Term
| indications for neuroprotective therapy in PD: |
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Definition
| dx w no fxnl impairment then focus becomes neuroprotective |
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Term
| 2 drugs for neuroprotective therapy in PD: |
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Definition
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Term
| therapy for tremor predominant PD pts >70yo |
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Definition
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Term
| therapy for tremor predominant PD pts <70yo |
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Definition
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Term
| therapy for non-tremor predominant PD pts <65yo: |
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Definition
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Term
| therapy for non-tremor predominant PD pt >65yo: |
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Definition
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Term
| therapy for non-tremor predominant PD in patients who are cognitively impaired: |
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Definition
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Term
| name 3 options for pts not responding to therapy in non-tremor dominant PD: |
|
Definition
1. increase dose of DA agonist or CD/LD
2. add CD/LD to regimine
3. consider another dx |
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Term
| when adding selegiline or rasagiline as an adjunct it is necessary to reduce the levodopa dose by: |
|
Definition
| 10-30% possibly as much as 50% to prevent involuntary movements or hallucinations |
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Term
| considering CD/LD therapy a DA agonist should be added when daily doses reach: |
|
Definition
| 500-800mg necessary for affect |
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Term
| when adding COMT therapy to CD/LD how should you dose adjust? |
|
Definition
| important to dose adjust levodopa downward 20-30% |
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Term
| steps in transitioning IR CD/LD to CR CD/LD: |
|
Definition
1. decrease frequency of administration by 50%
2. dose @ 100-120%
3. if wearing off persists but <60min then just increase the dose of the IR therapy
4. If wearing off persists >60min then increase the dose/frquency |
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Term
|
Definition
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Term
|
Definition
| MonoAmine Oxidase B inhibitors - MAO-B is the enzyme in the brain responsible for the breakdown of DA |
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|
Term
|
Definition
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|
Term
| SE of MAO-Bi's: GI,CNS,CV |
|
Definition
1. GI (N/V, constipation, dery mouth)
2. CNS (agitation, confusion, psychosis)
3. CV (hypotension, arrhythmias, palpitations) |
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Term
|
Definition
| reduces the need for high doses of L-dopa therefore alleviating some of the SE assoc w L-dopa |
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Term
| MOA for anti-cholinergics: |
|
Definition
| decrease the action of ACh in CNS helping to restore the ACh/DA balance |
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Term
| what do the Anti-cholinergics help with? not help with? |
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Definition
| mainly help with tremors and rigidity but not postural imbalance, bradykinesia, or gait problems |
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Term
| who is the prefered pt for anti-cholinergic therapy: |
|
Definition
| pt <70yo w tremor predominant and without akinesia |
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Term
|
Definition
1. dry mouth
2. constipation
3. dizziness
4. urinary retension
5. memory impairment |
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Term
|
Definition
1. increases DA synthesis,
2. blocks DA reuptake,
3. stimulates DA receptors and
4. has peripheral anticholinergic preperties. |
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Term
| role in therapy for amantidine: |
|
Definition
| effective in tx of akinesia and rigidity but less effective in the tx of tremors EXCEPT for those pts >70yo |
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|
Term
|
Definition
1. rare at rec doses
2. N/V/D, constipation, abd cramping
3. increse tremor, seixures, hallucinations
4. worsening CHF, arrhythmias
5. Livido Reticularis (diffuse rose colored motling of the skin) |
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Term
|
Definition
| LD is a precursor in DA syn and can be converted to DA in the CNS. CD stays in the periphery and inhibits LD conversion in the periphery, ensuring it goes where its needed |
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Term
|
Definition
1. Vomiting, PUD
2. orthostatic hypotension, arrhythmias
3. anxiety, confusion, hallucinations, hypersexuality, dyskinetic movements |
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|
Term
| Direct DA agonist's role in therapy: |
|
Definition
| monotherapy (although dosen't cover all sx) OR adjunct therapy w LD to reduce LD dosage. |
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|
Term
|
Definition
SE occur upon initiation of tx and tolerance develops over days-wks:
N/V, postural Hypotension, psychiatric sx, impulse control d/o (gambling, hypersexual, complusive shopping) |
