Pathophys 2

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Rx2013
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36665
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Pathophys 2
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2010-09-22 19:13:42
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Diseases aging
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Diseases of aging
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  1. Cognition
    sensory input that is transformed, reduced, elaborated, stored recovered and used.
  2. 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
  3. Storing Memories
    • Parahippocampal cortex
    • Peripheral cortex
    • Entorhinal cortex
    • Hippocampus
  4. Recalling memories
    • Hippocampus
    • Entorhinal cortex
    • Peripheral cortex
    • parahipocampal cortex
  5. Age 50
    decreased retrical speed of memories
  6. Impact of AD
    • 4th leading cause of death
    • 3rd most expensice illness in US
    • Affects 4 million at present with 250,000 afflicted/year
  7. 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)
  8. Criteria for Alzheimers Disease
    • impairment in social or occupational function
    • decline from previous level of function
    • gradual onset and continuing cognitive decline
  9. 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)
  10. Behavioral symptoms of AD
    • dilusions
    • hallucinations
    • depression
    • sundowning
    • other agitated behaviors
  11. AD occurs over ____ years
    2 to 10
  12. Various forms of memory that fall apart
    • episodic memory
    • short term memory (usually first)
    • memory of the meaning of words
    • procedural memory
  13. The end of AD
    all reasoning, attention and language abilities are disrupted
  14. 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
  15. Risk factors for developing AD
    • Age
    • Family history
    • Down syndrome (80%)
    • Head trauma
  16. Genes affected in AD
    • APP - chromosome 21
    • PS1 - chromosome 14
    • PS2 - chromosome 1
    • E4 on ApoE gene - chromosome 19
  17. Possible protective factors
    • education
    • exercise
    • word puzzels
    • reading
  18. cellular changes in AD
    • cortical atrophy
    • ventricular enlargement
    • plaques and tangles
    • decreased acetyl transferase (cleaves and activates acetylcholine)
  19. Available treatments for AD
    • Cholinesterase inhibitors (Blocks breakdown of acetylcholinesterase)
    • NMDA Antagonist (interferes with glutamatergic excitotoxicity)
    • -memantine
    • -prevents Ca2+ influx that causes apoptosis
  20. Delirium Presentation
    • Disturbance in consciousness
    • -awareness and attention
    • Change in cognition
    • -memory, disorientation, speech, perception
    • Evolves rapidly
    • -over the course of a day
  21. Clinical features of Delirium
    • Disturbance in sleep-wake cycle
    • Increase or decrease in psychomotor activity
    • Emotional disturbance
    • Behavioral disturbance
  22. Treatment of delirium
    • reverse insult
    • correct deficiencies
    • - B12 or electrolytes
    • Symptomatic treatment with medications (only when threatening others or self)
    • - sedative, anxiolytitcs, antipsychotics
  23. Stimulation of basal ganglia function
    • 1. Frontal cortex
    • 2. Putamen
    • 3. Globus Palidus
    • 4. Subthalamic nucleus
  24. Inhibition of motor function
    Substantia nigra inhibits basal ganglia via dopaminergic pathway
  25. Changes in basal ganglia resulting in parkinson's
    a deficiency in the dopaminergic projection of this modulating circuit
  26. Epidemiology and proposed etiology of PD
    • Age of onset ~62
    • Men > Women
    • 1-2%
  27. Etiology of PD
    • Genetic predisposition
    • Environmental factors
    • - rural living
    • - heavy metal or hydrocarbon exposure
    • Drut induced PD
    • - MPTP from crystal meth
  28. Hallmark Clinical symptoms of PD
    • Tremor at rest
    • Rigidity
    • Akinesia
    • Bradykinesia
    • Postural instability
    • idiopathic usually dominant side first, both if drug induced
  29. Other symptoms of PD
    • bradyphrenia (small words)
    • Hypophonia ( low voice)
    • micorgraphia
    • dysphagia
    • hypersalivation
    • decreased blink rate
    • diminished arm swing
    • shuffling gait
  30. Clinically possible diagnosis of PD
    • any one of the following:
    • 1. asymmetric resting tremor
    • 2. rigidity
    • 3. bradykinesia
  31. Clinically probable diagnosis of PD
    • any two of the following:
    • 1. asymmetric resting tremor
    • 2. rigidity
    • 3. bradykinesia
  32. Clinically definite diagnosis of PD
    • all of the following:
    • 1. asymmetric resting tremor
    • 2. rigidity
    • 3. bradykinesia
    • 4. response to anti-parkinson's drugs
  33. Differential Diagnosis of Multi-system atrophy
    • autonomic symptoms
    • speech dysfunction
    • falls backwards
    • lack of tremor
    • no response to DA therapy
    • MRI/CT
  34. Differential diagnosis of Progressice supranuclear palsy
    Eye movement disorder
  35. Hallmark feature on an autopsy of a PD patient
    lewy bodies
  36. Treatment for PD
    • Dopaminergic agents (carbidopa/levodopa)
    • catechol-O-methyltransferase inhibitors (COMT)
    • Monoamine Oxidase Inhibitors
    • NMDA receptor antagonist: amantidine
    • Anticholinergics: Benztropine
  37. COMT Inhibitors
    • Allows conversion of 3-O-Methyldopa to Levodopa
    • block degredation of DA and L-Dopa
  38. Levodopa
    Increases L-Dopa levels
  39. MAO Inhibitors
    stops breakdown of dopamine in the mitochondria
  40. Amantadine (NMDA receptor antagonist)
    stimulates the release of dopamine and inhibits reuptake of dopamine
  41. DA Agonists
    bind to DA receptors
  42. Acetylcholine inhibitors
    block action of ACh in striatum

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