Geriatrics Flashcards
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.
What are the core features of Lewy Body Disease?
- Waxing and waning of cognition, especially in the areas of attention and alertness.
- Visual hallucinations-usually vivid, colorful, well-formed images of animals or small people.
- Rapid eye movement (REM) sleep behavior disorder (not currently included in the DSM-5 core features)-violent movements during sleep in response to dreams, often of fighting.
- Development of extrapyramidal signs (Parkinsonism) - tremor, akinesia, rigidity, postural instability at least 1 year after cognitive decline becomes evident.
- Lewy is slow-y, sleepy, slippy and sees things (halLEWYcinations)
What are the suggestive features of Lewy Body Disease?
- Pronounced antipsychotic sensitivity (i.e., extra-pyramidal symptoms).
- Postural instability and recurrent falls.
- Loss of consciousness or transient unresponsiveness.
- Autonomic dysfunction.
- Diminished sense of smell.
- Non-visual hallucinations and delusions.
- Excessive sleepiness.
- Depression, anxiety, and apathy.
What are the indicative biomarkers of Lewy Body Disease?
- REM sleep without atonia (RWSA) demonstrated via polysomnography.
- Decreased 123 iodine-MIBG uptake on myocardial scintigraphy.
- Evidence of reduced dopamine receptor uptake in the basal ganglia via SPECT or PET.
Diagnosis of possible NCD with Lewy bodies?
Possible NCD with Lewy bodies: Only one core feature without evidence from indicative biomarkers OR one or more indicative biomarker(s), but no core clinical features.
Diagnosis of probable NCD with Lewy bodies?
Probable NCD with Lewy bodies: Two or more core features OR one core feature and one or more indicative biomarker(s).
Treatment of Lewy Body Disease?
- Cholinesterase inhibitors for cognitive and behavioral symptoms.
- Quetiapine or clozapine for psychotic symptoms. Monitor closely for adverse effects, such as extrapyramidal signs, sedation, increased confusion, autonomic dysfunction, and signs of Neuroleptic Malignant Syndrome (NMS).
- Levodopa-carbidopa for Parkinsonism - May exacerbate psychosis or REM sleep behavior disorder.
- Melatonin and/or clonazepam for REM sleep behavior disorder.
Frontotemporal Degeneration (FTD) includes a diverse group of clinical and pathological disorders that typically present between the ages of ____
45 & 65
Genetics of Frontotemporal Degeneration (FTD)?
Most often familial (40%) than AD – usually autosomal dominant, families can have coexistant ALS. Common mutations in FTD found in – progranulin (PGRN) - blood levels can be measured.
Behavioral variant (3+) of Frontotemporal Degeneration (FTD)
BEACH (behavioural disinhibition, empathy decrease, apathy, compulsions, hyperorality)
• Disinhibited verbal, physical, or sexual behavior.
• Overeating or oral exploration of inanimate objects.
• Lack of emotional warmth, empathy, or sympathy.
• Apathy or inertia.
• Perseveration, repetitive speech, rituals, or obsessions.
Pathology of Frontotemporal Degeneration (FTD)?
Marked atrophy of the frontal and temporal lobes.
Diagnosis of Frontotemporal Degeneration (FTD)?
- Definitive diagnosis cannot be made until autopsy.
- FTD is probable if frontotemporal atrophy is evident on structural imaging or hypoactivity is visualized on functional imaging in context of the characteristic clinical signs.
Treatment of Frontotemporal Degeneration (FTD)?
- Symptom-focused.
- Serotonergic medications (e.g., SSRIs, trazodone) may help reduce disinhibition, anxiety, impulsivity, repetitive behaviors, and eating disorders.
In Parkinson disease dementia (unlike in dementia with Lewy bodies), cognitive impairment that leads to dementia typically begins _____ after motor symptoms have appeared.
10 to 15 years
Parkinson disease dementia may affect multiple cognitive domains including attention, memory, and visuospatial, constructional, and executive functions. _______ typically occurs earlier and is more common in Parkinson disease dementia than in Alzheimer disease.
Executive dysfunction
What would you see on neuroimaging for normal pressure hydrocephalus?
Enlarged ventricles on neuroimaging
Language variant (primary progressive aphasia) of Frontotemporal Degeneration (FTD)?
- Difficulties with speech and comprehension.
* Relative sparing of learning/memory and perceptual-motor function.
Features that differentiate Frontotemporal Degeneration (FTD) from AD?
Features that differentiate from AD – loss of personal awareness, hyper-orality, stereotyped repetitive behaviours, decreased speech, visuospatial functions preserved.
Clinical manifestations of Frontotemporal Degeneration (FTD)?
