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Pharmacology and Therapeutics 2 Y2 > Anti-Parkinsonian Drugs and Neuroleptics > Flashcards

Anti-Parkinsonian Drugs and Neuroleptics Flashcards

1
Q

Describe DA synthesis

A
  • L-tyrosine -> (tyrosine hydroxylase) ->L-DOPA -> (DOPA decarboxylase) -> Dopamine (DA)
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2
Q

What is the rate limiting step in DA synthesis

A

Tyrosine hydroxylase

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3
Q

What removes DA from the synapse (2)

A

DA transporter and NA transporter

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4
Q

What metabolises DA (3)

A

Monoamine oxidase A (MAO-A) - metabolises DA, NE & 5-HT
MAO-B - metabolises DA
Catechol-O-methyl transferase (COMT) - wide distribution (glial cell, presynaptic terminal, CM of other cells), metabolises all catecholamines

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5
Q

What enzymes metabolises all catecholamines

A

COMT

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6
Q

What does MAOA metabolise?

A

DA, NE, 5-HT

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7
Q

4 major dopaminergic pathways?

A
  1. Nigrostriatal pathway - susbstantia nigra pars compacta (SNc) to the striatum Inhibition results in movement disorders (Parkinsons)
  2. Mesolimbic pathway - ventral tegmental area (VTA) to the Nucleus Accumbens (NAcc) Brain reward pathway (Schizophrenia)
  3. Mesocortical pathway - VTA to the cerebrum/frontal lobe. Important in executive functions & complex behavioural patterns (Schizophrenia)
  4. Tuberoinfundibular pathway - arcuate nucleus to the median eminence. Inhibition results in hyperprolactinaemia
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8
Q

Where is Nigrostriatal pathway from/to

A

susbstantia nigra pars compacta (SNc) to the striatum

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9
Q

What does inhibition of the Nigrostriatal pathway result in

A

Movement disorders (Parkinsons)

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10
Q

Where is Mesolimbic pathway from/to

A

ventral tegmental area (VTA) to the Nucleus Accumbens (NAcc)

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11
Q

Where is mesocortical pathway from/to

A

VTA to the cerebrum/frontal lobe

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12
Q

Where is tuberoinfundibular pathway from/to

A

arcuate nucleus to the median eminence

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13
Q

What is the pathway from susbstantia nigra pars compacta (SNc) to the striatum known as

A

Nigrostriatal pathway

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14
Q

What is the pathway from arcuate nucleus to the median eminence known as

A

tuberoinfundibular pathway

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15
Q

What is the pathway from VTA to the cerebrum/frontal lobe known as

A

mesocortical pathway

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16
Q

What is the pathway from ventral tegmental area (VTA) to the Nucleus Accumbens (NAcc) known as

A

Mesolimbic pathway

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17
Q

What does inhibition of the susbstantia nigra pars compacta (SNc) pathway to the striatum lead to

A

Movement disorders (Parkinsons)

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18
Q

What does dysfunction of the Mesolimbic pathway lead to

A

Schizophrenia

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19
Q

What does dysfunction of the mesocortical pathway lead to

A

Schizophrenia

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20
Q

What does dysfunction of the tuberoinfundibular pathway lead to

A

hyperprolactinaemia

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21
Q

What does pathway dysfunction of ventral tegmental area (VTA) to the Nucleus Accumbens (NAcc) lead to

A

Schizophrenia

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22
Q

What does pathway dysfunction of VTA to the cerebrum/frontal lobe lead to

A

Schizophrenia

23
Q

What does pathway dysfunction of susbstantia nigra pars compacta (SNc) to the striatum lead to

A

Parkinsons and other motor diseases

24
Q

What is the Mesocortical pathway important for

A

executive functions & complex behavioural patterns

25
Q

What is the mesolimbic pathway important for

A

Brain reward pathway

26
Q

Difference in causes of early and late stage onset of Parkinsons

A

Only early stage has genetic associations

27
Q

Similarity between Alzheimers and Parkinsons regarding their onset?

