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NU578 Unit 2 Class Discussion, Lecture notes of Nursing

University of South Alabama (USA)Nursing

NU578 in class discussion for exam 2

Typology: Lecture notes

2024/2025

Uploaded on 06/11/2025

caroline-ngo
caroline-ngo 🇺🇸

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Dugs for Parkinson’s/Dementia
How NTs Fit
Parkinson’s disease and Alzheimer’s dementia are two conditions that “cover” the NTs we have
been studying
Parkinsons is due to a decrease in DA—sympathetic
Alzheimer’s is due to decreased level of ACh…but Ach has been implicated
Treatment of each of these conditions may result in some easing of symptoms and in SE related
to enhancing or blocking certain NTs
What Causes Dementia?
Older theories on which treatment is based currently
oDementia is due to decrease ACh in certain parts of the brain
oThis affects speech, cognition, ADL, memory
oIncreasing ACh in the brain or decreasing rate of degeneration of ACh rich neurons are
treatment strategies
Newer Theories
oTau protein
oAmyloid plaques
oPoor dentition and gum disease
Porphyromonas gingivalis
Amyloid and tau proteins may be a response, not a cause—the bacteria release
enzymes called gingipains which destroy tissue
The amyloid and tau are “protecting” the brain…but they tangle neurons
resulting in dementia
oDoes this still mean Acetylcholine is involved?
Cholinesterase Inhibitors
oThese drugs work to increase ACh in the brain by decreasing its rate of breakdown
oModest improvements in behavior, cognition, and function are seen
oThese drugs are recommended for all AD patients with mild to moderate disease
oUsed in patients with mild to moderate symptoms
oOnly 25-30% respond
oThese drugs are NOT curative
oCholinergic SE include GI distress, HA, dizziness, bronchoconstriction
oDoses start low then increase to tolerance
oDonepezil, Galantamine, Rivastigmine
oDonepezil (Aricept): causes GI SE and bradycardia
oRivastigmine (Exelon): causes significant GI SE including weight loss, available as a patch
oGalantamine (Razadyne): GI SE and bronchoconstriction may be seen
oMemantine (Namenda)
NMDA receptor antagonist
This drug modulates the effect of glutamate at NMDA receptors, reducing the
destructive effects of this NT in the brain
This drug is reserved for moderate to severe AD
pf3

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Dugs for Parkinson’s/Dementia How NTs Fit  Parkinson’s disease and Alzheimer’s dementia are two conditions that “cover” the NTs we have been studying  Parkinsons is due to a decrease in DA—sympathetic  Alzheimer’s is due to decreased level of ACh…but Ach has been implicated  Treatment of each of these conditions may result in some easing of symptoms and in SE related to enhancing or blocking certain NTs What Causes Dementia?  Older theories on which treatment is based currently o Dementia is due to decrease ACh in certain parts of the brain o This affects speech, cognition, ADL, memory o Increasing ACh in the brain or decreasing rate of degeneration of ACh rich neurons are treatment strategies  Newer Theories o Tau protein o Amyloid plaques o Poor dentition and gum disease  Porphyromonas gingivalis  Amyloid and tau proteins may be a response, not a cause—the bacteria release enzymes called gingipains which destroy tissue  The amyloid and tau are “protecting” the brain…but they tangle neurons resulting in dementia o Does this still mean Acetylcholine is involved?  Cholinesterase Inhibitors o These drugs work to increase ACh in the brain by decreasing its rate of breakdown o Modest improvements in behavior, cognition, and function are seen o These drugs are recommended for all AD patients with mild to moderate disease o Used in patients with mild to moderate symptoms o Only 25-30% respond o These drugs are NOT curative o Cholinergic SE include GI distress, HA, dizziness, bronchoconstriction o Doses start low then increase to tolerance o Donepezil, Galantamine, Rivastigmine o Donepezil (Aricept): causes GI SE and bradycardia o Rivastigmine (Exelon): causes significant GI SE including weight loss, available as a patch o Galantamine (Razadyne): GI SE and bronchoconstriction may be seen o Memantine (Namenda)  NMDA receptor antagonist  This drug modulates the effect of glutamate at NMDA receptors, reducing the destructive effects of this NT in the brain  This drug is reserved for moderate to severe AD

 Now generic  A combination product with Donepezil is available—Namzaric  PO well tolerated  SE include dizziness, HA, confusion  Dosage starts at 5 mg/day for one week then builds to 20 mg (10mg BID) for maintenance Dementia Summary  No drug treats the disease—they only slow its progression  Drugs are most effective when started early  Cholinergic SE are most common o Drugs with anticholinergic SE may reduce these  Memantine is a newer class of drug for AD which may offer a neuroprotective effect; often used in combo with Donepezil  Adjunctive psychiatric drugs may be helpful in managing neuropsychiatric symptoms in these patients o Risperidone (Risperdal) and Olanzapine (Zyprexa) Parkinson’s Disease  This disease is caused by a decrease of DA in the nerves of the substantia nigra in the brain. As DA levels drop, ACh in this part of the brain starts to cause aberrant muscle movements such as tremor, bradykinesia, rigidity, blank facies, and post8ural instability. Treatment goals for this disease usually begins with blocking the excessive ACh activity  Anticholinergic drugs may be used for this, or drugs with anticholinergic SE (like antidepressants) may be used. As the disease progresses, a goal is to increase DA in the brain. Treatment is palliative, and drug holidays are encouraged so that treatment remains effective for as long as possible  Note: when DA is elevated in the brain, psychiatric symptoms will emerge! Drugs to Treat Parkinson’s Disease  Levodopa (L-Dopa): crosses BBB and is converted to DA  Carbidopa (Lodosyn): inhibits dopa decarboxylase in the periphery. Used together with L-dopa; may cause nausea, gait abnormalities, postural hypotension, arrhythmias.  The combo of these two drugs is called Sinemet. Paradopa is another formulation for ODT  L-Dopa is no longer sold as a single formulation drug. It is always combined with Carbidopa  Amantadine (Symmetrel): increases DA release from nerve terminals. Causes livedo reticularis (rose colored mottling of skin) on lower extremities and OH o This is an antiviral  Bromocriptine (Parlodel): stimulates DA receptors. Causes visual disturbances, dyskinesias, GI distress o Used in neonatal medicine  Selegiline (Eldepryl): prevents DA breakdown by blocking MAO-B. Causes agitation, insomnia  Trihexyphenidyl (Artane): anticholinergic. Causes tachycardia, mydriasis  Benztropine (Cogentin): anticholinergic. Same SE; useful in younger patients