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UWM Patho II Exam 4
Alzhiemer's Disease
Question | Answer |
---|---|
What is Alzheimer's disease? | A progressive, neurodegenerative disease characterized by: 1.loss of function & death of nerve cells in several areas of the brain 2.leads to a dementia |
What is the epidemiology of Alzheimer's disease? | 1.Is responsible for ~80% of all cases of dementia in both the presenile (<65 years) and the senile (>65 years) age bracket 2.Incidence: 2% at 65 years, doubles every 5 years. (4.5 million in USA in 2000) |
What are the risk factors for Alzheimer's disease? | 1.Aging 2.Gender women > men 3.Significant head trauma 4.Familial 5.Exposure to light metals(AL) 6.Low serum levels of folate & vitamin B12 (alcoholics) 7.Elevated plasma & total homocysteine 8.not much education 9.Lower income |
What is the etiology of Alzheimer's disease? | Associated with: 1.Reduced ACh levels in the cerebral cortex and hippocampus 2.Al toxicity 3.Chromosome 21 coding for amyloid precursor protein (APP) 4.(ApoE-ε4) located on chromosome 19 5.Abnormalities on chromosome 14 |
What is the most common cause of death of older patients with down syndrome? | Alzheimer's disease |
Neuritis (senile) plaques | 1.accumulation of amyloid plaques between nerve cells (neurons) 2.b-amyloid is a fragment of a protein cut from the amyloid precursor protein (APP). 3.In AD, the fragments accumulate to form hard, insoluble plaques instead of being broken down. |
What do neurofibrillary tangles consist of? | 1.Insoluble twisted fibers that consist of a tau microtubule-associated protein 2.microtubules help transport nutrients from one part of the nerve cell to another. 3.In AD, tau protein is abnormal and the microtubule structures collapse. |
What are the pathological findings of Alzheimer's disease? | 1.Dendrites deteriorate killing neurons 2.Hippocampus size reduced by 47% 3.Amygdala 26% decrease in volume 4.Cell density reduced by 75% (increase in ventricular size) 5.marked loss of cells in nucleus basalis of Meynert 6.Cortex has plaques & tan |
Symptoms of Alzheimer's disease | 1.Cells in the brain have difficult signal transmission 2.A person with AD has problems with memory, judgment, and thinking, which makes it hard for the person to work or take part in day-to-day life. |
How are memory and thinking affected by Alzheimer's disease? | 1.Impaired memory (short-term loss occurs first) 2.thinking disorientation and confusion |
What are the 10 Warning Signs of Alzheimer's Disease? | 1.Misplacing things 2.Abstract thinking 3.can't do familiar tasks 4.Changes in personality & behavior 5.Poor judgment 6.can't follow directions 7.Prob. with language Impaired visual and spatial skills Loss of motivation Loss of normal sleep patt |
What diagnostic tests are used to diagnose AD? | 1.No 1 diagnostic test that can detect AD. 2.diagnosis requires both amyloid plaques and tangles in excess of the abundance anticipated for age-matched healthy controls. 3.80~90% certainty of “probable” Alzheimer’s Disease |
How is diagnosis of AD made through cognitive impairment? | Cognitive impairment severe enough to cause social or occupational disability in at least two domains: 1.Memory 2.Language 3.Calculations 4.Orientation 5.Judgment |
What are the symptoms of mild AD? | 1.Loss of recent memory 2.Faulty judgment 3.Personality changes |
What are the symptoms of moderate AD? | 1.Verbal and physical aggression 2.Agitation 3.Wandering 4.Sleep disturbances 5.Delusions |
What are the symptoms of severe AD? | 1.Loss of all reasoning 2.Bedridden 3.Incontinence |
What is the mechanism of action in vaccination therapy (not available yet)used to treat AD? | Stimulates immune response against Ab peptides, leading to the peptides being cleared from the body |
What is the mechanism of action in b- and g-secretase inhibitors used to treat AD? | Inhibit b- and g-secretases, leading to decreased production of Ab proteins |
What is the mechanism of action in Cholesterol-lowering drugs(statins, HMG-CoA reductase inhibitors) used to treat AD? | 1.Increase processing of amyloid precursor protein (APP) by a-secretase, leading to decreased production of Ab proteins |
What is the mechanism of action in Copper/zinc chealator (clioquinol) used to treat AD? | 1.Decrease the interaction of copper and zinc with Ab peptides, leading to amyloid plaques being cleared |
What is the mechanism of action in Non-steroidal anti-inflammatory drugs (ibuprofen, indomethacin) used to treat AD? | Selectively inhibit the production of the Ab protein (however, evidence is insufficient to support treatment) |
What is the mechanism of action in Vitamin E and vitamin C used to treat AD? | Play a role in delaying the onset of AD |
What is the mechanism of action in Memantine used to treat AD? | an NMDA antagonist, interferes w/ glutamatergic excitotoxicity |
What can be used to prevent AD? | 1.Vaccination therapy 2. b- and g-secretase inhibitors 3.Cholesterol-lowering drugs (statins, HMG-CoA reductase inhibitors) 4.Copper/zinc chealator (clioquinol) 5.NSAIDS 6.Vitamins C and E 7. Memantine |
What is dementia? | Dementia is the progressive decline in cognitive function due to damage or disease in the brain |
Pick’s disease (frontotemporal lobar degeneration) | 1.Autosomal dominant 2.Clinically resembles AD 3. Pick’s bodies seen (round intracytoplasmic inclusions of neurofilaments) 4.marked cortical atrophy in the frontal and temporal lobes 5.Onset from 50~60 years of age 6.more frequent in women |
Multi-infarction dementia (Vascular dementia) | 1.Cerebral atherosclerosis 2.Sudden onset 3.intermittent signs of dementia and motor deficits 4. 2nd most common cause of dementia |
Diffuse Lewy body disease (dementia with Lewy bodies) | Lewy body within neurons of: 1.substantia nigra 2.basalis of Meynert 3.limbic cortex (esp. cingulate gyrus- hallmark) 4.memory loss 5.parkinsonism 6.visual hallucinations 7.exhibits clinical overlap between AD and PD |
What is the difference between PD, and Pick's disease? | 1.personality problems are more common in Pick's disease 2.memory problems are more common in Alzheimer's disease |
What is the pathology of Pick's disease? | 1."lobar atrophy" involving the frontal and temporal lobes 2.the posterior 2/3 of the superior temporal gyrus is spared. 3.The cerebral gyral atrophy in Pick's disease is so severe that some of the gyri are extremely thin (termed "knife blade atrophy") |