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Antiparkinsons and neuroleptics Flashcards

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1
Q

Differentiate neuroleptics and anti-psychotics and what tey are used to treat

A

SAME….. used to treat schizophrenia

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2
Q

Outline synthesis of dopamine a the dopamine receptor

A

L-tyrosine–> (TH) (i) L-DOPA –> (DOPA-D) (ii) Dopamine (DA)

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3
Q

Which is the rate limiting enzyme in dopamine production

A

TH (i.e you cant just add more tyrosine you have to increase tyrosine)

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4
Q

Outline the metabolism of dopamine

A
  1. DA removed from synaptic cleft by transporters (which?)
  2. Three enzymes beaking down DA:
    - Monoamine oxidase A (MAO-A): metabolises DA, NE & 5-HT
    - MAO-B: metabolises DA (more selective)
    - Catechol-O-methyl transferase (COMT): wide distribution, metabolises all catecholamines
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5
Q

Which transporters take up dopamine

A

dopamine transporter (DAT) & noradrenaline transporter (NET)

(as they are both monoamines)

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6
Q

Why do dopaminergic cells not produce NA which is produced by same pathways

A

Don’t contain the enzymes needed to convert the dopamine to the other MA

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7
Q

Where are MAOs usually found

A

Intracellular and on membrane of the mitochondria on the dopaminergic neuronal cell

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8
Q

Where is COMT found

A

Not just in neuon like the MOA,

found in glial cell, post synaptic membrane, and the neurone

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9
Q

What are the important dopaminergic pathways

A
  1. Nigrostriatal pathway
  2. Mesolimbic pathway
  3. Mesocortical pathway
  4. Tuberoinfundibular pathway
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10
Q

What locations do the nigrostriatal tract run

A

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

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11
Q

What locations do the mesolimbic tract run

A

ventral tegmental area (VTA) to the Nucleus Accumbens (NAcc). Brain reward pathway.

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12
Q

What locations do the mesocortical tract run

A

VTA to the cerebrum. Important in executive functions & complex behavioural patterns.

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13
Q

What locations do the tuberoinfundibular pathway tract run

A

arcuate nucleus to the median eminence. Inhibition results in hyperprolactinaemia

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14
Q

What conditions associated with each dopaminergic pathway

A
  1. Nigrostriatal pathway (movement)

2. Mesolimbic pathway (schizophrenia)

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15
Q

Compare parkinsons and schizophrenia

A

Parkinsons, like alzheimers, is NEURODEGENERATIVE

Schizophrenia is NEUROEFFECTIVE

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16
Q

Genetic component to parkinsons

A

SNCA, LRRK2

associated with the early onset parkinsons, not the late onset, whch is more prevalent

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17
Q

Pathophysiology of parkinsons

A

Severe loss of dopaminergic projection cells in SNc

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18
Q

What molecular signs are seen in parkinsons

A

Lewy bodies & neurites –> Found respectively within neuronal cell bodies & axons

these are associated with the neurodegeneraton

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19
Q

What are lewy bodies and neurites made up of

A

Consist of abnormally phosphorylated neurofilaments, ubiquitin & a-synuclein

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20
Q

Symptoms of parkinsons – motor

A

resting tremor, bradykinesia, rigidity, postural instability

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21
Q

Autonomic NS effects of parkinsons

A

olfactory deficits, orthostatic hypotension, constipation

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22
Q

Psychiatric symptoms of parkinsons

A

sleep disorders, memory deficits, depression, irritability

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23
Q

Progression of parkinsons)

A

Loss of smell (ANS deficit) as neurites start here

Motor

Neuropsychiatric (late stage)

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24
Q

What is the action of levadopa

A

Effecting the 20 % of remaining dopaminergic neurons

It is basically L-DOPA It is rapidly conerted to DA by DOPA decarboxylase (DOPA-D)

