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BRS 2 > psychiatry > Flashcards

psychiatry Flashcards

1
Q

what is a hallucination?

A

hearing/seeing something without any stimulus

i.e. if just at night, it it just an illusion

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2
Q

what is an adjustment reaction?

A

states of subjective distress and emotional disturbance, usually interferes with social functioning and performance

arises in the period of adaptation to a significant life change or a stressful life event

manifestations vary, include:

  • depressed mood
  • anxiety or worry (or mixture of these)
  • feeling of inability to cope, plan ahead, or continue in the present situation
  • some degree of disability in the performance of daily routine
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3
Q

what is an organic delusional disorder?

A

persistent or recurrent delusions dominate clinical picture

may be accompanied by hallucinations

some features suggestive of schizophrenia may be present (e.g. bizarre hallucinations or thought disorder)

organic = physical cause (e.g. start after a stroke)

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4
Q

what is the prevalence of post-stroke psychosis?

A

delusions: 4.67% (95% CI 2.30% to 7.79%)
hallucinations: 5.05% (95% CI 1.84% to 9.65%).

more common in right hemisphere strokes (5:1)

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5
Q

what are some common delusional themes in post-stroke psychosis?

A

persecutory

jealousy

environment

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6
Q

what is the interaction between physical and mental illness?

A

30% of those with long term medical conditions have a mental health problem

46% of those with mental health problems will have a long term condition

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7
Q

what are some some long term physical conditions associated with a definite causal link in increased risk of mental illness symptoms?

A

cardiovascular diseases - 3x risk of depression and anxiety

diabetes - 2x risk of depression

COPD - 10x risk of panic disorder

musculoskeletal disorders - 2x risk of depression

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8
Q

what are some some long term physical conditions that are associated with a discrete increased risk of mental illness symptoms (no definite causal link)?

A

thyrotoxicosis - anxiety, mania

thyroid deficiency - depression, dementia

Cushing’s disease - (excess cortisol) depression
- prednisolone, dexamethasone may lead to mania

infections (syphilis, HIV) - psychosis

cancer - depression

Parkinson’s disease - depression, anxiety, dementia

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9
Q

why may a long term physical condition cause mental illness symptoms?

A

increased social isolation

loss of quality of life

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10
Q

how may COPD increase risk of a panic disorder?

A

many people pant to get enough oxygen into their system

increased CO2 production - become alkalotic

this changes calcium metabolism

leads to anxiety

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11
Q

why may people with chronic mental illness be at greater risk of physical illness?

A

diet and exercise (association with poverty)

smoking, alcohol, drugs

medication side effects

generally die 20 years younger than general population

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12
Q

what factors may affect timely diagnosis of physical disorders in people with mental illness?

A

illness behaviour - help seeking (lack of recognition, more tolerance of symptoms)

diagnostic overshadowing - physical disorder is often mistaken as part of the mental illness

stigma - towards person, within health service

lack of resources - lack of funding

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13
Q

what is the Montreal Cognitive Assessment?

A

30 point assessment

visuospatial skills (drawing)

simple numerical manipulation

recognition

recall

orientation

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14
Q

what is delirium?

A

organic cerebral syndrome characterized by concurrent disturbances of:

  • consciousness and attention
  • perception
  • thinking
  • memory
  • psychomotor behaviour
  • emotion
  • sleep-wake schedule

duration is variable

degree of severity ranges from mild to very severe

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15
Q

what is the prevalence of delirium?

A

20% acute hospital patients >65 on admission

20% more develop delirium after admission

overall prevalence 30% on wards, 80% in intensive care

50% undetected, “hypoactive”

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16
Q

what are the practical implications of delirium?

A

psychiatric manifestation of a physical illness - impairs treatment

delays discharge

increases mortality if untreated

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17
Q

what causes delirium?

A

infection (urine, pneumonia, cellulitis, wound etc.)

change in environment (ITU, HDU, ward)

medication (opiates, anticholinergics, steroids)

alcohol withdrawal

surgery

pain

liver/ renal impairment

hypoxia

hyponatraemia

stroke

encephalitis

constipation

urine retention

dehydration

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18
Q

what are the predisposing factors for delirium?

A

advanced age

dementia (often undetected)

impaired activities of daily living

immobility

sensory impairment

urinary catheterization

malnutrition

alcohol

depression

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19
Q

how is delirium managed?

A

anticipate

modify risk factors if possible

early diagnosis

treat the causes

good nursing
- single room, well lit, familiar staff/family (in an ideal world)

medication (do not give)

wait

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20
Q

what are some potential examples of stigma in an acute case of delirium?

A

delay diagnosing underlying condition (not seen on every ward round)

may be interviewed by police if aggressive (meaningless, punitive)

detainment under Mental Health Act (unnecessary - Mental Capacity Act appropriate)

reluctance of care homes to take sufferers

friction between acute hospital staff and liaison team

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21
Q

what is stigma?

A

refers to challenges faced by people with mental illness related to knowledge, attitudes, and behaviour of people they meet

poor understanding of mental health

negative attitude

social exclusion

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22
Q

what are the practical effects of stigma?

A

leads to discrimination

increases disability caused by mental illness

creates disadvantage with personal relationships, education, and work

75% people with mental illness experience stigma

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23
Q

what are the 3 types of stigma in mental health?

A

intrapersonal stigma

  • direct effect on the individual
  • internalised discrimination
  • compounded by direct effects of illness

interpersonal stigma
- friends, family, colleagues

structural stigma

  • poor resources and funding
  • access to physical health care
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24
Q

what is psychosis?

A

descriptive term: difficulty perceiving and interpreting reality

can be caused by many disorders

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25
Q

what are some psychotic disorders?

A

schizoaffective disorder

depression with psychotic features

substance related

due to other medical condition

schizophrenia

delusional disorder

bipolar I

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26
Q

what are the two types of positive symptom of psychosis?

A

hallucinations - perceptions in absence of a stimulus

delusions - fixed, false beliefs, out of keeping with social/cultural background

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27
Q

what are the types of hallucination?

A

auditory

voices commenting on you, talking to each other

visual

somatic/tactile

olfactory (rare)

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28
Q

what are some examples of delusions?

A

persecutory

control

reference

mind reading

grandiosity

religious

guilt/sin

somatic

thought broadcasting

thought insertion

thought withdrawal

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29
Q

what are the 4 types of negative symptom of psychosis?

A

alogia - poverty of speech

anhedonia, asociality

avolition/apathy

affective flattening

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30
Q

what are the characteristics of alogia?

A

paucity of speech, little content

slow to respond

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31
Q

what are the characteristics of anhedonia/asociality?

A

few close friends

few hobbies/interests

impaired social functioning

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32
Q

what are the characteristics of avolition/apathy?

A

poor self-care

lack of persistence at work/education

lack of motivation

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33
Q

what are the characteristics of affective flattening?

A

unchanging facial expressions

few expressive gestures

poor eye contact

lack of vocal intonations

inappropriate affect

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34
Q

what are the two types of disorganisation symptom?

A

bizarre behaviour

thought disorder

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35
Q

what are the characteristics of bizarre behaviour?

A

bizarre social behaviour

bizarre clothing/appearance

aggression/agitation

repetitive/stereotyped behaviours

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36
Q

what are the characteristics of a thought disorder?

A

derailment

circumstantial speech

pressured speech

distractibility

incoherent/illogical speech

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37
Q

what is the epidemiology of psychosis in terms of onset?

A

can occur at any age

peak incidence in adolescence/early 20s

peak later in women

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38
Q

what is the epidemiology of psychosis in terms of course?

A

often chronic, episodic

very variable

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39
Q

what is the epidemiology of psychosis in terms of morbidity?

A

substantial, both from disorder itself and increased risk of common health problems e.g. heart disease

significant impact on education, employment and functioning

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40
Q

what is the epidemiology of psychosis in terms of mortality?

A

substantial

all-cause mortality 2.5x higher, ~15 years life expectancy lost

hgh risk of suicide in schizophrenia – 28% of excess mortality

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41
Q

what is important when taking a psychiatric history?

A

history of presenting concern

past psychiatric history

background history (family, personal, social)

past medical history and medicines

corroborative history

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42
Q

what is important when taking a psychiatric history of a presenting concern?

A

patient’s description of the presenting problem

  • nature
  • severity
  • onset
  • course
  • worsening factors
  • treatment received

circumstances leading to arrival to hospital

why now?

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43
Q

what is important when taking past psychiatric history?

A

any known diagnosis?

any treatment?

known to a community team?

any previous admissions to hospital?

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44
Q

what is important when taking past family history?

A

age of parents, siblings, relationship with them

atmosphere at home

mental disorder in the family, abuse, alcohol/drugs misuse, suicide

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45
Q

what is important when taking personal history?

A

mother’s pregnancy and birth

early development, separation, childhood illness

educational and occupational history

intimate relationships

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46
Q

what is important when taking social history?

A

living arrangements

financial issues

alcohol and illicit drug use

forensic history

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47
Q

what is important when taking past medical history and medicines?

A

regular medications?

compliance?

over the counter medications?

interactions?

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48
Q

what is important when taking corroborative history?

A

informants: relatives, friends, authority

confidentiality

consent

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49
Q

what is noted during a mental state examination?

A

appearance and behaviour

speech

mood

thoughts

perceptions

cognition

insight

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50
Q

what is noted about appearance and behaviour during a mental state examination?

A

general appearance

facial expression

posture

movements

social behaviour

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51
Q

what is noted about general appearance during a mental state examination?

A

neglect

  • alcoholism
  • drug addiction
  • dementia
  • depression
  • schizophrenia

weight loss

  • anorexia nervosa
  • depression
  • cancer
  • hyperthyroidism
  • financial issues/homelessness

bizarre or inappropriate clothing

poor personal hygiene

injuries/wounds - self inflicted? harm to self?

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52
Q

what is noted about facial expression during a mental state examination?

A

depressive, anxious

“wooden” Parkinsonian

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53
Q

what is noted about posture during a mental state examination?

