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Year 3 - Psychiatry (DP) > Development, Memory and Addiction > Flashcards

Development, Memory and Addiction Flashcards

1
Q

What brain structural changes in Schizphrenia result in a poorer prognosis?

A

Reduced frontal lobe volume
Reduced frontal lobe grey matter
Increased lateral ventricle volume

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2
Q

Where are there consistent reductions in brain structure in Schizophrenia?

A 
Temporal cortex (esp. Superior Temporal Gyrus)
Medial temporal lobe (esp. Hippocampus)
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3
Q

What is the neuropil composed of?

A

Mostly unmyelinated axons, dendrites and glial cells processes

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4
Q

What does neuropil form?

A

Synaptically dense region with a relatively low number of cell bodies:
- eg. Neocortex and olfactory bulb

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5
Q

When are grey matter abnormalities present in Schizophrenia?

A

Early

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6
Q

How can brain white matter be investigated?

A

Diffusion tensor imagine

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7
Q

What do higher numbers in fractional anisotropy indicate?

A

Healthy white matter tracts

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8
Q

What do higher numbers in mean diffusivity indicate?

A

Less healthy white matter tracts

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9
Q

Children showing impairment in what areas during infancy are more likely to develop Schizophrenia?

A

Behaviour
Motor development
Intellect

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10
Q

What does ventricular enlargement at diagnosis of Schizophrenia indicate?

A

It is non-progressive

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11
Q

What is the DA hypothesis in Schizophrenia?

A

Drugs which:
- Release DA (eg. Amphetamine) OR
- D2 receptor agonists (eg. Apopmorphine)
…both produce psychosis

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12
Q

According to the DA hypothesis, what effect does Amphetamine have on Schizophrenia?

A

Worsens it

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13
Q

According to the DA hypothesis, what effect do D2 receptor antagonists have in Schizophrenia?

A

Treat the symptoms

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14
Q

What DA pathways are overactive and may be related to Schizophrenia?

A

Tuberinfundibular (PRL release)
Mesolimbic/Cortical (Motivation and reward)
Nigrostriatal (Extrapyramidal motor system)

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15
Q

What do D1 family DA receptors (D1 and D5) do?

A

Stimulate cAMP

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16
Q

What do D2 family DA receptors (D2, D3 and D4) do?

A

Inhibit adenylyl cyclase
Inhibit voltage-gated calcium channels
Open potassium channels

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17
Q

What are the most abundant DA receptors?

A

D1

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18
Q

Where are D2 receptors also present?

A

Pituitary

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19
Q

What receptor is Bromocriptine an agonist of?

A

D2

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20
Q

What receptor is Raclopride an antagonist of?

A

D3

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21
Q

What receptor are Raclopride and Haloperidol antagonists of?

A

D2

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22
Q

What receptor is Quinpirole an agonist of?

A

D3

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23
Q

What receptor is Clozapine an antagonist of?

A

D4

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24
Q

What does subcortical DA hyperactivity result in?

A

Psychosis

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25
Q

What does mesocortical DA hypoactivity result in?

A

Negative and cognitive symptoms

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26
Q

What is the glutamatergic hypothesis?

A

Altered NMDA receptor subunit expression

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27
Q

What drug, which can cause psychosis, is explained by the glutamatergic hypothesis?

A

Ketamine

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28
Q

What is the serotonergic hypothesis?

A

Serotonin 2A binding potential in frontal cortex slightly small (by 16.3%) in schizophrenic patients

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29
Q

What gene alterations are indicated in psychosis?

A

Neuregulin
Dysbindin
DISC-1

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30
Q

What does Neuregulin do?

A

Signalling protein

Mediates cell-cell interactions and plays critical roles in growth and development

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31
Q

What does Dysbindin do?

A

Essential for adaptive neural plasticity

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32
Q

What does DISC-1 do?

A

Involved in neuritic outgrowth and cortical development via interactions with other proteins

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33
Q

What are some examples of typical (1st gen.) antipsychotics?

A 
Chlorpromazine
Thioridazine
Fluphenazine
Haloperidol
Zuclopentixol
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34
Q

How do typical antipsychotics work?

A

D2 inhibition:

  • Immediate blockaed
  • Delay in onset of effect
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35
Q

What are the side effects of typical antipsychotics?

A 
Dry mouth
Muscle stiffness and cramps
Tremor
Extrapyramidal signs:
- Akathisia
- Parkinsonism
- Dystonia
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36
Q

What is the definition of an atypical (2nd gen.) antipsychotic?

