Dementia Alzheimer (OWN) Ppt

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    Alzheimer Disease the most

    common of Dementia

    Kartika

    030.08.134

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    Introduction

    Dementia describes progressive decline of cognitive function,

    usually affecting the cortex as a whole, though sometimes

    patchily.

    Memory is especially affected, intellect gradually fails. There is

    loss of emotional control, deterioration of social behavior and

    loss of motivation.

    There are many causes of this syndrome. Dementia is a

    substantial cause of morbidity in any ageing population, with

    profound social and economic effects.

    Dementia affects some 10% of any population over 65, and

    20% over 80. The commonest causes are Alzheimers

    disease.(1)

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    What is Dementia?

    Dementia isn't a specific disease. Instead,

    dementia describes a group of symptoms

    affecting intellectual and social abilities

    severely enough to interfere with daily

    functioning.

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    Etiology

    Many cause of dementia, such us:

    degenerative disease, vascular, metabolic,

    vitamin deficiency, toxic, endocrine, infection,

    trauma. And many more

    But the most common of dementia is

    Alzheimer disease that include the generative

    disease about 60%

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    Symptoms

    The symptoms of dementia is divide into ABC

    A : activity of daily living

    B : behaviour/ behaviour psychologicalsyndrome of dementia (BPSD)

    C : cognition or cognitive defisicits

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    B/ Behaviour Psychological syndrome

    of dementia (BPSD)

    Paranoid: the people have taken his/hermoney, house in not oness home

    Hallucination:

    Depression:

    Anxiety:

    Social dysinhibition:

    Wandering

    Agitation

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    C/Cognitive deficits

    Memory: shortterm and longterm

    Orientation: time,person, place

    Language : Aphasia, anomian thingking,calculation, learning capacity

    Personality

    Judgement : ability to perform tasks insequence

    Reduce activity daily living

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    Risk factor

    Risk factors that can not be changed

    Age. The risk of Alzheimer's disease, vascular dementia andseveral other dementias increases significantly with age.However, dementia isn't a normal part of aging.

    Family history. People with a family history of dementia areat greater risk of developing it. However, many people witha family history never develop symptoms, and many peoplewithout a family history do.

    Down syndrome. By the time they reach middle age, most

    people with Down syndrome develop the plaques andtangles characteristic of Alzheimer's disease, according tostudies. Many, but not all, also develop dementia.(6)

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    Can be change Alcohol use. Consuming large amounts of alcohol appears to increase the risk

    of dementia.

    Atherosclerosis. This buildup of fats and other substances in and on your artery

    walls (plaques) is a significant risk factor for vascular dementia because it

    interferes with blood flow to your brain.

    Blood pressure. Blood pressure that's too high, and also possibly too low, can

    put you at risk of developing Alzheimer's disease and vascular dementia.

    Cholesterol. High levels of low-density lipoprotein (LDL) cholesterol, the

    "bad" cholesterol, can significantly increase your risk of developing vascular

    dementia.

    Depression. Although not yet well understood, late-life depression, may be an

    indication for the development of Alzheimer's-related dementia.

    Diabetes. If you have type 2 diabetes, you're at increased risk of developingboth Alzheimer's disease and vascular dementia.

    High estrogen levels. High levels of total estrogen in women have been

    associated with greater risk of developing dementia. This can be determined

    through a blood test.

    Smoking. Smoking likely increases the risk of developing dementia because itputs you at a higher risk of atherosclerosis and other types of vascular disease.(6)

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    DSM-IV criteria for the diagnosis of Dementia of the Alzheimer's Type(4)

    A. The development of multiple cognitive deficits manifested by both:

    1.Memory impairment (impaired ability to learn new information or torecall previously

    learned information)

    2.One or more of the following cognitive disturbances:

    (a) aphasia (language disturbance)

    (b) apraxia (impaired ability to carry out motor activities depite intactmotor function)

    (c) agnosia (failure to recognize or identify objects despite intactsensory function)

    (d) disturbance in executive functioning (i.e., planning, organizing,sequencing, abstracting)

    B. The cognitive deficits in criteria A1 and A2 each cause significantimpairment in social or

    occupational functioning and represent a significant decline from aprevious level of functioning.

    C. The course is characterized by gradual onset and continuing

    cognitive decline.

