Psychiatry Flashcards

1
Q

Mental Status Examination
categories

https://www.ncbi.nlm.nih.gov/books/NBK546682/

A
  • appearance
  • behavior
  • motor activity
  • speech
  • mood
  • affect
  • thought
  • process
  • thought content
  • perceptual disturbances (delusions, illusions, Hallucionations)
  • cognition (MMSE, MoCA)
  • insight
  • judgment.
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2
Q

Mental Status Examination
Irregular thought processes types

A
  • circumstantial
  • tangential
  • the flight of ideas
  • loose/disorganised
  • perseveration
  • thought blocking
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3
Q

Mental Status Examination
Circumstantial thought process

A

describes someone whose thoughts are connected but go off-topic before returning to the original subject

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4
Q

Mental Status Examination
Tangential thought process

A

Is a series of connected thoughts that go off-topic but do not return to the original topic.

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5
Q

Mental Status Examination
Flight of ideas thought process

A

Flight of ideas is a type of thought process similar to a tangential one in which the thoughts go off-topic, but without complting the thought or train of thoughts; and the connection between the thoughts is less obvious and challenging for a listener to follow.

Common in MANIA

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6
Q

Mental Status Examination
loose, disorganised thought process

A

No connection occurs between the thoughts AND no train of thought to follow.

it most often occurs in schizophrenia

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7
Q

Mental Status Examination
Perseveration

A

Perseverations are a thought process where the patient returns to the same subject, regardless of topic or question

May occur in DEMENTIA

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8
Q

Mental Status Examination
Thought Blocking

A

observed in psychosis when a patient has interruptions in their thoughts, making it challenging to either start or finish a thought.

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9
Q

Mental Status Examination
Affect - definition

A

affect reflects the person’s EXTERNAL emotional expression - which can be evaluated by the interviewer. It can be described as:
- EUTHYMIC (normal, well-balanced mood)
- DYSTHYMIC (sullen, flat)
- EUPHORIC (intensely elated mood)

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10
Q

Mental Status Examination
Mood - Definition

A

mood reflects person’s INTERNAL emotional experience (e.g. good, ok, frustrated, angry)

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11
Q

Mental Status Examination
Insight - Definition

A

It refers to a patient’s understanding of their illness and functionality. Insight is typically described as poor, limited, fair, or if a previous comparison depicts worsening versus improving

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12
Q

DEPRESSION Dx

A

2 core symptoms (depressed mood, low energy, anhedonia)
+
2 or more of the other symptoms
(<2 = mild; >2 + <5 moderate; >5 severe)
+
for at least 2 weeks

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13
Q

DEPRESSION Sx

A

Depressed mood (CORE) + SIGECAPS

– S = Sleep (decreased overall pattern and architecture)
– I = Interest/Enjoyment/
Anhedonia (low) (CORE)
– G = Guilt/Hopelessness/Pessimist/Self-blaming/Nihilistic
– E = Energy (low) (CORE)
– C = Concentration (decreased)
– A = Appetite (usually low, but can be increased)
– P = Psychomotor retardation
– S = Suicidal thoughts

typically, in depression, mood is worse in the morning and betters as the day progressed (this is called “diurnal variation”)

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14
Q

DEPRESSION
major depression with ATYPICAL features

A
  • mood remains reactive (lifting of depressive symptoms during happy life events)
  • reversed diurnal variation (i.e. evening are the most difficult time of the day for the mood)
  • feeling rejected and unloved (interpersonal rejection sensitivity)
  • leaden paralysis (dull/heavy limbs to lift)
  • hyperphagia/weight gain
  • hypersomnia

Rx: MAOi

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15
Q

Dysthymic Disorder (Persistent Depressive Disorder)

A

Chronic condition characterised by depressive symptoms that:
- occur for most of the day
- more days than not
- for > 2 years

common features:
- H: Hopelessness (despondency)
- E: Energy (decreased)
- S: Self-esteem (decreased)
- S: Sleep (decreased)
- A: Appetite (decreased)
- D: decision making (impaired)

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16
Q

DEPRESSION
Sleep disturbances features

A

MOST COMMON - waking up during the night and having trouble going back to sleep (also referred as middle insomnia). if successful [in going back to sleep], broken sleep thereafter

  • early morning wakening and being unable to get back to sleep at all (also referred as terminal insomnia)
  • increased REM stage
  • Decreased stage 3 non-REM stage (less stage 3 means less restorative periods => daylight tiredness)

LESS COMMON/UNCOMMON
- increased sleep latency (i.e. difficulty falling asleep) = MORE COMMON IN ANXIETY or associated with the use of nocturnal stimulants (e.g. caffeine)
- Hypersomnia and oversleeping
- Dramatic dreams (including dreams about death) ARE NOT TYPICAL OF DEPRESSION

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17
Q

DEPRESSION
Risk Factors

A
  • perfectionism
  • obsessionality
  • intellectual developmental delay
  • Family history of depression.
  • Family history of Autism
  • Substance Misuse.
  • Unemployment
  • Low socioeconomic status.
  • Elderly person with cognitive decline or bereavement.
  • All family members who have experienced family violence.
    – Experience of child abuse
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18
Q

DEPRESSION
groups are at higher risk of depression

A
  • Women
  • Postpartum women
  • Young rural males
  • Adolescents
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19
Q

DEPRESSION
Features in children/adolescents

A
  • Anhedonia/Apathy may be as severe or more apparent than mood abnormalities (often expressed as severe boredom)
  • impaired concentration
  • sadness(sad appearance)
  • psychomotor agitation (“jumpy”, not relaxed)
  • despondency (hopelessness)
  • excessive irritability
  • feeling rejected, unloved, inadequacy, worhtlessness (interpersonal rejection sensitivity)
  • somatic complaints (eg, headaches, abdominal pain, insomnia), and persistent self-blame.
  • anorexia, weight loss (or failure to achieve expected weight gain)
  • sleep disruption (including nightmares)
  • suicidal ideation
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20
Q

DEPRESSION
Firstline choice of treatment in children/adolescents

A

Fluoxetine

TCA’s, Mirtazapine, Venlafaxine are not recommended/approved for use in adolescents

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21
Q

DEPRESSION vs SCHIZOPHRENIA

A

***PATTERN

  • episodic
                                                 vs
  • progressive
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22
Q

DEPRESSION
Treatment according to the classification

A
  • Mild depression: CBT > antidepressants
  • Moderate depression: CBT = antidepressants
    (initial choice of therapy based on patient preference)
  • Moderate to Severe depression: Antidepressants > CBT
    (although concurrent psychological therapies may often be helpful if the patient can concentrate enough to participate in these.)
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23
Q

DEPRESSION
Antidepressants alone are ————— effective in patients with severe depression

A

50% to 60%

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24
Q

DEPRESSION
ECT indications

A

ECT indicated in some forms of severe depression:

  • psychotic depression
  • melancholic depression
  • voluntary patient with severe depression
  • If previous good response to ECT in patients
    with severe depression
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25
Q

DEPRESSION
Inpatient treatment indications:

A
  • depression with psychosis (ie with delusions or hallucinations);
  • significant risk of suicide, or homicide (eg ‘altruistic homicide’ by a woman suffering severe perinatal
    depression);
  • inadequate support at home;
  • seriously physically unwell

When the patient’s depression puts themselves or others at significant risk and the patient is not competent to agree to treatment, involuntary hospitalisation under the relevant mental health legislation must be considered

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26
Q

DEPRESSION
First-line drug options

A
  • SSRIs
  • SNRIs
  • Mirtazapine
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27
Q

DEPRESSION
When to assess response to antidepressant

A

after 2 to 4 weeks of treatment

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28
Q

DEPRESSION
% of patients with major depression that will respond to AT LEAST one antidepressant medication

A

80%

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29
Q

DEPRESSION
Management if there is PARTIAL initial response

A
  • increase the dose

⬇︎

  • reassess in 2 to 4 weeks

⬇︎

  • if no addtional response ➡︎ switch drug (first-line)
  • if additional response, but effect is still inadequate:
    ➡︎ increase the dose further if possible within the
    recommended dose range ➡︎ reassess in 2 to 4 weeks

➡︎ If a further dose increase is not possible, switch to a
different drug (first-line)

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30
Q

DEPRESSION
Management if there is No initial response

A
  • increase the dose

⬇︎

  • reassess in 2 to 4 weeks

⬇︎

  • if no addtional response ➡︎ switch drug (first-line)
  • if partial response, but effect is still inadequate:
    ➡︎ increase the dose further if possible within the
    recommended dose range ➡︎ reassess in 2 to 4 weeks

➡︎ If a further dose increase is not possible, switch to a
different drug (first-line)

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31
Q

DEPRESSION
Antidepressant-free interval recommended when changing from one SHORT-ACTING SSRI to ANOTHER SHORT-ACTING DRUG or FLUOXETINE

A

Nil

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32
Q

DEPRESSION
Antidepressant-free interval recommended when changing from FLUOXETINE to a SHORT-ACTING SSRI

A

1 week

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33
Q

DEPRESSION
Full recovery after favourable response to first-line therapy

A

6 weeks or longer

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34
Q

DEPRESSION
How long should treatment be for

A

If single episode of major depression = 6-12 months

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35
Q

DEPRESSION
Indications for long-term prophylatic therapy

A
  • 2 or MORE more depressive episodes within 5 years
  • 3 previous episodes,
  • single severe episode of psychotic depression
  • serious suicide attempt
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36
Q

DEPRESSION
duration of long-term treatment

A

at least 3 to 5 years
(including continuing work on vulnerability factors)

Some patients may require lifelong antidepressant therapy.

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37
Q

DEPRESSION
When to consider failure to respond to initial antidepressant therapy?

A

after unsuccessful trials of at least two first-line treatments (either drug or psychological)

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38
Q

DEPRESSION
Drug options for unsuccesful trial with First-line therapy

A
  • TCAs
  • MAOIs

both require specialist support

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39
Q

DEPRESSION
Discontinuation syndrome Sx

A
  • insomnia, nausea
  • postural imbalance
  • sensory disturbances
  • hyperarousal
  • flu-like symptoms.

SOME PATIENTS CAN EXPERIENCE THESE SYMPTOMS even after missing just 1 or 2 doses

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40
Q

DEPRESSION
Discontinuation Syndrome duration

A

these symptoms are mild, last 1 to 2 weeks
(usually does not require specific treatment)

If withdrawal symptoms occur due to abrupt discontinuation, symptoms are rapidly extinguished with the reinstitution of the antidepressant

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41
Q

DEPRESSION
Tapering regime to prevent Discontinuation syndrome

A

As a general rule

  • dose should be 1/2 every week
    ⬇︎
  • until the daily dose is half of the lowest unit strength available
    ⬇︎
    antidepressant can be stopped after 1 week on this dose.

In general, antidepressants should be tapered slowly, rather than stopped abruptly, to reduce the risk of discontinuation
syndrome. Antidepressant discontinuation syndrome is more likely to occur with a higher dose, a longer duration of treatment

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42
Q

DEPRESSION
If a patient, who has successfully been stable on prophylactic dose of a particular mood stabiliser, develops acute depression, what is the next best step in management?

A
  • Adding an antidepressant to the prophylactic mood stabilizer: the choices of the drug would be the same as for major depression. SSRls first line.
  • Increasing the dose of prophylactic mood stabilizer (ONLY if the patient’s psychosis is indicated in coming back, otherwise continue same dose)
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43
Q

DEPRESSION
Whcih antidepressive is considered appropiate in childhood/adolescence depression

A

FLUOXETINE

ABSOLUTE CONTRA-INDICATIONS ARE:
- TCAs = should not be used in children < 16 years.
- Mirtazapine = due to its effects of sedation and weight gain, may cause problems in this age group
- Venlafaxine = increased reports of hostility and suicide-related adverse effects such as suicidal ideation and self-harm.

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44
Q

DEPRESSION
Considerations regarding pharmacological tretment in childhood/adolescence depression

Trail, change of therapy, discontinuation

A
  • treatment trials should last:
    – for 3 to 4 weeks before considering a dose increase (as oposed to 2-4 weeks in adults)
    – and for 8 to 12 weeks before a change of therapy.
  • discontinuation trial should be considered **within 1 year **of starting treatment in children who have achieved a marked reduction in symptoms.
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45
Q

DEPRESSION
Patient with severe depression or suicidal ideation taking HCV treatment (interferon).
Management?

A

Stop interferon, start SSRI.
(Treat depression first. Recomence interferon once the depression is managed)

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46
Q

DEPRESSION
Drug of choice in post-cardiac depression

https://www1.racgp.org.au/ajgp/2023/november/incidence-and-impacts-of-post-cardiac-event-mental

A

Sertraline

Sertraline, citalopram, fluoxetine and mirtazapine in particular have been shown to be safe and effective for treating depression in cardiac patients. However, certain SSRIs, such as fluvoxamine, fluoxetine and paroxetine, can interact with antihypertensive medications, such as metoprolol and captopril, and should therefore be used with caution

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47
Q

Examples of Overvalued Ideas

A

Body dysmorphic disorder
Anorexia Nervosa
Hypochondriasis

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48
Q

BIPOLAR DISORDER
Dx

A

Elevated Mood + 3 of DIG FAST
or
Irritability + 4 of DIG FAST

FOR 1 week or more

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49
Q

BIPOLAR DISORDER
Sx

A
  • D – DISTRACTIBILITY
  • I – IMPULSIVITY (please seeking behaviours)
  • G – GRANDIOSITY
    (can border on the psychotic delusions and hallucinations.
  • F – FLIGHT OF IDEAS
  • A – ACTIVITY
    (psychomotor agitation/goal direct activity)
  • S – SLEEP = decreased need
  • T – TALKATIVINESS
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50
Q

BIPOLAR DISORDER
MANIA ≠ HYPOMANIA by following features

A
  • Minimum 7 days of symptoms
    (4 days for hypomania)
  • Marked functional impairment
    (no functional impairment in hypomania)
  • Delusions and hallucinations (psychotic features)
    (absent in hypomania)
  • Patient often requires hospitalisation
    (less commonly required in hypomania)
  • Insight and judgment are usually impaired in mania

“ELEVATED MOOD IS SEEN BOTH”

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51
Q

BIPOLAR DIORDER
Cyclothymia

A

≥ 2 years of fluctuating, mild hypomanic & depressive symptoms that do not meet criteria for hypomanic or
major depressive episodes

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52
Q

BIPOLAR DISORDER
Features more commonly seen in Bipolar Depression than in Unipolar Depression

A
  • Psychomotor retardation.
  • Increased appetite (hyperphagia)
  • Increased sleep (hypersomnia)
  • Positive family history of bipolar disorder
  • Early onset of first depression before 25 years of age.
  • Delusions and hallucinations (psychotic features)
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53
Q

BIPOLAR DISORDER
Suicidal Risk

A
  • 15 x more likely to commit suicide
  • 25% of BD patients will attempt suicide
  • history of drug taking is an important finding as it can be considered as suicide attempt
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54
Q

BIPOLAR DISORDER
MANIA vs PSYCHOTIC DISORDERS

A

***NATURE of delusions

  • grandiose
  • reward-oriented
    vs
  • conspiratorial thinking
  • paranoia
  • thought manipulation/control by outside force

***DISTINGUISHING SYMPTOMS

  • flight of ideas, distraction
                                                 vs
  • thought disorganisation + negative sx

***PATTERN

  • episodic
                                                 vs
  • progressive
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55
Q

BIPOLAR DISORDER
Hypomania vs HISTRIONIC PERSONALITY DISORDER

A

Some symptoms of hypomania overlap with histrionic personality disorder. These include:
- shallow emotions
- flirty nature

However:
- flirting in hypomania = increased sexuality
- flirting in histrionic personality disorder = attention seeking behaviour

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56
Q

BIPOLAR DISORDER
treatment of acute mania

A

1st OLANZAPINE VO

OR

1st RISPERIDONE VO

OR

2 HALOPERIDOL VO

OR

2 LITHIUM VO

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57
Q

BIPOLAR DISORDER

Treatment maitenance and recurrence prophylaxis

A

Lithium + CBT

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58
Q

BIPOLAR DISORDER
Duration of treatment following an acute mania episode

A

12 months

If an antipsychotic is used for acute treatment, it should be withdrawn within a few months after remission

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59
Q

BIPOLAR DISORDER
Acute mania Failure to respond to treatment

A
  • ensure that maximum tolerable drug concentration has been achieved.
  • switch to a different drug (eg from a second-generation antipsychotic to lithium)
  • combine drugs (eg a second-generation antipsychotic + lithium)
  • electroconvulsive therapy (ECT)—this is a proven treatment for mania and may be extremely effective even when patients fail to respond to one or more antimanic drugs
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60
Q

BIPOLAR DEPRESSION
Mx

A

1st Antidepressant (SSRI preferably)
+
Mood stabiliser

			    OR

1st Quetiapine Monotherapy

Mood-stabilising agents are SGAs (which carry the risk of metabolic syndrome. Although, for the acute resolution of symptoms agents from both classes have similar efficacy, SGAs may be slightly faster (possibly because of easier administration) and within the two classes
of agents there is a slight gradient of efficacy from lithium.

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61
Q

BIPOLAR DEPRESSION
When to cease antidepressant

A

preferably within 1 or 2 months of
successful resolution

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62
Q

BIPOLAR DEPRESSION
Treatment of ACUTE bipolar depression

https://www.racgp.org.au/afp/2013/september/bipolar-disorder

A

QUETIAPINE

Antidepressant monotherapy should be avoided due to the risk of inducing rapid cycling mania.

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63
Q

BIPOLAR DEPRESSION
Failure to respond to treatment

A
  • change to a different antidepressant or a
    different prophylactic drug
  • (ECT)
    —this is an effective treatment for bipolar depression and should be considered especially if the patient is psychotically depressed or displays significant psychomotorretardation or agitation
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64
Q

Schizophrenia
DX

A
  • 2 Sx ((at least ONE POSITIVE sx))
  • for at least 6 months

symptoms rarely have an acute onset. Instead, there is often a prodromal state followed by a progressive worsening of the symptoms

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65
Q

SCHIZOPHRENIA
Psychosis
definition

A
  • Psychosis is a loss of contact with reality - loss of insight into the fact that one is mentally ill
  • Some people with psychosis have false beliefs that can best be described as fearfulness and suspiciousness (paranoia);
  • They may have vague fears or complaints about others controlling their lives, but many describe consistent suspicions of very specific, elaborate, and persistent plots against THEM. Very often, these beliefs are directed at family members or friends.
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66
Q

SCHIZOPHRENIA - Delusions definition

A

false beliefs that are inconsistent with patient’s background and cannot be corrected by reasoning (result of an illness or illness process)

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67
Q

SCHIZOPHRENIA - Hallucinations definition

A

false perceptions in the absence of any external stimuli (e.g. auditory, visual) - no one else feels them

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68
Q

SCHIZOPHRENIA - Illusions definition

A

misperceptions of genuine stimuli, a specific form of sensory distortion because:
- individuals have been deliberately misled (e.g. by a magician);
- if their attention is diminished (e.g. delirium, fatigue, boredom or laziness)
- there is a lack of visual clarity (e.g. dim lighting, semi-darkness, fog)
- if they are intensely aroused by fear, passion or depression.

