PARKINSONS DRUGS

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ssilvis
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200848
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PARKINSONS DRUGS
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2013-02-19 16:26:08
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  1. PARALYSIS AGITANS-
    Another name for Parkinsons
  2. PATHOLOGY OF PARKINSONS-
    *There is a loss of dopamine-containing neurons in the substantia nigra-the dopamine inhibits firing of the cholinergic neurons the result is that the cholingeric neurons are now without their normal inhibitions ex: car going down hill with no brakes.
  3. WHAT IS THE BASAL GANGLIA?
    *Interconnected nuclei that includes the stratium, substantia nigra, globus pallidus and subthalmus in the brain.
  4. WHAT DOES THE BASAL GANGLIA DO?
    It is responsible for receiving input from entire cerebral cortex, processing this information, and giving feedback to motor area of cortex to give smooth coordinated body movements. Ex: walking and driving a car.
  5. PARKINSON IS CHARACTERIZED BY:
    Degeneration of dopaminergic neurons that arise from the substantia nigra, and other structures in the basal ganglia causes motor problems.
  6. NEUROGENIC PATHWAYS:
    • 1.  Direct pathway- responsible for excitatory movements.(decreased in PD)
    • 2.  Indirect pathway- responsible for  inhibitory movements. (increased in PD)
    • IN PD THE DIRECT PATHWAY HAS DECREASED IN ACTIVITY AND THE INDIRECT HAS INCREASED ACTIVITY.
  7. CHOLINERGIC NEURONS-
    -Cholinergic refers to a neuron that is capable of releasing Acetycholine which is used by the peripheral nervous system to send messages.
  8. IN PD IT LEADS TO EXCESS CHOLINERGIC ACTIVITY IN THESE PATHWAYS (ALL OF THESE PATHWAYS START TO DETERIORATE)-
    • 1.  Muscarinic- parasympthetic overactivity (rest and digest)
    • 2.  Nicotine- sympathetic overactivity (fight or flight)- neuromucular dysfunction- muscle fasciculations and muscle weakness.
    • 3.  Central effects- agitation, psychosis, confusion, coma and seizures.
  9. EXCESSIVE CHOLINERGIC ACTIVITY S/E's-
    • 1. Muscarinic effects - (parasympathetic overacitivy)-
    • -bradycardia
    • -pinpoint pupils
    • -sweating
    • -blurred vision
    • -excessive lacrimation
    • -excessive bronchial secretions
    • -wheezing
    • -dyspnea
    • -coughing
    • -vomitting
    • -abdominal cramping
    • -diarrhea
    • -urinary and fecal incontinence
    • 2.  Nicotine effects (Sympathetic overactivity)-
    • -tachycardia
    • -htn
    • -dilated pupils
    • -muscle fasciculation
    • -muscle weakness
    • 3.  Central effects-
    • -agitation
    • -psychosis
    • -confustion
    • -coma
    • -seizures
  10. ETIOLOGY OF PD-
    • -Unknown
    • -Environmental
    • -Oxidative stress theory- free radicals (molecules that lack an electron on their outer  orbits and take one from another molecule and are toxic to the dopaminergic neurons) cause disruption of molecular structure in the brain.
  11. CARDINAL FEATURES OF PE-
    • 1.  Resting tremor
    • 2.  Muscle rigidity
    • 3.  Bradykinesia (extreme slow movements)
    • 4.  Dementia
  12. GOAL OF THERAPY FOR PD-
    • -To replace dopamine that is missing
    • -To correct the imbalance of the cholinergic neurons in the striatum.
  13. 3 TYPES OF REPLACEMENT THERAPY FOR PD-
    • 1.  Dopamine replacement therapy
    • 2.  Dopamine agonist therapy- interfers with breakdown of dopamine and mimics the action of the lost dopamine.
    • 3.  Anticholinergic therapy- restores inhibition of the cholinergic neurons.
  14. DRUGS THAT INCREASE DOPAMINE LEVELS (DOMPAMINE REPLACEMENT THERAPY)-
    • 1.  Levodopa (Is Sinemet with Carbidopa)- Increases dopamine synthesis
    • 2.  Selegiline-
    • Inhibits dopamine breakdown
    • 3.  Amantadine- (drug to treat the flu)-
    • Increases dopamine release from neuron
    • 4.  Carbidopa-
    • Reduces peripheral metabolism of levadopa to increase the amount of levadopa that reaches the brain!
    • 5.  Tolcapone-
    • Enhance dopamine synthesis
  15. LEVADOPA-
    • -Precursor of dopamine that can cross the blood brain  barrier (Straight dopamine CAN'T)
    • -Competes with dietary amino acids to reduce transport of levodopa into the brain (do not eat protein and take pills)
    • -Large first pass effect!!!!
  16. INDICATIONS FOR LEVADOPA-
    -Alleviates motor dysfunction in patients
  17. WHAT VITAMIN IS NEEDED FOR ENZYME TO BREAK DOWN LEVADOPA?
    • -B6
    • -DO NOT TAKE VITAMIN  WITH LEVADOPA OR IT WILL BREAK IT DOWN AND IT WON'T WORK
  18. WHAT DOES LEVADOPA DO IN THE BRAIN?

