Geriatrics Flashcards
(151 cards)
Definition of Mild Neurocognitive Disorder (Mild Cognitive Impairment)?
Cognitive changes with measurable deficits in one or more cognitive domain
Peservation of independence or minimal impairment in ADLs and IADLs and not meeting criteria for major NCD
Investigations for Mild Neurocognitive Disorder (Mild Cognitive Impairment)?
Establish a baseline for follow-up
Clinical interview with patient and caregivers is the cornerstone of mild NCD evaluation
Neuropsychological testing
• MMSE (not sensitive to early cognitive change) or MoCA (more sensitive, score <26 is impaired); should not be used in isolation
• if abnormal, follow-up in one year to monitor cognitive and functional decline
Neuroimaging: role uncertain; a non-contrast brain CT is often ordered to evaluate for structural abnormalities (CVD, SDH, NPH, or mass lesion)
Most common subtype of Mild Neurocognitive Disorder?
Amnestic subtype is the most common and most associated with AD pathology
Treatment of Mild Neurocognitive Disorder?
Non-pharmacologic management: exercise training for 6mo is likely to improve cognition; insufficient evidence to support or refute cognitive intervention, it may improve outcome on select cognitive measures
No evidence for cholinesterase inhibitors, anti-inflammatory agents, vascular risk factor modification
Definition of Major Neurocognitive Disorder?
- Acquired, generalized, and (usually) progressive impairment of cognitive function associated with impairment in ADLs/iADLs (i.e. shopping, food preparation, finances, medication management)
- Diagnosis of major NCD requires presence of significant cognitive decline in at least 1 domain from a previous level of performance in one or more cognitive domains (complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition) based on:
• A) concern of the individual or a knowledgeable informant AND
• B) substantial impairment in cognitive performance either documented by standardized exam - Not due to other CNS, psychiatric, or systemic condition, drugs or delirium
Depression vs Dementia
Depression Dementia Motor Slowing + +/- Sad Mood + +/- Slow Responses + - Memory + + Recognition - + Cortical Deficits - +
Delirium vs Dementia
Delirium Dementia Rapid Onset + - LOC Change + - Fluctuating + +/- (DLB) Memory + + Motor Behaviour + - Medical Etiology + +/0
History that should be asked for Major Neurocognitive Disorder?
- “Geriatric Giants”
• confusion/incontinence/falls
• memory and safety (wandering, leaving doors unlocked, leaving stove on, losing objects, driving)
• behavioural (mood, anxiety, psychosis, suicidal ideation, personality changes, aggression)
• polypharmacy and compliance (sedative hypnotics, antipsychotics, antidepressants, anticholinergics) - ADLs and IADLs
- Cardiovascular, endocrine, neoplastic, renal ROS, head trauma history
- Alcohol, smoking
- Collateral history
Physical exam for Major Neurocognitive Disorder?
Blood pressure
Hearing and vision
Neurological exam with attention to signs of parkinsonism, UMN findings
General physical exam with focus on CVD, patient- specific risk factors, and history
MMSE or MoCA, clock drawing, frontal lobe testing (go/no-go, wordlists, similarities, proverb)
Ddx for Major Neurocognitive Disorder?
o Alzheimer’s Disease (Mixed/Vascular)
o Vascular Ischemic Dementia
o Dementia w/ Lewy Bodies
o Fronto-temporal Dementia
Investigations for Major Neurocognitive Disorder?
Blood Tests - Systemic/Metabolic: CBC (ESR optional), electrolytes, Glucose, LFTs, Renal Fcn, TSH, B12 (Folate optional)
Other Tests - Infectious/Neoplastic: CXR, UA, CSF, HIV, Syphilis
Imaging: Recommended in most situations - MRI
Definition of Alzheimer’s Disease?
