Parkinson's Dx

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  1. what is happening to the brain?
    This is a disease the affects the extra pyramidal system. This system controls and coordinate and modifies movements. This occur in the substantianigra, in the middle brain,  the neurons that originate there that produces dopamine, delivers the dopamine through the streatum to the globus palivus <= that’s the actual area that ends up converting the nerve impulses so that they coordinate out movements.
  2. what makes it a disorder of imbalance
    • not enough dopamine [dopamine producers are dying]
    • relatively to much Ach, in the siutation 
    • not enough GABA inhibition of the control center for movement coordination, the Globus Pallidus
    • uncontrolled neuron firing leading to DYSKINESIA, other symptoms of PD
  3. parkinson's Dx caused by


    brain damage
  4. PD cause: genetics
    problems with the destruction of alpha synuclein, a toxin that kills dopaminergic neurons. Alpha synuclein forms fibrils called Lewy bodies seen on autopsy, diagnostic for PD
  5. PD cause: environmental
    toxins, like cocaine, pesticides
  6. PD cause: brain damage
    due to vascular diseases (diabetes, etc.), tumors, viruses, encephalitis
  7. Parkinsonism
    (symptoms of Parkinson’s) caused by anti psychotic medications (reversible) – meds block dopamine receptors in the extrapyramidal system
  8. progressive death of dopaminergic neurons: early symptoms
    • tremors at rest, esp. a hand, on one side [uncontrollable]
    • "pill rolling"
    • head bobbing
  9. progressive death of dopaminergic neurons: late symptoms
    • rigidity, "cogwheel" movemet [jerky short movements] 
    • inability to initiate movement, "bradykinesia", "akinesia"
    • gait problem, hunched, forward leaning posture
    • balance problems since they're leaning so far forward they can't keep up with the motion so they have trouble stopping [high risk for fall]
  10. bradykinesia
    • slowness initiating movements
    • cannot stop easily 
    • shuffling gait
    • mucrographia [small handwriting]
    • cannot move slowly [fall risk]
  11. problems beside movement, gait
    • facial expression appears stiff, unemotional, less blinking so looks like staring
    • eating is dificult swallowing [aspiration precaution], drooling, prone to choking, difficulty to feed self [due to tremors]
    • speech is soft voice, poor articulation
    • emotions become labile, depression
    • weight loss - clothing become loose
  12. SE of too much Ach
    • diaphoresis - sweating
    • salivation - drooling
    • lacrimation - crying
    • sebaceous secretion - oily skin
    • constipation
    • urinary incontinence
    • prolonged urination
  13. how can this condition be treated
    • symptom control, vs. cure
    • medications - more dopamine, less Ach
    • nutrition - proteins inhibit absorption, Vit. B6 is needed to convert meds to dopamine 
    • activity - may respond to focused activated
    • surgery - med delivery, stem cell/transplants, brain stimulation, destruction of pallidus
  14. Goal for PD medication
    • goal: more stimulation of dopamin receptors in the striatum
    • goal: less Ach stimulation 

    • 1. make more dopamine
    • 2. recycle dopamine [reuptake inhibitor] 
    • 3. stimulate dopamine receptors without dopamine
    • 4. stop dopamine breakdown by stopping COMT ans MAO-B [inhibiting these enzymes slows the breakdown of dopamine]
  15. barriers to Tx - why can't we give them dopamine pills?
    b.c dopamine cannot cross the blood brain barrier
  16. most effective Tx: Levodopa or L-dopa
    • levodopa CAN cross the blood brain barrier 
    • levodopa gets converted into dopamine in a reaction using dopa decarboxylase enzymes <= this enzymes required Vit. B6 for the reaction to take place
  17. problems with levodopa Tx
    • destruction of neruona continues, so dose has to inc., and meds stop working in a few years
    • absoprtion rate: gradual and "on - off" phenomenon
    • levodopa is broken down peripherally [outside the brain] too, so only 2% actually reaches the brain => in the meantime your accumulating a lot of dopamine outside of the brain
    • needs Vit. B6 to change levodopa to dopamine, but higher B6 levels cause more peripheral breakdown
    • SE og excess dopamine [peripherally] itself are severe - dyskinesias, and psychosis
  18. ON-OFF phenomenon
    • dyskinesia suddenly turns to bradykinesia
    • large neutral amino acids in protein in foods compete with levodopa for abdorption
  19. remedies for ON-OFF phenomenon
    • nutritional - redistribute protein in evening meal
    • use implanted pump to deliver constant dose of levodopa
  20. levodopa SE
    • ALL directly related to dosage
    • nausea and vomiting - effect on chemoreceptor trigger zone in the brain 
    • Dyskinesias - like head bobbing, grimacing, ballismus, choreoathetosis [wave form movement in the muscle]
    • postural hypotension
    • dysrhythmias
    • psychosis - hallucinations, night terrors, paranoia [use clozapine]
    • darkening of urine, sweat
  21. what is drug holiday
    done in the hospital b.c it can be dangerous, this is where you stop the levodopa for a period of time and then putting them back on.
  22. adding carbidopa to levodopa effect?
    • it reduces total peripheral levodopa, and ALL SE
    • less need for Vit. B6
    • delivers 10 percent of levodopa dose to brain, NOT 2%
  23. drug of first choice for PD
    dopamine agonist
  24. dopamine agonist
    5 drugs, main one is pramipexole [Mirapex]

    less dyskinesia, but more chance of psychosis

    SE: sleep attacks, hallucinations, and postural hypotension

    first drug used in younger patients

    not good for older patients or those with advanced disease b.c they care more likely to develop psychosis
  25. other PD meds
    • COMT inhibitors
    • Seligiline
    • Amentadine
    • Central anticholinergics
  26. COMT inhibitors
    • ex: entacapone
    • stop breakdown of levodopa
  27. Seligiline
    MAO-B inhibitor, stops breakdown of dopamine, may stop destruction of dopamine neurons stopping PD progression
  28. Amantadine
    many actions, inhibits dopamine uptake and increase release
  29. central anticholinergics
    block cholinergic [Ach] receptors

    • SE includes
    • - dry mouth
    • - blurred vision
    • - tachycardia
    • - constipation
  30. non-medication Tx
    • transplant cells: stem cells and fetal brain cells
    • pallidotomy - getting tide of the globus pallidus on one side => unilateral
    • deep brain stimulation - reversible
    • nutritional - be careful about the protein intake
    • activity
Card Set:
Parkinson's Dx
2013-12-10 05:17:09
3220 final exam fall
3220 final exam fall
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