Neuro: Parkinson's Disease Flashcards
what non-drug treatments are avaialable for PD patients?
physiotherapy for balance/motor probs, speech and language therapy if the pt develops communication, swallowing or salive problems, occupational therapy for daily activities.
whats the 1st line options for PD patients whose motor symptoms affect their QoL?
levodopa with carbidopa or benserazide
what are the 1st line options for patients whose motor symptoms do not affect their quality of life?
levodopa
non-ergot derived dopamine agonists (pramipexole, ropinirole or rotigotine)
monoamine oxidase B inhibitors (rasagiline, selegiline)
what adverse reactions from antiparkinsonian drugs should you inform patient/carer about?
psychosis
excessive sleepiness
sudden onset of sleep
impluse control disorder with all dopaminergic therapy
what class of PD drug can cause sudden onset of sleep?
dopamine receptor agonists
why musn’t PD drug concentrations fall suddenly? - give 2 reasons why they might fall suddenly
to avoid potential for akinesia or neuroleptic malignant syndrome
due to poor absorption (constipation) or abrupt withdrawal
name 4 impulse control disorders
compulsive gambling, hypersexuality, binge eating, excessive shopping
breifly summarise the pathology behind PD
decreased dopamine due to loss of dopaminergic neurons in substantia nigra - presence of lewy bodies which contain alpha synuclein
why can’t dopamine be administered so why is levodopa given?
because dopamine does not pass BBB so would be metabolised in the gut so give LDOPA (the intermediate)
what’s the rate limiting step in the conversation of tyrosine to dopamine?
tyrosine hydorxylase - so means we can’t convert tyrosine to dopa even if we supplement with excessive amount of dopa
what converts l-dopa to dopamine?
what happens to dopamine if this conversion happens in the gut?
why is l-dopa never given on its own?
what is is given with?
- amino acid decarboxylase
- if this happens in the gut DA will be broken down by MAO and COMT
- because no DA would reach the brain if this occured
- given with a peripherally acting dopa decarboxylase inhibitor which blocks AADC in periphery allowing more l-dopa to cross the brain to be converted intp DA
name 2 peripheral dopa decarboxylasei nhibitors
carbidopa
benserazide
what class of drugs are impulse disorders associated with?
when are they used?
- dopamine D2 receptor agonists
- used alone in early (mild) disease to try and delay SE of L-dopa, or add on therapy with L-dopa to help balance SE
what’s secondary parkinsonism?
what type of drugs may be given to help?
is this the first port of call?
PD symptoms due to a cause other than idopathic PD - usually caused by drugs
- dopaminergic drugs can be given (levodopa, ropinerole, pramipexol)
- 1st line of action is to discontinue offending drug
what are the 2 types of D2 receptor agonists?
what’s the difference in their action?
what ones aren’t used often due to cardiac problems?
give examples
- ergot (cabergoline) and non-ergot (ropinerole, pramipexol)
- ergot are older and are more selective towards D1 and D2 wherear non-ergot are newer and have more selectivity to D2 and D3
- ergot ones have cardaic problems
what does COMT stand for?
give an example
what effect to COMT inhibitors have on the action of levodopa?
catechol methyl transferase
entacapone (formulated as stalevo)
increases duration of action of levodopa as help more get to brain
what therapy should be added if patients develop dyskineisa/motor fluctuations despite optimal levodopa therapy?
non-ergot receptor agonist, monoamine oxidase B inhibitor, or COMT inhibitor
when could you consider an ergot dopamine agonist?
what drug should be considered if dyskinesia is not managed by modifying existing therapy?
- only to be added to levodopa if symptoms are not adequtely controlled with anon-ergot dopamine agonist
amantadine hydrochloride
give 2 examples of monoamine oxidase B inhibitors
why aren’t drugs that inhibit MAOA used?
what interaction must you counsel patients on?
- rasagiline and selegiline
- becuase MAOB predominate in CNS and MAOA inhibitors would have more side effects
- interactio with dextramethorphan (antitussive) = increased hypertensive effect, risk of psychotic episode
what drug should be considered to help daytime sleepiness once reversible pharmacological and physical causes have been excluded?
modafinil
what is nocturnal akinesia?
what are the 1st and 2nd line treatment options?
- loss of ability to move muscles voluntarily at night
- levodopa or oral dopamine receptor agonists as first line
- rotigotine second line
what class of drug is rotigotine?
non-ergot receptor agonists
what are the pharmacological options to manage postural hypotension in PD once drug treatment has been reviewed?
1st line = midodrine hydrochloride
2nd = fludrocortisone (unlicensed)
how do you manage the psychotic symptoms of PD such as hallucinations/delusions?
what’s the 1st line?
is this a licensed use?
- don’t need to treat if hallucinations well tolerated
- otherwise, review dosage of PD drugs that may have triggered hallucinations
- quetiapine (unlicensed) can be considered
- if not effective then clozapine
