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RANZCP exam preparation > Schizophrenia > Flashcards

Schizophrenia Flashcards

1
Q

Structure of chlorpromazine

A

phenothiazine

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2
Q

Structure of haloperidol

A

butyrophenone

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3
Q

Structure of trifluoperazine

A

piperazine

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4
Q

Structure of thloridazine

A

piperidine

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5
Q

Structure of flupenthixol

A

thioxanthene

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6
Q

Structure of sulpride

A

benzamide

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7
Q

Structure of olanzapine

A

thienbenzodiazepine

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8
Q

Structure of clozapine

A

dibenzodiazepine

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9
Q

Structure of quetiapine

A

dibenzothiazine

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10
Q

Subtle differences in MOA of sulpride/amisulpride, risperidone, olanzapine/quetiapine, ziprasidone, aripiprazole

A

Sulpride/Amisulpride- presynaptic D4 at lower doses, d2 blockade at higher doses
Olanz/Queti- D2/5HT2 antagonists + H1 (sedative)
Risperidon- D2/5HT2 antagonists + a1 blockade (first dose hypotension)
Ziprasidone- 5HT/D2 antagonist, agonist at 5HT21A w/ monoamine reuptake inhibition
Aripiprazole- partial agonist D2, 5HT2 antagonist, partial agonist 5HT1A

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11
Q

What are the main principles of managing first episode psychosis

A

High index of suspicion
Proactive retention for the first 3-5 years
Initial treatment in outpatient setting
In patient if risk of aggression to self or others
In patient in least restrictive
24-48 hr wait and watch time
Commence low dose antipsychotic +/- benzo
Organic screen
Psychoeducation
Psychological treatment (CBT)
If no response with 2 antipsychotics, consider clozapine
Follow up in EPPIC or similar service

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12
Q

What are the risk factors for suicide in schizophrenia

A 
Individual:
Young, single, unemployed, male**
Caucasian
Depression and hopelessness**
Previous suicide attempt**
Drug and alcohol **
Insight retained**
Good premorbid function**
Akathisia
Deteriorating physical function

Social:
Social isolation
Unemployment
Hospitalisation close to roads or railway

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13
Q

Principles of managing suicidal ideation in schizophrenia

A 
1. Prompt initial assessment
Emergency medical treatment as required
Prompt initial assessment of SI/following attempt
Psychotic sx: command hallucinations, persecutory delusions, spy/conspiracy delusions
Depressive sx
Access to lethal means
Social support and supervision
2. Ensure immediate safety
Inpatient treatment with observation
Remove access to means of self harm
3. Appropriate management
Management of psychosis/depression
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14
Q

Poor prognostic factors

A 
poor premorbid
insidious
young onset
cognitive impairment
\+ventricle size
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15
Q

Good prognostic factors

A 
Elevation during
Affective
Female
FHx
Developed country
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16
Q

Number who have a prodrome

A

80-90%
Attenuated- late prodrome
= UHR mental state

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17
Q

Outcomes/prognosis in FEP (after 13 years)

A 
15-20% won't recur
Few in employment
52% >2 years sx free
52% no negative sx
55% good/reasonable social function
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18
Q

What are the factors affecting compliance in patients

A
  1. Patient factors
    - therapeutic alliance
    - attitudes toward medication, family attitudes
    - insight impaired
    - stigma
    - cultural factors
  2. Illness factors
    - delusions
    - hallucinations
    - cognitive impairment
    - depression
  3. Medication factors
    - lack of efficacy
    - side effects
    - complexity of regime
    - cost
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19
Q

Strategies to manage non-compliance

A
  1. Patient/family
    - psychoeducation
    - involve the family
    - CBT/IPT
    - compliance therapy/adherence therapy incorporating motivational interviewing
  2. Medication
    - dosette box, alarm, mobile phones, post it notes
    - normalise taking
    - depot
  3. Illness
    - treat illness aggressively
    If patient refuses: intensive follow up, inform GP, psychoeducation for family to detect early relapse sx, ofer trial of supervised medication, rather than abrupt cessation
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20
Q

Terms in schizophrenia: dementia precoce, manic depressive/dementia precox/catatonia/hebephrenia, schizophrenia, first rank. Names associated

A

Dementia precoce- Morel
Manic depressive/Dementia precox/Catatonia/Hebephrenia- Kraeplin
Schizophrenia- Bleuler
First rank- Schneider

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21
Q

Principles of managing treatment resistance

A
  1. Establish true resistance
  2. Treat pseudoresistance
  3. Clozapine is treatment of choice
  4. Dose: 300mg min effective, levels >350
22
Q

