can get HTN so monitor BP.
avoid MAOIs.

378
Q

how does mirtazapine work? how should it be used/what are the side effects to be aware of?

A

it’s a ‘noradrenaline and serotonin specific antidepressant’ - increases activity in noradrenaline/serotonin systems by blocking negative feedback of noradrenaline on presynaptic alpha-2-receptors. this also enhances serotonin release.
used as second-line treatment, or in combo with SSRIs for third line.
SEs - sedating, weight gain.

379
Q

how do TCAs work? how should they be used?

A

mostly used for people intolerance of SSRIs, can be helpful in people with chronic pain.
given at night or in divided doses. takes 1-2 weeks to feel effects as for SSRIs but reduction of anxiety and sedation occurs quickly.
to minimise initial side effects, start at low dose and increase over 10 days.

inhibit presynaptic noradrenaline and serotonin transporters.

380
Q

give some side effects of TCAs, according to which receptor blockade is responsible for them

A

muscarinic cholinergic receptor blockade = dry mouth, urinary retention, constipation, blurred vision, glaucoma, tachycardia, delirium, sexual dysfunction
alpha-1-adrenergic = postural hypotension, drowsiness, sexual dysfunction
histamine H1 = drowsiness, weight fain
other = arrhythmias, seizures

drowsiness = caution about driving/heavy machinery operation

381
Q

what cautions/contra-indications should you be aware of when prescribing TCAs?

A

avoid in glaucoma, prostatism, recent MI, heart failure, prophyria.
caution in epilepsy due to increased seizure frequency.
avoid combining with MAOIs.

dangerous in overdose - tachyarrhythmias, seizures, coma, death.

382
Q

how do MAOIs work? how should they be used?

A

monoamine oxidase inhibitors are third-line antidepressants - not as effective + more toxicity than others!
main indication is atypical/treatment resistant depression.

work by preventing breakdown of monoamines in presynaptic terminals by enzyme monoamine oxidase inhibitors, increasing transmitter availability.

if going to use - need a 2 week washout from TCAs or 5 weeks for SSRIs! prescribe in divided doses, educate pt about dietary restrictions.

383
Q

what are the potential side effects of MAOIs?

A

postural hypotension, insomnia, ankle oedema, dry mouth, dizziness, agitation, headache.
in overdose - hypertension, delirium, coma, death.

384
Q

what are the important cautions/contraindications for MAOIs?

A

MAO also metabolises tyramine, so have to avoid tyramine containing food - cheese, red wine, broad beans, pickled herrings, game, Marmite - can cause hypertensive crisis (headache, palpitations, fever, convulsions, coma)
can interact with - opiates, insulin, cold remedies, antiepileptics, SSRIs, TCAs.
avoid in heart/liver failure or porphyria.

385
Q

how does lithium work?

A

unclear mode of action, probably works on secondary messenger systems via phosphatidylinositol and glycogen synthetase kinase 3 (GSK3) pathways

386
Q

how is lithium used?

A

for relapse prevention in bipolar disorder, it works to prevent both manic and depressive relapses.
given as lithium carbonate.
need to give for >18 months for benefit to be clear.
can be effective in acute mania, although antipsychotics faster, and as adjunct in depression.

387
Q

what are the potential side effects of lithium at therapeutic levels and in overdose?

A

at therapeutic levels (0.5-1.0mmol/L) - fine tremor, metallic taste, dry mouth, thirst, mild polyuria, nausea, weight gain, hypothyroidism (in 20% women). renal impairment if prolonged use.
>1.5mmol/L toxic symptoms - coarse tremor, agitation, twitching, thirst, polyuria.
>2.5mmol/L - polyuric renal failure, seizures, coma, death.

toxic levels can occur from mild dehydration or low-salt diets.

388
Q

what do you have to do when starting/maintaining a patient on lithium?

A

discuss commitment and potential dangers.
measure U&Es, kidney function, TFTs, maybe an ECG.
measure lithium levels weekly to begin, then 3 monthly once stable.
titrate dose to maintain levels at 0.5-1.0mmol/L
test TFTs and renal function every 6 months.
if withdrawing - very gradual to avoid rebound mania.

