Card Set Information
Anti-parkinson Pharm V
Neurodegenerative disease involving extrapyramidal system (where specifically and e.g.)?!
substantia nigra and striatum
: Huntington's; also genetically determined
Neurodegenerative disease involving muscle weakness & atrophy? (e.g. and where?)
degenerate motor neurons in spinal cord and cerebral cortex
ALS (aka Lou Gehrigs)
Neurodegenerative disease characterized dementia (what it affects and e.g.)?
neurons in hippocampus and cerebral cortex
Factors in selective neurodegeneration? (4 main factors)
Genetic and environmental interaction
: genetic link (huntingtons), environmental toxins or viral
excessive glutamate release cause excessive influx of Ca++
drug-induced or age associated decline in metabolism; change membrange potentials, remove Mg2+ block of NMDA-receptor activation, increase Ca++
: eliminated by superoxide dimutase, glutathione, ascorbate ( can produce DNA, protein damage and lipid peroxidation of membranes)
Characteristics of Parkinson's?
tremors (at rest)
mask-like face and shuffling gait
inability to perform skilled tasks
Pathology of Parkinson's Disease?
degeneration of nigrostriatial dopamine (DA) neurons
project to striatum (caudate nucleus and putamen)
Lewy bodies (surviving neurons)
Etiology of Parkinson's?
aging, environmental and genetic
What are Parkinsonism disorders? (4 e.g.)
multiple small strokes
traumatic brain injury
antipsychotic drugs (chlorpromazine and haloperidol)
In the normal physiology of the Basal ganglia, what do D1 receptors control and how?
DA activates GABA
inhibit HABA neurons that project to thalamus
In the normal physiology of the basal ganglia, what do D2 receptors control and how?
DA inhibit indirect output
activate GABA neurons
inhibit Glut neurons
decrease GABA neurons that project to thalamus
What happens during abnormal functioning of the basal ganglia after degeneration of Dopaminergic Neurons?
Decrease DA acting on D1 and D2
: activate GABA nruons to the thalamaus
inhibit GLUT neurons to cortex
net decrease in excitator input ot the cortex
disruption of muscle control
What are the drugs that increase DA synthesis?
L-DOPA: availability? distribution?Peripheral side effects? CNS side effects?
precursor to DA
: symptoms; rigidity, tremors
oral, small intestine
"wearing off" effect
1-3% reaches brain (huge problem for side effects)
: peripher effects: n/v, anorexia, cardiac arrythmias, orthostatic hypotension
: visual and auditory hallucinations, dyskinesia, mood changes, depression, psychosis
Carbidopa actions and significance?
blocks peripheral metabolism of L-DOPA
so increase L-DOPA available to brain
allows to reduce dose by 4-5 fold
inhibitor of catechol-omethyltransferase
What are the drugs that decrease DA catabolism?
Selegeline: MOA, availability, metabolized?
inhibits monoamine oxidase type B (MAO-B)
decrease hydrogen peroxide, limiting free radicals
in combo with levodopa (little benefit when alone)
oral, renal excrete, half-life:7-9hrs
metabolized to methamphetamine and amphetamine (insomnia)
selective inhibitor of
not metabolized to amphetamine
What are the Dopamine receptor Agonists? (4)
: D2 ag + D1 partial ag
: D2+D3 ag
: D2+D3 ag
Dopamine Receptor Agonists: administration, side effects?
monotherapy in early stages
: low dose and gradual icnrease to therapuetic effect
: cardivascular (arrythmias, postural hypotension), neurological (depression, confusion, hallucinations, sleepiness, impulsivity), GI (n/v/),
: heart or mental problems!
Apomorphine: use, administration, side-effects?
acute tx w/ advanced disease for "off" periods (maked bradikinesia, immobility)
subQ (NO IV)
: n/v, arrythmias, postural hypotension, hallucinations, pronounced sleepiness
What are the muscarinic Antagonists: mechanism, side-effects? (2)
alleviate tremor and rigicity (not bradykinesia)
: loss of nigrostriatal neurons (inhibit Ach release) leads to increased firingof striatal cholinergic interneurons and overstimulation of muscarinic receptors; these will block this
: antimuscarinic effects: blurred vision, dry mouth, urinary retntion, constipation, aggravation of glaucoma, delirium, psychosis, memory impairment
Amantadine? use, MOA, side-effects?
bradykinesia and rigidity, prior to L-DOPA
: increase DA release, block cholinergic muscarinic receptors and glutamatergic NMDA receptors
: hallucinations, confusion, nasea, dizziness, rash of low extremeties
: CHF and glaucoma
developed as antiviral for influenza
Implications to dentistry: Musculature
hard to swallow
hard to brush teeth/floss
movements may complicate procedures
What drug can induce dyskinesia?
what drugs can sensitize to epi-induce arrythmias?
levodopa and MAO-B inhibitors
What drugs can reduce the elimination of Entacapone?
antibiotics: ampicillin, erythromycin
What are some side effects of the drugs that may effect oral health or appts?
nausea and vomiting
hope this was helpful, if there is anything wrong then just e-mail me and I think I can edit it...
Also, I hope I did this right due to the fact that I never use flashcards!