Parkinson's clinical Flashcards by kayleigh wootten

what is Parkinson’s disease

chronic, progressive neurodegenerative disease resulting from the loss of dopamine containing cells in the substantia nigra

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which pathway in the brain affects motor control

nigrostriatal pathway

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which pathway in the brain affects behaviour

mesolimbic and Mesocortical pathways

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which pathway in the brain affects endocrine control

Tuberhypophyseal pathway

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what are the motor symptoms of parkinsons disease

bradykinesia
muscle rigidity
tremor

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what is bradykinesia

slowness of voluntary movement that is asymmetrical and unpredictable

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what are the signs of bradykinesia

mask like face
soft voice - hypophonia
micrographia
shuffling gait
difficulty with fine actions

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what is muscle rigidity

increased tension
mainly in flexor muscles, trunk or limbs
stooping posture

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what are the signs of tremor

when resting, usually in hands - pill rolling movements
improves with concentration or voluntary movement

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which medicines can cause tremor

antipsychotics
beta agonists
anti-emetics

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what are the non-motor symptoms of parkinsons disease

depression
anxiety
fatigue
cognitive impairment
sleep disturbance
constipation
hyposmia
sialorrhea
excessive sweating
urinary issues
pain
hypotension

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what are the extrinsic environmental causes of parkinsons disease

drugs
- antipsychotics EPSEs
- antiemetic EPSEs
- reserpine
- recreational drugs

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how does reserpine cause parkinsons disease

depleted monoamines from presynaptic storage reduces dopamine release

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what are the extrinsic physical factors that can cause parkinsons disease

cerebral ischaemia
viral encephalitis
brainstem injury
dementia pugilistica from repeated head injury

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what are the intrinsic causes of parkinsons disease

genetic
age

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what mutations can cause parkinsons disease

alpha synuclein mutations
lewy body formation
parkin gene mutation

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what do alpha synuclein mutations do

causes lewy body formation, which causes DNA damage

what does the parkin gene do

neuroprotective gene - mutations are responsible for early onset

what are the exclusion factors for diagnosis of parkinsons

stroke
head injury
antipsychotics
encephalitis

supportive criteria for the diagnosis of parkinsons

unilateral onset
response to levodopa
progressive

what are the guidelines for the treatment of motor symptoms in PD

levodopa
when dyskinesia or fluctuations develop - add
- dopamine agonist
- monoamine oxidase B inhibitors
- catechol-o-methyl transferase inhibitors
- amantadine

which medications are co-administered with levodopa and why

Given with carbidopa or benserazide - reduces peripheral absorption Or COMT inhibitors such as entacapone

side effects of COMT inhibitors

red/orange urine
diarrhoea

what are the side effects of levodopa

nausea
anorexia
hypotension
sleep disturbances
psychological effects

how is levodopa to be taken

up to 800mg/day in divided doses 30-60 minutes after eating - inhibited by protein must be brand prescribed!

what are dopamine agonists and how do they work

mimics actions of dopamine ergot derived - bromocriptine (lots of s/e) non-ergot derived - ropinirole, pramipexole

dopamine agonist s/e

less dyskinesias but more s/e - especially ergot derived which should not be used unless absolutely necessary - N&V - heart and lung fibrosis

how are dopamine agonists taken

TDS usually but can get in MR formulations

what are monoamine oxidase inhibitors and how do they work

reduces metabolism of dopamine - may partially slow disease progression - selegeline - metabolised to amphetamine - rasagiline

what are the side effects of monoamine oxidase inhibitors

nausea postural hypotension dyskinesia confusion

how does amantadine work

increases dopamine levels in the brain - mild benefit to symptoms adjuvant only efficacy diminishes after a few months

what are the side effects of amantadine

hallucinations sleep disturbances N and V anorexia hypotension palpitations

what are impulse control disorders and how are they caused

caused by amantadine, dopamine agonists can last for 4-5 years post treatment - more likely to happen in younger males, with smoking or alcohol history

what happens if a dose of levodopa

acute akinesia or neuroleptic-like malignant syndrome

what is neuroleptic-like malignant syndrome

fever, rigidity, elevated CK and leucocytosis - caused by sudden drop in dopamine activity - more common in high levodopa doses

how are the non-motor symptoms of mental health treated in parkinsons

depression and anxiety - SSRI as per NICE dementia - rivastigmine (donepezil off label) impulse control - optimise therapy confusion/hallucinations - if severe quetiapine/clozapine

how are the non-motor symptoms of autonomic dysfunction treated in parkinsons

constipation - stimulant (PRN) and softener orthostatic hypertension if severe - midodrine/fludrocortisone dysphagia - optimise/switch meds excessive salivation and sweating - Glycopyrronium bladder issues - anti-muscarinic sexual dysfunction - sildenafil

how are the non-motor symptoms of N and V treated in parkinsons

1. domperidone 2. cyclizine or ondansetron protein free snacks before taking

how are the non-motor symptoms of pain treated in parkinsons

follow pain ladder consider s/e

how are the non-motor symptoms of sleep disturbances treated in parkinsons

○ Sedatives ○ Short term occasional - can cause falls etc ○ Daytime sleepiness - modafinil - specialist

how are patients medicines managed in parkinsons

- Review every 6-12m - Titrate to optimise - Sudden drug cessation may precipitate acute akinesia or neuroleptic malignant syndrome - Small doses of levodopa at increased intervals decrease peaks and troughs ○ Do not eat protein 30-60 mins before dose ○ Must be prescribed by brand

which OTC medications can worsen parkinsons symptoms

○ OTC avoid sympathomimetics (e.g. pseudoephedrine) with MAO-B inhibitors ○ OTC antihistamines ○ Calcium channel blockers – occasional EPSE, frequency unknown