389
Q

what cautions/contraindications are there to be aware of for lithium?

A

avoid if adherence likely to be variable/short-lived.
avoid in renal failure, pregnancy.
don’t combine with diuretics, ACE inhibitors, high-dose antipsychotics.
caution with NSAIDs.

390
Q

give some info on sodium valproate as used as a mood stabiliser

A

used when lithium not tolerated/contraindicated, or sometimes in combo with lithium.
blocks sodium channels and increases GABA turnover (in epilepsy)
start low and titrate up every few days to reach maintenance dose (no specific therapeutic range, decide based on adverse effects).
SEs - sedation, tiredness, tremor, GI upset.
teratogenic!!

391
Q

give some info on carbamazepine as used as a mood stabiliser

A

if lithium and sodium valproate hasn’t worked.
bocks sodium channels.
start low, titrate up. measure plasma levels if signs of toxicity (ataxia, confusion, blurred vision). check WCC after a week.
SEs - if erythematous rash/leucopenia then stop the drug. others incl. nausea, dizziness, drowsiness and hyponatraemia.

392
Q

give some info on lamotrigine as used as a mood stabiliser

A

prevents depressive episodes in bipolar, rarely used as monotherapy.
blocks sodium and calcium channels, decreases glutamate release.
very slow titration needed, every two weeks upped a tiny amount.
SEs - if rash, stop drug. also nausea, headache, tremor, dizziness.
cautions - be careful if combining with sodium valproate/carbamazepine.

393
Q

what are ‘anxiolytics’ also known as?

A

hypnotics/sedatives - drugs used to calm anxiety.

main ones are benzodiazepines - although only for short-term use (long term Rx = SSRIs/TCAs)

394
Q

how do benzodiazepines work?

A

potentiate inhibitory transmission via the benzodiazepine-binding sit of the GABA(a) receptor.

used to relieve acute anxiety/panic/insomnia. also for DTs/alcohol withdrawal, and to augment antipsychotics used for sedation in acute psychosis.

395
Q

give examples of short, intermediate and long acting benzodiazepines

A

short - midazolam, temazepam
intermediate - lorazepam, clonazepam
long - chlordiazepoxide, diazepam

396
Q

give some SEs of benzodiazepines

A

drowsiness, ‘hangover effects’, headache, nausea, ataxia, dysarthria, delirium.
shouldn’t be prescribed for 4+ weeks - dependency.
withdrawal symps - rebound anxiety, insomnia, visual and auditory hallucinations and seizures - manage by switching from short acting to diazepam and tapering dose down slowly.

397
Q

list the typical vs atypical antipsychotics

A
typical = haloperidol, chlorpomazine
atypical = risperidone, olanzapine, clozapine

atypical means an antipsychotic that doesn’t produce extrapyramidal side effects at clinical doses.

398
Q

generally speaking, how do antipsychotic drugs work?

A

blocking the D2 dopamine receptors - reverses the excess dopamine activity in mesolimbic system thought to cause psychotic symptoms.
usually effective in 70% of patients in treating positive psychotic symptoms within 6 weeks (clozapine is only one with greater efficacy). onset of action is gradual over those 6 weeks.

399
Q

apart from extrapyramidal symptoms, what side effects to typical/conventional antipsychotics cause?

A

prolactin elevation.
anticholinergic side effects
sedation
weight gain

400
Q

which antipsychotics cause prolactin elevation?

A

conventional:
haloperidol +++
chlorpromazine ++

atypical:
risperidone ++

401
Q

which antipsychotics cause anticholinergic side effects?what are these?

A

e.g. dry mouth, blurred vision, constipation, urinary retention.

conventional:
haloperidol +
chlorpromazine ++

atypical:
clozapine +

402
Q

which antipsychotics cause sedation as a side effect?

A

conventional:
haloperidol +
chlorpromazine ++

atypical:
olanzapine +++
clozapine +++

403
Q

which antipsychotics cause weight gain?

A

conventional:
chlorpromazine +

atypical:
risperidone ++
olanzapine +++
clozapine +++

404
Q

what are ‘extrapyramidal side effects’ (EPS)? what are the main four types?

