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PR3136 PT IV > Schizophrenia NBT > Flashcards

Schizophrenia NBT Flashcards

1
Q

what is the definition of psychosis?

A
  • acute and severe mental condition

- lack of insight; out of touch with reality

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2
Q

how is schizophrenia different from psychosis?

A

schizophrenia: more common forms of psychosis
- disorganised and bizzare thoughts, delusions, hallucinations, impaired psychosocial functioning
- higher incidence of comorbid conditions including HTN, DM, cardiac conditions, substance abuse disorders
- mortality higher
- onset: commonly adolescence or early adulthood

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3
Q

what are the different diagnoses/disorders with associated psychotic sx?

A
  1. organic disorders
    - Iatrogenic causes (drug related causes e.g. levodopa/dopamine agonist)
    - Psychosis related to alcohol & psychoactive substance misuse (e.g. methamphetamine or other CNS stimulants or alcohol/cocaine withdrawal)
    - epilepsy
    - cerebral lesions (tumors, stroke, trauma)
    - CNS infections; genetic/congenital
    - parkinson’s disease
    - dementia
    - any metabolic disorders affecting nervous system
    - endocrine disorders
  2. affective disorders presenting with psychotic smx: mania, psychotic depression, post-partum psychosis
  3. Schizophrenia itself
    - psychosis due to psychological development disorders or stress-related reactions
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4
Q

which neurotransmitters are dysregulated which can cause schizophrenia?

A
  • dopaminergic (DA)
  • serotonergic (5ht)
  • glutamatergic function
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5
Q

what are the etiology factors of schizophrenia?

A
  1. predisposing (factors from early life determining a person’s vulnerability to precipitating factors)
    - genetics (possible linkage)
    - neurodevelopmental effects
  2. precipitating (events that occur shortly before onset of disorder)
    - Drugs = alcohol, BZDs, barbiturates, dopamine agonist (levodopa)
    - CNS injury
  3. Perpetuating (factors that prolong course of disorder)
    - lack of support
    - poor adherence with antipsychotic medications

Most common reason admitted into hospital = substance/withdrawal, non-compliance)

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6
Q

what is the clinical presentation of schizophrenia based on the DSM-5 criteria (no need to memorise)

A
  1. two or more of the following, where each for at least a 1-month period:
    a. delusions
    b. hallucinations
    c. disorganised speech
    d. grossly disorganised or catatonic behaviour
    e. negative symptoms (affective flattening - zero expression on face; avolition - loss of motivation = can affect compliance)
  2. social/occupational dysfunction
  3. duration
    - continuous signs of the disorder for at least 6 months (inclusive of the 1 month sx in (1))
  4. schizoaffective or mood disorder has been excluded
  5. disorder NOT due to medical disorder or substance use
  6. if have pervasive development disorder, must have sx of hallucinations or delusions present for at least 1 mth
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7
Q

how to we diagnose/assess schizophrenia?

A
  1. Hx of present illness
  2. psychiatric Hx: any hx of neurosis or psychosis
  3. substance use hx: past use of cigarettes/ETOH/substances
  4. complete medical hx & medication hx
    - other med used
    - reassess adherence to med every visit
  5. family, social, developmental, occupational hx
    - esp 1st-degree family hx (as med they were taking could work for the pt)
  6. physical & neurological exam
  7. mental state exam (mse) [for accurate diagnosis]
    - assess for suicidal/homicidal ideations and risk
    - reassess MSE on every interview to evaluate efficacy & tolerability
  8. labs & other investigations
    - to exclude general medical conditions or substance-induced sx (e.g. depression, mania, anxiety, insomia, psychosis)
    - if patient have hx of unprotected sex: neurosyphilis (CNS infection) = check for WBC
    - fasting blood glucose for the 2nd gen anti-psy
    - urine toxicology for any substances
    - ensure electrolytes are balanced
    - ensure kidney is functioning
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8
Q

what is the non-pharmacological treatment?

A
  1. individual cognitive behavioural therapy (CBT)
    - in conjunct with med
    - can prevent psychosis in ‘at risk’ groups
    - …

2, electroconvulsive therapy (ECT)
- reserved for treatment-resistant schizophrenia

  1. repetitive transcranial magnetic stimulation (rTMS)
    - effective for reducing auditory hallucinations in schizophrenia
  2. Psychosocial rehabilitation
    - improve patient’s adaptive functioning
    - e.g. vocational: employment
    - CBT included
    - supportive/ counselling
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9
Q

what are the therapeutic goals of schizophrenia?

