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PHA333 > Schizophrenia (AS) > Flashcards

Schizophrenia (AS) Flashcards

1
Q

mortality with schizophrenia

A

mortality rate is higher

20% shorter life expectancy

causes of inc mortality:

  • inc suicide
  • inc circulatory conditions, infections, endocrine disorders
  • higher rates of CVD (MI)
  • inc physical health problems (smoking, obesity, diabetes)
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2
Q

2 factors that lead to the aetiology of schizophrenia

A

genetic

environmental

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3
Q

environmental factors that cause schizophrenia

A
  1. biological
    - advanced paternal age (>45yrs)
    - prenatal and perinatal events
    - > maternal infection
    - > maternal malnutrition
    - > pregnancy/birth complications, gestational diabetes, hypoxia, low birth weight, premature birth
    - season of birth
    - cannabis use
  2. psychosocial
    - urban birth/upbringing
    - migration
    - social disadvantage
    - exposure to engative life events
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4
Q

3 models of schizophrenia

A
  1. the dopamine hypothesis
  2. the glutamate hypothesis
  3. neurodevelopmental model
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5
Q

the dopamine hypothesis

A

schizophrenia results from the dysregulation of DAergic system in brain

positive Sx are a result of overactivity in the mesolimbic DAergic pathway

negative Sx from dec activity in mesocortical DAergic pathway

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6
Q

the glutamate hypothesis

A

schizophrenia results from the hypofunction of NMDA receptors in the brain

dec stimulation of GABA interneurons - disinhibition and hyperactivity of the mesolimbic DA pathway - positive Sx

dec stimulation and hypoactivity of mesocortical DA pathway - negative and cognitive Sx

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7
Q

3 types of schizophrenia Sx

A
  1. positive
  2. negative
  3. cognitive impairment
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8
Q

positive Sx of schizophrenia

A

hallucinations - audidory, visual, tactile

delusions - grandiosity, persecution, control

speech and thought disorder

disorganised motor behaviour - movements/mannerisms

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9
Q

negative Sx of schizophrenia

A

social withdrawal

anhedonia - inability to experience pleasure

flattening of emotional responses

loss of motivation and reluctance to perform everyday tasks (avolition)

impoverished speech and mental creativity (algogia)

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10
Q

cognitive impairment Sx of schizophrenia

A

disturbances in

  • memory
  • attention
  • sensory information processing
  • fluency of speech
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11
Q

2 diagnostic criteria for schizophrenia

A
  1. ICD-10 (internationl statistical classification of diseases)
  2. DSM-V (diagnostic and statistical manual of mental disorders
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12
Q

2 classes of antipsychotic drugs

A

1st generation - typical

2nd generation - atypical

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13
Q

What type of drugs are antipsychotics?

A

antagonists at DA receptors - schizophrenia inc activity in mesolimbic/mesocortical DAergic pathways

most effective against positive Sx (hallucinations, delusions)

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14
Q

FGAs classes

A
  1. phenothiazines
    - propylamine - chlorpromazine
    - piperidine - thioridazine
    - piperazine - fluphenazine
  2. butyrophenones
    - haloperidol
  3. thioxanthenes
    - flupentixol
    - zuclopentixol
  4. substituted benzamides
    - sulpride
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15
Q

MOA of FGAs

A

block DA receptors

  • D2 receptor blockade in mesolimbic pathway responsible for antipsychotic action
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16
Q

D2 receptor blockade in other parts of CNS (FGAs)

A

responsible for major adverse reactions

basal ganglia - acute extrapyramidal symptoms, movement disorders

hypothamalus-pituitary gland - inc prolactin secretion (endocrine effects)

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17
Q

blockage of other neurotransmitters (FGAs)

A

responsible for other major adverse effects

block alpha-adrenoceptor - postural hypotension, sexual dynfunction

block histmaine H1 receptor - sedation, weight gain

block muscarinic receptors - dry mouth, blurred vision, constipation, urinary retention, memory deficits

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18
Q

4 ‘on target’ adverse effects (of FGAs)

