Parkinson's Disease and Epilepsy Flashcards
what is the MOA of levodopa?
precursor of dopamine that is able to cross the BBB. it is taken up into dopaminergic neurons and converted to dopamine.
What needs to be given alongside levodopa in PD and why?
a peripheral dopa decarboxylase inhibitor (carbidopa or benserazide) to prevent levodopa being decarboxylated in teh peripheral tissues so there is more available to cross the BBB
name two side effects from having too much peripheral dopamine in the system
N&V due to stimulation of the CTZ in teh medullary vomiting centre whcih lies outside the BBB. And arrhythmias and vasodilation whcih can lead to postural hypotension and flushing
what can be given to patients who are getting severe side effects caused by peripheral dopamine?
domperidone, a peripheral DA antagonist.
what can excessive dopamine in the CNS cause?
dyskinetic involuntary movements, akathisia (restlessness), halluciantions, anxiety, confusion, pathological gambling, increased libido and psychosis. sedation
name 3 dopamine receptor agonists
pramipexole, ropinirole, rotigotine
name two selective monoamine oxidase type B inhibitors
rasagiline, selegiline
what role do MAOs have in treatmetn of PD?
they can prolong duration of action of DA and reduce levodopa dosage requirement, but only produce modest clinical benefit when used alone.
what is an example of a COMT inhibitor
entacapone
what is the MOA of COMT inhibitors?
COMT is responsible for the breakdown of levodopa. inhibition of COMT doubles the half-life of levodopa and increases motor response to a given dose.
what is often used as the initial treatment for younger pts with PD and why?
DA receptor agonist e.g. ramipexole due to less risk of dyskinesias in the long-term compared with levodopa
what can be used to treat parkinsonian psychosis?
atypical antipsychotics e.g. clozapine or quetiapine
why does drug-induced parkinsonism (e.g. by antipsychotics) respond poorly to levodopa-?
because the causative drug occupies the D2 receptors.
name three sodium channel blocking drugs that are used in epilepsy
carbamazepine, phenytoin, lamotrigine.
what teratogenic effects are associated with carbamazepine?
neural tube defects, cardiac and urinary tract abnormalities and cleft palate
what effect does carbamazepine have on cytochrome P450?
it induces it so it will reduce teh plasma concentration and efficacy of drugs metabolised by CYP enzymes such as warfarin, oestrogens and progestogens
how long do patients have to be seizure-free for before they can drive?
12 months
after changing epilepsy meds or stopping treatment, how many is it before they are allwoed to drive?
6 months
which seizure type does phenytoin not work for?
absences
what is the MOA of sodium valproate?
weak inhibitor of neuronal sodium channels, stabilising resting membrane potentials and reducing neuronal excitability. increases brain content of GABA.
name 4 unwanted effects of sodium valproate
nausea, gastric irritation, diarrhoea, tremor, ataxia, behavioural disturbances, thrombocytopenia, transient increase in liver enzymes
what is thought to be the MOA of levetiracetam
thoguht to modulate release of excitatory neurotransmitters, such as glutamate
what is the drug of choice for status epilepticus in hosptial?
IV lorazepam
after how many seizures is epilepsy usually diagnosed and drug treatment started?
2
name two first line drugs for partial seizures
carbamazepine, lamotrigine, oxcarbazepine, sodium valproate
what is first line for tonic-clonic seizure
carbamazepine, lamotrigine or sodium valproate