A
  1. acute stabilisation
    - minimise threat to self and others
    - minimise acute symptoms
  2. stabilisation
    - prevent relapse
    - promote medication adherence
    - optimize dose vs adverse effect
  3. Stable/maintenance phase
    - improve functioning and QOL
    - monitor for adverse effect (e.g. tardive dyskinesia)
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10
Q

why is maintaining antipsychotic treatment important?

A
  • reduces risk of relapse in stable illness to <30% per year
  • if w/o maintenance therapy:
  • -> 60-70% patients relapse within 1 yr
  • -> 90% patients relapse within 2 yrs
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11
Q

what are key things to take note for pharmacological treatment of schizophrenia?

A
  1. antipsychotic med = aka neuroleptic
    - tranquilizes w/o impairing consciousness and w/o paradoxical excitement
  2. short term: calm disturbed patients
  3. commonly used for schizophrenia (can be used for acute mania, agitated depression, toxic delirium)
  4. antipsychotics relieve symptoms of psychosis such as thought disorder, hallucinations and delusions, and prevent relapse
  5. long term treatment often necessary after first episode of psychosis and prevent illness from becoming chronic
    1. relapse often delayed for several weeks after cessation of treatment
  • -> adipose tissue are depot reservoir after chronic regular usage of antipsychotic
    1. Method to overcome poor treatment adherence:
      a. IM long-acting injections
      b. community psychiatric nurse (to adminster pills for them)
      c. patient and family (caregiver) education (to monitor them)
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12
Q

what is the MOA of antipsychotics?

A
  1. Mesolimbic tract
    - blockade of dopamine receptors the most common MOA for all antipsychotics
    - as overactivity in this region is responsible for positive symptoms of schizophrenia
  2. Mesocortical tract (MC) tract
    - responsible for higher-order thinking and executive functions
    - dopamine blockade/ hypofunction here results in negative symptoms
  3. Nigrostriatal (NS) tract:
    - modulates body movement
    - dopamine blockade here causes EPSE
  4. Tuberinfundibular (TI) tract
    - dopamine blockade of the anterior pituitary leads to hyperprolactinemia
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13
Q

which tract when blocked reduces the positive symptoms of schizophrenia?

A

Mesolimbic tract

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14
Q

which tract when blocked reduces the negative symptoms of schizophrenia?

A

Mesocortical tract

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15
Q

which tract when blocked reduces the extrapyramidal SE?

A

Nigrostriatal tract

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16
Q

which tract when blocked reduces gynecomastia, osteoporosis, sexual dysfunction, hyperprolactinemia?

A

Tuberoinfundibular tract

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17
Q

which receptor when antagonises improves the positive symptoms of schizophrenia?

A

D2 receptor antagonism

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18
Q

what are the side effects of D2 antagonism

A

D2 antagonism: EPSE, hyperprolactinemia

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19
Q

what is the therapeutic effect of 5-HT1A agonism?

A

anxiolytic

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20
Q

which receptor when antagonises improves the negative symptoms of schizophrenia?

A

5-HT2A

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21
Q

which drugs have more of the 5-HT2A antagonism?

A

the SGA (2nd gen anti-psy): aripiprazole, clozapine, risperidone

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22
Q

what SE does H1 antagonism cause?

A

sedation/weight gain

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23
Q

what SE does a1 antagonism cause

A

orthostasis (postural hypotension), sedation

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24
Q

what SE does 5-HT2C antagonism causes?

A

weight gain

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25
Q

what SE does M1 antagonism causes?

A

memory dysfunction, peripheral anticholinergic effects

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26
Q

what does IKr antagonism causes?

IKr = rapid delayed rectifier

A

QTc interval prolongation (pro-arrhythmic)

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27
Q

what is the hypothetical threshold for the anti-psychotic drug effects (D2 receptor blockade)

A

at 60% D2 receptor blockade: anti-psychotic effect threshold

at 70%: prolactin threshold

at 80%: EPS threshold

anti-psy that have weaker affinity can reach the anti-psy effect threshold vs high affinity anti-psy like haloperidol can reach the EPS threshold
–> thus v hard to know where is the threshold

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28
Q

what is the algorithm for schizophrenia treatment?

