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pharmacology of movement Flashcards

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1
Q

in parkinson’s, what pathway is there a shift to?

A

indirect pathway

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2
Q

describe the pathology seen in parkinson’s?

A
  • loss of dopaminergic cells in SNPC

- presence of Lewy bodies in neurons

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3
Q

what other disease is Lewy bodies found in?

A

dementia with Lewy bodies

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4
Q

what are Lewy bodies?

A

intracellular formations enriched in the protein a-synuclein

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5
Q

what is Dopamine transporter (DaT) imaging used for?

A

used to monitor gradual dopaminergic nigral cell loss

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6
Q

what is the dopamine transporter a marker of?

A

dopaminergic projections - can be labelled with SPECT ligands

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7
Q

what are the features of parkinson’s?

A

resting tremor
bradykinesia
rigidity
frozen facial expression and flexed posture
altered gait and postural changes
difficulty in initiating and stopping movement
gradual development of micrographia

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8
Q

what is the cardinal feature of parkinson’s?

A

bradykinesia

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9
Q

what is bradykinesia?

A

slowness of movement

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10
Q

what is micrographia?

A

small writing that cannot be deciphered

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11
Q

what are non-motor features of parkinson’s?

A 
•	Hyposmia
-       Depression
•	Psychotic symptoms
•	Cognitive dysfunction
•	Dementia (late phase)
•	Sleep disturbance
•	Autonomic dysfunction
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12
Q

what is hyposmia?

A

decreased sense of smell

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13
Q

why are non-motor symptoms useful?

A

Non-motor symptoms can be used to diagnose the condition 12-15 years earlier

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14
Q

what are the main genes involved in Parkinson’s

A

SNCA

LRRK2

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15
Q

what does the SNCA gene control?

A

involves the alpha-synuclein protein

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16
Q

what type of molecule is LRRK2?

A

kinase

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17
Q

what is the most common genetic contributor to PD?

A

LRRK2

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18
Q

what factors cause an increase in prevalence of PD?

A

age

male

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19
Q

what is MPTP?

A

methyl-phenyl-tetrahydropyridine

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20
Q

what is MPTP metabolised into?

A

MPP+

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21
Q

what is the problem with MPP+?

A

neurotoxic for dopaminergic neurons

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22
Q

what dysfunction can lead to increased oxidative stress?

A

Dysfunction of complex I in mitochondrial resp chain

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23
Q

why is increased oxidative stress bad in parkinson’s?

A

• Dopamine is v oxidizable – its metabolism forms free radicals and oxidation products e.g. H2O2
- leads to more monoamine oxidase (B isoform) so there’s less dopamine available

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24
Q

describe the biosynthesis of dopamine?

