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'B33CNS - Pharmacology & Therapeutics > Schizophrenia > Flashcards

Schizophrenia Flashcards

1
Q

When is the common onset of Schizophrenia?

A
  • Late adolescence
  • Early adulthood
    (acute onset over 2 - 3 weeks)
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2
Q

What is the median age of onset?

A

Median age of onset:
M: 23 years
F: 28 years

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3
Q

Is there a greater prevalence of Schizophrenia in one gender? Why could this be so?

A
  • More prevalent in males than females

- Oestrogen has a role in regulating dopamine receptor sensitivity, hence increased prevalence in males.

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4
Q

What is the environmental aetiology (cause) of Schizophrenia?

A
  • Males in urban areas are prone to schizophrenia
  • More prevalent in countries further from equator (cold weather; affects mothers e.g. viral infection, affects foetus)
  • Perinatal complications: severe malnutrition, exposure to stressful events, birth complications, altered brain development in early life
  • Early cannabis use
  • Advancing paternal age; germ cell (sperm) mutations increase risk of Schizophrenia in child.
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5
Q

What is the genetic aetiology of Schizophrenia?

A
  • Family history
  • Twin studies validates a genetic contribution; 50% chance other monozygotic twin has it if the other does

Susceptibility genes

  • Neuregulin & Dysbindin
  • Influence neurodevelopment and synaptic functioning
  • Can lead to Schizophrenia
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6
Q

What are the positive symptoms of Schizophrenia? How do they present?

A

Acute presentation:

  • Thought insertion
  • 3rd person auditory hallucinations
  • Thought disorder (e.g. cutting out mid-sentence, not knowing what’s happened after)
  • Delusional perception

Duration criteria:
- Symptoms persist for > 1 month

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7
Q

What are the exclusion criterion for positive symptom presentation of Schizophrenia?

A
  • Not secondary to mood disorder (exclude bipolar disorder e.g. ramblings)
  • No organic disease
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8
Q

What are the negative symptoms of Schizophrenia? How do they present?

A 
Chronic presentation:
- Flattened mood
- Indifference and loss of drive
- Social isolation
>>> (Similar to depression) 
- Poor self-care
- Poverty of speech

Negative symptoms are relatively nonspecific; could be passed off as ‘teenage years’ etc.

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9
Q

What else presents for Schizophrenia apart from positive and negative symptoms?

A

Cognitive impairment:

  • Affects attention, working and semantic memory (long-term memory not drawn from personal experience)
  • Link to dementia in elderly schizophrenic patients?
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10
Q

Define: working memory.

A

Working memory (can affect academia):

  • Temporary storage and manipulation of information
  • Necessary for tasks such as language comprehension, learning and reasoning
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11
Q

Define: semantic memory.

A
  • Long term memory that processes ideas and concepts

- Inclusive of common knowledge: colours, sounds of letters etc.

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12
Q

What sub syndromes of Schizophrenia are there?

A
  • Paranoid schizophrenia
  • Disorganised schizophrenia
  • Catatonic schizophrenia
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13
Q

What is paranoid schizophrenia?

A

Auditory delusions and hallucinations

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14
Q

What is disorganised schizophrenia?

A
  • Thought disorder
  • Odd behaviour
  • Inappropriate mood
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15
Q

What is catatonic schizophrenia?

A
  • Due to treatment of the condition (schizophrenia)
  • Rare form
  • Debilitating condition

Symptoms:

  • Unable to move or speak
  • Person stares
  • Holds body rigidly
  • Unaware of surroundings
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16
Q

How is schizophrenia diagnosed?

A

One or more of (if clear cut:

  • Delusions
  • Hallucinations

Two of:

  • Delusions
  • Hallucinations
  • Disorganised speech
  • Catatonic behaviour
  • Negative symptoms; flattened mood, inability to speak, general lack of drive
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17
Q

What is the dopamine theory of schizophrenia origin?

A
  • Excess dopamine
  • Excess dopamine receptors
    (Parkinson’s = opposite; depletion of DA)
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18
Q

What is the evidence to support the dopamine theory of schizophrenia?

A
  • Antipsychotic drugs = D2 receptor antagonists (too much DA)
  • DA agonists such as amphetamines, levodopa cause paranoid psychosis
  • CSF and brain studies of patients; abnormal levels of DA, its metabolites, enzymes or receptors
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19
Q

What is the evidence that DA is not the sole contributor to schizophrenia?