Beyond criterion for NCD, the core features of Alzheimer’s disease include an insidious onset and gradual progression of cognitive and behavioural symptoms
Typical presentation: amnestic
• Mild phase: impairment in memory and learning sometimes accompanied with deficits in executive function
• Moderate-severe phase: visuoconstructional/perceptual-motor ability and language may also be impaired
• Social cognition tends to be preserved until late in the course of the disease
Approximately 1% of AD results from an autosomal dominant single-gene mutation (_____, ______ or ______), which is associated with an early onset of symptoms.
Amyloid precursor protein, presenilin 1, or presenilin 2
Pathophysiology of Alzheimer’s Disease?
Accumulation of extraneuronal beta-amyloid plaques and intraneuronal tau protein tangles is associated with progressive brain atrophy.
Risk factors for Alzheimer’s Disease?
- Age is the greatest risk factor
- Genetic susceptibility polymorphism: apolipoprotein E4 increases risk and decreases age of onset
- Other factors include: traumatic brain injury, family history, Down syndrome, low education, and vascular risk factors (e.g. smoking, HTN, hypercholesterolemia, DM)
Clinical features of Alzheimer’s Disease?
Cognitive impairment
• memory impairment for newly acquired information (early)
• deficits in language, abstract reasoning, and executive function
Behavioural and psychiatric manifestations (80% of those with major NCD)
• Mild NCD: major depressive disorder and/or apathy
• Major NCD: psychosis, irritability, agitation, combativeness, and wandering
Motor manifestations (late) • gait disturbance, dysphagia, incontinence, myoclonus, and seizures
4As: amnesia, apraxia, agnosia and aphasia
Protection factors of Alzheimer’s Disease?
Protective Factors: Physical activity, diet, mental stimulation, social engagement, management of vascular RF
Treatment options for Alzheimer’s Disease?
- No cure or truly effective treatment.
- Cholinesterase inhibitors (e.g., donepezil, rivastigmine, and galantamine) may slow clinical deterioration by 6-12 months in up to 50% of patients with mild-to-moderate AD.
- The NMDA receptor antagonist, memantine, may provide a modest benefit to patients with moderate-to-severe disease.
- Antipsychotic medications are often used to treat agitation and aggression.
- Supportive care via behavioral, social, and environmental interventions.
- Care of the caregiver - refer to supportive services like the Alzheimer Society
- Advance directives and planning safety - driving – other driving options MARD/wandering/fire safety
- Treat depression, even with coexistent dementia.
Side effects of cholinesterase inhibitors?
S/E: Most common side effects are GI (primarily diarrhea, nausea and vomiting) – less so with donepezil. Anorexia/weight loss. Bradycardia and hypotension (enhanced vagal tone) - falls. Sleep disturbances (insomnia, vivid dreams – more common on donepezil)
Second most common single cause of major NCD after AD, accounting for approximately 20% of major NCDs.
Vascular Dementia (Vascular Cognitive Impairment)
Cognitive decline in vascular dementia occurs as a result of at least one of the following mechanisms:
Large vessel strokes, usually cortical.
Small vessel strokes (lacunar infarcts) to subcortical structures.
Microvascular disease affecting the periventricular white matter.
Major risk factors for Vascular Dementia (Vascular Cognitive Impairment)?
Major risk factors are the same as those for CVD (i.e. HTN, DM, smoking, obesity, high cholesterol levels, high homocysteine levels, other risk factors for atherosclerosis, atrial fibrillation, and conditions increasing risk of cerebral emboli)
Clinical manifestations of Vascular Dementia (Vascular Cognitive Impairment)?
- Presentation and progression of cognitive impairment are variable.
• Classically demonstrates a stepwise deterioration corresponding with the occurrence of micro-infarcts (i.e., multi-infarct dementia).
• May present with acute onset followed by partial improvement.
• May have an insidious onset with gradual decline similar to AD. - Complex attention and executive functions are the cognitive domains typically affected in small vessel disease.
- Confirmation of the diagnosis requires neuroimaging with findings that correlate to the clinical picture.
Treatment of Vascular Dementia (Vascular Cognitive Impairment)?
No cure or truly effective treatment.
Manage risk factors with a goal of preventing future strokes.
Symptomatic treatment is similar to AD.