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Pharmacology 4-8
| Question | Answer |
|---|---|
| What are neurodegenerative diseases characterized by? | Premature, primary death of specific nerve cell populations |
| What does neurodegeneration of functionally-linked areas produce? | -movement disorders and/or -personality changes |
| How is each disorder characterized? | Each disorder is distinct, progressive, and irreversible. |
| Do drugs cure neurodegenerative diseases? | No, and they don't prevent degeneration either. Neither do they stimulate recovery but some drugs may retard degradation. |
| What are the two main classes of neurodegenerative diseases that involve malfunction of the extrapyramidal system (particularly substantia nigra and striatum)? | Hypokinetic (ex: Parkinson's) and Hyperkinetic (Huntington's) |
| What kind of condition is Amyotrophic lateral sclerosis (ALS) or Lou Gehrig's disease an example of? | A neurodegenerative disease that involves muscle weakness and atrophy due to the degeneration of motor neurons in the spinal cord and cerebral cortex. |
| What is an example of a disease that is characterized by dementia due to degeneration of neurons in the hippocampus and cerebral cortex? | Alzheimer's disease |
| What are the factors for selective neurodegeneration? | -genetic and environmental interactions -excitotoxicity -energy metabolism -free radicals |
| What enzyme removes superoxide ions from the body and what do free radicals damage? | Superoxide dismutase. Free radicals may produce damage of DNA, proteins, lipid peroxidation of membranes. |
| What is excitotoxicity? | Excessive glutamate release which produces excessive influx of Ca 2+, that is excitation induced, into neurons |
| How does the environment and the genetics influence neurodegenerative diseases? | -there's a genetic link-ex: Huntington's disease -no widespread environmental link yet established to any neurodegenerative diseases -genetic predisposition and environmental toxins, or viral infections may contribute to Parkinson's disease |
| Explain what role does energy metabolism play in selective neurodegeneration | drug-induced or age associated decline in energy metabolism results in changes in membrane metabolism, removal of voltage dependent Mg 2+ , block of NMDA-receptor activationn and an increase in Ca 2+ influx |
| What is Parkinson's disease and what are some symptoms of that? | A progressive neurologic disorder of muscle movement, disorder of basal ganglia. Characterized by: bradykinesia, tremors, muscular rigidity, abnormal posture, shuffling gait, mask-like face, impaired speech, inability to perform skilled tasks |
| What does the pathology Parkinson's disease involve? | -presence of Lewy bodies (pathological oligomers of alpha-synuclein) in surviving neurons -degeneration of nigrostriatal dopamine neurons that project to the striatum |
| What is the etiology of Parkinson's disease | -cause not established -aging, environmental and genetic factors can contribute to development of the disease |
| Is Parkinsonism the same as Parkinson's disease? | No. Parkinsonism refers to disorders that resemble Parkinson's disease but have a known cause and variable rates of progression and responses to drug therapy -encephalitis lethargica -multiple small storkes -traumatic brain therapy -antipsychotic dru |
| What two pathways are involved in the normal physiology of basal ganglia? What receptors control them? | Direct and indirect pathways. D1 receptors control the direct pathway and D2 receptors control the indirect one. |
| What normally happens during the direct and indirect pathways of the basal ganglia? | Direct pathway: -DA activates the direct output pathway (GABA) -inhibits GABA neurons Indirect pathway: -DA inhibits the direct output pathway (GABA) -activates GABA neurons -inhibits Glut neurons decreases activity of GABA neurons |
| What happens in the basal ganglia in Parkinson's disease? | -reduced amount of DA acting on D1 and D2 -direct pathway inhibited and indirect pathway activated -GABA neurons activated, Glutamate neurons inhibited -net decrease in the excitatory input to the cortex -disruption of muscle control |
| Give examples of the major classes of drugs and the drugs that are used in the improvement of Parkinson's disease symptoms? | Increase DA synthesis: -L-Dopa -carbidpoa/L-dopa -entacapone -entacapone/L-Dopa/carbidopa Decrease DA catabolism: -selegiline -rasagiline DA receptor agonists: -bromocriptine -ropinirole -pramipexole -apomorphine Others: -amantadine |
| What are some antagonists of muscarinic and cholinergic receptors used with Parkison's disease? | benztropine and trihexyphenidyl |
| What are some characteristics of L-dopa? | -precursor of DA that passes BBB -decreases Parkinsonism symptoms (rigidity, tremor) -patients experience decline in response after 3-5 years -half life of 1-2 hours =orally available, rapidly absorbed from sm. intestine -only 1-3% reaches brain |
