Geriatrics

1. PUD
2. Hepatic disease
3. Renal disease
4. Bradycardia or AV block
5. Significant bronchospastic disease
6. Obstructive urinary disease
7. Epilepsy or history of seizure

Diarrhea
Nausea
Vomiting
Anorexia, weight loss
Dizziness, syncope, vertigo
Asthenia, fatigue, insomnia
Muscle cramps
Abnormal dreams
Headache
Peripheral oedema
Tremor

(Cochrane 2006 CI for AD)

Dizziness 6.3%
Headache 5.2%
Constipation 4.6%
Hypertension 4.1%
Somnolence 3.4%

(van Marum. Neuropsych Dis and Treatment 2009)

Memantine 5-10 mg bid

Renal excretion accounts for 65-90% of clearance. In patients with CrCl 10-30, maximum daily dose should be 5 mg bid.

Not subject to major hepatic metabolism.

No significant drug interactions, but alkaline urine can reduce renal excretion. Therefore, caution in patients taking sodium bicarbonate, carbonic anhydrase inhibitors, and severe UTI.

(van Marum. Neuropsych Dis and Treatment 2009)

Normal is +1 to -1 SD.
Below -1 is osteopenia.
Below -2.5 is osteoporosis.

A. Disturbance of attention (reduced ability to focus, sustain or shift attention), and awareness.
B. Disturbance develops over a short period of time (usually hours to days), represents a change from baseline attention/awareness, and tends to fluctuate in severity during the course of a day.
C. An additional change in cognition (memory, disorientation, language, visuospatial ability, or perception).
D. Not better explained by another NCD, and do not occur in the context of a severely reduced level of arousal, such as coma
E. There is evidence that the disturbance is caused by a medical condition, substance intoxication, or withdrawal, or exposure to a toxin, or is due to multiple etiologies.

Medications
Accidental
Neurological
Cardiovascular
Visual problems
Precipitants (infection, infarction, social stress)

1. Cognition - orientation and therapeutic activities protocols
2. Sleep - non-pharmacological sleep enhancement protocols
3. Immobility - early mobilization protocol
4. Vision protocol
5. Hearing protocol
6. Dehydration protocol

A. Meets criteria for major or mild NCD.

B. The disturbance has insidious onset and gradual progression.

C. Either (1) or (2):

1. Behavioral variant:

Three or more of the following:

- Behavioral disinhibition

- Apathy or inertia

- Loss of sympathy or empathy

- Perseverative, stereotyped or compulsive/ritualistic behavior

- Hyperorality and dietary changes

Relative sparing of memory and visuospatial functions

Prominent decline in social cognition and/or executive abilities

2. Language variant: prominent decline in language ability, in the form of speech production, word finding, object naming, grammar, or word comprehension.

D. Relative sparing of memory and perceptual-motor function.

E. Not better explained by CVD, another neurodegenerative disease, the effects of a substance, or another mental, neurological, or systemic disorder.

Core features:

-Impaired confrontation naming

-Impaired single-word comprehension

Other features:

-Impaired object knowledge, particularly for low-frequency or low-familiarity items

-Surface dyslexia or dysgraphia

-Spared repetition

-Spared speech production (grammar and motor speech)

Anterior temporal lobe atrophy

Core features

-Agrammatism in language production

-Effortful, halting speech with inconsistent speech sound errors (apraxia of speech)

Other features

-Impaired comprehension of syntactically complex sentences

-Spared single-word comprehension

-Spared object knowledge

Left posterior fronto-insular atrophy

Core features

-Impaired single-word retrieval in spontaneous speech and naming

-Impaired repetition of sentences and phrases

Other features

-Speech (phonologic) errors in spontaneous speech and naming

-Spared single-word comprehension and object knowledge

-Spared motor speech

-Absence of frank agrammatism

Left posterior perisylvian or parietal atrophy

Phosphorylated tau

Transactive response DNA-binding protein 43 (TDP-43)

Fused in sarcoma (FUS) protein

Programmed cell death, or "adaptive" aging. In this theory, aging is considered a beneficial aspect of evolution, to prevent overcrowding. Genes evolved that actively cause aging.

Non-adaptive theories (stochastic theories)

-Pleiotropic gene theory. There is a declining force of natural selection with age. Therefore, some genes that confer an advantage early in life will be favoured even if the same gene has deleterious effects later on (called pleiotropic genes).

-Disposable soma theory. Goal of an organism is to balance keeping itself going on a day-to-day basis, versus maintaining itself in the long-term. Optimum course of life is to invest fewer resources in the maintenance of somatic tissues, and deleterious effects of this are not seen until long after the organism would have died in the wild environment.

Werner's syndrome (DNA helicase)

Hutchinson-Gilford progeria (lamin A gene)

Human cells grown in culture have a limited life span. Telomeres are the structures at the ends of chromosomes, synthesized by telomerase. As cells divide, the length of telomeric DNA shortens until a lower limit is reached (called the Hayflick limit) at which point proliferation ceases.

1. Programmed cell death: reduction in telomere length and telomerase activity.

2. Stochastic theory of genomic instability (DNA mutations, gene repression, gene overexpression, genomic DNA damage, mitochondrial DNA damage).

