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Pharm Lehne Ch 20-25
CNS Drugs for Parkinson's, Alzheimer's, MS, Epilepsy & Muscle Spasms
| Question | Answer |
|---|---|
| How is the CNS different from the PNS with regard to neurotransmitters? (ch 20) | PNS has 3 compounds: acetylcholine, norepinephrine, and epinephrine, but CNS has at least 21 compounds that serve as neurotransmitters |
| Lipid-soluble agents and specific transport systems- cross blood-brain barrier? (ch 20) | Yes |
| Protein-bound drugs and highly ionized drugs- can cross blood-brain barrier? (ch 20) | No |
| Are infants more or less sensitive to CNS drugs than older children or adults? (ch 20) | Infants are much more sensitive to CNS drugs than are older children and adults |
| T/F We do not fully understand the brain in either health or disease (ch 20) | True |
| What are some of the adaptive changes during prolonged CNS drug exposure? (ch 20) | increased therapeutic effects, decreased side effects, tolerance, physical dependence |
| What type of disorder is Parkinson's Disease? (ch 21) | slowly progressive neurodegenerative disease |
| What is the most common degenerative disease of neurons? (ch 21) | Alzheimer's Disease |
| What is the second most common degenerative disease of neurons? (ch 21) | Parkinson's Disease |
| What are cardinal motor symptoms of Parkinson's Disease? (ch 21) | tremor, rigidity, postural instability, slowed movement |
| What are common nonmotor symptoms of Parkinson's Disease? (ch 21) | autonomic disturbances, sleep disturbances, depression, psychosis, dementia |
| What are early symptoms of Parkinson's disease? (ch 21) | loss of smell, excessive salivation, clumsiness of the hands, worsening of handwriting, bothersome tremor, slower gait, reduced voice volume |
| What is the underlying cause of motor symptoms in Parkinson's Disease? (ch 21) | loss of dopaminergic neurons in the substantial nigra |
| What is the most effective drug for Parkinson's Disease? (ch 21) | Levidopa, given in combination with Carbidopa (eventually becomes ineffective) |
| Motor symptoms in PD result from damage to what system? (ch 21) | Motor symptoms result from damage to the extrapyramidal system, a complex neuronal network that helps regulate movement |
| What are dyskinesias? (ch 21) | Dyskinesia = disorder of movement |
| What dyskinesias characterize PD? (ch 21) | tremor at rest, postural instability, bradykinesia |
| What is bradykinesia? (ch 21) | slowed movement |
| What contributes to the motor symptoms that characterize PD? (ch 21) | overactivity of GABAergic neurons (excitatory influence of ACh that goes unopposed b/c degeneration of neurons in substantia negra that supply dopamine to striatum) |
| How many neurons (that supply dopamine to striatum) must be lost before PD becomes clinically recognizable? (ch 21) | 70-80% |
| Levidopa - Adverse Effects (ch 21) | nausea & vomiting, dyskinesias (give amantadine?), postural hypotension, psychosis (clozapine, quetapine), anxiety, agitation, memory & cognitive impairment, nightmares, darken sweat and urine |
| Levidopa - Drug Interactions (ch 21) | First Gen Antipsychotic Drugs- decrease effects, MAO Inhibitors -> hypertensive crisis, Anticholinergics- enhance response to levodopa |
| Levodopa - Food interactions (ch 21) | high-protein meals can reduce therapeutic responses to levodopa (spread protein throughout the day) |
| contraindication for Levidopa (ch 21) | malignant melenoma |
| What is the action of carbidopa? (ch 21) | Carbidopa prevents decarboxylation of levodopa in intestine and PNS- preserves levodopa so more can cross the BBB |
| Pramipexole (ch 21) | DA receptor agonist, will not convert outside brain, doesn't need help, protein okay. *improves motor, good for restless leg |
| Pramipexole - adverse effects? (ch 21) | daytime somnolence, hallucinations, self-rewarding behaviors |
| Apomorphine (ch 21) | rescue treatment not given by mouth (acute tx fro trough) |
| Entracapone (ch 21) | COMT inhibitor used with levodopa, inhibits metabolism of levodopa before brain. can cause yellow/orange urine |
| Selegiline (ch 21) | MAO-B inhibitor used with levodopa, benefit decreases after 1-2 yr |
| Anticholinergics with Levodopa (ch 21) | reduce tremors but not bradykinesia, better for younger, not old. *potentially inappropriate for use in geriatric patients (benztropine, trihexyphenidyl) |
| Disease characterized by progressive memory loss, impaired thinking, neuropsychiatric symptoms, inability to perform routine activities of daily living (ch 22) | Alzheimer's disease |
| Where does neuronal degenerations start in early Alzheimer's Disease? (ch 22) | hippocampus (memory), cerebral cortex (speech, perception, reasoning) |
| What are acetylcholine levels like for Alzheimer's patients? (ch 22) | 90% below normal |
| neuritic plaques in Parkinson's Disease (ch 21) | Lewy bodies |
| neuritic plaques in Alzheimer's Disease (ch 22) | beta-amyloid, + neurofibrillary tabgles (tau twists) |
| risk factors for Alzheimer's (ch 22) | age, 90% 65 or older |
| Cholinesterase Inhibitors (ch 22) | donepezil, galantamine, rivastigmine approved for tx Alzheimer's |
| Donepezil, Galantamine, Rivastigmine (ch 22) | cholinesterase inhibitors approved for tx of Alzheimer's, increase availability of ACh, tx benefits 1 in 12, s/e nausea, vomiting, dyspepsia, diarrhea, dizziness, headache, bronchoconstriction *caution with COPD, can cause bradycardia |
| Cholinesterase Inhibitors- interactions (ch 22) | first gen antihistamines, tricyclic antidepressants, conventional antipsychotics |
| Memantine (ch 22) | NMDA receptor antagonist for moderate to severe Alzheimer's Disease, dizziness, headache, confusion, constipation |
| What kind of disorder is multiple sclerosis? (ch 23) | chronic, inflammatory, autoimune disorder that damages myelin sheath of neurons in the CNS, causing a wide variety of sensory, motor, and cognitive defects |
| What are paresthesias? (ch 23) | numbness, tingling, pins & needles |
| What are 4 types of MS? (ch 23) | relapsing-remitting (90%), secondary progressive, primary progressive, progressive-relapsing |
Created by:
cskrivanek
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