Some people have vivid imaginations and may see faces or figures in ordinary environmental features such as clouds, tree trunks, rock formations etc. This is quite common in children and is not considered

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69
Q

Schizophrenia
POSITIVE Sx
(should not be present, but are)

A

‘HD BS’

  • Hallucinations (auditory most common)
  • Delusions (paranoid or persecutory)
  • Thought Disorganisation = Behaviour (disorganised) + Speech (disorganised)
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70
Q

Schizophrenia
features of the auditory hallucination

A
  • comes from OUTSIDE of the head (as opposed to inside)
  • RIGHT side
  • commentary between speakers (as opposed to one voice)
  • mix of male and female voices
  • intermittent (rather than continuous)

Person will find specific REDUCING BEHAVIOURS (e.g. listening to radio/watching TV/talk to others very loud, wear headphones)
Person may seen reacting to what the voices are telling them (“RESPONDING TO INTERNAL STIMULI”)

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71
Q

SCHIZOPHRENIA
examples of Disorganised Behaviour

A
  • Motor perseveration (repeating same motions over and over)
  • echopraxia (copying someone’s movements)
  • Catatonia
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72
Q

SCHIZOPHRENIA
examples of Disorganised Speech

A
  • clang association ( words based on its sound/
    phonetics, like rhyming, rather than the actual meaning)
  • neologism
  • echolalia
  • perseveration (say the same word repeatedly w/o a purpose)
  • word salad (non-sense words)
  • concrete thinking (inability to think in abstract terms)
  • loosening association (Rapidly shifting from topic to topic, with no connection
    between one thought and the next)
  • Circumstantiality - an inability to answer a question without unnecessary and excessive detail
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73
Q

Schizophrenia
NEGATIVE Sx
(‘should be present but aren’t’)

A

The 5 A’s

  • Affect (flat/blunted)
  • Ambivalence/Avolition (difficulty making decisions/executing commands/poverty of thoughts)
  • Alogia (decreased or even absent speech)
  • Anhedonia
  • Asociality (social withdrawal)
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74
Q

Schizophrenia EPIDEMIOLOGY/PROGNOSIS

A
  • incidence general population 1/100 (1%)
  • men more affected than women 3/2 (1.5x)
  • earlier in men (18-25) than for in women (25-35)
  • men tend to exhibit more severe form and worse outcome
  • earlier onset
  • chances of recurrence after first episode (90% - similar to bipolar disorder)
  • SUICIDE: when it occurs, tends to happen in early stages when the insight is still preserved
  • negative symptoms are least likely to respond to medication.
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75
Q

Schizophrenia - RISK FACTORS

A
  • Monozygotic twin** 50%** chance of developing
  • Dizygotic twin has a 15% chance.
  • There is 48% chance if both parents are affected
  • There is 12 -13% chance if one birth parent is affected
  • There is increased risk with advanced paternal age, where the parent was aged over 55
  • Winter birth
  • Foetal hypoxia (Pre-eclampsia and emergency c-section)
  • use of illicit drugs (cannabis, amphetamines, cocaine, LSD)
  • Urban areas
  • stressful life experiences/migrants
  • physical/sexual abuse in childhood
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76
Q

Schizophrenia - Symptoms and different age groups

A

YOUNG PATIENTS (15-35 yo)
- spontaneous remission more common
- requires higher doses
- more likely to have “negative symptoms”

LATE ONSET (> 40-45 yo)
- less likely to remit spontaneously
- respond to lower doses
- persecutory delusions is most common symptom, along with accusative or abusive auditory hallucinations
- less likely to have thought disorder and negative symptoms

> 60 yo
- less likely to remit spontaneously
- visual hallucinations
- less likely to have thought disorder and negative symptoms

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77
Q

SCHIZOPHRENIA
Early signs suggestive of evolving psychosis in teenagers

A
  • Irritability or depressed mood (FIRST)
  • Deteriorating social or school function
    Withdrawal from friends and family
    A drop in performance at school
  • Increase in suspisciouesness
  • Hypervigilance
  • Ideas of reference and unsual rhoughts
  • Trouble sleeping
  • Lack of motivation
  • Strange behavior
  • Sudden and bizarre changes in emotions
  • Severe problems in making and keeping friends
  • Difficulty speaking, writing, focusing or managing simple tasks.
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78
Q

SCHIZOPHRENIA timeline DDx

A
  • Brief Psychotic disorder: > 1 day & < 1 month
  • Schizophreniform Disorder: > 1m & < 6 m
  • Schizoaffective Disorder
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79
Q

SCHIZOPHRENIA vs Schizoaffective Disorder

A

HATS:
- H: HALF or more of the time ill must be spent with mood sx
- A: psychotic sx must occur ALONE (i.e. w/o mood sx)
- T: psychotic sx must occur TOGETHER (i.e during an episode of mood disorder)
- S: exclude effect of SUBSTANCES or other medical conditions

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80
Q

SCHIZOPHRENIA vs BPD

A
  • stable or improving level of disfunction after early adulthood (as opposed to progressive decline over time seen in Schizophrenia)
  • affect instability of BPD involves rapidly emotional shifting (as opposed to weeks to months changes)
  • psychotic sx tend to be an sign of distress (experienced during times os stress)
  • Auditory hallucinations- if present - are described as inside (as opposed to outside) and vague/unclear (as opposed to clear/vivid)
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81
Q

SCHIZOPHRENIA vs Dementia

A

Demented patients usually have:

    • late onset
  • lack of prior psychiatric sx or signs
  • match average population in social milestones (school, work, marriage)
  • visual hallucinations
  • loss of recall of learnt information and visuospatial ability (schizophrenic patients have these intact)
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82
Q

SCHIZOPHRENIA
Secondary causes of acute-onset psychosis in children & adolescents

A
  • Metabolic/electrolyte disturbances
  • Urea cycle disorders
  • Acute intermittent porphyria
  • Wilson disease
  • Renal/liver failure
  • Hypoglycemia
  • Sodium/calcium/magnesium disturbances
  • SLE
  • Thyroiditis
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83
Q

Capgras syndrome

A
  • Also called delusional misidentification syndrome
  • Disorder in which a person believes that an identical-looking has replaced a friend, spouse, parent, or other close family member impostor
  • commonly occurs in patients with paranoid schizophrenia,
    dementia and brain injury
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84
Q

Cotard Syndrome

A

patient believes they have lost important body parts, blood, internal organs, or even their soul
- prevalent in schizophrenia, bipolar disorder, non-dominant temporo-parietal lesions and migraine.

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85
Q

Ekbom syndrome

A

Delusional infestation with parasites or worms in schizophrenic patients

Willis-Ekbom disease (WED); Witmaack-Ekbom syndrome or Restless leg syndrome (RLS) is characterised by a ‘compulsive’ restlessness or need to move the legs, often associated with paraesthesiae or dysaesthesiae. Symptoms at rest or disturbing sleep, quickly but temporarily relieved by standing and walking, with nocturnal worsening of symptoms.

https://litfl.com/karl-axel-ekbom/

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86
Q

FOLIE a DEUX

A

 Shared psychotic disorder
 Delusion developing in a person in close relationship with another person who has an established delusion (more common in mother-daughter or sister-sister relationships)
 Dominant person and submissive or
dependent person in the relationship is clearly established.
 Delusion similar in content.
 HAPPENS IN FAMILIES – GROUPS OF PEOPLE
– example is a cult.

Treatment:
 biggest challenge is getting the pair (or system) to accept the need for treatment.

 FIRST STEP IS to separate the person or people with the secondary disorder from the person with the primary disorder, as the secondary’s delusions often don’t persist following separation.

 Atypical antipsychotics aripiprazole and quetiapine most effective

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87
Q

Schizophrenia
first-episode psychosis treatment

A
  • Amisulpride

OR

  • Aripiprazole

OR

  • Olanzapine

OR

  • Paliperidone

OR

  • Quetiapine

OR

  • Risperidone

OR

  • Ziprasidone
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88
Q

Schizophrenia
Interventions additional to medication to prevent relapse and improve outcome

A
  • monitor for adverse drug effects
  • Shared-care programs
  • cognitive behavioural therapies (eg medication compliance therapy, motivational interviewing for substance abuse, coping strategies enhancement, symptom control interventions)
  • cognitive remediation for cognitive deficits, social skills programs, supported employment programs, accommodation and disability support options, education and training assistance, and social interventions to combat isolation
  • Manage comorbidities
  • monitor substance use
  • Maintain physical health and target cardiovascular risk factors
  • Work with family/carers
  • Carer assistance programs
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89
Q

Schizophrenia
period that requires symptoms to respond to treatment

A
  • Agitation = settles within days
  • Positive symptoms = may require several weeks, but some treatment response can be expected early (ie within 1 to 2 weeks of starting an antipsychotic)
  • Negative symptoms of schizophrenia are
    responsive to antipsychotics, but less so than positive symptoms
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90
Q

Schizophrenia
How long to wait before reevaluating if prescribed medication is working in a schizophrenic patient?

A

3 weeks
- Increase dose of the initial medication first,
- wait until 4-6 weeks

after 4-6 weeks

1 change to an alternate SGA, preferably (depending on positive/negative symptoms)

OR

2 change to FGA:
Haloperidol

OR

Chlorpromazine

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91
Q

SCHIZOPHRENIA
switchover regimen for antipsychotics

A

crossover phase of at least 1 to 2 weeks

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92
Q

Schizophrenia
Treatment duration

A
  • 2 years (Following a first psychotic episode)
  • ONLY if there has been full remission

Indefinite continuation of maintenance therapy is required for the majority of people with schizophrenia.

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93
Q

Schizophrenia
drug tapering regime

A
  • the antipsychotic can be cautiously tapered and discontinued over a period of at least 3 months.
  • monitor for early warning signs of relapse during this process and for a further 12 months after drug cessation.
  • If relapse occurs after cessation of maintenance therapy, longer-term treatment (ie at least 5 years) is required.
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94
Q

Schizophrenia
Main reason for relapse

A

drug discontinuation due to poor concordance

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95
Q

Schizophrenia
Risk factors for relapse

A
  • poor insight into the purpose of medication
  • psychosocial stressors
  • substance use (alcohol, cannabis, amphetamines more common)
  • premature lowering of the dose
  • discontinuation of antipsychotic treatment
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96
Q

Schizophrenia
Treatment Relapse Mx

A
  • commencing a depot antipsychotic
  • initiation of proceedings for involuntary community treatment
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97
Q

Schizophrenia
Treatment-resistant first step

A

identify any reasons for treatment resistance:

  • Is the diagnosis correct?
  • assess treatment concordance
  • Have possible underlying medical causes been identified and treated?
  • Is the patient reacting adversely to a current medication?
  • Have the drug dose and duration of administration been adequate?
  • assess abuse of alcohol and other drugs (eg cannabis, amphetamines)
  • Could an interacting drug be compromising the response?
  • Urine drug screening may be indicated, but this only identifies recent use and does not constitute a diagnosis of drug abuse or dependence,
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98
Q

Schizophrenia
Treatment Resistance definition

A
  • reasons in step one excluded

PLUS

  • drug trial of 6 to 12 weeks’ duration on optimal doses of at least TWO different antipsychotics
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99
Q

Schizophrenia
drug of choice for treatment resistance

A

Clozapine

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100
Q

Schizophrenia
Management of clozapine failure

A
  • augmenting strategies: (no drug has demonstrated to be the best)

– amisulpride VO
– haloperidol VO
– lamotrigine VO
– omega-3 fatty acids (in particular formulations high in eicosapentaenoic acid) 2 to 3

  • A trial of adjunctive ECT should be considered
    (However, the relapse rate is high after ceasing an acute course of ECT)
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101
Q

Schizophrenia
Indications for the use of Clozapine

A
  • severe and persistent positive and/or negative sx
  • persistent or frequently recurrent suicidal ideation and/or behaviours
  • severe and persistent EPS (eg tardive dyskinesia)
  • marked aggressive behaviour
  • severe comorbid substance abuse.
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102
Q

Schizophrenia
Mx of negative symptoms
(if not improved with first-line therapy)

A

Change to:

1 Amisulpride

OR

1 Clozapine

OR

1 a SGA other than clozapine
PLUS
an antidepressant (fluoxetine preferred)

OR

2 clozapine (
PLUS
an antidepressant (fluoxetine preferred)

OR

2 clozapine
PLUS
Lamotrigine

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103
Q

Hyperactive Delirium

A

Patients with hyperactive delirium demonstrate features of restlessness, agitation and hyper-vigilance. They often experience hallucinations and delusions but have no insight.

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104
Q

Lewy Body Dementia

A

 Dementia with Lewy Bodies is characterised: -impaired cognition
- fluctuating levels of awareness and attention
- Parkinsonism (ataxic gait)
- visual hallucinations
- sleep disorders
- tend to lack insight into the visual hallucinations

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105
Q

Behavioural emergencies
recommended methods necessary to gain control (from least invasive)

A
  • verbal de-escalation and early negotiation
    (including the offer of VO medication)
  • ‘show of force’
    (involves having a sufficient number of staff visibly backing up the clinician who is attempting to
    negotiate with the patient)
  • physical restraintv (immobilisation)
  • chemical restraint

NOTE: when weapons are involved or there is a high likelihood of extreme violence), security staff and/or police will be required to disarm and restrain the patient.

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106
Q

BEHAVIOURAL EMERGENCIES
What are the two types of treatment outcomes

A

-Tranquillisation
= defined here as a state of calmness (ie not showing anxiety, anger or other emotions)

-Sedation
= defined here as a state of rousable drowsiness.

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107
Q

BEHAVIOURAL EMERGENCIES
Oral Medication options

A
  • Diazepam VO
    (preferred in drug withdrawal and stimulant intoxication)
  • Olanzapine VO
    (preferred in acute psychosis)
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108
Q

BEHAVIOURAL EMERGENCIES
Intravenous medication option

Q.3.374

A
  • DIAZEPAM IV
    OR
  • MIDAZOLAM IV

If patient tolerant to benzodiazepine or if failure of first-line benzdiazepine USE: (in combiantion or single)

  • HALOPERIDOL IV
    OR
  • OLANZAPINE IV

If combination therapy is considered appropriate, each drug should be administered separately (ie do not combine drugs in the same syringe)

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109
Q

BEHAVIOURAL EMERGENCIES
Intravenous medication option

A
  • MIDAZOLAM IM

If patient tolerant to benzodiazepine or if failure of first-line benzdiazepine USE: (in combiantion or single)

  • HALOPERIDOL IM
    OR
  • OLANZAPINE IM

Diazepam is not recommended for intramuscular injection as absorption is poor and erratic.

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110
Q

ANXIETY DISORDERS
Generalised Anxiety Disorder (GAD) Dx

A

 Excessive anxiety/worry occurring on most days for at least 6 months (“chronic”)

 Associated with 3 or more of the 6 symptoms.

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111
Q

ANXIETY DISORDERS
Generalised Anxiety Disorder (GAD) Sx

A

MISERA-ble”

 M - Muscle tension
 I - Irritability
 S - Sleep (decreased)
 E - Energy (easy fatigue)
 R - Restlessness, feeling keyed up, on the edge
 A - Attention (Mind going blank or difficulty concentrating)

Not due to medical/ substance abuse/other
psychiatric disorders.

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112
Q

ANXIETY DISORDERS
Generalised Anxiety Disorder (GAD) Mx

A

 **Therapy CBT/SPS **(structured problem solving) - should always be first-line treatment

If severe or CBT ineffective after 3 months,
then SSRI can be introduced.

(SSRIs are decreased and ceased if patient is
symptom free for 6 months)

 Other options
- Buspirone - anxiolytic
- Benzodiazepines (short term of 2 weeks
and tapered over next 2 weeks; although it
has a more rapid effect it can easily lead to
physical dependence and should not be
used as long-term treatment)
- SNRI
- Beta blockers (PROPANOLOL) - if associated palpitation, tremors, for performance-only subtype

Individuals with performance-only social anxiety disorder do not fear nonperformance social situations and are not socially avoidant in general.

The pharmacologic treatment of performance-only social anxiety disorder includes as-needed beta blockers or benzodiazepines rather than maintenance medication.
- Beta blockers (eg, propranolol) on an as-needed basis help control the associated autonomic response (eg, tremors, tachycardia, diaphoresis).
- Due to their addictive potential, benzodiazepines (eg, diazepam, lorazepam) are generally avoided in patients with a personal or family history of substance use disorder. In addition, they are not preferred
when performance could be impaired by sedation and cognitive side effects (eg, giving a presentation, as in this case)

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113
Q

ANXIETY DISORDERS
Panic Attack Dx

A
  • Intense ACUTE fear or discomfort
  • in which 4 or more symptoms develop abruptly
  • reaches a peak in 5-10 minutes (crescendo-decrescendo pattern)
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114
Q

ANXIETY DISORDERS
**Panic Attack **
Sx

A

STUDENTS Fear C’s

 S - Sweating
 T - Trembling - shaking
 U - Unsteadiness or Dizziness/Faintness
 D - Derealisation/depersonalisation/
dissociation
 E - Elevated HR (Tachycardia/Palpitations)
 N - Nausea
 T - Tingling (Paresthesia)
 S - Shortness of breath/ smothering sensation

 FEAR - Fear of dying, Fear of loosing control or going crazy

 C’S
= Choking feeling
= Chills - hot flushes
= Chest pain/tightness

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115
Q

ANXIETY DISORDERS
*Panic Disorder *
Dx

A

1/6 people with panic attacks will develop panic disorder

Panic Disorder results from anxiety about having future panic attacks that impact one’s ability to lead a normal life

SURP-rise”

 S - Sudden (without a trigger)
 U - Unexpected
 R - Recurrent
 P - Panic attacks

Rise anxiety

Not associated with substance abuse

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116
Q

ANXIETY DISORDERS
*Panic Attack/Disorder *
Mx

A

FIRST: exclude medical condition. (acute
MI, asthma, thyrotoxicosis).