A

After diagnosis of schizophrenia:

  1. use single FGA or SGA (except clozapine)

if inadequate or no response/intolerable SE
2. use another single FGA or SGA (except clozapine) that was not prev tried

if still inadequate or no response/intolerable SE

  1. Clozapine = for treatment-resistant schizophrenia
    - -> 1% of granulocytosis –> death –> thus need to monitor full blood count
  2. Clozapine + (FGA or SGA or electroconvulsive therapy [ECT]) or
  3. (FGA + FGA or SGA + SGA) + either ECT or other agent (e.g. mood stabiliser)
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29
Q

how is the initial anti-psy med chosen for the patient?

A
  • individualised based on past response/failures on antipsychotics, efficacy and SE profiles of the therapy
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30
Q

what do we need to do to ensure that the antipsychotic drug used is working before changing it to another drug?

A

1- patient need to be compliant to the antipsychotic (except clozapine) for at least 2-6 weeks at optimal therapeutic doses before being considered as non-responder

2- if on clozapine: 3 months to confirm therapeutic response

3- if on clozapine + another anti-psy: 8-10 weeks required to confirm therapeutic response

4- manage any intolerable SE accordingly or switch to more suitable alternatives

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31
Q

IMPORTANT What dosage form should we consider when a patient is not completely compliant to the drug?

A

consider long-acting injectable antipsychotic if inadequately compliant, or if patient prefers (e.g. cannot swallow)

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32
Q

what are the long-acting IM anti-psychotics?

A 
All IM:
SGA
1. Risperidone microspheres
2. Paliperidone prolong release suspension
3. Aripiprazole LAI

FGA

  1. Haloperidol decanote
  2. Flupenthixol Decanoate
  3. Zuclopenthixol decanote
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33
Q

When can we consider giving clozapine as an anti-psy

A

only to those who are treatment-resistant

def: those who had failed >= 2 adequate trials of different antipsychotics (at least 1 should be a SGA)

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34
Q

what has to be monitored when a patient is on clozapine?

A

routine haematological monitoring
in sg: weekly for first 18 weeks, then monthly
monitor for WBC and ANC - leucopenia/agranulocytosis

(a treatment-refractory evaluation should be performed to reexamine diagnosis, substance abuse, medication adherence, and psychosocial stressors. CBT or psychosocial augmentation should be considered)

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35
Q

Which conditions we have to be pre-cautious about before the start of antipsychotic use?

A
  1. CV disease
    - CI: those with QTc prolongation
    - ECG required in those with CV risk factors, personal hx of CV disease, or patient is being admitted as inpatient
  2. Parkinson’s disease –> the EPS worsens by antipsychotic (can consider quetiapine as it is less likely to cause adverse drug-induced parkinsonism)
  3. Epilepsy & conditions predisposing to seizures
  4. depression
  5. myasthenia gravis
  6. prostatic hypertrophy
  7. angle-closure glaucoma
  8. severe resp disease
  9. Hx of jaundice
  10. Blood dyscrasias (blood disease) - esp for Clozapine
  11. Elderly with dementia - increased risk for mortality and stroke (black box warning)
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36
Q

in which patient antipsychotic use is a black box warning and needs to be documented with the family member?

A

elderly with dementia

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37
Q

what is the preferred drug for acute agitation (psychiatric emergency)?

A 
1. if patient is cooperative:
consider *oral* medication:
(a) oral **lorazepam** 1-2mg or
(b) oral antipsychotic:
- Haloperidol
- **Risperidone**
- Quetiapine
- Olanzapine
or
(c) oral-inhaled loxapine (CI in asthma/COPD)

(lorazepam or risperidone commonly used)

  1. if patient uncooperative and remains agitated/aggressive:
    consider fast-acting IM injection
    (a) IM Lorazepam 1-2mg or
    (b) IM Olanzapine (not to be given with IM Lorazempam within 1h of each other)
    (c) IM Aripiprazole (less hypotensive than IM Olanzapine)
    (d) IM Haloperidol
    (e) IM Promethazine
    (f) (a) + (d)
    (g) (d) + (e)
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38
Q

what drug can be given for catatonia?

(a group of symptoms that usually involve a lack of movement and communication, and also can include agitation, confusion, and restlessness. )

A

BZD: po/IM Lorazepam

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39
Q

what can be given for depressive sx and/or negative sx of chronic schizophrenia?

A

for depression: suitable antidepressant

for negative sx: some SSRIs have mild-moderate efficacy

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40
Q

which anti-psychotic drugs are to be taken with food?

