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BCPS study guide
Parkinson's and Multiple Sclerosis
| Question | Answer |
|---|---|
| cardinal signs of PD | akinesia/hypokinesia, rigidity, tremor, posture/gait abnormalities |
| secondary signs of PD | cognitive dysfunction, autonomic dysfunction, speech disturbances, micrographia, masked facies |
| can start pt on a dopamine agonist or levodopa. what are the primary symptom management advantages of each drug? | levodopa improves motor disability and dopamine agonists lessen motor complications. |
| MAOb inhibitors available for PD | selegiline and rasagiline |
| what problems arise with doses of selegiline greater than 10 mg daily | decrease MAOb selectivity |
| ADEs with selegiline | hallucinations, nausea, orthostatic hypotension, insomnia |
| what is the mechanism for insomnia with selegiline | it is metabolized to amphetamine |
| what drugs should be contraindicated with MAObs and why | tramadol, methadone, dextromethorphan, sympathomimetics, fluoxetine/fluvoxamine, meperidine due to serotonin syndrome risk. also cipro can double the concentration via cyp inhibition |
| purpose of carbidopa in PD | prevents peripheral levodopa conversion to dopamine allowing greater concentrations into the CNS. |
| dietary concerns with carbidopa/levodopa | high protein diets decrease absorption |
| acute adverse effects of Sinemet | GI, hypotension, cardiac arrhythmias, confusion, agitation, hallucinations |
| long term adverse effects of Sinemet | wearing off and on off, dyskinesias (involuntary movements) |
| return of PD symptoms before the next dose of Sinemet. How do you treat this? | wearing off. treat with amantadine. |
| profound unpredictable return of PD sx without respect to dosing interval. How do you treat this? | on-off. treat with entacapone, an MAOb inhibitors, pamipexole, ropinirole, apomorphine |
| typical ratio of carbidopa/levodopa | 25/100 mg |
| direct dopamine agonist options for treatment of PD | bromocriptine, pramipexole, ropinirole, rotigotine |
| ADEs associated with direct dopamine agonists | GI sx. postural hypotension, hallucinations, hypersexuality, compulsive behaviors. |
| contraindications with apomorphine | 5HT3 antagonists (ondansetron, palonosetron etc) and sulfite allergy |
| dosing concerns with apomorphine | poor PO bioavailability due to extensive first pass metabolism. given as a SQ shot. |
| ADEs associated with apomorphine | severe NV requires trt with trimethobenzamide before treatment and for at least 6 weeks during treatment. hypotension, hallucinations, dyskinesias |
| what is the role of anticholinergics in the treatment of PD and what drugs are used | tremor. trihexyphenidyl and benztropine |
| role of amantadine in treatment of PD. and ADEs | antidyskinesia agent. dizziness, insomnia, anxiety, livedo reticularis, nausea, nightmares |
| COMT inhibitor drugs used for PD and ADEs and role in therapy | used to decrease dopamine breakdown to increase levodopa in periphery. tolcapone. tolcapone req consent form due to hepatotoxicity. entacapone ADEs: dyskinesias, N/D-delayed up to 2 weeks, urine discoloration to orange, hallucinations and vivid dreams |
| preferred antipsychotics used in PD related to drug reactions or from disease | clozapine or quetiapine |
| how to treat dyskinesias associated with PD | lower levodopa dose or add amantadine |
| type of MS in which episodes of acute worsening of neurologic function are followed by a varying degree of recovery with a stable course between attacks. | relapsing remitting MS. common at diagnosis |
| type of MS in which initial relapsing remitting disease course is followed by progression with or without occasional relapses, minor remissions and plateaus | secondary progressive. presents in about half of patients after ~10 years. |
| type of MS in which gradual almost continuous worsening occurs with minor fluctuations but no distinct relapses. | primary progressive - ~10% of patients at diagnosis |
| type of MS in which disease is progressive from onset with clear acute relapses with or without recovery with periods between relapses characterized by continuing progression. | progressive-relapsing.of patients at diagnosis |
| how are acute relapses treated in MS | corticosteroids. methylpred IV 1 g QD x 3-5 days or PO prednisone 1250 mg QOD. IV ACTH |
| disease modifying drugs for MS | beta interferons (i.e. avonex, betaseron, extavia, rebif), dimethyl fumarate (Tecfidera), glatiramer acetate (Copaxone), fingolimod (Gilenya), Mitoxantrone (Novantrone), natalizumab (Tysabri), teriflunomide (Aubagio), |
| ADEs associated with beta interferons | injection site reactions, flu like symptoms (usually limited to first couple months), neutralizing antibodies (18-24 months of therapy and may increase relapse rates with pts with high antibody titers but may disappear with continued therapy) |
| ADEs associated with dimethyl fumarate (Tecfidera) | flushing helped with ASA and taking with food, starts 30 min after dose and ends after 30 mins. GI effects peak within first month. lymphocytes decrease by 30% in first year then stabilize |
| ADEs associated with glatiramer acetate (Copaxone) | injection site reactions, flusing, chest tightness, palpitations, anxiety, shortness of breath |
| ADEs associated with fingolimod (Gilenya) | bradycardia requiring monitoring for 6 hours after first dose and after any break over 2 wks in duration. AV conduction delays - first and second degree block, decrease in lymphocytes poss inc in infections. macular edema, resp effects, HTN, inc LFTs |
| ADEs associated with mitoxantrone (Novantrone) | potential for toxicity so only used for pts with rapidly advancing disease resistant to other therapies. cardiotoxicity requiring monitoring with ECG and not related to dose. acute leukemia in 0.8% of pts, |
| ADEs associated with Natalizumab (Tysabri) | hypersensitivity reactions, progressive multifocal leukoencephalopathy. reserved for failed therapies. |
| ADEs for teriflunomide (Aubagio) | liver tox, GI effects, alopecia, rash, infection including neutropenia and lymphopenia, preggers categpory X |
| due to the extremely long half live of terifunomide (Aubagio), what treatments can help to accelerate elimination | activated charcoal and cholestyramine |
| treatment for fatigue associated with MS | rest, assistive devices, cooling strategies, exercise, stress management, amantadine, methylphenidate |
| treatment for spasticity associated with MS | must be centrally acting. first line baclofen or tizanidine. second line dantrolene, diazepam. third line intrathecal baclofen. focal spasticity botox |
| treatment of walking impairment associated with MS |
Created by:
mjuhlin
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