A

hunched shoulders, downcast head and eyes – depressive

sitting upright, head erect, hands gripping the chair – anxious

overactive, restless – manic

inactive, slow - depressive

immobile, mute – stupor

tremors, tics, choreiform movements, dystonia, tardive dyskinesia
mannerisms, stereotypies

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54
Q

what is noted about social behaviour during a mental state examination?

A

disinhibited, overfamiliar

withdrawn, preoccupied

signs of impending violence: raised voice, clenching fists, pointed fingers, intrusion into personal space

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55
Q

what is noted about speech during a mental state examination?

A

quantity

rate

spontaneity

volume

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56
Q

what is noted about quantity of speech during a mental state examination?

A

less, more, mutism

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57
Q

what is noted about rate of speech during a mental state examination?

A

slow, fast, pressure of speech (keep talking)

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58
Q

what is noted about spontaneity of speech during a mental state examination?

A

latency

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59
Q

what is noted about volume of speech during a mental state examination?

A

quiet, loud

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60
Q

what are the two types of mood that are assessed during a mental state examination?

A

subjective

objective

  • predominant mood
  • constancy
  • congruity
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61
Q

what is noted about objective constancy during a mental state examination?

A

emotional lability/incontinence

reduced reactivity/blunting/flattening
irritability

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62
Q

what is noted about objective congruity during a mental state examination?

A

cheerful while describing sad events etc.

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63
Q

what is noted about thoughts during a mental state examination?

A

stream

form

content

  • preoccupations
  • morbid thoughts, suicidality
  • delusions, overvalued ideas
  • obsessional symptoms
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64
Q

what is noted about stream of thoughts during a mental state examination?

A

pressure, poverty, blocking

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65
Q

what is noted about form of thoughts during a mental state examination?

A

flight of ideas, loosening of associations, perseveration

disorganised thoughts may lead to disorganised speech (spontaneous speech that slips off track, difficulty holding train of thought)

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66
Q

what is noted about delusions and overvalued ideas (content of thoughts) during a mental state examination?

A

primary – occurs suddenly

secondary – arises from previous abnormal idea/experience (hallucination/mood/delusion)

delusional mood/perception/memory
shared delusion = folie à deux

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67
Q

how may delusional thoughts manifest?

A

paranoid

of reference

grandiose/ expansive

of guilt/ worthlessness

hypochondriacal

of jealousy

sexual/ amorous

religious

of control

concerning the possession of thought (insertion, withdrawal, broadcast)

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68
Q

what is noted about obsessional symptoms (content of thoughts) during a mental state examination?

A

obsessional thoughts: dirt and contamination, aggressive actions, orderliness, disease, sex, religion

compulsions: checking, cleaning, counting, dressing rituals

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69
Q

what is noted about perceptions during a mental state examination?

A

illusions (misperception of a real external stimulus)

hallucinations (perception in the absence of external stimulus)

distortions

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70
Q

what kind of hallucinations may be noted during a mental state exam?

A

1) true perception + 2) coming from outside the head
pseudohallucination = 1) OR 2)

hypnagogic (while falling asleep), hypnopompic (while waking up)

auditory – second person, third person

visual – Charles Bonnet syndrome (visual hallucinations caused by brain’s adjustment to significant vision loss)

olfactory

gustatory

tactile, of deep sensation

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71
Q

what is noted about cognition during a mental state examination?

A

consciousness

orientation

attention and concentration

memory

language functioning

visuospatial functioning

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72
Q

what is noted about insight during a mental state examination?

A

awareness of oneself as presenting phenomena that other people consider abnormal

recognition that these phenomena are abnormal

acceptance that these abnormal phenomena are caused by mental illness

awareness that treatment is required

acceptance of the specific treatment recommendations

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73
Q

what is the prodromal stage of psychosis?

A

early stage prior to a full-blown episode of psychosis

symptoms of this phase are often subtle - develop gradually and can be mistaken as “normal” behaviour (particularly in adolescents/young adults)

can include things like sleep schedule, social isolation etc.

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74
Q

what is a pseudohallucination?

A

not originating externally

i.e. “voices in my head” as opposed to “the people I see and hear talking about me”

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75
Q

what are the pharmacological options for treatment of psychosis?

A

antipsychotic medications (often mainstay of treatment)

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76
Q

what are the psychological options for treatment of psychosis?

A

CBT for psychosis

newer therapies like avatar therapy

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77
Q

what are the social support options for treatment of psychosis?

A

supportive environments, structures and routines

housing, benefits

support with budgeting /employment

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78
Q

typical vs

A

s

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79
Q

what are the differentials for psychosis?

A

schizophrenia

(mania, depression, schizoaffective disorder, puerperal psychosis, other psychotic disorders)

personality disorders

dementia

  • Alzheimer’s
  • vascular
  • Parkinson’s/Lewy body
  • Huntington’s

encephalopathy, acquired brain injury, stroke etc.

delirium

drugs (e.g. LSD)

metabolic (calcium, magnesium, B12 disorders)

endocrine (thyroid - Cushing’s, Addison’s)

infections (encephalitis, syphilis etc.)

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80
Q

what neurotransmitter system is most implicated in the mechanism of antipsychotics?

A

dopamine

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81
Q

what is the usual drug action on dopamine receptors to improve psychotic symptoms?

A

excessive dopamine can cause hallucinations etc.

antagonists lower dopaminergic neurotransmission

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82
Q

what are some extrapyramidal side effects caused by antipsychotics?

A

tardive dyskinesia

  • causes uncontrollable stiff, jerky movements of face and body
  • impaired buccal/lingual movements

akinesia
- loss of ability to move muscles voluntarily

akathisia

  • inner restlessness - feel compelled to move but does little to alleviate
  • can lead to overt restless movement
  • legs most commonly affected

dystonia

  • increased motor tone leads to sustained abnormal posture
  • can occur shortly after taking dopamine antagonist
  • can be acute, painful, even fatal (laryngeal dystonia)
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83
Q

what is a typical vs. atypical antipsychotic?

A

typical antipsychotics commonly cause extrapyramidal side effects at therapeutic doses (not based on drug mechanism)

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84
Q

how are the side effects of typical antipsychotics managed?

A

avoid in first place (atypical antipsychotics usually first line)

change medication

anticholinergic medications can help (e.g. procyclidine)

patients should be informed about risks

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85
Q

what are some potential side effects of antipsychotics on the CNS?

A

EPSEs (extra pyramidal side effects)

sedation

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86
Q

what are some potential haematological side effects of antipsychotics?

A

agranulocytosis

neutropenia

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87
Q

what are some potential metabolic side effects of antipsychotics?

A

increased appetite

weight gain

diabetes

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88
Q

what are some potential gastrointestinal side effects of antipsychotics?

A

constipation

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89
Q

what are some potential pituitary side effects of antipsychotics?

A

increased prolactin (release is generally suppressed by dopamine)

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90
Q

what are some potential cardiac side effects of antipsychotics?

A

dysrhythmia

long QTc

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91
Q

what is the long term management plan for psychosis?

A

some people after an episode of psychosis recover completely and remain well, majority follow an episodic course with periods of wellness and relapses

community follow-up

managing antipsychotic side effects (e.g. weight, diabetes - manage comorbidities in other specialties)

health promotion: reducing risk factors e.g. smoking, diet

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92
Q

what is a mood or affective disorder?

A

fundamental disturbance is a change in affect or
mood to depression (with or without associated anxiety) or to elation

usually accompanied by a change in the
overall level of activity

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93
Q

what causes mood disorder episodes?

A

mood disorders tend to be recurrent

onset of individual episodes often related to stressful events

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94
Q

what is the prevalence of major depressive disorder (MDD)?

A

10-20%

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95
Q

what is the prevalence of bipolar disorder (I and II), both lifetime and 12-month?

A

bipolar I - 1%

bipolar II - 1.1%

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96
Q

how has age of onset changed in major depressive disorder (MDD)?

A

increasing rate of MDD with earlier age of onset

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97
Q

what is the gender distribution of bipolar I disorder?

A

equal

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98
Q

what is the gender distribution of bipolar II disorder?

A

more women than men

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99
Q

what is the gender distribution of major depressive disorder (MDD)?

A

twice as many women than men

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100
Q

what percentage of mental/substance abuse disorders do MDD and bipolar disorders account for?

A

MDD - 40%

bipolar - 7%

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101
Q

what percentage of disability adjusted life years (DALYs) do mental and substance abuse disorders account for?

A

7%

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102
Q

what is low mood/depression characterised by?

A

circles of thought
- negative automatic thinking e.g. what’s the point?

behaviour

  • rumination
  • isolation (passive, stay at home)

physiological symptoms
- exhaustion/low energy

feelings

  • low, flat
  • irritability, agitation
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103
Q

what are the DSM-5 criteria for depressive episodes?

A

sustained, severe lowering in mood for at least 2 weeks

PLUS at least 4 from:

  • sleep alterations (insomnia or hypersomnia)
  • appetite alterations (increased or decreased)
  • diminished interest, anhedonia
  • decreased concentration
  • low energy/exhaustion
  • guilt
  • psychomotor changes (agitation or retardation)
  • suicidal thoughts
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104
Q

what is the basis of a longitudinal diagnosis of major depressive disorder (MDD)?

A

diagnosis of a major depressive episode by DSM-5 criteria

no past manic or hypomanic episodes

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105
Q

what are the 3 DSM-5 subtypes of major depressive disorder (MDD)?

A

atypical features

melancholic features

psychotic features

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106
Q

what are the features of the atypical subtype of major depressive disorder (MDD)?

A

mainly increased sleep and appetite

heightened mood reactivity

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107
Q

what are the features of the melancholic subtype of major depressive disorder (MDD)?

A

no mood reactivity

marked psychomotor retardation

anhedonia

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108
Q

what are the features of the psychotic subtype of major depressive disorder (MDD)?

A

presence of delusions or hallucinations

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109
Q

what are the 3 triads of depression?

