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NURS 660 Psychopharmacology 2025 Newest Exam 4 Correctly Answered Questions and Well Rated, Exams of Nursing

NURS 660 Psychopharmacology 2025 Newest Exam 4 Correctly Answered Questions and Well Accredited (Score A)-Maryville University

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2024/2025

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NURS 660 Psychopharmacology 2025 Newest
Exam 4 Correctly Answered Questions and
Well Accredited (Score A)-Maryville University
where in the brain is selective attention modulated?
the CSTC loop, Dorsal anterior cingulate cortex
issues with sustained attention are:
difficulty completing tasks
disorganization
trouble sustaining mental effort
issues with selective attention are:
difficulty with detail
carless mistakes
not listening
losing things
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NURS 660 Psychopharmacology 2025 Newest

Exam 4 Correctly Answered Questions and

Well Accredited (Score A)-Maryville University

where in the brain is selective attention modulated? the CSTC loop, Dorsal anterior cingulate cortex issues with sustained attention are: difficulty completing tasks disorganization trouble sustaining mental effort issues with selective attention are: difficulty with detail carless mistakes not listening losing things

being distracted forgetting things what part of the brain modulates impulsitivity? orbitofrontal cortex what symptoms of impulsitivity are observed? talking excessively blurting things out not waiting ones turn interrupting what part of the brain modulates hyperactivity? prefrontal cortex what are some key observations in the prefrontal cortex as it relates to ADHD? orbitofrontal cortex (OFC)-- impulsivity and hyperactivity DLPFC/DaCC-- sustained/selective attention issues

Increase DA what receptors does NE stimulate in the postsynapse? alpha 2 a; even better effect when beta1 receptors also stimulated what effect does DA have on receptors and what does this cause? decreases the noise and prevents inappropriate connections from taking place through stimulating D1 receptors what effect does NE have on receptors and what does this cause? increases the incoming signal and allows for increase connections between prefrontal networks through stimulation of alpha 2A receptors what effect do slow dose stimulants have? amplify tonic NE and DA signals block NET in PFC block DAT in nucleus accumbens

why do slow dose stimulants have less abuse potential? they dont occupy DAT too quickly or extensively, which is thought to reduce abuse potential what is salience provoked phasic firing?

  • bursts of DA release this can reinforce learning and reward conditioning which can lead to motivation to pursue rewarding experiences (education, career development) Can also lead to drug abuse.... how do pulsatile stimulants affect NE and DA? rapid increase in both can lead to feelings of euphoria and abuse ex: methylphenidate and amphetamine what is a big factor in if stimulants are abused?

sustained attention and problem solving linked to what area of the brain? DLPFC hyperactivity is linked to what area of the brain? prefrontal motor cortex what test assessing sustained attention? N-back test where is sustained attention modulated in brain? CSTC loop in the DLPFC insufficient activation in the DLPFC can cause inattention "sustaiNed attention- N back" what test assesses selective attention? Stroop test

"Selective, Stroop, Cingulate" what is the MOA of methylphenidate on DA neurons? works on DAT similarly to SSRI (blocks reuptake of DA into terminal) this leads to more DA availability -- not taken into the terminal itself what is the MOA of methylphenidate on NE neurons? works on NET adverse effects of stimulants (methylphenidate, amphetamine) generalized anxiety adverse affects of atomoxetine (strattera?) dysuria, erectile dysfunction, decreased libido, liver damage (rare)

  • tics what are examples of NET inhibitors for adhd? atomoxetine (strattera) buproprion (wellbutrin) venlafaxine (effexor) duloxetine (cymbalta) desvenlafaxine (prystiq) milnacipran (savella) desipramine nortriptyline what ADHD medication doesnt have abuse potential? atomoxetine (strattera) what drug class is atomoxetine? NE reuptake inhibitor How does Atomoxetine (Strattera) work? causes NE and DA levels to increase in PFC

relative lack of NETs in nucleus accumbens prevents atomoxetine from increasing DA and NE levels in the brain area, thus reducing abuse potential increases attention, decreases hyperactivity what ADHD medication can cause liver injury? strattera if a patient develops jaundice and evidence of liver injury while taking strattera, what should you do? stop the med and dont restart it what med metabolism pathway dose strattera work? CYP2D keep in mind when rx with paroxetine, fluoxetine, quinidine what causes guanfacine to absorb quicker?

Twice daily dosing w/ larger dose at bedtime what type of adhd symptoms might atomoxetine not work well with? inattentive in addition to ADHD, modafinil might help what? substance use disorder 2 alpha 2 adrenergic agonists are? clonidine guanfacine what is the pathology of alzheimers?

  • Extracellular amyloid plaque build up
  • Intracellular formation of neurofibrilary tangles (made up of Tau protein) what is the pathology of dementia with lewy bodies? alpha synuclein

what type of disorder is related to prion pathology? cruetzfeldt jacobs what are the clinical features of alzheimers? memory defict aphasia apraxia (inability to performed learned behavior) agnosia what are the clinical features of dementia with lewy bodies? memory issues, fluctuating attention extrapyramidal psychosis Frontotemporal Dementia Frontal and temporal regions degenerate, resulting in badly impaired emotional stability, decision-making and language use

•Problems with language •Disorientation regarding time or place •Impaired judgment •Problems with abstract thinking •Misplacing objects •Changes in mood or behavior •Changes in personality •Loss of initiative Processing of amyloid precursor protein enzyme B-secretase APP to form 2 peptides and through further process can form plaques what two key brain characteristics are present in alzheimers disease? beta-amyloid plaques neurofibrillary tangles which amyloid protein is soluble? a-APP

what is the strongest risk factor for alzheimers? age what two enzymes terminate acetylcholine? ACheE, BuChe Rivistigmine (Exelon) twice daily with meals AChe, BuChe GI side effects NO HEPATOTOXICITY no drug to drug interactions bc not metabolized by CYP available in a transdermal patch what dementia medication must be taken 4x daily? tacrine Tacrine (Cognex)

  • Cholinesterase Inhibitors

what medications would you use for mild-mod dementia/alzheimers? what classification are all these medications? donepezil, galantamine, rivastigamine cholinesterase inhibitors what medication would you give for moderate to severe alzheimers? memantine NMDA receptor agonist How do cholinesterase inhibitors work? The make acetylcholine more available by inhibiting enzymes from breaking it down. acetylcholine helps neurons communicate How does Memantine (Namenda) work? blocks excessive extrasynaptic activity of N-methyl-D-aspartate (NMDA) it is non-competitive, and low affinity

binds to magnesium site when it is open blocks the downstream release of glutamate by acting as a "plug" at the NMDA receptor site How does Donepezil (Aricept) work? It increases acetylcholine concentrations at receptor sites and inhibits acetylcholinesterase present in both central and peripheral nervous system in the CNS, acetylcholine can help with cognition in the gut/perihperal, causes GI side effects has a very long half life (once daily administration) How does rivastigmine work? inhibits AChE and BuChe RENALLY excreted