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Year 2 Pharmacology > Neurodegenerative disorders > Flashcards

Neurodegenerative disorders Flashcards

1
Q

what characterizes the deficits in Alzheimer’s disease?

A

loss of hippocampal and cortical neurons resulting in impaired memory formation and cognitive deficits

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2
Q

what characterizes the deficits in parkinson’s disease and huntington’s disease?

A

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

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3
Q

what characterizes the deficits in amyotrophic lateral sclerosis?

A

degeneration of cortical and spinal motor neurons resulting in muscular weakness

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4
Q

what are the protein accumulations associated with AD?

A

extracellular beta amyloid and intracytoplasmic neurofibrillary tangles

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5
Q

what are the protein accumulations associated with ALS and parkinsons?

A

intracytoplasmic aggregates

PD - alpha synuclein

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6
Q

what are the protein accumulations associated with huntingtons?

A

intranuclear inclusions of huntingtin protein

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7
Q

what are the cognitive symptoms associated with AD?

A 
loss of short term memory 
aphasia 
apraxia (inability to carry out motor activities) 
agnosia 
disorientation
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8
Q

what are the noncognitive symptoms associated with AD?

A

depression, psychotic

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9
Q

what is the cholinergic hypothesis of AD?

A

deficiency in Ach due to degeneration of subcortical cholinergic neurons (memory formation areas - hippocampus)

PRIMARY PATHOGENESIS HYPOTHESIS

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10
Q

what is the amyloid hypothesis of AD?

A

extracellular accumulations of beta amyloid peptides (BA) are toxic to neurons

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11
Q

does deposition of BA plaques correlate with neuronal loss?

A

no

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12
Q

early onset AD is associated with mutations in what genes? what is the result?

A

APP, PSEN1, PSEN2

overproduction of AB

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13
Q

what is the role of PSEN1 and PSEN2?

A

encode for membrane proteins involved in cleaving APP

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14
Q

what is the role of APP?

A

encodes amyloid B precursor peptides

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15
Q

what is the tau hypothesis in AD?

A

hyperphosphorylation of tau forms aggregates and neurofibrillary tangles

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16
Q

what is the result of tau hyperphosphorylation?

A

microtubular disintegration and instability
collapse of neuronal transport system
altered NT release and synaptic function
cell death

17
Q

what is the first line therapy for symptomatic treatment of cognitive impairments in mild to moderate AD? does it modify the progression?

A

cholinesterase inhibitors

no

18
Q

what is the MOA of the cholinesterase inhibitors?

A

reduce breakdown of endogenously released Ach, resulting in greater activation of postsynaptic Ach receptors

19
Q

what are the cholinesterase inhibitor agents for AD?

A

tacrine
donepezil
rivastigmine
galantamine

20
Q

donepezil inhibits primarily what enzyme?

A

AchE

21
Q

what is the MOA of rivastigmine?

A

inhibits AchE and BchE

22
Q

which AD agent appears selective for hippocampus and prefrontal cortex?

A

rivastigmine

23
Q

what is the route for rivastigmine?

A

transdermal pouch

24
Q

what are the cholinergic side effects of cholinesterase inhibitors?

A

SLUDGE

salivation 
lacrimation 
urinary incontinence 
diarrhea 
GI cramps 
emesis
25
Q

what is the main side effect associated with donepezil?

A

bradycardia

26
Q

what is the glutamate antagonist agent for AD?

A

memantine

27
Q

what is the MOA of memantine?

A

non-competitive antagonist of the NMDA glutamate receptor with long half life

provides neuroprotection by reducing intracellular calcium influx and glutamate induced neurotoxicity

28
Q

which hormone is used as replacement therapy in women with AD?

A

estrogen

29
Q

what is the main treatment options for the psychotic symptoms associated with AD?

A

atypical antipsychotics

risperidone, olanzapine, quetiapine

30
Q

what is the main treatment options for the depression symptoms associated with AD?

A

SSRIs

sertraline, citalopram

31
Q

which drugs should be avoided in treating the depression associated with AD? why?

A

TCAs

side effects - anticholinergic affects, orthostatic hypotension

Year 2 Pharmacology (70 decks)

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