Term
| What are the known causes of parkinsonisms that are not age reated? |
|
Definition
| brain disease or injury (tumors, trauma, encephalitis), and exposure to environmental toxins such as carbon monoxide and manganese |
|
|
Term
| Describe the neurochemical imbalance of parkinson's disease. |
|
Definition
| imbalance between the inhibitory effects of DA and the opposing stimulatory effects of ACh in the extrapyramidal system adn basal ganglia |
|
|
Term
| What are the different drugs given to directly replace DA? |
|
Definition
| levodopa, carbidopa or benserazide, cabidopa/levodopa |
|
|
Term
| Why can't you give dopamine to treat parkinsons? |
|
Definition
| DA itself does not cross the blood-brain barrier so you give precursors to dopamine |
|
|
Term
| What is the oral bioavailability of levodopa? |
|
Definition
| can be given orally and crosses the BBB but 90% is destroyed in the gut |
|
|
Term
| What is another name for carbidopa? |
|
Definition
|
|
Term
| What is the MOA of carbidopa? |
|
Definition
| inhibit DOPA decarbaxylase, the enzyme which converts levodopa to DA |
|
|
Term
| Why is it beneficial to give carbidopa/levodopa together? |
|
Definition
| a greater amout of DA leaves the gut and is thereofre available for transport to the brain |
|
|
Term
| What converts tyrosin to DOPA? |
|
Definition
|
|
Term
| What converts DOPA to dopamine? |
|
Definition
| aromatic amino acid decarboxylase |
|
|
Term
| What converts dopamine to norepinephrine? |
|
Definition
| dopamine beta hydroxylase |
|
|
Term
| What converts norepinephrine to epinephrine? |
|
Definition
| phenylethanolamine-N-methyltransferase |
|
|
Term
| What is the MOA of amantadine? |
|
Definition
|
|
Term
| When should amantadine be given? |
|
Definition
| early in disease course; not affective in advanced stages when stored pools of DA are low |
|
|
Term
| Name agonists at the postsynaptic DA receptor. |
|
Definition
| bromocriptine, pergolide, pramipexole, ropinirole |
|
|
Term
| Which DA receptor agonists are ergot derivatives? |
|
Definition
| bromocriptine and pergolide |
|
|
Term
| What's the difference between using DA direct replacement and agonists at post synaptic DA receptors? |
|
Definition
| DA agonists produce a greater incidence of psychiatric symptoms than L-DOPA |
|
|
Term
| What is the MOA of COMT inhibitors? |
|
Definition
| inhibit catechol-O-methyltransferase, an enzyme that is responsible for degrading dopamine |
|
|
Term
| Name some COMT inhibitors. |
|
Definition
|
|
Term
| What is the MOA of selegiline? |
|
Definition
|
|
Term
| What do you use after response to combination of carbidopa/levodopa begins to deteriorate? |
|
Definition
|
|
Term
| What are the metabolites of selegiline? |
|
Definition
| amphetamine and methamphetamine |
|
|
Term
| Name some anticholinergics that can be used to treat parkinson's disease? |
|
Definition
| trihexlphenidyl and benztropine |
|
|
Term
| What is the MOA of trihexylphenidyl and when do you use it? |
|
Definition
| inhibits ACh activity in key excitatory pathways and can be used for treating early, mild parkinsonism or more often as an adjunct with dopaminergic drugs |
|
|
Term
| What is the MOA of benztropine? |
|
Definition
| centrally acting antimuscarinic |
|
|
Term
| What other drugs besides direct/indirect DA and anticholinergics can be used to treat parkinsons? |
|
Definition
| diphenhydramine, ethopropazine, procyclidine |
|
|
Term
| What is the MOA of diphenhydramine in treating parkinsons? |
|
Definition
| antihistamine that also seems to block reuptake of DA |
|
|
Term
| What is the MOA of ethopropazine? |
|
Definition
| phenothiazine with marked anticholinergic properties (very atypical of this class of drugs) |
|
|
Term
| How does procyclidine treat parkinsons? |
|
Definition
| atropine-like activity that is particularly useful for alleviating rigidity and excessive salivation |
|
|
Term
| What is the medical term for excessive salivation? |
|
Definition
|
|
Term
| What are the most common side effects of drugs used to treat parkinsons? |
|
Definition
|
|
Term
| What are the side effects of drugs used to treat parkinson's disease? |
|
Definition
| nausea and vomiting, anorexia, choreiform movements, ataxia, orthostatic hypotension, tachycardia, neuroleptic malignant syndrome |
|
|
Term
| In what situation would a patient taking medications for parkinson's disease get neuroleptic malignant syndrome? |
|
Definition
| if levodopa is withdrawn abruptly |
|
|
Term
| What are the problems associated with long-term treatment of Parkinsons disease? |
|
Definition
| dyskinesias, end-of-dose failure, on-off phenomenon, secondary levodopa failure |
|
|
Term
| What is secondary levdopa failure? |
|
Definition
| effective drops off after 2-5 years |
|
|
Term
| What are the two most noteworthy drug interactions with parkinsons treatmetn? |
|
Definition
| interaction with MAOI's and other drugs affect dopamine neurotransmission (this is a very dangerous interaction that can lead to acute hypertensive episode and a stroke); an indirect interaction that results from high levels of vitamin B6 which by itself increases gastrointestinal dopa decarboxylase activity |
|
|
Term
| Which neurons degenerate in ALS? |
|
Definition
| spinal, bulbar and cortical neurons |
|
|
Term
| Name the treatments used for ALS (aka antispasmodics). |
|
Definition
| riluzole, baclofen, tizanidine, muscarinic receptor antagonists |
|
|
Term
| What is the MOA of riluzole? |
|
Definition
| drug with both presynaptic and post synaptic effects. This drug inhibits glutamate relese, but it also blocks postsynaptic NMDA and kainate-type glutamate receptors and inhibits voltage-dependent sodium channels |
|
|
Term
| How effective is riluzole? |
|
Definition
| modest but genuine effects on the survival of patients with ALS (60 days) |
|
|
Term
| What are the side effects of riluzole? |
|
Definition
| generally well tolerated, although nausea and vomiting may occur |
|
|
Term
| What is the MOA of baclofen? |
|
Definition
| a GABA(B) agonist that is a useful treatment for the spasticity observed in ALS patients |
|
|
Term
| What is the MOA of tizanidine? |
|
Definition
| alpha type 2 receptor agonist; reduces muscle spaciticity and is assumed to act by increasing presynaptic inhibition of motor neurons |
|
|
Term
| What is tizanidine used to treat? |
|
Definition
| used most widely in the treatment of spasticity in multiple sclerosis or after stroke but it may also be effective in patients with ALS |
|
|
Term
| What limits the dose of tizanidine that can be used? |
|
Definition
| side effects like drowsiness, asthenia, and dizziness |
|
|
Term
| Name the muscarinic receptor antagonists used to treat ALS? |
|
Definition
| dicyclomine, flavoxate, oxybutynin, oxyphencyclimine, trihexylphenidyl |
|
|
Term
| Which muscarinic receptor antagonists are used for urological disorders? |
|
Definition
|
|
Term
| What is the average age of onset of huntingtons? |
|
Definition
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