A
  1. Less likely to induce extrapyramidal symptoms
  2. High 5-HT2a:D2 ratio
    (3. Better efficacy against negative symptoms)
    (4. Effective if atypicals don’t work)
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37
Q

What are some examples of atypical antipsychotics?

A 
Olanzapine
Risperidone
Quetiapine
Clozapine
Aripiprazole
Amilsupride
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38
Q

What are the side effects of most/all atypical antipsychotics?

A 
Mostly metabolic:
- Weight gain
- Hyperglycaemia
- Dyslipidaemia and Hypertension
Sexual dysfunction
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39
Q

What atypical antipsychotics can cause extrapyramidal symptoms at high doses?

A

Olanzapine
Risperidone
Amilsupride

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40
Q

What side effect can olanzapine have?

A

Increase PRL at high doses

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41
Q

How does an acute dystonic reaction present?

A

Muscle spasms

Within hours-days of initiation of antipsychotics

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42
Q

How are acute dystonic reactions treated?

A

Ach antagonists:

  • Prochlorperazine
  • Procyclidine
  • Orhphenadine
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43
Q

What is tardive dyskinesia?

A

Repetitive, involuntary movements:

  • Grimacing
  • Sticking tongue out
  • Lip smacking
  • Pursing lips
  • Blinking
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44
Q

How long does tardive dyskinesia take to develop?

A

Years to develop

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45
Q

What effect does stopping medications have on tardive dyskinesia?

A

It often continues

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46
Q

What do drugs with a high affinity for 5-HT2 receptors cause?

A

Hallucinations

Thought disturbance

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47
Q

What drugs have a high affinity for 5-HT2 receptors?

A

Hallucinogenic indoleamines

Phenylethylamines

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48
Q

How is 5-HT2 receptors binding affected in Schizophrenia?

A

Reduced

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49
Q

Blockade of what histamine receptor causes sedation?

A

H1

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50
Q

How does histamine blockade affect appetite?

A

Increases it

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51
Q

Why are newer anti-histamines not as sedative?

A

Do not cross BBB

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52
Q

What is histamine involved in?

A

Appetite
Pain perception
Regulation of pituitary hormon secretion
Reducing nausea and vomiting

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53
Q

What serious side effect can Clozapine have?

A

Agranulocytosis

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54
Q

How are the side effects of Clozapine monitored and prevented?

A

FBC:

  • Weekly for first 6 months
  • Fortnightly for next 6 months
  • Every 4 weeks thereafter
  • For 1 months after cessation
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55
Q

If a patient has a sore throat while on Clozapine, what must be done?

A

FBC!!

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56
Q

How does Clozapine cause myocarditis?

A 
IgE-mediated Type 1 sensitivity
OR
Cytokine release
OR
Hypercatecholaminaemia
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57
Q

How is myocarditis monitored/prevented while on Clozapine?

A

Regular ECGs:

- May show nonspecific ST segment changes

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58
Q

What is the first line treatment of Schizophrenia?

A

An atypical antipsychotic (risperidone or olanzapine):

- Continue for 2 weeks

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59
Q

During the first line treatment of Schizophrenia, if there is no improvement by what point should an alternative therapy be considered?

A

4 weeks

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60
Q

During the first line treatment of Schizophrenia, if there is only partial improvement by what point should an alternative therapy be considered?

A

8 weeks

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61
Q

If there is remission of the first episode of Schizophrenia, how long should maintenance therapy be continued for?

A

> =18 months

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62
Q

If no response to the first line antipsychotic in Schizophrenia, what can be prescribed?

A

A different atypical antipsychotic
OR
Chlorpromazine (or another typical low-potency antipsychotic)

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63
Q

What drug is used in treatment-resistant Schizophrenia? When is Schizophrenia deemed treatment-resistant?

A

Clozapine

Poor response to 2 antipsychotics (one of which must be an atypical antipsychotic)

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64
Q

How can aggression in hospital be predicted?

A

Body language

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65
Q

How can aggression in hospital be prevented?

A

De-escalation
Observations
Room layout

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66
Q

How can aggression in hospital be treated?

A

Restraint
Seclusion
Rapid tranquilisation

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67
Q

How is a person who has or appears to have a mental disorder defined under section 329 of the Mental Health Act (Scotland)?

A

Any mental illness
Personality disorder
Learning disability

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68
Q

Who can approve a short-term detention or a CTO under the Mental Health Act?

A

Approved medical practitioner:
- Register practitioner who is either a member/fellow of the Royal College of Psychiatrists OR have 4 yers of continuous psychiatric experience and are sponsored by a local medical director

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69
Q

What is the only treatment authorised under Emergency Detention?

