Class 1 Flashcards

1
Q

Symptoms of Psychosis

A
  1. Positive symptoms: delusions, hallucinations,
    thought disorganization, hostility
  2. Negative symptoms: affective blunting, thought
    impoverishment, aboulia (diminished motivation),
    anhedonia (?)
  3. Cognitive symptoms: attention/concentration,
    executive planning, memory
  4. Impulsive symptoms: aggressiveness, suicidality,
    substance abuse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Symptoms of Psychosis that can be “Pseudopsychotic”

A

• Delusions: a fixed belief or a “fluid” belief or an overvalued idea or an obsessional idea with a “psychotic” flavor (personality/cultural issues; obsessive-compulsive disorder)
• Persecutory, referential, grandiose, somatic, guilt
• Hallucinations: perceptual disturbances unrelated to the external environment – auditory, visual, olfactory, gustatory, somatic, synaesthetic
• Many non-psychotic people can hear at one or more times in their life simple “voices” (periodic paralysis, mourning); childhood sexual abuse with dissociations (including but not usually associated with borderline
personality disorder); associated with substance abuse (auditory may predominate, but visual, olfactory, gustatory are more pronounced);
associated with various neurological diseases (visual olfactory, gustatory, somatic more pronounced)
• Negative symptoms: neuroleptic effect of medication
(too much dopamine blockade); over sedation;
comorbid major depression (30% of patients with
schizophrenia); comorbid anxiety (generalised
anxiety, panic/agoraphobia); hoarding/OCD; social
phobia)
• Hypothyroidism, anaemia, psychodynamic/social
difficulties
• Thought disorganization: difficulty to follow the train of thought of the patient; thought blocking is rare but delay of response is common (negative symptom) – poor sleep, substance abuse, but not affective disorders, rarely aphasia
• Cognitive symptoms: acute intoxication, acute neurologic event, dissociative episode (no memory for different alter), comorbid attention deficit disorder, comorbid anxiety disorder
• Impulsive symptoms: substance abuse (e.g. ups and downs of stimulant abuse, alcohol intoxication and suicidality); personality factors/intermittent explosive disorder; family history of substance abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

synasthetic: more

A

more psychedelic drug experience, feel sounds, taste things that you see

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

borderline and voices

A

don’t have a delusional explanation for the voices, voices don’t respond to antipsychotic rx, never have negative symptoms of schizophrenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

schizotypal vs psychosis

A

schizotypal don’t necessarily share same ethipathological than psychosis. Seems like they’re on the autistic spectrum in their interpersonal relationships, overvalued ideas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Etiopathology of Psychotic Disorders

A
  • DSM-IV/DSM-5 categories of no predictive therapeutic value
  • RDoCs (Research Domain Criterias) supposedly more “scientific” in finding biological correlates that would lead to more homogeneous groups in order to study treatment has been unhelpfully unpredictive
  • No specific biological workers
  • Specific genes for medication responsiveness or symptoms prediction have been disappointing
  • European consortium : 108 genes identified for schizophrenia and many overlapped with bipolar disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

A new Paradigm for Schizophrenia Therapeutic Markers

A

• Hyperdopaminergia: 70-80% of all patients who respond to dopamine blocking antipsychotics
• Normodopaminergia: 20-30% of all patients “treatment
resistant schizophrenia” or clozapine-responsive
schizophrenia
• Normodopaminergia: 5-10% first episode psychosis – partial response to clozapine/ECT7
• But resistance to clozapine increases over time to 40-70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Etiopathology of Schizoaffective Disorders and Delusional Disorders

A

• Schizoaffective disorder : the psychotic part is likely reflected in the etiopathology of schizophrenia, including pharmacoresistance
• Mania is essentially also a hyperdopaminergic problem
• Genetics of bipolar/schizoaffective disorder are quite variable and share many areas with schizophrenia
• Delusional Disorder – no evidence for a clear
biological/genetic etiopathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Psychosocial Aspects of Etiology of Psychotic Disorders

A

• In more well-defined and common psychotic disorders (schizophrenias, schizoaffective disorders), there are clear familial risks, even if the exact genes are not known in a given case
• For example, the well-known Danish Adoption Study suggested that the heritability of schizophrenia if one parent were affected would be 10-15%, and > 40% if two parents were affected
• In terms of more clear cut psychosocial aspects of etiology of psychoses, the following factors have some (unquantifiable) influence:
o Immigration
o Deafness, blindness
• On the other hand, childhood sexual and psychological abuse has an unclear association

