Parkinson's clinical Flashcards
what is Parkinson’s disease
chronic, progressive neurodegenerative disease resulting from the loss of dopamine containing cells in the substantia nigra
which pathway in the brain affects motor control
nigrostriatal pathway
which pathway in the brain affects behaviour
mesolimbic and Mesocortical pathways
which pathway in the brain affects endocrine control
Tuberhypophyseal pathway
what are the motor symptoms of parkinsons disease
bradykinesia
muscle rigidity
tremor
what is bradykinesia
slowness of voluntary movement that is asymmetrical and unpredictable
what are the signs of bradykinesia
mask like face
soft voice - hypophonia
micrographia
shuffling gait
difficulty with fine actions
what is muscle rigidity
increased tension
mainly in flexor muscles, trunk or limbs
stooping posture
what are the signs of tremor
when resting, usually in hands - pill rolling movements
improves with concentration or voluntary movement
which medicines can cause tremor
antipsychotics
beta agonists
anti-emetics
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
what are the extrinsic environmental causes of parkinsons disease
drugs
- antipsychotics EPSEs
- antiemetic EPSEs
- reserpine
- recreational drugs
how does reserpine cause parkinsons disease
depleted monoamines from presynaptic storage reduces dopamine release
what are the extrinsic physical factors that can cause parkinsons disease
- cerebral ischaemia
- viral encephalitis
- brainstem injury
- dementia pugilistica from repeated head injury
what are the intrinsic causes of parkinsons disease
- genetic
- age
what mutations can cause parkinsons disease
alpha synuclein mutations
lewy body formation
parkin gene mutation
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
- domperidone
- 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
