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Published byBryan Howard Modified over 9 years ago
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Memory Fact memory Skills memory
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Cortical Sensory Area Amygdala Hippocampus Diencephalon Prefrontal Cortex Basal Forebrain
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Cortical Sensory Area Corpus Striatum Motor Cortex Cerebellum Extrapyramidal Motor Nuclei
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Alzheimer’s Features Etiology Pathophysiology Manifestation Diagnosis All of this is in your lab book!!
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Features degenerative most common dementia 4th most common cause of death not a normal part of ageing
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Etiology no gender differences risk increases with age –c–can be 40 - 50 –m–most over 65 prevalence = 20% by 80 10-15% of cases potentially attributed to depression
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Slow virus - incubation period 2 - 30 years, transmission difficult to prove An auto immune process - increased levels of brain reactive antibodies Aluminium toxicity - aluminium deposits have been identified in some patients.
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Etiology Genetic predisposition - 10 - 30% of patients have familial association +ve correlation with fat defect on chromosome 21 implicated supported by Downs developing AD in 4th decade SDAT families produce 3x normal numbers of Downs children
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The 7 Dietary Principles to Reduce Alzheimer's Risk PCRM 1. Minimize saturated fats and trans fats. 2. Vegetables, legumes (beans, peas, and lentils), fruits, and whole grains should be the primary staples of the diet. 3. One ounce of nuts or seeds (one small handful) daily provides a healthful source of vitamin E. 4. A reliable source of vitamin B 12, such as fortified foods or a supplement providing at least 2.4 μg per day for adults) should be part of the daily diet. 5. Choose multivitamins without iron and copper, and consume iron supplements only when directed by your physician. 6. Avoid the use of cookware, antacids, baking powder, or other products that contribute dietary aluminium. 7. Engage in aerobic exercise equivalent to 40 minutes of brisk walking 3 times per week.
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Pathophysiology severe loss of hippocampal and cortical neurons (hippocampus becomes isolated and functionless) presence of granulovacuolar degeneration, diffuse neurofibrillary tangles and senile plaques
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Pathophysiology last 2 changes also found in lead encephalopathy and Downs suggested that enzymes metabolising neurotransmitters are involved; choline acetyltransferase is reduced severity of dementia directly related to reduction in brain ACh
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Manifestations insidious and progressive loss of memory, disorientation, impaired abstract thinking, changes in personality Three stages:
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Manifestations 12 - 4 yrs –subjective memory deficit, random forgetfulness, get lost easily –lack of spontaneity –subtle personality changes (loss of sense of humour) –disorientation to time and date
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Manifestations 2Confusional - may last several years –impaired cognition and abstract thinking –restlessness and agitation –wandering - "Sundown Syndrome” –inability to carry out daily living activities
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Manifestations 2Confusional (cont’d) –impaired judgement –inappropriate social behaviour –lack of insight –repetitive behaviour –voracious appetite
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Manifestations 3Terminal - 1 - 2 yrs –indifference to food leads to emaciation –inability to communicate –urinary and faecal incontinence –seizures –death usually the result of malnutrition or infection
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Diagnosis absence of definitive test diagnosis only by microscopic examination of tissue from cerebral biopsy or autopsy patient presenting should be tested to detect potentially reversible nutritional, endocrine, and infectious causes of symptoms (eg. B 12 deficiency, thyroid dysfunction and electrolyte imbalance)
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Diagnosis requires presence of dementia established by clinical examination and documented by results of a Mini-mental status test, Blessed dementia test, or similar to yield deficits in 2 or more areas of cognition and progressive worsening of memory or other cognitive functions
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