NURS 8024 Pharm neuro Study Guide Questions with Verified
Answers
Neuropharmacology
Parkinson’s Disease: (neurodegenerative)
• etiology/patho, symptoms, treatment strategies,
o progressive neuro disorder of muscle movement, characterized by
tremors, muscle rigidity, bradykinesia and postural and gait
abnormalities
o Etiology: destruction of dopaminergic neurons in the substantia nigra
▪ Reduction of dopamine action in brainaffects
motor control
o Symptoms: r/t imbalance between excitatory cholinergic
neurons and greatly diminished numbers of inhibitory
dopaminergic neurons
o Therapy: restore dopamine in basal ganglia and
antagonizing the excitatory effect of acetylcholine at the
muscarinic receptors
• pharmacologic therapy- levodopa/carbadopa (why combined), mechanism
of
action, absorption/metabolism, effects, ADE, how long does it work for most
patients
o levodopa and carbidopa (Sinemet)
▪ Enhances synthesis of dopamine in surviving neurons of
the substantia nigra conversion of levodopa to
dopamine
▪ Very therapeutic response in new patients
▪ Relief is only symptomatic and only lasts while the drug is
present in body
▪ MOA:
• Levodopa
o Attempts to replace dopamine that is deficient
o Can cross BBB and convert to dopamine in brain
• Carbidopa
o Enhances effect of levodopa via diminishing
metabolism of levodopa in GI tract and
peripheral
▪ Action: decreases rigidity, tremors, and other symptoms
, ▪ Typical decline in response in 3rd to 5th year of treatment
▪ Absorption:
• Rapid GI absorption on empty stomach
• Extremely short half-life
▪ On-off phenomenon – causes sudden loss of normal
mobility, tremors, cramps, immobility
▪ Meals interfere w/ transport into CNS – take on empty stomach
▪ ADE: n/v, anorexia, tachycardia, PVCs, postural
hypotension, mydriasis
▪ Contraindicated in history of psychosis
• Dopamine receptor agonists
o Pramipexole and Ropinirole
, ▪ Effective w/ mild parkinsonism
▪ Used in combination w/ levodopa
▪ Used in restless leg syndrome
▪ ADE: n/v, anorexia, postural hypotension, dyskinesia,
hallucination, impulsivity
• Psyche ADE more common than w/ levodopa
• anticholinergic agents (Cogentin)- cautions/warnings,
o Cogentin
▪ Caution in elderly, BPH, urinary retention, liver, renal,
GI/GU disease
▪ Can precipitate narrow-angle glaucoma
• info on slide “General Points in Treatment”
•
Alzheimer’s Disease: (neurodegenerative)
• Types/patho, aim of pharmacologic therapy
o Therapy
▪ Aimed at improving cholinergic transmission w/in the CNS
▪ Preventing excitotoxic actions resulting from
overstimulation of NMDA-glutamate receptors
o Pharmacologic intervention is palliative and provides modest
short term benefit
• acetylcholinesterase inhibitors- indications, mechanism of action, ADE,
precautions, effects/ expectations of therapy
o Indication: mild to moderate Alzheimer’s
o MOA: block enzyme that degrades acetylcholinemore
acetylcholine at the synaptic cleftenhances
cholinergic
transmission
o Effects: diminishes s/s of dementia
o Improves function and mildly slows progression of symptoms
Answers
Neuropharmacology
Parkinson’s Disease: (neurodegenerative)
• etiology/patho, symptoms, treatment strategies,
o progressive neuro disorder of muscle movement, characterized by
tremors, muscle rigidity, bradykinesia and postural and gait
abnormalities
o Etiology: destruction of dopaminergic neurons in the substantia nigra
▪ Reduction of dopamine action in brainaffects
motor control
o Symptoms: r/t imbalance between excitatory cholinergic
neurons and greatly diminished numbers of inhibitory
dopaminergic neurons
o Therapy: restore dopamine in basal ganglia and
antagonizing the excitatory effect of acetylcholine at the
muscarinic receptors
• pharmacologic therapy- levodopa/carbadopa (why combined), mechanism
of
action, absorption/metabolism, effects, ADE, how long does it work for most
patients
o levodopa and carbidopa (Sinemet)
▪ Enhances synthesis of dopamine in surviving neurons of
the substantia nigra conversion of levodopa to
dopamine
▪ Very therapeutic response in new patients
▪ Relief is only symptomatic and only lasts while the drug is
present in body
▪ MOA:
• Levodopa
o Attempts to replace dopamine that is deficient
o Can cross BBB and convert to dopamine in brain
• Carbidopa
o Enhances effect of levodopa via diminishing
metabolism of levodopa in GI tract and
peripheral
▪ Action: decreases rigidity, tremors, and other symptoms
, ▪ Typical decline in response in 3rd to 5th year of treatment
▪ Absorption:
• Rapid GI absorption on empty stomach
• Extremely short half-life
▪ On-off phenomenon – causes sudden loss of normal
mobility, tremors, cramps, immobility
▪ Meals interfere w/ transport into CNS – take on empty stomach
▪ ADE: n/v, anorexia, tachycardia, PVCs, postural
hypotension, mydriasis
▪ Contraindicated in history of psychosis
• Dopamine receptor agonists
o Pramipexole and Ropinirole
, ▪ Effective w/ mild parkinsonism
▪ Used in combination w/ levodopa
▪ Used in restless leg syndrome
▪ ADE: n/v, anorexia, postural hypotension, dyskinesia,
hallucination, impulsivity
• Psyche ADE more common than w/ levodopa
• anticholinergic agents (Cogentin)- cautions/warnings,
o Cogentin
▪ Caution in elderly, BPH, urinary retention, liver, renal,
GI/GU disease
▪ Can precipitate narrow-angle glaucoma
• info on slide “General Points in Treatment”
•
Alzheimer’s Disease: (neurodegenerative)
• Types/patho, aim of pharmacologic therapy
o Therapy
▪ Aimed at improving cholinergic transmission w/in the CNS
▪ Preventing excitotoxic actions resulting from
overstimulation of NMDA-glutamate receptors
o Pharmacologic intervention is palliative and provides modest
short term benefit
• acetylcholinesterase inhibitors- indications, mechanism of action, ADE,
precautions, effects/ expectations of therapy
o Indication: mild to moderate Alzheimer’s
o MOA: block enzyme that degrades acetylcholinemore
acetylcholine at the synaptic cleftenhances
cholinergic
transmission
o Effects: diminishes s/s of dementia
o Improves function and mildly slows progression of symptoms
