Psychosis Flashcards
HCR 20
Historical factors
H1 Previous violence
H2 Young age at first violence
H3 Relationship instability
H4 Employment
H5 Substance Use
H6 Major Mental Disorder - psychotic/mood/other
H7 Psychopathy
H8 Early maladjustment
H9 Personality disorder
H10 Prior supervision failure
Clinical Items
C1 Lack of insight
C2 Negative attitudes
C3 Active sx of MI
C4 Impulsivity
C5 Unresponsive to treatment
Risk mx
R1 Professional services and plans - feasibility
R2 Exposure to destabilisers
R3 Personal support
R4 Noncompliance with remediation attempts
R5 Stress/coping
Qtc
start of QRS and end of T interval
class 1 and 3 antiarrhythmic drugs - sotalol, amiodarone
antibiotics - azithro, erythro, ciprofloxacin
hyponatremia, K, recent infection
kidney problems, liver problems
RISK BENEFIT ANALYSIS
Clozapine, RFs for myocarditis
At least 6 weeks of 300mg CPZ equivalent,two trials one of SGA, CBT offered
At least 12 month trial to allow for late responders
Risperidone/amisulpride augmentation to cloz for residual pos
Smoking reduces plasma levels up to 50% via inductionof hepatic enzymes particularly CYP1A2
SES: sedation, constipation, hypersalivation, nausea, nocturnal enuresis
Complications:
1. Neutropenia, agranulocytosis (extremely low neutrophils) - 18 weeks
Yellow: WBC <3.5, Neuts <2 - twice weekly FBC until green
Red: WBC <3, Neuts <1.5 - Stop. FBC every 24 hours until green
- Myocarditis: risks: epilim, rapid titration
Trop and CRP weekly for 6 weeks
HR>120 or increase by 30, CRP50-100, Trop <2ULN - daily CRP, trop, ECG - most common sinus tachy, non specific ST and T wave changes, other variable changes - prolonged QRS, QT, TWI
CRP>100, Trop>2ULn - Stop, Echo, cardio - Cardiomyopathy - SOB, fatigue, abdo swelling or ankle oedema - cardio, no specific guidelines - beta, ACE
- metabolic - weight, BMI, BP monthly
6 month metabolic bloods
Cloz levels if poor response, non adherence, concurrent meds e.g. fluvox, changed smoking, hepatic disease. Aim 350-600 trough level, toxicity >1000
Pretx: FBC with neuts 10 days before
Blood group, UEC, fasting glucose and lipids, LFT, CRP, trop, CK, baseline ECho, ECG. Given verbal and written info
Retitration - 48-72 hours - half of dose in two divided doses, then 75% day 2, normal day 3
72 hours -1 week - 12.5 or 25 then increase over >3 days
>1 week - normal titration 12.5 or 25, 25 or 50, increase by 25-50 daily until 300 by week 3. 50-100 every 3-7 days
Abrupt cessation - benztropine can help with cholinergic rebound symptoms - agitation, malaise, insomnia, nausea, diarrhea
Lithium - precautions, SES. levels. toxicity
Li - anti manic 6-10 days
antidepressant effect 6-8 weeks
Precautions -
1. Hyponatremia - increases risk of toxicity . Avoid in vomiting, diarrhea, diuretic use, Addison’s dehydration
2. Hypothyroidism
3. Hyperparathyroidism
4. Psoriasis
5. Renal impairment
6. Elderly - age related renal fn decline, more sensitive to toxicity and more comorbidities
7. Pregnancy - avoid in first trimester. clearance increases in second half of pregnancy - dose adjustments. mothersafe. check level more often. in breastfeeding - a relative but not absolute contraindication
8. Severe cardiac disease
SES
1. Most common - initial GI discomfort - nausea and diarrhea, vertigo, muscle weakness - disappear after stabilisation
2. Persistent - fine tremor, fatigue, thirst, polyuria, wt gain
3. Nephrogenic diabetes insipidus with polydipsia and polyuria - affects about 10% of pts treated for >15 years. Can cause dehydration, Li toxicity, renal fn decline - refer to renal. ESRD of 2-7% for >15 years
Some evidence once daily lithium less likely for renal damage
Li level 5-7 days after each dose change, then every 3-6 months. Within 2 weeks of a dose increase
