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eLCRS - 팜 > Anti-Parkinson drugs & Neuroleptics > Flashcards

Anti-Parkinson drugs & Neuroleptics Flashcards

1
Q

describe the synthesis of dopamine

A

L-tyrosine –> converted to L-DOPA (via Tyrosine hydroxylase)
–> which is then converted to Dopamine (DA) (via DOPA decarboxylase)

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2
Q

Describe the metabolism of dopamine

A

method 1 :
DA = removed from synaptic cleft by dopamine transporter (DAT) + noradrenaline transporter (NET)

method 2: enzyme metabolism (3)

  • Monoamine oxidase A (MAO-A): –> metabolises DA, NE & 5-HT
  • MAO-B: metabolises DA
  • Catechol-O-methyl transferase (COMT): wide distribution, metabolises all catecholamines
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3
Q

What is the rate limiting step/ enzymes in the synthesis of dopamine

A

Tyrosine hydroxylase)

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4
Q

Where are the 4 major locations of the dopaminergic pathways?

A

Nigrostriatal pathway

  • -> from susbstantia nigra pars compacta (SNc) to the striatum.
  • -> Inhibition results in movement disorders

Mesolimbic pathway

  • -> from ventral tegmental area (VTA) to the Nucleus Accumbens (NAcc).
  • -> Brain reward pathway.

Mesocortical pathway

  • -> from VTA to the cerebrum.
  • -> Important in executive functions & complex behavioural patterns.

Tuberoinfundibular pathway

  • -> arcuate nucleus to the median eminence.
  • -> Inhibition results in hyperprolactinaemia
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5
Q

5% of Parkinson’ disease cases = due to mutations in certain genes:

A
  • SNCA

- LRRK2

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6
Q

Describe the pathophysiology of parkinson’s disease

A
  • there is Severe loss of dopaminergic projection cells in SNc
  • -> Lewy bodies & neurites = Found respectively within neuronal cell bodies & axons

–> Consist of abnormally phosphorylated neurofilaments, ubiquitin & a-synuclein

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7
Q

What are clinical presentation of parkinson’s disease?

A

Motor symptoms –> resting tremor, bradykinesia, rigidity, postural instability (cardinal symptoms)

Autonomic nervous system effects –> olfactory deficits, orthostatic hypotension, constipation

Neuropsychiatric –> sleep disorders, memory deficits, depression, irritability

sequence = ANS effects –> Motor symptoms –> Neuropsychiatric

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8
Q

What are methods to treat parkinson’s disease

A
  1. Dopamine replacement (gold standard)
    - e.g Levodopa (L-DOPA)
    - -> converted to DA by DOPA decarboxylase
    - - acts on D2receptor
    - -> crosses BBB
  2. dopamine receptor agonists
    a) Ergot Derivatives:
    e.g Bromocriptine & Pergolide
    Act as potent agonists of D2 receptors
    –> Associated with cardiac fibrosis

b) Non-ergot derivatives:
e. g Ropinirole & Rotigotine
- -> Ropinirole also available as extended-release formulation
- -> Rotigotine also available as a patch
- -> non associated with cardiac fibrosis

  1. Monoamine oxidase B (MAOb) inhibitors
    e. g Selegiline
    - -> Reduces dosage of L-DOPA required
    - -> Can increase the amount of time before levodopa treatment is required
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9
Q

What are long term side effects of L-DOPA?

A
  • Dyskinesias + On&off effects
  • -> not disease modifying

–> there is peripheral breakdown by DOPA-D - triggers Chemoreceptor trigger zones
(can cause nausea + vomiting)

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10
Q

L-DOPA can cause nausea + vomiting, how is this overcome?

A

via adjuncts

a) DOPA decarboxylase inhibitors: Carbidopa & Benserazide
- Do not cross BBB –> prevent peripheral breakdown of levodopa
- Reduce required levodopa dosage

b) COMT inhibitors: Entacapone & Tolcapone
increase amount of levodopa in the brain

a) + b) –> increases effect of levodopa

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11
Q

what receptors can dopamine act on?