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|
Term
|
Definition
| inhibit COMT which breaks down levodopa in the CNS |
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|
Term
|
Definition
| reduce the wearing off phases in CD/LD therapy seen in late stage PD |
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Term
| Adverse Effects of COMTi: 5 |
|
Definition
1. diarrhea
2. discoloration of urine
3. nausea
4. HA
5. somnolence |
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|
Term
| COMTi that runs a risk of severe hepatocellular injury including acute fulminant liver failure. |
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Definition
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Term
| normal doses for selegine |
|
Definition
1. eldepryl 5mg
2. zelepar 1.25
10mg/day for both |
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Term
| normal doses for amantidine: |
|
Definition
| symmetrel 100mg (200-300mg/d) |
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|
Term
| normal dosing for IR CD/LD |
|
Definition
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|
Term
| normal dosing for CR CD/LD |
|
Definition
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|
Term
| which is the desintegrating tablet of CD/LD |
|
Definition
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|
Term
|
Definition
| entacapone 200mg (600-2000mg/d) |
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Term
| define "delayed on response" |
|
Definition
| delay of absorption of med through the BBB. LD uses neutral AA transporters to get thru BBB not taking med on empty stomach increases competition for these xporters |
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|
Term
| define "wearing off phenom" |
|
Definition
| loss of response to dose before the next is due. - from either decreased absorption/penetration (GI/BBB) OR degeneration of presynaptic DA neurons resulting in decreased DA storage (late PD) |
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|
Term
| control measures for wearing off:3 |
|
Definition
1. increase the freq and/or dose of LD
2. add DA agonist
3. add COMTi |
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Term
|
Definition
| rapid fluctuation from sx free to extreme sx; occur in 40% of pts after 5yrs |
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Term
| control measures for on-off phenom: |
|
Definition
1. direct DA agonist
2. extra levodopa
3. chewing an IR between CR doses |
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Term
|
Definition
| unable to initiate a coplete movement |
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|
Term
|
Definition
| uknown pathophys; can occur during on or off phenoms and is unrelated to dose timing and unresponsive to dose changes. |
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Term
| control measures for freezing: |
|
Definition
| guessing game; an atempt to find a relationship to meds and recommend an increase or decrease |
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Term
|
Definition
| PD meds; the therapeutic window for eliciting motor responses without causing a dyskineasia decreases w the progression of PD |
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Term
| control methods for dyskinesia:5 |
|
Definition
1. switch from CR to Ir
2 reduce or eliminate selegine or COMTi
3. reduce LD/CD
4. add amantidine
5. consider surgery |
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Term
| define diphasic dyskinesia: |
|
Definition
| dyskinesia occuring during dose absorption or when dose is wearing off |
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Term
| control of diphsic dyskinesias: |
|
Definition
prolonging the on state by:
1. increasing dose/frequency
2. add DA agonist
3. consider surgery |
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Term
|
Definition
| can be the presenting sign of PD; foot posturing upon awakening |
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|
Term
|
Definition
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Term
| etiology of neuropsychiatric problems in PD: |
|
Definition
| can be a manefestation of dz or Rx |
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Term
| control measures for cognitive impairment in PD: |
|
Definition
1. tx any underlying probs (inf, lytes)
2. remove any unecessary Rx
3. decrease/dc PD rx |
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Term
| in the case of controling cognitive impairment in PD, in what order do you d/c PD meds: |
|
Definition
1. anitcholinergics
2. amantidine
3. selegine
4. DA |
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Term
| control of hallucinations/delirium in PD: |
|
Definition
discontinue:
1. anticholinergics
2. amantidine
3. selegine
4. DA
in that order |
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|
Term
| what is the Rx for psychosis in PD? |
|
Definition
1. clozapine
2. quetiapine |
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Term
| in PD pts >70 amantidine increases: |
|
Definition
| chances for cognitive impairment |
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|
Term
| in PD pts <70 CD/Ld therapy is generally reserved for: |
|
Definition
| when there is marked impairment of ADLs |
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Term
| CD/LD in PD pts >70 increases risks for: |
|
Definition
| hallucinations, confusion, psychosis |
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