A
  • Lurasidone & Ziprasidone
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41
Q

which anti-psychotics are CYP3A4 metabolised?

A

FGA:
Chlorpromazine, Haloperidol,

SGA:
Aripiprazole, Brexpiprazole, Clozapine, Cariprazine, Olanzapine, Quetiapine, Lurasidone, Ziprasidone

NOT: risperidone, paliperidone

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42
Q

what are the FGA?

A

Chlorpromazine, Haloperidol, sulpride, trifluoperazine

(Note haloperidol v potent and dosed BD or TDS compared to most anti-psy which is OD)
(0.5-3mg BD/TDS, total dose/day is 5-15mg)

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43
Q

what are the SGA?

A
  1. Amisulpride
  2. Aripiprazole
  3. Brexpiprazole
  4. Cariprazine
  5. Clozapine (max dose 900mg/day v high)
  6. Lurasidone (w food)
  7. Olanzapine (5-20mg/day)
  8. Paliperidone
  9. Quetiapine (max dose 800mg/day vhigh)
  10. Risperidone (2-6mg/day)
  11. Ziprasidone (w food)
  12. Asenapine
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44
Q

what are the FGA IM long-acting antipsychotics

A
  1. Flupenthixol decanoate
  2. Haloperidol decanoate –> can cause high EPSE
  3. Zuclopenthixol decanoate

not that impt (grey):
Fluphenazine decanoate

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45
Q

what are the SGA IM long-acting antipsychotics?

A
  1. risperidone (every 2 weeks) (supplement with oral dose during 1st 3 weeks)
  2. Paliperidone PR suspension for injection (every 4 weeks or every 3 months)
  3. Aripiprazole ER suspension (every 4 weeks/ every month)
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46
Q

FGA have more of what side effects than SGA?

A

EPSE and increase prolactin

due to D2 block

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47
Q

Which SGA have weight gain as the most important SE?

A

Clozapine, Olanzapine

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48
Q

which SGA dont have the weight gain SE

A
  1. Lurasidone
  2. Ziprasidone
  3. Aripiprazole
  4. Brexipiprazole
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49
Q

how do we manage the EPSE (dystonia) SE?

A
  • Dystonia: muscle spasms, stiffness
  • caused by high-potent antipsy (e.g. haloperidol), neuroleptic-naive patients, young M
  • thus, use IM anticholinergics (e.g. benztropine, diphenhydramine)
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50
Q

how do we manage the EPSE (Pseudo-parkinsonism) SE?

A
  • pseudo-parkinsonism: tremors, rigidity, bradykinesia
  • seen in elderly F, w prev neurological damage (head injury, stroke)
  • thus, reduce antipsychotic dose (not v practical) or switch to SGA
  • anticholinergics PRN (e.g. trihexyphenidyl (benzhexol), benztropine
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51
Q

how do we manage the EPSE (Akathisia) SE?

A

Akathisia - restlessness

  • due to high potency antipsychotics (e.g. haloperidol) > Risp > Olan > Quetiapine/Clozapine
  • management:
  • -> reduce antipsy dose or switch to SGA
  • -> clonazepam (low dose) PRN
  • -> propranolol
  • -> anticholinergics NOT helpful
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52
Q

how do we manage the EPSE (tardive dyskinesia) SE?

A
  • irreversible, lip chewing, tongue protrusion
  • due to:
  • -> FGA > SGA
  • -> worsen with anticholinergic drugs
  • solution:
  • -> discontinue any anticholinergics
  • -> decrease antipsychotic dose, or switch to SGA (clozapine possibly effective)
  • -> Valbenazine 40-80mg/day (reversible VMAT2 inhibitor)
  • -> Clonazepam PRN
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53
Q

how do we manage the hyperprolactinemia SE?

A
  • gynecomstia in Male, lactation

risk:

  • FGAs, and
  • Paliperidone > Risperidone > other SGAs

solution:

  • decrease FGA dose
  • dopamine agonist (amantadine, bromocriptine)
  • switch to aripiprazole
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54
Q

how do we manage the metabolic SE?

A
  • weight gain, diabetes, increase lipids

risk:
- high: Olanzapine. Clozapine

  • moderate: chlorpromazine, quetiapine, risperidone
  • low: Aripiprazole, Haloperidol, Lurasidone, Ziprasidone

solution:

  • lifestyle modification: diet, exercise
  • treat DM (e.g. w metformin), hyperlipidemia
  • *switch to lower risk agents = ari, lura, zip, halo
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55
Q

what are the cardiovascular side effects of antipsychotics?

