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Sem 3 > schizophrenia > Flashcards

schizophrenia Flashcards

1
Q

What is the definition of schizophrenia by ICD-10?

A

a severe and enduring disorder, with fundamental and characteristic distortions of thinking and perception, and affects that are inappropriate or blunted. clear consciousness and intellectual capacity are usually maintained, although cognitive deficits may evolve in the course of time
+ accompanied by high levels of social dysfunction, inability to maintain employment, depression and suicide

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2
Q

What are the different symptoms in schizophrenia?

A
  • -> positive symptoms (psychosis)
  • delusions
  • hallucinations
  • thought disorder
  • -> negative symptoms (deficit)
  • flat or blunted affect and emotion
  • poverty of speech (logia)
  • anhedonia (inability to experience pleasure)
  • associability (lack of desire to form relationships)
  • avolition (lack of motivation)
  • -> cognitive impairements
  • particularly memory and executive function
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3
Q

What is the difference between hallucination and delusion?

A
  • delusion: fixed, false belief, unshakeable by superior evidence to the contrary, and out of keeping with a person’s cultural norms
  • hallucination: a perception, internally generated, in the absence of an external stimulus
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4
Q

What types of delusions do you see in schizophrenia?

A
  • reference: believe things are directed at yourself when they are not
  • persecution: people are out to get you
  • control: people are controlling you
  • bizarre and impossible
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5
Q

What types of hallucinations are typically seen in schizophrenia?

A

auditory

+ telling them to do things/ negative things about themselves, are very distressing

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6
Q

What is the prevalence of schizophrenia in a population?

A
  • 10-20 per 100000 adult population per year

- UK prevalence: 0.4%

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7
Q

What is the modal age of onset?

Median age?

A

modal: 20
median: 26 (male, 29 (females)

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8
Q

What is the male:female ratio for schizophrenia?

A

1.4:4

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9
Q

What is the genetic risk in schizophrenia?

A

-7% risk in 1st degree relative
-2.3% in second degree relative
-10% dizygotic co-twins
-45% monozygotic co-twins
(SZ inherited not learned)

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10
Q

What is the genes involved in Sz?

A
  • over 200
  • connected to glutamate, dopamine and GABA neurotransmitter function, neuronal structures, plasticity, general synaptic function, or to inflame/immune response
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11
Q

What are the environmental risk involved in Sz?

A
  • child abuse, taken into care
  • cannabis or other substances misuse
  • second generation of UK ethnic minority
  • migration
  • peri-natal oxygen deprivation, maternal starvation while in utero
  • urban living, overcrowded parental separation, general deprivation as a child
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12
Q

How is the onset and presentation of Sz?

A
  • preceded by subtle social and cognitive impairment, even in infant
  • (prodromal/at risk state): often progresses over years from vague symptoms of depression, anxiety, insomnia or negative symptoms to vague but psychotic symptoms and then full psychosis

–> you can manage to not develop psychosis (early development or prodromal stages)

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13
Q

What are the diagnosis criteria under ICD-10?

A
  • -> at least 1 first rank symptom for at least 1 month:
    1. thought echo, thought insertion, thought withdrawal, thought broadcasting
    2. delusions of control, influence or passivity, clearly referred to body or limb movements or specific thoughts, actions and sensations
    3. auditory hallucinations giving a running commentary or discussing the patient between themselves, hallucinatory voices from parts of the body
    4. persistent delusions that are completely impossible
  • -> OR at least 2 second rank symptoms (for a mouth)
    1. other persistent hallucinations in any modality
    2. thought disorder (neologisms, loosening or breaks in he train of though resulting in incoherent or irregular speech)
    3. catatonic behaviour
    4. negative symptoms, not due to depression or medications
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14
Q

What are the four major projections of the dopamine system?

A
  1. nigrostriatal pathway
    2 mesolimbic pathway
  2. mesocortical pathway
  3. tuberoinfundibulnar pathway
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15
Q

What are the components of the nigrostriatal pathway projection in Sz?

A

substantia nigra (SNc;A9) to striatum

  • -> SNc to sensiromotor (dorsal) striatum: motor (involuntary) control
  • -> SNc to associative (mid) striatum: cognition, volition, emotion
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16
Q

What are the components of the mesolimbic pathway projection in Sz?

A
  • ventral tegmental area (VTA, A10) in midbrain to limbic regions associated with reward, motivation, affect and memory
  • includes ventral striatum (nucleus accubens), amygdala, hippocampus and medial prefrontal cortex
17
Q

What are the components of the mesocortical pathway projection in Sz?

A

VTA to frontal cortex, including dorsolateral prefrontal cortex (DLPFC)
–> cognitive function, motivation and emotional response

18
Q

What are the components of the tuberoinfundibular pathway projection in Sz?

A 
puberal region (hypothalamus) to median eminence (infundibular region at top of pituitary stalk)
--> DA acts to inhibit prolactin release from pituitary
19
Q

What are the different types of dopamine receptors and where do you find them?