A

acute extrapyramidal s/e (EPSE)

tardive dyskinesia (TD)

hyperprolactinaemia and sexual dysfunction

neuroleptic malignant syndrome (NMS)

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19
Q

acute EPSE

A

D2 blockade in basal ganglia

early onset in 50-90% of patients

several forms:
- akathisia/motor restlessness: repeptitive purposeless actions, pacing, rolling -> reduce dose

  • dystonic reactions: abnormal movements of fact and body (procyclidine)
  • psrudoparkinsonsm: tremor, bradykinesia, rigidity, gradual onset over weeks
20
Q

tardive dyskinesia

A

late onset movement disorder
prolonged use of antipsychotic
rhythmical, involuntary movements
can sometimes worsen on Tx withdrawal

21
Q

hyperprolactinaemia and sexual dysfunction

A

D2 receptor blockade in pituitary gland

inc prolactin and reduced gonadotropin release

men - gyaecomastia, failure of ejactulation, dec libido, impotence

women - lactation/galactorrhoea, anovulaton, amenorrhoea, dec libido, infertility

22
Q

NMS - neuroleptic malignant syndrome

A

rare, life threatening syndrome

90% of cases within 10 dyas of starting antipsychotic

most commonly associated with high potency agents

characterised by catatonis, rigidity, stupor, fever, autonomic instability

myoglobinaemia and death in 10%

related to DA D2 receprot polymorphism

possibly due to receptor blockade in corpus striatum and hypothalamus

23
Q

mesolimbic pathway fxn and Da antagonism action

A

emotion and sensations of pleasure

hyperactivity responsible for psychosis

-> reduction in posive Sx

24
Q

mesocortical pathway fxn and Da antagonism action

A

cognitive fxn

hypoactivity can casue negative and cognitive Sx

-> worsening of negitive and cognitive Sx

25
Q

nigrostriatal pathway fxn and Da antagonism action

A

controls movement

-> EPSE, akathisia, dystonai, tardive dyskinesia

26
Q

tuberoinfundibular pathway fxn and Da antagonism action

A

controls prolactin release

-> hyperprolactinaemia and sexual dysfunction

27
Q

off targer adverse effects

A

blockade of muscarinic receptors - memory deficits and sedation, constipation, dry mouth, blurred vision,urinary retention, tachycardia

blockade of alpha-adrenoceptors - postural hypotension, faulire of ejaculation, sedation

blockade of central histamine receptors - sedation, weight gain

28
Q

exammples of SGAs

A 
clozapine
risperidone
olanzapine
quetiapine
aripipazole
paliperidone
amisuplride
29
Q

PD classification of SGAs

A
  1. serotonin-DA antagonisis SDA
    - high selecitvity for 5-HT2A, D2 receptors (and alpha1-adR)
    - risperidone, paliperidone
  2. multi-acting R targeted antipsychotics MARTA
    - affinity for 5-HT2A, D2 R and R in other systems (cholinergic, H, 5HT1A, 5HT1C)
    - clozapine, olanzapine, quetiapine
  3. combined D2/D3 DDA receptor antagonists
    - preferentially block D2 and D3 subtypes of D2-like R
    - amisulpride
  4. partial DA R antagonists
    - aripipazole
30
Q

MOA of SGAs

A

block D2 receptors - antipsychotic effects

block 5-HT2 receptors - antipsychotic effectcs (relief of -ve Sx?)

31
Q

Why are SGAs better than FGAs?

