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AC- CNS lectures > Schizophrenia 1.5.1 > Flashcards

Schizophrenia 1.5.1 Flashcards

1
Q

What are some negative symptoms of schizophrenia?

A
  • Emotional withdrawal
  • Social withdrawal
  • Lack of pleasure/ motivation
  • Poor grooming/ hygiene- unkempt, BO
  • No goal- directed behaviour- amotivation
  • Alogia- talks little, uses few words
  • Apathy
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2
Q

What are some positive symptoms of schizophrenia?

A
  • Delusions- neighbour poisoning him
  • Hallucinations- insect sensation
  • Disorganised speech- “hard to comprehend”
  • Disorganised behavior
  • Agitation
  • Insomnia
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3
Q

How do we diagnosis schizophrenia?

A
  • There is no clear test to diagnose schizophrenia
  • Mental state examination (interview patient)
  • History from patient/family/friends
  • MRI, CT scan and blood tests are generally used to rule out physical illness
  • Drug testing - to exclude drug induced psychosis
  • DSM 5 Criterion: TWO or more symptoms present for a significant portion of time during a 1 month period including delusions, hallucinations, disorganised speech (incoherence), grossly disorganised, negative symptoms (avolition, diminished emotional expression)
  • Continuous signs of the disturbance persist for at least 6 months. This 6-month period must include at least 1 month of symptoms (or less if successfully treated) that meet Criterion A (i.e., active-phase symptoms) and may include periods of prodromal or residual symptoms
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4
Q

How do you get the positive symptoms?

A
  • an excess of dopamine in the mesolimbic pathway
  • dopamine travels from the midbrain tegmental area to the nucleus accumbens
  • increased activity in this pathway
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5
Q

How do you get negative symptoms?

A
  • due to insufficient dopamine activity in mesocorticol pathway
  • decreased activity in the pathway that goes from the midbrain to the prefrontal lobe cortex* can cause
    • apathy
    • withdrawal
    • lack of motivation & pleasure
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6
Q

What causes extrapyrimidal SE of antipsychotic drugs?

A
  • the pathway from the substantia nigra to the striatum is involved in the coordination of body movements
  • inhibition of this pathway causes EPSE
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7
Q

How do you get elevated serum prolactin levels?

A
  • the pathway from the hypothalamus to the pituitary
  • D2 stimulation –> inhibits the release of prolactin
  • inhibition of this pathway leads to elevated serum prolactin levels
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8
Q

What is the dopamine theory of schizophrenia?

A
  • most antipsychotic drugs block dopamine receptors
  • psychotic symptoms can be induced by drugs that increase dopaminergic activity anti-parkinsonian agents
  • single positive electron tomography ligand scans show an increase in D2 receptors in nucleus accumbens of schizophrenia patients
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9
Q

Which drugs mimic positive, negative & cognitive symptoms of schizophrenia?

A
  • phencyclidine
  • ketamine
    • they are glutamate NMDA receptor antagonists
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10
Q

Which drugs mimic positive symptoms of schizophrenia? How?

A
  • amphetamine, methamphetimine
  • psilocybin, LSD
  • phencyclidine, ketamine
  • they release dopamine & inhibit its reuptake
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11
Q

Which drugs are good in treating negative symptoms?

A
  • 5HT2A receptor antagonists produced by SGAs
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12
Q

Which drugs are good in treating positive symptoms of schizophrenia?

A

Positive symptoms respond well to D2 receptor antagonism produced by FGAs & SGAs

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13
Q

Why does it take 1-3 weeks for antipsychotic agents to have therapeutic effect?

A
  • there are 3 time-dependent changes in dopamine neurotransmission
    • immediate effects: an increase in dopamine synthesis, release and metabolism but NO therapeutic effect
    • prolonged effects (1-3wks): depolarization blockade–> reduced dopamine release from mesolimbic and nigrostriatal neurons –> alleviate the positive symptoms of schizophrenia while causing EPSs
    • extended prolonged effects: dopamine receptor up-regulation and supersensitivity to dopamine agonists
    • —>>may contribute to the development of a delayed type of EPS called tardive dyskinesia
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14
Q

What are the FGAs used to treat antipsychotics?

A
  • chlorpromazine
  • haloperidol
  • droperidol
  • flupentixol
  • periciazine
  • zuclopenthixol
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15
Q

What are the SGAs used to treat schizophrenia?

A
  • clozapine
  • olanzapine
  • quetiapine
  • risperidone
  • paliperidone
  • amisulpride
  • aripiprazole
  • asenapine
  • ziprasidone
  • lurasidone
  • brexipiprazole
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16
Q

What is the difference between FGAs & SGAs?

A
  • incidence of EPSE
  • efficacy in treatment- resistant groups of patients
  • efficacy against negative symptoms
    • FGAs not effective
  • receptor selectivity
  • pharmacological properties
  • FGAs- positive sxs
  • SGAs- postive & negative sxs
17
Q

What is the MOA of antipsychotics?

A
  • D2 receptor antagonism is essential
  • 5HT2A receptor antagonism enhances/ complements D2 receptor antagonism
  • 5HT2A receptor antagonism by SGAs
18
Q

What happens in the mesocortical pathway?