A. Evidence of modest decline from previous level of performance in one or more cognitive domains based on:

(i) concern of the individual, a knowledgeable informant, or the clinician; and

(ii) a modest impairment on neuropsychological testing or other quantified clinical assessment

B. The cognitive deficits do not interfere with everyday activities.

C. Does not occur in the context of delirium

D. Not explained by another mental disorder (e.g. depression, schizophrenia)

A. Evidence of significant cognitive decline in one or more cognitive domains based on:

(i) concern of individual, knowledgeable informant, or clinician; and

(ii) substantial impairment in cognitive performance on standardized neuropsychological testing or other quantified clinical assessment

B. The cognitive deficits interfere with independence in everyday activities

C. Not in context of a delirium

D. Not better explained by another mental disorder

A. Criteria met for dementia

B. Clinical features are consistent with a vascular etiology, as suggested by either:

(i) Onset of cognitive deficits is temporally related to one or more cerebrovascular events

(ii) Evidence for decline is prominent in complex attention (including processing speed) and frontal-executive function

C. There is evidence of cerebrovascular disease from history, physical exam, and/or neuroimaging considered sufficient to account for the neurocognitive deficits.

D. The symptoms are not better explained by another brain disease or systemic disorder.

Probable vascular neurocognitive disorder is diagnosed if one of the following is present; otherwise possible vascular neurocognitive disorder should be diagnosed:

1. Clinical criteria are supported by neuroimaging evidence.

2. Neurocognitive syndrome is temporally related to one or more documented cerebrovascular events.

3. Both clinical and genetic (e.g. CADASIL) evidence of cerebrovascular disease is present.

A. Criteria met for major or mild NCD

B. Insidious onset, and gradual progression in one or more cognitive domains (for major NCD, at least 2 domains must be impaired)

C. Criteria are met for either probable or possible AD as follows:

For major NCD, probable AD is diagnosed if either of the present is following is present; otherwise possible AD should be diagnosed:

1. Evidence of a causative AD genetic mutation from family history or genetic testing.

2. All three of the following are present:

a. Clear evidence of decline in memory and learning and at least one other cognitive domain

b. Steadily progressive, gradual decline in cognition, without extended plateaus

c. No evidence of mixed etiology

For mild NCD:

Probable AD is diagnosed if there is evidence of a causative AD genetic mutation from either genetic testing or family history

Possible AD is diagnosed if there is no evidence of a causative AD genetic mutation from either genetic testing or family history, and all three of the following are present:

1. Clear evidence of decline in memory and learning

2. Steadily progressive, gradual decline in cognition, without extended plateaus.

3. No evidence of mixed etiology

D. The disturbance is not better explained by cerebrovascular disease, another neurodegenerative disease, the effects of a substance, or another mental, neurological, or systemic disorder.

Probable AD dementia, use when meets criteria for dementia, and in addition, has the following characteristics:

-Insidious onset, over months to years, not sudden over hours or days;

-Clear-cut history of worsening cognition by report or observation; and

-The initial and most prominent cognitive deficits are evident on history and examination in one of the following categories

Amnestic presentation

Nonamnestic presentation (language, visuospatial, executive dysfunction)

Possible AD dementia, should be used in either of these circumstance:

-Atypical course: sudden onset of cognitive impairment or demonstrates insufficient historical detail, or objective documentation of progressive decline.

-Etiologically mixed presentations

Stroke temporally related; or presence of extensive infarcts or severe white matter disease

Features of DLB

Evidence of another neurological disease, non-neurological medical comorbidity, or medication use that could have a substantial effect on cognition

JAMA 2014: older age, fewer years of education, stroke, diabetes, amnestic type MCI

From CCCDTD4

1. Age less than 60 years

2. Rapid (e.g., 1 or 2 months) unexplained decline in cognition or function

3. “Short” duration of dementia (less than 2 years)

4. Recent and significant head trauma

5. Unexplained neurological symptoms (e.g. new onset of severe headache or seizures)

6. History of cancer (especially in sites and types that metastasize to the brain)

7. Use of anticoagulants or history of bleeding disorder

8. History of urinary incontinence and gait disorder early in the course of dementia (as may be found in normal pressure hydrocephalus)

9. Any new localizing sign (e.g., hemiparesis or a Babinski reflex)

10. Unusual or atypical cognitive symptoms or presentation (e.g. progressive aphasia)

11. Gait disturbance

Central feature: progressive cognitive decline, dementia

Core features: fluctuations, visual hallucinations, parkinsonism

- 1 feature for possible DLB, 2 features for probable

Suggestive features: REMSBD, neuroleptic sensitivity, dopamine transporter imaging

- 1 feature for possible, or 1 suggestive + 1 core for probable

Supportive features (undetermined diagnostic specificity)

-repeated falls

-syncope or transient loss of consciousness

-autonomic failure

-hallucinations in other modalities

-systematized delusions

-depression

-relative preservation of medial temporal lobe on MRI or CT

-generalized low uptake on SPECT or PET with reduced occipital activity

-abnormal uptake on MIBG cardiac scintigraphy

-prominent slow wave activity and temporal lobe transient sharp waves on EEG

1. Daytime drowsiness and lethargy

2. Daytime sleep >2 hours

3. Disorganized speech

4. Duration of episodes last seconds to days

5. Staring into space for long periods

(see original DLB consensus)

Tools include:

Clinician Assessment of Fluctuation scale

One Day Fluctuation Assessment scale

Mayo Fluctuations Composite scale

Axial tendency, with greater postural instability, gait difficulty, facial immobility.

Resting tremor less common

Less levodopa responsive

For mild vascular NCD, single stroke or extensive white matter disease is generally sufficient.