A
  • orthostatic hypotension
  • QTc prolongation
  • VTE/PE
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56
Q

how does the CV SE of orthostatic hypotension occur? which drugs are higher risk?

A
  • chlorpromazine, clozapine > Risperidone, Paliperidone, Quetiapine > Olanzapine, Ziprasidone, Aripiprazole, Sulpride
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57
Q

how can we manage orthostatic hypotension?

A
  • switch to lower risk agents

- get up slowly from sitting or lying position

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58
Q

which drugs have a higher risk to cause QTc prolongation

A

Thio > chlorpromazine > Zip > Halo > iloperidone (llo) > Quet > Risp > Olanzapine

  • high doses, IV haloperidol, decreased K+, IHD
59
Q

how can we manage QTc prolongation?

A

if QTc > 440ms (for M) and >470ms (for F): switch to lower risk agents, refer cardio if >500ms

60
Q

which drugs increase the risk of VTE/PE?

A

Low potency > SGA > FGA > high potency, Aripiprazole

61
Q

how can we manage VTE/PE

A

manage emergent DVT

62
Q

what are the CNS SE of antipsychotics?

A
  • sedation
  • seizure
  • neuroleptic malignant syndrome (NMS)
  • psychogenic polydipsia
  • temperature dysregulation
63
Q

which drugs have a higher risk of causing sedation?

A

chlorpromazine, cloz > quet > olan > risp, pali, zip, ari

64
Q

how to manage the sedation SE?

A

switch to a lower risk agents

65
Q

which drugs have a higher risk of causing seizure?

A
  • cloz, chlorpromazine > other SGAs

- high doses, rapid titration, Hx of epilepsy

66
Q

how to manage the seizure SE?

A
  • switch to high-potency agents (e.g. halopiderol)
67
Q

what is neuroleptic malignant syndrome (NMS) and which drugs have a higher risk of causing NMS?

A
  • muscle rigidity, fever, autonomic dysfunction (increase PR, labile BP, diaphoresis = sweating), altered consciousness, increase creatinine kinase (CK)
  • lead-pipe rigidity, fever, high CK
  • high-potency antipsychotics
  • rare, but potentially lethal
  • onset: hours to 3 days (within 30 days)
68
Q

how do we manage neuroleptic malignant syndrome (NMS)?

A
  • IV Dantrolene 50mg TDS
  • oral dopamine agonist (e.g. amantadine, bromocriptine), supportive measures
  • switch to SGA, low dose, least potent
69
Q

which drugs increases the risk of psychogenic polydipsia

A
  • def: increase intake of water

- anticholinergics causes it

70
Q

what can be the management of psychogenic polydipsia?

A
  • fluid restriction, discontinue drugs w anticholinergic properties
71
Q

which drugs increase the risk of temperature dysregulation?

A
  • anticholinergics
72
Q

what can be the management of temperature dysregulation

A
  • hydration. appropriate clothing/shade
73
Q

what is the hepatic SE of antipsychotics?

A

increase LFTs (usually benign), cholestatic jaundice

74
Q

which drugs can cause increase LFTs?

A
  • chlorpromazine, olan, quet > other SGAs
75
Q

what is the management of increase LFT?

A

if jaundice develops, discontinue antipsychotics

76
Q

what ophthalmologic SE can be caused by antipsychotics?

A

cornea/lens changes, pigmentary retinopathy

77
Q

which drugs increase the risk of cornea/lens changes, pigmentary retinopathy?

A

Phenothiazines (chlorpromazine, thio), Quet

78
Q

what is the management for the ophthalmologic SE?

A

if on Quet, eye exam q6 months

79
Q

what dermatological SE can be caused by antipsychotics?

A

maculopapular rash, photosensitivity, pigmentation

80
Q

which drugs increase the risk of the dermatological SE?

A

Phenothiazines (chlorpromazine)

81
Q

what is the management of the dermatological SE?

A

protective clothing, sunscreens

- consider switch to other antipsychotics

82
Q

IMPORTANT what is the hematological SE of using antipsychotics

A
  • decrease WBC

- Agranulocytosis –> decrease absolute neutrophil count

83
Q

which drug can cause the hematological SE?