At the time of attack:
- slow breathing technique (if
hyperventilating)
- distraction methods
- benzodiazepines

** Treatment to prevent further attack**
- CBT (stress management, exposure and
desensitisation)
- avoid caffeine

 if Psychotherapy is not working
- SSRI or buspirone.
- should be used in conjunction with CBT

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117
Q

ANXIETY DISORDERS
Agoraphobia

A

It is generally a specific coping mechanism that arises in response to having panic attacks/disorder where one begins to avoid going out at all preferring to stay in the safety of their own home (become housebound) where they feel less vulnerable to panic attacks - however, it can occur alone

it develops in about 1/4 of people with Panic Disorder (it is a marker of severe Panic Disorder

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118
Q

ANXIETY DISORDERS
Social Phobia/ Social Anxiety Disorder

A

Persistent fear of interpersonal rejection

Affected individuals avoid social or performance situations in fear they’ll embarrass themselves or be judged as anxious or stupid

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119
Q

ANXIETY DISORDERS
Disorders that often present with anxiety as chief complaint and their differences

A
  • OCD (obsessional thoughts)
  • Somatisation ( anxiety to physical sx)
  • PTSD (re-experiencing trauma)
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120
Q

ANXIETY DISORDERS
Medical conditions that often present as anxiety

A

 Pheochromocytoma (rare)

 Diabetes Mellitus
(Hypoglycaemia is the commonest underlying organic cause of anxiety symptoms)

 Arrhythmias (Paroxysmal supraventricular tachycardias)

 Temporal epilepsy

 Hyperthyroidism

 Alcohol withdrawal

 Drug intoxication or withdrawal

NOTE:
Carcinoid does not cause anxiety.
Carcinoma of the bronchus and hyperparathyroidism are more likely to present with depression.

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121
Q

OCD
Definition of Compulsion

A

Compulsive behaviours are:

  • repetitive actions driven by anxiety or distress;
  • They often serve as a coping mechanism to alleviate stress or prevent a feared event or situation through a repeated behaviour
  • Associated with negative reinforcer (taking something - ie anxiety - away)

Impulsive behaviour are:
- spontaneous actions performed without forethought or consideration of the consequences
- These behaviours are driven by immediate desires
- Associated with positive reinforcer ( often meaning is pleasurable)

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122
Q

OCD
Are patients egosyntonic or ego-dystonic with how they view their disorder?

A

Ego-dystonic = recognise one’s intrusive thoughts are not reflective (discordant) of their true desires (insight is preserved)

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123
Q

OCD
Clinical features

A
  • obsessive thoughts and compulsive rituals
  • Compulsions are “repetitive purposeful”, “intentional” behaviours conducted to prevent an adverse outcome
  • While OBSESSIONS are REQUIRED for the diagnosis, COMPULSIONS are OPTIONAL (not everyone with obsessions will develop compulsions; however, everyone with compulsions will have obsessions)

  • Obsessions:
    Recurrent, intrusive, anxiety-provoking thoughts, urges, or images
  • Compulsions
    Response to obsessions with repeated behaviors or mental acts. Behaviors not connected realistically with preventing feared event
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124
Q

OCD
Obsessive thoughts characteristics

A

I MURDER

 I - Intrusive
 M - Mind-based (not thought insertion)
 U - Unwanted
 R - Resistant
 D - Distressing
 E - Ego-dystonic
 R - Recurrent

  • Time-consuming (>1 hr/day) or causing significant distress or impairment
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125
Q

OCD
Epidemiology

A
  • Men and women are “EQUALY” affected
  • once of symptoms often during childhood or young adulthood (< age of 20-30)
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126
Q

OCD
Mx

A

optimal management always include a combination of both:

               CBT  **(ERP = exposure & response prevention) **

                \+

               SSRI

NOTE: Alcohol makes OCD symptoms feel better for a while, however, it is not recommended as a therapy due to the risk of alcohol abuse

NOTE: “CLOMIPRAMINE” is a TCA and can be used as a second-line alternative if CBT+SSRI have failed or in more severe cases of OCD

NOTE Neurosurgery (i.e cynguloctomy) is reserver for severe/refractory cases

SINGLE THERAPY IS NOT EFFECTIVE IN CBT - combination therapy is always the first line treatment

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127
Q

Risks of developing Obsessive Compulsive Disorder

A
  • Anxiety
  • Depression
  • Alcohol or substance misuse
  • Eating disorders
  • Body dysmorphic disorders
  • Chronic physical health problems (skin problems due to excessive hand washing)
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128
Q

BODY DYSMORPHIC DISORDER
Key features

A

FIX ME DOC

 FIX - Fixation on perceived flaw
 M - Medical care-seeking
 E - Ego-Syntonic
 D - Disabling
 O - Obsessive thoughts
 C - Compulsive behaviours

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129
Q

BODY DYSMORPHIC DISORDER
patients are ego-syntonic or ego-dystonic with how they view their disorder?

A

Ego-syntonic
Patient does not admit that their fears and preoccupations are extreme or excessive

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130
Q

BODY DYSMORPHIC DISORDER Mx

A

CBT ± SSRI

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131
Q

Comorbid conditions found with BDD

A
  • Anxiety
  • Social Phobia
  • OCD
  • Delusional disorder
  • Alcohol or substance misuse
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132
Q

GENDER DYPHORIA (GD)
Clinical features

A
  • Experiences persistent (>6 months) incongruence between assigned & felt gender
  • Desires to be another gender
  • Dislikes own anatomy, desires sexual traits of another gender
  • discomfort with the development of unwanted secondary sexual characteristics.
  • Believes feelings/reactions are of another gender
  • Feels significant distress/impairment
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133
Q

GENDER DYPHORIA (GD)
Management

A
  • Assessment of safety
  • Support; psychotherapy (individual, family)
  • Referral to specialist Gender identity-affirming care services (medical & mental health multidisciplinary)
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134
Q

HYPOCHONDRIASIS Dx
vs
Illness Anxiety Disorder

A

fears and symptoms persist for ≥ 6 months

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135
Q

HYPOCHONDRIASIS
features

A
  • Preoccupation with or fear of having (as opposed to getting) a serious disease, despite medical reassurance, leading to significant distress/impairment.
  • often present with a (self)-diagnosis
  • Ego-syntonic (involuntary/non-volitional & unconsciously)
  • Often involves history of prior physical disease.
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136
Q

HYPOCHONDRIASIS Mx

A
  • group therapy ± SSRI
  • schedule regular appointments with the patient’s primary caregiver (if existing)
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137
Q

Difference between Hypochondriasis & Somatisation

A

Hypochondriasis:
patient presents with a diagnosis
focus on the disease, not a particular symptom
failure to respond to reassurance

                     Somatisation:   - presents with a variety of unexplained sx - primary focus of  preoccupation/concern with the symptoms themselves
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138
Q

HOARDING DISORDER

Management

A

CBT and SSRI

nonetheless, patient usually don’t respond well

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139
Q

HOARDING DISORDER
Define Diogenes syndrome

A
  • squalor and decline in personal hygiene
  • sometimes hoarding useless items
  • significant frontal lobe impairment
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140
Q

PTSD
Signs & Symptoms

A

TRAUMA

 T - Trauma core
 R - Re-experiencing core
 A - Arousal core
 U - Unable to function
 M - Month ( present > 4 weeks)
 A - Avoidance core

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141
Q

PTSD
Trauma features

A

Must be:
- life-threatening
- actual or threatened physical and/or sexual violence
- secondary exposure to a traumatic event (such as about a spouse or family member) also qualifies

NOTE: other non-life-threatening events such as harassment and non-violent bullying do not “qualify” as trauma per DSM-5 (despite these being distressing and resulting in S/S indistinguishable from PTSD) and ADJUSTMENT DISORDER with ANXIOUS MOOD should be considered

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142
Q

PTSD
Arousal phenomenon

A

Persistent (chronic) and generalised

  • Hyper-arousal State:
    increased anxiety and awareness
  • hyper-vigilance:
    constant scanning of their environment for
    clues to the presence of danger
  • MISERA-ble = MUSCLE tension, IRRITABILITY, trouble with SLEEP, low ENERGY, RESTLESSNESS, inability to pay ATTENTION (poor concentration and memory) to non-trauma related stimuli
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143
Q

PTSD
Duration

A

Symptoms must be present for at least 1 month

NOTE: it does not necessarily mean that symptoms have to present in the first month after the trauma occurs (delayed onset is more characteristic)

ACUTE: symptoms last < 3 months

CHRONIC: symptoms last > 3 months

DELAYED ONSET: Sx appear at least 6 months
after traumatic event

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144
Q

**PTSD **
vs
ACUTE STRESS DISORDER

A

When the core trauma-related symptoms have not yet reached ONE month in length

NOTE: the presence of ASD immediately following a traumatic event does not rule in later development of PTSD, nor does its absence rule it out

NOTE: the presence of ASD immediately following a traumatic event does not rule in later development of PTSD, nor does its absence rule it out

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145
Q

PTSD
Avoidance features

A

– physical avoidance (people, places, things)
– Psychological avoidance (emotional numbing)
an attempt to self-protect against strong negative
emotions; however, interferes with ability to
experience positive emotions such as joy (flattening
affect), satisfaction, love (detachment from others)

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146
Q

PTSD
Risk factors

A
  • alcohol and drug abuse
  • previous history of depression
  • previous history of sexual abuse.
  • Victims of domestic violence
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147
Q

PTSD
Features that predict a higher chance of having PTSD one year from the incident

A
  • the intentional nature of the trauma
    (eg sexual abuse/rape/assassination attempt)
  • Experiencing the trauma alone
  • lack of social support network
  • presence of at least one pre-trauma psychiatric diagnosis

NOTE: Onset of symptoms soon after the traumatic event (ie ACUTE DISTRESS DISORDER)

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148
Q

PTSD Mx

A
  • CBT (FIRST-LINE TREATMENT)
    • trauma-based psychotherapy, crisis
      intervention therapy,
    • EMDR (eye movement desensitisation and
      reprocessing therapy)
  • Life-style modifications (sleep hygiene,
    relaxation techniques)

NEXT STEP
- If not responding, then SSRI (it does not help specifically with either sleep or nightmares)

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149
Q

PTDS
Initial response to an acutely traumatised state

A
  • provide a comforting and consoling presence
  • to listen empathically

Most people following traumatic events recover spontaneously without specific psychological interventions

NOTE:
the current consensus is that debriefing is not clinically
indicated as an immediate intervention and may even be harmful
.

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150
Q

ADJUSTMENT DISORDER
with ANXIOUS MOOD or DEPRESSIVE MOOD
features:

A

Diagnostic criteria:
onset of anxiety/depression symptoms within 3 months of identifiable psychosocial stressor(s)

which:
- are time-limited (Once the stressor or its consequences have terminated, the symptoms do not persist for more than 6 months)

  • Aren’t severe enough to meet criteria for MDD or GAD and incurs in response to as stress that isn’t life-threatening or violent enough to be trauma
  • are in excess of normal expectations of reaction to the stressor(s)
  • are not due to another identifiable mental disorder
  • are not part of a continuing pattern of overreaction to stress impair social or occupational functioning.
  • Significant impairment in social,
    occupational, or other important areas of
    functioning
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151
Q

ADJUSTMENT DISORDERS
Mx

A
  • primary interventions = psychological supportive therapy including counselling, relaxation, problem solving, stress management, and (CBT)
  • short-term pharmacotherapy (usually < 2 wks) with BZ = if the symptoms are severe, if significant impairment of functioning and there is inadequate response to psychological interventions.

NOTE: Most drugs used to treat anxiety (ie [SSRIs]) take a number of weeks to produce an effect, thus in this situation the use of a BZP may be appropriate

NOTE: Intermittent use, on occasional days when there is a severe exacerbation of anxiety, may suffice and is preferable to continuous treatment.

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152
Q

ADDICTION/SUBSTANCE ABUSE
overall pattern

A
  • Repeated use
  • Reinforcers (Positive)
  • Repercussions (Njuegative)
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153
Q

ADDICTION/SUBSTANCE ABUSE
vs
OCD

A

Compulsive vs. Impulsive:

The primary difference between compulsive and impulsive behaviours lies in their motivation and execution.

  • Compulsive behaviours stem from an internal drive to alleviate the fear and anxiety triggered by obsessive thoughts
  • Impulsive behaviours are spontaneous and often driven by desires.
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154
Q

ADDICTION/SUBSTANCE ABUSE
Tobacco
The stages of intervention

A

the 5As framework
ask (about smoking)
assess (motivation & nicotine dependence)
advise (to quit)
assist (with cessation)
arrange follow-up

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155
Q

ADDICTION/SUBSTANCE ABUSE
Tobacco
Nicotine dependence levels

A

— high dependence
— moderate dependence
— low-to-moderate dependence
— low dependency

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156
Q

ADDICTION/SUBSTANCE ABUSE
Tobacco
Nicotine HIGH Dependence

A

waking at night to smoke

                 or

smoking within the first 5 minutes after waking

= usually smokes > 30 cigarettes daily

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157
Q

ADDICTION/SUBSTANCE ABUSE
Tobacco
Nicotine MODERATE Dependence levels

A

smoking within 30 minutes after waking

= usually smokes 20- 30 cigarettes daily

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158
Q

ADDICTION/SUBSTANCE ABUSE
Tobacco
Nicotine LOW-TO- MODERATE Dependence levels

A

not needing to smoke within the first 30 minutes after waking

usually smokes 10-20 cigarettes daily

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159
Q

ADDICTION/SUBSTANCE ABUSE
Tobacco
Nicotine LOW Dependence levels

A

not needing to smoke in the 1st hour after waking

usually smokes < 10 cigarettes daily.

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160
Q

ADDICTION/SUBSTANCE ABUSE
Tobacco
When to intervene for stopping smoking with pharmacotherapy

A

Recommended for:
- moderately to highly nicotine-dependent smokers
&

  • who express an interest in quitting
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161
Q

ADDICTION/SUBSTANCE ABUSE
Tobacco
Interventions for smoking cessation

A

Best results are usually achieved when pharmacotherapy is combined with counselling and support

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162
Q

ADDICTION/SUBSTANCE ABUSE
Tobacco
Smoking cessation First-line pharmacotherapy options

A
  • Nicotine Replacement Therapy (NRT)
  • Varenicline
  • Bupropion
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163
Q

ADDICTION/SUBSTANCE ABUSE
Tobacco
NRT
indications/suitability

A

– Combination NRT (ie patch and oral form) preferred
(*Combination NRT is as effective as varenicline and more effective than single types of NRT.)

  • can be used by people with cardiovascular disease (Caution is advised for people in hospital for acute cardiovascular events, but NRT can be used under medical supervision if the alternative is active smoking.)
  • NRT may be considered in women who are pregnant if they were unsuccessful in stopping smoking without pharmacotherapy. If NRT is used, the benefits and risks should be explained carefully to the patient by a suitably qualified health professional. The clinician supervising the pregnancy should also be consulted.
  • NRT (ie patch, intermittent) is considered an option for breastfeeding mothers. Infant exposure to nicotine can be reduced further by taking intermittent NRT immediately after breastfeeding.
  • cannot be used in children aged < 12 years
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164
Q

ADDICTION/SUBSTANCE ABUSE
Tobacco
Varenicline
indications/suitability

A
  • The most effective single-form pharmacotherapy for smoking cessation
  • not recommended for pregnant and breastfeeding women, nor for adolescents.
  • causes nausea in 30% of patients
  • requires caution in CKD patients
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165
Q

ADDICTION/SUBSTANCE ABUSE
Tobacco
Bupropion
indication/suitability

A
  • less effective than varenicline for smoking cessation.
  • contraindicated in patients with a history of seizures, eating disorders and those taking monoamine oxidase inhibitors
  • not recommended for women who are pregnant or breastfeeding
  • Should be used with caution in people taking medications that can lower seizure threshold (eg antidepressants, antimalarials, oral hypoglycaemic agents)
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166
Q

ADDICTION/SUBSTANCE ABUSE
Alcohol Use Disorder
CAGE questionnaire in Alcohol Use Disorder (AUD):

A

“YES” to 2 or more is a POSITIVE screen:

 C - CUT
Have you ever felt you should Cut down on your drinking?

 A - ANNOYED
Have people Annoyed you by criticising your drinking?

 G - GUILTY
Have you ever felt bad or Guilty about your drinking?

 E - Have you ever had a drink first thing in the morning to steady your nerves or to get rid of a hangover? (Eye-opener)

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167
Q

ADDICTION/SUBSTANCE ABUSE
Alcohol Use Disorder
Overdose/Intoxication
Mx

A

Treatment of intoxication and overdose is supportive and symptomatic, with careful monitoring of:
- BAC
- airway
- level of consciousness and responsiveness
- oxygen saturation
- hypoglycaemia and metabolic acidosis
- Alcoholic Hallucinations

Stimulants should not be given.

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168
Q

ADDICTION/SUBSTANCE ABUSE
Alcohol Use Disorder
ACUTE Alcohol withdrawal syndrome

A

Symptoms usually appear within 6-24 hours of the last consumption of alcohol (BAC ≤ 0.1%). can last up to 72 hours

The signs and symptoms may be grouped into three major classes: autonomic, gastrointestinal, and CNS changes that represent manifestations of sympathetic hyperactivity.

AUTONOMIC:

  • Sweating
  • Fever
  • Tachycardia
  • Hypertension
  • Tremor

GASTROINTESTINAL:

  • nausea and vomiting
  • Dyspepsia
  • Anorexia

CNS
- Anxiety
- agitation
- Delusions/Hallucinations
- Insomnia and vivid dreams
- Seizures (occasionally - 5% - observed, grand mal type = generalised, not focal)

LAB
- ↑ GGT
- ↑ AST/ALT RATIO

Seizures is the hallmark feature of Acute Alcohol Withdrawal (in contrast to Delirium Tremens which normally does not present with seizures) and the most concerning intercurrence

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169
Q

ADDICTION/SUBSTANCE ABUSE
Acute Alcohol withdrawal” Mx

A
  • Diazepam VO
    – Oxazepam VO (if liver disease)
  • Thiamine (IM or IV)
  • AVOID antipsychotics (which lower seizure threshold).

