NUR 425 Test 2 Review Notes PDF

**[NUR 425 - Test 2 Review Notes ]** **[Week 5: Headache, Parkinson's Disease, & Dementia ]** **[Parkinson's Disease ]** - Progressive, neurodegenerative disorder - Characterized by bradykinesia (slow movement), inc muscle tone, tremor at rest and impaired gait and a lack of the neurotra...

**[NUR 425 - Test 2 Review Notes ]** **[Week 5: Headache, Parkinson's Disease, & Dementia ]** **[Parkinson's Disease ]** - Progressive, neurodegenerative disorder - Characterized by bradykinesia (slow movement), inc muscle tone, tremor at rest and impaired gait and a lack of the neurotransmitter dopamine - Unknown cause, thought to be related to environment and genetics - Most often affects individuals over the age of 60 ***Basal Ganglia*** - Group of structures involved in coordination of movement - Motor control - Affected in parkinson's - ***Substantia nigra*** - Part of the basal ganglia - Located in the midbrain (part of the brainstem) - Has dopaminergic neurons, they produce dopamine - In parkinson's disease, there is degeneration of these neurons - Leads to dec release of dopamine - **Degeneration of dopaminergic neurons** - Dopamine inhibits acetylcholine - **Decrease release of dopamine → inc release of acetylcholine** - **Disrupts balance between dopamine & acetylcholine, leading to inc acetylcholine** - The imbalance between dopamine and acetylcholine can lead to muscle overexcitement, which causes tremors and jerking movements. ***Clinical Manifestations*** - Seen with loss or impairments of 60-80% of the dopaminergic neurons - Tremor, rigidity, akinesia, postural instability - Non-motor symptoms: loss of smell, sleep dysfunction, mood disorders, anxiety, depression, memory changes, constipation ***Evaluation*** - Based on patient history and physical exam - Diagnosis is going to begin w/ detailed hx or symptoms - When they started, how long they've been going for, the progression - Looking for key symptoms - tremor, rigidity, etc. - Comprehensive med hx - family hx, current/past meds, and any potential neurological disorders - Physical exam - motor function - Rapid alt movement - Observe tremors at rest - have them put their hands out - Postural instability - assess gait - Romberg test - No specific confirmation with lab tests of imaging - imaging/tests rules out other things that mimic Parkinson's ***Management of Parkinson's Disease*** - Medication therapy - Enhancing release or supply of dopamine - Blocking the effects of acetylcholine ***Levodopa-Carbidopa*** - Dopamine precursor - it is converted into dopamine in the basal ganglia - However, levodopa is broken down (metabolized) by the enzyme dopa decarboxylase (before it reaches the brain) - Carbidopa inhibits the enzyme dopa decarboxylase, and is prescribed with levodopa (allows more levodopa to reach the brain) - L-C decreases symptoms - May take several weeks to months to become effective - improvement can take several weeks to months - Considerations: Urine, sweat & saliva can appear darker (red, brown, or black) - Harmless but frightening to see - Avoid taking with high protein meals (take meds 30 mins before meals or 1-2 hrs after) as this can interfere with drug absorption - If pt exp nausea, take it with light carb snack - Lack of effectiveness after 5-10 years, may be secondary to disease progression - AE: hallucinations, orthostatic hypotension, dyskinesia, paranoid ideation - About 80% of patient can develop dyskinesia (abnormal involuntary movements) within the first few years of treatment ***Dopamine Antagonists*** - Stimulate dopamine receptors - Can be used with levodopa-carbidopa - Ex: apomorphine (not used routinely, short term use only for "off" episode), pramipexole, rotigotine, ropinirole - AE: hallucinations, daytime sleepiness, postural hypotension ***MAO-B Inhibitors*** - Monoamine oxidase type B inhibitors - MAO-B is an enzyme that inactivates dopamine and prevents breakdown of tyramine - Can be used with levodopa-carbidopa - Ex: rasagiline, selegiline - Like all MAO inhibitor meds, must avoid food high with tyramine (aged cheese, smoked or cured meats, fermented foods, beer) - Too much tyramine → release of large amts of norepinephrine → constricts blood vessels and inc bp - Can cause dangerous inc in bp (avoid MAO inhibitor meds with food high with tyramine) ***COMT Inhibitors*** - Catechol-O-methyltransferase inhibitor - COMT breaks down dopamine → COMT inhibitors inc availability of dopamine in the brain - Used with levodopa-carbidopa, helps levodopa to work longer - Example: entacapone - AE: liver failure (rare), dyskinesias, postural hypotension, nausea, vomiting - Entacapone can cause yellow-orange discolouration of urine ***Amantadine*** - No longer used as an antiviral for influenza A - Thought to stimulate dopamine release (inc levels of dopamine in the brain) and block the reuptake of dopamine - Can help to manage dyskinesia caused by long term use of levodopa - Often prescribed with levodopa ***Anticholinergic medications*** - Works by blocking the action of the neurotransmitter acetylcholine - This helps to inhibit involuntary muscle movements, decreases rigidity - Little or no effect on bradykinesia - Limited effectiveness, multiple side effects - Benztropine (Cogentin) most common - AE: dry mouth, blurred vision, photophobia, urinary retention, constipation, tachycardia ***Nutrition considerations for Parkinson's*** - Dysphagia & bradykinesia highlight need for foods that are easy to chew & swallow - Adequate fibre to reduce constipation (constipation is common issue due to slow GI motility) - Watch protein intake with levodopa - Protein can interfere w levodopa absorption - be mindful of when you're taking the meds vs. when you're eating protein foods **[Dementia]** - Progressive decline in cognitive functioning - Affects memory, judgment, reasoning, ability to communicate, ability to carry out purposeful movements - Affects mood & behaviour - Risk factors include aging and family history (but not a normal part of aging) ***Dementia: 4 Most Common Types*** - Alzheimer's disease - Vascular dementia - Dementia with Lewy bodies - Frontotemporal dementia ***Alzheimer's Disease*** - Characterized by: - Neuronal degeneration - Hippocampus: early in the disease; plays important role in memory - Cerebral cortex: seen later in the disease; affects speech, perception & memory - Later stages: affects bladder & bowel control, ADLs - Amyloid plaques - Amyloid plaques are abnormal clusters of protein fragments - Build up between neurons and disrupt cell-to-cell communication - Causes inflammation by activating immune responses - Leads to neuronal damage - Neurofibrillary tangles - Neurofibrillary tangles - twisted fibers of TAU proteins - In healthy neurons, TAU helps stabilize microtubules - TAU proteins become broken apart from tangles, disrupts entire network → cell death - A diagram of a brain cell Description automatically generated - Loss of connections between neurons - Gradual loss of connections b/w neurons caused by amyloid plaques, neurofibrillary tangles, and associated neuro-inflammation → damage & death of neurons → brain atrophy (cognitive decline) ***Alzheimer's: Decreased production of Acetylcholine*** - Acetylcholine is a neurotransmitter that plays an important role in memory - Helps to convert short term memory into long term memory - Important for learning and attention - Acetylcholine is formed by the cholinergic neurons - There is a loss of cholinergic neurons in Alzheimer's disease - Widespread reduction of acetylcholine levels - causes pts to have difficulty forming memories, retrieving memories, overall cognitive decline - Linked with memory loss in later disease ***Other Factors (involved in Alzheimer's)*** - **Apolipoprotein e4 (APOE)** refers to a gene linked to Alzheimer's disease - 3 different forms - The APOE e4 has been found to inc the risk of Alzheimer's - **Endoplasmic reticulum-associated binding protein** - Elevated in the brains of Alzheimer's patients - Has been found to be toxic to neurons (involved in formation of amyloid plaques) ***Vascular Dementia*** - Damage stems from CVD that leads to decreases in blood & oxygen delivery to the brain, leading to cell ischemia - Patient may have a hx of a stroke or multiple strokes - Can present with a sudden onset - Risk factors: smoking, HTN, CAD, diabetes, dyslipidemia ***Dementia with Lewy Bodies*** - Characterized by presence of Lewy bodies - Found in cerebral cortex contributing to cognitive decline and hallucinations ***Frontotemporal Dementia*** - Degeneration of the frontal lobe, temporal lobe or both - Usually affects behaviour & language - Associated with an accumulation of abnormal proteins in the neurons - Typical age of onset is between 40-65 years of age ***Presentation of Dementia*** - Gradual onset usually - Disease can last 3-20 years - May have mild cognitive impairment prior to dementia ------------------------------------------------------------------------------------------------------ ----------------------------------------------------------------------------------------- **8 As of Dementia** **Anosognosia** - pt unaware of their neurological deficit or psychiatric condition **Agnosia** - Inability to process sensory info **Aphasia** - language difficulty, difficulty finding words, understanding language or communicating **Apraxia** - Unable to perform tasks or movements when asked **Altered Perception** - Leads to misinterpretation or confusion **Attentional Deficits** - Problems focusing, leads to difficulty completing tasks **Apathy** - Lack of interest, socially withdrawn **Amnesia** - Memory loss, can be early memory, recent memory, or even long term memory ------------------------------------------------------------------------------------------------------ ----------------------------------------------------------------------------------------- ***Dementia Evaluation*** - Based on history, interview with patient & family/caregivers - Cognitive tests: MMSE, MoCA - Ruling out delirium, depression - Imaging with CT scan, MRI of head may be considered - Imaging won't capture specifics but we may see brain atrophy or tumors/abnormalities - Imaging won't give definitive diagnosis ***Medications*** +-----------------------+-----------------------+-----------------------+ | **Cholinesterase | **NMDA Receptor | **Combination Therapy | | Inhibitors** | Antagonist** | of the 2** | +-----------------------+-----------------------+-----------------------+ | Donepezil | Memantine | Helpful for moderate | | | | to severe disease | | | | | | | | Enhances ability to | | | | do ADLs | +-----------------------+-----------------------+-----------------------+ | Rivastigmine | | | +-----------------------+-----------------------+-----------------------+ | Galantamine | | | +-----------------------+-----------------------+-----------------------+ ***Cholinesterase Inhibitors*** - Leads to inc levels of acetylcholine in the brain - Indications - Alzheimer's disease (mild, moderate and sometimes severe cases) - Vascular dementia (some evidence supporting use of donepezil) - Lewy body dementia - Not used in frontotemporal dementia (ineffective) - mild, short-limited benefits in quality of life & cognitive function - AE: nausea, diarrhea, vivid dreams, leg cramps, dizziness, headache - Bradycardia is rare but can lead to syncope ***Memantine*** - Can be used with cholinesterase inhibitor in Alzheimer's disease - **Not used in frontotemporal dementia** - Less AE and better tolerated than cholinesterase inhibitors - Modest benefits in moderate-severe Alzheimer's disease - Memantine regulates effect of glutamate - glutamate is important for learning and memory - protection from cytotoxicity ***Nonpharmacologic Strategies for Dementia*** - Exercise - Social Engagement - Cognitive stimulation - MIND diet (hybrid of Mediterranean diet & dietary approaches to stop hypertension (DASH) diet) - Recent RCT found lack of evidence for MIND diet