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psychiatry Flashcards

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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
what are some psychotic disorders?
schizoaffective disorder depression with psychotic features substance related due to other medical condition schizophrenia delusional disorder bipolar I
26
what are the two types of positive symptom of psychosis?
hallucinations - perceptions in absence of a stimulus delusions - fixed, false beliefs, out of keeping with social/cultural background
27
what are the types of hallucination?
auditory voices commenting on you, talking to each other visual somatic/tactile olfactory (rare)
28
what are some examples of delusions?
persecutory control reference mind reading grandiosity religious guilt/sin somatic thought broadcasting thought insertion thought withdrawal
29
what are the 4 types of negative symptom of psychosis?
alogia - poverty of speech anhedonia, asociality avolition/apathy affective flattening
30
what are the characteristics of alogia?
paucity of speech, little content slow to respond
31
what are the characteristics of anhedonia/asociality?
few close friends few hobbies/interests impaired social functioning
32
what are the characteristics of avolition/apathy?
poor self-care lack of persistence at work/education lack of motivation
33
what are the characteristics of affective flattening?
unchanging facial expressions few expressive gestures poor eye contact lack of vocal intonations inappropriate affect
34
what are the two types of disorganisation symptom?
bizarre behaviour thought disorder
35
what are the characteristics of bizarre behaviour?
bizarre social behaviour bizarre clothing/appearance aggression/agitation repetitive/stereotyped behaviours
36
what are the characteristics of a thought disorder?
derailment circumstantial speech pressured speech distractibility incoherent/illogical speech
37
what is the epidemiology of psychosis in terms of onset?
can occur at any age peak incidence in adolescence/early 20s peak later in women
38
what is the epidemiology of psychosis in terms of course?
often chronic, episodic very variable
39
what is the epidemiology of psychosis in terms of morbidity?
substantial, both from disorder itself and increased risk of common health problems e.g. heart disease significant impact on education, employment and functioning
40
what is the epidemiology of psychosis in terms of mortality?
substantial all-cause mortality 2.5x higher, ~15 years life expectancy lost hgh risk of suicide in schizophrenia – 28% of excess mortality
41
what is important when taking a psychiatric history?
history of presenting concern past psychiatric history background history (family, personal, social) past medical history and medicines corroborative history
42
what is important when taking a psychiatric history of a presenting concern?
patient’s description of the presenting problem - nature - severity - onset - course - worsening factors - treatment received circumstances leading to arrival to hospital why now?
43
what is important when taking past psychiatric history?
any known diagnosis? any treatment? known to a community team? any previous admissions to hospital?
44
what is important when taking past family history?
age of parents, siblings, relationship with them atmosphere at home mental disorder in the family, abuse, alcohol/drugs misuse, suicide
45
what is important when taking personal history?
mother’s pregnancy and birth early development, separation, childhood illness educational and occupational history intimate relationships
46
what is important when taking social history?
living arrangements financial issues alcohol and illicit drug use forensic history
47
what is important when taking past medical history and medicines?
regular medications? compliance? over the counter medications? interactions?
48
what is important when taking corroborative history?
informants: relatives, friends, authority confidentiality consent
49
what is noted during a mental state examination?
appearance and behaviour speech mood thoughts perceptions cognition insight
50
what is noted about appearance and behaviour during a mental state examination?
general appearance facial expression posture movements social behaviour
51
what is noted about general appearance during a mental state examination?
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?
52
what is noted about facial expression during a mental state examination?
depressive, anxious “wooden” Parkinsonian
53
what is noted about posture during a mental state examination?
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
54
what is noted about social behaviour during a mental state examination?
disinhibited, overfamiliar withdrawn, preoccupied signs of impending violence: raised voice, clenching fists, pointed fingers, intrusion into personal space
55
what is noted about speech during a mental state examination?
quantity rate spontaneity volume
56
what is noted about quantity of speech during a mental state examination?
less, more, mutism
57
what is noted about rate of speech during a mental state examination?
slow, fast, pressure of speech (keep talking)
58
what is noted about spontaneity of speech during a mental state examination?
latency
59
what is noted about volume of speech during a mental state examination?
quiet, loud
60
what are the two types of mood that are assessed during a mental state examination?
subjective objective - predominant mood - constancy - congruity
61
what is noted about objective constancy during a mental state examination?
emotional lability/incontinence reduced reactivity/blunting/flattening irritability
62
what is noted about objective congruity during a mental state examination?
cheerful while describing sad events etc.
63
what is noted about thoughts during a mental state examination?
stream form content - preoccupations - morbid thoughts, suicidality - delusions, overvalued ideas - obsessional symptoms
64
what is noted about stream of thoughts during a mental state examination?
pressure, poverty, blocking
65
what is noted about form of thoughts during a mental state examination?
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)
66
what is noted about delusions and overvalued ideas (content of thoughts) during a mental state examination?
primary – occurs suddenly secondary – arises from previous abnormal idea/experience (hallucination/mood/delusion) delusional mood/perception/memory shared delusion = folie à deux
67
how may delusional thoughts manifest?
paranoid of reference grandiose/ expansive of guilt/ worthlessness hypochondriacal of jealousy sexual/ amorous religious of control concerning the possession of thought (insertion, withdrawal, broadcast)
68
what is noted about obsessional symptoms (content of thoughts) during a mental state examination?
obsessional thoughts: dirt and contamination, aggressive actions, orderliness, disease, sex, religion compulsions: checking, cleaning, counting, dressing rituals
69
what is noted about perceptions during a mental state examination?
illusions (misperception of a real external stimulus) hallucinations (perception in the absence of external stimulus) distortions
70
what kind of hallucinations may be noted during a mental state exam?
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
71
what is noted about cognition during a mental state examination?
consciousness orientation attention and concentration memory language functioning visuospatial functioning
72
what is noted about insight during a mental state examination?
