Neurocognitive Disorders

types of neurocognitive disorders

Delirium

Dementia (Alzheimer's and other NCD's)

Frontotemporal lobe disease

Lewy bodies

Vascular dementia

Traumatic brain injury

delirium vs dementia

type of delirium

hyperactive: agitation, restlessness

hypoactive: apathy, quiet

mixed: combination

unclassified: manifestations dont fit in either category

delirium causes

nursing interventions for delirium

Prevent physical harm due to confusion, aggression, or fluid and electrolyte imbalance.

Perform comprehensive nursing assessment to aid in identifying cause.

Assist with proper health management to eradicate underlying cause.

Use supportive measures to relieve distress.

#1 Nursing Priority is SAFETY and getting the underlying cause of the delirium treated!

Ex: Terry's story of delirium after his heart surgery - YouTube

dementia characteristics

Insidious onset

Slow, progressive development

Usually a primary disorder, but might be related to other illnesses

Impaired short-term memory

Long-term memory slowly failing

Level of consciousness unchanged

Thought content normal initially, later confusion

Eventual loss of ability to abstract

Misidentification, delusions

Affect alterations 12

dementias, neurocognitive disorders

Alzheimer’s (AD or DAT)

Vascular: if the question mentions cardiac history

Diffuse Lewy Body Disease

AIDS Dementia Complex

Frontotemporal Lobe Dementia (Pick’s Disease)

Parkinson’s Disease: neurological

Creutzfeldt-Jakob Disease: mad cow disease

Huntington’s Disease: chorea, hereditary genetic

Wernicke-Korsakoff: wet brain, thiamine deficiency in alcoholics

Traumatic Brain Injury

alzheimers disease

Alzheimer’s disease (AD) is the most common form of dementia in the elderly affecting more than 5 million Americans.

Cognitive deficits appear and progress gradually/slowly

Loss of short-term memory is an essential feature of AD and is usually its first manifestation.

Loss of memory for _recent events__ is an essential feature of AD and is usually its first manifestation.

Diagnosis is made after all other disorders have been ruled out.

Age is the most significant risk factor; rarely diagnosed before age 60

Hx of head injury, cardiovascular disease, lower levelsof education, and being female are also risk factors.

etiology of alzheimers

Cholinergic Deficit: What neurotransmitter? ach: neurotransmitter used in the PNS and CNS (cognition, memory, concentration)

Neuronal Loss: cerebral cortex, hippocampus, amygdala, forebrain

Neurofibrillary Tangles: cellular nutrition transport

Beta Amyloid Plaques: oxidative stress, free radicals

Genetics

diagnosis of AD

Diagnosis is based primarily on clinical features.

Autopsy of brains of individuals with AD reveals extracellular deposition of amyloid-beta protein, neurofibrillay tangles, senile (neuritic) plaques, and loss of neurons.

affected areas of the brain alzheimers

Frontal lobe- impaired problem solving, poor judgment, personality changes, aggressiveness

Parietal lobe- inability remain oriented in environment

Temporal lobe- inability to recall words, inability to use words correctly (language comprehension), late stages contributes to delusions and hallucinations

Occipital lobe-unable to recognize familiar objects, impaired language interpretation

Hippocampus- impaired memory STM initially, late stages-unable to form new memories

Amygdala-impaired emotions

four A's of AD

1. Amnesia: memory (both old and new)

2. Aphasia: language

1. Expressive: broca, written or oral: know what they want to say, just cant say it

2. Receptive: wernicke, speak normal, no understanding, content doesent make sense

3. Apraxia: movement

4. Agnosia: Recognition of objects, people

classic behaviors of AS

Word-finding difficulty

Difficulty concentration

Misinterpreting the environment: visual hallucinations (late)

Delusions: dead relatives alive, pathologic jealousy

Pathological jealousy

Stealing odd things

Illusions

Somatic preoccupations

Misidentification

Sundowning- severe (Stage 6); symptoms seem to worsen in the late afternoon and evening (increased confusion and agitation)

Loss of ability to care for oneself

defense mechanisms AD

Denial - Client/Family refuse to believe that changes are taking place

Confabulation - Client makes up stories when questioned about events or activities that they do not remember, can be unconscious attempt to save self esteem

Perseveration - repeats phrases/behaviors

Avoidance of questions

stages of AD: mild

Decreased short-term memory

Word-finding difficulties

Decreased decision-making, concentration, reasoning, judgment

Difficulty performing usual activities

Denial

Getting lost/misplacing objects

Repetitive questioning

stages of AD: moderate

aphasia, Apraxia, agnosia, poor comprehension

Disorientation

Blunted affect

Misidentification

Sleep disturbance

Delusions (later in mild)

Needs help with activities of daily living, supervision with meals

Emotional lability

Wanders

Urinary incontinence

stages of AD: severe

Gait disturbance

Unable to feed self

Urinary and bowel incontinence

Bedridden/require turning q2h

Swallowing difficulty

24-hour supervision

stages of AD

stages of AD cont

screening assessment tools

Mini-mental status examination (MMSE)

Confusion Assessment Method (CAM)