    • -Converts levadopa to dopamine
    • -Increases dopamine
    • -Replacement therapy
    • -Counteracts effects of PD
  19. PROBLEMS WITH LEVADOPA?
    • 1.  Wearing off effect-
    • The med will wear off before the next dose, so med has to keep being increased until reaches max dose and then what?
    • 2.  On-off phenomenon-
    • Severe motor flucuations that occur rapidly.  Ex: moving fine and then completely stiff for a few minutes and then you can move again.
  20. LEVADOPA ADVERSE EFFECTS- (ARE FROM DOPAMINE THAT IS GENERATED BY PERIPHERALE DECARBOXYLATION)-
    • -N/V
    • -Orthostatic hypotension
    • -Cardiac arrhythmias
    • *CARBIDOPA REDUCES THESE EFFECTS
    • -Hallucinations
    • -agitation
    • -delirium
    • -vivid dreams
    • -nightmares
    • -Dyskinesias- involuntary movements
  21. LEVADOPA INTERACTIONS-
    • 1.Drugs that delay gastric emptying can slow levadopa absorption and its peak serum concentration
    • 2.MAO inhibitors- Phenelezine can cause a hypertensive crisis
    • 3.Drugs that promote gastric emptying- Antacids can increase bioavability.
  22. LEVADOPA CAN TREAT THESE PROBLEMS-
    • 1. Idiopathic PD
    • 2.  Postencephalitic parkinsoism
    • 3.  Parkinsonism cause by toxins:
    • -Carbon monoxide poisioning
    • -Manganese intoxication
    • -Cerebral arteriosclerosis
  23. CARBIDOPA-
    -Is a dopamine decarboxylase inhibitor that does not cross the blood-brain barrier- it decreases the peripheral metabolism of Levadopa and increases the amount of Levadopa that reaches the brain.
  24. WHY IS CARBIDOPA USED WITH LEVADOPA?
    -Because it decreases the s/s.  It blocks the peripheral formation of dopamine and IF NOT BLOCKED can lead to cardiac arrthymias!!!
  25. CARBIDOPA MODE OF ACTION:
    • 1. Inhibits conversion of levodopa in peripheral tissues
    • 2. Increases amount of levodopa that enters the brain
    • 3. Reduces gastrointestinal and CV s/e's
    • 4.  ALLOWS 75% REDUCTION OF LEVADOPA DOSAGE
    • 5. SR  and IR formulations.
  26. SYMMETREL (Amantadine)-
    • -Used to treat early or mild cases of PD
    • -Adjunct to levodopa
    • -Adverse effects-
    • -Sedation
    • -restlessness
    • -vivid dreams
    • -nausea
    • -dry mouth
    • -hypotenstion
    • -LIVEDO RETICULARIS- mottling of skin with edema.
  27. SELEGILINE-
    • -INHIBITS MONOAMINE OXIDASE (MAO) THAT SLOWS THE BREAKDOWN OF DOPAMINE
    • -Deprenyl/ Eldepryl
    • -Prevents breakdown of dopamine, increases dopamine levels in  basal ganglia
    • -Possible inhibits the progression of PD
    • -Adverse effects-
    • -Confusion
    • -Dyskinesias
    • -Hallucination
    • -Hypostension
    • -Insomnia
    • -Nausea
    • Interaction-
    • Meperidine, SSRI's (fluoxetine)
  28. TOLCAPONE-
    • - is a Catechol-o-mehtyltransferace (COMT)
    • -Tasmar
    • -Used to enhance effectiveness of levodopa
    • -Inhibits breakdown of levadopa- produces twofold increase in oral bioavailability and half-life of levadopa
    • ADVERSE EFFECTS-
    • -diarrhea
    • -nausea
    • -hepatitis!!!!!!!!!!!!!!!!!!
    • INTERACTIONS-
    • -Comtan
  29. DOPAMINE RECEPTOR AGONISTS MEDS-
    • 1.  Bromocriptine (parlodel)
    • 2.  Pergolide (permax)
    • 3.  Pramiprexole
    • 4.  Ropinirole
  30. WHAT DO DOPAMINE RECEPTOR AGONIST DO?
    • -Interfers with neuronal pathway between striatum and thalamus; increases thalamic stimulation of the cortex
    • -Mimics action of dopamine- IMMITATOR
    • -It doesn't rely on functional dopaminergic neurons- good because they are deteriorating!!!
    • -D2 receptor agonist
    • -Useful in wearing off and on-off fluctations in advanced PD!!!!!!!!!!
  31. BROMOCRIPTINE AND PERGOLIDE ADVERSE EFFECTS-
    • -Nausea
    • -Confusion
    • -Dyskinesias
    • -Sedation
    • -Vivid dreams
    • -Hallucinations
    • -Orthostatic hypotension
    • -Dry mouth
    • -DECREASED PROLACTIN LEVELS
  32. PRAMIPREXOLE AND ROPINIROLE-
    • -Mirapex and Requip
    • -Activates D2 receptors
    • -Ropinirole- also activates D3 receptors
    • -Used in early and late disease
    • ADVERSE EFFECTS-
    • -dizziness
    • -hallucination
    • -insomnia
    • -N/V
    • -Sedation!!!!!!!!!!!!
  33. WHAT ARE DOPAMINE AGONISTS?
    -drugs that bind to and activate dopamine receptors.
  34. ACETYLCHOLINE RECEPTOR ANTAGONISTS-
    • -Use for adjunt therapy
    • -REDUCE TREMORS! and may reduce bradykinesias and rigidity
    • -Used in early and late PD
    • -Reduce effectiveness of uninhibited cholinergic neurons in the basal ganglia.
  35. ACTEYLCHOLINE RECEPTOR ANTAGONIST DRUGS-
    • 1.  Trihexyphenidyl- Artane
    • 2.  Benztropine- Cogentin
    • 3.  Biperiden- Akineton
    • 4.  Diphenhydramine- Benadryl
    • SIDE EFFECTS-
    • -dry mouth
    • -constipation
    • -urinary retention
    • -confusion
  36. GENERAL TREATMENT CONSIDERATIONS-
    • EARLY DISEASE-
    • 1.  Diet and exercise
    • 2.  Education
    • 3.  ST,OT,PT
    • 4.  Effects of drugs may not be noted until 2-3 weeks!!!!

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