A

Only early stage has genetic associations

28
Q

Pathophysiology of Parkinsons? (loss of what where, what is found to be present/abnormal)

A
  • Severe loss of dopaminergic projection cells in SNc – nigrostriatal pathway
  • Lewy bodies & neurites -> Found respectively within neuronal cell bodies & axons
  • Consist of abnormally phosphorylated neurofilaments, ubiquitin & a-synuclein
29
Q

Motor symptoms of Parkinsons?

A

resting tremor, bradykinesia (slowness in movement), rigidity, postural instability (cardinal symptoms) (4)

30
Q

ANS deficits of Parkinson’s? (3)

A

olfactory deficits, orthostatic hypotension, constipation

31
Q

Neuropsychiatric presentations of Parkinsons?

A

sleep disorders, memory deficits, depression, irritability

32
Q

3 Main methods of treating Parkinsons?

A
  1. Dopamine replacement
  2. Dopamine receptor agonists
  3. Monoamine oxidase B (MAOB) inhibitors
33
Q

Adjuncts given alongside DA replacements?

A

DOPA decarboxylase inhibitors

COMT inhibitors

34
Q

Example of dopamine replacement?

A

L-DOPA

35
Q

Side effects (short and long term) of DA replacement?

A

ST: nausea & vomiting
LT: dyskinesias & ‘on-off’ effects

36
Q

How does L-DOPA work?

A
  • Rapidly converted to DA by DOPA decarboxylase (DOPA-D)
  • Can cross blood-brain barrier (BBB)
  • Basically works by flooding the remaining neurons that have survived the neurodegeneration with dopamine which acts on the D2 receptor D2R.
  • Peripheral breakdown by DOPA-D ® Leads to activation of the CTZ chemoreceptor trigger zone and so nausea & vomiting
37
Q

Purpose of DOPA decarboxylase inhibitors given as adjuncts with L-DOPA?

A

does not cross BBB -> prevents peripheral breakdown of levodopa and then separates with it at the BBB
Reduces levodopa dosage needed

38
Q

Receptors that L-DOPA activates post-cleavage?

A
  • Dopamine (DA) can act on D1,5(Gs linked) or D2-4 (Gi-linked) receptors
  • DA is re-uptaken by the dopamine transporter (DAT) & metabolised by monoamine oxidase (MAO) enzymes
39
Q

problem with DA receptor agonists? (which type of DA agonist?)

A
  • Associated with cardiac fibrosis

Ergot derivatives

40
Q

Which type of DA receptor agonist is associated with cardiac fibrosis and which one isn’t

A

Ergot derivatives are

Non-ergot aren’t

41
Q

Life expectancy of schizophrenics?

A

30 years less than usual

42
Q

Predisposing factors of schizophrenia

A

Genetics and afro-carribeans

43
Q

What is the reason for the different life expectancy of schizophrenics?

A

recreational drug use to alleviate symptoms kills people early

44
Q

‘Positive’ symptoms of schizophrenia (4)

A
  • Increased Mesolimbic dopaminergic activity
  • Hallucinations- Auditory & visual
  • Delusions- Paranoia
  • Thought disorder- Denial about oneself
45
Q

‘Negative’ symptoms of schizophrenia? (4)

A
  • Decreased Mesocortical dopaminergic activity
  • Affective flattening- lack of emotion
  • Alogia- lack of speech
  • Avolition/apathy- loss of motivation
46
Q

Most effective antipsychotic?Why is it the most effective?

A

Clozapine as it treats both positive and negative symptoms of schizophrenia

47
Q

second gen antipsychotic examples? (3)

A

Clozapine, risperidone, quetiapine

48
Q

quetiapine e.g. of?

A

Second gen antipsychotic

49
Q

risperidone e.g. of?

A

Second gen antipsychotic

50
Q

Clozapine e.g. of?

A

Second gen antipsychotic

51
Q

Antipsychotic receptor targets?

A

5-HT, D2 receptors, H1 receptors

52
Q

MOA of clozapine

A
  • Very potent antagonist of 5-HT2A receptors
53
Q

MOA of risperidone

A

5HT and D2 antagonist

54
Q

MOA of quetiapine

A

Potent H1 antagonist

Pharmacology and Therapeutics 2 Y2 (24 decks)

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