A

L-tyrosine –> L-Dopa –> dopamine

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25
describe the metabolism of dopamine
Dopamine  DOPAC via MAO + aldeyhyde dehydrogenase DOPAC  Homovanilic acid via COMT
26
why is L-Dopa given instead of dopamine?
1. Dopamine is broken down and inactivated 2. Hydrophilic – can pass through the BBB 3. Dopamine makes you sick in large amounts
27
why does dopamine make you sick in large amounts?
it stimulates dopamine receptors in the chemoreceptor trigger zone outside the BBB  induces vomiting
28
why does an L-dopa carboxylase inhibitor need to be given with L-Dopa carboxylase?
stops L-dopa from being peripherally converted into dopamine
29
name the dopaminergic pathways in the CNS?
nigrostriatal mesocortical mesolimbic
30
where is the nigrostriatal pathway?
from the SNPC to the striatum
31
where is the mesocortical pathway?
ventral tegmental area to the cingulate cortex
32
where is the mesolimbic pathway?
ventral tegmental area to the ventral part of the striatum
33
which dopaminergic pathway should be targeted by treatment?
nigrostriatal
34
what type of receptors are dopamine receptors?
GPCRs
35
what are the 2 main groups of dopamine receptors?
D1-like | D2-like
36
what are the D1-like receptors?
D1 and D5
37
what are the D2-like receptors?
D2, D3 and D4
38
what are the main treatment methods for parkinson's?
1. Dopaminergic compounds 2. MOAB inhibitors 3. Anticholinergic compounds 4. Amantadine 5. COMT inhibitors
39
how do dopaminergic compounds help in PD?
compensate directly for the dopamine deficit
40
what is the most common dopaminergic compound given in PD?
L-Dopa (Levodopa) | Biosynthetic precursor
41
what does L-Dopa need to be combined with?
a peripherally acting DOPA decarboxylase inhibitor
42
name DOPA decarboxylase inhibitors
carbidopa | benserazide
43
name dopaminergic agonists
ropinirole, pramipexole, rotigotine, pergolide, bromocriptine, cabergoline
44
how is rotigotine administered?
transdermal patch
45
how is apomorphine administered?
infusion for major motor fluctuations
46
how do MAOB inhibitors work?
protect residual dopamine against oxidation
47
name MAOB inhibitors
Rasagiline, selegiline
48
why should anticholinergic compounds be given in PD?
dopamine loss leads to hyperactivity of cholinergic cells
49
name anticholinergic compounds
Orphenadrine, procyclidine, trihexyphenidyl
50
why is amantadine given in PD?
inhibits dopamine reuptake | increases dopamine release
51
why are COMT inhibitors given in PD?
used in combination with L-Dopa to enhance its effects
52
name COMT inhibitors
Entacapone, tolcapone
53
list adverse effects of L-Dopa
* Nausea/vomiting * Postural hypotension * Psychosis * Impulse-control disorders * Excessive day-time sleepiness
54
what are the motor complications of L-Dopa?
- on-off effect - wearing off - dyskinesia - dystonia
55
what is the on off effect?
unpredictable mobility associated with regular intake of L-DOPA
56
what is dyskinesia?
uncontrollable involuntary movement
57
what is dystonia?
muscles contracting uncontrollably
58
what should PD patients have access to?
o monitoring and alteration of medication o a continuing point of contact o a reliable source of information Physiotherapy, speech and language therapy and occupational therapy should be available
59
what are other treatment approaches to PD other than pharmacological treatments?
- human embryonic mesencephalic graft - graft releases dopamine after metamphetamine is given - surgical approach
60
what surgical approaches are there to PD?
- stimulation of subthalamic nucleus - pallidotomy - thalamotomy - deep brain stimulation
61
what is a thalamotomy?
destruction of part of the thalamus to fix a tremor
62
when is deep brain stimulation used?
used in people with advanced PD whose symptoms aren’t controlled by pharmacology therapy
63
what is Huntington's chorea?
involuntary jerky movements
64
what pathology causes Huntington's?
Major degeneration of striatal neurons and cortical atrophy loss of medium spiny neurons (striato-pallidal and striato-nigral pathways)
65
how is huntington's inherited?
autosomal dominant
66
what gene is affected in huntington's and what chromosome is this found on?
huntingtin gene on chromosome 4
67
how does the affected gene in Huntington's present?
o Genes presents w abnormal number of repeats of glutamine (CAG codon) in the protein sequence – gain of function mutation - mutated protein aggregates inside cells
68
what are the mechanisms underlying neurodegeneration in huntington's disease?
* Excitotoxicity * Loss of neurotrophic factors * Accumulation of aggregates of mutant huntingtin protein * Dysregulation of transcription * Increased oxidative stress * Abnormalities in axonal transport * Synaptic abnormalities
69
what are symptoms of HD?
* Choreic movement (early to mid-stage disease) * Gait abnormalities * Lack of coordination * Cognitive impairment: poor attention, memory difficulties * Psychiatric disturbances * Sleep disturbance * Weight loss
70
how long does HD take to progress from onset?
12-15 years
71
what is the pharmacological treatment for HD?
no treatment - mainly palliative and symptomatic o Tetrabenazine: inhibitor of vesicular amine transporter o Haloperidol, Olanzapine: antidopaminergic/antipsychotic drugs o Imipramine, Amitriptyline: antidepressant drugs.

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