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Pharmacology > Unit 3 Neurodegenerative > Flashcards

Unit 3 Neurodegenerative Flashcards

1
Q

Neurodegenerative Disorders main characteristics

A

progressive & irreversible loss of neurons from brain regions, injury of specific type of neurons & locations, due to both genetic & environmental factors, pathology includes cellular aggregation of misfolded proteins

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2
Q

Alzheimer’s Disease

A

loss of hippocampal & cortical neurons results in impaired memory formation & cognitive deficits

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3
Q

Parkinson’s disease & Huntington’s disease

A

loss of dopaminergic neurons in basal ganglia leads to altered movement control

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4
Q

Amyotrophic Lateral Sclerosis (ALS)

A

Degeneration of control & spinal motor neurons results in muscular weakness

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5
Q

Alzheimer’s protein accumulation

A

extracellular beta-amyloid plaques & intracytoplasmic neurofibrillary tangles (tau protein)

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6
Q

ALS & Parkinson’s protein accumulation

A

Intracytoplasmic aggregates

Parkinson’s = alpha synuclein

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7
Q

Huntington’s protein accumulation

A

Intranuclear inclusions of huntingtin protein

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8
Q

Prion disease protein accumulation

A

extracellular prion amyloid plaques in different brain regions

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9
Q

Neurodegenerative disorders occur at what stage in life

A

later - over age of 65

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10
Q

Alzheimer’s cognitive symptoms

A

Loss of short-term memory, Aphasia, Apraxia, Agnosia, Disorientation

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11
Q

Alzheimer’s noncognitive symptoms

A

Depression, psychotic symptoms, behavioral disturbances

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12
Q

Alzheimer’s diagnosis

A

Based on clinical assessment - requires dementia (cognitive impairments beyond normal for their age)
Neuroimaging (CT & MRI)
Mild cognitive impairment (MCI) - initial diagnosis/manifestation of disease

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13
Q

MCI (mild cognitive impairment)

A

Can progress to Alzheimer’s but doesn’t always
Initial manifestation of progressive degeneration dementia
Cognitive impairment not reducing function (prefrontal cortex may be effected)

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14
Q

Most common cause of dementia in people 65 yrs or older

A

Alzheimer’s disease

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15
Q

Patients usually die within _____ of AD onset

A

6-12 years

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16
Q

Mild stage AD

A

First 3 years
Progressive loss of memory, impaired judgement, confusion, decreased concentration
Areas of brain effected are increasing

17
Q

Moderate stage AD

A

2-10 years
Language impairments, decreased comprehension, sleep disorders, disorientation
Requires increase level of care

18
Q

Severe stage AD

A

8-12 years
Most of brain affected, large amount of atrophy
Dependence, delusions, agitation, incapacitation (noncognitive disorders as well)
Needs to be in a care facility

19
Q

Pathology of AD

A

Massive tissue damage & decreased brain volume from neuronal degeneration & atrophy, neuritic plaques, & neurofibrillary tangles

20
Q

Cholinergic hypothesis of AD

A

Deficiency of ACh in certain brain areas due to degeneration of subcortical cholinergic neurons in hippocampus

21
Q

Amyloid hypothesis of AD

A

Extracellular accumulations of beta-amyloid peptides that are toxic to neurons
Cleaved from APP & produced faster than cleared

22
Q

Early-onset AD

A

Rare, related to mutations in APP & PSEN1/2 (cleave APP)

Overproduction of beta-amyloid

23
Q

Late-onset AD

A

Common, epsilon4 allele of APOE - not as effective at clearing beta-amyloid
increases risk of AD 3x

24
Q

Tau hypothesis of AD

A

Hyperphosphorylation of tau causes aggregates & forms neurofibrillary tangles
Causes microtubular instability, collapse of transport system, altered NT release & synaptic function, and cell death

25
Q

AD treatment goals

A

Slow down progression, treat cognitive difficulties & preserve function, treat behavioral & psychiatric symptoms

26
Q

Cholinesterase inhibitors used for

A

First line for symptomatic treatment of cognitive impairments in mild to moderate AD
Slows decline of cognitive & behavioral function

27
Q

Cholinesterase inhibitors MOA

A

block AChE &/or BChE-mdiated breakdown of ACh to choline & acetate
Increase activation of postsynaptic ACh receptor

28
Q

Cholinesterase inhibitors include

A

Tacrine, Donepezil, Rivastigmine, Galantamine

29
Q

Tacrine

A

Cholinesterase inhibitor

No longer used - had extensive side effects & needed to be taken 4x per day (short 1/2 life) = bad compliance

30
Q

Donepezil

A

Cholinesterase inhibitor
Primarily inhibits AChE
Long 1/2 life - once day dose
Improve cognition & clinical function, delay symptomatic progression

31
Q

Rivastigmine

A

Cholinesterase inhibitor
Inhibits both AChE & BChE
2x per day dose
Transdermal patch can be used - has improved GI effects

32
Q

Galantamine

A

Cholinesterase inhibitor
similar to Donepezil & Rivastigmine
2x per day dose
Main side-effects GI

33
Q

Cholinesterase inhibitors side effects

A

GI effects main problem (nausea, vomiting, diarrhea)
Other side effects related to ACh: salivation, sweating, urinary incontinence, dizziness, muscle weakness, bradycardia
SLUDGE

34
Q

Memantine

A

Glutamate antagonist
Non-competitive antagonist of NMDA glutamate receptor
Neuroprotection by reducing intracellular Ca influx & glutamate induced excitotoxicity
long 1/2 life
Commonly used in moderate-severe AD
Often used with other drug
Main side-effects are dizziness, headaches, depression

35
Q

Preferred treatment of non-cognitive symptoms of AD are

A

non-pharmacologic approaches

36
Q

Treatment options for Psychosis/agitated behavior in AD

A

Atypical antipsychotics

37
Q

Treatment options for depression & anxiety in AD

A

SSRI - safe for elderly, better side effects (sertraline & citalopram)
Avoid tricyclics = confusion & falls

38
Q

Treatment options for sleep disturbances

A 
Antidepressants, atypical neuroleptics
Avoid benzodiazepines (long acting) & antihistamines (anti-cholinergic)

Pharmacology (8 decks)

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