A

D1,5 (Gs linked)

D2-4 (Gi linked)

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12
Q

What are symptoms of schizophrenia?

a) Positive symptoms
b) Negative symptoms

A

Positive symptoms

  • increase in Mesolimbic dopaminergic activity
  • Hallucinations: Auditory & visual
  • Delusions: Paranoia
  • Thought disorder: Denial about oneself

Negative symptoms

  • decrease in Mesocortical dopaminergic activity
  • Affective flattening: lack of emotion
  • Alogia: lack of speech
  • Avolition/ apathy: loss of motivation
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13
Q

Neuronal pathways

Nigrostriatal pathway: inhibition results in =

Mesolimbic pathway: activation associated with =

Mesocortical pathway: inhibition associated with =

Tuberoinfundibular pathway: inhibition results in =

A

Neuronal pathways
- Nigrostriatal pathway: inhibition results in movement disorders

  • Mesolimbic pathway: activation associated with positive schizophrenia symptoms
  • Mesocortical pathway: inhibition associated with negative schizophrenia symptoms
  • Tuberoinfundibular pathway: inhibition results in hyperprolactinaemia
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14
Q

NOTE:

Disease probability of schizophrenia increases with the presence of one person in family with the disease

A

-

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15
Q

Onset age of schizophrenia =

A

15 - 35 years

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16
Q

NOTE schizophrenic patients –> deaths = more linked to drug use to alleviate symptoms

A

-

17
Q

What are the drugs used to treat schizophrenia?

6 types

  • give an overview of how each work
A

a) chlorpromazine
–> possibly D2 receptor antagonism
Side Effect =
- High incidence : anti-cholinergic, especially sedation
- Low incidence : extrapyramidal side-effects (EPS)

b) Haloperidol
–> potent D2 antagonist
Side Effect =
High incidence - EPS

c) Clozapine
–> most effective antipsychotic
–> potent antagonist of 5-HT2A receptors
Side Effect = can cause potentially fatal neutropenia, agranulocytosis, myocarditis & weight gain

d) Risperidone
–> potent antagonist of 5-HT2A & D2 receptors
SIDE Effect = More EPS & hyperprolactinaemia than other atypical antipsychotics

e) Quetiapine
–> potent antagonist of H1 receptors
Side Effect = Lower incidence of EPS than other antipsychotics

f) Aripiprazole
–> Partial agonist of D2 & 5-HT1A receptors
Side Effects = Reduces incidences of hyperprolactinaemia & weight gain than other antipsychotics

18
Q

Increased DA in mesolimbic pathway:

Reduced DA in mesocortical pathway:

A

Increased DA in mesolimbic pathway: Positive symptoms –> hallucinations

Reduced DA in mesocortical pathway: Negative symptoms –> affective flattening

19
Q

give a brief overview of how chlorpromazine works? on schz

A

Chlorpromazine: phenothiazine causing antimuscarinic side-effects

20
Q

give a brief overview of how haloperidol works? on schz

A

Haloperidol: potent D2 antagonist causing extrapyramidal side-effects

21
Q

give a brief overview of how clozapine works ? on schz

A

Clozapine: very effective but causes agranulocytosis

22
Q

give a brief overview of how risperidone works? on schz

A

Risperidone: effective but associated with weight gain & EPS

23
Q

give a brief overview of how quetiapine works ? on schz

A

Quetiapine: low incidence of EPS

24
Q

give a brief overview of how Aripiprazole works? on schz

A

Aripiprazole: partial agonist, low incidence of hyperprolactinaemia

25
Q

PD: L-DOPA & carbidopa & selegiline - used in conjunction to

A
  • used in conjunction to reduce side-effects & required dosage

eLCRS - 팜 (36 decks)

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