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Neurocognitive disorders
temporary or permanent damage to neurons
Types of cognitive impairment disorders
delirium, dementia, amnestic disorders
Delirium according to DSM-5
disturbance in attention and awareness (reduced orientation to environment)
Disturbance develops over short period of time, represents an acute change from baseline and tends to fluctuate in severity during the course of a day
Delirium develops over a short time and is
reversible if underlying cause is identified and treated quickly
Pts with delirum experience
Changes in cognition and mental status → pt doesn’t know where they are, may not recognize familiar objects, or unable to carry a conversation
Risk factor for delirium
AIDS, pneumonia, bone fracture, meds, preexisting dementia, advanced age
Drugs that cause delirium
Perscription drugs
Sedative hypnotics (benzodiazepines), anticonvulsants (barbiturates), antiparkinsonian agents (benzotropine)
Analgesics → narcotics, NSAIDS
Antihistamines
Abx
Antinauseants → scopolamine, dimenhydrinate
Psychotropic meds → lithium
Cardiac meds → digitalis
GI meds → H2-blockers
other meds that cause delirium
Liquid meds containing alcohol, mandrake, henbane, jimson weed, atropa belladonna extract
When doing physical assessment on pt with delirum always
Consider medical first
Physical assessment
Substance use hx
Interview caregivers
Hx of onset, duration, range, and intensity (always consider medical first)
Meds (cold meds can cause confusion)
Neuro assessment to rule out TIA
Assess for infections, labs
Physiological needs for delirum
Respiratory and cardiovascular
Safety/behavioral for delirum
They have combative behavior so de-escalation is a priority
Nursing interventions for delirum
Safe therapeutic environment
Maintenance of fluid and electrolyte balance
Prevention of aspiration, skin breakdown
Psychosocial interventions
Frequent interaction and support
Encouragement to express fears and discomforts
environment al control → adequate lighting, reasonable noise level, easy-to-read calendars and clocks
Frequent verbal orientation
Alzheimer disease 2 subtypes
Early onset and late onset
Early onset is
Age 65 yrs and younger, more rapid progression
Late onset is
Age older than 65 yrs, more common
Risk factors for AD
Genetics, metabolic syndrome, down syndrome
Amyloid precursor protein
peptides can accumulate as amyloid plaques, promoting neurodegeneration
Beta-amyloid plaques
clump together in the brain and destroy cholinergic neurons
Neurofibrillary tangles
when microtubules disintegrate, the neuron’s transport system collapses, resulting in cell death
Synpatic micron RNA and neurotransmission
several major neurotransmitters are affected such as ACh, norepi, serotonin
Etiology of AD
Amyloid precursor protein, Beta-amyloid plaques, Neurofibrillary tangles, Synpatic micron RNA and neurotransmission, Oxidative stress, free radicals, mitochondrial dysfunction, Inflammation, Gut-brain axis alteration
Gut-brain axis alteration
exposure to exotoxins that pass BBB
AD
degenerative, progressive, neuropsychiatric disorder, cognitive impairment, emotional and behavioral changes, physical and functional decline
s/sx of AD
memory loss, recent, remote, disorientation, decreased ability to concentrate or learn new material, difficulty making decisions, poor judgement
Aphasia
alterations in language
Apraxia
inability to execute motor activities despite intact motor function
Agnosia
failure to recognize objects despite intact sensory function
Hyperorality
excessive, compulsive preoccupation with oral sensations involving putting objects in the mouth, chewing, sucking, biting, or smacking lips
Pharm interventions for AD
acetylcholinesterase inhibitors, NMDA antagonists, memantine and donepezil combination, mood stabilizers, antianxiety meds, antidepressants
Donepezil
prevents breakdown of ach in the brain
Galantamine
Prevents breakdown of acetylcholine and modulates nicotinic receptors that release ach in the brain
Memantine
Blocks toxic effects of excess glutamate and regulates glutamate activation