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BB CC > Pharmacology of Movement > Flashcards

Pharmacology of Movement Flashcards

1
Q

Parkinson’s Pathology

A

Loss of dopaminergic cells in substantia nigra pars compacta
Lewy bodies in neurones- intracellular formations enriched in the protein alpha-synuclein
GABA inhibitory drive to thalamus becomes stronger

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2
Q

Dopamine Transporter (DaT) imaging

A

Help monitor gradual dopaminergic nigral cell loss

In striatum

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3
Q

Cardinal Parkinson’s signs

A

Resting tremor
Bradykinesia
Rigidity
Gait and postural changes

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4
Q

Parkinson’s other changes

A 
Frozen facial expression
Flexed posture
Stop/Start movement
Microphagia
Depression
Sleep disturbance
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5
Q

Non-motor features parkinsons

A

May precede by 12-15 years the onset of atypical Parkinsonian motor symptoms

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6
Q

SNCA gene

A

Used to make alpha-synuclein

Rare SNCA mutations, duplications or triplications cause autosomal dominant familial PD

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7
Q

Prevalence PD

A

2nd most common neurodegenerative disorder
100-180 in 100,000
M > F

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8
Q

Mitochondrial toxicity

A

MPTP= methyl-phenyl-tertrahydropyridine
Compound MPTP can be transformed into metabolite MPP+ which is neurotoxic for dopaminergic neurones
MPP+ taken up into neurone
Causes dysfunction of Complex 1 of the mitochondrial respiratory chain –> increased oxidative stress

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9
Q

Oxidative stress

A

Increased in Parkinson’s
Dopamine is highly oxidizable + its metabolism produces free radicals + oxidation products e.g. H2O2
MAO (b isoform) critically involved in oxidation processes

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10
Q

Dopamine biosynthesis

A

L-tyrosine –> L-Dopa

L-Dopa –> Dopamine

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11
Q

Dopaminergic pathways in CNS

A

Mesocortical
Mesolimbic
Nigrostriatal

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12
Q

Dopamine receptors

A

G protein coupled receptors

Dopamine binds to two types- D1-like and D2-like

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13
Q

D1-like receptor subtypes

A

D1 and D5

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14
Q

D2-like receptor subtypes

A

D2, D3, D4

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15
Q

L-Dopa

A

Biosynthetic precursor

Combined with peripherally acting DOPA decarboxylase inhibitors (carbidopa, benserazide)

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16
Q

Dopaminergic agonists

A 
Ropinirole
Pramipexole
Rotigotine- transdermal patch
Apomorphine- infusion
Pergolide
Bromocriptine
17
Q

MAOB inhibitor

A

Protect residual dopamine against oxidation
Rasagiline
Selegiline

18
Q

Anticholinergic (antimuscarinic) compounds

A

Dopamine loss leads to hyperactivity of cholinergic cells
Orphenadrine
Procyclidine

19
Q

Amantidine

A

Inhibits dopamine reuptake

Increases dopamine release

20
Q

COMT inhibitors

A

Used in combination with L-Dopa to enhance its effects
Entacapone
Tolcapone

21
Q

L-Dopa adverse effects

A 
Nausea/vomiting
Postural hypotension
Psychosis
Impulse-control disorders
Excessive day time sleepiness
22
Q

L-Dopa motor complications

A

On-off effect
Wearing-off
Dyskinesia
Dystonia

23
Q

Treatment stratergy

A

Mild- MAO-B inhibitor
Mild/moderate- Dopamine agonist
Moderate/severe- Levodopa + COMTI

24
Q

Human embryonic mesencephalic graft

A

Graft is functional and releases dopamine

25
Q

Surgical approaches to PD

A

Stimulation subthalamic nucleus
Thalamotomy
Pallidotomy
DBS - advance PD whose symptoms not adequately controlled by optimised pharmacological therapy

26
Q

Huntington’s disease

A

Autosomal dominant
Changes in gene encoding protein huntingtin on chromosome 4
Gene presents with abnormal no. of repeats of glutamine in protein sequence
–> abnormal gene contains >36 repeats
–> gain of function mutation
–> mutated protein aggregates inside cells
Major degeneration of striatal neurones and cortical atrophy

27
Q

Huntington’s disease pathological changes

A

Cortical atrophy
Prominent striatal degeneration
Loss of medium spiny neurones (striato-pallidal and striato-nigral)

28
Q

Huntingtons- mechanisms underlying neurodegeneration

A 
Excitotoxicity
Loss of neurotrophic factors
Accumulation of aggregates of mutant huntingtin protein
Dysregulation of transcription
Increased oxidative stress
29
Q

Huntington’s symptoms

A 
Choreic (jerky) movements
Gait abnormalities
Lack of coordination
Cognitive impairment- bad attention and memories
Sleep disturbance
Weight loss
Psychiatric disturbances
30
Q

Huntington’s pharmacological management

A

Vesicular amine transporter inhibitor- tetrabenazine
Antidopaminergic drugs- haloperidol, olanzapine
Antidepressant drugs- imipramine, amitriptyline

BB CC (29 decks)

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