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Name the Psychotic Disorders

A
• Schizophrenia
o Schizophreniform disorder
o Schizophrenia multi-episodes
• Schizoaffective Disorder
• Brief Psychotic Disorder
• Substance-induced Psychotic Disorder
• Catatonia
• Delusional Disorder
• Schizotypal Personality Disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Schizophreniform Disorder criteria

A

• Two or more of the following for at least one month but less than six months
1) Delusions
2) Hallucinations
3) Disorganized speech
4) Grossly disorganized or catatonic behaviour
5) Negative symptoms
• Not attributable to substance abuse or medical conditions
• Absence of blunted affect and good premorbid functioning are good prognostic features

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Schizophreniform Disorder epidemiology

A

• About a third of individuals will recover within the six
months period
• Two thirds will eventually receive a diagnosis of schizophrenia
• Epidemiology and genetic risk is same as
schizophrenia
• Functional consequences are similar for
schizophrenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Schizophrenia epidemiology

A
• Prevalence : 0.3-0.7%
• Sex ratio differs across samples
• Poor prognosis factors – males
• Late onset cases (over 40 years old) over represented
by females
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Schizophrenia Development and course:

A

o Psychotic features in late teens up to mid-thirties, males earlier than females
o Slow gradual onset in most; 15-20% have favourable outcome
o Psychotic symptoms tend to decline in late middle and old age due to normal age-related declines in dopamine activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Risk factors schizophrenia

A

late winter / early spring birth (?),
urban environment, pregnancy and birth
complications with hypoxia, greater paternal age
Cultural/linguistic factors in misidentifying symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Suicide risk schizophrenia

A

5-6% die by suicide; 20% attempts; highest risk in comorbid substance abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Differential Diagnosis schizophrenia

A
• Major affective disorder with psychosis or catatonic
features
• Delusional disorder
• Schizotypal personality disorder
• Obsessive compulsive disorder and body dysmorphic
disorder
• Post traumatic stress disorder
• Autism Spectrum disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Schizoaffective Disorder epidemiology

A

• Prevalence 0.3%, higher in females than males
• Development and course – early adulthood mostly
• Increased risk: first degree relatives with
schizophrenia
• Suicide risk: 5% with presence of depressive
symptoms correlating for higher risk of suicide;
higher in North America (?)

19
Q

Brief Psychotic Disorder

A

• Lasts more than one day and remits by one
month; specifier with or without marked stressor
• 9% of cases of first episode

20
Q

Substance-Induced Psychotic Disorder

A

• Presence of hallucinations and/or delusions
• Symptoms develop during or soon after a substance
intoxication or withdrawal; substance able to produce
hallucinations and delusions
• Specifiers: onset during intoxication, onset during withdrawal
• Alcohol, cannabis, phencyclidine, other hallucinogens,
inhalants, amphetamines, cocaine, sedative/hypnotics
• Prevalence 7-25% of first episode psychosis
• Evolution to chronic psychoses

21
Q

Catatonia

A
  • Can be seen in many disorders
  • Clinical picture:
  • Stupor: motionless
  • Catalepsy: stiffness
  • Waxy flexibility: put them in a position and they keep it there
  • Mutism
  • Negativism: they do the opposite of what you want them to do
  • Posturing: adopting a posture for a long period of time
  • Mannerism: clothing, movements that stand out
  • Agitation
  • Grimacing, echolalia, echoproxia
22
Q

Delusional Disorder

A

• Presence of one or more delusions with a duration of at least one month
• Hallucinations if present, are not prominent
• Apart from impact of delusions, functioning/behaviour not impaired
• Erotomanic, grandiose, jealous, persecutory, somatic
• Specifiers: first episode, multiple episodes, continuous
• Prevalence – 0.2%; no gender differences
Give antipsychotic + antidepressant

23
Q

Schizotypal Personality Disorder

A
  • Pervasive pattern of social/interpersonal deficits marked by acute discomfort with and reduced capacity for close relationships
  • Cognitive or perceptual distortions
  • Eccentricities of behaviour
  • Beginning in early adulthood
  • Symptoms – ideas of reference, magical thinking/odd beliefs, unusual perceptual experience, including bodily illusions, odd thinking, suspiciousness or paranoid ideation
  • Constricted affect, odd appearance, lack of close friends, excessive social anxiety
  • Prevalence 0.6-4.6%; infrequent in clinical populations 0-1.9%
  • Rare to develop schizophrenia
24
Q

