Parkinson's and Alzheimers Flashcards
what are the 4 major clinical features of parkinson’s disease
- bradykinesia
- muscular rigidity
- resting tremor
- impairment of postural balance, gait
what class is Selegiline (Deprenyl®) in
- MAO-B inhibitor
- inhibit MAO-B in CNS
- reduces striatal metabolism of DA
- does not affect peripheral metabolism of DA by MOA-A
what class is Rasagiline (Azilect®) in
MAO-B inhibitor
- inhibit MAO-B in CNS
- function: reduces striatal metabolism of DA
- does not affect peripheral metabolism of DA by MOA-A
what class is Tolcapone (Tasmar®) in
COMT inhibitor
what class is Entacapone (Comtan®) in
COMT inhibitor
List the Dopamine receptor agonists
- Bromocriptine (Parlodel®)
- Pramipexole (Mirapex®)
- Ropinirole (Requip®)
- Apomorphine (Apokyn®)
what class is Amantadine (Symmetrel®) in
dopamine releasers
what class is Benztropine (Cogentin®) in
anticholinergic
what class is Trihexyphenidyl (Artane®) in
anticholinergic
List the L-Dopa drugs used in parkinson’s disease
- Levodopa (Dopar®; Larodopa®)
- Carbidopa (Lodosyn®)
- Carbidopa/levodopa (Sinemet®)
List the drugs to tx alzheimers dz
- Donepezil (Aricept®)
- Rivastigmine (Exelon®)
- Galantamine (Reminyl®)
- Memantine (Namenda®
What causes parkinson’s dz
- characterized by the degeneration of dopamine (DA) neurons projecting from the substantia nigra (SN) to the corpus striatum (nigrostriatal pathway).
- symptoms = 70- 80% decrease in striatal dopamine neurons
What happens to DA/ACh balance in parkinson’s ? what is the overall effect
- Degeneration of DA neurons in the SN leads to an imbalance between DA and acetylcholine (ACh), such that the ACh pathways are now dominant.
- DA pathways normally inhibit GABA output from the striatum, whereas acetylcholine stimulates it.
- Loss of DA thus leads to overactivity of inhibitory GABA neurons
what is responsible for metabolism of dopamine
- MAO-B
- COMT
MOA of L-Dopa (Levodopa; dopar; larodopa)
- increase dopamine levels
- “replacement” therapy
- L-dopa crosses BBB and is converted into DA in the neuron
peripheral effects of L-Dopa (Levodopa; dopar; larodopa)
- severe nausea and vomiting
clinical uses of L-Dopa
- improves PD for 3-4 years
- effectiveness will go down over time
- does not affect progression, DA neurons continue to degenerate
- not effective in drug induced parkinsonism
why does L-Dopa need to be administered in high doses
- only 1-3% gets into the CNS
- short half life: taken 3-4 x /day
MOA of Carbidopa
-
dopa decarboxylase inhibitor that does not cross the blood brain barrier
- Therefore, it inhibits the synthesis of DA from l-dopa in the periphery, but does not affect DA synthesis in the brain
effect of combining L-Dopa with Carbidopa (sinemet)
- decreases dose of L-Dopa needed
- decreases peripheral effects -> nausea