A
  • -> D1 receptor family
  • D1 (motor, associative, ventral striatum + cerebral cortex)
  • D5 (hippocampus and hypothalamus)
  • -> D2 receptor family
  • D2 (L+S) (motor, associative, ventral striatum)
  • D3 (ventral and associative striatum, hippocampus and amygdala)
  • D4 (frontal cortex, medulla, midbrain and amygdala)

auto receptors on terminals (SNc and VTA):
D2S: DA synthesis, metabolism and release
D3: DA release

20
Q

Which are the receptors that are heterogeneously dispersed in the brain?

A

D1 and D2: seen in all functional subdivisions of the striatum
D4: seen most in frontal cortex

21
Q

What are the DA abnormalities in Sz and how does it relate to symptoms?

A
  1. excessive DA release in the striatum (associative): positively correlates with positive symptoms and with good treatment response to antipsychotic drugs
  2. inadequate release of dopamine in the frontal cortex: associated with deficits in cognitive function (DLPFC)
    (3. normal to decrease DA in ventral striatum (limbic))
22
Q

What is the primary abnormality in Sz?

A

GABA or glutamate systems:

NMDA receptor is hypofunctional

23
Q

by what mechanisms of dysfunction does decrease NMDAr function cause Sz?

A
  • excessive glutamate release: causing excitotoxicity (impaired neuronal development, makes disease progression worse): neg symptoms
  • DA dysregulation via glu-DA interactions: postive symptoms
24
Q

What is the GLU-DA interaction hypothesis?

A
  1. neurodevelopmentally hypofunctional NMDA receptor mediated synapse on parvalbumin-containing GABA neurones (cortex)
  2. GABA release is low and doesn’t adequately suppress portico-brainstem glutamate outflow
  3. excessive direct glutamate stimulation of SNc DA interneuron cell bodies leads to increase DA in associative striatum and sensorimotor striatum
  4. excessive indirect glutamate stimulation of mesocortical/mesolimbic DA neurones cell bodies in VTA (increase GABA interneurone)
  5. decrease DA release in cortex
25
Q

What is the pharmacological treatment for Sz?

A

Antipsychotics:

  • low dose antipsychotics (if not agitated): are all reversible true D2 receptors antagonists.
  • need to get over 65% threshold D2 receptor occupancy in associative striatum for the drug to be efficient
  • don’t need the receptor occupancy for the whole 24 hours, (only for adequate proportion of the time and does not have to be continuous)
26
Q

What are the adverse effects of D2R antagonism?

A
  1. mesolimbic pathway: worsening go negative symptoms
  2. nigrostriatal motor pathway: parkinsonism and other EPSE
  3. mesocortiyal pathway: exarcerbating cognitive function
  4. tuberoinfundibulnar pathway: hyperprolactonaemia (sexual function, reproductive function, breast pathology, hypergonadism)
27
Q

On what other receptors do antipsychotics bind to?

A 
AChM
H1
alpha2
alpha1
5-HT 2A
5-HT 2C
28
Q

what are the anticholinergic (M1 antagonism) side effects?

A 
dry mouth
sore throat
blurred near vision
tachycardia
urinary retention
abuse potential
acute confusion in overdose

(if you block M1 receptors, you can alleviate some EPSE)

29
Q

What are the alpha adrenergic antagonism side effects?

A
  • orthostatic hypotension and reflex tachycardia

- small pupils

30
Q

What are the cardiotoxicity side effects and which receptors are involved?

A
  • delayed conduction
  • M1 antagonism
  • alpha-adrenegic antagonism
31
Q

Which receptors are involved in sedation side effect?

A
  • H1 antagonism

- alpha adrenergic antagonism

32
Q

Which receptors are involved in weight gain side effect and what is the effect?

A
  • H1, 5-Ht2A, 5-HT2C, AChM3, adrenergic alpha 1 and 2 antagonism
  • -> effect on leptins
33
Q

Which are the antipsychotics you should not give unless completely need to?

A

clozapine and olanzopine (due to weight gain)

34
Q

When do you use clozapine?

A

treatment resistant SZ (RTRS): when two antipsychotics fail or can’t be tolerated at full dose

35
Q

What are the psychosocial treatment in Sz?

A
  • family intervention (CBT approach + education about illness, at least 12 sessions over 6 months and patient must be present to at least half the sessions: helps in relapse outcome)
  • CBT (treatment of residual symptoms
36
Q

What are the different services provided for people with Sz?

A
  • early intervention service: minimise delay in first treatment, focus on return to work and training, reconstruct family relationships and social networks (non-stigmatisation: offices in community)
  • community mental health teams: thereafter early intervention service
  • crisis resolution teams: for him treatment of acute exacerbations
37
Q

What are signs of poor prognosis in Sz?

A 
slow onset
premorbid disability
longer psychotic before treatment 
continued substance misuse
poor adherence
family criticism

Sem 3 (20 decks)

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