A
  • DA changes Glu transmission downstream
  • Signalling via NMDA is implicated
  • NMDA receptor antagonists e.g. ketamine, phencyclidine (PCP) produce schizophrenia-like syndrome
  • Thus depletion of Glu = schizophrenia symptoms
20
Q

What other theories aside from the DA/Glu theory are there for the cause of schizophrenia?

A

Functional imaging studies:

  • Abnormalities in cerebral blood flow and metabolism - impairment of neuronal circuits
  • Specific impairment in frontal cortex, hippocampus, thalamus and cerebellum (hence delusions)

Structural brain changes:
- Enlargement of lateral ventricles
- Slight decrease in size of brain
- Histology; altered neuronal and synaptic organisation, affected white matter, no gliosis (absence of neurodegenerative process) THUS
»> schizophrenia = neurodevelopmental, not neurodegenerative.

21
Q

What is the management strategy for schizophrenia?

A 
Based on stage of illness:
Intervention:
- Physical (pharmacological therapy)
- Psychological
- Social (family, care home)

Initial assessment:

  • Compulsory admission required (upon initial psychiatric event)
  • Drug free if possible; might have to give benzodiazepine to calm them down
22
Q

How is schizophrenia managed? How long do antipsychotics take to take effect? What do they combat?

A
  • Antipsychotics effective against most positive symptoms
  • Gradual onset of therapeutic effect (2-3 weeks(
  • Investigate context; substance misuse (cannabis) may contravene treatment
  • Family support is key
    »> Early intervention; CBT, antipsychotics
23
Q

What is the mechanism of action for antipsychotics?

A
  • Inhibit D2 receptors

- Reverse excess DA activity in mesolimbic system; site for psychosis symptoms

24
Q

How long is antipsychotic treatment continued for after initial psychosis? How does treatment change over time?

A
  • 12-24 months; after ONE single episode.

- Tail off medication if improvement noted; tardive dyskinesia and other S/Es.

25
Q

What is tardive dyskinesia?

A

Involuntary movement of the tongue, lips, face, tongue and extremities.

26
Q

Do antipsychotics have effect against positive symptoms?

A
  • Yes; within 6 weeks in 70% of patients

- Useful in prevention of psychosis relapse in delirium (mental confusion) and severe depression

27
Q

How is antipsychotic drug therapy chosen?

A
  • Informed by patient presentation
  • Patient’s choice (in conjunction w/HCP, carer)
  • S/E profile
  • Treatment history

> > > 6 week trial at adequate dosage to assess treatment response (switch to another after 2 weeks if not even minimal improvement)

28
Q

What should be avoided when receiving antipsychotic drug therapy?

A
  • Co-administration w/anticholinergic/antimuscarinic agents

- Combinations of antipsychotics; exacerbate antimuscarinic S/Es

29
Q

Which symptoms do antipsychotics treat the best?

A
  • Positive symptoms

- Antipsychotics have minor effects on negative and cognitive symptoms

30
Q

Why are atypical (second generation) antipsychotics generally preferred to typical (first generation) antipsychotics?

A
  • Atypicals do not produce extrapyramidal S/Es (Parkinson’s-like tremors) at clinical doses
  • Similar profile to typicals otherwise
31
Q

What is the hierarchy of atypical antipsychotics, and their advs/disadvs?

A

1) Risperidone; availible as depot too
2) Olanzapine; sedative effects useful, BUT may cause metabolic syndrome (HBP, diabetes, obesity)
3) Amisulpride; some efficacy against negative symptoms
4) Quetiapine; quite sedating, beneficial in treating bipolar depression
5) Aripiprazole; acts as DA partial agonist, ‘stabilises’ DA, antagonises DA when levels are high, mimics DA when levels are low.

32
Q

What are the S/Es w/atypical antipsychotics?

A

Weight gain:

  • Mean weight gain of 5kg over 6 months
  • Genetic polymorphism of 5-HT2C receptor?

Hyperglycaemia and Type 2 DM:

  • Increased incidence of Type 2 DM
  • Occurs from drug-induced hyperglycaemia and insulin resistance

Metabolic syndrome:
- Screening required prior to and during treatment.