A

Emergency treatment

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70
Q

What is the first step of the Tayside Rapid Tranquilisation Policy?

A

Consider non-drug approaches:

  • Distraction
  • Seclusion
  • Conversation
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71
Q

For the second step of the Tayside Rapid Tranquilisation Policy, what drug can be used if any of the following are met:

  • Unknown PMHx or DHx
  • Heart disease
  • No Hx of typical antipsychotics
  • Current illicit drug use
A

PO Lorazepam 1-2mg

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72
Q

For the second step of the Tayside Rapid Tranquilisation Policy, what drugs can be used if there is a confirmed history of significant typical antipsychotic exposure?

A

PO Lorazepam 1-2mg
AND/OR
PO Haloperidol 5mg

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73
Q

When can the third stage of the Tayside Rapid Tranquilisation Policy be initiated?

A

If PO therapy unsuccessful
OR
Effect required within 30 minutes

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74
Q

For the third step of the Tayside Rapid Tranquilisation Policy, what drug can be used if any of the following are met:

  • Unknown PMHx or DHx
  • Heart disease
  • No Hx of typical antipsychotics
  • Current illicit drug use
A

IM Lorazepam 1-2mg:

- Mixed 1:1 in water or NaCl

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75
Q

For the third step of the Tayside Rapid Tranquilisation Policy, what drugs can be used if there is a confirmed history of significant typical antipsychotic exposure?

A 
IM Lorazepam 1-2mg:
- Mixed 1:1 in water or NaCl
AND/OR
IM Haloperidol 5mg:
- Not in same syringe as Lorazepam
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76
Q

What monitoring is required in IM Haloperidol is used in the Tayside Rapid Tranquilisation Policy? How frequently and for how long?

A

Respiratory rate
Pulse rate
BP
Every 5-10 minutes for 1 hour

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77
Q

When can the fourth step of the Tayside Rapid Tranquilisation Policy be initiated? What is the fourth step?

A

After waiting 30 minutes, another IM injection can be given

If this fails, get senior help

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78
Q

How can inner experience and behaviours deviating from the expectations of the individuals be manifested in the diagnosis of a Personality Disorder?

A 
Cognition (perceiving/interpreting self and others)
Affectivity (of emotional response):
- Range
- Intensity
- Lability
- Appropriateness
Interpersonal functioning
Impulse control
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79
Q

How is the enduring pattern of behaviour changes in a Personality Disorder described?

A

Inflexible

Pervasive

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80
Q

What do the behaviour changes in a Personality Disorder lead to?

A

Clinically significant distress
OR
Impairment in social/occupational/other functioning

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81
Q

What personality disorder is characterised by feelings of excessive doubt and caution, preoccupation with lists/rules, perfectionism, excessive scrupulousness, pedantry, stubbornness and unreasonable insistence that others submit to their way of doing things?

A

Anankastic (F60.5)

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82
Q

What kinds of personality disorders are classed as Cluster A; ‘Odd and Eccentric’ in DSM-V?

A

Paranoid
Schizoid
Schizotypical

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83
Q

What kinds of personality disorders are classed as Cluster B; ‘Dramatic, emotional, erratic’ in DSM-V?

A

Antisocial
Borderline
Histrionic
Narcissistic

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84
Q

What kinds of personality disorders are classed as Cluster C; ‘Anxious and fearful’ in DSM-V?

A

Avoidant
Dependent
Obsessive-Compulsive

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85
Q

What personality disorder is characterised by distrust and suspicion of others. It begins in early adulthood and presents with >=4 of the following:

  • Suspecting others of exploiting/harming them
  • Preoccupied with unjustified doubts of others loyalty
  • Reluctance to confide in others
  • Reads hidden meanings from benign remarks
  • Persistently bears grudges
  • Feels attacked and quickly reacts angrily
  • Recurrent suspicions regarding partner’s fidelity
A

Paranoid personality disorder

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86
Q

What personality disorder is characterised by detachment from social relationships, restricted range of emotional expression, beginning in early adulthood and presents with >=4 of the following:

  • Doesn’t desire/enjoy close relationships
  • Chooses solitary activities
  • Little interest in sex
  • Takes pleasure in few/no activities
  • Lacks close friends
  • Appears indifferent to praise/criticism
  • Emotional detachment or flat affect
A

Schizoid personality disorder

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87
Q

What personality disorder is characterised by disregard for and violation of the rights of others, occurs since around 15 years of age and is present with >=3 of the following:

  • Failure to conform to social norms (forensic Hx)
  • Deceitfulness
  • Impulsivity
  • Aggressiveness
  • Reckless disregard for safety of self/others
  • Consistent irresponsibility (ccupations/finances)
  • Lack of remorse
A

Antisocial personality disorder

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88
Q

What personality disorder is characterised by instability of interpersonal relationships, self-image and affects, marked impulsivitiy, beginning by early adulthood and presenting with >=5 of the following:

  • Frantic efforts to avoid abandonment
  • Unstable/Intense interpersonal relationships
  • Identity disturbance
  • Impulsivity in two areas (sex, spending, substance abuse, reckless driving, binge eating)
  • Recurrent DSH/suicidal ideation
  • Marked reactivity of affect
  • Chronic feelings of emptiness
  • Inappropriate, intense anger
  • Transient, stress-related paranoid ideation or severe dissociation
A

Borderline personality disorder

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89
Q

What personality disorder is characterised by social inhibition and feeling inadequate, beginning in early adulthood and presenting with >=4 of the following:

  • Avoiding occupational activities
  • Unwilling to socialise unless knowing you’ll be liked
  • Restraint with intimacy
  • Preoccupation with being rejected
  • Inhibited in new social situations
  • Views self as socially inept or inferior
  • Unusually resistant to engage in new activities
A

Avoidant personality disorder

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90
Q

What personality disorder is characterised by excessive need to be taken care of, beginning in early adulthood and presenting with >=5 of the following:

  • Needs excessive advice for everyday decisions
  • Needs others to assume responsibility
  • Difficulty expressing disagreement
  • Difficulty being independent
  • Goes to excessive lengths to obtain support
  • Feels helpless when alone
  • Urgently seeks another relationship for support
  • Unrealistically preoccupied with fears of being left to take care of themselves
A

Dependent personality disorder

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91
Q

What personality disorder is characterised by a preoccupation with orderliness, perfectionism and interpersonal control at the expense of flexibility and openness. It begins in early adulthood and presents with >=4 of the following:

  • Preoccupied with rules, lists etc
  • Perfectionism affecting task completion
  • Excessively devoted to work
  • Inflexible about morality/ethics/values
  • Hoarding
  • Reluctance to delegate
  • Frugal
  • Stubborn
A

Obsessive-Compulsive personality disorder

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92
Q

What is the most common personality disorder?

A

Obsessive-Compulsive personality disorder (1.9% prevalence)

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93
Q

How is avoidant PD treated?

A

Social skills training

Antidepressants

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94
Q

How is borderline PD treated?

A

Dialectical Behavioural Therapy
‘Mentalism’ (Interpret own actions as meaningful)
Medication is usually for comorbidities

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95
Q

Borderline PD is over-represented in atypical depression, what drugs may help?

A

MAOIs:

- Phenelzine also for hostility

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96
Q

What is the IQ range for a mild learning disability?

A

50-69

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97
Q

What is the IQ range for a moderate learning disability?

A

35-49

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98
Q

What is the IQ range for a severe learning disability?

A

20-34

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99
Q

What is the IQ range for a profound learning disability?

A

<20

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100
Q

What is the IQ range for a borderline learning disability?

A

> =70 (-84)

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101
Q

What is the most commonly used psychometric assessment scale?

A

Wechsler Adult Intelligent Scale

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102
Q

What are O’Brien’s Principles?

A

Essentially that those with learning disabilities continue to grow and are worthy of all the dignity and rights of any citizen

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103
Q

What do people with a mild learning disability usually have problems with?

A

Delayed speech

Difficulties reading and writing

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104
Q

What do people with a moderate learning disability usually have problems with?

A

Slow comprehension and language
Limited achievements
Delayed self-care and motor skills

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105
Q

What common comorbidities are seen in moderate learning disorders?

A

Epilepsy

Physical disability

106
Q

What are some prenatal aetiologies of learning disability?

A

Genetic
Chromosomal
Intrauterine

107
Q

What are some perinatal aetiologies of learning disability?

A

Birth trauma

Anoxia

108
Q

What are some postnatal aetiologies of learning disability?

A

Infection

Head injury

109
Q

What is the incidence of Down’s Syndrome at maternal age 30?

110
Q

What is the incidence of Down’s Syndrome at maternal age 40?

111
Q

What is the incidence of Down’s Syndrome at maternal age 50?

112
Q

What is the typical IQ range in Down’s Syndrome?

113
Q

What is Down’s Syndrome associated with?

A

Schizophrenia

114
Q

What is Patau Syndrome?