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
73
what is the prodromal stage of psychosis?
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.
74
what is a pseudohallucination?
not originating externally i.e. "voices in my head" as opposed to "the people I see and hear talking about me"
75
what are the pharmacological options for treatment of psychosis?
antipsychotic medications (often mainstay of treatment)
76
what are the psychological options for treatment of psychosis?
CBT for psychosis newer therapies like avatar therapy
77
what are the social support options for treatment of psychosis?
supportive environments, structures and routines housing, benefits support with budgeting /employment
78
typical vs
s
79
what are the differentials for psychosis?
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.)
80
what neurotransmitter system is most implicated in the mechanism of antipsychotics?
dopamine
81
what is the usual drug action on dopamine receptors to improve psychotic symptoms?
excessive dopamine can cause hallucinations etc. antagonists lower dopaminergic neurotransmission
82
what are some extrapyramidal side effects caused by antipsychotics?
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)
83
what is a typical vs. atypical antipsychotic?
typical antipsychotics commonly cause extrapyramidal side effects at therapeutic doses (not based on drug mechanism)
84
how are the side effects of typical antipsychotics managed?
avoid in first place (atypical antipsychotics usually first line) change medication anticholinergic medications can help (e.g. procyclidine) patients should be informed about risks
85
what are some potential side effects of antipsychotics on the CNS?
EPSEs (extra pyramidal side effects) sedation
86
what are some potential haematological side effects of antipsychotics?
agranulocytosis neutropenia
87
what are some potential metabolic side effects of antipsychotics?
increased appetite weight gain diabetes
88
what are some potential gastrointestinal side effects of antipsychotics?
constipation
89
what are some potential pituitary side effects of antipsychotics?
increased prolactin (release is generally suppressed by dopamine)
90
what are some potential cardiac side effects of antipsychotics?
dysrhythmia long QTc
91
what is the long term management plan for psychosis?
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
92
what is a mood or affective disorder?
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
93
what causes mood disorder episodes?
mood disorders tend to be recurrent onset of individual episodes often related to stressful events
94
what is the prevalence of major depressive disorder (MDD)?
10-20%
95
what is the prevalence of bipolar disorder (I and II), both lifetime and 12-month?
bipolar I - 1% bipolar II - 1.1%
96
how has age of onset changed in major depressive disorder (MDD)?
increasing rate of MDD with earlier age of onset
97
what is the gender distribution of bipolar I disorder?
equal
98
what is the gender distribution of bipolar II disorder?
more women than men
99
what is the gender distribution of major depressive disorder (MDD)?
twice as many women than men
100
what percentage of mental/substance abuse disorders do MDD and bipolar disorders account for?
MDD - 40% bipolar - 7%
101
what percentage of disability adjusted life years (DALYs) do mental and substance abuse disorders account for?
7%
102
what is low mood/depression characterised by?
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
103
what are the DSM-5 criteria for depressive episodes?
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
104
what is the basis of a longitudinal diagnosis of major depressive disorder (MDD)?
diagnosis of a major depressive episode by DSM-5 criteria no past manic or hypomanic episodes
105
what are the 3 DSM-5 subtypes of major depressive disorder (MDD)?
atypical features melancholic features psychotic features
106
what are the features of the atypical subtype of major depressive disorder (MDD)?
mainly increased sleep and appetite heightened mood reactivity
107
what are the features of the melancholic subtype of major depressive disorder (MDD)?
no mood reactivity marked psychomotor retardation anhedonia
108
what are the features of the psychotic subtype of major depressive disorder (MDD)?
presence of delusions or hallucinations
109
what are the 3 triads of depression?
core symptoms biological symptoms psychological symptoms
110
what are the 3 core symptoms of depression?
low mood anergia anhedonia
111
what are the 3 biological symptoms of depression?
sleep libido appetite
112
what are the 3 psychological symptoms of depression?
the world oneself the future
113
what are the behaviours associated with a typical cycle of low mood (unipolar/bipolar depression)?
rumination isolation (passive, stay at home)
114
what are the thoughts associated with a typical cycle of low mood (unipolar/bipolar depression)?
circles of thought - negative automatic thinking e.g. what's the point?
115
what are the physiological symptoms associated with a typical cycle of low mood (unipolar/bipolar depression)?
exhaustion/low energy
116
what are the feelings associated with a typical cycle of low mood (unipolar/bipolar depression)?
low, flat irritability, agitation
117
what are the behaviours associated with a typical cycle of high mood (mania)?
impulsivity increased activity
118
what are the thoughts associated with a typical cycle of high mood (mania)?
grandiose, self related thinking e.g. "I can do anything, I'm the best"
119
what are the physiological symptoms associated with a typical cycle of high mood (mania)?
increased energy racing sensation (related to behaviours, thoughts)
120
what are the feelings associated with a typical cycle of high mood (mania)?
refreshing - euphoria, elation, excitement tips over into more aggressive feelings - agitation, irritability, confusion
121
what are the DSM-5 criteria for manic episodes?
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)
122
what is the basis of a diagnosis of a type I bipolar disorder?
manic symptoms according to DSM-5 for at least 1 week with notable functional impairment (i.e. manic episode)
123
what is the basis of a diagnosis of a hypomanic episode?
manic symptoms according to DSM-5 for at least 4 days but without notable functional impairment
124
what is the basis of a diagnosis of a type II bipolar disorder?
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
125
what is the basis of a diagnosis of an unspecified bipolar disorder?
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)
126
what caveats are given for a diagnosis of a hypomanic episode (i.e. manic episode is diagnosed instead)?