A

core symptoms

biological symptoms

psychological symptoms

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110
Q

what are the 3 core symptoms of depression?

A

low mood

anergia

anhedonia

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111
Q

what are the 3 biological symptoms of depression?

A

sleep

libido

appetite

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112
Q

what are the 3 psychological symptoms of depression?

A

the world

oneself

the future

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113
Q

what are the behaviours associated with a typical cycle of low mood (unipolar/bipolar depression)?

A

rumination

isolation (passive, stay at home)

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114
Q

what are the thoughts associated with a typical cycle of low mood (unipolar/bipolar depression)?

A

circles of thought - negative automatic thinking e.g. what’s the point?

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115
Q

what are the physiological symptoms associated with a typical cycle of low mood (unipolar/bipolar depression)?

A

exhaustion/low energy

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116
Q

what are the feelings associated with a typical cycle of low mood (unipolar/bipolar depression)?

A

low, flat

irritability, agitation

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117
Q

what are the behaviours associated with a typical cycle of high mood (mania)?

A

impulsivity

increased activity

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118
Q

what are the thoughts associated with a typical cycle of high mood (mania)?

A

grandiose, self related thinking

e.g. “I can do anything, I’m the best”

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119
Q

what are the physiological symptoms associated with a typical cycle of high mood (mania)?

A

increased energy

racing sensation (related to behaviours, thoughts)

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120
Q

what are the feelings associated with a typical cycle of high mood (mania)?

A

refreshing - euphoria, elation, excitement

tips over into more aggressive feelings - agitation, irritability, confusion

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121
Q

what are the DSM-5 criteria for manic episodes?

A

euphoric or irritable mood

PLUS 3 or more from

  • decreased need for sleep with increased energy
  • distractibility
  • grandiosity or inflated self-esteem
  • flight of ideas or racing thoughts
  • increased talkativeness or pressured speech
  • increased goal-directed activities or psychomotor agitation
  • impulsive behaviour (sexual impulsivity, spending sprees)
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122
Q

what is the basis of a diagnosis of a type I bipolar disorder?

A

manic symptoms according to DSM-5 for at least 1 week with notable functional impairment (i.e. manic episode)

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123
Q

what is the basis of a diagnosis of a hypomanic episode?

A

manic symptoms according to DSM-5 for at least 4 days but without notable functional impairment

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124
Q

what is the basis of a diagnosis of a type II bipolar disorder?

A

manic symptoms according to DSM-5 for at least 4 days but without notable functional impairment (i.e. hypomanic episode)

no manic episodes in history (only hypomanic)

at least 1 major depressive episode

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125
Q

what is the basis of a diagnosis of an unspecified bipolar disorder?

A

manic symptoms occur for fewer than 4 days

or other specific thresholds are not met for manic or hypomanic episodes

bipolar disorder can manifest with many different patterns (different frequencies, amplitudes, distribution of manic vs. depressive episodes)

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126
Q

what caveats are given for a diagnosis of a hypomanic episode (i.e. manic episode is diagnosed instead)?

A

presence of psychotic features (e.g. hallucinations/delusions) - these features involve functional impairment by definition

hospitalisation - even if manic symptoms last fewer than 4 days

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127
Q

what is the most consistent clinical feature for diagnosing mood disorders?

A

psychomotor changes

mood can be variable in these conditions - e.g. MDD can be without sad mood and mania can be without euphoria

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128
Q

what is the diagnosis if manic or hypomanic episodes are caused by antidepressants?

A

bipolar disorder

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129
Q

what is cyclothymia?

A

significant mood swings

do not reach the extreme levels of mania or depression

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130
Q

how does mood in bipolar I disorder change with respect to mania and depression?

A

first episode is usually depressive

severe mood swings to extremes of mania and depression

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131
Q

how does mood in bipolar II disorder change with respect to mania and depression?

A

severe mood swings

does not reach extremes of mania

reaches extremes of depression

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132
Q

how does bipolar disorder change over time?

A

people largely autonomous in between episodes (50-60% relapse within 1 year after recovering from a mood episode)

long term (prospective study over 12 years)
- just over half the time symptom free
- about 1/3 of the time in depressive episodes
(varies depending on individual)

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133
Q

how does anxiety interact with bipolar disorder?

A

anxiety prevalent amongst bipolar individuals

worse prognosis and outcomes

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134
Q

why were bipolar and unipolar disorder defined as separate entities in DSM-III?

A

age of onset
- bipolar had earlier onset (19yrs vs. late 20s)

episode duration
- shorter depressive episodes in bipolar (<3 months) compared to unipolar (6-12 months)

course
- more frequent episodes in bipolar than unipolar (rapid cycling - 4 or more per year)

genetic specificity
- manic episodes found in FHx of people with manic episodes but not in FHx of people with unipolar depression

treatment

  • unipolar depression - antidepressants
  • mania - neuroleptics, lithium
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135
Q

why are bipolar and unipolar disorders more difficult to separate than they were in DSM-III?

A

age of onset
- MDD commonly diagnosed in children (onset below mean of late 20s)

episode duration and course
- brief depressive episodes that occur multiple times yearly are diagnosed in MDD - if MDD and bipolar disorders were further apart this would be a rare occurrence

genetic specificity
- depressive episodes (without mania) in FHx of bipolar individuals and vice versa

treatment
- overlaps (neuroleptics and lithium)effective in mania, unipolar and bipolar depression

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136
Q

how does heritability differ between bipolar and unipolar mood disorders?

A

bipolar has higher heritability

depression is about half as heritable as bipolar

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137
Q

how does insight differ between bipolar and unipolar mood disorders?

A

often preserved in depression but impaired in mania

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138
Q

how does insight present in bipolar mood disorders?

A

about half of patients with severe mania and most patients with hypomania deny having symptoms despite them being observable

insight has a U-shaped curve in relation to severity (i.e. most impaired in hypomania and severe mania, but more preserved in moderate states)

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139
Q

what mood disorder diagnosis can easily be missed (and what is the likely misdiagnosis)?

A

lack of insight in mania/hypomania may cause misreporting of bipolar disorders

patient may end up with an MDD diagnosis despite a history of mania

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140
Q

how can misdiagnosis of bipolar disorders as MDD due to lack of insight be avoided?

A

collateral history (friends, family)

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141
Q

what is a problematic consequence of misdiagnosing bipolar disorder as MDD?

A

treatment issues - i.e. choose to treat with antidepressants (standard for depressive episode without mania)

antidepressants appear to be mostly ineffective in acute bipolar depression and
prophylaxis

cause acute manic/hypomanic episodes

worsen long-term course of bipolar illness (especially those with a rapid-cycling course)

in rapid-cycling cases - appear to lead to more mood episodes, (including
depressive states) over time

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142
Q

what are the attention biases in depression?

A

biases in maintaining/shifting attention

difficulties for depressed people to disengage from negative material

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143
Q

one study showed prolonged maintenance of attention over negative pictures - what does this demonstrate?

A

reduced attention allocation to positive stimuli

long term effects - seen in individuals with high risk of depression, people with depression and remitted depressed adults

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144
Q

how does an fMRI work?

A

detects changes in blood oxygenation and flow in response to neural
activity via BOLD signals

(when an area is more active more oxygen is consumed, blood flow increases to meet increased demand)

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145
Q

what are the physiological changes that allow an fMRI to be taken?

A

neural activity systematically associated with changes in relative concentration of
oxygen in local blood supply

oxygenated blood has different magnetic susceptibility relative to
deoxygenated blood

changes in the ratio of oxygenated/de-oxygenated blood
(haemodynamic response function) can be inferred with fMRI by measuring the blood-oxygen level dependent (BOLD) response

fMRI can be used to produce activation maps showing which parts
of the brain are involved in a particular mental process

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146
Q

which parts of the brain display different activity in depression which can be seen using an fMRI?

A

sustained amygdala response to negative stimuli

prefrontal cortex:
- sustained perigenual anterior cingulate cortex (ACC) activity (BA 24, 25, and 32)
appears to mediate negative attentional biases
- increased activity in lateral inferior frontal cortex (associated with impaired ability
to divert attention from task-irrelevant negative information)

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147
Q

how does depression affect memory processes?

A

preferential recall of negative material compared to positive material

increased negative memory bias
- ability to recall memory related to negative words 10% more easily than positive words

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148
Q

who do memory biases present in?

A

individuals at risk (high on personality trait measure of neuroticism)

recovered depressed individuals

individuals with depression

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149
Q

what does the facial expression recognition test show in depression?

A

increased recognition of sad faces and/or decreased recognition of happy faces

(can be seen in healthy individuals with high levels of neuroticism)

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150
Q

what do the results of the facial expression recognition test demonstrate?

A

emotion recognition deficits in MDD

reduced recognition of all basic emotions except for sadness

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151
Q

what effect does incidental/passive viewing of emotional facial expressions have in depression?

A

enhanced amygdala response to negative faces

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152
Q

what is the function of the amygdala?

A

involved in perception and encoding of stimuli relevant to current or chronic affective goals

ranges from reward/ punishment to facial expressions of emotion to aversive/pleasant images

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153
Q

where is the amygdala found?

A

medial temporal lobe region

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154
Q

when does the amygdala show bias?

A

generally sensitive to detecting and triggering responses to arousing stimuli

shows bias towards detecting cues signalling potential threats (e.g. expressions of fear)

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155
Q

how does an acute single dose of noradrenergic antidepressant (e.g. reboxetine, duloxetine) affect facial expression recognition in healthy volunteer models?

A

better recognition of happy faces

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156
Q

how does an acute single dose of serotonergic antidepressant (e.g. SSRIs, mirtazapine) affect facial expression recognition in healthy volunteer models?

A

overall affect negative emotional face processing

mirtazapine - decreased recognition of fearful faces

SSRIs (e.g. citalopram) - mixed results, can sometimes increase fear recognition (both increased and decreased amygdala response)

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157
Q

how does 7 days treatment of serotonergic or noradrenergic antidepressant affect facial expression recognition in healthy volunteer models?