If hallucinations are not responding to Benzodiazepines alone, add:
- Olanzapine VO

other meaures include:
- Nursing in well-lit and quiet environment
- Monitoring for and treating hypoglycaemia
- Rehydration
- High calorie high carbohydrate diet,

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170
Q

ADDICTION/SUBSTANCE ABUSE
Alcoholic Hallucinosis vs DTs

A

Alcoholic Hallucinosis
* develop 6 - 24 hours of the last drink
* typically persist for up to 72 hours
* transient visual, auditory hallucinations
* Usually benign
* Associated with Alcohol intoxication

DTs
* occurs 24-72 hours after stopping/significantly reducing alcohol consumption
* Autonomic instability (↑ BP, ↑ HR)
* Usual course is 3 days, but persist for up to 14 days
* Associated with withdrawal

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171
Q

ADDICTION/SUBSTANCE ABUSE
Delirium Tremens (DTs)” Ddx

A

Delirium tremens is a diagnosis by exclusion, so before commencing treatment, screen for other factors contributing to delirium, in particular:

  • subdural haematoma
  • head injury
  • Wernicke’s encephalopathy
  • hepatic encephalopathy
  • hypoxia
  • sepsis
  • metabolic disturbances
  • intoxication with or withdrawal from other drugs
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172
Q

ADDICTION/SUBSTANCE ABUSE
Benzodiazepines use & intercurrent illness

A
  • IV Diazepam should be avoided if possible.
    – Onset of action isn’t much faster than with
    VO
    – there is a greater likelihood of causing
    severe adverse effects such as respiratory
    depression.
    – If an injection is necessary, it must not be
    diluted and it must be given slowly over
    several minutes to minimise the risk of
    respiratory depression or arrest. Close
    cardiorespiratory monitoring is essential.
  • If Severe liver disease
    – Oxazepam VO
  • Severe chronic airflow limitation
    Use benzodiazepines with caution and with
    close monitoring.
    – Midazolam IV
    or
    – Short acting Benzodiazepine = Temazepam
    or Oxazepam
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173
Q

ADDICTION/SUBSTANCE ABUSE
Thiamine

A
  • Initial dosing is with IV or IM thiamine
    (absorption of oral thiamine is slow and may be incomplete in patients with poor nutritional status)
  • Administer thiamine before giving any form of glucose when possible. A carbohydrate load in the presence of thiamine deficiency risks precipitating Wernicke’s encephalopathy.
174
Q

ADDICTION/SUBSTANCE ABUSE
Long-term management of alcohol dependence

A
  • acamprosate
  • naltrexone
  • disulfiram
                         \+

best used in conjunction with psychosocial therapy

For each of these drugs, treatment
duration of 6 months or more is recommended.

175
Q

ADDICTION/SUBSTANCE ABUSE
AUD - Acamprosate

A
  • started following cessation of the acute phase of alcohol withdrawal, ie approximately 1 week after cessation of drinking
  • Treatment should continue even if the patient lapses;

INDICATIONS
- moderate to severe AUD
- Does not interact with alcohol
- compliance may be challenging due to dosing regimen

CONTRAINDICATIONS
- hypersensitivity to the drug
- renal insufficiency
- severe hepatic failure
- Tetracyclines may be rendered inactive by the calcium component in acamprosate.

  • Modulates GABA/glutamate
176
Q

ADDICTION/SUBSTANCE ABUSE
AUD - Naltrexone

A

INDICATIONS
- moderate to severe AUD

CONTRAINDICATIONS
- acute hepatitis or severe liver failure.
- There are no well controlled studies of the
safety of naltrexone during pregnancy or
lactation.
- not suitable for people who are opioid
dependent or who have pain disorders/
require opioid analgesia

  • blocks the effect of endogenous opioids released following alcohol intake
177
Q

ADDICTION/SUBSTANCE ABUSE
AUD - Disulfiram

A
  • most effective with supervised
    administration
  • Careful monitoring of cardiac and liver condition is recommended if disulfiram treatment is started. Liver tests should be performed fortnightly for 2-3 months, particularly in those with abnormal tests at baseline.

INDICATIONS
- appropriate for patients who are motivated to ABSTAIN from alcohol. It should not be prescribed for patients who have a goal of reduced alcohol intake.
- It is beneficial for patients that accept a need for an external control on their drinking and are prepared to be supervised in the daily dosing of the medication.

CONTRAINDICATIONS
- cardiovascular, hepatic or pulmonary disease
- Safe use of disulfiram during pregnancy or lactation has not been established
- Patient has not consumed alcohol in the previous 24 hours

  • primarily works by inhibiting the action of aldehyde dehydrogenase - enzyme involved in the second step in the metabolism of alcohol, that converts acetaldehyde to acetate. This leads to the accumulation of acetaldehyde following consumption of alcohol while on disulfiram. The resulting symptoms are unpleasant
178
Q

Pyromania
Features

A
  • impulse control disorder
    (an impulse to set fires and involves deliberate and purposeful fire setting with anxiety prior to the act and gratification or relief following the act of setting the fire)
  • They do not do it to seek public attention.
  • They do not like to play with fire
  • The fire is not set for monetary gain out of any sense
    of revenge or anger (which is arsoning)
179
Q

**ADHD **
Inattention signs:

A

DETaILS OFF

 D - Details are sloppy
 E - Easily distracted
 T/A - Task Avoidance
 I - Ignores instructions
 L - Loses things
 S - Sustained attention (poor)

 O - Organisation (poor)
 F - Forgetful
 F - Fails to finish tasks

180
Q

ADHD
Hyperactivity signs:

A

HE RILED UP

 H - Hiperactive
 E - Energetic

 R - Running around
 I - Interrups/Impulsivity
 L - Loud
 E - Effusive
 D - Delay Intolerance

 U - Unseated
 P - Prematurely answers questions

181
Q

ADHD Dx:

A
  • Does not require symptoms of both domains (Inattention or Hyperactivity) to co-exist
  • It’s a diagnosis of exclusion
  • ADHD = Inattention and hyperactivity that is excessive, unrelated to other disorders and has been observed in multiple settings from a young age (in case of divorced parents, it is important to obtain colateral history from the other parent that is not present on the first assessment)
  • symptoms are chronic (as opposed to episodic and fluctuating) - must be present for at least 6 monyhs
  • symptoms must’ve been present before age of 7 y

FIDGETY

 F - Functionally impairing
 I - Inattention
 D - Disinhibition
 G - Greater than normal
 E - Exclude other disorders
 T - TWO or more settings
 Y - young age (12 or less)

  • ADHD does not present with failure to achieve developmental milestones
  • ADHD can maintain the ability to focus on activities they find intrinsically interesting or enjoyable
182
Q

ADHD
Tools to assist on the diagnosis

A
  • Behavioral Rating Scale
  • Visual & Hearing Assessments
  • Classroom Observation
  • Psychometric Assessment

Behavioural rating scales give an objective measure of the symptoms across various domains and can assist in
determining if symptom criteria for ADHD have been met. It is recommended that they be obtained from home and school at least. However they are not diagnostic. The person completing the scales should have known the subject person for at least a month.

Psychometric assessment can exclude
**intellectual impairment **and learning disorders. ADHD has a high rate of comorbidity with learning disorders, so there will need to be a review of the child’s academic competency.

183
Q

ADHD
Risk factors

A
  • Male: Female 2:1
  • Family history of ADHD
  • in utero tobacco exposure
  • maternal stress
  • premature delivery
  • low birth weight
  • poverty
184
Q

ADHD
Prognosis

A
  • Predominant inattentive subtype is more common ( ~ 2/3)
  • Combined subtype 20%
  • Predominant hyperactive subtype 10%
  • Hyperactive subtype often prominent during school and decreases with age
  • Inattentive subtype persists at same level throughout life

60% will continue to exhibit symptoms into
adulthood

185
Q

ADHD
Adult main features

A

Symptoms are more subtle, and are subject to change:

  • Hyperactivity may be replaced with restlessness
  • impulsivity may be replaced with inability to control emotions or social inappropriateness.
186
Q

ADHD
Treatment

A
  • CBT (behavioural management and training) + family therapy

+/-

  • Pharmachological
    • 1st line: Stimulants (methylphenidate,
      dexamphetamine
      )
      • 2nd line: Atomoxetine

drugs alone may not have a longer-term benefit on academic performance

The alternative stimulant should be considered if the maximum dose of the first drug is reached and there is no significant improvement
- after ** ONE month ** of treatment
or
- if there are major adverse effects.

With rare exceptions, do not use stimulants in children aged younger than 4 years

187
Q

Mechanism of action of ADHD medication

A
  • STIMULANTS:
    Inhibition of dopamine and norepinephrine reuptake
  • ATOMOXETINE:
    Selective Noradrenaline reuptake inhibitor
188
Q

ADHD
Stimulants side-effects
and Mx

A
  • headache
  • abdominal discomfort

However, many children become tolerant to these effects without the need to reduce doses.

  • Increased sleep latency
  • appetite suppression are common.

Due to the anorectic properties of these drugs, doses should be given at or after breakfast and lunch

  • growth restriction (relatively minor)

The weight and height of children should be monitored routinely during their treatment. When there is concern about a child’s growth, drug holidays may be appropriate at times when some increase in symptoms may be acceptable (eg weekends and school holidays)

  • Social withdrawal and tearfulness

may be indicators of an excessive dose.

189
Q

ADHD
Contra-indication/precautions

A
  • should be used with caution in children with:
    • structural cardiac abnormalities, serious heart
      problems or those with conditions that may be
      exacerbated by increased pulse rate or BP
      • family history of sudden death, syncope
        —-»> An assessment by a cardiologist is suggested.
        —-»> Promptly evaluate children who develop
        exertional chest pain, unexplained syncope or
        other cardiovascular symptoms.
  • Avoid stimulants in children with a history of psychosis as a psychosis may be precipitated.
190
Q

ADHD
Comorbid mental disorders

A
  • oppositional defiant disorder
  • conduct disorder
  • learning and language problems
  • autism
  • GAD
  • OCD
191
Q

ADHD
DDx that can mimic

A

PAN LID NOISE

 PAN - Parenting, Abuse, and Neglect
 LID - Learning, Intellectual, and Developmental
Disabilities (these conditions do not respond to
the treatment for ADHD; in addition, they
present with failure to reach milestones

 N - Nutrition
 O - Other conditions (DM, Seizures, MDD, ODD, CD)
 I - Intoxication
 S - Sleep
 E - Environment

192
Q

ADHD
vs ODD/CD

A
  • ADH has no intention to misbihave or be disruptive
  • ADH have remorse if they realise they’ve upset others
  • ADH disruptive behaviours rarely escalate to the level of fraglant disregard to rules and others rights like in CD
193
Q

AUTISM SPECTRUM DISORDER (ASD)
core symptoms

A
  • deficitis in social communication (Austistic Aloness)
  • restrictive and repetitive interests & activities (Insistence upon Sameness)

Two domains

194
Q

AUTISM SPECTRUM DISORDER (ASD)
Dx

A

both core symptoms
social communication
&
Restricted interests and behaviours

+
Developmental (1-3 years old) onset

“the criteria for diagnosing is in the name of the disorder: “ASD

195
Q

AUTISM SPECTRUM DISORDER (ASD)
Signs/Symptoms deficits social communication domain

A
  • speech delays/Lack of speech
  • difficult understanding and using non-verbal communication
  • Overly literal
  • indifference to the presence of others
  • Reciptocity (absent)
  • Turn-taking (absent)
  • Sharing (absent)

ASD is most strongly associated with delays in speech-related milestones rather than motor milestones. These deficits often do not begin until the age of 1 at the earliest.

196
Q

AUTISM SPECTRUM DISORDER (ASD)
Signs/Symptoms Restricted interests and activities domain

A
  • paticular fixations and fascinations
  • stereotyped or repetitive movements or posturing of body, arms, hands or fingers
197
Q

AUTISM SPECTRUM DISORDER (ASD)
Other sings and symptoms

A

although common (occurring in 60-80% of cases), they are not required for a diagnosis
- disturbance in sensory perception
* hypersensitivity* = aversion to sounds or textures
* hypopsensistivity* = high tolerance to pain or
temperature

  • motor sings
    • poor coordination
    • low muscle tone
    • unusual gait
198
Q

ASD vs ADHD

A
  • patterns must be observed in multiple settings from early childhood FOR BOTH conditions
  • ONLY ASD is associated with milestone delays
199
Q

AUTISM SPECTRUM DISORDER (ASD)
Mx

A
  • beihavioural training
    = teach specific adaptive skills
  • speech language therapy
    = teaching skills to overcome communication deficits

medications play no role in improving outcomes in autism

200
Q

ASD
Risk Factors

A
  • family history (1st degree relative)
  • childreen of older fathers
  • M>F (4x)
201
Q

ASD
and other causes for speech delays

A

“APHASIC”

 A - Autism
 P - Physical deficits
 H - Heating impairment
 A - Abuse/neglect
 S - Selective Mutism
 I - Intelctual Disability
 C - Cerebral Palsy

For many patients, speech delay is the initial reason for a formal evaluation of autism. Hence, other causes of speech delay must be ruled out

202
Q

PERSONALITY DISORDERS
Five personality traits

A

OCEAN

 O - Openness to experience
 C - Conscientiousness (tendency to act in
accordance with both personal and societal
expectantions)
 E - Extroversion (tendency to engage with the
external environment/other people)
 A - Agreeableness ( priority that one places on
getting along with other people)
 N - Neuroticism (tendency to experience
negative emotions over positive ones)

203
Q

PERSONALITY DISORDERS
DDx

A

The dysfunction seen in personality disorders is chronic and enduring - rather than transient and episodic

the characteristic patterns of a disordered personality tend to develop early in life - if it had started 2-3 yrs
back in adulthood, it is likely not a personality disorder

As with all personality disorders, a diagnosis of histrionic personality disorder requires that the patient demonstrate a persistent pattern of problematic behavior since early adulthood and across multiple contexts.

People with ONE personality disorder often meet criteria for ANOTHER

204
Q

PERSONALITY DISORDERS
CLUSTER A

what happens when people from each cluster are invited to a party

A

PaSS” the invitation as they:
tend to shy away from social interaction

 P - Paranoid
 S - Schizoid
 S - Schizotypal

common shared base

Cluster A resembles psychosis

205
Q

PERSONALITY DISORDERS
CLUSTER B

what happens when people from each cluster are invited to a party

A

BAHNed” from future parties for:
engaging in overly emotional, self-centered, manipulative, or even downright antisocial behaviour

 B - Borderline
 A - Antisocial
 H - Histrionic
 N - Narcisitic

all but histrionic have a shared base

Cluster B resembles mood

206
Q

PERSONALITY DISORDERS
CLUSTER C

what happens when people from each cluster are invited to a party

A

party will be “DOA” (Dead On Arrival) given their tendency:
to be highly neurotic, which will drag down the spirit of the party

 D - Dependent
 O - Obsessive-compulsive
 A - Avoidant

no shared bases between disorders

Cluster C resembles anxiety

207
Q

PERSONALITY DISORDERS A
Paranoid Personality Disorder
Features

A
  • Low agreeableness (tends to see people’s motives with skepticism or suspisciousness)
  • fear
  • mistrust
  • suspiciousness
  • There some social engagement
  • usually labelled as “angry”
208
Q

PERSONALITY DISORDERS A
Paranoid Personality Disorder
vs
Paranoid Delusions in Schizophrenia

A
  • Paranoia in Schizophrenia involves a stable pattern sticking to one belief (fixed and enduring belief system)
  • PPDs tend to jump between various paranoid ideas (constant stream of new paranoid thoughts)
209
Q

PERSONALITY DISORDERS A
Schizoid Personality Disorder
Features

A
  • Low extroversion (lack of interest in social relationships)
  • preference for solitary activities (the happy loner fine being on their own)
  • Aloof
  • lack of self-confidence
  • indiference to praise or criticism from others
210
Q

PERSONALITY DISORDERS A
Schizoid Personality Disorder
vs
Avoidant Personality Disorder

A

unlike in Avoidant Personality Disorder, the lack of social contact doesn’t appear to bother one with Schizoid Personality Disorder. They generally find that being alone is preferable to the constant demands for connection and intimacy that others put upon them.

211
Q

PERSONALITY DISORDERS A
Schizoid Personality Disorder
vs
Asociality in Schizophrenia

A

The Asociality in Schizoid Personality Disorder is more conscious and intentional - ego-syntonic.
In contrast, someone with schizophrenia tends to avoid social connection due to a lack of motivation and inability to connect with others due to negative symptoms

212
Q

PERSONALITY DISORDERS A
Schizotypal Personality Disorder
Features

A
  • odd beliefs (magical) & ensitive perceptions (quasi
    delusional beliefs)
  • difficulty relating to other people (emotionally distant)
  • eccentric behaviour
  • loneliness/isolation (“isolated hippie”)
213
Q

PERSONALITY DISORDERS A
Schizotypal Personality Disorder
vs
Schizoid Personality Disorder

A

In Schizotypal Personality Disorder, the social avoidance is often out of fear that others will judge them for their odd beliefs, strange maneirisms, or unconventional manner of dress

214
Q

PERSONALITY DISORDERS B
Narcissistic Personality Disorder

A
  • High Neuroticism (focuses on negative stimulli, thinks about mistakes from the past)
  • inflated self-importance (grandiosity, superiority, entitlement)
  • repeatedly boasting about one’s sefl-accomplishment
  • inability to empathise (haughty, aloof)
  • exploits others
  • craves for attention and admiration
  • dificulty tolerating criticism

any peoplee with narcissistic personality disorder will exagerate their claims, the disorder does not preclude them from being highly successfu, and it should nnot be assumed that they are making up or embellishing their success

Although patients with (NPD) also need to be the center of attention, they typically do not exhibit the dramatic emotional displays (seen in this patient) that are a key feature of histrionic personality disorder.

