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16 Cards in this Set
- Front
- Back
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Define Alzeihmers.
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A progressive, irreversible dz associated with neuronal loss and loss of neuronal function.
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Name four degenerative of the CNS that cause dementia.
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1. Most common are Alzeihmers Dz and Parkinsons Dz
2. Frontotemporal dementias ( Pick's dz, Progresssive surpranuclear palsy), 3. Vascular Dz (Multi-infarct dementia) 4. Lewy Body Dementia 5. Structural CNS disorders- brain tumor hydrocephalus |
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What is more common Alzeihmers of Parkinsons?
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Alzeihmer's Dz is 10X more prevalent.
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What are some risk factors predisposing Alzeihmer's Dz.
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1. Age
2. Trisomy 21 3. Head injury 4.. Family History 5. E-4 allele for apoprotein E is associated with late onset PD 6. HLA-A2 |
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Discuss the amyloid hypothesis in relation to AD.
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Accumulation of 42 aa frag of amyloid (A beta 1-42) concentrated in plaques in Alzeihmers are toxic to brain...thus current therapy is aimed at removing this amyloid.
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True/False. Frontotemporal dz lack tauopathies.
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True. tauopathies are amyloid plaques....neurofibrillary changes associated with abnormal phosphorylation of tau protein.
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What are the normal changes in brain anatomy characteristic of senescence /aging?
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Reduction in size and dilation of ventricles. Loss of cortical neurons is NOT a normal aging process.
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Characterize the typical prognosis of Alzeihmers from onset.
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Patients live 7 years from time of Dx.
1. Dz restricted to cognition and behavior (memory, orientation, judgement, language, insight) 2. Advancing symptoms include aphasic and gait abnormalities. 3. Eventually progressses to total loss of autonomy (bladder/bowel incontinence, loss of circadian rythms) |
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What is MMSE?
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Mini-mental state examination. A technique for assesing the decline resultant of Parkinsons.
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What is the sole method of Dx of Alzeihmers Dz?
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Tissue examination. Biopsy/autospsy. However, careful clinical assesment can proviide a correct Dx 90% of the time.
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Name six abnormalities occuring as a result of Alzeihmers Dz.
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1. Neuronal loss- atrophy of temporal lobes including hippocampi
2. Neurofibrillary tangles 3. granulovaculor degeneration 4. Hirano bodies- rod-like eosiniphilic intracellular inclusions made of proteins and actin 5. amyloid depostion in vessel walls (angiopathy) 6.neuritic "senile" plaques |
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What is the association between AD and trisomy 21?
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The Amyloid precursor gene is located on chromosome 21. Patients living beyond the age of 40 will develop Alzheimers dementia in addition to their mental retardation.
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How would you differentiate clinically between the various causes of dementia?
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1. Alzeihmers- memory, word finding
2. Frontotemporal- Personality change (Pick's) psychosis, judgement 3, Vascular etiologies present as episodic stepwise dementia |
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What is currently the treatment for AD?
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1. Memantine- selectively blocs pathological activation of NMDA receptors
2. Cholinesterase inhibitor |
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What is the funciton of memantine?
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Excess glutamate in the brain leads to exitotocitiy. Memantine protects cells from glutamate by blocking NMDA receptors and minimizing oxidative damage.
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What antioxidants are preventative for AD?
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Vitamin E & C...water soluble EC restores E to its reduced state.
1. also increased folic acid intake and reduced homocysteine |