A

reduced recognition of anger and fear

reduced amygdala and medial prefrontal cortex response

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158
Q

how does clinical response to antidepressants change over time?

A

early changes in positive processing (facial expression recognition after single dose) are predicative of later response

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159
Q

what changes in the anterior cingulate cortex predict a positive response to treatment of depression (medication, neurostimulation, CBT)?

A

elevated baseline ACC activity during tasks that probe affective circuitry (also executive functions or self-referential processes such as the resting state)

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160
Q

where are the nuclei from where the serotonergic neurons project located?

A

raphe nuclei in midbrain

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161
Q

how many different serotonin receptors are there?

A

14

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162
Q

what is serotonin also known as?

A

5-hydroxytryptamine (5-HT)

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163
Q

where does serotonin reuptake occur?

A

proteins located on pre-synaptic membrane

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164
Q

what does the monoamine deficiency hypothesis of depression postulate?

A 
depressive symptoms arise from insufficient levels of monoamine
neurotransmitters
- serotonin/5-HT
- norepinephrine
- dopamine
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165
Q

how does use of reserpine (antihypertensive) provide indirect evidence of 5-HT hypofunction in depression?

A

reserpine (antihypertensive) can lead to 5-HT depletion - causes depressive symptoms

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166
Q

how does use of clinically useful antidepressants provide indirect evidence of 5-HT hypofunction in depression?

A

all help with depressive symptoms through mediating increase in synaptic monoamine
(some selectively 5-HT) concentrations

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167
Q

how does use of PET scanning provide indirect evidence of 5-HT hypofunction in depression?

A

shows lower levels of 5-HT1A and 5-HT4 receptors in brains of people with depressive symptoms

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168
Q

how do monoamine oxidase A levels provide indirect evidence of 5-HT hypofunction in depression?

A

increased levels of monoamine oxidase A in MDD (more degradation of 5-HT)

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169
Q

how does blocking serotonin synthesis provide indirect evidence of 5-HT hypofunction in depression?

A

inhibition of tryptophan hydroxylase (converts tryptophan to serotonin) with p-chlorophenylalanine prevents antidepressant effects of MAOIs and TCAs

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170
Q

how does tryptophan depletion provide indirect evidence of 5-HT hypofunction in depression?

A

depletes synthesis of serotonin via tryptophan hydroxylase

can trigger relapse in MDD

171
Q

how do mood changes provide indirect evidence of 5-HT hypofunction in depression?

A

correlation between monoamine depletion and decreased mood (i.e. the lower the serotonin levels, the lower the mood)

both in at-risk individuals and individuals with MDD in remission

172
Q

how does serotonergic transmission in vulnerability marker traits provide indirect evidence of 5-HT hypofunction in depression?

A

traits such as pessimism, dysfunctional attitudes in people with MDD, negativism and neuroticism in healthy individuals (vulnerability markers) positively correlated with levels of 5-HT2A receptor (inversely proportional to serotonin levels)

173
Q

what are the disadvantages of PET imaging in comparison to fMRI?

A

invasive

radioactive

expensive

less optimal temporal and spatial resolution

174
Q

what are the advantages of PET imaging in comparison to fMRI?

A

more selective (fMRI gives no information about molecules or transmitters involved in increased or decreased brain activity)

175
Q

how does PET imaging work?

A

injection of a radioactive
pharmaceutical tracer

tracer travels through blood across blood brain barrier

binds to specific target that it has affinity for, accumulation on target occurs

decay causes tracers to release positrons

positrons meet electrons - sets photons 180 degrees from each other

sends data into PET scanner - can determine site of decay as tracer has specific target (density will be high near target)

176
Q

how can PET imaging be used practically?

A

measure dopamine levels and dopamine release in brain

177
Q

how can PET imaging be used to compare dopamine levels and release (quantify dopamine receptors)?

A

take baseline PET scan

scan later in the day after you have given a pharmacological challenge (e.g. amphetamines like ritalin methylphenidate) that releases dopamine from presynaptic site

high levels of dopamine after amphetamine challenge competes with the radioactive tracer

subtract both scans, see difference in binding of tracer to the receptors - difference gives a measure of how much dopamine was released from the challenge given

178
Q

why has usage of PET imaging to measure 5-HT levels by issuing a pharmacological challenge not been successful so far?

A

tracers used are all antagonists (i.e. not as sensitive to changes in synaptic levels of the transmitter)

179
Q

how may usage of PET imaging to measure 5-HT levels by issuing a pharmacological challenge be successful in the future?

A

development of agonist PET tracer targeting 5-HT2A receptor

test with amphetamine as pharmacological challenger to increase serotonin levels

can see ‘real time’ release of serotonin

180
Q

what has PET imaging with a pharmacological challenge shown about serotonin thus far?

A

patients with MDD release less serotonin in response to pharmacological challenge in comparison to healthy individuals

lower levels of serotonin associated with more depression

(aligns with serotonin hypothesis - i.e. hypofunction of serotonin system causes depressive symptoms)

181
Q

what are the advantages of being able to measure serotonin levels in the brain directly (e.g. PET imaging with pharmacological challenge)?

A

predict treatment response

understand treatment resistance and give target medication based on this

182
Q

what is important in taking a past psychiatric history in suspected depression?

A

previous episodes of depression?

did previous episode(s) resolve with or without treatment?

history of any other mental illness? (important to rule out manic episodes)

previous admissions? (informal versus under the mental health act)

collateral history (mainly important when risks / patient being guarded)

183
Q

what is important in taking family history in suspected depression?

A

any mental illness?

who (e.g. first degree relative?)

what are the family relationships like?

184
Q

what is important in taking medication history in suspected depression?

A
  • antidepressants? antipsychotics? mood stabilisers?
  • side effects?
  • ECT?
  • psychology?

substance misuse

  • cannabis / alcohol / cocaine / heroin (opiates) / hallucinogens
  • self medication?

details:

  • when treated?
  • for how long?
  • what exact medication?
  • what doses?
  • how well tolerated?
  • did it help?
185
Q

what is important in taking forensic history in suspected depression?

A

arrests

cautions

incarcerations

forensic mental health act admissions

probation officer

186
Q

what is important in taking personal history in suspected depression?

A

birth, early life

school, qualifications, higher/further education

employment

psychosexual history

premorbid personality

187
Q

what risk assessment is taken in suspected depression?

A

to self:

  • current suicidal ideation/plans/intent
  • previous attempts (method/how many episodes/how did they feel when they survived
  • self harm/cutting
  • self neglect/poor care of physical illness

to others:

  • more rare in depression but still ask!
  • thoughts/plans to harm others?

from others:
- vulnerability to exploitation

188
Q

what are the differentials in a suspected case of depression?

A

bipolar vs unipolar?

bipolar (and depression) vs borderline personality disorder?

bipolar vs schizophrenia?

bipolar vs attention deficit disorder?

189
Q

what is cluster A of personality disorders according to DSM-5?

A

paranoid: pattern of irrational suspicion and mistrust of others, interpreting motivations as malevolent
schizoid: lack of interest and detachment from social relationships, apathy, and restricted emotional expression
schizotypal: extreme discomfort interacting socially, and distorted cognition and perceptions

190
Q

what is cluster B of personality disorders according to DSM-5?

A

antisocial: pervasive pattern of disregard for and violation of the rights of others, lack of empathy, bloated self-image, manipulative and impulsive behaviour
borderline: pervasive pattern of abrupt mood swings, instability in relationships, self-image, identity, behaviour andaffect, often leading to self-harm and impulsivity
histrionic: pervasive pattern ofattention-seekingbehaviour and excessive emotions
narcissistic: pervasive pattern ofgrandiosity, need for admiration, and a perceived or real lack of empathy

191
Q

what is cluster C of personality disorders according to DSM-5?

A

avoidant: pervasive feelings of social inhibition and inadequacy, extreme sensitivity to negative evaluation.
dependent: pervasive psychological need to be cared for by other people.

obsessive-compulsive personality disorder: rigid conformity to rules, perfectionism, and control to the point of satisfaction and exclusion of leisurely activities and friendships (distinct fromobsessive-compulsive disorder)

192
Q

what are the similar traits between bipolar affective disorder and borderline personality disorder?

A

rapid mood swings

unstable interpersonal relationships

impulsive sexual behaviour

suicidality

193
Q

how can you differentiate between bipolar affective disorder and borderline personality disorder?

A

BPAD:

  • runs in family; heritability +++
  • grandiosity
  • mood states typically less affected by environment

BPD:

  • poor self image
  • fear of abandonment
  • feelings of emptiness
194
Q

what are the similar traits between bipolar affective disorder and schizophrenia?

A

hallucinations (present in 50% of mania & 10% of depression)

cognitive impairment

depression, negative symptoms of schizophrenia (apathy, lack of affect, low energy, and social isolation)

schizoaffective shares features of both BPAD and schizophrenia

195
Q

how can you differentiate between bipolar affective disorder and schizophrenia?

A

BPAD:
- episodic delusions/hallucinations

schizophrenia:
- chronic delusions/hallucinations

196
Q

what are the similar traits between bipolar affective disorder and attention deficit disorder?

A

impaired concentration

impairment of executive function

abnormal working and short term memory

197
Q

how can you differentiate between bipolar affective disorder and attention deficit disorder?

A

family history (heritability+++)

recurrent depressive episodes

amphetamines worsen mania

198
Q

what are some endocrine causes of symptoms of depression?

A

hyperthyroidism, hypothyroidism

hyperparathyroidism, hypoparathyroidism

hyperadrenocorticism, hypoadrenocorticism

hypoglycaemia

Cushing’s syndrome

Addison’s disease

199
Q

what are some systemic conditions that may lead to symptoms of depression?

A

viral infections

systemic lupus erythematosus

HIV infection

pancreatic (and other) cancer

200
Q

how may systemic diseases lead to causes of depression?

A

cytokines manifested in systemic diseases are considered to be a cause of depression

201
Q

what are some deficiencies that may lead to symptoms of depression?