215
Q

PERSONALITY DISORDERS B
Narcissistic Personality Disorder vs Bipolar Disorder

A

Look at the timing of signs and symptoms as these will be:
- enduring in Narcissistic Personality Disorder
- episodic in Bipolar Disorder

216
Q

PERSONALITY DISORDERS B
Histrionic Personality Disorder
core Features

A
  • excessive or exagerated behaviours intended to draw
    attention to one’s self or to gain approval of others
    (dramatic, flitartious, sexually provocative)
  • although it comes shallow and provocative
  • Self-dramatisation, theatricality, exaggerated
    expression of emotions (with facial expressions and
    hand gestures)
  • Shallow/vague speech and labile affectivity
  • Continually seeking to be the centre of attention
  • Inappropriate disinhibition/flirtiness
  • Over-concern with their physical attractiveness (Uses
    appearance to draw attention)
  • easily influenced by others (suggestible)
  • Considers relationships more intimate than they are
217
Q

PERSONALITY DISORDERS B
Histrionic Personality Disorder
other Features

A
  • Approximately 2-3% of the population has HPD
  • least impairing disorder in Cluster B
  • does not have association with child abuse
  • F > M
  • Tends to run in families
  • There’s a genentic link between alcoholism and HPD
218
Q

PERSONALITY DISORDERS C
Dependent Personality Disorder
Features

A
  • high agreeableness (place other’s interests
    ahead of their own)
  • overreliance upon other people (clinging behaviour)
  • avoids conflcts
  • difficulty in making decisions in multiple areas of life
    (small and large)
  • seeks reassurance constantly
  • extremely deferential (reverential, respectful, obedient)
  • suggestible (can be easily influenced by other people)
219
Q

PERSONALITY DISORDERS C
Obsessive-Compulsive Personality Disorder (OCPD)
Features

A
  • high conscientiousness (tend towards planned
    behaviours)
  • low openness to new experiences (value
    pragamatism)
  • emotional rigidity and controlling behaviour
  • reluctant to delegate
  • Scrupulous
  • Inflexible about matters of morality
220
Q

PERSONALITY DISORDERS C
OCPD vs OCD

A
  • OCPD
    • ego-systonic (feel that they are right/correct)
  • OCD
    • ego-dyntonic (rituals that cause feelings of distress, rather than satisfaction)
221
Q

PERSONALITY DISORDERS C
Obsessive-Compulsive Personality Disorder (OCPD)
Management

A
  • CBT
  • Interpersonal Therapy (addressing the effect that
    rigidity has on others)
222
Q

PERSONALITY DISORDERS C
Avoidant Personality Disorder
Features

A
  • creepling sense of disaproval
  • avoidance of social engagements
  • unwilingness to meet new people
    • alone but wants connection
  • tendency to avoid getting into intimate relatioships
  • constant worries about being criticised or rejected
  • inhibited behaviour in interpersonal situatiions
  • a view of oneself as inept or inferior
  • reluctance to take risks or do anything potentially
    embarrassing
223
Q

PERSONALITY DISORDERS C
Avoidant Personality Disorder vs Schyzoid Personality Disorder

A
  • Schyzoid
    • happy loner
  • Avoidant
  • still desire human contact
224
Q

PERSONALITY DISORDERS C
Avoidant Personality Disorder
Mx

A
  • SSRIs
  • CBT
225
Q

PERSONALITY DISORDERS
BPD Sings & Symptoms:

A

9 key criteria: I DESPAIR

 I - Identity
 D - Dysphoria
 E - Emotinal Instability (affective lability)
 S - Suicide/Self-harm
 P - Psychosis/Dissociative
 A - Anger
 I - Impulsivity
 R - Relationships (Unstable/Sensitivity to
abandonment) = highly sensitive and specific

226
Q

PERSONALITY DISORDERS
BPD Sings & Symptoms:

A

Psychosis-like symptoms are different from primary psychosis:

– auditory hallucinations
- (voices come from inside and are vague, as
opposed to the typical auditory hallucinations
psychosis where they they com from outside their
head and are clear
- often transient and tend to occur in times of stress

– paranoid ideations
related to extreme interpersonal sensitivity as opposed to complex delusinal belief system

227
Q

PERSONALITY DISORDERS
BPD Sings & Symptoms:

A

Impulsivity

Someone with extreme and erratic emotions would also engage in extreme and erractic behaviours

these actions help to temporarily relieve the chronic state of dysphoria (as opposed to extreme bahaviours seen in mania where it is purely pleasure-seeking behaviours)

228
Q

PERSONALITY DISORDERS
BPD Sings & Symptoms:

A

Splitting

Tendency to see the world in extremes or black-and-white terms. Relatives, friends, and HCPs interacting with BPD patients often find themselves on one side or the other of a split: they are either “the best person ever” or “the cruelest person ever to walk on the face of the earth”

229
Q

PERSONALITY DISORDERS
BPD Dx:

A

Is characterised by chronic instability in the domains of identity, mood, affect, behaivour, relashionship, and and one need 5 out of 9 sx to be diagnosed.

230
Q

PERSONALITY DISORDERS
Difference between BPD and Cyclothymic disorder?

A

BPD:
- impulsivity in at least two areas that are potentially self-damaging
- A pattern of unstable and intense interpersonal relationships characterized by alternating between extremes of idealization and devaluation

Cyclothymic:
- many periods of depressed mood and many
episodes of hypomanic mood for at least 2 years
- During the above 2-year period (1 year in children and adolescents), the hypomanic and depressive periods have been present for at least half the time and the individual has not been without the symptoms for more than 2 months at a time

231
Q

PERSONALITY DISORDERS
Difference between Dysphoria and dysthymia

A
  • Dysphoria = reactive state
    people with dysphoria may express their disocontent through anger outbursts. They externalise their dissatisfaction thorough blaming others.
  • Dysthymia = non-reactive to circumstances
    people with depression/dysthymia may be more passive in their attempts to cope. They blame themselves and feel guilt
232
Q

PERSONALITY DISORDERS
BPD Mx

A

Dialectical behaviour therapy (DBT)

  • mindfullness
  • distress tolerance
  • emotional regulation
  • interpersonal effectiveness

downsides
- small pool of available providers (as it requires training)
- Costly
- time consuming (requires 1-2 years of treatment before meaningful improvements are seen)

Pharmacological
If medications must be be used, they should only be for symptomatic treatment of specific symptoms and are used adjunctively:
- Anticonvulsants = reduce anger and impulsivity
- Antipsychotics = alleviate paranoid or dissociative sx

This teaches specific skills targeted towards core sympyoms that BPD patients tend to struggle with

233
Q

PERSONALITY DISORDERS
BPD and Comorbidities Mx

A

People with BPD often meet criteria for multiple other conditions:

  • depression
  • anxiety
  • bipolar disorder
  • PTSD

Treatment of BPD should come first. It tends to improve related symptoms.

The only exception is if there is an immediate threat to the health of the patient or if not treating these conditions it would interfere with the ability of the patient to engage in therapy

234
Q

PERSONALITY DISORDERS
BPD other features:

A
  • evident in adolescence/early adulthood
  • less common in old age groups
  • traumatic events in child are correlated (but not causative)
  • F=M (although in clinical settinhs it tends to be F>M)
  • Family history/high inheritability (50% risk)
  • Complete remission is quite rare (interpersonal sensitivity tends to persist)
235
Q

PERSONALITY DISORDERS
Antisocial Personality Disorder (ASPD) Sings & Symptoms:

A

8 criteria “ACID LIAR

 A - Adult (diagnosis > age of 18)
 C - Criminality
 I - Impulsivity (low conscientiousness)
 D - Disregard for safety

 L - Lying
 I - Irresponsibility
 A - Aggression
 R - Remorselessness

236
Q

PERSONALITY DISORDERS
Antisocial Personality Disorder (ASPD)
other features

A
  • emotinal instability (anger, sadness, irritability)
  • impulsive aggression
  • difficulties in relationships
  • isolation and loneliness
  • premaditated acts
237
Q

PERSONALITY DISORDERS
Antisocial Personality Disorder (ASPD) Dx

A

Adult age + 3 or more of the core symptms

238
Q

OPOSITIONAL DEFIANT DISORDERS (ODD)

A

DOs
- Argumentativeness (frequently argues/stubbornness)
- purposefully do things to upset others
- vindictiveness
- defiance/testing limits (ignore rules)
- Failing to accept responsibility for one’s own actions
and blaming others for one’s own mistakes.

DON’Ts
- violate others rights
- no overt violence
- no aggression
- no theft

must occur for at least 6 months

239
Q

OPOSITIONAL DEFIANT DISORDERS (ODD)
Other features

A
  • average onset age 6-8 years (can continue into adolescence)
  • M > F (2x)
  • persistent anger and irritability (losing one’s temper)
  • believe that they are justified in their actions
240
Q

CONDUCT DISORDER (CD)

A
  • Flaglrant disregard to others’ rights
  • overt violence (physical cruelty)
  • aggression (fights)
  • robbery, fire setting, property damage
  • sexual coercion

conceptualised as a precursor to ASPD

241
Q

CONDUCT DISORDER (CD)
other features

A
  • almost all patiets show signs by the age of 10
  • M > F (4x)
  • believe that they are justified in their actions
242
Q

Externalising Disorders (ODD,CD)
Mx

A
  • family therapy
  • behavioural training for the child
  • medications are geneerally not helpful

CD reponds to a lesser extent than ODD to these therapies

243
Q

Eating Disorders
Eating disorders are commonly associated with what patient profiles (history)

A

– Female Adolescent
– Low self-esteem
– Personal or family history of depression
– Family history of obesity
– High personal expectations
– Family history of eating disorders
– Disturbed family interactions
- Social factors
- Childhood sexual abuse
- Perfectionism and obssessionality

244
Q

Eating Disorders
Anorexia Nervosa core patterns

A

UNDER-exia”

 U - Underweight (BMI < 17.5)
 N - Nervous/fearful about gaining weight
 A - Distorted self-perceptions about weight (ego-syntonic)
 A - Exercise/purging/other behaviours to burn calories and lose weight
 A - Restricting caloric intake

245
Q

Eating Disorders
Anorexia Nervosa
Lab features

A
  • Significant electrolyte disturbance (K < 3.0 or Na < 130)
  • Hypercholesterolemia
  • Raised liver enzymes and Albumin < 35g/L
  • Vitamin deficiencies
  • LOW WBC
  • Hypochloraemic Alkalosis
  • ESR is LOW or Normal
246
Q

Eating Disorders
Anorexia Nervosa
Clinical features

A
  • Bradycardia. (< 40bpm)
  • Hypotension (< 90mmHg)
  • Dehydration (excessive exercise/abuse of laxatives)
  • osteoporosis
  • Amenorrhoea/Infertility (abscence of 3 consecutive cycles)
    – secondary amenorrhoea due to low levels LH/FSH (hypogonadotropic Hypogonadism)
  • Constipation
  • Cachexia (less than 85% of ideal body weight)
  • Hypothyroidism
    – Hypothermia
    – Cold intolerance
  • mood swings, anxiety
  • Suicide (single most deadly mental ilness, with up to 20% of people dying)

https://pubmed.ncbi.nlm.nih.gov/22349551/

can be associated with:
-Depression
-OCPD

247
Q

Eating Disorders
Anorexia Nervosa
Indications for hospital admission

A

 Low weight (85% or less of expected weight and/or less than the third percentile for BMI)

Physiologic decompensation including, but not limited to, the following:
 severe electrolyte imbalance (life-threatening risks created by sodium and potassium derangements),
 cardiac disturbances or other acute medical disorders
 orthostatic differential > than 30/min
 Temperature < than 36°C
 Pulse < 45 bpm
 Significant oedema

 altered mental status or other signs of severe malnutrition
 Psychosis or a high risk of suicide

248
Q

Eating Disorders
Anorexia Nervosa vs OCD

A
  • Anorexia = ego-syntonic (lack of insight)
  • OCD = ego-dystonic
249
Q

Eating Disorders
Anorexia Nervosa & OCPD

A
  • ego-syntonic
  • rigitiy of behaviour (little variation)
  • high conscientiousness (act in accordance with societal expectations

Anorexia has a high rate of comorbity with OCPD

250
Q

Eating Disorders
Anorexia Nervosa Epidemiology/Risk Factors

A
  • F > M (10x)
  • begins around puberty (13-14y) and young adulthood (17-18y)
  • Associated with careers/hobbies that can produce extrem pressure to be thin (modeling, gymnastics, ballet, and running)
  • low self-esteem
  • high socioeconomic status (SES)
251
Q

Eating Disorders
Anorexia Nervosa Mx

A
  • nutritional rehabilitation
  • psychitherapy (CBT)
  • Medications are of no proven benefit for the primary anorexia nervosa itself.
252
Q

Eating Disorders
Anorexia Nervosa severe complication related to re-initiation of nutrition

A

Refeeding Syndrome

The manifestations of refeeding syndrome are mainly caused by hypophosphataemia, precipitated by increased glycolysis when carbohydrate replaces body fat as the main source of energy.

In chronic malnutrition, phosphate stores are already low. When the individual is suddenly fed again, insuline is released causing further uptake of phosphate into cells and leads to even grater hypophosphatemia. The low availability of phosphate prevents metabolic intermediates from being produced, leading to hypoxia and muscle disfunction.

253
Q

Eating Disorders
Refeeding Syndrome

A
  • cardiovascular collapse, cardiac failure
  • rhabdomyolysis and muscle weakness (which in turn may lead to ventilatory failure, seizures or delirium)
  • Hypokalaemia and hypomagnesaemia can cause cardiac arrhythmias
  • glycolysis-induced thiamine depletion can lead to Wernicke encephalopathy
254
Q

Eating Disorders
Refeeding Syndrome
Patients at high risk of developing refeeding syndrome if they have:

A

one or more of the following:
- BMI < 16
- loss > 15% of body weight in the last 3-6 months
- little or no nutritional intake for > 10 days
- low concentrations of potassium, phosphate or magnesium before reintroduction of nutrition

                 OR

two or more of the following:
- BMI < 18.5
- loss > 10% of body weight in the last 3-6 months
- little or no nutritional intake > 5 days
- history of hazardous alcohol use or drug use (including insulin, chemotherapy, antacids or diuretics).

255
Q

Eating Disorders
Refeeding Syndrome
Management of refeeding syndrome

A
  • Give thiamine (at least 100 mg IV or 300 mg VO, daily) before starting and for the first 7-10 days of feeding.
  • Measure serum electrolytes (including potassium, phosphate, and magnesium) before starting feeding, and supplement as required. Check serum electrolytes at least daily for the first week after reintroduction of nutrition.
  • Start feeding slowly (30-50% of estimated caloric requirement) then, if electrolytes are stabilised, increase gradually over 5 to 7 days to the patient’s estimated needs. For severely malnourished patients, start at 5-10 kcal/kg/day.
  • Give a multivitamin (once daily for at least 7 days).
  • In the first week of refeeding, monitor vital signs and (in high-risk patients) cardiac rhythm, and look for signs of oedema, heart failure and a deteriorating mental state.
256
Q

Eating Disorders
Bulimia Nervosa Signs & symptoms

A

Bowl-emia

 B - Binge eating (impulsive/out of control)
 O - Off-setting behaviours (purging)
 W - Weekly (or more) for a period of 3 months
 L - Linked to self-steem

Purging (methods inteded to rid the body of the effects of calories) can take form in different behaviours:
- self-induced vominting (most common)
- Laxatives/diuretic/enema abuse
- driven exercise and/or fasting

257
Q

Eating Disorders
Bulimia Nervosa complications due to purging

A
  • Kidney injury due to dehydration
  • Metabolic Alkalosis (loss of stomach acid)
  • gastric ulcers
  • Boerhaave Syndrome
  • changes in hormone levels (amenorrhoea is common, but no hirsutism)
  • abnormalities in liver and thyroid function, and anemia are a result of malnutrition seen in Anorexia nevorsa, hence less likely Bulimia Nervosa

Physical exame:
- Patients have normal weight or are overweight (BMI > 18)
- erosion of dental enamel/dental decay
- swollen salivary glands
- injury of the knuckles (Russell’s sign)

The menstrual and ovulatory abnormalities are due to suppresed sex hormone secretion as a consequence of fasting and prolonged dietary restriction

258
Q

Eating Disorders
Bulimia Nervosa Epidemiology/Risk Factors

A
  • F > M (10x)
  • peak onset at 18 (but can begin in adolescene, or as old as 25 years)
  • Family history of eating disorder
  • associated with sexual abuse
  • often comorbid with BPD
259
Q

Eating Disorders
Bulimia Nervosa Mx

A
  • CBT + Interpersonal Therapy
  • SSRIs (for both depressed and not depressed patients)
260
Q

Eating Disorders
Bulimia Nervosa Mx
which SSRI must be avoided and why?

A

Bupropion

  • Increases the risk of seizures
261
Q

Somatoform Disorders
Somatic Symptom Disorder Dx

A

History of many physical complaints begining before the age of 30

SOME-ATTIC

 S - Symptoms
 O - One or multiple
 M - Medically unexplained (“no outward sign”)
 E - Excessive

 A - Anxiety about health or symptoms
 T - Thinking about the seriousness of symptoms
 T - Time and energy devoted to these symptoms or health concerns
 I - Impaired or distressed resulting in significant disruption of daily life
 C - Chronic the state of being symptomatic is
persistent, lasting months to years (typically more than 6 months)

-gastrointestinal tract is the most commmon location for somatic symptoms in ALL PATIENTS
-gynecologic complaints are the second most common symptom IN WOMEN

  1. FOUR Pain symptoms:
    Headaches, abdominal pains, back and joint pain, pain during menstruation or sexual
    intercourse, chest pain.
  2. TWO GI symptoms:
    Nausea, bloating, vomiting other than during pregnancy, diarrhea or intolerance to several foods.
  3. ONE sexual symptom:
    Erectile dysfunction, irregular menses, excessive menstrual bleeding, vomiting throughout the pregnancy.
  4. ONE Pseudoneurologic symptom: Conversion symptoms such as impaired coordination or balance, paralysis or localized weakness, difficulty in swallowing, lump in throat, aphonia, hallucinations, loss of sensations, visual problems, urinary retention etc.

Either of the following:
1.After appropriate investigations, symptoms not adequately explained by known general medical condition.
2.When related to a general medical condition, symptoms are In excess of what would be expected from history, physical examination and investigations.

262
Q

Somatoform Disorders
Somatic Symptom Disorder Mx

A
  • Regular visits (minimises the idea of only seeing the doctor when sick)
  • CBT
  • Midnfulness therapy
  • physiotherapy & rehabilitation
  • TCA’s and SNRIs (smaller effect)

Analgesia is usually not helpful

263
Q

Somatoform Disorders
Conversion Disorder Dx

A

CAN’T-version

 C - Clinically unexplained
 A - medical Abnormality
 N - involving Nervous System
 T - usually (~50%) brought on by a Trigger

Patient is not manufacturing or faking the symptoms (unconscious & Involuntary)

264
Q

Somatoform Disorders
Conversion Disorder Features of neurologic sx

A
  • subjectively reported symptoms
    (blindness, blurry vision, loss of sensation)
  • objectively observed signs
    (weakness, imbalance, shaking)

OR

  • absence of function
    (as in motor paralysis)
  • presence of dysfunction
  • (as in convulsions)

NOTE: given the features above, the conversion disorder diagnosis would not be appropriate a patient presenting with abdominal pain or chest discomfort)

265
Q

Somatoform Disorders
Conversion Disorder Mx

A
  • Educate patient about conversion disorder
  • overall majority of cases resolve spontaneously
  • physical/occupational therapy can be helpfu for patients with motor deficit (even in the absence of objective neurologic pathology)
  • 25% relapse within a year

NOTE: CBT and medication are not helpful

266
Q

Somatoform Disorders
Factitious Disorder Signs & Symtpoms

A

unexplained symptoms intentionally feigned

  • intentional production of symtpoms voluntary
  • Unsconscious goal is primary gain (desire the sympathy and attention that accompanies having an illness)
  • Recurrent presentations
  • rejects being discharged
  • Knowledge of illness (50% work in the medical field)\
  • No insight (can hurt themselves; desire to remain in the sick role over and above preserving their own bodily integrity)

FAC

  • F - Factitious
  • A - Always
  • C - come back

as their primary motivation is in the medical care itself

267
Q

Somatoform Disorders
Factitious Disorder associated with self-harm?