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
127
what is the most consistent clinical feature for diagnosing mood disorders?
psychomotor changes | mood can be variable in these conditions - e.g. MDD can be without sad mood and mania can be without euphoria
128
what is the diagnosis if manic or hypomanic episodes are caused by antidepressants?
bipolar disorder
129
what is cyclothymia?
significant mood swings do not reach the extreme levels of mania or depression
130
how does mood in bipolar I disorder change with respect to mania and depression?
first episode is usually depressive severe mood swings to extremes of mania and depression
131
how does mood in bipolar II disorder change with respect to mania and depression?
severe mood swings does not reach extremes of mania reaches extremes of depression
132
how does bipolar disorder change over time?
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)
133
how does anxiety interact with bipolar disorder?
anxiety prevalent amongst bipolar individuals worse prognosis and outcomes
134
why were bipolar and unipolar disorder defined as separate entities in DSM-III?
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
135
why are bipolar and unipolar disorders more difficult to separate than they were in DSM-III?
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
136
how does heritability differ between bipolar and unipolar mood disorders?
bipolar has higher heritability depression is about half as heritable as bipolar
137
how does insight differ between bipolar and unipolar mood disorders?
often preserved in depression but impaired in mania
138
how does insight present in bipolar mood disorders?
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)
139
what mood disorder diagnosis can easily be missed (and what is the likely misdiagnosis)?
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
140
how can misdiagnosis of bipolar disorders as MDD due to lack of insight be avoided?
collateral history (friends, family)
141
what is a problematic consequence of misdiagnosing bipolar disorder as MDD?
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
142
what are the attention biases in depression?
biases in maintaining/shifting attention difficulties for depressed people to disengage from negative material
143
one study showed prolonged maintenance of attention over negative pictures - what does this demonstrate?
reduced attention allocation to positive stimuli long term effects - seen in individuals with high risk of depression, people with depression and remitted depressed adults
144
how does an fMRI work?
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)
145
what are the physiological changes that allow an fMRI to be taken?
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
146
which parts of the brain display different activity in depression which can be seen using an fMRI?
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)
147
how does depression affect memory processes?
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
148
who do memory biases present in?
individuals at risk (high on personality trait measure of neuroticism) recovered depressed individuals individuals with depression
149
what does the facial expression recognition test show in depression?
increased recognition of sad faces and/or decreased recognition of happy faces (can be seen in healthy individuals with high levels of neuroticism)
150
what do the results of the facial expression recognition test demonstrate?
emotion recognition deficits in MDD reduced recognition of all basic emotions except for sadness
151
what effect does incidental/passive viewing of emotional facial expressions have in depression?
enhanced amygdala response to negative faces
152
what is the function of the amygdala?
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
153
where is the amygdala found?
medial temporal lobe region
154
when does the amygdala show bias?
generally sensitive to detecting and triggering responses to arousing stimuli shows bias towards detecting cues signalling potential threats (e.g. expressions of fear)
155
how does an acute single dose of noradrenergic antidepressant (e.g. reboxetine, duloxetine) affect facial expression recognition in healthy volunteer models?
better recognition of happy faces
156
how does an acute single dose of serotonergic antidepressant (e.g. SSRIs, mirtazapine) affect facial expression recognition in healthy volunteer models?
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)
157
how does 7 days treatment of serotonergic or noradrenergic antidepressant affect facial expression recognition in healthy volunteer models?
reduced recognition of anger and fear reduced amygdala and medial prefrontal cortex response
158
how does clinical response to antidepressants change over time?
early changes in positive processing (facial expression recognition after single dose) are predicative of later response
159
what changes in the anterior cingulate cortex predict a positive response to treatment of depression (medication, neurostimulation, CBT)?
elevated baseline ACC activity during tasks that probe affective circuitry (also executive functions or self-referential processes such as the resting state)
160
where are the nuclei from where the serotonergic neurons project located?
raphe nuclei in midbrain
161
how many different serotonin receptors are there?
14
162
what is serotonin also known as?
5-hydroxytryptamine (5-HT)
163
where does serotonin reuptake occur?
proteins located on pre-synaptic membrane
164
what does the monoamine deficiency hypothesis of depression postulate?
``` depressive symptoms arise from insufficient levels of monoamine neurotransmitters - serotonin/5-HT - norepinephrine - dopamine ```
165
how does use of reserpine (antihypertensive) provide indirect evidence of 5-HT hypofunction in depression?
reserpine (antihypertensive) can lead to 5-HT depletion - causes depressive symptoms
166
how does use of clinically useful antidepressants provide indirect evidence of 5-HT hypofunction in depression?
all help with depressive symptoms through mediating increase in synaptic monoamine (some selectively 5-HT) concentrations
167
how does use of PET scanning provide indirect evidence of 5-HT hypofunction in depression?
shows lower levels of 5-HT1A and 5-HT4 receptors in brains of people with depressive symptoms
168
how do monoamine oxidase A levels provide indirect evidence of 5-HT hypofunction in depression?
increased levels of monoamine oxidase A in MDD (more degradation of 5-HT)
169
how does blocking serotonin synthesis provide indirect evidence of 5-HT hypofunction in depression?
inhibition of tryptophan hydroxylase (converts tryptophan to serotonin) with p-chlorophenylalanine prevents antidepressant effects of MAOIs and TCAs
170
how does tryptophan depletion provide indirect evidence of 5-HT hypofunction in depression?
depletes synthesis of serotonin via tryptophan hydroxylase can trigger relapse in MDD
171
how do mood changes provide indirect evidence of 5-HT hypofunction in depression?
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
how does serotonergic transmission in vulnerability marker traits provide indirect evidence of 5-HT hypofunction in depression?
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
what are the disadvantages of PET imaging in comparison to fMRI?
invasive radioactive expensive less optimal temporal and spatial resolution
174
what are the advantages of PET imaging in comparison to fMRI?
more selective (fMRI gives no information about molecules or transmitters involved in increased or decreased brain activity)
175
how does PET imaging work?
