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Pharmacology and Therapeutics > Anti-parkinsonian drugs and neuroleptics > Flashcards

Anti-parkinsonian drugs and neuroleptics Flashcards

1
Q

Mesocortical pathway

A

Dopaminergic pathway

  • ventral tegmental area to the cerebrum
  • important in executive functions and complex behavioural patterns
  • inhibition associated with negative schizophrenia symptoms (stimulation has opposite effect with positive)
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2
Q

Mesolimbic pathway

A

Dopaminergic pathway

  • ventral tegmental area to the nucleus accumbens
  • ‘the brain reward pathway’
  • involved in emotion
  • activation associated with positive schizophrenia symptoms (inhibition has opposite effect with negative)
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3
Q

Nigrostriatal pathway

A

Dopaminergic pathway

  • substantia nigra pars compacta to the striatum
  • inhibition results in movement disorders (involved in movement regulation)
  • degenerates to give Parkinson’s disease
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4
Q

Tuberoinfundibular pathway

A

Dopaminergic pathway

  • arcuate nucleus of the hypothalamus to the median eminence
  • inhibition leads to hyperprolactinaemia (prolactin release regulation from the anterior pituitary gland)
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5
Q

L-DOPA adjuncts

A

Increases efficacy and safety of L-DOPA by preventing peripheral breakdown

DOPA-D inhibitors (eg: Carbidopa, Benserazide)
-inhibition of peripheral DOPA-D only to prevent peripheral L-DOPA breakdown
-can’t cross the blood brain barrier
-reduces required L-DOPA dosage
COMT inhibitors (eg: Entacapone, Tolcapone)
-increases L-DOPA levels reaching the brain by inhibiting peripheral metabolism
-reduces ‘on-off’ long term side effect

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6
Q

L-DOPA limitations

A

Peripheral breakdown by DOPA-D
-poor efficacy (low DOPA-D levels reach the brain)
-peripheral L-DOPA breakdown by DOPA-D=stimulate the chemoreceptor trigger zone (N&V)
Long-term side effects
-dyskinesias
-on-off effects (depends on plasma L-DOPA levels)

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7
Q

Dopamine receptor agonist examples

A
  • Ergot derivatives

- Non-ergot derivatives

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8
Q

Ergot derivatives

A
  • Act as potent agonists of Dopamine D2 receptors
  • Associated with cardiac fibrosis
  • Eg: Bromocriptine and Pergolide
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9
Q

Non-ergot derivatives

A
  • Eg: Ropinirole and Rotigotine
  • Ropinirole also available as extended-release formulation
  • Rotigotine also available as patch
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10
Q

Monoamine oxidase B inhibitors

A
  • Eg: Selegiline (Deprenyl) and Rasagiline
  • reduces the dosage of L-DOPA required
  • Can increase the amount of time before Levodopa (L-DOPA) treatment is required
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11
Q

First generation antipsychotics

A
  • Chlorpromazine

- Haloperidol

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12
Q

Second generation antipsychotics

A
  • Clozapine
  • Risperidone
  • Quetiapine
  • Aripiprazole
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13
Q

Chlorpromazine

A

First generation antipsychotic

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14
Q

Haloperidol

A

First generation antipsychotic

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15
Q

Schizophrenia positive symptoms

A

Increased mesolimbic dopaminergic activity associated with positive symptoms

  • hallucinations (auditory and visual)
  • delusions (paranoia)
  • thought disorder (denial about oneself)
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16
Q

Schizophrenia negative symptoms

A

Decreased mesocortical dopaminergic activity associated with negative symptoms

  • affective flattening (lack of emotion)
  • alogia (lack of speech)
  • avolition/apathy (loss of motivation)
17
Q

Quetiapine

A

Second generation antipsychotic

18
Q

Aripiprazole

A

Second generation antipsychotic

19
Q

Chlorpromazine

A

First generation antipsychotic
-discovered during new antihistamine development

Side effects:

  • High incidence= of anti-cholinergic, especially sedation
  • Low incidence of extrapyramidal symptoms
20
Q

Haloperidol

A

First generation antipsychotic

  • very potent dopamine D2 receptor antagonist (~50 times more potent than Chlorpromazine)
  • Therapeutic effects develop over 6-8 weeks
  • Little impact on negative symptoms

Side effects:
-High incidence of extrapyramidal symptoms

21
Q

Clozapine

A

Second generation antipsychotic

  • Most effective antipsychotic
  • Very potent 5-HT2A receptor antagonist
  • Only drug to show efficacy in treatment resistant schizophrenia and negative symptoms

Side effects:
-potentially fatal neutropenia, agranulocytosis, myocarditis and weight gain

22
Q

Risperidone

A

Second generation antipsychotic
-Very potent 5-HT2A receptor and dopamine D2 receptor antagonist

Side effects:
-More extrapyramidal symptoms and hyperprolactinaemia than other atypical antipsychotics

23
Q

Quetiapine

A

Second generation antipsychotic
-Very potent H1 receptor antagonist

Side effects:
-Lower extrapyramidal symptom incidence compared to other antipsychotics

24
Q

Aripiprazole

A

Second generation antipsychotic

  • Partial dopamine D2 receptor and 5-HT2A receptor agonist
  • No more effective than typical antipsychotics

Side effects:
-reduced incidences of hyperprolactinaemia and weight gain compared to other antipsychotics

25
Q

Dopamine synthesis

A

1) L-tyrosine converted to L-DOPA by Tyrosine hydroxylase
2) L-DOPA converted to Dopamine by DOPA decarboxylase

OCCURS IN THE NEURONE

26
Q

Dopamine metabolism

A

-dopamine removed from synaptic cleft by dopamine transporter and noradrenaline transporter

3 enzymes metabolising dopamine:

1) Monoamine oxidase A (MAO-A) metabolises dopamine, NE, and 5-HT
2) Monoamine oxidase B (MAO-B) metabolises dopamine
3) Catechol-O methyl transferase (COMT)=wide distribution and metabolises all catecholamines

27
Q

Parkinson’s disease epidemiology

A
  • 1 to2% of individuals over 60 years old

- around 5% of cases are due to mutations in certain genes (eg: SNCA, LRRK2)

28
Q

Parkinson’s disease pathophysiology

A
  • severe loss of dopaminergic projection cells in substantia nigra pars compacta
  • Lewy bodies and Lewy neurites=found respectively within neuronal cell bodies and axons
  • neurofilaments and proteins (ubiquitin and alpha-synuclein) become abnormally phosphorylated, aggregating within Lewy bodies and Lewy neurites
29
Q

Parkinson’s disease clinical presentation

A 
MOTOR (BEFORE NON-MOTOR/COGNITIVE SYMPTOMS)
-resting tremor
-bradykinesia
-rigidity
-postural instability
-stooped, shuffling gait
-loss of arm swing 
-hypomimia
-micrographia
NON-MOTOR (AUTONOMIC)
-anosmia (olfactory deficits)
-orthostatic hypotension
-constipation
-erectile dysfunction
-urinary incontinence
-hypersalivation
NON-MOTOR (NEUROPSYCHIATRIC)
-insomnia (sleep disorders)
-cognitive decline 
-dementia (memory deficits)
-depression
-anxiety
-irritability
30
Q

Schizophrenia epidemiology

A

/

31
Q

Receptor activation in Parkinson’s disease

A

/

32
Q

Dopamine replacement

A

L-tyrosine converted to dopamine

-rate limiting enzyme is tyrosine hydroxylase

Pharmacology and Therapeutics (30 decks)

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