Alzheimer's Disease and Delirium: Clinical Manifestations and Mechanisms PDF

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ExceedingLyre3525

Uploaded by ExceedingLyre3525

University of Windsor

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Alzheimer's disease delirium cognitive impairment neurology

Summary

This document provides a comparison of Alzheimer's disease and delirium. It differentiates the conditions on the basis of clinical manifestations, disease progression, causative agents, contributing factors, and pathophysiological mechanisms. The content covers cognitive changes, memory loss, and related neurological impacts.

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5 Altera)on in Cogni)on: Delirium and Demen)a Differen)ate between Alzheimer’s disease and delirium on the basis of clinical manifesta)ons, disease progression, causa)ve agents, contribu)ng factors and pathophysiological mechanisms. Clinical Manifesta)ons: Alzheimer’s Disease (AD):...

5 Altera)on in Cogni)on: Delirium and Demen)a Differen)ate between Alzheimer’s disease and delirium on the basis of clinical manifesta)ons, disease progression, causa)ve agents, contribu)ng factors and pathophysiological mechanisms. Clinical Manifesta)ons: Alzheimer’s Disease (AD): o Characterized by progressive memory loss, disorienta8on, confusion, impaired problem-solving, and difficul8es with language and judgment. Behavioral symptoms include irritability, agita8on, mood swings, depression, and anxiety. Delirium: o Manifests as acute changes in cogni8on and aCen8on, fluctua8ng levels of consciousness, disorganized thinking, and perceptual disturbances (e.g., hallucina8ons or delusions). Hyperac8ve delirium presents with restlessness and agita8on, while hypoac8ve delirium involves lethargy and reduced motor ac8vity. Disease Progression: Alzheimer’s Disease: o Gradual and progressive onset. Ini8al symptoms are mild (e.g., forgeKulness), but they worsen over years, leading to severe cogni8ve impairment and dependency. The disease course can extend for several years to a decade or more. Delirium: o Rapid onset, typically developing within hours or days. The condi8on fluctuates in severity throughout the day and can resolve quickly with treatment or underlying cause correc8on, though it may persist in some cases if the trigger remains. Causa)ve Agents: Alzheimer’s Disease: o No single causa8ve agent. Associated with amyloid-beta plaques and neurofibrillary tangles (tau protein aggregates), mitochondrial dysfunc8on, and chronic inflamma8on. Delirium: o OSen triggered by reversible factors such as infec8ons (e.g., pneumonia, urinary tract infec8ons), metabolic disturbances, drug intoxica8on or withdrawal, and post-surgical states. Contribu)ng Factors: Alzheimer’s Disease: o Age, gene8c predisposi8ons (e.g., APOE ε4 allele), cardiovascular risk factors (e.g., hypertension, high cholesterol, diabetes), trauma8c brain injury, and estrogen deficiency in females. Delirium: o Older age, preexis8ng cogni8ve impairment, visual or hearing impairment, mul8ple medica8ons, recent surgery, dehydra8on, and infec8ons are common contribu8ng factors. Pathophysiological Mechanisms: Alzheimer’s Disease: o Accumula8on of amyloid-beta leads to plaque forma8on, tau protein hyperphosphoryla8on forms neurofibrillary tangles, and chronic neuroinflamma8on causes synap8c loss and neuronal death. Reduced cerebral blood flow and mitochondrial dysfunc8on exacerbate the damage. Delirium: o Disrup8on of neurotransmiCer balance, especially acetylcholine deficiency and dopamine excess, contributes to altered cogni8on and aCen8on. Inflamma8on and metabolic disturbances also play a role, par8cularly when related to infec8ons or other acute condi8ons. This dis8nc8on highlights the progressive and irreversible nature of Alzheimer’s compared to the acute, reversible nature of delirium when the underlying cause is managed.

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