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Neurodegenerative disease involving extrapyramidal system (where specifically and e.g.)?!
- substantia nigra and striatum
- Hypokinetic (rigid): Parkinsonism
- Hyperkinetic (choreic): 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
- Excitotoxicity: excessive glutamate release cause excessive influx of Ca++
- Energy Metabolism: drug-induced or age associated decline in metabolism; change membrange potentials, remove Mg2+ block of NMDA-receptor activation, increase Ca++
- Free Radicals: eliminated by superoxide dimutase, glutathione, ascorbate ( can produce DNA, protein damage and lipid peroxidation of membranes)
Characteristics of Parkinson's?
- tremors (at rest)
- muscular rigiddity
- abnormal posture
- mask-like face and shuffling gait
- impaired speech
- 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.)
- encephalitis lethargica
- 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?
- direct pathway
- 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?
- indirect pathway
- 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
- inhibit direct
- activate indirect: 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
- tx: symptoms; rigidity, tremors
- oral, small intestine
- "wearing off" effect: 3-5yrs
- 1-3% reaches brain (huge problem for side effects): peripher effects: n/v, anorexia, cardiac arrythmias, orthostatic hypotension
- CNS: 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 BRAIN MAO-B
- not metabolized to amphetamine
What are the Dopamine receptor Agonists? (4)
- Bromocriptine: D2 ag + D1 partial ag
- Ropinirole: D2+D3 ag
- Pramipexole: D2+D3 ag
Dopamine Receptor Agonists: administration, side effects?
- monotherapy in early stages
- oral: low dose and gradual icnrease to therapuetic effect
- adverse: cardivascular (arrythmias, postural hypotension), neurological (depression, confusion, hallucinations, sleepiness, impulsivity), GI (n/v/),
- Contra: heart or mental problems!
Apomorphine: use, administration, side-effects?
- acute tx w/ advanced disease for "off" periods (maked bradikinesia, immobility)
- subQ (NO IV)
- side-effects: n/v, arrythmias, postural hypotension, hallucinations, pronounced sleepiness
What are the muscarinic Antagonists: mechanism, side-effects? (2)
- Benztropine, Trihexyphenidyl
- alleviate tremor and rigicity (not bradykinesia)
- MOA: loss of nigrostriatal neurons (inhibit Ach release) leads to increased firingof striatal cholinergic interneurons and overstimulation of muscarinic receptors; these will block this
- side-effects: 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
- MOA: increase DA release, block cholinergic muscarinic receptors and glutamatergic NMDA receptors
- Side-effects: hallucinations, confusion, nasea, dizziness, rash of low extremeties
- contra: CHF and glaucoma
- developed as antiviral for influenza
Implications to dentistry: Musculature
- hard to swallow
- tongue muscles
- 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
- orthostatic hypotension
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!