A

vitamin B12 or folic acid

202
Q

what are some neurological conditions that may lead to symptoms of depression?

A

multiple sclerosis

Alzheimer’s

Parkinson’s

203
Q

what are some medications that may lead to symptoms of depression?

A

beta-blockers

steroids

anti-Parkinson’s

anti-cholinergics (e.g. dicyclomine for IBS)

some antibiotics (e.g. ciprofloxacin)

statins

oestrogen

opiate pain killers

acne medications

204
Q

who is vascular depression/early sub-cortical dementia common in?

A

later life

205
Q

what is vascular depression associated with?

A

white matter hyperintensities

206
Q

how do white matter hyperintensities increase risk of vascular depression?

A

impact on cognitive function

makes the individual more vulnerable to stressors

207
Q

what are vascular risk factors that could increase risk of vascular depression?

A

diabetes

hypertension

smoking

alcohol use

208
Q

what features are prominent in post-stroke depression?

A

retardation in thinking and behaviour

209
Q

lesions in which areas of the brain can cause post-stroke depression?

A

left frontal lobe

basal ganglia

210
Q

how does the position of a lesion affect the severity of post-stroke depression?

A

the more frontal the lesion, the more severe the symptom

211
Q

what questions should be asked about drug abuse?

A

drug being abused

quantities taken? frequency taken? (some drugs can have therapeutic effects at certain doses but harmful effects at others)

over the counter? prescription? internet? illegal?

212
Q

what are the 4 broad categories of drug?

A

depressant

stimulant

hallucinogenic

cannabinoid

213
Q

why may someone take a drug recreationally?

A 
positive reinforcement
('gain positive state' - want to gain something from the drug)
- get high
- like it
- stay awake
- escapism
negative reinforcement
('overcome adverse state' - want to overcome something unpleasant)
- boredom
- to get to sleep
- to feel better
- to reduce anxiety

other:

  • why not?
  • to rebel
  • curiosity
  • to fit in/everyone does it
214
Q

how can recreational use of a drug lead to dependency?

A

“like” - recreational usage, people can leave at any point

shift in motivational desire to “want” - ‘necessary’ to have drug available

“need” - regular usage

spiral into dependence (for normal function) - must have the drug, dominates life

(neuroadaptations)

215
Q

what proportion of people that recreationally use a drug will become dependent?

A

“funnel” shaped progression

people use recreationally/to alleviate negative feelings

as feelings recede (i.e. drugs take effect) drug use usually recedes

smaller number spiral into dependence

216
Q

how is harmful substance use defined according to ICD-10?

A

pattern of substance use causing actual damage to health (mental or physical) of the user in the absence of diagnosis of dependence syndrome

adverse social consequences

includes bingeing on substances (does not include ‘hangover’ alone)

e.g. someone who has fallen, someone who has got into a fight, heavy smoker with recurrent chest infections

217
Q

how is hazardous substance use defined according to ICD-10?

A

one step before harmful substance use

i.e. likely to become harmful if they carry on in the same manner

218
Q

what are the 6 criteria that define dependence syndrome according to ICD-10?

A

strong desire or sense of compulsion to take the substance

difficulties in controlling substance taking behaviour in terms of its onset, termination, or levels of use (key aspect of dependence)

  • who has control, you or ‘the drug/behaviour’?
  • when did you last have a drink/drug?

physiological withdrawal state when substance use has stopped or been reduced
- a ‘negative’ state (from uncomfortable to intolerable) so user takes drug/alcohol to get relief from it or ‘treat’ it

evidence of tolerance: need to take more to get same effect

progressive neglect of alternative interests

persisting with substance use despite clear evidence of overtly harmful consequences

219
Q

what is a ‘binge’?

A

may use a substance relatively rarely, but do not have control once they begin (large quantities of substance taken in short period of time)

220
Q

what is necessary for a diagnosis of dependence syndrome (ICD-10)?

A

meet 3 ICD-10 criteria within a period of 12 months

221
Q

what is the difference between addiction and dependence?

A

addiction

  • compulsive drug use despite harmful consequences
  • characterized by an inability to stop using a drug
  • failure to meet work, social, or family obligations
  • (depending on the drug) tolerance and withdrawal

dependence

  • (biology/pharmacology) refers to a physical adaptation to a substance (neurochemistry, body adapts to presence)
  • tolerance/withdrawal
  • can be dependent and not addicted - no behaviours around it (no drug seeking, taking more than needed, no failure to make other commitments)
222
Q

how does a drug produce psychoactive effects?

A

enters brain

223
Q

what property of drugs affects its addictive potential?

A

speed of entry into brain

faster entry = more “rush”, more addiction

(difference in intake method of coca leaves vs cocaine vs crack)

224
Q

what 3 things contribute to the speed of entry of a drug into the brain (and therefore higher addictive potential)?

A

speed of reaching the brain

speed of crossing the blood-brain barrier

lipophilicity of drug

225
Q

what 3 elements are involved in substance use and addiction?

A

social, environmental factors (access, social norms, cost etc.)

personal factors (genetics, personality traits like impulsivity, family history)

drug factors (kinetics, formulation taken)

226
Q

what factors influence pre-existing vulnerability to addiction?

A

family history

age

227
Q

how may age influence pre-existing vulnerability to addiction?

A

the earlier you tend to use a drug, the more likely you are to become dependent on it

young brains not fully formed in terms of myelination (more synaptic plasticity) - therefore more vulnerable

228
Q

what factors influence increased drug exposure in addiction?

A

compensatory
neuroadaptations
to maintain
brain function

resilience (i.e. being able to take a drug and not experience many detrimental effects)

229
Q

how may acute use of alcohol help users to sleep or reduce anxiety?

A

alters balance between brain’s inhibitory system (GABA-A system, involves GABA-A ion channel) and excitatory system (glutamate system, involves NMDA ion channel)

alcohol boosts inhibitory system (leads to anxiolysis, sedation) - i.e. GABA

alcohol blocks excitatory system (leads to impaired memory, alcoholic blackouts)

230
Q

how may chronic use of alcohol affect the GABA and glutamate systems?

A

neuroadaptations to allow GABA and glutamate systems to remain balanced in presence of alcohol (allows normal function)

reduced function of inhibitory system: switches subunit type within GABA-A receptor to a subtype that is less sensitive to alcohol

upregulation of excitatory system: more NDMA receptors

231
Q

how may genetics affect the GABA-A receptor and therefore alcohol tolerance?

A

less sensitive GABA-A receptor

feel fewer adverse effects - can drink more, therefore damage is greater

232
Q

in the absence of alcohol (withdrawal) after chronic use, how do the GABA and glutamate systems react?

A

in absence of alcohol GABA and glutamate systems are no longer in balance - reduced function in inhibitory system, upregulated excitatory system

NMDA receptor - increase in Ca2+ entering cell - toxicity leads to hyperexcitability (seizures) and cell death (atrophy)

233
Q

how can withdrawal symptoms after chronic alcohol usage be treated?

A

benzodiazepines

boost function of GABA system

counteract glutamatergic hyperactivity, restore balance

234
Q

how can magnetic resonance spectroscopy demonstrate the effects of benzodiazepines in treating alcohol withdrawal?

A

higher synaptic and metabolic glutamate levels in people that use alcohol

glutamate levels in anterior cingulate cortex (frontal cortex) raised one day after withdrawal

14 days on benzodiazepines - glutamate levels reduced closer to healthy controls

235
Q

how does acamprosate help people to abstain from alcohol?

A

reduces NMDA function

reduces toxicity in brain, potentially neuroprotective (idiopathic improved cognitive function, reduced seizure risk)

236
Q

why may anticonvulsants be able to treat alcohol withdrawal?

A

affect glutamate and GABA systems

237
Q

what are the 3 models of addiction?

A

reward deficiency (positive reinforcement)

overcoming adverse state, negative reinforcement (e.g. withdrawal, anxiety)

impulsivity/compulsivity

238
Q

how does the reward deficiency model work?

A

natural rewards increase dopamine levels in ventral striatum - pleasure, reward, motivation

drugs of abuse also increase dopamine levels

lack of control increases as dependence increases - less about pleasure/reward, more about motivation

therefore addiction conceptualised as “reward-deficient” state

239
Q

what does the reward (dopaminergic) system look like?

A

dopaminergic projections in ventral tegmental area (VTA) of brain stem project into ventral striatum and frontal cortex

240
Q

how does the opioid system act as a key modulator for the dopamine system?

A

mediates pleasurable effects (e.g. of alcohol) - produces endorphin rush that modulates dopamine system

241
Q

what are some modulators of the dopamine system?

A

GABA-B

cannabinoids

glutamate

242
Q

how does cocaine interact with the dopamine system?

A

block post-synaptic dopamine re-uptake channel

more dopamine in the synapse, more of a signal

243
Q

how do amphetamines interact with the dopamine system?

A

block post-synaptic dopamine re-uptake channel - more dopamine in the synapse, more of a signal

enhances release of dopamine

244
Q

why do drugs of abuse like cocaine or amphetamines (stimulants) have such a potent effect on addiction and the reward process?

A

directly target dopamine synapse

245
Q

how do drugs of abuse like alcohol, opiates or nicotine interact with the dopamine system?

A

increase dopamine neuron firing in ventral tegmental area (VTA) by altering tonic inhibitory responses

(indirect effects)

246
Q

how does the reward-deficient addiction model work with respect to availability of dopamine receptors?

A

people with higher availability of D2 receptors do not like the effect of stimulants

people with lower availability may have lower level of dopaminergic function in natural pleasure-reward system - drug-induced increase of dopamine increases feeling of pleasure

in people with higher availability increased dopamine levels could cause anxiety, paranoia etc. (important when considering psychotic states e.g. in schizophrenia)

247
Q

how can reward deficiency in adolescence be linked to vulnerability to problematic drug use?

A

blunted brain activation in striatum when winning money aged 14 as part of IMAGEN study linked to problematic drug use at 16

reward deficient model

248
Q

how does the reward system appear in abstinent addicts as compared to healthy controls?

