neurodegenerative disorders Flashcards
(17 cards)
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?
1%
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
ADRs of centrally acting antimuscarinics?
like peripheral antimuscarinics: dry mouth, constipation, urinary retention, impaired vision