A

Trisomy 13

115
Q

What is the incidence of Patau Syndrome?

116
Q

How many Patau Syndrome patients survive 1 year?

117
Q

What is Edward’s Syndrome?

A

Trisomy 18

118
Q

How does Cri du chat syndrome present and what causes it?

A

Microcephaly
Profound/Severe learning disability
Chromosome 5p deletion

119
Q

How does Angelman syndrome present and what causes it?

A 
Learning disability
Ataxia
Paroxysms of laughter
Chromosome 15q(11-13) deletion:
- Maternally derived
120
Q

How does Prader-Willi syndrome present and what causes it?

A 
Learning disability
Over-eating
Self-injurious behaviour
Chromosome 15q(11-13) deletion:
- Paternally derived
121
Q

How does DiGeorge syndrome present and what causes it?

A 
50% have learning diability
Cleft palate
Cardiac abnormalities
Abnormal facies
Chromosome 22q11.2 deletion
122
Q

What else can DiGeorge syndrome be called?

A

Velo-Cardiofacial syndrome

123
Q

What is Turner’s syndrome?

124
Q

What is Klinefelter’s syndrome?

125
Q

What is the incidence of Fragile X?

126
Q

What causes Fragile x?

A

Faulty FMR1 gene

127
Q

What genetic protein defect is a cause of severe learning disability?

A

Phenylketonuria

128
Q

What genetic carbohydrate defect is a cause of severe learning disability?

A

Mucopolysaccharidoses

129
Q

What genetic lipid metabolism defect is a cause of severe learning disability?

A

Neurolipidoses

130
Q

How is Tuberous Sclerosis inherited?

A

Autosomal dominant

131
Q

What does TSC1 code for?

A

Hamarton

On chromosome 9q34

132
Q

What does TSC2 code for?

A

Tuberin

On chromosome 16p13.3

133
Q

How is Lesch-Nyhan syndrome inherited?

A

X-linked recessive

134
Q

What causes Lesch-Nyhan syndrome?

A 
Mutations in HPRT1 gene:
- Codes for hypoxanthine-guanine phosphoribosyltransferase
Results in uric acid build up:
- Gout
- Kidney problems
135
Q

What else does Lesch-Nyhan syndrome result in?

A

Neurological dysfunction
Cognitive and behavioural disturbances:
- Including self-mutilation

136
Q

What causes holoprosencephaly?

A

Prosencephalon (forebrain) fails to divide into two hemispheres

137
Q

What prenatal maternal infections can cause learning disabilities?

A

Rubella
CMV
Toxoplasmosis

138
Q

What is Foetal Alcohol Spectrum Disorder associated with?

A

Mild learning disability

ADHD

139
Q

What perinatal infections are associated with learning disabilities?

A

Neonatal septicaemia
Pneumonia
Meningitis/Encephalitis

140
Q

What newborn complications (other than infections) can result in learning disabilities?

A

Respiratory destress
Hyperbilirubinaemia
Hypoglycaemia
Extreme prematurity

141
Q

What is the Flynn Effect?

A

Average IQ in the US rises 3 points per decade:

- Therefore ~10 points per generation

142
Q

What factors contribute to underdiagnosis of psychotic comorbidities in learning disability?

A

Intellect
Diagnostic overshadowing
Compliance (‘Talked out of’ symptoms)
Eager to please

143
Q

When might antipsychotics be used in the context of learning disability?

A

Psychosis
Behavioural disturbance
Autism
ADHD

144
Q

When might antidepressants be used in the context of learning disability?

A

Depression
Anxiety disorders
Self-harm
Autism

145
Q

When might anticonvulsants be used in the context of learning disability?

A

Bipolar affective disorder

Episodic dyscontrol

146
Q

When might stimulants be used in the context of learning disability?

147
Q

When might opiate antagonists be used in the context of learning disability?

A

Repetitive self-harm

148
Q

When might anti-libidinal drugs be used in the context of learning disability?

A

Sexual offending

149
Q

When might beta-blockers be used in the context of learning disability?

A

Autonomic arousal

150
Q

How does Schizophrenia present in learning disability?

A

3 times more common
Early onset (mean age 23)
Negative symptoms more common
Main presentation may be change in behaviour

151
Q

How does Schizophrenia present in severe learning disability?

A 
Unexplained aggression
Bizarre behaviour
Social withdrawal
Mood lability
Increased mannerisms/stereotypes
152
Q

How common is bipolar affective disorder in learning disability?

153
Q

How common is a depressive disorder in learning disability?