33
Q

What is Metabolic syndrome?

A

Dyslipidemia and hypertension make up metabolic syndrome, in addition to Type 2 DM and hyperglycaemia

34
Q

How effective is the atypical, clozapine?

A
  • Effective in 30% of patients resistant to other drugs
  • Used when failure to respond to two 6 week trials
  • Reduces suicide risk in schizophrenia
  • Mechanism of greater efficacy not known
35
Q

Why is clozapine reserved as a 3rd line agent, given its efficacy? What precautions must be taken as a result?

A

Agranulocytosis: bone marrow suppression (suppressing WBCs inc. neutrophils = prone to infection)
- Thus reserved for treatment-resistant patients
»> Weekly blood tests mandatory

Other S/Es:

  • Weight gain
  • Metabolic syndrome
  • Hypersalivation
  • Sedation
  • Seizures (at high doses)
36
Q

What are some typical (first generation) antipsychotics? What advantages do they have?

A
  • Chlorpromazine
  • Haloperidol
    »> Cheap and efficacious BUT S/E profile
37
Q

What is the characteristic side effect of typical antipsychotics?

A

Extrapyramidal symptoms; motor abnormalities related to receptor blockade in basal ganglia (normally coordinates movement, filters out unnecessary movements etc..

38
Q

List the side effects associated w/typical antipsychotics.

A
  • Acute dystonia
  • Parkinsonism
  • Akathisia
  • Tardive dyskinesia
  • Neuroleptic malignant syndrome
  • Prolongation of the QT interval (ECG)
39
Q

What is Acute dystonia? Treatment?

A
  • Painful contractions of muscles in the neck, jaw or eyes (spasms set of by ACh)
  • Young men given high doses of typical antipsychotics particularly vulnerable; onset within hours or days
    »> Treatment: IM or IV anticholinergic agents
40
Q

What does Parkinsonism entail? Treatment?

A
  • Decreased facial movements, shuffling gait, stiffness, sometimes tremor
  • Common in early weeks of treatment
    »> Treatment: reduce dose (too little DA = symptoms), or administer anticholinergic agent
41
Q

What does Akathisia entail? Treatment?

A
  • Feeling of restlessness and need to walk around
  • Very unpleasant, occurs in first few months
    »> Treatment: lower dose, or propanolol
42
Q

What does Tardive Dyskinesia (TD) entail? Treatment?

A
  • Uncontrollable grimacing movements of face, tongue, upper body
  • Distressing and disabling
  • Occurs in 5% of patients taking long-term typicals
  • No way of predicting
  • Can be irreversible
    »> Treatment: no reliable treatment availible; titrate down dose after patient presents w/TK
43
Q

What is Neuroleptic malignant syndrome? Treatment?

A
  • 1 in 500 (Fatal in 10%)
  • Pyrexia, stiffness, autonomic instability (tachycardia, fluctuating BP) and seizures; leading to coma.
  • Characteristics: raised serum creatine kinase (byproduct of muscle damage), metabolic acidosis (low pH), leucocytosis (elevated leukocytes)
    »> Treatment: just stop the drug, monitor if patient develops fever w/o a clear cause
  • After an episode; restart treatment gradually, switch to atypical, careful monitoring
44
Q

What does prolongation of the QT interval mean?

A
  • Predisposes to serious arrhythmia

- Inhibition of specific cardiac K+ channels

45
Q

What other drugs are involved in the pharmacological management of schizophrenia?

A

Benzodiazepines:
- Short term treatment (target negative symptoms)

Antidepressants:
- Treatment administered as recommended by NICE

Electroconvulsive treatment
- Not effective unless in catatonic schizophrenia (treatment-induced)

46
Q

What does psychological treatment entail for schizophrenia?

A

Family therapy:

  • Focus; educate family, changing their behaviour
  • Effectiveness; modest
  • Challenges; difficult to implement widely due to financial constraints

CBT:
- Some efficacy against auditory hallucinations and delusions
- Adopted as integral component of schizophrenia management
- Hallucinations can also benefit from simple practical manoeuvres; use of ear plugs or personal stereos “drown out noise”
»> But can be counter-productive; voices saying “Why are you trying to get rid of me?” etc.

'B33CNS - Pharmacology & Therapeutics (13 decks)

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