| What are side effects of L-dopa in the PNS? | caused by the peripheral conversion of DA to NE: -nausea -vomiting -anorexia -cardiac arrhythmias -orthostatic hypotension |
| What are side effects of L-dopa in the CNS? | -visual and auditory hallucinations -abnormal involuntary movements (dyskenesia) -may cause mood changes (depression, psychosis, anxiety) |
| Which medication is the medication of choice for symptomatic treatment of Parkinson's disease? | Levedopa/Carbidopa-blocks peripheral metabolism of L-Dopa and increases L-Dopa availability in brain -allows to reduce dose and allows for less side effects of peripheral DA |
| What is Entacarpone/Levodopa/Carbidopa? | A medication used to treat symptoms of Parkinson's disease. Inhibits cathechol-O-methyltransferase, decreases peripheral metabolism of L-Dopa at periphery and increases L-Dopa availability in the brain |
| What is Selegiline (deprenyl)? | An anti-parkinson's symtpoms drug used as adjunct treatment,inhibits MAO-B, decreases production of H2O2 (and free radicals), little benefit when taken alone, may cause insomnia (caused by amphethamine/methamphetamine which is a metabolite) |
| What is Rosagiline? | A drug used to treat symptoms of Parkinson's, selectively inhibits MAO-B in brain, not metabolized to amphetamine like Selegiline (amphetamine is what causes insomnia) |
| What are Bromocriptine, Ropinirole, Parmipexole? | All treat Parkinson's symptoms. Bromocriptine- D2 agonis, D1 partial agonist Ropinirole-D2 and D3 agonist Pramipexole-D2 and D3 agonist |
| How are DA receptor agonists used clinically? | -effective in monotherapy in early stage of disease or as adjunct therapy to L-Dopa in later stages of the disease -orally active -begin with low doses then increase gradually, usual maintenance dose is 10-30 mg/day. |
| What are some side effects presented with DA receptor agonists? | -cardiovascular effects-cardiac arrhythmias, postural hypotension -neurological effects: depression, confusion, sleepiness, hallucinations, impulsivity -GI problems- nausea, vomiting -contraindicated in patients with heart or mental problems |
| What is Apomorphine? | A DA receptor agonist drug.Acute treatment for patients with advanced disease for "off" periods. Administered subQ. Side effects; nausea, vomiting, arrhythmias, postural hypotension, hallucinations, pronounced sleepiness |
| What are Benztropine and or Trihehyphenidyl? | Muscarinic antagonists. Alleviate tremor and rigidity (not very helpful for bradykinesia) as monotherapy or along with other drugs -block overstimulation of muscarinic receptors -side effects: blurred vision, dry mouth, urinary retention, constipation |
| What is Amantadine? | -used to alleviate bradykinesia and rigidity in Parkinson's in patients with mild to moderate disease prior to initiation of L-Dopa. Moderately increase DA release, blocks cholinergic muscarinic receptors and glutamatergic NMDA receptors. |
| What are some side effects of Amantadine (used for Parkinson's)? | Hallucinations and confusion, nausea, dizziness, rash of the low extremities, special caution taken when prescribing to patients with CHF and glaucoma -was originally developed as antiviral to treat influenza |
| What is Alzheimer's disease? | -progressive dementing disorder, results from widespread degeneration of synapses and neural in cerebral cortex and hippocampus, impaired short-term memory and cognition. |
| What are signs and symptoms of Alzheimer's? | memory loss, language deterioration,impaired ability to mentally manipulate visual information, poor judgement, confusion, restlessness and mood swings -degeneration of basal forebrain cholinergic neurons, presence of amyloid senile plaques |
| What are some risk factors for Alzheimer's? | Age, incidence increases with age, eight leading cause of death for people over 65. Genes-mutation of the amyloid precursor protein (APP gene), 10% of cases are inherited, mutation in presenilin 1(PS1)a more agressive form of FAD,mutation in presenilin 2 |
| What are ways to treat Alzheimer's? | No cure and no way to slow progression of disease. Symptoms improved with drugs. AChE inhibitors (donezepil, galantamine, rivastigmine, tacrine) or NMDA receptor inhibitors (memantine) |
| What are Donezepil and or Rivastigmine? | AChE inhibitors. Block ACh degradation, increase ACh, benefits may be reatined for several years, good oral bioavailability, variable half-life. Donezepil and galantamine metabolized by P450s, rivastigmine metabolized by ChE |
| What are some side effects of AChE inhibitors? | -tremors -bradychardia -nausea, vomiting -diarrhea -anorexia |
| What is Memantine? | Used to treat symptoms of Alzheimer's. MNDA receptor antagonist (low affinity) derivative of amantadine.Protects neurons from Ca2+ overload (excitotoxicity. Improved daily activites and cognitive function, benefits additive when given with donezepil. |
| What are some side effects of Memantine (Alzheimer's)? | Dizziness, headache, confusion, agitation, constipation. |
Created by:
rcernetchi
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