154
Q

What anxiety disorder is more common in learning disability?

155
Q

What anxiety disorder is less common in learning disability?

A

Agoraphobia

156
Q

What is the M:F ratio of autism?

157
Q

What are the triad of symptoms in autism?

A

Abnormal social interaction
Communication impairment
Rigid/Restricted or repetitive behaviour, interests and activities

158
Q

How many units of alcohol indicate higher risk drinking?

A

> 35 units per week (regularly)

159
Q

How many units of alcohol indicate increased risk drinking?

A

15-35 units per week

160
Q

How many units of alcohol indicate low risk drinking?

A

=<14 units per week spread over >=3 days

161
Q

What does the AUDIT tool aim to do?

A

Detect hazardous drinking

162
Q

What does the CAGE tool aim to do?

A

Detect alcohol abuse and dependence

163
Q

What does the TWEAK tool aim to do?

A

Screens for alcohol problems in pregnant women

164
Q

What does the MAST tool aim to do?

A

Full version useful for psychiatric settings

165
Q

What do the PAT and FAST tools aim to do?

A

A+E testing

166
Q

What does GGT indicate?

A

Degree of liver injury

167
Q

What does Carbohydrate Deficient Transferrin indicate?

A

Identifies men drinking >=5 units per day for >=1 years

168
Q

What is FRAMES in regard to alcohol abuse?

A

Feedback - Review problems due to alcohol
Responsibility - Patient is responsible for change
Advice - Reduction/Abstinence
Menu - Provide options for change
Empathy
Self efficacy - Encourage optimism for change

169
Q

When should referral be considered in alcohol abuse?

A

Signs of moderate-severe alcoholism
Failure to benefit from structured brief advice and want more help
Signs of severe alcohol impairment or comorbidity

170
Q

What are some specialist interventions for alcohol abuse?

A

Detoxification
Relapse prevention:
- Psychosocial
- Pharmacological

171
Q

What channels does alcohol inhibit? What does chronic use result in?

A

Excitatory NMDA-glutamate ion channels

Chronic use -> Receptor upregulation

172
Q

What channels does alcohol potentiate? What does chronic use result in?

A

Inhibitory GABAa controlled ion channels

Chronic use -> Receptor downregulation

173
Q

What does alcohol withdrawal result in?

A

Excess glutamate activity -> Nerve cell toxicity

CNS excitability

174
Q

When do alcohol withdrawal symptoms peak?

A

24-48 hours

175
Q

When does delirium tremens tend to occur?

A

Usually within 24 hours

176
Q

How long does it take for alcohol withdrawal symptoms to resolve?

177
Q

How can delirium tremens cause death?

A

Cardiovascular collapse

Infection

178
Q

What benzodiazepines are used in alcohol withdrawal and why?

A

Long-acting agents:

  • Diazepam
  • Chlordiazepam
179
Q

How do BZDs work in alcohol withdrawal?

A

Cross tolerant with alcohol:

- At on GABAa

180
Q

How long is the BZD dose reduced over in alcohol withdrawal?

181
Q

How is BZD therapy guided in alcohol withdrawal?

182
Q

Why can Thiamine be prescribed in alcohol withdrawal?

A

Prophylaxis against Wernick’e Encephalopathy

183
Q

How is Thiamine given in alcohol withdrawal?

A

Parenteral only

184
Q

What is the first line drug for relapse prevention in alcohol abuse? How does it work?

A

Naltrexone
Opioid antagonist:
- Reduces reward from alcohol

185
Q

How does Disulfiram prevent alcohol abuse relapse?

A

Inhibits acetylaldehyde dehydrogenase:

- Acetylaldehyde accumulates if alcohol consumed

186
Q

What symptoms does Disulfiram cause if alcohol is consumed?

A 
Flushed skin
Tachycardia
Nausea and vomiting
Arrhythmias
Hypotension
187
Q

How does Acamprosate work in preventing alcohol abuse relapse?

A

Acts centrally on glutamate and GABA systems

Reduces cravings

188
Q

When is Acamprosate started?

A

As soon as detoxification finishes

189
Q

When there is a relapse, what happens to acamprosate?

A

Continued throughout

190
Q

What are the side effects of acamprosate?

A

Headache
Diarrhoea
Nausea

191
Q

When would detoxification be used for opiate abuse?

A

Shorter history
Uncomplicated
Relatively stable socially
Detoxing TO something (not from something)

192
Q

When is opiate blockade used for opiate abuse?

A

If an impulsive relapser

193
Q

What drugs can be prescribed to assist with detoxification from opiate abuse?