Neelon/Champagne (NEECHAM) Confusion Scale

Functional Dementia Scale

Brief Interview for Mental Status (BIMS)

Functional Assessment Screening Tool (FAST)

Global Deterioration Scale

Blessed Dementia Scale: uses a secondary sourcelike family

MMSE

AD involves the death of

brain cells, neurodegenerative

AD risk factors

age, genetics, lifestyle

nursing interventions for AD

Articulate words clearly/provide short simple directions

A calm approach works best

Avoid arguing and go along with the concern followed by therapeutic distraction

Provide prompts and reminders for patients with short-term memory loss

Provide reality orientation for those with higher cognitive functioning

Provide a structured environment with a set schedule

Do not rush the patient

nursing interventions cont

Do not shout if the patient is hard of hearing

Observe patient during ADLs and determine the need for assistance

Set realistic goals – goals will need to be adjusted as the patient’s cognition declines.

Monitor physical needs – assess for visual acuity, hydration, nutritional needs, ability to communicate needs, ability to function safely in environment.

Allow patient to be as independent as possible, as longas possible

Intervene early when the patient begins to escalate

MORE nursing interventions

Interventions are based on the patient’s ability to participate in self-care.

Set realistic goals, dependent on the patient’s level of functioning.

Safety is a special concern, because of abnormal posture and movement.

Be patient and allow extra time for tasks.

Begin safety, fall precautions as needed.

Monitor sleep, hydration, nutrition, elimination, and physical status.

Encourage ventilation of feelings

milieu management AD

Observe patient preference for temperature and lighting

Reduce noxious sounds

TV: purposeful viewing only

Match personalities of roommates when possible

Memory aids

Calendar, notes, illustrated directions

Large-print directions, pill boxes3

community resources for AD

Transportation services

Supervision and care when the primary care giver is out of the home

Information on support groups in the community

Meals on Wheels

Information on respite and residential services

Telephone numbers for help lines

Home health services

Caregiver support

goals for dementia treatments

Restore neurotransmitter loss

Chiefly, acetylcholine (Ach)

Glutamate

Halt neuronal death

psychopharmacology: AD

Acetylcholinesterase inhibitors: for mild to moderate disease

Tacrine (Cognex)

Donepezil (Aricept)

Rivastigmine (Exelon)

Galantamine (Razadyne)

Memantine (Namenda)—for moderate to severe disease; the only approved medication for Alzheimer disease that is not an AChE inhibitor

enzymes

Produced via genetic coding

Drive energy production and material for building blocks of life

Catalyst of metabolic change

Cholinesterase (ChE) breaks down Ach

- ACh can no longer activate cholinergic receptors

- Treatment goal: prevent ACh breakdown by blockingChE37

cholinergic pathways

Selectively destroyed in Alzheimer disease (AD)

1. Inflammation drives selective dysfunction.

2. Immune cells synthesize and degrade Ach.

3. Anti inflammatory cholinergic pathway mediates immunoregulation via cortico-limbic system and nicotinic receptors.

4. Loss of ACh in (a) hippocampus and (b) amygdala causes memory loss.

psychopharmacology

Majority of Alzheimer medications work within CNS (cerebral cortex)

Acetylcholinesterase (AChE) & butyrylcholinesterase (BuChE) are enzymes that terminate the actions of acetylcholine.

Used in mild to moderate AD

Acetylcholine loss occurs in people with Alzheimer’s Disease. The goal of these meds is to increase the level of acetylcholine and therefore slow disease progression and improve cognition.

Cholinesterase inhibitors

- Aricept (donepezil) - (AChE) inhibitor

- Exelon (rivastigmine) - (AChE) & (BuChE) inhibitor

- Razadyne (galantamine) - (AChE) inhibitor

Adverse effects: _facial flushing, leg cramps, GI (n/v and diarrhea),bradycardia, syncope (take Aricept at night to sleep through theside effects of that cause fainting from the irregular heartbeat)

Contraindicated: Asthma/COPD-increase Ach can lead to bronchoconstriction

cholinesterase inhibitors

Elevate ACh levels to prolong cognitive abilities.

Temporarily mask neurodegeneration.

Improve function but do not slow disease

what are the cholinesterase inhibitors

Tacrine—Cognex

- Inhibited both AChE and BChE

- Discontinued: severe hepatotoxicity

Donepezil—Aricept

- More selective for AChE; reversible inhibitor

Rivastigmine—Exelon

- Irreversible inhibitor of ChE

Galantamine—Razadyne

- Preference for AChE over BChE

- Can stimulate presynaptic muscarinic receptors: fewerSEs42

agents that may retard neurodegeneration

NMDA receptor inhibitors

- Memantine—Namenda

- Could theoretically prevent neuronal death

Secretase inhibitors

- Serious side effects with these drugs

Dihydropyridine calcium channel blockers

- Possible new preventive tools to slow vessel changes

namenda (memantine)

possible drugs to prevent AD

Strategies being tested to modify progression include

NSAIDs

Statins

Estrogen

Antioxidants

B and E vitamins

Antiamyloid immunotherapy