Can cross the BBB

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25
What is the consequence of levadopa being converted to dopamine in the periphery
Because DOPA decarboxylase is present in periphery It can make dopamine from the levadopa This can act on areas outsde the BBB.... ie the CTZ and can activate comiting
26
Why can L-tyrosine not be given as PD treatment
The rate limiting step is TH so you need to surpass this step
27
What are the long term effects of levadopa
dyskinesias & ‘on-off’ effects. NOT disease-modifying On/off refers to the changes from motor control to lack of motor control near to end of dose Dyskinesia is muscle movements that people with Parkinson’s can’t control. They can include twitches, jerks, twisting or writhing movements https://www.parkinsons.org.uk/information-and-support/wearing-and-dyskinesia
28
Adjuncts given with levadopa
DOPA decarboxylase inhibitors COMT inhibitors
29
Name 2 DOPA decarboxylase inhibitors and how they help in parkinsons
Carbidopa & Benserazide Do not cross BBB .... this prevent peripheral breakdown of levodopa into dopamine but not that in the CNS Reduce required levodopa dosage
30
Name the different COMT inhibitors
Entacapone & Tolcapone
31
What does COMT do to help in parkinsons
Increase amount of levodopa in the brain
32
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33
Which receptors can dopamine act on
Dopamine (DA) can act on D1,5(Gs linked) or D2-4 (Gi-linked) receptors
34
Second treatment of PD other than levadopa
DOPAMINE RECEPTOR AGONISTS Ergot derivatives: Bromocriptine & Pergolide Non-ergot derivatives: Ropinirole
35
How do dopamine receptor agonists work
Act as potent agonists of D2 receptors
36
Disadvantage or ergot derivative dopamine receptor agonist
Cardiac fibrosis
37
Third treatment of PD
Monoamine oxidase B (MAOB) inhibitors (i.e. the MAO specific to dopamine) Selegiline (deprenyl) & Rasagiline
38
Why are MAO used in PD
Reduce the dosage of L-DOPA required Can increase the amount of time before levodopa treatment is required
39
Outline the formulatins of the non-ergot derivatives
Ropinirole also available as extended-release formulation | Rotigotine also available as a patch
40
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41
Onset of symptoms of schizophrenia
Onset of symptoms: between 15-35 years
42
T/f schizophrenia is 100% genetic
F.. in twin studies with monozygotic twins there is 50% concordance so genetic and environmental factors
43
Higher incidence of schizophrenia in which populations
Higher incidence in ethnic minorities (eg Afro-Caribbean immigrants)
44
Patient's life expctancy with schizophrenia
- 20-30 years lower than average
45
Positive symptoms of schizophrenia
Inceased mesolimbic dopaminergic activity Hallucinations: Auditory & visual Delusions: Paranoia Thought disorder: Denial about oneself memory aid that increased mesolimbic is like drugs do cos of reward and drugs lead to simlar things
46
Negative symptoms of schizophrenia
Reduced Mesocortical dopaminergic activity Affective flattening: lack of emotion Alogia: lack of speech Avolition/ apathy: loss of motivation memory aid that these are cortical function
47
Why is schizophrenia associated with early death
More recreational drug use to alleviate symptoms
48
Pathophysiology of schizophrenia
Increase mesolimbic dopaminergic activity Reduced mesocortical dopamiergic activity
49
What aspects of schizophrenia do the drugs deal with
Only the positive ones
50
Outline types of neuropleptics
=antipsychotic first generation= typical second generation= atypical
51
Action of chlorpromazine
Discovered by serendipity Primary mechanism of action – possibly D2 receptor antagonism. This Gi linked. Reduced AC, cAMP and PKA (also histamine antagonist)
52
Side effects of chlorpromazine
High incidence - anti-cholinergic, especially sedation Low incidence - extrapyramidal side-effects (EPS)
53
Outline mecahnism of haloperidol action
Very potent D2 antagonist (~ 50x more potent than chlorpromazine) Therapeutic effects develop over 6-8 weeks Little impact on negative symptoms
54
Side effects of haloperidol
High incidence of EPS (in contrast to the chlorpromazine which has low EPS and high anticholinergic)
55
Action of clozapine
MOST EFFECTIVE ANTI-PSYCHOTIC Potent antagonist of 5-HT2A receptors
56
T/f clozapine has highest affinity for the 5-HT2A receptor
F.... it binds M1 most effectively but the 5-HT2A is where the effect lies
57
What is the effectiveness of clozipine
Only drug to show efficacy in treatment resistant schizophrenia & negative symptoms (most liit positive systems but not negatie)
58
Side effects of clozapine
Can cause potentially fatal neutropenia, agranulocytosis, myocarditis & weight gain
59
If clozapine is most effective why not used as first line
Because of the side effects, patients ahve to be monoted on them
60
Difference btween first and second generation antipsychtics
first mostly anti D2 | second mostly 5HT angatonist
61
Action of risperiodne
Very potent antagonist of 5-HT2A & D2 receptors
62
Side effects of risperiodone
More EPS & hyperprolactinaemia than other atypical antipsychotics
63
Ation of quetiapine
Very potent antagonist of H1 receptors
64
Side effects of quetiapine
Lower incidence of EPS than other antipsychotics
65
T/F these drugs have good selectivity
F..... they are dirty drugs
66
What is the problem with dopamine antagonist drugs
They are blocking mesolimbic system which is good because this is increased dopamine in schiz but it is also reducing dopamine in the mesocortical system, which is bad because these levels are already reduced in schiz
67
Outline the mechanism of aripiprazole
Partial agonist of D2 & 5-HT1A receptors
68
Why was aripirazole thought to be more effective , and was it
Because it is partial agonist so would incrase dopamine action at the mesocortical tract (where dopamine it is reduced in schiz) but reduce it where dopamine is too high (i.e. mesolimbic) No more efficacious than typical antipsychotics (ie first line)
69
Side effects of aripirazole
Reduced incidences of hyperprolactinaemia & weight gain than other antipsychotics

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