A
  • CLOZAPINE
84
Q

what is the management for the hematological SE?

A
  • discontinue antipsychotic if severe: WBC < 3x10^9/L or ANC <1.5x10^9/L

ANC = absolute neutrophil count

85
Q

when do we monitor BMI in patients taking antipsychotics?

A
  • if the concerned SE is weight gain
  • weekly for 1st six weeks or every visit (at least monthly x 3 months for SGA) x 6 months
  • q3 months when dose stabilised
86
Q

when do we monitor waist circumference in patients taking antipsychotics?

A
  • when the concerned SE is obesity

- every visit x 6 mths, then annually

87
Q

when do we monitor for fasting blood sugar in patients taking antipsychotics?

A
  • when the concerned SE is diabetes mellitus
  • for low-risk patients: annually
  • for high-risk patients: 4 mths after initiating new antipsychotic (or 3 months after initiating SGA), then annually
88
Q

when do we monitor for lipid panel in patients taking antipsychotics?

A
  • when concerned SE is hyperlipidemia
  • low risk patients: q2-5 yrs
  • high risk patient: (3 months after initiating SGA), q6mths
89
Q

when do we monitor for plasma prolactin in patients taking antipsychotics?

A
  • when concerned SE is hyperprolactinemia

- monitor at baseline

90
Q

when do we monitor for blood pressure in patients taking antipsychotics?

A
  • when concerned SE is increase or decrease BP

- monitor q3 months after initiating SGA, then annually

91
Q

when do we do a EPSE exam for rigidity, tremors, akathisia, tardive dyskinesia in patients taking antipsychotics?

A

when EPSE is a concerned SE

  • weekly for 1st 2 weeks after initiation new antipsychotic or until dose stabilised
  • low risk patients: FGA q6mths, SGA q12mths
  • high-risk patients: FGA q3mths, SGA q12mths
92
Q

when do we monitor for WBC and ANC (absolute neutrophil count) in patients taking antipsychotics?

A
  • when CLOZAPINE is taken and
    leucopenia/agranulocytosis is a concerned SE
  • in SG: weekly for first 18 weeks, then monthly
93
Q

when do we monitor for ECG in patients taking antipsychotics?

A
  • when patient taking Ziprasidone and QTc prolongation is a concerned SE
  • repeat ECG if symptoms of QTc prolongation (e.g. syncope)
94
Q

most SGA need to monitor for _ mths

A

3mths for BMI, and lipid panel, then followed by q6 mths

3mths for fasting blood sugar, lipid, blood pressure, then annually

q12mths for EPSE

95
Q

in pregnancy, which drugs are of concern?

A
  • olanzapine, clozapine, to watch for gestational diabetes
96
Q

what drugs are suitable in breastfeeding

A
  • olanzapine or quetiapine
97
Q

what drugs is not suitable in breastfeeding?

A
  • clozapine should be continued and not breastfeed
98
Q

which drug is preferred in renal impaired patients?

A

PO Aripiprazole

99
Q

which drugs to avoid in renal impaired patients?

A
  • avoid sulpride and amisulpride
100
Q

which drugs are preferred in hepatic impaired patients

A
  • sulpride and amisulpride
101
Q

what drugs are to be avoided in elderly*

A
  • avoid drugs with high a1-adrenergic blockade (orthostatic hypotension)
    = chlorpromazine, clozapine
  • avoid drugs with anticholinergic SE (constipation, urinary retention, delirium)
    = benztropine, diphenhydramine, benzhexol (aka trihexyphenidyl), other F/SGAs
  • avoid adverse interactions - go for simple regime
  • avoid long T1/2 drugs
  • start low go slow
102
Q

what is the dosing for elderly?

A
  • start low go slow

- simplify regime

103
Q

what is the precaution for elderly with dementia?

A

FGA/SGAs reported to increase mortality and CVAs

104
Q

what are the PD drug interactions that are of concern?

A

– increase CNS depression by combining 2 CNS depressants; increase risks of seizures by combining drugs that lower seizure thresholds

  • additive effect = agonistic + agonistic effect

2 drugs affect same organ system but by different mechanisms:
- synergistic = potentiation

  • antagonism: 2 drugs reduce each other’s effect
105
Q

what drug-disease interaction is of concern

A

antipsychotics worsen Parkinson’s disease sx

106
Q

Drugs with CNS depressant effects + antipsychotics causes

A
  • Additive CNS effects

e. g. BZDs and Clozapine –> reduce RR and BP

107
Q

drugs with CNS depressant effects?

