Flashcards in neurodegenerative disorders Deck (17):
Features of Alzheimer's disease
- increased cerebral Glut levels, decreased cholinergic neurons
- neurofibrillary tangles develop, malformation of cytoplasmic microtubules
- appearance of deposits of cell debris and excessive amounts of beta-amyloid protein
Drugs used for Alzheimer's
- AChE inhibitors (may improve in early stages, 6months-2 years)
- NMDA receptor antagonist (for mod-severe Alzheimer's)
- immune therapy
ADRs of AChE
GI disturbances common, dose-related
MOA of NMDA receptor antagonists
inhibit prolonged activation of receptor
ADRs of NMDA receptor antagonists
agitation, drowsiness, dizziness, headache
MOA of immune therapy
mop up Beta-amyloid by inhibiting its formation and enhancing its clearance
drugs for Parkinson's disease
L-dopa, DDC inhibitors, COMT inhibitors, amantadine, D2 agonists, MAO-B inhibitors
How much of the L-dopa dose is converted to DA in the brain?
ADRS of L-dopa
nausea, vomiting, anorexia, orthostatic hypotension, cardiac dysrhythmias, writhing involuntary movements
MOA of DDC inhibitors?
improve L-dopa CNS delivery by inhibiting peripheral enzyme
MOA of COMT inhibitors?
improves L-dopa CNS delivery by inhibiting peripheral enzyme: inhibition of DDC causes compensatory increase in activity of COMT: products compete with L-dopa in crossing the BBB)
ADRs of L-dopa + DDCi + COMT-i?
delusions, hallucinations, confusion, insomnia, nightmares
MOA of amantadine?
causes release of DA from neurons still working + inhibits DA reuptake
Uses of D2 agonists, MAO-B inhibitors and centrally acting antimuscarinics
adjunct to L-dopa therapy, D2 agonists and MAO-B specifically in on-off phenomena
ADRs of D2 agonists?
nausea, hypotension, psychotic symptoms, inhibits prolactin release
MOA of centrally acting antimuscarinics?
inhibit dopamine storage use for early minor symptoms