A

blunted activation of reward system

249
Q

how does the reward system appear in poly drug users as compared to healthy controls?

A

blunted activation of reward system

250
Q

how does the reward system appear in relapsed addicts as compared to abstinent addicts?

A

substantial blunting of reward system

not in all individuals

251
Q

theoretically, how could risk of relapse be mitigated when treating addiction?

A

medication that boosts dopamine system to counter naturally blunted reward system activation

252
Q

what are the 3 stages involved in the cycle of addiction?

A

binge/intoxication - positive reinforcement

withdrawal (negative affect, negative reinforcement)

preoccupation/anticipation - craving

253
Q

which region of the brain does withdrawal affect?

A

hypothalamus and brainstem effectors (autonomic, somatic, neuroendocrine)

amygdala

254
Q

what effects does withdrawal produce due to its impact on the amygdala?

A

highly aroused, anxious state

255
Q

how can the change from positive to negative reinforcement be described as dependence develops?

A

non-dependent: “high” produced, declines into negative (withdrawal state), returns to homeostatic set point eventually

neuroadaptations take place as drug use/ tolerance increases

dependent: smaller “high” produced, greater negative withdrawal state - returns to allostatic set point lower than homeostatic set point

256
Q

what is an addict’s motivation when taking a drug after reaching a point of negative reinforcement?

A

need to overcome greater withdrawal state rather than achieve pleasure

fear/anxiety apparent without access to drug - cannot counter negative state

257
Q

how does dysregulation of the amygdala affect the ‘reward’ system?

A

reduced dopamine and mu opioid function

258
Q

how does dysregulation of the amygdala affect the ‘stress’ system?

A

increased activity

  • arousal system (noradrenaline)
  • CRF system (cortisol)
  • kappa system (dynorphin)

decreased ‘anti-stress’ neurotransmitters (e.g. oxytocin, nociceptin)

259
Q

what is the kappa opioid/dynorphin system?

A

opposite to mu opioid/dopamine system which produces endorphins

260
Q

what kind of state is produced by stimulation of the kappa opioid/dynorphin system?

A

produces aversive, dysphoric state

261
Q

how can dysregulation of the amygdala in addiction be demonstrated using aversive images and fMRI?

A

heightened brain response to aversive images in left amygdala for abstinent polydrug addicts

(but not in alcoholism)

262
Q

what transition in the brain takes place during the change from voluntary drug use to compulsive drug use?

A

executive control moves deeper from prefrontal cortex to striatum

specifically - move from ventral (limbic/emotional) to dorsal (habitual) striatum

263
Q

what does the balance between the prefrontal cortex and the striatum usually moderate?

A

internal drives

264
Q

what disease is associated with the dorsal striatum?

A

Parkinson’s

265
Q

which part of the brain is highly associated with craving?

A

hippocampus (memory)

266
Q

how can neurocircuitry involved in inhibitory control be assessed?

A

go - no go task with fMRI

267
Q

where can activity be seen in a go - no go task with fMRI?

A

putamen (dorsal striatum and inferior frontal gyrus)

268
Q

what does a go - no go task with fMRI show in abstinent addicts?

A

greater activity in putamen

higher in abstinent alcoholics when compared to abstinent poly drug users and controls

269
Q

what does a higher level of activity in the putamen shown in an fMRI of abstinent addicts indicate?

A

greater response associated with longer abstinence

i.e. greater activity during inhibitory control, facilitates staying sober

270
Q

how can units of alcohol be calculated?

A

% strength x ml/1000

271
Q

what is the excretion rate of alcohol?

A

1 unit per hour

272
Q

what are the symptoms of opiate withdrawal?

A

tachycardia

sweating

restlessness

dilated pupils

bone aches

runny nose

GI upset

tremor

yawning

anxiety/irritability

gooseflesh skin

273
Q

what drugs can be given to aid abstinence of alcohol?

A

acamprosate

disulfiram (antabuse)

naltrexone

nalmefene

274
Q

how does acamprosate help alcohol abstinence?

A

increases GABA, NMDA antagonist

275
Q

how does disulfiram (antabuse) help alcohol abstinence?

A

inhibits acetaldehyde dehydrogenase

therefore feel nauseous/flushes if mixed with alcohol

276
Q

how does nalmefene help alcohol abstinence?

A

opioid antagonist

given on days at high risk of drinking, in those dependent but without withdrawal, to reduce alcohol intake

277
Q

what drugs can be given to aid abstinence of opioids?

A

methadone

buprenorphine

278
Q

what are the DSM-5 criteria for opioid/alcohol use disorder?

A

taken in larger amounts/over a longer period than intended

persistent desire or unsuccessful efforts to cut down

great deal of time spent obtaining, using and recovering from it

craving to use

recurrent use results in failure to fulfil major obligations (work, school, home)

continued use despite persistent social/interpersonal problems caused or exacerbated by usage

important social, occupational or recreational activities are given up due to use

recurrent use in situations where it is physically hazardous

continued use despite knowledge of having a persistent physical/psychological disorder caused or exacerbated by usage

tolerance, either:

a) need for increased amounts to achieve intoxication/desired effect
b) diminished effects with continued use of same amount of drug

withdrawal, either:

a) characteristic withdrawal syndrome
b) same/similar substance taken to avoid or relieve withdrawal

279
Q

how is opioid/alcohol use disorder categorised according to DSM-5?

A

2 symptoms - opioid/alcohol use disorder

mild: 2-3 symptoms
moderate: 4-5 symptoms
severe: 6+ symptoms

280
Q

what does a history taking look like in substance misuse?

A

presenting complaint (PC) – snapshot of main problem/s

history of presenting complaint (HPC) – length of current problem/s, onset, causes, signs and symptoms etc

substance misuse history (following areas should be assessed for each substance):

  • length of current use and when last used
  • current amount (units/grammes per day) and for how long at this level
  • total length of use, max use, and any periods of abstinence
  • mode/method of use
  • evidence of withdrawals and severity (e.g. seizures, admissions)
  • any previous treatments - medication, psychotherapy, detox, rehab
  • any previous substance overdoses (accidental vs deliberate)
  • assess triggers to use substances/alcohol
  • assess motivation to change/engage in treatment

family history – include mental illnesses and addiction disorders, often history of trauma (neglect, abuse)

screen for developmental disorders, especially ADHD (25% of substance use disorders have comorbid ADHD), assess developmental and educational history

social/personal history

  • relationships
  • accommodation
  • money, employment
  • forensics (cautions, convictions etc.)
281
Q

what are some common comorbid conditions with substance use disorders?

A

depression

anxiety

suicidality

personality disorder

PTSD

bipolar disorder

282
Q

what are the major causes of morbidity and mortality associated with substance abuse?

A

trauma (e.g. fractures)

road traffic accidents

homicide

suicide

overdose (deliberate, and frequently accidental)

cirrhosis (alcohol)

endocarditis (IV)

abscesses (IV)

BBV: hepatitis B/C & HIV (IV)
(ask about vaccinations)

283
Q

what is drug induced psychosis?

A

cluster of psychotic phenomena occurring during or immediately after substance use, especially stimulants

(e.g. crack, methamphetamine)

284
Q

how may drug induced psychosis present?

A

vivid hallucinations, often auditory

paranoid delusions (can be severe)

285
Q

how long does drug induced psychosis take to resolve?

A

within 1-6 months

286
Q

why must diagnosis of drug induced psychosis be done carefully?

A

care not to diagnose something like a schizophrenic episode, which may be ‘triggered’ by substance abuse

287
Q

what features of alcohol abuse should be noted during examination?

A

jaundice

anaemia

clubbing

cyanosis

oedema

ascites

lymphadenopathy

DVT

288
Q

what investigations should be done in suspected alcohol abuse?

A

fibro scan /ultrasound

bloods (LFT, GGT, lipids, U&E, amylase)

breathalyser

urine drug screen

289
Q

what features of opioid abuse should be noted during examination?

A

collapsed veins / track marks

endocarditis

skin abscesses

hepatitis / HIV

pneumonia

290
Q

what investigations should be done in suspected opioid abuse?

A

bloods (LFT, GGT, U&E, glucose)

breathalyser

urine drug screen

sexual health screening/BBV

291
Q

what is CAGE screening (alcohol assessment)?

A

have you ever felt you needed to CUT DOWN on your drinking?

have people ANNOYED you by criticizing your drinking?

have you ever felt GUILTY about drinking?

have you ever felt you needed a drink first thing in the morning (EYE-OPENER)?

292
Q

what is an AUDIT test?

A

alcohol use disorders identification test - 10 questions about alcohol intake

293
Q

how can AUDIT test results be categorised?

A

0-7 = low risk

8-15 = increasing risk (brief advice to reduce risk)

16-19 = higher risk

20+ = possible dependence (consider referral to specialist alcohol harm assessment)

294
Q

what are the immediate effects of alcohol on the CNS?

A

impaired reaction time and motor co ordination

impaired judgement

sedation

(coma and death)

295
Q

what are the immediate effects of alcohol on the senses?

A

less acute

296
Q

what are the immediate effects of alcohol on the stomach?

A

nausea

inflammation

bleeding

297
Q

what are the immediate effects of alcohol on the skin?

A

flushing

sweating

heat loss and hypothermia

formation of broken capillaries

298
Q

what are the immediate effects of alcohol on sexual functioning?

A

reduced erection response

reduced vaginal lubrication

299
Q

what are the chronic effects of alcohol on the brain?

A

damaged brain cells

reduced brain size

impaired memory

loss of sensation in limbs

brain atrophy

300
Q

what are the chronic effects of alcohol on the cardiovascular system?

A

weakened cardiac muscle

elevated blood pressure

irregular heartbeat

increased stroke risk

301
Q

what are the chronic effects of alcohol on the breast?

A

increases risk of breast cancer

302
Q

what are the chronic effects of alcohol on the immune system?

A

lowered disease resistance

303
Q

what are the chronic effects of alcohol on the digestive system?

