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Parkinson Disease
degenerative progressive disorder of the CNS cause by the depletion of dopamine ]. it usually effects adults over 50. it takes years for the symptoms to develop. meds therapy is the cornerstone for treatment
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Four classic features
- 1. Tremor- resting tremor
- 2. bradykinesia- slow movements
- 3. muscle rigidity- hard to flex and extend
- 4. postural instability- problem with balance more fall
slowness weakness
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Pathology of Parkinson's disease and how meds can decrease this?
Dopamine is not functioning correctly; and ach is release (helps one nerve cell talk to another but with parkinson this goes down)
place arole with coordination
the drugs restore dopamine function and block cholinergic activity in the nigrostriatal pathway
dopamine and ach is messed
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name two classification for Parkinson disease
- Dopaminergic- increase dopamine
- anticholin- decrease ach bring up dopamine
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Congentin
- initial therapy
- then used as an adjunct
- dopamine does not cross the brain blood barrier
- block ach and raise the dopamine
- increase dopamine
- does not cross the brain blood barrier
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Congentin Se
similar to anticholinergic SE
Dry mouth, tachycardia, urinary retention, constipation, increase temp, decrease sweating, blurried vision
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dopaminergic
Sinemet- levodopa/carbidopa (carbidopa stops enzyme from breaking up levodopa- helps more of the levodopa get into the brain. no real function but that and all se come from levodopa)
this the choice for Parkinsonism
SE: increase anxiety, insomnia, nightmare, GI N/v weight loss, CV hypotension neuro- dykinesia abnormal involuntary movements to increase dopamine
toxcity dyskinesias uncontrolled movements- muscle twitching and spasm of the eye
early sign of toxcity-
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other Parkinson agents
Dopamine agonist
Antiviral agent
adjunct
- Dopamine agonist (mirapex and requip)- directly activate the dopamine receptors. requip had been seen to have better control dyskinesia
- SE: nausea, constipation, headache, hypotension, sudden sleep disturbances
- Antiviral agent (amantadine): cause release of dopamine from nerve terminals.
- SE: dizziness, lightheadedness, anxiety, sleep disturbance, difficulty concentration
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Alzheimer;s disease
progressive degenerative disease. a main characteristic of dementia. etiology is not fully understood, research: enviromental factors, development of amyloid plaques and neurofibrillary tangles, chronic brain inflammation, immune factors, virus
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AD s/s
- inabiltiy to remember and to recall information,
- impaired memory and judgement, disorientation, inability to recognize family and friends, and anxiety
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Pathology and meds effects of AD
- AD - abnormal structures in the brain.
- neurons die
- the brain shrinks
- memory loss
med- cholinesterase inhibits- increase ach
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Acetylcholinesterase (achE)
most widely used
AchE inhibitor are indirect acting cholinergic drugs
AchE is the enzyme that breaks up ach
what the meds do it replace it.
- start immediately upon dx
- most effective early one
- with time the effects decrease
- it is individual- some pts will have a great response and some mild
- common side effects GI- diarrhea
- NI- takes a month for full of effects, d/c slowly take them off
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Aricept (donepezil)
- has as a cholinergic effect
- increase ach- abd cramping.diarrhea
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Other agents for AD
Namenda- NMDA receptor agent, reduces high levels of glutamate- glutamate destroys neurons. used for moderate to severe AD
Vit E- increase oxydation so cells can grow
- Cox 2- decrease inflammation
- Atypical Antipsychotic agents- decrease agitation, hallucination (last resort)
- Antianxiety agents- mood stabilizer: treat anxiety and depression (last resort)
- the two have CNS effects be careful with this...
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