A
  • Munchausen Syndrome
    (intentional self-inflicted harm to provide evidence of illness. Can also be someone who knownly has a condition but refuses treatment to gain others’ sympathy)
  • Munchausen Syndrome by proxy
    (harm imposed on another)
268
Q

Somatoform Disorders
Factitious Disorder Mx

A
  • poor prognosis
  • neither medications nor psychotherapy are effective
  • Refer to specialist
269
Q

Somatoform Disorders
Malingering Signs & Symtpoms

A

intentional and Conscious production of signs and symptoms for obvious secondary gains.

    • goal is extrinsic to the role of being sick (disability payments, excuse from work/military service, lighter sentence in a criminal case, financial compensation from a fake injury, admission to hospital)

MAL

  • M - Malingering
  • A - Always
  • L - Leave

once their need has been met, because there is no longer reason for them to seek medical care

270
Q

Somatoform Disorders
Malingering Mx

A

No clear treatment

271
Q

Difference between Complicated Grief Disorder & Avoidant personality disorder?

A

Complicated grief:
- symptoms persist longer than six months
- Avoidance of situations that serve as reminders of the loss is also common

Avoidant Personality Disorder:

272
Q

CATATONIA symptoms

A
  • lmmobility or excessive purposeless activity
  • Mutism, stupor (decreased alertness & response to stimuli)
  • Negativism (resistance to instructions & movement)
  • Posturing (assuming positions against gravity)
  • Waxy flexibility (initial resistance, then maintenance of new posture)
  • Echolalia, echopraxia (mimicking speech & movements)

Rx: Hospitalisation + Benzodiazepines

273
Q

CATATONIA
most often develops in
the context of??

A

a mood disorder (eg, bipolar disorder, major depressive disorder)

274
Q

CATATONIA
1st line treat for malignant catatonia?

A

ECT

275
Q

Tardive dyskinesia vs Parkinsons disease

A

identical symptoms:
- rigidity
- bradykinesia
- postural instability

Differentiating symptoms:
- involuntary movements of face and tongue (tardive)
- Stiffness

276
Q

Dementia
Dx

A

DIRE

 D - Decline in cognition (memory, language, hability to plan) - screening tools (e.g. MMSE, MoCA)

 F - Functional Impairment (IADLs 1st > ADLs 2nd)

 R - Rule out Delirium

 E - Exclude other mental health conditions

277
Q

Dementia
vs
Normal aging

A

Normal aging Preserved cognitive domains
- language
- recognition of faces and situations
- awareness of memory loss

Normal aging Impaired cognitive domains

  • deficits in short-term memories
  • declarative memories (recalling)
  • attention
  • processing speed
  • concrete thinking (as opposed to ability to think abstractly)
278
Q

Dementia
What are IADL’s

A

Intrumental Activities of Daily Living
(first signs of the impact of cognitive impairments)
SHAFT

 S - Shopping
 H - Housekeeping
 A - Accouting
 F - Food Preparation
 T - Transportation

279
Q

Dementia
What are the ADL’s”

A

Activities of daily living:
(signs of late stage cognitive impairment)
DEATH

 D - Dressing
 E - Eating
 A - Ambulating
 T - Toileting
 H - Hygiene

280
Q

Dementia
What is MMSE

A

Screening tool to assess cognitive skills

281
Q

Dementia
What are the 5 main areas assessed on the MMSE

A

ORRAL

 O - Orientation (time/space)
 R - Registration (“name 3 objects)
 R - Recall (ask for the 3 objects repeated above)
 A - Attention/Concentration & Calculation
 L - Language

282
Q

Dementia
Examples of methods used to assess Attention/Concentration on the MMSE

A
  • serial 7’s (from 100 - 0) not a memory test
  • spelling a word backwards not a memory test
  • serial 3’s (from 100-70) not a memory test
  • Digit span memory test
  • Recitation of the days of the week/mothns of year in reverse order) not a memory test
283
Q

Dementia
What MMSE score would indicate a normal test?

A

25-30

284
Q

Dementia
What would a score of 24 on an MMSE indicate?

A

pseudodementia/depression

285
Q

DEMENTIA
Difference between dementia & pseudodementia?

A

Cognitive impairment due to the presence of a mood-related mental health concern, most often depression (giving up).

Pseudodementia have INSIGHT

286
Q

Dementia
If patient has scored just below the normal threshold of MMSE due to sight impairment. What should be done?

A

Correct sight impairment and redo test, or perform other cognitive tests that do not require sight (Six-item Cognitive Impairment Test)

287
Q

Dementia
What does a score < 25 on the MMSE indicate?

A

Cognitive decline

288
Q

Dementia
After MMSE is done to determine cognitive decline what investigation is best indicated?

A

it is improtant to:
- rule out delirium
- exclude other psychiatric conditons (e.g. depression)
- CT (PET) scan (the presence of brain tissue degeneration, such as atrophy, can confirm dementia)

289
Q

Dementia
What is the Clock Drawing Test (CDT)

A

Although it is part of a screening tool for congnitive impairment (MoCA), the CDT t is a tool that measures dementia severity

strong indicator of early dementia, but it can’t diagnose the type of dementia or rule out other conditions

290
Q

Dementia
What cognitve(s) domain(s) is(are) assessed on the Clock Drawing Test

A
  • Frontal functioning
  • Temporo-parietal Functioning
291
Q

Dementia
Types of dementia

A
  • Alzheimer’s Dementia (50% to 70%)
  • Non-Alzheimer’s Dementias
    – Frontaltemporal dementias (up to 10%)
    – Dementia with Lewy Bodies and Parkinson disease dementia (up to 10%)
    – Vascular Dementia (10% to 20%)
    – alcohol-related dementia (up to 5%).
292
Q

Dementia
Alzheimer’s Dementia S/Sx + Dx

A

No single test to diagnose Alzheimer’s

GRANdPA U OK

 G - Gradual decline
 R - Relentless (unremiting, steady downward
Trajectory)
 A - Amnesia ( + Neurocognitive deficits = 4 A’s)  Nd - Neurocognitive deficits
 P - Psychiatric (mood changes, psychosis-like sx)
 A - Activity (losses in complex behaviours,
increase in purposeless behaviours)
 U - Unable to function
 O - Objective biomarkers
 K - Knowledge of Illness (patients are unware of their cognitive defits)

293
Q

Dementia
Alzheimer’s Dementia the 4 A’s of Neurocognitive Deficits

A

 4 A’s of Alzheimer’s:

Amnesia (EARLY SYMPTOM defining feature of the condition)
Aphasia (LATER FINDING; language impairment - sepaking, reading, writing, and receptive)
Apraxia (LATER FINDING; inability to perform motor activities)
Agnosia (LATER FINDING; inability to translate what we percieve with our senses into a cohesive signal to be acted upon)

Progression of cognitive impairment follows this order:
Amnesia > Aphasia, > Apraxia > Agnosia

294
Q

Dementia
Alzheimer’s Dementia Amnesia features

A
  • FIRST and MOST affected cognitive domain
  • both retrograde and anterograde memories affected (with the former being impacted earlier and more severely)

these distintinctions tend to breakdown as the disease progresses

295
Q

Dementia
Alzheimer’s Dementia What is “sundowning

A

State of confused restlessness/agitation/wandering that is more prominent in the evening

Endeavour to manage sundowning
through nonpharmacological interventions.

296
Q

Dementia
Alzheimer’s Dementia Imaging

A

CT scan
– widespread cortical atrophy
– widespread decrease in brain cells metabolic activity
– hypocampus atrophy (low Acetylcholine activity)

297
Q

Dementia
Alzheimer’s Dementia Pathology Biomarkers

A

 pathology (not routinely done)
* cerebral spinal fluid
– B-amyloid protein
– Tau Protein

  • biopsy
    – senile plaques (clumps of B-amiloid ptrotein)
    – neurofibrilary tangles (Tau Protein)
298
Q

Dementia
Alzheimer’s Dementia genetic Biomarkers

A

 genetic testing (autosomal dominant)
* APOE4 gene (codes for a poorly fuctioning version of APO-LIPOPROTEIN E which clears B-amyloid protein)
— 1 copy = 3x more risk
— 2 copies = 15x more risk

299
Q

Dementia
Alzheimer’s dementia
Epidemiology/Prognosis

A
  • early onset considered < 65 years
  • risk 3% in population > 65 years
  • risk doubles every 5 years
  • Steadily progressive; No cure
  • highly lethal (death occuring with 10 years of dx)
300
Q

Dementia
Alzheimer’s dementia
Nonpharmacological Mx

A

**goals of treatment are:
- paliative
- symptom reduction
- preservation of function

Psychotherapy not effective (cognitive deficits prevent patient from meaningfully engaging in treatment)

 Behavioural modifications
– education
– self-care (bathing, dressing, toileting)
– exercise

 Sensory stimulation- music, pets.
 Social interaction- regular visits from family,
friends.

Patients with a clinical suspicion for dementia should not be permited to driveor operate complex machinery that could potentially put their own lives or the lives of others at risk.

301
Q

Dementia
Alzheimer’s dementia
Pharmacological Mx

A
  1. Cholinesterase inhibitors (AChEi)
    (donepezil, galantamine, rivastigmine)
  2. NMDA receptor antagonist
    (memantine)

  • These drugs improve alertness and function and can maintain cognitive scores at or above the baseline for up to 12 months;
  • Not all patients benefit from cholinesterase inhibitors; some have modest benefit and a few show significant improvement.
  • Patients should be treated for at least 2 months at the maximum recommended dose (if tolerated) before a final assessment of response is made.
  • If patients tolerate and appear to benefit from cognitive enhancing drugs then the drug should not be ceased until the patient is in an advanced state of dementia (usually having lost independent mobility)
302
Q

Dementia
Alzheimer’s dementia
Pharmacology: Tocxicity of AChE Inhibitors

A

DUMBBEELSS

 D - Diarrhoea
 U - Urination (urinary incontinence)
 M - Miosis
 B - Bradycardia
 B - Bronchocontriction
 E - Emesis
 E - Excitation (tremor, insomnia,vivid dreams)
 L - Lacrimation
 S - Salivation
 S - Sweating

other side associated with prominent adverse effects are:

  • anorexia, weight loss
  • depression
  • lethargy, fatigue, drowsiness

Take care when introducing these drugs in patients with:
- asthma, chronic obstructive pulmonary disease (Bronchoconstricion)
- cardiac conduction abnormalities (particularly atrioventricular block) (Bradycardia)
- peptic ulcer disease

303
Q

Dementia
Alzheimer’s dementia
Pharmacology:
NMDA Inhibitors adverse effects

A
  • confusion
  • dizziness
  • drowsiness
  • headache
  • insomnia (If present, memantine can be taken earlier in the day)
  • agitation and hallucinations

NOTE: reduce dose in kidney failure (RENAL EXCRETION)

304
Q

Dementia
Dementia with Lewy Bodies (DLB)” S/Sx

A

C’N STUPH

 C - Cognitive deficits fluctuation (memory isn’t the most prominent cognitive domain that is affected - in contrast to Alzheimer’s)
 N - Neuroleptic sensitivity ( poor response and at higher risk of developing side effects to antipsychotics) AVOID!
 S - Sleep bahviour (REM Sleep Behaviour disorder - patients acting out on their dreams) - very specific sign
 T - Timing (earlier onset, rapid decline)
 U - Unstable (rapid fluctiation in cognition, waxing and waning alertness and lucidity) - very specific
 P - Parkinsonism (tremor, rigidity, slow movement, postural imbalance)
 H - Hallucinations (visual)

305
Q

Dementia

DLB” vs “Alzheimer’s dementia

A

Alzheimer’s
- onset usually > 65
- gradual and progressive decline (years)
- memory is usually the first cognitive domain to be affected

DLB
- earlier onset (~50s)
- rapid cognitive decline (months)
- cognitive domains other than memory are prominently affected
- Fluctuating confusion
- visual hallucinations
- EPS

306
Q

Dementia
DLB” vs “Schizophrenia” hallucinations

A

DLB
- insight is usually preserved (patient not bothered)
- Typically visual hallucinations

Schizophrenia
- no insight, severely disturbed
- Auditory hallucinations are prevalent

307
Q

Dementia
Dementia with Lewy Bodies (DLB)” Mx

A

Similar to Alzheimer’s dementia (but less effective and impose greater side effect burden)

  • anti-Parkinson’s drugs to treat motor symptoms
308
Q

Dementia
Charles-Bonnet Syndrome (CBS):

A

 Intact cognition/preserved insight
 Ocular Pathology (BLIND or, commonly, macular degeneration) or occipital disease - NOT psychiatric
 Visual Hallucination
- vivid, colourful, and well-organised hallucinations
- experience may last for seconds or hours at a time
- patient has good insight
- hallucinations are not distressing, but may be quite engaging

309
Q

Dementia
Frontotemporal Dementia (FTD)” S/SX

A

OH DEAR

 O - Obliviousness (loss of sympathy and empathy)
 H - Hyperorality (preference for carbohydrate-rich foods, consumption of inedible objects)
 D - Disinhibition (impulsivity, hypersexuality, loss of social awareness)
 E - Executive dysfunction (language difficulty, inability to plan and execute complex ideas)
 A - Apathy
 R - Restrictive/ritualistic behaviour

  • Insidious onset and slow progression
  • early changes are in personality & behaviour
  • memory and visuospatial abilities are relatively preserved (to laste-stage disease) - in constrast with Alzheimer’s
  • not same fluctiation seen in DLB
    *
310
Q

Dementia
Frontotemporal Dementia (FTD)” Dx

A
  • (Clock Drawing Test) CDT is a screening tool and a cognitive deficit score (SCORE ≥ 3) on this test can indicate FDT
311
Q

Dementia
Frontotemporal Dementia (FTD)” Mx

A
  • tailored behavioural management strategies
  • TG does not recomend any pharmacotherapy for FTD
312
Q

Dementia
Vascular Dementia” Clinical Features

A
  • sudden cognitive decline in a step-wise manner (each drop in functional ability represents another ischemic event)
  • emotinal lability
  • gait abnormalities
  • urinary dysfunction
  • Parkinson motor features
  • Hallucinations are rare/not present
  • Vascular lesions on CTI/MRI
313
Q

Dementia
Vascular Dementia” Risk Factors

A
  • HAS
  • DM
  • CVD
  • smoking
  • hyperlipedemia
314
Q

Dementia
Reversible causes of dementia-like symptoms

A

DEMENTIAS

 D - Dringking & Drugs
 E - Endocrine (thyroid, parathyroid, pituitary, adrenal)
 M - Metabolic (disglycemia, electrolytes, vitamin b12 deficiency)
 E - Ears & Eyes (sensory impairment)
 N - Neoplasias
 T - Trauma (subdural hematoma)
 I - Infection meningitis, encephalitis, Endocarditis, syphilis, HIV)
 A - Autoimmune

315
Q

Dementia
Normal Pressure Hydrocephalus

A

Triad “DIG

 D - Dementia
 I - Incontinence
 G - Gait

Mx: shunt to drain excess fluid

316
Q

Dementia
Treatment of mood and behavioural disturbances in dementia

A
  • AVOID First-Generation Antipsychotics (FGA)
  • Anxiety and agitation
    – Oxazepam VO
  • hallucinations, delusions or seriously disturbed
    – 1 Risperidone VO
    OR
    – 2 Olanzapine VO
  • Depression
    Avoid antidepressants with anticholinergic
    adverse effects (i.e. TCA’s)
    (exaggerate the cognitive deficits due to central
    acetylcholine deficiency in Alzheimer disease)
317
Q

Dementia
Wernicke’s Encephalopathy
Pathophysiology

A

Acute neuropsychiatric reaction to severe thiamine deficiency. It is a type of delirium and is usually reversible

318
Q

Dementia
Wernicke’s Encephalopathy” Sx:

A

TRIAD:

  • CONFUSION
  • GAIT ATAXIA (Lack of coordination)
  • OPHTHALMOPLEGIA (horizontal nystagmus, abducens palsy, or conjugate gaze disorder all typical).

– **All three elements of this triad need not be present in order to make the diagnosis.
**

319
Q

Dementia
Wernicke’s Encephalopathy
Conditions that can lead to B1 deficiency

A

Thiamine deficiency may be secondary to:

  • alcoholism
  • Hyperemesis gravidarum
  • restrictive eating disorders + vomiting
  • cannabis hyperemesis Syndrome
  • dietary deficiency associated with Mg insufficiency
  • gastric carcinoma
320
Q

Dementia
Wernicke’s Encephalopathy” Mx:

A

urgent IV thiamine

321
Q

Dementia
Wernicke’s Encephalopathy” if not treated?

A

but the majority will develop a chronic Korsakoff syndrome.

322
Q

Dementia
Korsakoff syndrome
Pathophysiology

A

Irreversible damage to the mammillary bodies
(region associated with memory and recall) leading to Dementia

323
Q

Dementia
Korsakoff syndrome” Sx

A
  • profound anterograde amnesia
  • Confabulation (due to memory gaps)
324
Q

Dementia
Huntington’s Disease”

A
  • 20 - 50 years old
  • Dementia
  • Chorea
325
Q

Dementia
Creutzfeldt-Jakob Disease (CJD)” Sx

A
  • mid-aged adults
  • rapidly progressive dementia (weeks - months)
  • Myoclonus
326
Q

Delirium
(“Acute Confusional State”)
Screening/Dx

A

The Confusion Assessment Method (CAM) considers that a diagnosis of delirium is likely if the following are present:

  • acute onset and fluctuating course
  • impaired attention span (or inattention)
  • disorganized thinking or an altered level of consciousness.
327
Q

Delirium
Risk Factors

A
  • age > 65 years
  • pre-existing dementia
328
Q

Delirium
Precipitants

A

 D - Drugs & Drug Withdrawal
– prescription and over-the-counter medicines, and
alcohol and illicit drugs
– withdrawal states - alcohol and benzodiazepines;
(suspect alcohol withdrawal if tremors, sweating and
visual hallucinations are present)
 E - Epilepsy & Endocrine
– seizures and postictal states
– DM, Thyroidism
 L -
 I - Infections
(UTI most common in AUS)
 R -
 I - Intracerebral events
(subdural haematoma, haemorrhage, stroke)
 U - Unpleasantness
(pain and discomfort, urinary retention, constipation)
 M - Metabolic disturbance & Malignancy
(hypoglycaemia, hyperglycemia, hyponatraemia)

 organ failure:
kidney failure, liver failure, and respiratory failure with hypoxia/hypercapnia
 cardiac events: MI, arrhythmia, CHF

329
Q

Delirium
Drugs and drug groups commonly implicated in delirium

A

 A - alcohol and illicit drugs (eg cannabis, methamphetamine).
 A - Anticholinergics
 B - Benzodiazepines
 C - corticosteroids
 D - dopaminergic drugs

  • NSAIDs
  • Opioids
  • sotalol and propranolol (unlikely with other beta blockers)
330
Q

Delirium
Emergency Mx

A

DRABCDE

+

TONGF

The delirious patient must be observed at all times.

