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Homework answers / question archive / University of Illinois, Chicago NURS 531 Chapter 40: Neurodegenerative diseases MULTIPLE CHOICE 1)An essential factor in neuronal excitotoxicity is   depletion of intracellular calcium excessive levels of intracellular calcium depletion of adenosine triphosphate inhibition of intracellular proteases depletion of intracellular glutamate     2

University of Illinois, Chicago NURS 531 Chapter 40: Neurodegenerative diseases MULTIPLE CHOICE 1)An essential factor in neuronal excitotoxicity is   depletion of intracellular calcium excessive levels of intracellular calcium depletion of adenosine triphosphate inhibition of intracellular proteases depletion of intracellular glutamate     2

Nursing

University of Illinois, Chicago

NURS 531

Chapter 40: Neurodegenerative diseases MULTIPLE CHOICE

1)An essential factor in neuronal excitotoxicity is

 

  1. depletion of intracellular calcium
  2. excessive levels of intracellular calcium
  3. depletion of adenosine triphosphate
  4. inhibition of intracellular proteases
  5. depletion of intracellular glutamate

 

 

2.    The accumulation of b-amyloid protein is believed to cause neuronal degeneration in

 

  1. Huntington’s disease
  2. Parkinson’s disease
  3. Creutzfeldt-Jakob disease
  4. amyotrophic lateral sclerosis
  5. Alzheimer’s disease

 

 

3.    Levodopa is usually administered with a peripheral dopa decarboxylase inhibitor such as

 

  1. carbidopa

 

  1. selegiline
  2. entacapone
  3. amantadine
  4. pergolide

 

 

4.    Factors that contribute to the development of Alzheimer’s disease include

 

  1. absence of Ab40 peptides
  2. decreased proportion of Ab42 peptides
  3. mutations in the apoE4 gene
  4. increased expression of a-secretase
  5. decreased expression of g-secretase

5.    The use of selegiline in Parkinson’s disease is based on its ability to

 

  1. selectively inhibit type A monoamine oxidase
  2. slow progression of Parkinson’s disease
  3. inhibit peripheral degradation of levodopa
  4. protect dopamine from intra-neuronal degradation
  5. exert the neuroprotective effects shown in clinical trials

6.    Memantine may produce a small improvement in cognitive function in persons with Alzheimer’s disease because it acts to

 

  1. inhibit cholinesterase
  2. activate cholinergic nicotinic receptors
  3. block N-methyl-D-aspartate receptors
  4. activate N-methyl-D-aspartate receptor
  5. activate dopamine D1 receptors

 

 

7.    Entacapone reduces “end of dose” motor fluctuations in Parkinson’s disease because entacapone inhibits the degradation of levodopa by

 

  1. catechol-O-methyltransferase
  2. monoamine oxidase-A
  3. monoamine oxidase-B
  4. dopa decarboxylase
  5. dopamine b-hydroxylase

 

 

8.    Expansion of CAG (cyotosine-adenine-guanine) trinucleotide repeats in certain genes occurs in persons with

 

  1. spongiform encephalopathy
  2. Parkinson’s disease
  3. Alzheimer’s disease
  4. amyotrophic lateral sclerosis
  5. Huntington’s disease

 

 

 

 

9.    In the treatment of Alzheimer’s disease, rivastigmine typically causes

 

  1. rapidly irreversible inhibition of acetyl- and butyryl-cholinesterase
  2. slowly reversible inhibition of acetyl- and butyryl-cholinesterase
  3. allosteric enhancement of nicotinic receptor activation
  4. allosteric enhancement of muscarinic receptor activation
  5. cholinergic side effects that increase over time

 

 

10.   The acute side effects of levodopa in Parkinson’s disease patients include

 

  1. involuntary writhing movements
  2. rapid fluctuations in clinical state
  3. nausea and anorexia
  4. hypertension
  5. urinary retention

 

 

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