logging in or signing up Dementia benjatchison Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 104 Category: Entertainment License: All Rights Reserved Like it (0) Dislike it (0) Added: October 12, 2011 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript Module 6:Dementia: Module 6:Dementia OT 3740 Disabling ConditionsDSM-IV Definition: DSM-IV Definition “multiple cognitive deficits with the main deficit being impairment of memory” Dementia no longer referenced by APA as “organic” Senile dementia no longer used by medical communityDelirium and Dementia: Delirium and Dementia Cognitive disorders most commonly seen by OT’s Differ in course and prognosis yet easily mistaken for each otherDSM-IV Diagnostic Criteria: DSM-IV Diagnostic Criteria Disturbed consciousness Change in cognition Rapid onset Related to medical condition OR Intoxication or withdrawal from substances (American Psychiatric Association, 2000)Etiology of Delirium: Etiology of Delirium 1 or > medical conditions Varied to include: Infection, burns, metabolic problems Adverse reaction to medication; toxic substances Post surgical complicationIncidence and Prevalence: Incidence and Prevalence Commonly under recognized 1% of adults; 10% of ER patients,40% terminally ill; 50% hospitalized patients ( Samuals & Neugroschel,2004)Delirium Signs and Symptoms: Delirium Signs and Symptoms Emerging Signs ( Prodromal ) Restlessness Anxiety Sleep disturbance IrritabilitySigns and Symptoms: Signs and Symptoms Altered perceptions Decrease attention, impaired memory Disorientation to time and place Disorganized thinking and speechSigns and Symptoms: Signs and Symptoms Dysgraphia Constructional Apraxia Dysnomic Aphasia AsterixisCourse and Prognosis of Delirium: Course and Prognosis of Delirium Rapid Onset Fluctuation Sundowning TRANSIENTMedical Management: Medical Management Treat underlying cause Withdraw sedatives that act on CNS Except when related to alcohol w/d Also may prescribe neuroleptics Vigilant, supportive care Avoid long term decisions until delirium clearedDEMENTIA: DEMENTIA Memory most prominent; STM Aphasia, apraxia , agnosia Topographical disorientation Poor judgement /insightPotential Etiologies of Dementia: Potential Etiologies of DementiaAlzheimer’s Disease: Alzheimer’s Disease Most common form of dementiaPathomechanics of AD : Pathomechanics of AD Neuropathology of the Neuron: Plaques and TanglesAmyloid Plaques: Amyloid Plaques APP is a normal protein aids in neuronal growth Enzymes called secretases clip APP into shorter pieces to create sticky deposits called plaqueAmyloid Plaques: Amyloid Plaques Betta and gamma secretase team up to cleave the APP molecule This generates an A-beta protein which drifts from cell membraneAmyloid Plaques: Amyloid Plaques Most A-beta dissolves in the fluid surrounding the neuron Some of it folds into fibrils which cluster together.Amyloid Plaques: Amyloid Plaques Clusters of A Beta gradually expand to form larger plaques This displaces brain cells and destroys themNeurofibrillary Tangles: Neurofibrillary Tangles The branches from neurons (neurites) contain microtubules These perform many critical tasksNeurofibrillary Tangles: Neurofibrillary Tangles Each microtubule is reinforced by tau proteins. These proteins hold the microtubule togetherNeurofibrillary Tangles: Neurofibrillary Tangles Lacking proteins to hold them together, microtubules disintegrate Neurons then shrink and diesWhat Causes This Process?: What Causes This Process? Not known-no biologic marker identified Neuronal loss is most significant in cortexGenetic Considerations: Genetic Considerations Three identified for rare, early onset type of AD Chromosome 21 Chromsome 14 Chromosome 1 If one parent diagnosed:children have 50% chance of early onsetGenetic Considerations: Genetic Considerations Apoliprotein E gene on Chromosome 19 Down Syndrome due to extra Chromosome 21 Chromosome 21 carries the APPP gene Brains of most with DS show changes >41Neurotransmitter Abnormalities: Neurotransmitter Abnormalities Autopsies show destruction of cholinergic tracts Choline acetlytransferase reductionVascular Risk Factors: Vascular Risk Factors Cardiovascular disease linked to AD 60-90% of AD cases have cerebrovascular pathologiesIncidence and Prevalence: Incidence