  • SGAs
A
  • 5-HT2 receptors inhibit presynaptic dopamine release
  • by blocking these receptors this may increase dopamine release in this pathways – this may alleviate the –ve Sx
  • 5HT2A antagonist enhance / complements action of D2 antagonist to reduce positive symptoms
  • may protect against EPS by preserving nigrostriatal DA activity
  • also alleviate anxiety and insomnia in schizophrenia
19
Q

What happens in the mesolimbic pathway?

  • FGAs
A
  • dopamine D2 receptor blockers inhibit effect of dopamine in mesolimbic pathways thereby reducing the positive Sx
  • Affinity for D2 receptors cause of EPS (extrapyramidal side- effects)
  • Affinity for D2 receptors is strongly correlated with alleviation of positive symptoms and cause of EPS (extrapyramidal side-effects)
  • FGAs alleviate positive symptoms of schizophrenia (delusions, hallucinations & disturbed thinking)
  • FGAs are quite ineffective in treating negative & cognitive symptoms and EPS may become intolerable
20
Q

What are therapeutic effects of SGAs?

A
  • alleviation of negative & cognitive symptoms as well as positive symptoms
  • lower incidence of EPS and generally better tolerated
  • SGAs are superior to FGAs interact with 5-HT2A and D2 receptors
  • Antagonism of D3, D4 and other receptors may also contribute to the favourable clinical profile of SGAs
21
Q

What are some ADV of antipsychotics?

A
  • blockade of a1 receptors
    • hypotension, reflex tachycardia
  • blockade of histamine H1-receptor
    • sedation & weight gain
  • blockade of 5HT2C & H1 receptors
    • weight gain
  • anticholinergic effects
    • blurred vision, dry mouth, constipation, urinary

retention

  • ADV due to immune reaction
    • hypersensitivity, dermatitis, rashes, photosensitivity, urticaria
  • ADV due to individual drug
    • clozapine cause agranulocytosis -neutropenia, bone marrow depression
  • idiosyncratic rxn
    • neuroleptic malignant syndrome
22
Q

What are some EPSE?

A
  • acute dystonia
    • involuntary muscle spasms
    • hyperextension of trunk, neck
    • arching of back
    • lock jaw
  • akathesia
    • muscle quivering, restlessness, inability to sit still
  • parkinsonism
  • neuroleptic malignant syndrome
    • fever, encephalopathy, vtals unstable, elevated enzymes, rigidity of muscles
    • dantrolene tx
23
Q

Chlorpromazine as a FGA…

A
  • low potency antipsychotic
  • EPS can become troublesome
  • prominent sedation, hypotension & antimuscarinic effects
  • can cause obstructive jaundice and photosensitivity leading to sunburn
  • useful when sedation is desired
  • administered orally, IV or IM
24
Q

Flupenthixol decanoate as a FGA

A
  • depot preparation that can be administered IM every 2-4 weeks
  • Minimal sedation & hypotension, but prominent EPS
25
Q

Haloperidol as a FGA…

A
  • high potency antipsychotic
  • EPS is a main problem
  • Favoured when sedation, hypotension, and antimuscarinic effects are undesirable (elderly patients)
  • Administered orally or IM
26
Q

What are long acting depot injections used for?

A
  • for patients who don’t reliably take oral antipsychotic medication
27
Q

What are clinical uses of SGAs?

A
  • Treatment of acute and chronic psychoses (e.g. schizophrenia)
  • Acute mania (olanzapine, quetiapine, risperidone)
  • Organic psychoses (e.g. dementia- associated agitation)
  • Severe behavioural disorders in children
28
Q

Olanzapine as a SGA…

A
  • Does not cause agranulocytosis
  • Convulsions can occur
  • Side-effects include: sedation, weight gain, impaired glucose regulation, hypotension and antimuscarinic effects
  • widely prescribed
29
Q

Risperidone as a SGA…

A
  • positive, negative, cognitive symptoms of schizchoprenia
  • above therapeutic doses (>4-6mg/day), can produce EPS
  • Does not cause agranulocytosis
  • Antimuscarinic effects are minimal
  • Side-effects include: mild sedation, mild weight gain & impaired glucose regulation, hypotension, hyperprolactinaemia
  • widely prescribed
30
Q

Aripiprazole as a SGA…

A
  • Improve positive symptoms and reduce relapse rates after an acute episode
  • Does not cause agranulocytosis
  • Side-effects include: sedation, weight gain, impaired glucose regulation, hypotension and antimuscarinic effects
  • Precautions:
    • Recent history of MI, unstable heart
    • Treatment with CYP3A4
    • Poor metaboliser - CYP2D6
  • indicated for schizophrenia & BPAD as monotherapy
31
Q

Quetiapine as a SGA…

A
  • can treat positive, negative & cognitive symptoms without producing EPS
  • Does not cause agranulocytosis
  • Side-effects include sedation, dry mouth, constipation, hypotension, mild weight gain & impaired glucose regulation
  • good for schizophrenia
32
Q

Receptor affinities for antipsychotics, 5HT2, D1, D2

A

AC- CNS lectures (28 decks)

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