Common Comorbid Disorders

A

• Anxiety disorders in up to 50% of schizophrenias,
schizoaffective disorders
• Substance use disorder, including alcohol use
disorder 50-80%
• Patients still have their own personality traits

25
Q

Medical and Psychosocial Complications

A
  • Schizophrenias and schizoaffective disorders
  • Poorer general health
  • Decreased longevity (particularly with no treatment), related to poor lifestyle choices and poverty
  • Decreased dental health
  • Decreased occupational functioning (related to number of relapses, intensity of follow-up)
  • Decreased social functioning
  • Some illnesses, like diabetes, appear to be linked genetically
26
Q

Psychosocial Treatments for Psychotic Disorders

A

• Many interventions have historically been helpful (Dr Heinz Lehmann’s “East House” Project in 1950’s), but have not produced lasting results – patient requires
continuous accompaniment and coaching
• Modern interventions:
o Motivational interviewing (adherence) and relapse prevention
o Cognitive behaviour therapy (anxiety > delusion/hallucination resolution)
o Case management approach
o Supported work programs
o Psychosocial rehabilitation activities (emphasising patient strength)
o Psychoeducation (patient and family)
• Not all patients are accessible to these interventions and response rates are harder to measure because of smaller numbers in studies and selection biases
• No evidence that CBT will replace antipsychotics

27
Q

Risk Factors for Relapse

A
• Medication non-adherence 4-5X
- < 25% of prescribed dose for > 2 weeks
• Substance abuse : 3X
• High emotional expression: 2-3X
• Low premorbid functioning: 2X
28
Q

Medication non-adherence: Risk Factor

A
  • Physician over estimate
  • Insight
  • Beliefs about medication
  • Polypharmacy
  • Secondary effects
  • Stigmatization
29
Q

Recovery in Psychosis

A

• Very medical definitions equate symptom remission and
recovery, but this leaves the same hopeless level of 13%
today, as in Kraepelin’s time
• Quality of life scales show improvement with symptom
remission
• Non-medical definitions of recovery emphasize approach and process more than results, to encourage hope in patients, families, and clinicians

30
Q

Principles of Recovery

A
  • Hope
  • Agency/Autonomy
  • Symptom management
  • Spiritual recovery
  • Subjective well-being
  • Belonging to a social group
  • Societal integration
  • Accepting limits imposed by the illness
  • Fighting stigmatization
31
Q

Pharmacotherapy and Recovery

A

• Pharmacotherapy is the corner stone on which
other psychosocial interventions are laid
• Patients themselves feel this
• Untreated or sub-optimally treated illness
becomes more and more resistant

32
Q

Biological Treatments for Psychotic Disorders

A
  • Antipsychotics dopamine blockers and clozapine are effective for most psychotic conditions
  • Adjunctive “boosters” such as anticonvulsants/mood stabilizers are unclearly useful
  • Delusional disorders often tend to be relatively pharmacoresistant – unclear etiopathology and not clearly hyperdopaminergic
  • With dopamine blockers, it is important not to pass the “neuroleptic threshold” = patient has just a soupçon of parkinsonism/akathisia
  • Antipsychotic effect occurs at roughly 60% dopamine blockade in the striatum, while akathisia/hyper-prolactineamia occurs at 72% and parkinsonism at 78-80%
33
Q

neuroleptic threshold

A

neuroleptic threshold: overdose
1/3 - 1/2 of average dose we give = minimal effective dose = 2,5 mg zyprexa. average dose = 15 mg
average dose: pt doesn’t have any extrapyramidal symptoms

34
Q

How long treatment

A

• Treatment is essentially for the adult life of the patient
• Therefore, while efficacy is always the primary concern,
tolerability of the long-term treatment ends up being more important
• De-stigmatization (no obvious side effects – sedation,
parkinsonism, tardive dyskinesia, obesity)
• Better adherence through shared decision-making
• Better comfort (constipation, sexual side effects, hypersalivation)

35
Q

Efficacy of Pharmacologic Interventions on positive, negative, neurocognitive, affective and impulsive symptoms