and Prevalence Expected to QUADRUPLE in next 50 years 1: 45 Americans Prevalence increases with age Women have higher incidenceRisk Factors: Risk Factors Low educational level Head trauma Depression Late maternal age Environmental/occupational exposure ECTRisk Factors: Risk Factors Alcohol abuse Analgesic abuse Long standing physical inactivity Vascular risk factors Type II Diabetes African American/Hispanic High waist to hip ratiFactors May Reduce Risk: Factors May Reduce Risk Antioxidants, e.g. Vitamin E Regular consumption of fish Estrogen replacement therapy NSAIDS Statins Histamine blockers Physical activity Education, cognitive training, and mental stimSigns and Symptoms: Signs and Symptoms Hallmark=Memory Loss Impact all performance skills Three Stages Clinical Dementia Rating(CDR)Mild Cognitive Impairment: Mild Cognitive Impairment Five Criteria: C/O memory problems Abnormal for persons age ADL’s not affected Other cognitive abilities are intact No dementia presentAD: Early Stage: AD: Early Stage Memory: STM Emergence of LTM impairment Procedural Memory Semantic MemoryAD : Early Stage: AD : Early Stage Language Visuospatial Executive FunctionsAD : Middle Stage: AD : Middle Stage Memory: Deteriorates further Language Visuospatial Psychiatric Signs & Symptoms Behavior DisturbancesAD: Late Stage: AD: Late Stage 8-12 years No new memories Language Motor Skills Psychiatric SymptomsCourse and Prognosis: Course and Prognosis Progressive disease Average survival time is 4-6 years Some live 20 years post dx Death 2 infection, dehydration, nutritionMedical Management: Medical Management DSM-IV Diagnostic Protocol NIH 3 Criteria: Multiple Cognitive Deficits Significant Impairment Course is gradual onset; progressive decline 5 Steps Detailed history Interviews with family and close friends Physical Examination CT Scan/MRI Neuropsychologic TestsGeneral Treatment Approach: General Treatment Approach Four Pillars of Complete Dementia Care Supportive care for patient Supportive care for family/caregiver Disease Treatment Treatment of Symptoms/SignsNext….: Next…. Please view all short videos posted in module You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.
Dementia benjatchison Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 104 Category: Entertainment License: All Rights Reserved Like it (0) Dislike it (0) Added: October 12, 2011 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript Module 6:Dementia: Module 6:Dementia OT 3740 Disabling ConditionsDSM-IV Definition: DSM-IV Definition “multiple cognitive deficits with the main deficit being impairment of memory” Dementia no longer referenced by APA as “organic” Senile dementia no longer used by medical communityDelirium and Dementia: Delirium and Dementia Cognitive disorders most commonly seen by OT’s Differ in course and prognosis yet easily mistaken for each otherDSM-IV Diagnostic Criteria: DSM-IV Diagnostic Criteria Disturbed consciousness Change in cognition Rapid onset Related to medical condition OR Intoxication or withdrawal from substances (American Psychiatric Association, 2000)Etiology of Delirium: Etiology of Delirium 1 or > medical conditions Varied to include: Infection, burns, metabolic problems Adverse reaction to medication; toxic substances Post surgical complicationIncidence and Prevalence: Incidence and Prevalence Commonly under recognized 1% of adults; 10% of ER patients,40% terminally ill; 50% hospitalized patients ( Samuals & Neugroschel,2004)Delirium Signs and Symptoms: Delirium Signs and Symptoms Emerging Signs ( Prodromal ) Restlessness Anxiety Sleep disturbance IrritabilitySigns and Symptoms: Signs and Symptoms Altered perceptions Decrease attention, impaired memory Disorientation to time and place Disorganized thinking and speechSigns and Symptoms: Signs and Symptoms Dysgraphia Constructional Apraxia Dysnomic Aphasia AsterixisCourse and Prognosis of Delirium: Course and Prognosis of Delirium Rapid Onset Fluctuation Sundowning TRANSIENTMedical Management: Medical Management Treat underlying cause Withdraw sedatives that act on CNS Except when related to alcohol w/d Also may prescribe neuroleptics Vigilant, supportive care Avoid long term decisions until delirium clearedDEMENTIA: DEMENTIA Memory most prominent; STM Aphasia, apraxia , agnosia