A
  • alcohol, opioids, other psychotropics
108
Q

drugs with antimuscarinic, anti-H1, a1 blockade or dopamine blockade + antipsychotic

A
  • additive adverse effect
109
Q

dopamine-augmenting agents (e.g. levodopa, bromocriptine) + antipsychotic

A

mutual antagonism with antipsychotic

110
Q

antihypertensives/trazodone + antipsychotics

A

increases hypotensive effects

111
Q

CYP1A2 inducers (rifampicin, phenobarbitone, phenytoin, cigarette smoking) + antipsychotic

A

decreases phenothiazines (CPZ), Halo, Cloz, Olan, Zip

112
Q

CYP 1A2 inhibitors (fluvoxamine, quinolones, macrolides (except azithromycin), isoniazid, ketoconazole) + antipsychotics

A

increases phenothiazines (CPZ), Halo, Cloz, Olan, Zip

113
Q

carbamazepine + clozapine

A

agranulocytosis

114
Q

what are the CYP1A2 inducers

A

rifampicin, phenobarbitone, phenytoin, cigarette smoking

115
Q

what are the CYP1A2 inhibitors

A

fluvoxamine, quinolones, macrolides (except azithromycin), isoniazid, ketoconazole

116
Q

what are the CYP2D6 inducers?

A
  • rifampicin, phenobarbitone, phenytoin, carbamazepine
117
Q

what happens when CYP2D6 inducers + antipsychotics

A

decreases phenothiazines (chlorpromazine), halo, risp, ari, Olan, Zuclopenthixol

118
Q

what are the CYP2D6 inhibitors?

A

fluoxetine, paroxetine, duloxetine

119
Q

what happens when CYP2D6 inhibitors + antipsyhotics

A

increases phenothiazines (chlorpromazine), halo, risp, ari, Olan, Zuclopenthixol

120
Q

what are the CYP3A4 inducers?

A
  • barbiturates, carbamazepine, phenytoin
121
Q

what happens when CYP3A4 inducers + antipsychotics

A

decreases Quet, Zip, Ari, Risp

122
Q

what are the CYP3A4 inhibitors

A

fluvoxamine, norfluoxetine, TCAs, imidazoles, isoniazid, macrolides

123
Q

what happens when CYP3A4 inhibitors + antipsychotics

A

increases Quet, Zip, Ari, Risp

124
Q

what happen when 5-HT augmenting agents are added with antipsychotics

A

may antagonise 5-HT2a receptor blockade –> decrease dopamine release and worsening EPSEs

125
Q

how do we monitor for effectiveness of therapy?

A

Mental Status exam (MSE)

psychiatric rating scales

  • 4-item positive sx rating scale (PSRS) and brief negative symptom assessment (BNSA)
  • easy to administer, 15min
126
Q

what do we monitor in terms of adverse effects?

A
  • metabolic parameters: fasting plasma glucose, lipids, body weight, BP
  • EPSE
  • -> drug-induced pseudo parkinsonism: simpson-angus rating scales
  • -> akathisia: Barnes akathisia scale
  • -> tardive dyskinesia: AIMS, DISCUS
127
Q

what is the time course of treatment response

A
  1. early improvements
    - 1st week –> reduced agitation, aggression, hostility
    - 2-4 weeks –> decrease paranoia, hallucinations
  2. late improvements
    - 6-12 weeks –> decrease delusions, negative sxs may improve
    - 3-6 months –> cognitive sx may improve (with SGAs)
128
Q

SUMMARY

what are the clinical features of schizophrenia

A
  • positive sx, negative sx, functional impairment
  • accurate diagnosis necessary to guide treatment and subsequent monitoring

schizophrenia aka thought disorder

129
Q

SUMMARY

what is the MOA of the antipsychotics (aka thought organisers)

A
  • FGA & SGA
  • D2 antagonism (in mesolimbic dopamine tract) improves +ve sxs
  • SGA only
  • 5HT2A antagonism may improve mood sxs, and possibly also negative sxs
130
Q

SUMMARY

what is the clinical differences between SGA and FGA?