For major vascular NCD, two or more strokes, a strategically placed stroke (angular gyrus, thalamus, basal forebrain), or a combination of white matter disease and one or more lacunes is generally necessary.

DSM V, page 622

1. Abrupt deterioration within 3 months after stroke, and fluctuating or stepwise course

2. History of gait disorder, or frequent falls

3. Urinary frequency and incontinence early in the course of the dementing illness

4. Neurological findings (focal deficit, sensory loss, pseudobulbar syndrome, extrapyramidal signs, psychiatric symptoms)

From the NINDS-AIREN vascular dementia diagnostic criteria 1993 paper

NIA-AA 2011 workgroup:

Evidence of brain amyloid-beta (Aβ) protein deposition:

-Low CSF Aβ42

-Positive PET amyloid imaging

Evidence of downstream neuronal degeneration or injury:

-Elevated CSF tau, both total tau and phosphorylated tau (p-tau)

-Decreased FDG uptake on PET in temporoparietal cortex

-Disproportionate atrophy on structural MRI in medial, basal and lateral temporal lobe, and medial parietal cortex

Structural alterations in brain are seen in anxiety disorders (limbic system, hippocampal and prefrontal regions)

Reduced neurotransmitter function (serotonin, acetylcholine)

HPA-axis dysregulation (chronic high cortisol may damage the hippocampus)

Genetic vulnerability (serotonin transmitter, Apo e4 allele)

DSM-V:

Content of worry - older adults report greater concern about well-being of family or their own physical health.

Frail elderly may also worry about safety, such as falling, and limit their abilities.

Chronic physical disease may be a potent issue for excessive worry in elderly.

Linked with cognitive impairment, and what may appear to be excessive worry, such as the whereabouts of things, may be due to cognition.

1. Ophthalmoplegia (vertical > horizontal)

2. Saccadic intrusions into fixed gaze (square wave jerks)

3. Loss of optokinetic nystagmus

4. Loss of convergence

5. Blepharospasm

6. Eyelid-opening apraxia

Criteria must be fulfilled for last 3 months, with symptom onset at least 6 months before diagnosis.

1. 2 or more of the following:

-straining during at least 25% of defecations

-lumpy or hard stools in at least 25% of defecations

-sensation of incomplete evacuation for at least 25% of defecations

-sensation of anorectal obstruction/blockage for at least 25% of defecations

-manual manoeuvres to facilitate at least 25% of defecations

-fewer than 3 defecations/week

2. Loose stools are rarely present without the use of laxatives

3. Insufficient criteria for IBS

Adverse effects include bloating, flatulence, abdominal pain, diarrhea. These effects are most often with lactulose, because of its metabolism by colonic bacteria to carboxylic acids. Patients can also develop an aversion to sweet taste of lactulose.

(Gandell 2013)

Antacids containing calcium or aluminum

Calcium supplements

NSAIDs

Oral iron

Antihistamine

Opioids

CCB

Antiparkinsonian agents

Anticholinergic

Diuretics

Antipsychotics

TCA

Metabolic

-Diabetes

-Hypothyroidism

-Hypercalcemia

-Hypokalemia

GI

-CRC

-Stricture

Neurologic

-Stroke

-Parkinson disease

-Dementia

-MS

-Autonomic neuropathy

Psychiatric

-Depression

-Anxiety

-Somatization

Connective tissue

-Systemic sclerosis

-Amyloidosis

Family history of colorectal cancer

Hematochezia

Anemia

Weight loss ≥ 5 kg in previous 6 months

Positive result of fecal occult blood test

Persistent constipation unresponsive to treatment

Acute onset of constipation

Osmotic agents (lactulose, PEG, Mg, sodium phosphate)

Bulk agents (psyllium, methylcellulose)

Stimulants (sennosides, bisacodyl)

Stool softeners (docusate)

Prokinetic agents (prucalopride)

Enemas or suppositories

Guanylate cyclase C agonist (linaclotide)

Any complaint of difficulty passing stool, incomplete passage of stool, or diminished frequency.

Straining is the most commonly identified symptom.

-Ensuring adequate time to toilet

-Positioning knees at or above level of the hips for mechanical advantage

-Taking advantage of the gastrocolic reflex by guiding cognitively impaired patients to toilet following meal

-Biofeedback (electromyographic), for dyssynergistic defecation

No great evidence for physical activity or fluid intake, but still encouraged.

Decreased renal plasma flow

Decreased bladder contractility

Increased bladder overactivity

Decreased bladder capacity (lower voiding volumes)

Higher pressure threshold for voiding

Decreased detrusor muscle to collagen ratio

Impaired sphincteric function

Sympathetic (T10 - L2), via the hypogastric nerve (mostly storage function)

Parasympathetic (S2 - S4) via the pelvic splanchnic nerve (mostly voiding function)

Somatic (S2 - S4) via the pudendal nerve (controls the external urethral sphincter)

1. Identify the main symptom (frequency, straining, incomplete evacuation)

2. Look for secondary causes

3. Exclude fecal impaction

4. Optimize behavioural factors

5. Trial of dietary modifications

6. Trial of previously preferred laxatives, followed by other laxatives

1. Identify the issue

2. Identify appropriate measures that will allow use to test our hypothesis

3. Determine ideas to improve those measures

4. Test the idea using four steps

- Plan

- Do

- Study

- Act

5. Sustain - ensure the process is sustainable

Infection, erosion, UTIs, retention, incomplete resolution of symptoms.