How do you manage pseudoresistance

A 
Reassess diagnosis
Rule out organic
Optimise dose
Serum levels
Assess compliance
Check for pharmakokinetic/pharmacodynamic interactions
Screen for co-morbidities
23
Q

What are the negative sx in schizophrenia

A 
Abulia*
Alogia*
Apathy
Affective blunting*
Anhedonia
Social withdrawal
24
Q

What are the causes of negative symptoms

A 
Primary- schizophrenia
Secondary-
Severe positive sx
Depression, demoralisation (post-psychotic depression)
Post remission exhaustion syndrome
Medication/EPSE
Drug misuse
Organic
25
Q

Crow two syndrome hypothesis

A 
1. Mostly Positive sx
Good premorbid
Normal cognition
Good treatment response
2. Negative sx
Poor function
Impaired cognition
Brain structural abnormalities
3. Syndrome
- psychomotor poverty
- disorganisation
- reality distortion
26
Q

Subtypes of schzophrenia

A 
Catatonic
Paranoid
Disorganised
Undifferentiated
Post-schizophrenia depression
Residual
Simple
27
Q

Components of family therapy in schizophrenia

A 
Therapeutic alliance with family
Psychoeducation
Address high EE
Increase problem solving capacity of family
Enhance communication through circular questions
Boundary setting
Promote individual independence
Allow venting
Involve family in relapse prevention
28
Q

What are the components of CBT in schizophrenia

A
  1. Therapeutic alliance
  2. Challenging assumptions
  3. Reconceptualisation of symptoms
  4. Mood modification
  5. Anxiety modification
  6. Compliance therapy
  7. Coping strategies and problem solving
29
Q

Techniques in adherence therapy

A 
Use reflective listening
Summarising statements
Inductive questions (conclusions from observations)
Explore ambivalence
Use normalising rationales
30
Q

Components of cognitive remediation therapy

A
  1. Assessment
  2. Treatment to remediate impairments
  3. Cognitive mediation- errorlesss learning, easy discrimination of components being learnt, individual should not experience failure, extremely gradual increase of difficulty of task to be learnt
31
Q

Components and principles of social skills trainings

A

Social skills deficits model- deficits cause vulnerability to psychiatric illness
Stress-vulnerability model- social skills protect againts psychiatric disorder
Targets
1. Non verbal
2. Para-linguistic
3. Linguistic
Modelling, feedback and opportunities to generalise behaviour

Efficacy- Meta-analysis Schiz Bull 2006 showed skills can be learned and maintained in artificial environment, but generalisation rarely occurs, it must be programmed.

32
Q

Important trials

A

CATIE
CutLASS
EUFEST

33
Q

What are the criteria for prodromal states

A

Attenuated= sub threshold symptoms over period of 1 week to 5 years
Schizotypal disorder trait or first degree rel with schizophrenia + decrease in GAF over period of 1 month to 5 years
BLIPS (brief intermittent psychotic symptoms)- at least one psychotic sx for <1 week over past year

  1. Trait + attenuated
  2. Trait or attenuated < 5 years
  3. Trait or attenuated or BLIPS + GAF <60

Any of the above predict psychosis over 12 months

34
Q

Consequences of untreated psychosis

A 
Slower and less complete recovery
Higher relapse rates
Treatment resistance
Increased negative symptoms
Functional impairment
Substance misuse
Higher suicide
Decreased quality of life
Neuropsychological deficits
35
Q

Important management points dystonia

A

Benztropine IV or IM 1-2mg

36
Q

Important risk factors/management points pseudoparkinsonism

A

Can assess with Simpson-Angus rating scale
Differentiated by Parkinson’s by bilateral tremor
Risk factors: elderly females, pre-existing neurological

Reduction of dose, change to atypical if on typical, prescribe anticholinergic

37
Q

Important management points akathisia

A

Measured by Barnes Akathisia Scale
Incraeses suicide risk

Reduce dose
Change to atypical
Benzt may help if other antiparkinsonian sx present
Propranolol
Cyproheptadine
Benzo
Clonidine
38
Q

Important risk factors/ management points TD

A

Lip smacking, tongue protrusion, choreiform, pelvic thrusting
Measured by AIMS
Risks: diabetes, typicals, organic neuro, female, smoking

Stop anticholinergic
Reduce dose
Change to atypical
If untreated, clozapine

Tetrabenazine (Huntington’s)
Benzo
Vit E

39
Q

Tips for restarting antipsychotic after NMS

A
  1. Wait 2 week
  2. Lower potency (Olanzapine, questiapine) lower dose, titrate slowly
  3. Avoid co-administration with Lithium
  4. Avoid dehydration
  5. Monitor for sx
40
Q