A

Alpha-2 adrenergic agonists:

- Lofexidine

194
Q

What adjunct drugs can be prescribed in detoxification from opiate abuse?

A

Loperamide
Hypnotics
NSAIDs

195
Q

What are some opioid substitution therapies?

A

Methadone

Buprenorphine

196
Q

What effect does mephedrone have?

A

Inhibits reuptake of serotonin, NA and DA
DA release
Stimulant (Self-confidence, talkative)
Empathogenic (Intimacy, openness, dancing)

197
Q

What is sympathetic toxidrome?

A

Acute toxic effects of amphetamine-type substances

198
Q

What are the symptoms of serotonin syndreom?

A 
Agitation
Hyperreflexia
Tremor
Myoclonus
Sweating
Diarrhoea
Shivering
Ataxia
Fever
Confusion
Hypomania
Confusion
199
Q

What drugs can cause serotonin syndrome?

A 
Antidepressants
OTC cough medications
Antimigraines
Antibiotics
Tramadol
Herbal products
200
Q

What is methiopropamine?

A

Structural analogue of methamphetamine

201
Q

How does methipropamine work?

A

NA and DA reuptake inhibitor

202
Q

What is CHING?

A

Cocaine substitute
79% ethylphenidate
Cut with lidocaine

203
Q

How does CHING work?

A

DA and NA reuptake inhibitor

204
Q

What effects do synthetic cannabinoids have over cannabis?

A 
Psychosis
Increased agitation
Increased hallucinations
Sympathemimetic effects (2-3x as likely)
CVS problems
205
Q

What primary effect does ketamine have?

206
Q

What is a ketamine bladder?

A

Urge incontinence
Reduced volume
Detrusor over-activity
Painful haematuria

207
Q

How does ketamine work?

A

NMDA receptor antagonist

208
Q

How do we do urine toxicology?

A

20ml urine in white universal container

209
Q

What does a urine immunoassay detect?

A 
Benzodiazepines
Meth
Opiates
Amphetamines
Barbituates
Cocaine
Cannabinoids
Alcohol
210
Q

What CAGE score indicates the possibility of alcoholism?

A

> =2 Yes repsonses

211
Q

What sensation does the mesolimbic pathway produce?

212
Q

What does the mseolimbic pathway connect?

A

Ventral Tegmental Area to the Nucleus Accumbens

213
Q

What does the mesolimbic pathway release?

A

DA into the Nucleus Accumbens -> Reward

214
Q

What effect does DA have in the Nucleus Accumbens?

A

Motivating signal
Incentivises behaviour
Involved in normal pleasurable experiences

215
Q

What drugs increase DA release?

A

Amphetamine
Cocaine
Nicotine
Morphine

216
Q

In fMRI studies, non-addict controls (gambling) had increased blood flow to striatum after winning. Addicts had a lower response. What does this suggest? What is the potential mechanism?

A

Tolerance to reward:

  • Repeated DA release -> DA receptor downregulation
  • Threshold for reward increased (during abstinence)
  • Normal pleasurable experiences don’t evoke reward
217
Q

What are the initial stages of drug-taking driven by?

A

Reward (positive reinforcement)

218
Q

What are the late stages of drug-taking driven by?

A

Becomes a thirst:

- Negative reinforcement

219
Q

What happens to orbitofronal cortex activation in addicts when presented with drug cues? What does this correlate with?

A

Increased activation:

  • Correlates with self-reported drug cravings
  • Changes persists into abstinence
220
Q

What is the role of the prefrontal cortex in behaviour?

A

Helps intention-guided behaviour
Modulates powerful effects of reward system
Sets goals and focuses attention
Keep emotions and impulses under control:
- Long term goal achievment

221
Q

How does an adolescents response to reward compare to an adults?

A

Equivalent

Strong stimulus reward

222
Q

How does an adolescents prefrontal cortex control compare to a childs? What does this mean?

A

Equivalent
Reduced attention:
- Minimal judgement and impulse control

223
Q

In terms of memory and habit forming, what parts of the brain are important in acquisition, consolidation and expression of drug stimulus learning?

A

Hippocampus
Striatum
Amygdala

224
Q

What type of learning is the striatum responsible for?

225
Q

What type of learning is the hippocampus responsible for?

A

Decelerative

226
Q

What effects does stress have on DA release?

A

Increased release in neural reward pathway

227
Q

What do the following parts of the brain belong to:

  • Hippocampus
  • Fornix
  • Mamillary bodies
  • Anterior thalamic nuclei
  • Cingulate gyrus
  • Enterohinal cortex
A

Circuit of Papex

228
Q

What is the function of the right side of the amygdala?