Oxybutynin

Fesoterodine

Solifenacin

Tolterodine

Darifenacin

Mirabegron

Weight loss

Adequate fluid intake

Appropriately timed fluids

Dietary changes (avoid excess caffeine, alcohol, artificial sweeteners, concentrated sugars)

Behavioural strategies such as urge suppression, bladder retraining, appropriate containment products, manage constipation, strengthening pelvic floor muscles)

Prompted or timed voiding

Pelvic floor exercises

Pessary

Surgical procedures (e.g. mid-urethral sling)

Multi-component group/home-based exercises

Tai Chi

Multifactorial interventions, including individual risk assessment

Vitamin D (in trials that only enrolled patients with low vitamin D)

Home safety assessment/modification

Pacemakers in people with CSS

First eye cataract in women

Gradual withdrawal of psychotropic meds

Prescribing modification program for primary care physicians

Anti-slip shoe device in icy conditions

Multifaceted podiatry

(Cochrane 2012)

1. Address medical issues

2. Medication review

3. Assess fracture risk

4. Review home environment

5. Provide appropriate walking aid

6. Gait and balance exercise training

(Dr. Dian's slides)

1. Assess your community's needs

2. Establish your program's purpose, goals, and objectives. Goals should be quantitative with objectives that can be easily measured

3. Determine what risk factors your program will address (single intervention programs vs multifaceted intervention programs)

4. Collaborate with partners to address additional risk factors

5. Decide who will implement the various program components (physician, optometrist, NP, pharmacist, RN, PT, OT, SW, certified exercise instructor, Tai Chi instructor)

6. Find a location to conduct the program (home, physician's office, hospital/clinic, PT facility, pharmacy, seniors center, gym/fitness centre, senior housing facility)

7. Evaluate your program

8. Promote your program

9. Sustain your program

Falls

Pressure ulcers, perineal infections

Depression

Sexual dysfunction

Increased caregiver burden

(Up-to-date)

Hip fracture

Fear of future falls

Social isolation

Economic cost

Nursing home admission

Mortality

(Up-to-date)

Reduced falls, improved cognition (withdrawal of psychotropic drugs and benzos)

Fewer cardiovascular events and death (inappropriate antihypertensives)

Reduced emergency visits

Reduced annual mortality and referrals to acute care hospital in LTC (Garfinkel 2007)

Patient-reported global improvement in health (Garfinkel 2010)

Reduced days in hospital

1. Ascertain all drugs and the reasons for taking them

2. Consider overall risk of drug-induced harm in determining the required intensity of deprescribing intervention

3. Assess each drug for its eligibility to be discontinued

4. Prioritize drugs for discontinuation

5. Implement and monitor drug discontinuation regiment

(Scott IA. JAMA Int Med 2015)

Clinical complexity

Limited consultation time

Fragmented care among multiple prescribers, incomplete information (on past rationales for, and patient tolerance of drugs)

Ambiguous or changing care goals

Uncertainty about benefits and harms of continuing or discontinuing specific drugs

Community/professional attitudes toward more rather than less use of drugs

Fear of withdrawal effects

Recommendations within disease-specific clinical guidelines. Less applicable to older, multimorbid patients with polypharmacy.

(Scott IA. JAMA Int Med 2015)

Absorption

-not much change

-absorption of B12, calcium, and iron may be reduced, whereas absorption of levodopa may be increased

-reduction of salivary amylase may decrease buccal absorption

Distribution

-fat increases, water decreases

-water soluble drugs (digoxin) have smaller Vd, therefore higher concentration

-lipid soluble drugs (diazepam) have larger Vd, therefore longer half-life

-decreased albumin, which may increase serum levels of acidic drugs (furosemide, phenytoin, warfarin, salicylic acid)

Metabolism

-decreased liver mass

-decreased liver blood flow

-toxicity due to decreased metabolism

-decreased first-pass metabolism may increase bioavailability of drugs such as propanolol and labetalol. Some ACE inhibitors are prodrugs (enalapril and perindopril), and require activation in the liver. Their first-pass activation may be reduced.

Excretion

-decreased renal function

-increases half-life of many drugs (diuretics, digoxin)

Cardiovascular disease

Kidney disease

Liver disease

CNS disease

Bone disease

Non-AIDS-associated malignancies (cervical/anal carcinoma, HCC, EBV-related lymphoma, NHL, lung cancer)

May be 1) direct effect of HIV, 2) effect of traditional risk-factors in HIV-positive individuals, 3) effect of antiretroviral therapy.

(JAMA 2013)

1. Statins and protease inhibitors (increased statin exposure)

2. Benzodiazepines (midazolam, alprazolam, diazepam) and protease inhibitors and efavirenz (increased benzodiazepine exposure)

3. PPI and atazanavir (decreased atazanavir absorption)

4. Opiates (methadone) and ritonavir-boosted protease inhibitors (decreased methadone exposure)

5. Corticosteroids (systemic, inhaled, or intranasal) and ritonavir (increased fluticasone and budesonide exposure; decreased protease inhibitor exposure with dexamethasone)

6. Rivaroxaban and protease inhibitors (increased rivaroxaban)

7. Warfarin and protease inhibitors (increased or decreased warfarin effect)

(JAMA 2013)

Septra inhibits CYP 2C9, which increases risk of hypoglycemia with glyburide.