0.6-1 for mania or 0.6-0.8 for elderly. considerable interpatient variability for maintenance, for most 0.6-0.8 some 0.4-0.6, others 0.8-1.0, elderly 0.4-0.8
TFT , Ca, PTH yearly
Li toxicity >1.5 and potentially >1.2(1.2 elderly) - GI symptoms, rarely major problems
CNS effects such as coma and seizures with chronic poisoning
QT prolongation
Mild toxicity sx: blurred vision, nausea, diarrhea, vomiting, muscle weakness, drowsiness, apathy, ataxia, flu like
severe: increased muscle tone, hyperreflexia, myoclonic jerks, coarse tremor, dysarthria, disorientation, psychosis, seizures and coma
counselling about N+V , extreme thirst, polyuria
Beware NSAIDS, diuretics, ACE
Ethical issues in pt wanting to stop depot
- Autonomy
-pt’s insight
-pt’s attitude to treatment
-does pt consent to CTO, capacity to consent
-power of attorney for medical decision making - Benefience
-is CTO best interest of the pt (justification) - Non mal
-CTO can have a negative impact on therapeutic alliance
-may undermine the autonomy of the pt (recovery model)
-pt can still relapse
Confidentiality and privacy
-family members involvement is important in tx
-autonomy and MHA takes precedence over family wishes
-family wishes are conveyed to tribunal
Justification for CTO
-Treatable mental illness that has to be treated i.e. scz/SAD
-Medication and tx proposed is in best interest of patient as reduces risk of relapse and treats symptoms
-Refusal to take medication, which is likely to help improve sx and reduce the risk of relapse
-Previous treatment in hospital has not been sufficiently effective to lead to remission or improvement
-Discharge from hospital has resulted in relapse
-Patient understands role of CTO and accepts
-Least restrictive option
-Lack of insight and is non adherent - current or past
-Previous risk when unwell
-Lacks capacity to make decision with refusal to take treatment
-Illness significantly impacts on functioning, accommodation, employment, relationships
Evidence for CTOs
A legal framework where there is stipulation to take meds, attend appts to enhance compliance of medications to treat mental illness and to prevent risk of harm to self and others and to help recovery
Evidence:
-best interests (benefience)
-least restrictive option to avoid hospital admission
-evidence suggests they can improve under a CTO which reduces risk of relapse and improve pt outcomes
-clinical studies have shown benefits. patients or families may choose/prefer CTO
Evidence against:
-against recovery principles as it may be considered as a violation of human rights
-may undermine the autonomy, a key tenet of recovery model
-can disrupt therapeutic alliance, which is associated with outcomes
-despite CTO, patients may relapse
-increases health service use and higher resource allocation
-negative and conflicting results as independent RCT shown no benefits
Pt wants to stop cloz - what info needed
-Current clozapine level (350-600 ng/ml) -may be elevated due to a range of interactions, smoking habits or recently stopped(reduces levels), caffeine habits (increases), other meds such as cipro or erthyro or fluvoxamine which may increase levels (CYP1A2 inhibitor)
Past psych hx
-past history of MI
-nature of illness
-severity of illness
-risks when unwell
-compliance
Previous side effects and how managed?
New or previously complained?
Past insight and compliance
Organic cause of SEs
Current MSE
-delusions or hallucinations leading to sleep or agitation
-depression causing tireness and fatigue, memory issues
-cannabis use (amotivational syndrome)
How to have safe transition from cloz to another APT
Strong antihistamingeric antagonism and anticholinergic properies
Sudden cessation can cause antih and antich rebound that presents with severe rebound insomnia, r affective symptoms and r psychosis (with physical and autonomic sx that resemble NMS) +/- anticholinergic delirium.
