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Tx PD and MS
Pharm-II
| Question | Answer |
|---|---|
| What is PD caused by | nigrostratal dopamine neurons loss |
| What is key in clinical improvements and AE’s | activation of D2 receptor |
| How do we dx PD | Bradykinesia + ≥2 of the following, limb muscle rigidity, resting tremor, postural instability, micrographia (also, lack of other neuro impairment, responsive to L-dopa, R/o drug induced parkinson’s |
| Staging of PD (name) | 0-V: restricted to bed/wheelchair called the Hoehn and Yahr staging |
| Tx goals of PD | maintain pt independence, alleviate sxs, minimize response fluctuations, limit med AE’s |
| Three ways to approach pd tx | lifestyle changes, nutrition, exercise, pharm, and surgical txs |
| 4 dopamine enhancement drugs | levodopa/carbidopa, amantadine, MAO-B inhibitors, COMT inhibitors |
| 3 types of drug categories to tx PD | Dopamine enhancers, dopamine agonists, anticholinergics |
| Fxn of cabidopa | inhibits peripheral conversion of levodopa to dopamine |
| Why do we need to titrate this combination slowly | to avoid N/V and hypotension |
| MOA of amantadine | blocks DA reuptake and stimulates DA receptors, sedation and confusion common |
| MOA of MOA-B inhibitors | prevent breakdown of DA via MAO-B |
| Two MAO-B inhibitors | selegiline and rasagiline (more inxs w/ rasagline) |
| Drug/food intxs w/ MAO-B I’s | TCA, SSRI, SNRI, Meperidine: CNS tox, autonomic instability, HTN ↑temp, death, MAOI: HTN crisis , and tyramine foods, HTN crisis |
| MOA of COMT I’s | inhibit breakdown of levodopa, INCREASE T1/2 OF LEVODOPA BY 50%, GOOD ADDITIVE DRUG |
| Two COMT I’s | entacapone and Tolcapone : catecholo-o-methyltransferase inhibitors |
| What is the mechanism of therapy for dopamine agonists | delay need for use of levodopa in early dz, or ↓ dose of levodopa in advanced dz’s |
| Two dopamine agonists | pramipexole and ropinirole |
| AE’s and pt ed for dopamine agnosits | confusion, dizziness, hallucinations, orthostasis, nausea, asthenia, syncope (falling asleep at the wheel must educate) |
| CNS effects of excess dopamine | confusion, hallucinations |
| Systemic effects of excess dopamine | GI complaints, orthostatic hypotension |
| What behavioral AE’s are associated w/ dopamine agnoists | ↑ irribility, agitation, pshyce, more in patients that are susceptible to psych or impulse d/o |
| MOA of anticholinergics | relative ↑ in striatal cholinergic activity →tremor |
| MC used anticholinergic drug | Benztropine (Cogentin) Se’s: confusion, memory loss, anti-slud, |
| As PD progresses, what occurs | ↑ loss of DA-producing neurons, so more dependence on meds to ↑ DA more med SE’s |
| What is the initial tx if PD | selegiline or rasagiline (potent) aka MOA-b I’s |
| Are there current neuroprotective therapies | no, but exercise may ↑motor fxn, speech therapy ↑ speech vol. |
| 1st line tx for pshychosis in dementia | quetiapine (Seroquel) |
| What does the definition of MS mean | M: many affected areas of the brain, S: plaques or slerosed areas |
| Tx’s for Mild, mod, severe exacerbations | Mild: may need none, Mod: oral corticosteroids (prednisone), Severe: IV methylprednisolone |
| When do we use corticosteroids for exacerbations, why? | severe ones w/ fxn consequences, the effects decrease w/ repeated use |
| AE’s of corticosteroids | short term: GI , insomnia, mood swings |
| Tx for severe attacks | hemiplegia, paraplegia, etc, don’t respond to Corticosteroid tx: plasma exchange 7tx for effects |
| What is PML | progressive multifocal leukoencephalopathy |
| What is AML | acute myelogenous leukemia |
| What med might improve demyelinated nerve conduction | Dalfampridine |
Created by:
becker15
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