NMS: sx, Ix, risks, management

A

Sx: Diaphoresis, fever, rigidity, fluctuation consciousness, autonomic instability (fluct BP, tachyC)

Ix: CK++, leukocytosis, altered LFTs

Risks: high potency typicals, abrupt dose change, abrupt withdrawal of anticholinergic, parkinson’s/organic, hyperthyroid, dehydration, psychomotor agitation, ID

Management:

  1. Medical emergency
  2. Withdrawl AP
  3. monitor vitals
  4. Rehydration, bromocriptine, dantrolene, benzo’s
  5. Cooling blankets, artifical ventilation if required
  6. ECT
  7. Restart antiP with caution
41
Q

Hematological SE clozapine

A

Agranulocytosis
Neutropenia
TE/PE

42
Q

CV SE clozapine

A 
Myocarditis
CM
TachyC- high % benign
Prolonged QTc
PeriC
Pericardial effusion
Cardiac failure
MV insufficiency
43
Q

Core facts: prevalence, mortality, comorbidity, heritability, risk with Identical, both parents, 1 parent, genetic association

A

Prev: 15-19/1000
Mortality: 20% reduced life expectancy
Co-morbid: HIV/HEP B/HEP C + men in first year, epilepsy, IHD, celiac substances
Heritability: 60-80% (Neureglin, NRGI, dysbindin, DISCI, COMT Val158Met)
Identical twin- 46%
both parents- 40%
1 parent- 15%

44
Q

Metabolic syndrome sx and management

A 
Central adiposity
Raised TG/LDL
Reduced HDT
T2DM, glucose intolerance
Hypertention

Management:
1. Baseline monitoring
2. FHx obesity, DM, dyslipidemia, HTN, CVD
3. BMI, waist, BP, FGL, lipids- every 3-6 months
4. Treat with SGA with least weight gain potential
5. Psychoeducation
6. Lifestyle modification- dietician, exercise
7. Pharmacotherapy if required
(orlistat, sibutramine (MAORI), rimonabant (Cannabinoid receptor antagonist, topiramate, metformin)

45
Q

Mechanism of AP induced weight gain in schizophrenia

A

Individual factors

  • increased body fat
  • alcohol
  • leptin dysfunction
  • ghrelin dysfunction
  • insulin resistance

Meds:

  • 5HT2c antagonist, H1 antagonist
  • reduced energy expenditure
46
Q

Characteristics of late onset schizophrenia, compared to early-onset schizophrenia

A 
Onset >45, or >65 in very late
Greater sensory impairment
Social isolation
Eccentric premorbid
Greater likelihood of visual hallucinations
Encapsulated delusions
Partition delusions
Greater female preponderance
Greater risk of developing TD
Lesser genetic risk
No past hx
Less formal TD
Less affective blunting
47
Q

Contributory factors to psychosis in old age

A 
Sensory impairment
Social isolation
Neurocognitive changes, neurochemical
Age related deterioration in frontal and temporal cortices
Pharmacokinetic/pharmacodynamic changes
Polypharmacy
48
Q

Common misidentifying delusions in AD

A

Capgras
Phantom boarder
Mirror sign
TV sign

49
Q

DSM V criteria SZP

A 
2 or more, >1 month (must have 1,2, or 3)
Delusions
Hallucinations
Disorganised speech
Grossly disorganised/catatonic behaviour
Negative symptoms
Continuous disturbance for >6 months

Schizophreniform= >1month, less than 6
Brief psychotic= >1 day, <1 month
Delusional disorder= one or more delusions >1 month, and criteria A for schizophrenia has never been met

50
Q

DSM V for Schizoaffective

A
  1. Major mood + criteria A of schizophrenia
  2. Delusions or hallucination for 2 + weeks in absence of major mood episode
  3. Criteria for mood are filled during active and residual periods of illness
51
Q

Aetiology of schizophrenia

A
  1. Biochemical:
    - DA
    - Glutaminergic hyperactivity
    - 5HT +(LSD, cloz)
    - a-adrenergic ++
    - GABA -ve (leads to + NE/5HT/DA)
  2. Neurodevelopmental- obstetric compl, motor/cognitive problems, cerebral structure, dysmorphic
  3. Disconnection hypothesis= -ve grey matter, memory/frontal lobe impairment, -ve white matter in frontal lobes

RANZCP exam preparation (119 decks)

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