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
how can PET imaging be used practically?
measure dopamine levels and dopamine release in brain
177
how can PET imaging be used to compare dopamine levels and release (quantify dopamine receptors)?
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
why has usage of PET imaging to measure 5-HT levels by issuing a pharmacological challenge not been successful so far?
tracers used are all antagonists (i.e. not as sensitive to changes in synaptic levels of the transmitter)
179
how may usage of PET imaging to measure 5-HT levels by issuing a pharmacological challenge be successful in the future?
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
what has PET imaging with a pharmacological challenge shown about serotonin thus far?
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
what are the advantages of being able to measure serotonin levels in the brain directly (e.g. PET imaging with pharmacological challenge)?
predict treatment response understand treatment resistance and give target medication based on this
182
what is important in taking a past psychiatric history in suspected depression?
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
what is important in taking family history in suspected depression?
any mental illness? who (e.g. first degree relative?) what are the family relationships like?
184
what is important in taking medication history in suspected depression?
- 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
what is important in taking forensic history in suspected depression?
arrests cautions incarcerations forensic mental health act admissions probation officer
186
what is important in taking personal history in suspected depression?
birth, early life school, qualifications, higher/further education employment psychosexual history premorbid personality
187
what risk assessment is taken in suspected depression?
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
what are the differentials in a suspected case of depression?
bipolar vs unipolar? bipolar (and depression) vs borderline personality disorder? bipolar vs schizophrenia? bipolar vs attention deficit disorder?
189
what is cluster A of personality disorders according to DSM-5?
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
what is cluster B of personality disorders according to DSM-5?
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 and affect, often leading to self-harm and impulsivity histrionic: pervasive pattern of attention-seeking behaviour and excessive emotions narcissistic: pervasive pattern of grandiosity, need for admiration, and a perceived or real lack of empathy
191
what is cluster C of personality disorders according to DSM-5?
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 from obsessive-compulsive disorder)
192
what are the similar traits between bipolar affective disorder and borderline personality disorder?
rapid mood swings unstable interpersonal relationships impulsive sexual behaviour suicidality
193
how can you differentiate between bipolar affective disorder and borderline personality disorder?
BPAD: - runs in family; heritability +++ - grandiosity - mood states typically less affected by environment BPD: - poor self image - fear of abandonment - feelings of emptiness
194
what are the similar traits between bipolar affective disorder and schizophrenia?
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
how can you differentiate between bipolar affective disorder and schizophrenia?
BPAD: - episodic delusions/hallucinations schizophrenia: - chronic delusions/hallucinations
196
what are the similar traits between bipolar affective disorder and attention deficit disorder?
impaired concentration impairment of executive function abnormal working and short term memory
197
how can you differentiate between bipolar affective disorder and attention deficit disorder?
family history (heritability+++) recurrent depressive episodes amphetamines worsen mania
198
what are some endocrine causes of symptoms of depression?
hyperthyroidism, hypothyroidism hyperparathyroidism, hypoparathyroidism hyperadrenocorticism, hypoadrenocorticism hypoglycaemia Cushing's syndrome Addison's disease
199
what are some systemic conditions that may lead to symptoms of depression?
viral infections systemic lupus erythematosus HIV infection pancreatic (and other) cancer
200
how may systemic diseases lead to causes of depression?
cytokines manifested in systemic diseases are considered to be a cause of depression
201
what are some deficiencies that may lead to symptoms of depression?
vitamin B12 or folic acid
202
what are some neurological conditions that may lead to symptoms of depression?
multiple sclerosis Alzheimer's Parkinson's
203
what are some medications that may lead to symptoms of depression?
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
who is vascular depression/early sub-cortical dementia common in?
later life
205
what is vascular depression associated with?
white matter hyperintensities
206
how do white matter hyperintensities increase risk of vascular depression?
impact on cognitive function makes the individual more vulnerable to stressors
207
what are vascular risk factors that could increase risk of vascular depression?
diabetes hypertension smoking alcohol use
208
what features are prominent in post-stroke depression?
retardation in thinking and behaviour
209
lesions in which areas of the brain can cause post-stroke depression?
left frontal lobe basal ganglia
210
how does the position of a lesion affect the severity of post-stroke depression?
the more frontal the lesion, the more severe the symptom
211
what questions should be asked about drug abuse?
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
what are the 4 broad categories of drug?
depressant stimulant hallucinogenic cannabinoid
213
why may someone take a drug recreationally?
``` 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
how can recreational use of a drug lead to dependency?
"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
what proportion of people that recreationally use a drug will become dependent?
"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
how is harmful substance use defined according to ICD-10?
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
how is hazardous substance use defined according to ICD-10?
one step before harmful substance use i.e. likely to become harmful if they carry on in the same manner
218
what are the 6 criteria that define dependence syndrome according to ICD-10?
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
what is a 'binge'?
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
what is necessary for a diagnosis of dependence syndrome (ICD-10)?
meet 3 ICD-10 criteria within a period of 12 months
221
what is the difference between addiction and dependence?
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
how does a drug produce psychoactive effects?
enters brain
223
what property of drugs affects its addictive potential?
speed of entry into brain faster entry = more “rush”, more addiction (difference in intake method of coca leaves vs cocaine vs crack)
224
what 3 things contribute to the speed of entry of a drug into the brain (and therefore higher addictive potential)?
speed of reaching the brain speed of crossing the blood-brain barrier lipophilicity of drug
225
what 3 elements are involved in substance use and addiction?
social, environmental factors (access, social norms, cost etc.) personal factors (genetics, personality traits like impulsivity, family history) drug factors (kinetics, formulation taken)
226
what factors influence pre-existing vulnerability to addiction?
family history age
227
how may age influence pre-existing vulnerability to addiction?