A

SGAs have low affinity for binding or rapid dissociation from D2 receptor in the basal ganglia

significantly milder extrapyramidal symptoms

bettter adverse effect profile and patient compliance

32
Q

4 major groups of adverse efects

A
  1. neurological s/e (EPSE)
    - assocated with most FGAs and some SGAs
    - more pornounced with high potency FGAs *haloperidol), some SGAs (risperidone)
  2. cardiometabolic s/e
    - weight gain, induction of DM, hyperlipidaemia
    - both FGAs and SGAs
    - most pronounced with some SGAs (clozapine, olanzapine, quetiapine, risperidone)
  3. prolactin elevation and sexualdysfunction
    - most pornounced with high potency FGAs and some SGAs (esp amisulpride, risperidone)
  4. cardiovascular s/e
    - ECG abnormalities, AQ prolongation, tachycardia, orthostatic hypotension
    - FGAs and SGAs
    - significant QT prolongation with some SGAs (sertindole, ziprasidone)
33
Q

investigations to undertake before starting antispychotic

A
  • weight (plotted on chart)
  • waist circumference
  • pulse, BP
    fasting blood glucose, HbA1c, blood lipid profile, prolactin levels
  • assessment of any movement disorders
  • assessment of nutritional status, diet, level of physical activity
34
Q

When to offer ECG before antipsychotic Tx?

A
  • if specified on SPC
  • physical exam ID specific CV risk (hypertension)
  • Hx of CVD
  • pt admitted as an inpatient
35
Q

monitiring during antipsychotic Tx

A
  • repsonse to Tx, changes in Sx/behaviour
  • s/e of Tx and impact on functioning
  • emergence of movement disorders
  • weight: weeky for first 6 weeks, than at 12 weeks, at 1yr, annually (plotted on chart)
  • waist circumference (plotted on chart)
  • pulse, BP at 12 weeks, 1yr, annually
  • fasting blood glucose, HbA1c, blood lipid levels at 12 weeks, 1yr, annually
  • adherence
  • overall physical health
36
Q

depot/long acting antipsychotic formulations (LAIs)

A

slow release formulations given by deepIM inhection every 1-4 weeks

used in maintenance Tx for schizophrenia

FGAs and SGAs available

37
Q

FGAs available as depot/long acting antipsychotic formulations

A 
haloperidol
flupenthixol
fluphenazine
zuclopenthixol
pipothiazine
38
Q

SGAs available as depot/long acting antipsychotic formulations

A

olanzapine
riperidone
paliperidone
aripiprazole

39
Q

advantages of depot/long acting antipsychotics

A
  • consistent bioavailability and predictable dosage plasma drug level relationship
  • imporved PK profile, lower dose, reduced risk of s/e
  • anhanced medication adherance and avoidanc of covert non-adherance
  • rule out poor med adherance as possible cause fo ecaxerbation of pt Sx/relapse
  • reduced risk of inadvertent/deliberate OD
  • regular contact with hc prof, review opportinuty for Sx/s/e, rpovision of psychosicial support
40
Q

disadvantages of depot/long acting antipsychotics

A
  • mainly rlated to PK properties
  • dose titration against reponse proteacted process
  • inc risk relapse after ereduction in dose/extension of injection interval not immediatelt evident
  • long elim half life, lack of flexibility in dealing with emergent s/e

uncmfortable local reactions at site of injection, painful, inflammation

41
Q

important practice points for antipsychotics

A
  • avoid high dose antipsychotic drug therapy - except after adequate sequential trial of 2+ diff drugs
  • avoid antipsychotic drug combination (except for short periods when cross-tapering)
  • when switching antipsychotic meds, gradual cross-tapering of dosages of 2 drugs
  • ensure regular monitirong of effect of antipsychotic Tx on physical health of pt
42
Q

When is clozapine offered?

A

when schizophrenia not responsed to Tx despite sequential use of 2+ diff antipsychotics

at least one should be non-clozapine SGAs

43
Q

serious adverse effects with clozapnie

A

agranulocytosis
neutropenia
myocarditis - full physical exam and MHx before initiation

44
Q

counselling for clozapine

A

stick to same brand

report signs of infection

leucocyte and differential blood counts must be normal before starting

  • every week for 18 weeks
  • then at least every 2 mths
  • after 1yr, at least every 4 weeks
  • 4 weeks after discontinuation
45
Q

leukocyte and neutrophil count with clozapine

A

if leukocyte count below 3x10^9/L

or absolute neutrophil count below 1.5x10^9/L

  • discontinue permamently and refer to haematologist

PHA333 (27 decks)

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