Risk benefit analysis
-risk of stopping: evidence based in treatment resistant scz. Olanzapine may be appropriate according to evidence (and has antihistaminergic and anticholinergic to reduce rebound but similar SES) but newer metabolically friendly antipsychotics may be considered however these have less evidence in TR (ad brex/lur lack antich and antih and this risk of relapse). Cloz should be reduced whilst pt is stabilised on adequate dose of a non antihistaminergic antipsychotic
-or augment with dopamine agonist with lower dose of cloz
-inpt admission to prevent risk of relapse OR assertive outreach approach
-psychoed about risks and benefits, early relapse signs
-involvement of family to detect early relapse signs
Stopped very slowly over 6 weeks. Or 3-6 mths for high risk pts. Even slowing tapering due to hyperbolic curve at lower doses
Withdrawal and discontinuation syndromes from stopping an antipsychotic
How to do it
Sx mainly due to dopaminergic, antihistaminergic and anticholinergic rebound
Olanz/quet/cloz have strong antic and antih - discontinuation may lead to rebound insomnia, affective sx and psychotic sx with relapse of illness
Reduction should be done in graded manner. Switching tool such as NPS switching tool
If switching to antihistaminergic antipsychotic, can do direct cross titration as this reduces risk of antih and antic rebound
Close monitoring should be in place when considering changeover. Appropriate choice of APT should be considered when transitioned
Cholinergic W sx - agitation, insomnia, anxiety, depression
dizziness, lightheadedness, tachy
nausea, vomiting
confusion, disorientation
tremor, restlessness
hallucinations
rigidity, hypothermia sweating
Dopaminergic
-Nigrostriatal: withdrawal dyskinesia, parkinsonism, NMS, akathisia, dystonia
-Mesolimbic: AHs, delusions, catatonia, other psychotic sx
Histaminergic
-Irritability, insomnia, agitation
-Depressed affect
-Loss of appetite and nausea
-Tremulousness/incoordination
Serotonin Withdrawal Symptoms
-Flu like sx
-Dizziness, lightheadedness or tachy
-Paresthesia
-Sweating or chills
-anxiety, agitation
-N+V
-confusion
Adrenergic
-headache, anxiety, agitation
-HTN, tachycardia
-angina, palpitations,
-sweating, tremulousness
Causes of pseudoresistance
- Extra Pyramidal Side Effects (EPSE)
- Non-compliance with medications
- Drug misuse
- Pharmacokinetic effects – Fluvoxamine, smoking:
* The prevalence of smoking in patients with schizophrenia is 71% in males and 44% in
females. Thus, tobacco smokers have a lower serum concentration of haloperidol,
olanzapine and clozapine, especially clozapine, as it is metabolised by CYP1A2.
Caffeine also affects levels by inducing the same enzyme.
* Rifampicin, carbamazepine and phenytoin – CYP3A4 metabolises quetiapine,
aripiprazole and risperidone and to a lesser extent ziprasidone
* Also relevant is a predisposition for rapid metabolism occurring in those with
CYP2D6 and most South Europeans, Saudi Arabians and Ethiopians have this.
Tx of Negative sx
Pharmacological – newer antipsychotics
* Glycine – mixed results
* D-Cycloserine
* Fluvoxamine
* Mirtazapine
Psychosocial therapies
* Psychoeducation – group and family
* Social skills training
* Cognitive Behavioural Therapy
* Cognitive remediation
* Group family therapy
Mx of pseudoparkinsonism, rfs
- Pseudoparkinsonism is characterised by tremor, bradykinesia, rigidity, bradyphrenia (thought slowing)
- Differentiated from Parkinson’s disease by presence of bilateral tremor and rigidity
- Pseudoparkinsonism can be assessed by the Simpson-Angus rating scale
- Risk factors for Pseudoparkinsonism include being an elderly female, and pre-existing
neurological impairment - Management includes reduction of dose, change to atypical if on typical and prescribe
anticholinergic (e.g. Benztropine)
Akathisia mx
- Measured by Barnes Akathisia Scale
- Increases suicide risk
- Management in following order:
Reduce dose
Change to atypical if on typical
Benztropine may help if other Parkinsonian symptoms present
Propranolol
Cyprohepatadine
Benzodiazepine
Clonidine
TD mx, rfs
- Lip smacking, tongue protrusion, choreiform hand movements, pelvic thrusting
- Measured by AIMS
- Risk factors include diabetes, typical antipsychotics, organic neurological impairment,
female, diabetes, smoking - Management in following order
Stop anticholinergic
Reduce dose of antipsychotic
Change to atypical drug if on typical
If untreated, Clozapine
Other strategies include:
Tetrabenazine – depressogenic, useful in Huntington’s
Benzodiazepine
Vitamin E