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
what factors influence increased drug exposure in addiction?
compensatory neuroadaptations to maintain brain function resilience (i.e. being able to take a drug and not experience many detrimental effects)
229
how may acute use of alcohol help users to sleep or reduce anxiety?
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
how may chronic use of alcohol affect the GABA and glutamate systems?
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
how may genetics affect the GABA-A receptor and therefore alcohol tolerance?
less sensitive GABA-A receptor feel fewer adverse effects - can drink more, therefore damage is greater
232
in the absence of alcohol (withdrawal) after chronic use, how do the GABA and glutamate systems react?
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
how can withdrawal symptoms after chronic alcohol usage be treated?
benzodiazepines boost function of GABA system counteract glutamatergic hyperactivity, restore balance
234
how can magnetic resonance spectroscopy demonstrate the effects of benzodiazepines in treating alcohol withdrawal?
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
how does acamprosate help people to abstain from alcohol?
reduces NMDA function reduces toxicity in brain, potentially neuroprotective (idiopathic improved cognitive function, reduced seizure risk)
236
why may anticonvulsants be able to treat alcohol withdrawal?
affect glutamate and GABA systems
237
what are the 3 models of addiction?
reward deficiency (positive reinforcement) overcoming adverse state, negative reinforcement (e.g. withdrawal, anxiety) impulsivity/compulsivity
238
how does the reward deficiency model work?
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
what does the reward (dopaminergic) system look like?
dopaminergic projections in ventral tegmental area (VTA) of brain stem project into ventral striatum and frontal cortex
240
how does the opioid system act as a key modulator for the dopamine system?
mediates pleasurable effects (e.g. of alcohol) - produces endorphin rush that modulates dopamine system
241
what are some modulators of the dopamine system?
GABA-B cannabinoids glutamate
242
how does cocaine interact with the dopamine system?
block post-synaptic dopamine re-uptake channel more dopamine in the synapse, more of a signal
243
how do amphetamines interact with the dopamine system?
block post-synaptic dopamine re-uptake channel - more dopamine in the synapse, more of a signal enhances release of dopamine
244
why do drugs of abuse like cocaine or amphetamines (stimulants) have such a potent effect on addiction and the reward process?
directly target dopamine synapse
245
how do drugs of abuse like alcohol, opiates or nicotine interact with the dopamine system?
increase dopamine neuron firing in ventral tegmental area (VTA) by altering tonic inhibitory responses (indirect effects)
246
how does the reward-deficient addiction model work with respect to availability of dopamine receptors?
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
how can reward deficiency in adolescence be linked to vulnerability to problematic drug use?
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
how does the reward system appear in abstinent addicts as compared to healthy controls?
blunted activation of reward system
249
how does the reward system appear in poly drug users as compared to healthy controls?
blunted activation of reward system
250
how does the reward system appear in relapsed addicts as compared to abstinent addicts?
substantial blunting of reward system | not in all individuals
251
theoretically, how could risk of relapse be mitigated when treating addiction?
medication that boosts dopamine system to counter naturally blunted reward system activation
252
what are the 3 stages involved in the cycle of addiction?
binge/intoxication - positive reinforcement withdrawal (negative affect, negative reinforcement) preoccupation/anticipation - craving
253
which region of the brain does withdrawal affect?
hypothalamus and brainstem effectors (autonomic, somatic, neuroendocrine) amygdala
254
what effects does withdrawal produce due to its impact on the amygdala?
highly aroused, anxious state
255
how can the change from positive to negative reinforcement be described as dependence develops?
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
what is an addict's motivation when taking a drug after reaching a point of negative reinforcement?
need to overcome greater withdrawal state rather than achieve pleasure fear/anxiety apparent without access to drug - cannot counter negative state
257
how does dysregulation of the amygdala affect the 'reward' system?
reduced dopamine and mu opioid function
258
how does dysregulation of the amygdala affect the 'stress' system?
increased activity - arousal system (noradrenaline) - CRF system (cortisol) - kappa system (dynorphin) decreased 'anti-stress' neurotransmitters (e.g. oxytocin, nociceptin)
259
what is the kappa opioid/dynorphin system?
opposite to mu opioid/dopamine system which produces endorphins
260
what kind of state is produced by stimulation of the kappa opioid/dynorphin system?
produces aversive, dysphoric state
261
how can dysregulation of the amygdala in addiction be demonstrated using aversive images and fMRI?
heightened brain response to aversive images in left amygdala for abstinent polydrug addicts (but not in alcoholism)
262
what transition in the brain takes place during the change from voluntary drug use to compulsive drug use?
executive control moves deeper from prefrontal cortex to striatum specifically - move from ventral (limbic/emotional) to dorsal (habitual) striatum
263
what does the balance between the prefrontal cortex and the striatum usually moderate?
internal drives
264
what disease is associated with the dorsal striatum?
Parkinson's
265
which part of the brain is highly associated with craving?
hippocampus (memory)
266
how can neurocircuitry involved in inhibitory control be assessed?
go - no go task with fMRI
267
where can activity be seen in a go - no go task with fMRI?
putamen (dorsal striatum and inferior frontal gyrus)
268
what does a go - no go task with fMRI show in abstinent addicts?
greater activity in putamen higher in abstinent alcoholics when compared to abstinent poly drug users and controls
269
what does a higher level of activity in the putamen shown in an fMRI of abstinent addicts indicate?
greater response associated with longer abstinence i.e. greater activity during inhibitory control, facilitates staying sober
270
how can units of alcohol be calculated?
% strength x ml/1000
271
what is the excretion rate of alcohol?