A

cirrhosis

inflammation of stomach and pancreas

increased risk of lip, mouth, larynx, oesophagus, liver, rectal and stomach cancers

304
Q

what are the chronic effects of alcohol on the kidney?

A

kidney failure associated with end stage liver disease

305
Q

what are the chronic effects of alcohol on nutrition?

A

nutrient deficiencies

obesity

306
Q

what are the chronic effects of alcohol on the reproductive system?

A

menstrual irregularities

increased risk of children with foetal alcohol syndrome

impotence

testicular atrophy

307
Q

what are the chronic effects of alcohol on bone?

A

increased risk of osteoporosis

increased risk of fractures (frequent falls)

308
Q

how does alcohol withdrawal present over time?

A

Worsening pattern of symptoms

onset usually from 6 hours

hallucinations can occur any time

delirium tremens is a late sign

309
Q

what are the 2 effects of opioids?

A

analgesic effect

sense of euphoria

310
Q

what are some examples of opioid agonists that affect mu, delta and kappa opioid receptors?

A

heroin, methadone, fentanyl, codeine

311
Q

what are some examples of partial opioid agonists that affect mu, delta and kappa opioid receptors?

A

buprenorphine

312
Q

what are some examples of opioid antagonists that affect mu, delta and kappa opioid receptors?

A

naltrexone

313
Q

what is the difference between opiates and opioids?

A

opiates: naturalopioids (e.g. morphine,codeine, heroin to some extent)
opioids: all natural, semisynthetic (e.g. heroin, oxycodone),andsynthetic (e.g. fentanyl, methadone)opioids

314
Q

what are the 4 types of treatment in psychiatry, with examples?

A

chemical
- drugs, medicines

electrical stimulation

  • ECT for depression
  • neurostimulation for pain syndromes

structural rearrangement
- psychosurgery/deep brain stimulation for severe depression

talking therapy

  • CBT
  • exposure therapy for phobias
315
Q

what are the advantages of classifying psychiatric drugs based on chemical structure?

A

each drug has unique structure, easy to allocate data

316
Q

what are the disadvantages of classifying psychiatric drugs based on chemical structure?

A

no use in clinical decision making

317
Q

what are the advantages of classifying psychiatric drugs based on what illnesses they treat (antidepressant, antipsychotic etc.)?

A

easy for doctors to choose as they make the diagnosis

318
Q

what are the disadvantages of classifying psychiatric drugs based on what illnesses they treat (antidepressant, antipsychotic etc.)?

A

many medicines treat several disorders (some antidepressants also treat anxiety and OCD etc.)

most disorders have multiple symptoms - a single medication may not treat them all
(e.g. depression may present with anxiety, insomnia, loss of libido - all have different neurotransmitter mechanisms)

319
Q

what do psychiatric medicines target?

A

1 (maybe 2) of 4 different systems

  • receptors
  • neurotransmitter reuptake sites
  • ion channels
  • enzymes
320
Q

how can psychiatric drugs produce unwanted side effects?

A

targets are in the brain but drugs can affect systems elsewhere (especially liver enzymes)

321
Q

how are neurotransmitters create/inhibit an action potential in the receiving neuron?

A

action potential moves down axon

neurotransmitters released across synapse

activate receptors on post-synaptic membrane

322
Q

how are neurotransmitters released across the synapse?

A

action potential arrives and depolarises the terminal region

depolarisation allows calcium to flow into terminal region

calcium activates enzymes that allows vesicles containing neurotransmitter to fuse with the cell membrane to release neurotransmitters

323
Q

what happens to neurotransmitters after acting on post synaptic receptors?

A

most taken back up in the pre synaptic neuron through transporter/re-uptake site

324
Q

which neurotransmitter is not taken back up through re-uptake proteins?

A

acetylcholine

325
Q

how is acetylcholine broken down?

A

degrading enzymes outside the terminal

326
Q

how are autoreceptors involved in inhibition of action potentials?

A

neurotransmitter attaches to autoreceptors inside first neuron and activates them

activation causes inhibition of calcium influx

causes inhibition of action potential - terminal does not fire

327
Q

how do monoamine oxidase inhibitors act on enzymes to treat anxiety and depression?

A

block the breakdown of 5-HT and noradrenaline

328
Q

how do acetylcholinesterase inhibitors act on enzymes to treat dementia?

A

block the breakdown of acetylcholine

deficiency of acetylcholine in dementia

329
Q

how does lithium act on enzymes to treat bipolar disorder?

A

blocks glycogen synthase kinase

stabilises neurones to produce mood stability

330
Q

how do dopamine blockers act on receptors to treat schizophrenia?

A

antagonists

331
Q

how do serotonin receptor subtype antagonists act on receptors to treat depression?

A

augment effects of SSRIs

332
Q

how do benzodiazepines act on receptors to promote sleep and reduce epilepsy?

A

agonists

enhance inhibitory transmitter GABA

333
Q

how does guanfacine act on receptors to control ADHD?

A

enhances noradrenaline

334
Q

what is the principle behind psychiatric drugs that target reuptake sites?

A

block them to increase neurotransmitter concentration in the synapse to enhance post-synaptic receptor activity

some switch the reuptake site direction to enhance release

335
Q

what are 3 examples of drugs that target reuptake sites?

A

citalopram

  • SSRI, enhances serotonin
  • used for depression and anxiety

desipramine

  • noradrenaline reuptake inhibitor, enhances noradrenaline
  • used for depression

methylphenidate

  • dopamine reuptake inhibitor, enhances dopamine
  • used for ADHD
336
Q

why is the 5-HT1A receptor targeted in treatment of depression?

A

increased stimulation of receptor inhibits activity in neurons with these receptors

337
Q

why is the 5-HT2 receptor targeted in treatment of schizophrenia, sleep regulation and eating?

A

psychedelic drugs act on 5-HT2 to produce hallucinations, disturbance of consciousness

targeting this is thought to regulate receptor activity in mental disorders with similar effects

338
Q

what is the principle behind psychiatric medication targeting ion channels?

A

block channels to reduce neuronal excitability

339
Q

how do drugs like sodium valproate and carbamazepine aid treatment of epilepsy by targeting ion channels?

A

block sodium channels

block transmission of information down the axon

prevention of action potentials prevents process of recruiting neurones in an epileptic focus that would cause a seizure

340
Q

how do drugs like sodium valproate and carbamazepine aid mood stabilisation in bipolar disorder by targeting ion channels?

A

block sodium channels

block transmission of information down the axon

prevention of recurrent cyclical activity between groups of neurones helps stabilise mood

341
Q

how do drugs like gabapentin or pregabalin aid treatment of epilepsy and anxiety by targeting ion channels?

A

block calcium channels in terminal region of axons (synapse)

prevent neurotransmitter release

342
Q

how can neurotransmitters be divided into 2 categories?

A

fast acting (on-off)

slow acting (neuromodulators)

343
Q

what kind of fast acting neurotransmitter is glutamate?

A

excitatory

344
Q

where is glutamate present?

A

80% of all neurons

pyramidal cells (regulation of brain function)

345
Q

what kind of fast acting neurotransmitter is GABA?

A

inhibitory

346
Q

where is GABA present?

A

15% of all neurons

interneurons (connect other neurons together, make up network of brain)

347
Q

what is the balance between glutamate and GABA responsible for?

A

content of everything

e.g. memory, movement, vision

348
Q

what is the role of neuromodulators?

A

adds emotions, drives, valence to content created by fast acting neurons

349
Q

what is valence?

A

attractiveness/”good”-ness (positive valence) or averseness/”bad”-ness (negative valence) of an event, object, or situation

350
Q

what does excess glutamate cause?

A

epilepsy

alcoholism

351
Q

how can epilepsy caused by excess glutamate be treated?

A

perampanel (glutamate receptor blocker)

352
Q

how can alcoholism caused by excess glutamate be treated?

A

acamprosate, ketamine (glutamate receptor blocker)

353
Q

what does deficient GABA cause?

A

anxiety

354
Q

how can anxiety caused by deficient GABA be treated?

A

benzodiazepines (GABA enhancer)

355
Q

what does deficient 5-HT cause?

A

depression

anxiety

356
Q

how can anxiety and depression caused by deficient 5-HT be treated?

A

SSRIs and MAOIs (serotonin enhancers)

357
Q

what does excess dopamine cause?

A

psychosis

358
Q

how can psychosis caused by excess dopamine be treated?

A

dopamine receptor blockers

359
Q

what does excess noradrenaline cause?

A

nightmares (e.g. in PTSD)

360
Q

how can nightmares caused by excess noradrenaline be treated?

A

prazosin (noradrenaline receptor blocker)

361
Q

what does deficient acetylcholine cause?

A

impaired memory/dementia

362
Q

how can impaired memory caused by deficient acetylcholine be treated?

A

acetylcholinesterase enzyme blockers

363
Q

when can partial agonists be safer than full agonists?

A

improved safety in overdose

364
Q

how can a partial agonist act as a modulator?

A

effect of partial agonist determined by level of neurotransmitter

excess neurotransmitter - blocks receptor (acts as an antagonist)

neurotransmitter deficit - acts as an agonist

365
Q

why is a partial agonist’s action as a modulator better than that of a full antagonist?

A

blocking all effects of a neurotransmitter may have more side effects

366
Q

how can a partial agonist be used in treating heroin addiction?

A

buprenorphine

  • heroin alternative
  • used to treat pain and addiction syndromes
367
Q

how can a partial agonist be used in treating depression?

A

full antagonist (haloperidol) may produce extrapyramidal side effects

aripiprazole prevents side effects, can also allow normal motor function by acting as an agonist if dopamine is deficient

368
Q

how can a partial agonist be used in treating nicotine addiction?

A

varenicline

- replacement therapy for tobacco

369
Q

what is an inverse agonist?

A

opposite effect to an agonist

e.g. GABA has inhibitory effect, inverse agonist has excitatory effect

370
Q

how can an inverse agonist be used to improve memory (e.g. in alcoholism)?