A

Negative emotions:

  • Fear
  • Sadness
229
Q

What is the function of the left side of the amygdala?

A

Both pleasant and unpleasant emotions

Reward

230
Q

What are the three stages of memory?

A

Encoding -> Storage -> Retrieval

231
Q

In the multi-store model of memory, what commits a sensory memory to short-term memory?

232
Q

In the multi-store model of memory, what commits a short-term memory to long-term memory?

233
Q

In the multi-store model of memory, what recalls a long-term memory to short-term memory?

234
Q

In the multi-store model of memory, what is recall?

A

The ability to recollect something from the short-term memory

235
Q

How long does sensory memory last for?

236
Q

How long does short-term memory last for?

237
Q

What are the two types of long-term memory?

A

Explicit (conscious)

Implicit (unconscious)

238
Q

What are the two types of explicit memory?

A

Episodic (events, experiences)

Semantic (facts, concepts)

239
Q

What is the type of implicit memory? What does it allow us to undertake?

A

Procedural memory:

  • Skills
  • Tasks
240
Q

What features need to be present to diagnose Alzheimer’s?

A
  1. Presence of dementia
  2. Insidious onset and slow deterioration
  3. Absence of clinical/investigation evidence of a biological cause
  4. Absence of a sudden, apopleptic onset or of focal neurological damage early in illness
241
Q

What biological causes may be differential diagnoses for Alzheimer’s?

A 
Hypothyroid
Hypercalcaemia
Vit B12 deficiency
Niacin (Vit B3) deficiency - ie. Pellagra
Neurosyphilis
Normal pressure hydrocephalus
Subdural haematoma
242
Q

What is the neuropathology of Alzheimer’s?

A

Amyloid plaques

Neurofibrillary tangles

243
Q

How can vascular dementia present?

A

Abrupt onset or stepwise deterioration in:

  • Memory loss
  • Intellectual impairment
  • Focal neurological signs
244
Q

How are insight and judgement affected in vascular dementia?

A

Often preserved

245
Q

How can vascular dementia be confirmed?

A

CT

Neuropathology

246
Q

What are associated features in vascular dementia?

A

Hypertension
Carotid bruit
Emotional lability

247
Q

What is the central feature of Lewy Body Dementia?

A

Progressive dementia;

- Deficits in attention and executive functions

248
Q

What are the core features in Lewy Body Dementia?

A 
Fluctuating cognition:
- Pronounced variations in attention and alertness
Complex visual hallucinations:
- Well formed
- Detailed
Spontaneous Parkinsonism
249
Q

What are some suggestive features of Lewy Body Dementia?

A

REM sleep behaviour disorder (years before onset)
Severe neuroleptic sensitivity (50%)
Low DA transporter uptake in basal ganglia:
- SPECT
- PET

250
Q

What are some supportive signs in Lewy Body Dementia?

A

Repeated falls
Transint loss of consciousness
ANS dysfunction

251
Q

What indicates a probable diagnosis of Lewy Body Dementia?

A 
Dementia PLUS >=2 core features
OR
Dementia PLUS:
- 1 core features AND
- >=1 suggestive features
252
Q

What indicates a possible diagnosis of Lewy Body Dementia?

A

Dementia PLUS 1 core feature
OR
Dementia PLUS >=1 suggestive features

253
Q

What are Lewy Bodies?

A

Alpha-synuclein proteins in cytoplasm of neurones

254
Q

Where is DA lost in Lewy Body Dementia?

A

Substantia nigra

255
Q

What other neurones are lost in Lewy Body Dementia?

A

Ach-producing

256
Q

What are the three types of Fronto-Temporal Dementia?

A

Behavioural variant
Semantic dementia
Progressive non-fluent aphasia

257
Q

What are usually preserved in FTD?

A

Memory
Perception
Spatial skills
Praxis

258
Q

What are Pick Bodies?

A

Tau-positive spherical cytoplasmic neuronal inclusions composed of straight filaments

259
Q

What are Pick Cells?

A

Ballooned neurones with dissolution of chromatin

260
Q

Apart from Pick’s Disease, what else are Pick Bodies and Cells seen in?

261
Q

How is alcohol-related dementia diagnosed?

A

Memory impairment plus >=1 of the following:

  • Apraxia
  • Aphasia
  • Agnosia
  • Disturbance in executive functioning
  • Functional impairment

Year 3 - Psychiatry (DP) (4 decks)

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