1 unit per hour
272
what are the symptoms of opiate withdrawal?
tachycardia sweating restlessness dilated pupils bone aches runny nose GI upset tremor yawning anxiety/irritability gooseflesh skin
273
what drugs can be given to aid abstinence of alcohol?
acamprosate disulfiram (antabuse) naltrexone nalmefene
274
how does acamprosate help alcohol abstinence?
increases GABA, NMDA antagonist
275
how does disulfiram (antabuse) help alcohol abstinence?
inhibits acetaldehyde dehydrogenase therefore feel nauseous/flushes if mixed with alcohol
276
how does nalmefene help alcohol abstinence?
opioid antagonist given on days at high risk of drinking, in those dependent but without withdrawal, to reduce alcohol intake
277
what drugs can be given to aid abstinence of opioids?
methadone buprenorphine
278
what are the DSM-5 criteria for opioid/alcohol use disorder?
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
how is opioid/alcohol use disorder categorised according to DSM-5?
2 symptoms - opioid/alcohol use disorder mild: 2-3 symptoms moderate: 4-5 symptoms severe: 6+ symptoms
280
what does a history taking look like in substance misuse?
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
what are some common comorbid conditions with substance use disorders?
depression anxiety suicidality personality disorder PTSD bipolar disorder
282
what are the major causes of morbidity and mortality associated with substance abuse?
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
what is drug induced psychosis?
cluster of psychotic phenomena occurring during or immediately after substance use, especially stimulants (e.g. crack, methamphetamine)
284
how may drug induced psychosis present?
vivid hallucinations, often auditory paranoid delusions (can be severe)
285
how long does drug induced psychosis take to resolve?
within 1-6 months
286
why must diagnosis of drug induced psychosis be done carefully?
care not to diagnose something like a schizophrenic episode, which may be 'triggered' by substance abuse
287
what features of alcohol abuse should be noted during examination?
jaundice anaemia clubbing cyanosis oedema ascites lymphadenopathy DVT
288
what investigations should be done in suspected alcohol abuse?
fibro scan /ultrasound bloods (LFT, GGT, lipids, U&E, amylase) breathalyser urine drug screen
289
what features of opioid abuse should be noted during examination?
collapsed veins / track marks endocarditis skin abscesses hepatitis / HIV pneumonia
290
what investigations should be done in suspected opioid abuse?
bloods (LFT, GGT, U&E, glucose) breathalyser urine drug screen sexual health screening/BBV
291
what is CAGE screening (alcohol assessment)?
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
what is an AUDIT test?
alcohol use disorders identification test - 10 questions about alcohol intake
293
how can AUDIT test results be categorised?
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
what are the immediate effects of alcohol on the CNS?
impaired reaction time and motor co ordination impaired judgement sedation (coma and death)
295
what are the immediate effects of alcohol on the senses?
less acute
296
what are the immediate effects of alcohol on the stomach?
nausea inflammation bleeding
297
what are the immediate effects of alcohol on the skin?
flushing sweating heat loss and hypothermia formation of broken capillaries
298
what are the immediate effects of alcohol on sexual functioning?
reduced erection response reduced vaginal lubrication
299
what are the chronic effects of alcohol on the brain?
damaged brain cells reduced brain size impaired memory loss of sensation in limbs brain atrophy
300
what are the chronic effects of alcohol on the cardiovascular system?
weakened cardiac muscle elevated blood pressure irregular heartbeat increased stroke risk
301
what are the chronic effects of alcohol on the breast?
increases risk of breast cancer
302
what are the chronic effects of alcohol on the immune system?
lowered disease resistance
303
what are the chronic effects of alcohol on the digestive system?
cirrhosis inflammation of stomach and pancreas increased risk of lip, mouth, larynx, oesophagus, liver, rectal and stomach cancers
304
what are the chronic effects of alcohol on the kidney?
kidney failure associated with end stage liver disease
305
what are the chronic effects of alcohol on nutrition?
nutrient deficiencies obesity
306
what are the chronic effects of alcohol on the reproductive system?
menstrual irregularities increased risk of children with foetal alcohol syndrome impotence testicular atrophy
307
what are the chronic effects of alcohol on bone?
increased risk of osteoporosis increased risk of fractures (frequent falls)
308
how does alcohol withdrawal present over time?
Worsening pattern of symptoms onset usually from 6 hours hallucinations can occur any time delirium tremens is a late sign
309
what are the 2 effects of opioids?
analgesic effect sense of euphoria
310
what are some examples of opioid agonists that affect mu, delta and kappa opioid receptors?
heroin, methadone, fentanyl, codeine
311
what are some examples of partial opioid agonists that affect mu, delta and kappa opioid receptors?
buprenorphine
312
what are some examples of opioid antagonists that affect mu, delta and kappa opioid receptors?
naltrexone
313
what is the difference between opiates and opioids?
opiates: natural opioids (e.g. morphine, codeine, heroin to some extent)  opioids:  all natural, semisynthetic (e.g. heroin, oxycodone), and synthetic (e.g. fentanyl, methadone) opioids
314
what are the 4 types of treatment in psychiatry, with examples?
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
what are the advantages of classifying psychiatric drugs based on chemical structure?
each drug has unique structure, easy to allocate data
316
what are the disadvantages of classifying psychiatric drugs based on chemical structure?
no use in clinical decision making
317
what are the advantages of classifying psychiatric drugs based on what illnesses they treat (antidepressant, antipsychotic etc.)?
easy for doctors to choose as they make the diagnosis
318
what are the disadvantages of classifying psychiatric drugs based on what illnesses they treat (antidepressant, antipsychotic etc.)?
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
what do psychiatric medicines target?
1 (maybe 2) of 4 different systems - receptors - neurotransmitter reuptake sites - ion channels - enzymes
320
how can psychiatric drugs produce unwanted side effects?
targets are in the brain but drugs can affect systems elsewhere (especially liver enzymes)
321
how are neurotransmitters create/inhibit an action potential in the receiving neuron?
action potential moves down axon neurotransmitters released across synapse activate receptors on post-synaptic membrane
322
how are neurotransmitters released across the synapse?
