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32 Cards in this Set
- Front
- Back
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aphasia
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deterioration in language function
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apraxia
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imparied ability to execute motor activities despite intact motor function
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agnosia
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failure to recognize or identify objects despite intact sensory
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reversible causes of dementia
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etoh, chronic lung diseases, iron deficiency, subdural hematoma, arthritis syndromes, CHF, hydrocephalus, thyroid disease, UTI!!
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what drugs may induce dementia/delirium?
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alcohol, anticholinergics, antidepressants, antihypertensives, antiparkinsons, antipsychotics, anxiolytics, corticosteroids
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what is the age of onset for dementia?
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>65
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what are some behavior disturbances associated with dementia?
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agitation, disturbed affect/mood, hallucinations, insomnia, aggression, anxiety, altered perceptions, appetite changes, withdrawal
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what is the patho of alzheimer's?
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neuritic plaques in the brain, neurofibrillary tangles (apo lipoprotein), genetic mutations on chromosome 21, loss of cholinergic neurons
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what role do inflammatory mediators have in Alzheimers?
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reduced risk of the disease with NSAIDS and corticosteroid use
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how are the serotonergic neurotransmitters affected in alzheimers?
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decreased
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how are noradrenergic NTs affected in alzheimers?
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cells in locus cerulus are lost
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how is GABA affected in alzheimer's?
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normal or moderately decreased
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how is MAO-B affected by alzheimer's
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increased
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if the disease process in alzheimers in primary neuronal injury resulting in neuritic plazues and neurofibrillary tangles what are the treatment options?
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none
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is the disease process in alzheimer's is neuronal injury causing neuronal death through processes of oxidative stress, loss of nerve growth factor and inflammation, how is it treated?
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vitamin E, selegiline, NSAIDS, estrogen, and gingko biloba
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if the disease process of alzheimers is neuronal dealth causing neurotransmitter loss in temporal, parietal and frontal lobes, how is it treated?
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cholinesterase inhibitors and cholinergic agonlists
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If the disease process of alzheimer's is neurotransmitter loss which causes mental symptoms of depression, delusions, hallucinations, aggreassion and sleep-wake disturbances, how is it treated?
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antidepressants, antipsychotics, anticonvulsants, and sedatives
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MOA of cholinomimetic therapy in AD
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increases acetylcholine at synapse to counteract the decline in cholinergic function by blocking the hydrolysis of acetylcholine at the synapse
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what are the S/E's of tacrine (cognex)?
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hepatotoxicity and GI toxicity
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caution using tacrine in these disorders
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peptic ulcer disease, bradycardia, bronchial secretions
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how is cognex administered?
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multiple daily dosing requiring slow titration
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what are the s/e's of aricept?
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similar to cognex but with no hepatotoxicity and little GI toxicity
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what are some interactions with cognex
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same but less than tacrine
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how does Rivastigmine (exelon) work?
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increased inhibitory effect in hippocampus and cortex which are most affected
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S/E's of exelon
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n/v/d, dizziness, abdominal affects (take w/food)
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How does metrifonat (promen) work?
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irreversible inhibitor of acetylcholinesterase and betacholinesterase with higher selectivity for betacholinesterase
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S/E's of promen
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muscle weakness, n/v/d, dizziness, abd pain, leg cramps, decreased BP/pulse
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what is a common symptom with cholinesterase inhibitors?
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nausea
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how does namenda work?
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blocks NMDA receptor which is normally a target of glutamate (a chemical messanger involved in storing, processing, and retreiving brian cells from an imbalance of chemicals and electrolytes like calcium. Over exidation of NMDA causes nerve damage
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when is namenda contraindicated?
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In patients iwth seizures and kidney disease
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what are the DI's with namenda?
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antihistamines, cold/flu, amantadine or other NMDA receptor antagonists, drugs excreted through kidneys, sodium bicarb
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adverse effects of namenda
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agitation, restlessness, confusion, dizziness, hallucination, not being able to hold urine, swelling in throat, rash, vomiting.
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