Clarithromycin is a P-glycoprotein inhibitor. Dabigatran is a substrate that has moderate affinity for the P-glycoprotein transport system. Leads to increased serum concentration of dabigatran.

Amiodarone enhances anticoagulant effect of warfarin. The primary mechanism of this interaction is likely related to the ability of amiodarone to inhibit one or more of the enzymes responsible for warfarin metabolism.

Inhibition of COX-2 in the kidneys, which reduces sodium excretion and increases intravascular volume

(Up-to-date: NSAIDs and acetaminophen: Effects on blood pressure and hypertension)

Carbemazepine reduces serum concentration of warfarin. Carbamazepine induces enzymes responsible for warfarin metabolism (CYP 1A2, CYP 3A4, CYP 2C9).

They both have FARM: fever, autonomic instability, rigidity, mental status changes.

Typical features in serotonin syndrome that are not often seen in NMS are shivering, hyperreflexia, myoclonus, and ataxia. Nausea, vomiting, and diarrhea are also a common part of the prodrome in serotonin syndrome, and are rarely described in NMS.

DIC, rhabdomyolysis, myoglobinuria, metabolic acidosis, renal failure, ARDS.

(Up-to-date)

Sluggishness, ataxia, confusion, tremor, agitation, seizure, encephalopathy, nephrogenic DI.

(Up-to-date)

1. Balance and strength (resistance) exercise

2. Individualized

3. Progressive

4. 2-3 times per week

5. Continued over 50 hours

6. Delivered by specially trained instructors

Functional Assessment Staging tool (FAST):

1. Stage 7c (unable to ambulate independently) or beyond on FAST.

2. Patient must have had at least one of the following in the last year (mnemonic: PAUSER)

i. Pressure ulcer, multiple, stage 3 or 4

ii. Aspiration pneumonia

iii. UTI (pyelonephritis or other upper UTI)

iv. Septicemia

vi. Eating problems, defined as food or fluid intake insufficient to sustain life

v. Recurrent fever after treatment with antibiotics

NEJM 2015 "Advanced Dementia"

Reduced number and duration of episodes of delirium in hospitalized older patients.

1. Functional status
2. Aortic aneurysm surgery
3. Thoracic surgery
4. Age > 70
5. Metabolic abnormalities (markedly abnormal sodium, potassium, glucose)
6. Alcohol abuse
7. Cognitive status

Mnemonic: FATAMAC

(JAMA 1994)

1. Sitting balance

2. Arises

3. Attempts to arise

4. Immediate standing balance

5. Standing balance

6. Nudged

7. Eyes closed

8. Turning 360 degrees

9. Sitting down

1. Initiation of gait

2. Step length and height

3. Step symmetry

4. Step continuity

5. Path

6. Trunk (amount of sway)

7. Walking stance (?wide-based)

Reduced FEV1

Reduced FVC

Reduced FEV1/FVC

Reduced DLco

Increased RV

Increased FRC

Reduced VO2max

Decreased MIP, MEP, SNIP

Consequences:

1. Increased frequency of pneumonia

2. Increased risk of hypoxia

3. Decreased max O2 uptake

1. Flexed posture

2. Reduced toe-floor clearance

3. Reduced length of stride

4. Slightly broad base

5. Excessive flexion at hips and knees

Brocklehurst chapter 16.

More fragmented sleep (periods of wakefulness)

Decreased sleep duration

Decreased slow wave sleep (stage 3/4)

Decreased REM sleep

Decreased sleep efficiency

Lower auditory awakening thresholds

Sleep desynchronized from circadian rhythm

Decreased hearing of higher frequencies

Decreased speech discrimination

Increased pure tone threshold averages

1. Prolonged hospital stay

2. Persistent cognitive impairment

3. Functional decline

4. Mortality

5. Admission to institution

On admission (Arch Int Med 1993):

1. Vision impairment

2. Severe illness

3. Cognitive impairment

4. BUN/Cr ratio high

During hospitalization (JAMA 1996):

1. Physical restraints

2. Malnutrition

3. Meds > 3

4. Bladder catheter

5. Iatrogenic event

Performance oriented mobility assessment (POMA)

Berg balance scale

TUG

Hierarchical assessment of balance and mobility (HABAM)

Functional reach

Dementia (OR 2.3, 95% CI1.4-3.7)

Vision impairment (OR 2.1, 95% CI 1.3-3.2)

Functional impairment (OR 1.7, 95% CI 1.2-3.0)

High comorbidity (OR 1.7, 95% CI 1.1-2.6)

Use of physical restraints during delirium (OR 3.2, 95% CI 1.9-5.2)

VPD-CF

Sun exposure

Diabetes

Alcohol

Steroids

Smoking

Metabolic syndrome

(Up-to-date)

Hypernatremia

Increased serum osmolality

Increased serum vasopressin

Decreased urine osmolality

NEJM 1984 Reduced Thirst after Water Deprivation in Healthy Elderly Men. Paddy P et al

1. Decreased renal tubular secretion of potassium

2. Obstructive uropathy can lead to renal tubular acidosis

3. Hyporeninemic hypoaldosteronism may occur in elderly, in association with diabetes and renal insufficiency

4. Drug-induced hyperkalemia

Blurred vision

Scotoma

Visual distortions (on Amsler grid)

Decreased contrast sensitivity

Abnormal dark adaptation

Need for brighter light or additional magnification to read small print

(NEJM 2008 review)

Dry AMD: gradual, insidious vision loss with central or pericentral scotomas, over months to years.