A

motor abnormalities due to dopaminergic receptor blockade in basal ganglia by conventional antipsychotics (and to some extent, risperidone)

1) acute dystonia
2) Parkinsonism
3) akathisia
4) tardic dyskinesia

405
Q

what is acute dystonia (an EPS)?

A

painful contractions of muscles in neck, jaw or eyes - particularly occurs in young men given high doses.
onset is hours-days.
Rx with IM/IV anticholinergic agents e.g. benztropine, procyclidine

406
Q

what is Parkinsonism?

A

reduced facial movements (mask like), shuffling gait, stiffness, tremor.
common in early weeks of treatment.
Rx - reduce dose, temporarily add anticholinergic.
can be mistaken for depression/negative schizophrenia symptoms.

407
Q

what is akathisia?

A

feeling of restlessness, need to walk around.
very unpleasant.
occurs in first months of treatment.
mistaken for psychotic behaviour.
Rx - lower dose, temporarily add propranolol

408
Q

what is tardive dyskinesia?

A

uncontrollable grimacing movements of face, tongue or upper body.
occurs in 5% of patients taking long-term antipsychotics each year.
no treatment, can be irreversible.

409
Q

what are the side effects of risperidone?

A

causes extrapyramidal side effects, prolactin and weight gain

410
Q

what are the side effects of olanzapine?

A

sedation and weight gain - metabolic syndrome/diabetes risk

411
Q

what are the side effects of clozapine?

A

sedation and weight gain, some anticholinergic side effects (dry mouth, blurred vision, constipation, urinary retention etc) - metabolic syndrome/diabetes risk

412
Q

what serious complication can clozapine cause that you would detect via blood test?

A

agranulocytosis - they have basically 0 white blood cells so massive infection risk - this is why clozapine is reserved for when patients are unresponsive to everything else!!
weekly FBCs to monitor WCC - pt must be registered with and engaged with monitoring service - drug has to be stopped if WCC falls - makes it expensive!

other SEs - weight gain, metabolic syndrome, hypersalivation, sedation. seizures if high dose.

413
Q

give some features of lithium toxicity

A

vision loss, D&V, hypokalaemia, ataxia, dysarthria, coma, polyuria/polydipsia, hypo/hyperthermia

414
Q

how do you treat lithium toxicity?

A

ABCDEs, fluids, haemodialysis if needed

415
Q

what is neuroleptic malignant syndrome? how does it present? how is it managed?

A

uncommon, life-threatening neuroleptic (antipsychotic) induced disorder
symps - fever, muscle rigidity, delirium and autonomic instability. markedly raised serum creatinine kinase.
Rx -
stop antipsychotic
IV fluids to prevent renal failure
dantrolene* may be useful in selected cases
bromocriptine, dopamine agonist, may also be used

416
Q

what is serotonin syndrome? signs and symptoms?

A

caused by medications that increase serotonergic activity e.g. SSRIs or when drugs used in combinations.
signs = tachycardia, HTN, hyperthermia, agitation, ocular clonus, dilated pupils, tremor, akathisia, hyperreflexia, muscle rigidity, bilateral Babinski signs, dry mucous membranes, flushed skin, increased bowe sounds

417
Q

how do you treat serotonin syndrome?

A
  • stop serotonergic agents
  • benzodiazepines
  • cardiac monitoring, may need ITU
  • IV fluids/O2
  • cooling for hyperthermia
  • if more severe - serotonin antagonists e.g. chlorpromazine/crypoheptadine
418
Q

what are the three key features of a patient’s “disorder” that need to be true for you to use the MHA?

A

must be a:

  • mental disorder
  • of a nature or degree of severity requiring inpatient admission
  • and causing a risk to themselves, others or their physical health
419
Q

who may release a patient from a section?

A
  • nearest relative
  • responsible clinician (usually the Sect. 12 approved consultant)
  • mental health act review tribunal
  • hospital managers
420
Q

list some social interventions that might be put in place for someone with a psychiatric disorder

A
  • benefits
  • care packages
  • cultural support
  • help with housing
  • help with meaningful activity e.g. volunteer work
  • safeguarding
  • person-centered care
  • access/support with education
  • social integration