A

alpha-5IA acts as inverse agonist for GABA

acts in hippocampus, increases activity/functionality to reverse amnesiac effects

371
Q

how can an inverse agonist be used to improve attention (e.g. in ADHD)?

A

histamine blockers cause sedation

inverse agonists have opposite effect

372
Q

what is the most common GABA-A receptor sub-type?

A

2 alpha, 2 beta, 1 gamma proteins

373
Q

what are the components of a GABA-A receptor?

A

5 separate proteins combined in multiple ways to form different receptor sub-types

374
Q

where is the most common type of GABA-A receptor found?

A

cortex

375
Q

how are different GABA-A receptors arranged at the synapse?

A

alpha-1 - synaptic

alpha-2 - proximal segment of synapse

alpha-5 - extra synaptic

376
Q

how does the arrangement of alpha-1 GABA-A receptors at the synapse relate to their function?

A

alpha-1 - synaptic

regulates inhibition from the GABA inter-neurons onto these pyramidal cells

377
Q

how does the arrangement of alpha-2 GABA-A receptors at the synapse relate to their function?

A

alpha-2 - proximal segment of synapse

control the output of the pyramidal cells - inhibition of proximal segment prevents firing of pyramidal cell to control overall activity

378
Q

how does the arrangement of alpha-5 GABA-A receptors at the synapse relate to their function?

A

alpha-5 - extra synaptic

produce a tonic activity (dampen down tonic activity in the brain)

379
Q

how is the GABA-A alpha-5 receptor distributed in the brain?

A

highly expressed in ‘emotionally rich’ areas

cingular cortex, hippocampus

380
Q

why is the tonic activity of GABA-A alpha-5 in emotionally rich areas of the brain (cingular cortex, hippocampus) important with reference to conditions like addiction or anxiety?

A

tonic activity necessary to maintain equilibrium

lack of function may contribute to anxiety, addiction etc.

381
Q

what is an orthosteric site/orthosteric receptor?

A

receptor/site that the original transmitter binds to

382
Q

how does the binding of GABA to its receptor produce an effect?

A

GABA-A receptor is ion-channel linked receptor

GABA binds to GABA receptor (orthosteric site)

binding enhances chloride ion conductance, therefore inhibits neurons to calm the brain

383
Q

how does the binding of benzodiazepines to the GABA-A receptor produce an effect? (also barbiturates, neurosteroids, ethanol)

A

bind to GABA receptor (allosteric site)

enhances action of GABA (sedation)

therefore help with sleep, anxiety reduction, anti-epilepsy

384
Q

why does haloperidol cause side effects in treatment of schizophrenia with reference to its selectivity?

A

highly selective for D2 receptor

(minor effects of alpha-1 receptor)

adverse effects due to full dopamine receptor block

385
Q

why does clozapine cause side effects like sedation and weight gain in treatment of schizophrenia with reference to its selectivity?

A

non-selective for D2 receptor (lower affinity than haloperidol)

has actions at histamine receptors as an antagonist (also 5-HT1A receptor as a partial agonist, alpha-2 receptors as an antagonist)

histamine blockade causes sedation, weight gain

386
Q

why does clozapine cause side effects like constipation in treatment of schizophrenia with reference to its selectivity?

A

non-selective for D2 receptor (lower affinity than haloperidol)

has actions at cholinergic muscarinic receptors as an antagonist (also 5-HT1A receptor as a partial agonist, alpha-2 receptors as an antagonist)

causes constipation, maybe paralytic ileus (lethal)

387
Q

why does amitriptyline cause side effects in treatment of depression with reference to its selectivity?

A

derived from tricyclic structure compounds, therefore not very selective (not specific to 5-HT and noradrenaline receptors/transporters)

also blocks histamine receptors, is a muscarinic anticholinergic blocker

adverse effects from histamine and acetylcholine receptor blockade

388
Q

why may the side effects of amitriptyline cause death?

A

overdose may lead to cardiac and brain toxicity

389
Q

why is citalopram preferred to amitriptyline with reference to its selectivity?

A

selective for 5-HT reuptake transporters

adverse effects solely driven by increased serotonin (therefore limited)

390
Q

how can dementia be described?

A

degenerative disease of the brain

with cognitive and behavioural impairment

sufficiently severe to interfere significantly with social and occupational function

391
Q

what are amyloid plaques?

A

insoluble β-amyloid peptide deposits as senile plaques or β-pleated sheets

392
Q

where are amyloid plaques found?

A

hippocampus

amygdala

cerebral cortex

393
Q

how do amyloid plaques relate to the pathophysiology of dementia?

A

increased density with advanced disease

394
Q

what are neurofibrillary tangles (NFTs)?

A

consist of phosphorylated tau protein

395
Q

where are neurofibrillary tangles (NFTs) found?

A

cortex

hippocampus

substantia nigra

396
Q

how are amyloid plaques and neurofibrillary tangles (NFTs) related to the pathophysiology of dementia?

A

co-occurrence of amyloid plaques and NFTs now accepted as a hallmark of dementia

(NFTs are also found in normal ageing)

397
Q

how are the neurons affected in the pathophysiology of dementia?

A

up to 50% loss of neurons and synapses in cortex and hippocampus

398
Q

how is chromosome 21 implicated in development of dementia?

A

gene for amyloid precursor protein (APP) found on the long arm

(also implicated in Down’s syndrome)

399
Q

how is chromosome 19 implicated in development of dementia?

A

codes for apolipoprotein E4

presence of E4 alleles increases risk of Alzheimer’s

400
Q

how is chromosome 14 implicated in development of dementia?

A

codes for presenilin 1

implicated in B-amyloid peptide

401
Q

how is chromosome 1 implicated in development of dementia?

A

codes for presenilin 11

implicated in B-amyloid peptide

402
Q

what is the cholinergic hypothesis?

A

the pathological changes lead to degeneration of cholinergic nuclei in the basal forebrain (nucleus basalis of Meynert)

this results in reduced cortical acetylcholine (ACh)

403
Q

how may drugs such as donepezil be used in treatment of dementia?

A

acetylcholinesterase inhibitor

increased levels of cortical acetylcholine

404
Q

how may drugs such as memantine be used in treatment of dementia?

A

NMDA receptor antagonist

high levels of glutamate in Alzheimer’s causes damage to neurons due to overactivity, increased calcium

memantine prevents glutamate from binding to neurons (i.e. inhibit calcium release to prevent action potentials)

405
Q

what are the early signs of dementia?

A

absent-mindedness

difficulty recalling names and words

difficulty learning new information

disorientation in unfamiliar surroundings

reduced social engagement

406
Q

what are the signs of progressive dementia?

A

marked memory impairment

reduced vocabulary

loss of less complex speech patterns.

mood swings and/or apathy

decline in activities of daily living and social skills

emergence of psychotic phenomena

407
Q

what are the signs of advanced dementia/Alzheimer’s?

A

monosyllabic speech

psychotic symptoms

behavioural disturbance

loss of bladder and bowel control

reduced mobility

408
Q

what are some psychiatric symptoms of dementia?

A

delusions (15%) -(usually of a paranoid nature)

auditory and/or visual hallucinations (10–15%)(may be simple misidentification, and indicate rapid cognitive decline)

depression (requires treatment in up to 20% of patients)

409
Q

what are some behavioural disturbances seen in dementia?

A

aggression

wandering

explosive temper

sexual disinhibition

incontinence

excessive eating

searching behaviour.

410
Q

what are some personality changes seen in dementia?

A

often reflects an exaggeration of premorbid traits with coarsening of affect and egocentricity

411
Q

why is differential diagnosis of Alzheimer’s difficult/inexact?

A

due to mixed nature of dementia pathologies

e.g. AD frequently occurs in the presence of vascular changes, indicating coexisting vascular dementia

412
Q

what are the criteria for a clinical diagnosis of ‘probable Alzheimer’s disease’?

A

presence of dementia

insidious onset

deterioration from the individual’s baseline

not more likely to be accounted for by another cause (e.g. other types of dementia, neurological, medical or psychiatric comorbidities etc.)

413
Q

how does dementia differ from delirium and depression in terms of onset?

A

dementia - insidious (months to years)

delirium - acute (hours to days)

depression - acute or insidious (weeks to months)

414
Q

how does dementia differ from delirium and depression in terms of course?

A

dementia - progressive

delirium - fluctuating

depression - may be chronic

415
Q

how does dementia differ from delirium and depression in terms of duration?

A

dementia - months to years

delirium - hours to weeks

depression - months to years

416
Q

how does dementia differ from delirium and depression in terms of consciousness?

A

dementia - usually clear

delirium - altered

depression - clear

417
Q

how does dementia differ from delirium and depression in terms of attention?

A

dementia - impaired

delirium - normal (except in severe dementia)

depression - may be decreased

418
Q

how does dementia differ from delirium and depression in terms of psychomotor changes?

A

dementia - often normal

delirium - increased or decreased

depression - may be slowed in severe cases

419
Q

how does dementia differ from delirium and depression in terms of reversibility?

A

dementia - irreversible

delirium - usually

depression - usually

420
Q

why are routine dementia investigations done?

A

exclude reversible causes of cognitive deterioration

421
Q

what blood tests are done as part of routine dementia investigations?

A

FBC, ESR, CRP - anaemia, vasculitis

T4 and TSH - hypothyroidism

biochemical screen - hypercalcaemia or hypocalcaemia

urea and creatinine - renal failure, dialysis dementia

glucose

B12 and folate - vitamin deficiency dementia

clotting and albumin - liver function

(midstream urine test if delirium is likely)

422
Q

why is imaging a part of routine dementia investigations?

A

exclude other cerebral pathologies

may help to identify treatable causes (e.g. subdural haematoma, normal pressure hydrocephalus, cerebral tumours)

help establish subtype of dementia

423
Q

how is an MRI useful as a part of routine dementia investigations?

A

assists with early diagnosis

detects subcortical vascular changes

(CT scanning could also be used)

BRS 2 (10 decks)

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