A

for efficacy:
- SGA effective for BOTH positive sx and mood sx

  • FGA effective mainly for positive sx

for toxicity:

  • FGA: more ‘muscle SE’ = EPSE
  • SGA more ‘metabolic SE’ (except aripiprazole, brexpiprazole, lurasidone, ziprasidone)
131
Q

SUMMARY

which SGAs are more sedating, more weight gain?

A

the ‘ines’ = Clozapine, Olanzapine, Quetiapine

vs

‘ones’ or ‘piprazoles’= risperidone, lurasidone, ziprasidone, aripiprazole)
- less sedating, less weight gain

132
Q

SUMMARY

what is the non-pharmacological management for schizophrenia?

A

supportive counselling, social skills therapies, rehab, vocational training

133
Q

SUMMARY

what is the pharmacological treatment like for schizophrenia?

A
  • 1st line: suitable non-clozapine antipsychotic (SGA or FGA) and titrate
  • choose the antipsychotic formulation:
  • -> Oral (immediate release, oral dispersible, oral soln, oral extended release)

–> intramuscular:
- IM rapid acting (e.g. IM Haloperidol or IM Olanzapine)
(for v agitated)

  • IM long acting (e.g. Haloperidol decanoate)
134
Q

SUMMARY

what is the duration for an adequate antipsychotic trial?

A
  • at least 2-6 weeks at recommended therapeutic dosing range

- clozapine trial may require 3 mths

135
Q

SUMMARY

what are the adjunctive treatments for schizophrenia?

A
  • BZDs (for agitation)

- antidepressants (for depression)

136
Q

SUMMARY

what is treatment resistant schizophrenia (TRS)

A
  • not responsive to at least TWO adequate trials of antipsychotics, of which one is a SGA
  • Clozapine is the drug of choice for TRS
  • -> monitor baseline and periodic FBC (full blood count) with ANC (absolute neutrophil count) due to risk of agranulocytosis
137
Q

SUMMARY

What is the acute stabilisation phase?

A
  • goal: reduce agitation, aggression hostility; improve sleep
  • if acutely agitated/aggressive:
    1st: de-escalate
    2nd: consider oral antipsychotic +/- BZD
    3rd: if refuse or not possible to administer oral med –> consider FAST-acting IM alternative w monitoring:
  • -> IM haloperidol 5mg w ECG + IM Lorazepam 2mg
  • monitor for treatment-emergent adverse effects
    e. g. dystonia, pseudo-parkinsonian SE - treat accordingly (oral or IM benztropine 2mg)
  • monitor vitals (BP/HR/RR/oximetry, temp, pain, hydration status)
138
Q

SUMMARY

what is the stabilisation and maintenance phase

A
  • goal: minmise/prevent relapse, maintain baseline functioning
  • monitor and manage adverse effects
  • if poor adherence to oral med, or if pt prefers IM, consider:
  • -> IM long-acting antipsychotic: IM Haloperidol Decanoate
  • -> community psychiatric nurse referral
139
Q

SUMMARY

how do we manage dystonia, tremors/rigidity EPSE?

A
  • anticholinergics (benzotropine/ diphenhydramine/ trihexyphenidyl (benzhexol))
    or
  • switch to lower-potency antipsychotics (e.g. quetiapine, sulpride)
140
Q

SUMMARY

how do we manage akathisia EPSE?

A
  • clonazepam and/or propranolol, or

- switch to a SGA or lower-potency antipsychotic

141
Q

SUMMARY

how do we manage tardive dyskinesia EPSE?

A
  • can be irreversible if detected late in advanced stages
  • discontinue any anticholinergics
  • switch to low potency SGA
  • treat with valbenazine
  • clonazepam PRN
142
Q

SUMMARY

how do we manage the metabolic SE

A

metabolic SE; weight gain, elevated fasting lipids, glucose profiles

  • maintain on current antipsychotics to prevent relapse but treat the emergent diabetes, dyslipidemia with lifestyle and med (e.g. metformin for DM, statins for hyperlipidemia) or
  • switch to aripiprazole, brexpiprazole, lurasidone, ziprasidone, haloperidol
143
Q

SUMMARY

how do we manage the daytime sedation SE?

A
  • administer dose in early evening (e.g. 7pm) for sedation to wear off
  • consolidate to once-nightly dosing whenever possible (EXCEPT for clozapine or quetiapine due to risk of seizures and severe hypotension)
144
Q

SUMMARY

how do we manage dizziness (orthostatic hypotension) SE

A
  • rise up slowly from a lying/sitting position

PR3136 PT IV (17 decks)

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