Wet AMD: may have sudden, profound visual loss within days to weeks as a result of subretinal hemorrhage or fluid accumulation secondary to choroidal neovascularization. Responsible for 80% of cases of severe visual loss or legal blindness from AMD.

(NEJM 2008 review)

Advanced age

White race

Heredity

History of smoking in the past 20 years

Obesity

High dietary intake of vegetable fat

Low dietary intake of antioxidants and zinc

Dry, or atrophic age-related MD - retinal pigment epithelium and choriocapillaris underlying the macula appears to degenerate, resulting in dysfunction of overlying photoreceptors.

Wet, or exudative age-related MD - neovascular net emanates under the macular region of the central retinal from choroidal circulation, proliferating between the retina and the underlying retinal pigment epithelium. Leakage of plasma components and frank subretinal hemorrhage or scarring cause loss of vision.

(NEJM review 2008)

1. Female gender

2. Not smoking

3. Moderation of alcohol

4. Dietary factors

5. Exercise

6. Genetics

7. Compressed morbidity

8. Compressed disability

9. Social factors (emphasis of time spent with friends and family)

High IL-6, IL-8, S-100 ß

High cortisol, CRP

Low IGF-1

(Khan, JAGS 2011)

Dry skin

Immunosenescence

Peripheral neuropathy

86% sensitivity, 93% specificity

(JAMA 2010)

The Likelihood Ratio (LR) is the likelihood that a given test result would be expected in a patient with the target disorder compared to the likelihood that that same result would be expected in a patient without the target disorder

Positive LR = sensitivity / (1-specificity)

Negative LR = (1-sensitivity) / specificity

Relative risk is the ratio of the probability of developing an outcome with vs without a given risk factor or intervention.

Attributable risk is the absolute difference in incidence between an exposed and unexposed group.

Aspiration pneumonia

Fracture

Dental and tongue injuries

Headache ← most common complication

Nausea

Memory loss (anterograde and retrograde amnesia)

(Up-to-date)

Unstable or severe cardiovascular disease
Space-occupying intracranial lesion with evidence of elevated intracranial pressure
Recent cerebral hemorrhage or stroke
Bleeding or otherwise unstable vascular aneurysm
Severe pulmonary condition
American Society of Anesthesiologists (ASA) Class 4 or 5

(Up-to-date: medical consultation for ECT)

Physical trauma

Malignancy

Chronic lung or kidney disease

HIV

Lymphoma (HL, NHL)

Patients on immunosuppressive therapy

1. Do you have decrease in libido

2. Do you have a lack of energy?

3. Do you have a decrease in strength or endurance?

4. Have you lost height?

5. Have you noticed a decreased “enjoyment in life”?

6. Are you sad and/or grumpy?

7. Have you noticed a recent deterioration in your ability to play sports?

8. Are you falling asleep after dinner?

9. Has there been a recent deterioration in your work performance?

If you answer yes to number 1 or 7 or if you answer yes to more than 3 questions, you may have low testosterone

Predisposing risk factors

1. Female gender

2. Widowed or divorced

3. Previous history of depression

4. Brain changes due to vascular problems

5. Personality type, such as avoidant or dependent personality and lifelong problems developing close relationships

6. Major physical and chronic disabling illnesses

7. Taking medications, such as centrally acting antihypertensive drugs (e.g. BB, CCB, digoxin), analgesics, steroids, antiparkinsonians, benzodiazepines, and antipsychotics

8. Excessive alcohol

9. Social factors (e.g. social disadvantage and low social support)

10. Providing care to a significant other person affected by a major disease (e.g. dementia)

Precipitating risk factors

1. Recent bereavement

2. Moving to an institution, such as nursing home, particularly in the first year of placement

3. Adverse life events (e.g. separation, losses, financial crisis)

4. Chronic stress associated with declining health, family, or marital problems and social isolation

5. Persistent sleep difficulties

(CCSMH 2006 2.1.1)

Cognitively intact: GDS, SELFCARE self-rating scale, and the Brief Assessment Schedule for the Elderly (BASDEC).

Cornell Scale for Depression in Dementia

Citalopram

Sertraline

Venlafaxine

Bupropion

Mirtazapine

Minimize dietary restrictions

Optimize energy intake (high energy foods at best meal of the day, eating smaller meals more often, eating favourite foods and snacks, providing finger foods)

Optimize and vary dietary texture

Avoid gas-producing foods

Ensure adequate oral health

Nutritional supplements

Take supplements between meals

Eat in company or with assistance

Use flavour enhancers

Participate in regular exercise

Take a multivitamin

Use community nutritional support services

(CMAJ 2005, unintentional weight loss in elderly patients)

Non-modifiable riskfactors

1. Old age

2. Male gender

3. Being widowed or divorced

4. Previous attempt at self harm

5. Losses (e.g. health, status, role, independence,significant relations)

Potentially modifiable

1. Social isolation

2. Presence of chronic painful condition

3. Abuse/misuses of alcohol or other medications

4. Presence and severity of depression

5. Presence of hopelessness and suicidal ideation

6. Access to means, especially firearms

(CCSMH 2006)

1. Agitation

2. Giving personal possessions away

3. Reviewing one's will

4. Increase in alcohol consumption

5. Non-compliance with medical treatment

6. Taking unnecessary risk

7. Preoccupation with death

(CCSMH 2006)

