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Cognition
sensory input that is transformed, reduced, elaborated, stored recovered and used.
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Normal Cognitive Aging
- short term memory preserved with slow processing
- long-term memory preserved
- decreased efficiency with retrieval and processing
- greater impact on recollection - hippocampus
- rely more heavily on entorhinal cortex
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Storing Memories
- Parahippocampal cortex
- Peripheral cortex
- Entorhinal cortex
- Hippocampus
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Recalling memories
- Hippocampus
- Entorhinal cortex
- Peripheral cortex
- parahipocampal cortex
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Age 50
decreased retrical speed of memories
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Impact of AD
- 4th leading cause of death
- 3rd most expensice illness in US
- Affects 4 million at present with 250,000 afflicted/year
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Criteria for diagnosis of dementia
- Can't learn new info or recall old info
- and at least one of the following:
- aphasia (language)
- apraxia (carying out motor function)
- Agnosia (recognition of objects)
- Disturbed executive function (planning and sequencing)
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Criteria for Alzheimers Disease
- impairment in social or occupational function
- decline from previous level of function
- gradual onset and continuing cognitive decline
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it's not AD if
- CNS misfunction
- Systemic conditions known to cause dementia
- substance-induced condition
- occurs only during the course of a delirium
- is associated with another Axis 1 disorder (depression, bipolar, schiz)
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Behavioral symptoms of AD
- dilusions
- hallucinations
- depression
- sundowning
- other agitated behaviors
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AD occurs over ____ years
2 to 10
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Various forms of memory that fall apart
- episodic memory
- short term memory (usually first)
- memory of the meaning of words
- procedural memory
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The end of AD
all reasoning, attention and language abilities are disrupted
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Timeline of AD
- 1. Forgetfulness
- 2. Memory loss impairs work social functions
- 3. Recent memory imparied, withdrawl from difficult tasks
- 4. Frequently disoriented to time, some details of past are missing
- 5. Need help with ADLs
- 6. Cannot speak, walk or feed self
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Risk factors for developing AD
- Age
- Family history
- Down syndrome (80%)
- Head trauma
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Genes affected in AD
- APP - chromosome 21
- PS1 - chromosome 14
- PS2 - chromosome 1
- E4 on ApoE gene - chromosome 19
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Possible protective factors
- education
- exercise
- word puzzels
- reading
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cellular changes in AD
- cortical atrophy
- ventricular enlargement
- plaques and tangles
- decreased acetyl transferase (cleaves and activates acetylcholine)
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Available treatments for AD
- Cholinesterase inhibitors (Blocks breakdown of acetylcholinesterase)
- NMDA Antagonist (interferes with glutamatergic excitotoxicity)
- -memantine
- -prevents Ca2+ influx that causes apoptosis
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Delirium Presentation
- Disturbance in consciousness
- -awareness and attention
- Change in cognition
- -memory, disorientation, speech, perception
- Evolves rapidly
- -over the course of a day
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Clinical features of Delirium
- Disturbance in sleep-wake cycle
- Increase or decrease in psychomotor activity
- Emotional disturbance
- Behavioral disturbance
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Treatment of delirium
- reverse insult
- correct deficiencies
- - B12 or electrolytes
- Symptomatic treatment with medications (only when threatening others or self)
- - sedative, anxiolytitcs, antipsychotics
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Stimulation of basal ganglia function
- 1. Frontal cortex
- 2. Putamen
- 3. Globus Palidus
- 4. Subthalamic nucleus
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Inhibition of motor function
Substantia nigra inhibits basal ganglia via dopaminergic pathway
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Changes in basal ganglia resulting in parkinson's
a deficiency in the dopaminergic projection of this modulating circuit
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Epidemiology and proposed etiology of PD
- Age of onset ~62
- Men > Women
- 1-2%
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Etiology of PD
- Genetic predisposition
- Environmental factors
- - rural living
- - heavy metal or hydrocarbon exposure
- Drut induced PD
- - MPTP from crystal meth
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Hallmark Clinical symptoms of PD
- Tremor at rest
- Rigidity
- Akinesia
- Bradykinesia
- Postural instability
- idiopathic usually dominant side first, both if drug induced
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Other symptoms of PD
- bradyphrenia (small words)
- Hypophonia ( low voice)
- micorgraphia
- dysphagia
- hypersalivation
- decreased blink rate
- diminished arm swing
- shuffling gait
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Clinically possible diagnosis of PD
- any one of the following:
- 1. asymmetric resting tremor
- 2. rigidity
- 3. bradykinesia
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Clinically probable diagnosis of PD
- any two of the following:
- 1. asymmetric resting tremor
- 2. rigidity
- 3. bradykinesia
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Clinically definite diagnosis of PD
- all of the following:
- 1. asymmetric resting tremor
- 2. rigidity
- 3. bradykinesia
- 4. response to anti-parkinson's drugs
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Differential Diagnosis of Multi-system atrophy
- autonomic symptoms
- speech dysfunction
- falls backwards
- lack of tremor
- no response to DA therapy
- MRI/CT
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Differential diagnosis of Progressice supranuclear palsy
Eye movement disorder
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Hallmark feature on an autopsy of a PD patient
lewy bodies
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Treatment for PD
- Dopaminergic agents (carbidopa/levodopa)
- catechol-O-methyltransferase inhibitors (COMT)
- Monoamine Oxidase Inhibitors
- NMDA receptor antagonist: amantidine
- Anticholinergics: Benztropine
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COMT Inhibitors
- Allows conversion of 3-O-Methyldopa to Levodopa
- block degredation of DA and L-Dopa
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Levodopa
Increases L-Dopa levels
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MAO Inhibitors
stops breakdown of dopamine in the mitochondria
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Amantadine (NMDA receptor antagonist)
stimulates the release of dopamine and inhibits reuptake of dopamine
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DA Agonists
bind to DA receptors
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Acetylcholine inhibitors
block action of ACh in striatum
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