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
what happens to neurotransmitters after acting on post synaptic receptors?
most taken back up in the pre synaptic neuron through transporter/re-uptake site
324
which neurotransmitter is not taken back up through re-uptake proteins?
acetylcholine
325
how is acetylcholine broken down?
degrading enzymes outside the terminal
326
how are autoreceptors involved in inhibition of action potentials?
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
how do monoamine oxidase inhibitors act on enzymes to treat anxiety and depression?
block the breakdown of 5-HT and noradrenaline
328
how do acetylcholinesterase inhibitors act on enzymes to treat dementia?
block the breakdown of acetylcholine | deficiency of acetylcholine in dementia
329
how does lithium act on enzymes to treat bipolar disorder?
blocks glycogen synthase kinase stabilises neurones to produce mood stability
330
how do dopamine blockers act on receptors to treat schizophrenia?
antagonists
331
how do serotonin receptor subtype antagonists act on receptors to treat depression?
augment effects of SSRIs
332
how do benzodiazepines act on receptors to promote sleep and reduce epilepsy?
agonists enhance inhibitory transmitter GABA
333
how does guanfacine act on receptors to control ADHD?
enhances noradrenaline
334
what is the principle behind psychiatric drugs that target reuptake sites?
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
what are 3 examples of drugs that target reuptake sites?
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
why is the 5-HT1A receptor targeted in treatment of depression?
increased stimulation of receptor inhibits activity in neurons with these receptors
337
why is the 5-HT2 receptor targeted in treatment of schizophrenia, sleep regulation and eating?
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
what is the principle behind psychiatric medication targeting ion channels?
block channels to reduce neuronal excitability
339
how do drugs like sodium valproate and carbamazepine aid treatment of epilepsy by targeting ion channels?
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
how do drugs like sodium valproate and carbamazepine aid mood stabilisation in bipolar disorder by targeting ion channels?
block sodium channels block transmission of information down the axon prevention of recurrent cyclical activity between groups of neurones helps stabilise mood
341
how do drugs like gabapentin or pregabalin aid treatment of epilepsy and anxiety by targeting ion channels?
block calcium channels in terminal region of axons (synapse) prevent neurotransmitter release
342
how can neurotransmitters be divided into 2 categories?
fast acting (on-off) slow acting (neuromodulators)
343
what kind of fast acting neurotransmitter is glutamate?
excitatory
344
where is glutamate present?
80% of all neurons pyramidal cells (regulation of brain function)
345
what kind of fast acting neurotransmitter is GABA?
inhibitory
346
where is GABA present?
15% of all neurons interneurons (connect other neurons together, make up network of brain)
347
what is the balance between glutamate and GABA responsible for?
content of everything e.g. memory, movement, vision
348
what is the role of neuromodulators?
adds emotions, drives, valence to content created by fast acting neurons
349
what is valence?
attractiveness/"good"-ness (positive valence) or averseness/"bad"-ness (negative valence) of an event, object, or situation
350
what does excess glutamate cause?
epilepsy alcoholism
351
how can epilepsy caused by excess glutamate be treated?
perampanel (glutamate receptor blocker)
352
how can alcoholism caused by excess glutamate be treated?
acamprosate, ketamine (glutamate receptor blocker)
353
what does deficient GABA cause?
anxiety
354
how can anxiety caused by deficient GABA be treated?
benzodiazepines (GABA enhancer)
355
what does deficient 5-HT cause?
depression anxiety
356
how can anxiety and depression caused by deficient 5-HT be treated?
SSRIs and MAOIs (serotonin enhancers)
357
what does excess dopamine cause?
psychosis
358
how can psychosis caused by excess dopamine be treated?
dopamine receptor blockers
359
what does excess noradrenaline cause?
nightmares (e.g. in PTSD)
360
how can nightmares caused by excess noradrenaline be treated?
prazosin (noradrenaline receptor blocker)
361
what does deficient acetylcholine cause?
impaired memory/dementia
362
how can impaired memory caused by deficient acetylcholine be treated?
acetylcholinesterase enzyme blockers
363
when can partial agonists be safer than full agonists?
improved safety in overdose
364
how can a partial agonist act as a modulator?
effect of partial agonist determined by level of neurotransmitter excess neurotransmitter - blocks receptor (acts as an antagonist) neurotransmitter deficit - acts as an agonist
365
why is a partial agonist's action as a modulator better than that of a full antagonist?
blocking all effects of a neurotransmitter may have more side effects
366
how can a partial agonist be used in treating heroin addiction?
buprenorphine - heroin alternative - used to treat pain and addiction syndromes
367
how can a partial agonist be used in treating depression?
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
how can a partial agonist be used in treating nicotine addiction?
varenicline | - replacement therapy for tobacco
369
what is an inverse agonist?
opposite effect to an agonist e.g. GABA has inhibitory effect, inverse agonist has excitatory effect
370
how can an inverse agonist be used to improve memory (e.g. in alcoholism)?
alpha-5IA acts as inverse agonist for GABA acts in hippocampus, increases activity/functionality to reverse amnesiac effects
371
how can an inverse agonist be used to improve attention (e.g. in ADHD)?
histamine blockers cause sedation inverse agonists have opposite effect
372
what is the most common GABA-A receptor sub-type?
2 alpha, 2 beta, 1 gamma proteins
373
what are the components of a GABA-A receptor?
5 separate proteins combined in multiple ways to form different receptor sub-types
374
where is the most common type of GABA-A receptor found?
cortex
375
how are different GABA-A receptors arranged at the synapse?
alpha-1 - synaptic alpha-2 - proximal segment of synapse alpha-5 - extra synaptic
376
how does the arrangement of alpha-1 GABA-A receptors at the synapse relate to their function?
alpha-1 - synaptic regulates inhibition from the GABA inter-neurons onto these pyramidal cells
377
how does the arrangement of alpha-2 GABA-A receptors at the synapse relate to their function?