- Cognitive deficits in attention, abstraction, planning, and problem solving.
- Behavioral variant (3+): BEACH (behavioural disinhibition, empathy decrease, apathy, compulsions, hyperorality)
- Decline in social cognition and/or executive abilities.
- Language variant (primary progressive aphasia):
- Many individuals have features of both the behavioral and language variants.
- Increased sensitivity to adverse effects of antipsychotics.
Normal pressure hydrocephalus triad?
Wet, wacky, and wobbly
- Triad of dementia, gait disturbance and urinary incontinence
- Gait is unique – cant lift legs off ground, but if lying down can mimic walking
What is frailty?
Frailty: clinically – recognizable state of decreased reserve in older adults with increased vulnerability to acute stressors resulting from functional decline across multiple physiologic system
What is the etiology of frailty?
o Medications
o Environmental/Social (e.g., isolation, poverty, elder abuse, neglect)
o Medical disease
o Malnutrition (e.g., from poor dentition, malabsorption, dysphagia – skeletal atrophy in first 1/3 of esophagus)
o Psychiatric (e.g., mild cognitive impairment, dementia, depression, psychosis)
o Changes in visual acuity
o Changes in auditory acuity
o Decreased mobility
What are the symptoms of frailty?
Symptoms include generalized weakness, exhaustion, slow gait, poor balance, decreased physical activity, cognitive impairment, and weight loss
What is included in the comprehensive geriatric assessment?
- Includes: Past Medical History, Medications (optimization), Allergies, Social History, Function, Physical Exam, and Geriatric Review of Systems (cognition, mood, sleep, pain, nutrition, falls, continence, vision/hearing, skin, and safety)
- Screen for elder abuse and neglect
- Assessment of the impact of symptoms on activities of daily living
- Caregiver support
Which scale can be used to estimating severity of frailty and can guide GOC?
Clinical Frailty Scale
Which scale can be used to define frailty components?
Edmonton Frail Scale
Which cardiovascular medications should you avoid in the geriatric population?
Alpha blockers for HTN (doxazosin)
Central alpha agonists for HTN (clonidine)
Digoxin for 1st line afib/HF
Amiodarone for 1st line afib
Who qualifies for Supportive Living SL3?
- Individuals who are medically and physically stable
- Living with physical disability, mental health diagnoses, or mild dementia with no known risk of wandering, and who are not a risk to self or others
- Must be able to move independently or with the assistance of one other person
- Could be experiencing increased healthcare needs that cannot be scheduled
- Are able to use a call system to get help
Which endocrine medications should you avoid in the geriatric population?
Sliding scale insulin
Long acting sulfonylureas
Which CNS medications should you avoid in the geriatric population?
Anticholingeric antidepressants (e.g. TCAs)
Antipsychotics
Benzos
Z drugs (zopiclone)
Which GI medications should you avoid in the geriatric population?
Metoclopramide or long term PPIs
Which GU medications should you avoid in the geriatric population?
Anticholinergics or alpha blockers
Which pain medications should you avoid in the geriatric population?
NSAIDs or opioids as 1st line
Who qualifies for Supportive Living SL4/D?
- Individuals who have more complex medical needs that are predictable and safely managed with onsite, professional nursing (LPN level) and the direction of the case manager
- May require chronic disease management
- May require the following types of assistance with daily activities:
- Complete meal assistance including tube feeds
- Mechanical lift transfers
- Two person transfers
- Medication assistance or administration
- DSL4D is for individuals with moderate to severe dementia, who may have a high risk of wandering and unpredictable behaviours but who are not a safety risk to themselves or others
What are the topics to discuss for a dying patient?
Goals of Care: disease vs. symptom management
▪ Advance directives, power of attorney, public guardian, and trustee)
▪ Location (e.g. hospice, home, palliative care facility, etc.
▪ Patient wish (medical assistance/feasibility to fulfill)
▪ Physician assisted death (patient-initiated discussion)
▪ Treatment options and likelihood of success
Common Medical Interventions: mechanical ventilation, antibiotic therapy, feeding tubes
Resuscitation Options: and likelihood of success, i.e. Full Code vs. DNR states incl. preferences for CPR, intubation, ICU admission, artificial hydration)
SDM: If wishes unknown, act in the patient’s best interest, taking the following into account
- Values and beliefs held by the patient while capable
- Whether well-being is likely to improve with vs. without treatment
- Whether the expected benefit outweighs the risk of harm
- Whether a less intrusive treatment would be as beneficial as the one proposed
What are Instructional Advance Directives
The patient sets out his/her decisions about future health care, including who he/she would allow to make treatment decisions on his/her behalf and what types of interventions he/she would want