1. Excessive feelings of guilt not related to the deceased and self-devaluation

2. Psychomotor retardation

3. Active suicidal ideation (more than a passive wish to have died first or with the deceased)

4. Presence of mood-congruent delusions

5. Significant functional limitations impairing one’s routine daily activities beyond the first 2 months of the loss

6. Reaction out of proportion with the degree of loss

(CCSMH 2006, page 20)

1. Psychotic depression

2. MDD with need for rapid response

3. MDD with medical comorbidities that prevent the use of antidepressant medication

4. Previous response to ECT

5. Refractory or resistant to antidepressant therapy

6. Catatonia

7. Persistent suicidal intent

8. Bipolar depression or mania

(Up-to-date: overview of ECT for adults)

1. Sleep hygiene

2. Stimulus control

3. Relaxation strategies

4. Sleep restriction

1. Less likely to endorse feelings of sadness and/or guilt

2. Prominent somatic complaints

3. Loss of interest, apathy common

4. Anxiety, worry

5. Cognition impairment more likely

6. Unexplained functional impairment

FACADS: function, apathy, cognition, anxiety, depression (less), somatic

5 question GDS (2 out of 5 is considered a positive screen)

1. Are you basically satisfied with your life?

2. Do you often get bored?

3. Do you often feel hopeless?

4. Do you prefer to stay at home rather than going out and doing new things?

5. Do you feel pretty worthless the way you are now?

SHHWB - satisfied, hopeless, home, worthless, bored

OR 1.54, AR 1.2

(JAMA 2005)

Most deaths due to cardiovascular and infectious diseases.

Female
Recent adverse life events
Chronic physical and mental health disorders
Poverty
Parental loss or separation
Low affective support during childhood
Mental health problems in parent

1. Differentiates MCI from normal aging

2. Differentiates different types of dementia

3. Differentiates dementia from mood disorder

4. Following patient with MCI or subjective cognitive concerns over time

5. Assessing changes in cognition following TBI

6. Supporting patients or their families with behavioural strategies and education about their disease

(BCMJ 2011)

Behavioural therapy

CBT

Interpersonal therapy

Problem solving therapy

Reminiscence therapy

Brief psychodynamic therapy

(BCMJ 2017, and CCSMH 2006)

Probable MSA

Sporadic, progressive, adult (>30 y)- onset disease with:

1. Autonomic failure (urinary incontinence, erectile dysfunction, or orthostatic decrease of 30/15 AND

2. Poorly levodopa-responsive parkinsonism OR

3. Cerebellar syndrome

Possible MSA

Sporadic, progressive, adult (>30 y)- onset disease with:

1. Parkinsonism OR

2. Cerebellar syndrome AND

3. At least one feature suggesting autonomic dysfunction AND

4. At least one of the additional features of possible MSA-P or MSA-C

Possible MSA-P or MSA-C

1. Babinski sign with hyperreflexia

2. Stridor

Possible MSA-P

1. Rapidly progressive parkinsonism

2. Poor response to levodopa

3. Postural instability within 3 y of motor onset

4. Gait ataxia, cerebellar dysarthria, limb ataxia, or cerebellar oculomotor dysfunction

5. Dysphagia within 5 y of motor onset

6. Atrophy on MRI of putamen, middle cerebellar peduncle, pons, or cerebellum

7. Hypometabolism on FDG-PET in putamen, brainstem, or cerebellum

Possible MSA-C

1. Parkinsonism (bradykinesia and rigidity)

2. Atrophy on MRI of putamen, middle cerebellar peduncle, or pons

3. Hypometabolism on FDG-PET in putamen

4. Presynaptic nigrostriatal dopaminergic denervation on SPECT or PET

Second consensus statement on diagnosis of MSA. Neurology 2008.

2.8%

(Rising tide, 2010)

Higher education

Better vascular risk factor control

Changes in diet

Physical activity

(NEJM2016: Incidence of dementia over three decades)

1. Disinhibition

2. Apathy or inertia

3. Lack of empathy or sympathy

4. Perseverative, stereotyped, or compulsive/ritualistic behavior

5. Hyperorality and dietary changes

6. Neuropsychological profile: executive deficits, with relative sparing of memory and visuospatial deficits

1. Refer to a specialist and diagnostic centre with the expertise and access to diagnostic facilities to mount an organized and comprehensive diagnostic procedure.

2. Exclude delirium and other evident underlying causes.

3. Focus diagnostic strategy on reversible causes such as infections, immune-mediated, and toxic-metabolic causes.

1. Patient or proxy decides to stop

2. Non-adherent, and no way of rectifying the problem

3. Rate of cognitive, functional or behavioural decline is greater on the medication than prior to starting it

4. Side effects that are definitely or probably related to the CI

5. Comorbidities of the patient make continuation of the CI too risky or futile (e.g. terminally ill)

6. Dementia is at a stage where there would be no clinically meaningful benefit (e.g. GDS stage 7)

1. Similarities (conceptualization)

2. Verbal fluency

3. Luria test

4. Conflicting instructions

5. Go, no-go

6. Prehension behavior (do not take my hands)

1. Memory

2. Speech & language

3.Recognition of family members

4. Orientation to time

5. Orientation to place

6. Decision making ability

7. Social and community activity

8. Home activities and responsibilities (IADLs)

9.Personal care/cleanliness

10. Eating

11. Continence

12. Mobility

Cognitive training

Vascular risk factor modification (BP control)

Exercise

Diet (Mediterranean diet)

Treat comorbidities (hypothyroidism, depression)

1. Core clinical criteria provides good diagnostic accuracy and utility in most settings

2. More research needed to ensure properly designed criteria

3. No standardized values from one locale to another

4. Not readily accessible

5. Cost effectiveness (invasive, expensive, risk of false positives)

Stage1: No cognitive decline

· Experiences no problems in daily living.