331
Q

Delirium
Pharmacological management

A

Haloperidol VO (single dose)

OR

olanzapine VO (single dose)

OR

Risperidone VO (single dose)

*onset of action can be delayed from 30-60 minutes after administration

*second doses should not be given for at least 30 minutes

332
Q

Delirium
Pharmacological management

If oral administration is impossible and symptoms are severe

A

Haloperidol IM (single dose)
OR
Olanzapine IM (single dose)

*onset of action can be delayed from 30-60 minutes after administration

*second doses should not be given for at least 30 minutes

333
Q

Delirium
What drug should be avoided

A

benzodiazepines should be avoided in delirium (especially in patients with significant respiratory depression)

except for cases due to alcohol withdrawal or seizures

334
Q

Delirium Tremens
(or Alcohol Withdrawal Delirium) Sx:

A
  • It usually commences 72 to 96 hours (3-7 days) after cessation of drinking.
  • characterised by:
    gross tremors
    – fluctuating levels of agitation
    hallucinations (usually tactile)
    – disorientation and impaired attention
    – Fever
    – tachycardia
    – hypertension
    – dehydration

it is usually associated with:
– infections
– anaemia
– metabolic disturbances
– head injury

335
Q

Delirium Tremens
Mx:

A

1 diazepam VO

2 midazolam IV (if agitation)

If an antipsychotic drug is required, use:

  • VO Haloperidol

AVOID chlorpromazine
(it lowers seizure threshold)

If extrapyramidal adverse effects (EPS) emerge:
- benztropine VO or IM

IV diazepam should be avoided if possible
– Onset of action is not much faster than with VO
– there is a greater likelihood of causing severe adverse effects such as respiratory depression
– If an injection is necessary, it must not be diluted and it must be given slowly over several minutes to minimise the risk of respiratory depression or arrest.

336
Q

Delirium Tremens
Mx:

For severe psychotic symptoms when VO not possible

A
    • Haloperidol IM, as a single dose.
      (less likely to lower seizure threshold)

OR

    • Droperidol IM, as a single dose
      (similar to haloperidol but is more sedating)
337
Q

Sleep Disorders
Insomnia” types

A
  • Idiopathic (Primary) Insomnia
  • Secondary Insomina

According to duration:

  • Acute Insominia (< 30 days)
  • Chronic Insomina (> 30 days)
338
Q

Sleep Disorders
Insomnia
Idiopathic Insomnia mechanism

A
  • over-reactivation of HPA axis
  • Hypervgillance about falling asleep
339
Q

Sleep Disorders
Insomnia
Secondary Insomnia mechanism

A

A symptom of other disorders
* due to somatic symptoms (pain)
* Psychiatric Conditions (mood and anxiety disorders)
* Drug use (caffeine, alcohol, nicotine being more common)
* Intrisic Sleep Disorders ( sleep apnoea, restless legs syndrome)

340
Q

Sleep Disorders
Insomnia
FIRST LINE Mx

A

Primary treatment goals are to improve sleep quality and quantity, and to relieve insomnia-related daytime
impairment.

  • Management of underlying problems
  • Good sleep practices (sleep Hygiene)
    – Sleep–wake activity regulation
    – Sleep setting and influences
    – Sleep-promoting adjuvants
  • Psychological and behavioural interventions
    (most often used for chronic insomnia as they do not
    work immediately and require practise and
    persistence)
    – Relaxation therapy
    — e.g. hypnosis, meditation
    — can be of benefit for both acute and chronic
    problems– Cognitive therapy (CBTi - “i” for insomnia)
    — targets dysfunctional beliefs about sleep– Stimulus control
    — limit the amount of time spent in bed awake
    — useful for people who have difficulty falling asleep– Sleep restriction
    — goal is to reduce the amount of time spent awake
    — suitable for people who have difficulty staying
    asleep due to poor sleep drive.
341
Q

Sleep Disorders
Insomnia” Pharmacologic Mx indications

A
  • short-term management of acute insomnia
  • chronic insomnia when the nonpharmacological
    strategies are not effective.
342
Q

Sleep Disorders
Insomnia” hypnotic drugs

A

1 Temazepam VO (before bedtime)
(idel for patients with sleep onset insomnia)

OR

1 Zolpidem VO
(less morning sedation)

OR

1 Zopiclone VO

OR

2 Melatonin VO (before bedtime) for patients > 55 years
(there is insufficient evidence to support treatment > 3 wks)

Contra-indicated if history of:
- addiction and dependence
- OSA
- use of other substances (e.g alcohol, CNS depressants)

Complaints of use of BZ include:
- sleeping is not refreshing
- reduced daytime alertness

343
Q

Sleep Disorders
Insomnia” Treatment duration and Mx of long-term hypnotic use

A
  • treatment should be limited to < 2 weeks.
  • Intermittent therapy may be considered in severe longstanding insomnia that is not relieved by non-pharmacological management

The patient with chronic insomnia should be reviewed weekly for 4-6 weeks period for these psychological and behavioural treatments.

344
Q

Sleep Disorders
Parasominas” Definition

A

Dysfunctions associated with

sleep, sleep stages or partial arousal
+
abnormal motor, behavioural or sensory experiences.

345
Q

Sleep Disorders
Parasominas” main Types

A
  • occurring in non-REM sleep
    – associated with stages 3 and 4
    – typically occur in the first half of the sleep period
    – eg sleepwalking, sleep terrors
  • associated with REM sleep
    (eg nightmares, REM sleep behaviour disorder)
346
Q

Sleep Disorders
Sleepwalking” features

A
  • sleeper performs some repetitive activity in bed
  • sleeper can walk freely from the bed
  • more common in children
  • can be associated with some hypnotics
347
Q

Sleep Disorders
Sleepwalking” Mx

A
  • Usually no treatment is required
  • if frequent, and presents danger sleeper, the sleeping environment should be made safe.
  • Adults with recurring episodes may need to seek
    specialist assistance.

Hypnotics may be considered if:
* have injured themselves or others
* serious risk of doing so
* whose quality of life is significantly affected.

348
Q

Sleep Disorders
Night (Sleep) Terrors” features

A
  • sharp screams
  • violent thrashing movements
  • autonomic discharge with sweating and tachycardia.
  • The subject may or may not wake
  • there is usually no recall of the event (as they occur in non-REM sleep states)
349
Q

Sleep Disorders
Night (Sleep) Terrors” Mx

A
  • Usually no treatment is required (vast majoirty do not persist into adulthood)
  • reassurance is typically sufficient
  • Adults with recurring episodes may need to seek
    specialist assistance.

Hypnotics may be considered if:
* have injured themselves or others
* serious risk of doing so
* whose quality of life is significantly affected.

350
Q

Sleep Disorders
Nightmares” features

A
  • dream-related anxiety episodes
  • Recurrent stereotyped nightmares are commonly associated with PTSD
  • can be associated with the discontinuation of REM-suppressing drugs (eg alcohol, antidepressants and some hypnotics)
  • A number of drugs can also cause vivid dreams or nightmares (eg B-blockers, SSRIs, benzodiazepines, levodopa)
351
Q

Sleep Disorders
Nightmares” Mx

A
  • Psychological evaluation and therapy are required if associated with PTSD
352
Q

Sleep Disorders
REM Sleep Behaviour Disrder (RBD)” features

A
  • complex and elaborate motor activity in association with dreams
  • may result in violent behaviour during sleep
  • **frequently associated with neurodegenerative (eg Parkinson’s and Lewy Bodies Dementia **

Diagnosis can be made by a sleep study and specialist evaluation is recommended.

353
Q

Sleep Disorders
(RBD)” Mx

A
  • reassurance
  • improving sleep practices
  • interventions as necessary to address safety issues
  • If more severe, and if there is concern about physical injury occurring -»> low-dose clonazepam.
354
Q

Sleep Disorders
Narcolepsy” features

A
  • appear between adolescence and the age of 30 years
  • chronic daytime sleepiness

+

CHAP

 C - Cataplexy - specific sign
(sudden loss of muscle tone during wakefulness, associated with or without strong emotion)
 H - Hallucinations
(often visual) on falling asleep (hypnagogic) or waking (hypnopompic)
 A - Attacks
(sudden unpredictable episodes of sleep; it can last secs to mins) - most common sign
 P - Sleep Paralysis
muscle paralysis on falling asleep or waking

all symptoms need not to be present

355
Q

Sleep Disorders
Narcolepsy” Dx

A
  • clinical history
  • absence of other sleep disorders (particularly OSA) on overnight sleep study
  • objective evidence of excessive daytime sleepiness (using a multiple sleep latency test or maintenance of
    wakefulness test)
356
Q

Sleep Disorders
Narcolepsy” Mx

A
  • Non-pharmacologic
    – Scheduled naps can help, but seldom suffice as primary therapy
    – Advise the patient to follow good sleep practices.
    – Advise patients with severe sleepiness to avoid dangerous activities at home and at work. They should not operate a motor vehicle until sleepiness is adequately managed and they satisfy the Australian standards of fitness to drive
  • Pharmacologic
    – Modafinil
    (first-line drug therapy for reducing daytime sleepness and sleep attacks)
            OR
    
      -- dexamphetamine and methylphenidate. 

If Cataplexy, sleep paralysis and hallucinations

– TCAs or SSRI can be added
– GHB is also effective (not mentioned by the ATG)

357
Q

Sleep Disorders
Obstructive Sleep Apnoea
Predictive Factors/Symptoms

A

SAD BBANG TF

 S - Snoring
 A - Apnoea (observed by someone else)
 D - Daytime sleepness/irritability/ poor attention

 B - BP (HIGH)
 B - BMI (HIGH)
 A - Age (OLDER)
 N - Neck Circumference (LARGE)
 G - Gender (MALE)

 T - Thyroid disease
 F - Family History

358
Q

Sleep Disorders
Obstructive Sleep Apnoea
Dx

A
  • overnight in-laboratory polysomnogram (standard)
  • Simplified home-based assessments may be appropriate in some settings as a screening tool for patients with high pre-test probability of obstructive sleep apnoea (eg sleepy obese patients who snore and take antihypertensive drugs)
    – Home-based tests can be useful to rule in
    OSA in these patients, but not to rule out OSA (the
    tests have high specificity and low sensitivity)
  • patients who require urgent assessment are those
    with:
    – unstable cardiovascular status (eg nocturnal angina
    or recurring cardiogenic pulmonary oedema)
    – hypercapnic respiratory failure
    – high pre-test probability of OSA who are about to
    undergo major surgery
    – history of significant drowsiness while driving.

A polysomnogram calculates the number and severity of obstructive apnoeas and hypopnoeas with desaturation and arousal.

359
Q

Sleep Disorders
OSA
Polysomnopraphy Results

A
  • Minimal OSA
    – is indicated by an apnoea–hypopnoea index of LESS
    than 5 events per hour
  • Significant OSA
    – is indicated by an apnoea–hypopnoea index of
    MORE than 5 events per hour
  • Severe OSA
    – more than 30 events per hour.
360
Q

Sleep Disorders
OSA” Treatment

A
  • Mild disease WITHOUT intercurrent HAS or CVD and NO DAYTIME DYSFUNCTION
    – General Measures
    — Weight reduction
    — Avoidance of alcohol and drugs that affect sleep
    — Positional therapy (supine –> lateral position)
    — Reduced nasal resistance (with smoking cessation
    and using intranasal corticosteroid spray)
  • CPAP + General Measures
  • Mandibular advancement splints + General Measures
    (effective only in mild to moderate OSA)
361
Q

Sleep Disorders
OSA” CPAP INDICATIONS

A
  • severe OSA (apnoea–hypopnoea index > 30)
  • mild to moderate OSA with symptoms of daytime
    dysfunction
  • mild to moderate OSA with HAS or other CVD.
362
Q

Sleep Disorders
Restless legs syndrome (RLS)” Sx

A

URGE

 U - Urge to move
 R - Rest worsens
 G - Gets better with activity
 E - Evening is worse

363
Q

Sleep Disorders
Restless legs syndrome (RLS)” Sx

A
  • limb discomfort at rest, followed by an urge to move the affected part
    – Symptoms affect both arms and legs in about 50%
    – symptoms confined to the arms are uncommon
    – can be bilateral (more common) and unilateral
  • may describe the sensation as creeping, crawling, itching, burning, searing, tugging, pulling, drawing, aching, hot and cold, electric current–like, restless or painful.
  • Usually, symptoms occur when the patient has been lying quietly, and last for a few minutes or an hour
  • can also occur when the patient is sitting quietly, but this is rare
  • When the patient is more mentally rested and
    physically quiet, the symptoms are more intense
  • The syndrome is worse from the evening to the early hours of the morning, whether or not the patient is asleep.
364
Q

Sleep Disorders
Restless legs syndrome (RLS)” Dx

A
  • clinical criteria (a sleep study is not usually needed)
  • can be idiopathic or secondary (more common)
365
Q

Sleep Disorders
Restless legs syndrome (RLS)“common causes

A

— iron deficiency (most common cause seen in 20%)
— DM
— pregnancy
— end-stage kidney disease
— Some drugs (eg antidepressants, antihistamines) can exacerbate the condition.

366
Q

Sleep Disorders
Restless legs syndrome (RLS)“Mx

A
  • Most cases are mild and don’t need treatment
  • Mild, infrequent symptoms —»> lifestyle changes:
    – physical exercise
    – good sleep practices
  • Exclude iron deficiency
    – Replace iron so the serum ferritin > 50 micrograms/L.
367
Q

Sleep Disorders
Restless legs syndrome (RLS)” Pharmacologic Mx

A
  • Mild, infrequent (if LSC not sufficient)
    – Levodopa VO
  • More severe symptoms
    – Pramipexole VO (dopamine agonist)
    OR
    – Gabapentine
    OR
    – Pregabalin
368
Q

Berievement & Grief
(Normal)
1st Stage, timframe, features

A

DENIAL

From event to hours to several days

– disbelief
– emotional numbness

Anxiolytics or hypnotics may be helpful for a brief period in acute grief to control excessive anxiety or assist with sleep for a few nights
(usually for fewer than 7 nights), but there is a risk that ‘brief’ use can become long-term

369
Q

Berievement & Grief
(normal)
2nd Stage, timframe, features

A

Grief and despair

few weeks to 6 months

– separation distress—preoccupation with thoughts or images of the deceased, especially yearning for the deceased
– intense sadness, tearfulness, guilt, blame
– loss of usual levels of activity and capacity to undertake normal tasks
– withdrawal from others
–physical symptoms, including fatigue and loss of appetite
– sleep disturbance, restlessness
– fleeting images (illusions, even hallucinations) about the deceased
– anxiety (about the future)
– anniversary reaction (resurgence of acute grief triggered by the anniversary of the death)

370
Q

Berievement & Grief
(normal)
3rd Stage, timframe, features

A

ACCEPTANCE

After 6 months following the death (usually resolves within 12 months)

  • Only memories of good times left.
371
Q

Berievement & Grief
(normal) Mx

A
  • Supportive psychotherapy and counselling.
  • Short acting sleeping agents, if severe problem with sleep
372
Q

Berievement & Grief
(Abnormal/complicated)
Features

A

Symptoms of stage 2 that:
– persist more than 6 months after the death
– impact on day-to-day functioning

Clinical features of complicated grief include:

  • Persistent, intense yearning, longing, and sadness.
  • maladaptive thoughts and behaviours related to the death or the deceased
  • Rumination is common and is often focused on angry or guilty recrimination related to circumstances of the death.
  • continuous emotional dysregulation about the death
  • social isolation
  • Hallucinations
  • suicidal ideation.
373
Q

Berievement & Grief
(Abnormal/complicated)
Risk Factors

A

-History of mood or anxiety disorders.
-History of alcohol or drug abuse.
-Multiple losses
-History of depression
-Development of depression early in bereavement
-there are concurrent losses and other significant stresses
-the relationship with the deceased was ambivalent, conflicted or overly interdependent
-family/friends are unsupportive or in conflict.