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
how does the arrangement of alpha-5 GABA-A receptors at the synapse relate to their function?
alpha-5 - extra synaptic produce a tonic activity (dampen down tonic activity in the brain)
379
how is the GABA-A alpha-5 receptor distributed in the brain?
highly expressed in 'emotionally rich' areas cingular cortex, hippocampus
380
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?
tonic activity necessary to maintain equilibrium lack of function may contribute to anxiety, addiction etc.
381
what is an orthosteric site/orthosteric receptor?
receptor/site that the original transmitter binds to
382
how does the binding of GABA to its receptor produce an effect?
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
how does the binding of benzodiazepines to the GABA-A receptor produce an effect? (also barbiturates, neurosteroids, ethanol)
bind to GABA receptor (allosteric site) enhances action of GABA (sedation) therefore help with sleep, anxiety reduction, anti-epilepsy
384
why does haloperidol cause side effects in treatment of schizophrenia with reference to its selectivity?
highly selective for D2 receptor (minor effects of alpha-1 receptor) adverse effects due to full dopamine receptor block
385
why does clozapine cause side effects like sedation and weight gain in treatment of schizophrenia with reference to its selectivity?
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
why does clozapine cause side effects like constipation in treatment of schizophrenia with reference to its selectivity?
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
why does amitriptyline cause side effects in treatment of depression with reference to its selectivity?
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
why may the side effects of amitriptyline cause death?
overdose may lead to cardiac and brain toxicity
389
why is citalopram preferred to amitriptyline with reference to its selectivity?
selective for 5-HT reuptake transporters adverse effects solely driven by increased serotonin (therefore limited)
390
how can dementia be described?
degenerative disease of the brain with cognitive and behavioural impairment sufficiently severe to interfere significantly with social and occupational function
391
what are amyloid plaques?
insoluble β-amyloid peptide deposits as senile plaques or β-pleated sheets
392
where are amyloid plaques found?
hippocampus amygdala cerebral cortex
393
how do amyloid plaques relate to the pathophysiology of dementia?
increased density with advanced disease
394
what are neurofibrillary tangles (NFTs)?
consist of phosphorylated tau protein
395
where are neurofibrillary tangles (NFTs) found?
cortex hippocampus substantia nigra
396
how are amyloid plaques and neurofibrillary tangles (NFTs) related to the pathophysiology of dementia?
co-occurrence of amyloid plaques and NFTs now accepted as a hallmark of dementia (NFTs are also found in normal ageing)
397
how are the neurons affected in the pathophysiology of dementia?
up to 50% loss of neurons and synapses in cortex and hippocampus
398
how is chromosome 21 implicated in development of dementia?
gene for amyloid precursor protein (APP) found on the long arm (also implicated in Down’s syndrome)
399
how is chromosome 19 implicated in development of dementia?
codes for apolipoprotein E4 presence of E4 alleles increases risk of Alzheimer's
400
how is chromosome 14 implicated in development of dementia?
codes for presenilin 1 | implicated in B-amyloid peptide
401
how is chromosome 1 implicated in development of dementia?
codes for presenilin 11 | implicated in B-amyloid peptide
402
what is the cholinergic hypothesis?
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
how may drugs such as donepezil be used in treatment of dementia?
acetylcholinesterase inhibitor increased levels of cortical acetylcholine
404
how may drugs such as memantine be used in treatment of dementia?
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
what are the early signs of dementia?
absent-mindedness difficulty recalling names and words difficulty learning new information disorientation in unfamiliar surroundings reduced social engagement
406
what are the signs of progressive dementia?
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
what are the signs of advanced dementia/Alzheimer's?
monosyllabic speech psychotic symptoms behavioural disturbance loss of bladder and bowel control reduced mobility
408
what are some psychiatric symptoms of dementia?
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
what are some behavioural disturbances seen in dementia?
aggression wandering explosive temper sexual disinhibition incontinence excessive eating searching behaviour.
410
what are some personality changes seen in dementia?
often reflects an exaggeration of premorbid traits with coarsening of affect and egocentricity
411
why is differential diagnosis of Alzheimer's difficult/inexact?
due to mixed nature of dementia pathologies e.g. AD frequently occurs in the presence of vascular changes, indicating coexisting vascular dementia
412
what are the criteria for a clinical diagnosis of 'probable Alzheimer's disease'?
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
how does dementia differ from delirium and depression in terms of onset?
dementia - insidious (months to years) delirium - acute (hours to days) depression - acute or insidious (weeks to months)
414
how does dementia differ from delirium and depression in terms of course?
dementia - progressive delirium - fluctuating depression - may be chronic
415
how does dementia differ from delirium and depression in terms of duration?
dementia - months to years delirium - hours to weeks depression - months to years
416
how does dementia differ from delirium and depression in terms of consciousness?
dementia - usually clear delirium - altered depression - clear
417
how does dementia differ from delirium and depression in terms of attention?
dementia - impaired delirium - normal (except in severe dementia) depression - may be decreased
418
how does dementia differ from delirium and depression in terms of psychomotor changes?
dementia - often normal delirium - increased or decreased depression - may be slowed in severe cases
419
how does dementia differ from delirium and depression in terms of reversibility?
dementia - irreversible delirium - usually depression - usually
420
why are routine dementia investigations done?
exclude reversible causes of cognitive deterioration
421
what blood tests are done as part of routine dementia investigations?
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
why is imaging a part of routine dementia investigations?
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
how is an MRI useful as a part of routine dementia investigations?
assists with early diagnosis detects subcortical vascular changes (CT scanning could also be used)

BRS 2 (10 decks)

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