A

 Positive symptoms : up to 87% in first episode psychosis acute treatment, although response rates can be lower
o Less effective in relapse prevention, but still highly effective
 Negative symptoms
o Small statistical efficacy in studies does not translate to meaningful efficacy clinically
o Prevention of worsening at lowest effective dose
 Neurocognitive symptoms
o Small statistical efficacy in studies does not translate to meaningful efficacy clinically
o Prevention of worsening : role of anticholinergic antipsychotics and use of antiparkinsonians. bradymentina: mind slowing, parkinsonised mentally
anticholingeric: cognitive effects
Affective/anxiety symptoms
o Statistical efficacy in studies, but difficult for patients to
differentiate this effect between first and second generation antipsychotics
o Known comorbidity up to 45% requiring specific intervention
Impulsive symptoms (suicide, violence, drug abuse)
o Clozapine in suicidality, violence, drug abuse
o Long-acting injectable antipsychotics in drug abuse

36
Q

Cognitive deficits

A

 Multiple relapses often lend to continuing neurodegeneration
 However, many patients will show cognitive deficits that do not deteriorate over time
 Treatment response declines with each relapse
 Each unsuccessful trial of an antipsychotic before clozapine decreases 8-11% of response to clozapine
 Many, probably most patients who stop treatment and then relapse fail to regain prior level of function5
more relapses, brain bounces back less

37
Q

Clozapine study

A

risperdal/ zyprexa to clorazil 75% response
risperdal/ zyprexa to risperdal/zyprexa less than 20% response
most its who go off clozapine relapse, don’t do well

38
Q

Hyperdopaminergia and normodopaminergia are not yet anchored as therapeutic concepts, Result:

A

polypharmacy of antipsychotics (e.g. use of two dopamine blockers in a patient with likely normodopaminergic illness)

high dose antipsychotic treatment (variable definitions – e.g. olanzapine > 25-40 mg/d which is unlikely to produce an improvement in more than 5-10% of cases

Inherent “hypofrontality” hypodopaminergia already in many cases of schizophrenia makes excessive dopamine blockade problematic.

39
Q

Consequences of too much Dopamine Blockade

A

 It has been known for decades that clinical results with lower doses of first generation antipsychotics was likely attributable to better adherence due to lower side effect burden, even if motor side effects are covered by antiparkinsonian medication
 Very low doses can prevent relapses and “wake up” patients even with risk of symptomatic return
 Increasing striatal dopamine blockade was associated with decreased subjective well being
 Positive affect also decreases with increased striatal binding
 Neuroleptic threshold: dose where a hint of induced parkinsonism is noted
  risk of extrapyramidal side effects (acute and tardive) by going beyond neuroleptic threshold, even if EPSE are covered by antiparkinsonians
 Patients “stabilized” already should also be assessed for this since PET scans show that once threshold is passed, reducing the dose can improve cognition
 If D2 blockade > 80% - cognition is worse
 46,7% of patients in remission after 6 months had D2 receptor occupation < 65% and 8/30 with > 65% lost their remission

40
Q

Weight gain

A

 “Weight gain, metabolic and cardiovascular complications with decreased mortality are unavoidable”
 Schizophrenia is recognized as a risk factor for diabetes
 Most first generation antipsychotics have weight gain
potential (> 7% of body weight) and like second generation medications, this usually starts early and worsens over time
 Weight gain can occur with low doses (e.g. quetiapine
25 mg hs) and higher doses do not increase weight gain
 While it is true that cardio-metabolic, risks are present even before treatment and that obesity itself can be associated with cognitive dysfunction over the long term, there is no reason to augment the risks with metabolically – unfavorable medication
 Psychiatrists have a poor record in metabolic monitoring
 Weight gain > 7% body weight among antipsychotics :
lurasidone/asenapine 5%; ziprasidone 10%; aripiprazole 8%; risperidone 18%; quétiapine 23%; olanzapine 29%, clozapine 30%
 Switching AP does not always reverse weight gain

41
Q

Patients who require complex care are more likely to have xxxx services

A

inadequate

42
Q

ECT and psychosis

A

 Electroconvulsive therapy is almost as effective as
antipsychotics in antipsychotic responsive schizophrenia
 In ultra-resistant schizophrenia (non response to
antipsychotics and clozapine), electroconvulsive therapy
is effective in 50% of cases

43
Q

rTMS and psychosis

A

Transcranial magnetic stimulation is held to be effective in positive and negative symptoms, but has little availability and studies on long-term efficacy are lacking

44
Q

Pregnancy and psychosis

A

o With improved care, more women with psychotic condition are experiencing pregnancy and motherhood
o Antipsychotics are safe during pregnancy from a teratogenic point of view
o Near delivery, doses may need to be diminished or even stopped for a few days because the baby’s liver enzyme metabolizing system will not be as effective and the baby could be sedated or even mildly parkinsonized
o Genetic risk counselling is a must