374
Q

Berievement & Grief
(Abnormal/complicated) Mx

A

 Psychiatrist referral
 CBT and counselling (First-Line)
 SSRI/ Antipsychotics.
 ECT

375
Q

ECT
Indications

A
  • severe depression
    – if features of severe depression are present;
    – if ECT is the preferred method of treatment in a
    voluntary patient with severe depression
    – If previous good response to ECT in patients
    with severe depression
  • treatment-resistant mania
  • treatment-resistant bipolar depression
  • treatment-resistant acute schizophrenia
  • schizoaffective psychoses in the acute phase
376
Q

ECT
Features of severe depression that meet criteria for ECT

A
  • psychotic depression (ECT is more effective than antidepressants combined with antipsychotics)
  • melancholic depression unresponsive to antidepressants
  • depressive stupor, severe psychomotor retardation (catatonia) leading to severe self-neglect, or life-threatening anorexia
  • severe postnatal depression and psychosis
  • strong suicidal ideation

ECT is superior to any other therapy (ie CBT an/or Antidepressants) in the treatment of Severe Depression

377
Q

ECT
Overall response rate

A

60-90%

378
Q

ECT
Contra-indication

A

Raised Intracranial pressure (ICP) - ONLY ABSOLUTE CONTRAINDICATION

 SITUATIONS OF HIGH RISK: (warrants specialist review)
- Hypertension
- Myocardial Infarction <3 m
- Bradyarrythmias
- Cardiac Pacemakers
- Intracranial Pathology (Aneurysms, Epilepsy)
- Skull Defect
- Retinal Detachment
- Osteoporosis

379
Q

ECT
Legislation

A

Mental Health Act in Australia

  • Patient is able to give CONSENT
    – at least two authorized medical practitioners,
    one of them must be a psychiatrist, should agree that ECT is indicated and right treatment option.
    – The same rule aplies even if a voluntary patient presents for ECT
    – If medical practitioner is concerned about the capacity of the patient to decide, an application to Mental Health Review Tribunal should be made
  • Patient is INCOMPETENT ehich precludes their ability to consent or refuse treatment
    – must be detained involuntarily in hospital and kept safe with 24 hour constant nursing supervision and given supportive care while application to a Mental Health Review Tribunal (or equivalent independent statutory authority) is made
    Relatives must be informed of the treatment plan
    Relatives are not legally able to consent or
    refuse on patients behalf
    even under enduring power of attorney
380
Q

ECT
Adverse effects

A

Most common adverse effects
- muscle aches and pains (from the muscle relaxant)
- headaches and transient confusion for ~ 1 hour after treatment.

other adverse effects include
- reversible short-term retrograde memory loss
(particularly of autobiographical memories (memories of personal experiences), for the period of treatment and to a lesser degree for antecedent events.
- in generall, new learning appears unaffected after ECT and is often improved after recovery from depression.
- Cognitive adverse effects are greater with bilateral than right unilateral treatment.
- Some patients with post-ECT confusion have ongoing ictal activity (non-convulsive status epilepticus) than can be shown on EEG monitoring, and it can be stopped with
agents like midazolam

  • There is NO CONTINUED memory impairment once treatment is completed
  • DEMENTIA IS NOT LISTED AS AN ADVERSE EFFECT
381
Q

ECT and psychotropic drugs

A

**Where possible, it is usually desirable to cease psychotropic drugs **

  • Benzodiazepines should be tapered and ceased
    — they raise the seizure threshold and may impair the efficacy of ECT
  • taper and discontinue all antidepressants
    – There is little to be gained from continuing failed antidepressants during acute ECT and there is some
    evidence it may increase adverse effects.
  • Lithium should be ceased
    – Although Lithium does not impair the effectiveness of ECT, it may occasionally result in severe postictal confusion even at a low serum concentration
  • Antiepileptics
    – In patients with epilepsy, not usually withdrawn (high risk of spontaneous seizures)
    – In patients taking antiepileptics for the management of bipolar disorder, are preferably withdrawn (before or early in the course of ECT). They can be quickly reinstated at the conclusion of the course of therapy if necessary, with the exception of lamotrigine, which requires the usual slow dose titration to reduce the risk of skin rash.
  • Antipsychotics
    – may be continued unless clearly ineffective or interacting adversely with ECT (eg prolonged seizures with clozapine)
  • Non-benzodiazepine hypnotics (eg. Zolpidem, Zopiclone) can be used if needed (eg. procedure-related anxiety)
382
Q

CBT principals

A
  • cognitions may control feelings and behaviour
  • behaviours affect thought patterns and emotions
383
Q

CBT
useful in..

A

– Psychosis.
– Depression.
– Anxiety
– Phobias (Exposiure Therapy)
– Personality diosrder.(DBT in BPD)
– Eating disorders
– Insomnias (but not Parasomnias)
– Grief

384
Q

SUICIDE
Risk Assessment

A

S - SEX MALE (1)
A - AGE < 20 & > 45 (1)
D - DEPRESSION (2)

P - PYSCHIATRIC HX (1)
(PREVIOUS ATTEMPTS)
E - EXCESSIVE DRUG USE (1)
R - RATIONALITY LOSS (2)
(PYCHOSIS or SEVERE DEPRESSION)
S - SEPARATED (1)
O - ORGANIZED PLAN (2)
N - NO SUPPORT (1)
S - SICKNESS (1)

385
Q

SUICIDE
When is the period at which patient with a mental health disorder is at their highest risk of suicide?

A

On discharge from the hospital

  • The risk of suicide in the 4 weeks after psychiatric inpatient care is around 100 times greater than that for the general population.
  • This risk declines rapidly over subsequent weeks.
  • The strongest risk factor for self-harm after discharge is an
    admission for self-harm in the previous 12 months.
386
Q

SUICIDE
How soon after discharge should patient who attempted suicide be followed up?

A

1 WEEK

387
Q

SUICIDE
2 questions that MUST be asked to assess suicidal ideation

A
  1. Do you feel hopeless?
  2. Have you felt that you’ve lost interest in your usual activities?
388
Q

Defence Mechanisms
Imature (types)

https://pmc.ncbi.nlm.nih.gov/articles/PMC8555762/

hierarchically ordered

A
  • Acting out (externalisation of regression, thus imature)
    Acting in (internalisation of anxiety)
  • Passive aggression (demonstrating hostile feelings in a nonconfrontational manner)
  • Regression (reversion to an earlier stage of development)

——————————————————————————

  • Sppliting (an individual is unable to integrate mixed feelings (eg, seeing others as alternately “all bad” and “all good”)

——————————————————————————

  • denial (refuse to recognise or acknowledge a threatening situation)
    compensation or counter dependency (respond to limits being recommended on one’s behaviour by taking on even more work/responsibilities. - a renunciation is adopted to evade anxiety out of one’s impulses)
  • Projection(disguising one’s own unacceptable impulses/thuoghts/feelings/motives by attributing to another person. Eg, one is angry but say the other person is angry)
  • Rationalisation (attempting to justify or excuse a behavior or decision rather than acknowledging the true motives, significance, or consequences of it- The subject avoids feelings of guilt or shame)

——————————————————————————

  • Neurotic (displacement, Dissociation, reaction formation, regression, intellectualisation)
389
Q

Defence Mechanisms
Neurotic

A
  • displacement (redirection of emotions or impulses onto a neutral person or object unrelated with the episode)
  • reaction formation (transforming an unacceptable feeling or impulse into its extreme opposite - it does not provide satisfaction)
  • Intellectualisation (transformation of a distressing event into a situation devoid of emotion to avoid confrontation of uncomfortable emotional components)
390
Q

Defence Mechanisms
Mature defensive category
(no impairment of insight)

A

SASH

  • S - SUBLIMATION (person channels unacceptable thoughts or impulses into socially acceptable behavior, which is similar to the original thoughtlimpulse and provides satisfaction)
  • A - ALTRUISM (alleviating nrgative feelings via unsolicited generodity, through unselfish devotion, or service to others - which provides gratification)
  • S - SUPRESSION (intentionally withholding an idea/feeling from conscious awareness but only temporarily (vs repression which is permanently) and no changes in personality (vs dissociation which is accompanied by drastic changes)
  • H - HUMOR (Lightheartedly expresing uncomfortable feelings to shift the internal focus away from the distress)
391
Q

which are the** five stages **of human development according to Freud’s theory of psychosexual development

A

O - Oral
first stage, which takes place from birth-one year old

A - Anal
second stage, which takes place from 1-3 years old

P - Phallic
third stage, which takes place from 3-6 years old

L - Latency
fourth stage, which takes place from 6-12 years old

G - Genital
fifth stage, which takes place from 13-18 years old

392
Q

Erikson’s Stages of Psychosocial Development

https://www.ncbi.nlm.nih.gov/books/NBK556096/

A

1 Trust vs. Mistrust (0-18 months):
Developing trust through consistent caregiving

2 Autonomy vs. Shame (18 months-3 years):
Learning independence and self-control

3 Initiative vs. Guilt (3-5 years):
Exploring and taking action in the world

4 Industry vs. Inferiority (5-12 years):
Developing competence through achievements

5 Identity vs. Role Confusion (12-18 years):
Forming personal identity and life direction

6 Intimacy vs. Isolation (18-40 years):
Building meaningful relationships

7 Generativity vs. Stagnation (40-65 years):
Contributing to society and future generations

8 Integrity vs. Despair (65+ years):
Reflecting on life and finding meaning

393
Q

SEXUAL DYSFUNCTION
PREMATURE EJACULATION

A

Choice of treatment depends on the couple’s preference.

  • Topical preparations
    – (lidocaine+prilocaine) 10 to 20 minutes before intercourse.
  • **SSRIs **
    – single dose before sexual activity
    (less likely to be associated with adverse effects (eg
    anorexia, reduced libido and/or anejaculation)
    &raquo_space;> DAPOXETINE VO
    OR
    &raquo_space;> PAROXETINE VO
    OR
    &raquo_space;> SERTRALINE VO– continuous/daily dosing
    &raquo_space;> PAROXETINE VO
    OR
    &raquo_space;> SERTRALINE VO

NOTE:
- Relaxation
- squeeze method
- sex therapy with partner

HAVE DUBIOUS LONGTERM BENEFIT

394
Q

Other personality disorders

A

Personality Change:
- Labile type
- Masochistic
- Disinhibited type
- Aggressive type
- Passive Aggressive type
- Apathetic type
- Combined type
- Unspecified type

395
Q

Pyromania is a one of _______ disorder

A

Several impulse control disorders

396
Q

Diagnosis of chronic insomnia

A
  1. A self-reported complaint of poor sleep quality
  2. Sleep difficulties occur despite adequate sleep opportunity.
    Impaired sleep produces deficits in daytime function.
  3. Sleep difficulty occurs three nights per week and is present for three months
397
Q

How much time should infants exposed to SSRI’s be observed for

A

3 days (monitoring for serotonin syndrome)

398
Q

Difference between Adjustment Disorder & Regular Grief

A

Grief usually occurs after loss of something like any close relative or property, however, there are l**ess behavioural symptoms **and it is a self-limiting
condition

399
Q

Perception - definition?

A

one’s ability to accurately take in information about the world. Most common:
- illusions
- Hallucinations

400
Q

Risk Factors for suicide?

A
  • Guns
  • Recent suicide attempts
  • Ongoing thoughts of suicide
  • Self-harm
  • Ethanol
  • Substances

mnemonic “Guns & ROSES”

401
Q

Healthy BMI

A

20=25

402
Q

Underweight BMI

A

18

403
Q

Overweight BMI

A

25-29

404
Q

Obese BMI

A

30-39

405
Q

Morbidly obese BMI

A

< 40

406
Q

PREGNANCY
Antidepressants
Which should be avoided?

A
  • Paroxetine
  • Fluoxetine

Concern about harm–benefit analysis for their use in the perinatal period is commonly encounteredconcern about harm–benefit analysis for their use in the perinatal period is commonly encountered however, there is no evidence to recommend any particular SSRI over another during pregnancy. There are six areas of concern: terato-genicity, spontaneous abortion and premature labour, low birth weight/small-for-gestational age, poor neonatal adaptation, persistent pulmonary hypertension of the newborn, and neurodevelopmental difficulties in older children. There were limitations and inconsistencies in published findings, and the overall consensus is that concern about teratogenicity should not deter prescription of
SSRIs during pregnancy for treatment of moderate-to-severe major depression and anxiety disorders

  • Paroxetine is linked to reports of increased risk of cardiovascular malformations. As the absolute risk is low, women who find themselves unexpectedly pregnant should not be advised to abruptly stop the drug.
  • Fluoxetine (due to its longer half-life)
407
Q

PREGNANCY
Antipsychotics
which one should be avoided and reason

A

OLANZAPINE

increased risk of maternal gestational diabetes

There is not sufficient evidence to recommend any one antipsychotic over another during pregnancy. Drug choice should be made with consideration of previous effective treatment and patient preference. During pregnancy, switching from one antipsychotic to another puts the patient at risk of relapse and of potential adverse effects to the fetus from exposure to multiple drugs.

There are extensive data available about the safety of haloperidol used as an antipsychotic. However, first-generation antipsychotics may lead to extrapyramidal symptoms in the neonate Anticholinergic drugs should be avoided if possible during pregnancy.

408
Q

PREGNANCY
Bipolar Disorder
Mx in PLANNED PREGNANCY in MILD disorder

A
  • Slow withdrawal of Lithium (3-4 weks) before conception (if stable, and not severe symptoms)
  • If relapse of symptoms:
    – Antipsychotics
    OR
    – Lithium can be reinstated ~ 50 days of conception (after cardiogenesis)
    OR
    – ECT
409
Q
A
410
Q

PREGNANCY
Bipolar Disorder
Mx in PLANNED PREGNANCY in SEVERE disorder

A
  • continue with Lithium
  • consider ECT

The benefits of lithium prophylaxis during pregnancy, in cases of severe bipolar disorder, may outweigh the risks, and lithium has been considered as a first-line treatment during pregnancy for some such women.

For patients who are currently treated with valproate or carbamazepine, it is suggest switching treatment avoid the teratogenic effects of these two antiepileptics.

The absolute risk of teratogenesis is much less with lithium than that found with valproate, carbamazepine and lamotrigine.

According to Royal Australian and New Zealand College of Psychiatrists guidelines, if the use of a mood stabiliser is essential, lithium is the safest option as compared to other treatment options.

411
Q

PREGNANCY
Bipolar Disorder
Mx in UNPLANNED PREGNANCY

A
  • Continue treatment
  • investigate for any anomaly
412
Q

PREGNANCY
Mood Stabiliser
Risk associated with the use of Lithium and the stage of pregnancy

A

Ebstein’s anomaly

  • Lithium use during the first trimester of pregnancy

Tricuspid valve are displaced downwards towards the apex of the right ventricle of the heart.

413
Q

PREGNANCY
Mood Stabiliser
Risk of developing Ebstein’s anomaly on patients on lithium?

A

approximately 1 in 1000 to 2000
compared with 1 in 20000 in the general population.

414
Q

PREGNANCY
Mood Stabiliser
What investigation should done in any patient exposed to Lithium during pregnancy?

A
  • High-resolution US at around 18-20 weeks
    Refer to Ebstein Centre if any anomaly is detected
415
Q

PREGNANCY
Mood Stabiliser
Mx of Lithium at delivery?

A
  • 24 to 48 hours before delivery (if the delivery is planned)
  • withheld at the onset of labour (if delivery is not planned)
  • Restart lithium at the prepregnancy dose after delivery

To avoid floppy baby syndrome due to neonatal toxicity

416
Q

PREGNANCY
Anxiety disorders
Mx

A

For anxiety and insomnia, the first-line
treatment should be
nonpharmacological.

417
Q

PREGNANCY
Anxiety disorders
Risks associated to exposure to BZ drug in the 1st Trimester

A
  • First trimester exposure to benzodiazepines is associated with increased risk of cleft lip and/or palate.

  • The first 8 weeks of pregnancy is the period of highest risk. A high-resolution US examination at 18 to 20 weeks.
418
Q

PREGNANCY
Anxiety disorders
Risks associated to exposure to BZ drug in the 3rd Trimester

A

If benzodiazepines taken in late pregnancy, they can cause
- neonatal drowsiness
- respiratory depression
- poor temperature regulation
- poor feeding
- hypotonicity (the ‘floppy infant syndrome’).
- Neonatal withdrawal symptoms can present

419
Q

PREGNANCY
Psychiatric Syndromes that occur following childbirth

A
  • postpartum blues: ~ 5 days after delivery
  • postpartum depression: within weeks/months after delivery
  • postpartum psychosis: within 2-4 weeks after delivery
420
Q

Breastfeeding
Postpartum Blues
Features & Rx

A
  • peak within 4-5 days
  • generally time-limited
  • spontaneously remit with 10-14 days
  • if symptoms last for more than 2 weeks, postpartum depression should be considered

  • Occurs in 80% of mothers following delivery (considered normal)
421
Q

Breastfeeding
Postpartum Depression
clinical features

A
  • peak at 12 weeks
  • occurs between 6-12 months after the delivery,

Sx:
- marked mood swings
- irritability towards the family
- guilty thoughts about being a bad mother,
- excessive anxiety about the wellbeing of
the baby
- irritability towards the family
- agitation
- poor memory and concentration
- depressed mood and weight loss

  • prevalence 10-15%
422
Q

Breastfeeding
*Postpartum Depression *
Mild-to-Moderate
Rx

A

CBT

423
Q

Breastfeeding
Postpartum Depression
Severe
Rx

A

SSRI
(Sertraline || Paroxetine)

From published data, sertraline and paroxetine appear to
have the lowest transmission into breastmilk and fluoxetine, escitalopram and citalopram the highest. Venlafaxine gives a higher mean relative infant dose than the SSRIs; however, for some women venlafaxine may have been prescribed during pregnancy or earlier due to lack of efficacy of other antidepressants. For these women, if they have a full-term infant who is otherwise well, breast-feeding should be encouraged.

424
Q

Breastfeeding
Postpartum Depression
which SSRIs should be avoided

Due to the risk of excretion into breastmilk

A
  • Fluoxetine (due to its longer half-life)
  • Citalopram
  • Escitalopram

  • Fluoxetine, escitalopram and citalopram have the highest transmission into breastmilk
  • Fluoxetine has the potential to accumulate in the breastfed infant, and been associated with low weight gain, irritability, difficulty settling and infant gastrointestinal dysfunction.
425
Q

Breastfeeding
*Postpartum Psychosis *
Risk Factors

A
  • previous episode of postpartum psychosis
  • history of bipolar disorder (highest risk).
  • maternal suicide (20%) = rule out by psych eval first (notify child services & consult psychiatrist)
  • child harm & Infanticide (4%)

Postpartum psychosis is rare (1 to 2 cases per 1000 live births);

426
Q

Breastfeeding
*Postpartum Psychosis *
clinical features

A
  • postpartum psychosis: within** 2-4 weeks** after delivery

 Symptoms include:
- agitation
- elation (if an episode of bipolar disorder)
- confusion
- thought disorganisation
- sleep disturbance
- psychosis (hallucinations and delusions)
- affective symptoms.

427
Q

Breastfeeding
*Postpartum Psychosis *
Management

A

 The presentation is acute and usually
requires inpatient management.

Treatment in ACUTE MANIA – PSYCHOTIC EPISODE is:
- antipsychotics and/or ECT, (for quick resolution)

 depending on the underlying Dx –
antipsychotics + Lithium/antiepileptics
may be added or antidepressants.

 If (+) hx of previous episode of postpartum psychosis = PROPHYLACTIC USE LITHIUM after delivery reduces the likelihood of a recurrence.

428
Q

Breastfeeding
Safe Anti-psychotic

Overall safe drug in case of FIRST Mania/Psychosis episode

A

Haloperidol

  • In lower dose, ie less than 10 mg haloperidol daily or equivalent, they are usually regarded as safe
429
Q

Breastfeeding
Anti-psychotics to avoid

A
  • Olanzapine
  • Clozapine

  • Additional studies are required to definitively establish safety, and the association of OLANZPINE with some reversible adverse effects (jaundice, impaired weight gain, sedation, irritability and tremor) in a small series of breastfed babies has led the manufacturer to recommend against breastfeeding while taking olanzapine.
  • CLOZAPINE should not be used while breastfeeding (due to high concentration in breastmilk and the theoretical risk of agranulo-cytosis occurring in the infant).
  • The first-generation antipsychotics, especially at high dose, have occasionally been associated with adverse reactions in breastfed infants (eg urinary retention, dystonic reactions).
430
Q

Breastfeeding
what is the recommendation while breastfeeding if taking Olanzapine

A
  • continuation of clozapine for maternal wellbeing

PLUS

  • the use of formula feeding rather than breastfeeding.
431
Q
A