Topographical disorientation Poor judgement /insightPotential Etiologies of Dementia: Potential Etiologies of DementiaAlzheimer’s Disease: Alzheimer’s Disease Most common form of dementiaPathomechanics of AD : Pathomechanics of AD Neuropathology of the Neuron: Plaques and TanglesAmyloid Plaques: Amyloid Plaques APP is a normal protein aids in neuronal growth Enzymes called secretases clip APP into shorter pieces to create sticky deposits called plaqueAmyloid Plaques: Amyloid Plaques Betta and gamma secretase team up to cleave the APP molecule This generates an A-beta protein which drifts from cell membraneAmyloid Plaques: Amyloid Plaques Most A-beta dissolves in the fluid surrounding the neuron Some of it folds into fibrils which cluster together.Amyloid Plaques: Amyloid Plaques Clusters of A Beta gradually expand to form larger plaques This displaces brain cells and destroys themNeurofibrillary Tangles: Neurofibrillary Tangles The branches from neurons (neurites) contain microtubules These perform many critical tasksNeurofibrillary Tangles: Neurofibrillary Tangles Each microtubule is reinforced by tau proteins. These proteins hold the microtubule togetherNeurofibrillary Tangles: Neurofibrillary Tangles Lacking proteins to hold them together, microtubules disintegrate Neurons then shrink and diesWhat Causes This Process?: What Causes This Process? Not known-no biologic marker identified Neuronal loss is most significant in cortexGenetic Considerations: Genetic Considerations Three identified for rare, early onset type of AD Chromosome 21 Chromsome 14 Chromosome 1 If one parent diagnosed:children have 50% chance of early onsetGenetic Considerations: Genetic Considerations Apoliprotein E gene on Chromosome 19 Down Syndrome due to extra Chromosome 21 Chromosome 21 carries the APPP gene Brains of most with DS show changes >41Neurotransmitter Abnormalities: Neurotransmitter Abnormalities Autopsies show destruction of cholinergic tracts Choline acetlytransferase reductionVascular Risk Factors: Vascular Risk Factors Cardiovascular disease linked to AD 60-90% of AD cases have cerebrovascular pathologiesIncidence and Prevalence: Incidence and Prevalence Expected to QUADRUPLE in next 50 years 1: 45 Americans Prevalence increases with age Women have higher incidenceRisk Factors: Risk Factors Low educational level Head trauma Depression Late maternal age Environmental/occupational exposure ECTRisk Factors: Risk Factors Alcohol abuse Analgesic abuse Long standing physical inactivity Vascular risk factors Type II Diabetes African American/Hispanic High waist to hip ratiFactors May Reduce Risk: Factors May Reduce Risk Antioxidants, e.g. Vitamin E Regular consumption of fish Estrogen replacement therapy NSAIDS Statins Histamine blockers Physical activity Education, cognitive training, and mental stimSigns and Symptoms: Signs and Symptoms Hallmark=Memory Loss Impact all performance skills Three Stages Clinical Dementia Rating(CDR)Mild Cognitive Impairment: Mild Cognitive Impairment Five Criteria: C/O memory problems Abnormal for persons age ADL’s not affected Other cognitive abilities are intact No dementia presentAD: Early Stage: AD: Early Stage Memory: STM Emergence of LTM impairment Procedural Memory Semantic MemoryAD : Early Stage: AD : Early Stage Language Visuospatial Executive FunctionsAD : Middle Stage: AD : Middle Stage Memory: Deteriorates further Language Visuospatial Psychiatric Signs & Symptoms Behavior DisturbancesAD: Late Stage: AD: Late Stage 8-12 years No new memories Language Motor Skills Psychiatric SymptomsCourse and Prognosis: Course and Prognosis Progressive disease Average survival time is 4-6 years Some live 20 years post dx Death 2 infection, dehydration, nutritionMedical Management: Medical Management DSM-IV Diagnostic Protocol NIH 3 Criteria: Multiple Cognitive Deficits Significant Impairment Course is gradual onset; progressive decline 5 Steps Detailed history Interviews with family and close friends Physical Examination CT Scan/MRI Neuropsychologic TestsGeneral Treatment Approach: General Treatment Approach Four Pillars of Complete Dementia Care Supportive care for patient Supportive care for family/caregiver Disease Treatment Treatment of Symptoms/SignsNext….: Next…. Please view all short videos posted in module