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    D. The cognitive deficits in Criteria A1 and A2 are not due to any

    of the following:

    (1) other central nervous system conditions that causeprogressive deficits in memory and cognition (e.g.,

    cerebrovascular disease, Parkinson's disease, Huntington's

    disease, subdural hematoma, normal-pressure hydrocephalus,

    brain tumor)

    (2) systemic conditions that are known to cause dementia (e.g.,

    hypothyroidism, vitamin B or folic acid deficiency, niacin

    deficiency, hypocalcaemia, neurosyphilis, HIV infection)

    (3) substance-induced conditions

    E. The deficits do not occur exclusively during the course of a

    delirium.

    F. the disturbance is do not better accounted for by another axis

    I disorder (e.g., major depressive disorder, schizophrenia) (2)(4)

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    Test in Dementia

    Blood test: full blood count, ESR, C-reactiveprotein, urea, electrolytes, blood glucose, liverbiochemistry, serum calcium, vitamin B12, folate,T3 T4, HIV serology.

    Imaging : Chest X-rays, CT scan, MRI brain Other: genetic studies, EEG, CSF, brain biopsy.

    Psychiatric evaluation/neuropsychiatri:

    MMSE(mini mental states examination)CDT (clock drawing test)

    IADL

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    What is Alzheimer Disease?

    Alzheimers disease is an irreversible,

    progressive brain disease that slowly destroys

    memory and thinking skills.

    This is the commonest dementia, a

    degenerative disease of the cortex, accounting

    for over 65% of dementia in any age group.(3)

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    Etiology

    AD develops when genetic, lifestyle, and

    environmental factors work together to cause

    the disease process to start.

    In recent years, scientists have discovered

    genetic links to AD. They are also investigating

    other factors that may play a role in causing AD

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    Genetic

    The two main types of AD are early-onset and late-onset:

    Early-onset AD is rare, usually affecting people aged 30to 60 and usually running in families. Researchers haveidentified mutations in three genes that cause early-onset AD.

    Late-onset AD is more common. It usually affectspeople over age 65.

    Researchers have identified a gene that produces aprotein called apolipoprotein E (ApoE). Scientistsbelieve this protein is involved in the formation of beta-amyloid plaques.

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    To understand Alzheimers disease, its

    important to know about the brain

    Cerebellum in charge of balance and coordination

    Brain Stem connects the spinal cord with the brain

    relays and receives messages to and from muscles, skin, and

    other organs

    controls automatic functions such as heart rate, blood

    pressure, and breathing.

    Hippocampus: where short-term memories are converted to

    long-term memories

    Thalamus: receives sensory and limbic information and sends tocerebral cortex

    Hypothalamus: monitors certain activities and controls bodys internalclock

    Limbic system: controls emotions and instinctive behavior (includes

    the hippocampus and parts of the cortex)

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    Neuropathology

    Amyloid plaque : which are dense deposits of

    protein and cellular material that accumulate

    outside and around nerve cells

    Neurofibrillary tangles : which are twisted

    fibers that build up inside the nerve cell

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    Beta-amyloid PlaquesAmyloid precursor protein (APP) is theprecursor to amyloid plaque.

    1. APP sticks through the neuronmembrane.

    2. Enzymes cut the APP into fragmentsof protein, including beta-amyloid.

    3. Beta-amyloid fragments cometogether in clumps to form plaques.

    1.

    2.

    3.

    AD and the Brain

    In AD, many of these clumps form,

    disrupting the work of neurons. This

    affects the hippocampus and other areas

    of the cerebral cortex.

    Slide 17

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    NeurofibrillaryTangles

    Neurons have an internal support structure partly made up of

    microtubules. A protein called tau helps stabilize microtubules. In AD,

    tau changes, causing microtubules to collapse, and tau proteins clump

    together to form neurofibrillary tangles.

    AD and the Brain

    Slide 18

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    Amyloid accumulation and Neurofibrillary

    tangles nerve cell death neurochemical

    deficiency cognitive and behaviour changes

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    Conclusion

    Alzheimer's disease is the most common cause of dementiain people age 65 and older.

    Symptoms usually appear after age 60, but early-onsetforms of the disease can occur, usually as the result of adefective gene.

    Alzheimer's disease usually progresses slowly, over seven toten years, causing a gradual decline in cognitive abilities.

    Caring for a person with Alzheimers disease can have highphysical, emotional, and financial costs.

    The demands of day-to-day care, changing family roles, anddifficult decisions about placement in a care facility can behard to handle. (8)