Stage 2: Very mild cognitive decline

· Forgets names and locations of objects.

· May have trouble finding words.

Stage 3: Mild cognitive decline

· Has difficulty traveling to new locations.

· Has difficulty handling problems at work.

Stage 4: Moderate cognitive decline

· Has difficulty with complex tasks (finances, shopping, planning dinner for guests).

Stage 5: Moderately severe cognitive decline

· Needs help to choose clothing.

· Needs prompting to bathe.

Stage 6: Severe cognitive decline

· Loss of awareness of recent events and experiences.

· Requires assistance bathing; may have a fear of bathing.

· Has decreased ability to use the toilet or is incontinent.

Stage 7: Very severe cognitive decline

· Vocabulary becomes limited, eventually declining to single words.

· Loses ability to walk and sit.

· Requires help with eating.

Severe renal impairment

Severe hepatic impairment

Previous allergic reaction

Midlife obesity

High total cholesterol

High systolic blood pressure

Were all significant risk factors for dementia, with OR of 2 for each, and they increased the risk additively (OR 6.2 for the combination)

Syst-Eur. Lancet 1998. Prevention of dementia in randomised double-blind placebo-controlled Systolic Hypertension in Europe (Syst-Eur) trial

· Randomized to placebo, versus nitrendipine 10-40 mg daily, with possible addition of enalapril 5-20 mg and HCTZ 12.5 – 25 mg daily

· Target was to reduce SBP by at least 20 mm Hg to reach a value below 150 mmHg.

· 21 vs 11 patients (7.7 to 3.8 cases per 1000 patient-years)

PROGRESS. Arch Intern Med 2003. Effects of BP lowering with perindopril and indapamide therapy on dementia and cognitive decline in patients with cerebrovascular disease

1. Disclosure should begin as soon as possibility of cognitive impairment is suspected

2. Consider the disclosure as opportunity for education/discussion

3. Potential for adverse psychological consequences must be assessed and addressed through education

4. Disclose the diagnosis in a manner consistent with the expressed wishes of the patient

5. Follow-up plans must be made and discussed

CYP 3A4, 2D6.

3A4 inducers: carbamazepine, phenytoin, glucocorticoids, rifampin

2D6 inducers: dexamethasone, rifampin

CSF Aβ 42

CSF tau/p-tau

CSF Aβ oligomers

CSF dendritic protein neurogranin (a synaptic biomarker)

CSF presynaptic protein SNAP25

(Alzheimer's disease. Lancet 2016)

1. Attentional deficits

2. Executive dysfunction

3. Visuospatial dysfunction

4. Preserved confrontation naming, and short and medium term recall as well as recognition

5. Greater impairment on verbal fluency, visual perception and performance tasks

Serotonin and dopamine neurotransmitter deficiencies.

Antidepressants may improve behavioral symptoms in FTD, but not cognitive symptoms.

Antipsychotics have also been shown to decrease NPI score.

Explicit (or declarative) memory -"knowing what". Facts and events. Refers to memories that can be consciously recalled. Further divided into semantic and episodic memory.

Semantic memory - facts, meanings, concepts, and knowledge about the external world. Examples: types of food, capital cities, social customs, functions of objects, vocabulary.

Episodic memory - events and experiences.

Implicit (procedural) memory - "knowing how". The unconscious memory of skills and how to do things, like riding a bike, tying shoelace.

Wandering

Exit-seeking behaviours

Excessive noisiness

Inappropriate voiding

Hiding/hoarding

Inappropriate undressing

Eating inedible objects

(BC Best Practices for accommodating and managing BPSD in residential care, 2012)

Intrinsic risk factors:

1. Advanced age

2. Poor nutrition

3. Vascular disease

4. Immobility

5. Incontinence

Extrinsic risk factors

1. Pressure

2. Moisture

3. Shear force

4. Friction

1. Regular skin inspection

2. Supportive surfaces

3. Repositioning schedule

4. Nutrition

5. Staff education

6. Treat incontinence, wound drainage

US NIA description:

1. Weight loss

2. Decreased appetite and poor nutrition

3. Inactivity

4. Dehydration

5. Depressive symptoms

6. Impaired immune function

7. Low cholesterol

1. Lower frailty index

2. Fewer steps to do 180 degree turn

3. Higher Functional Independence Measure (FIM)

4. Higher score on MMSE; better ability to pass clock test

5. Higher serum albumin

Mnemonic: SCAFF (steps, cognition, albumin, FIM, frailty index)

(Age Ageing 2012; 41:242-246)

3 physical findings

1. Muscle wasting

2. Edema, ascites

3. BMI

4 biochemical markers

1. Low albumin

2. Low transthyretin (prealbumin)

3. Low transferrin

4. Lymphopenia

5 adverse outcomes

1. Death

2. Infections

3. Pressure sores

4. Falls

5. Fracture

(Royal College example questions)

Toileting needs

Delirium

Agitated depression

Social isolation

Hunger/thirst

1. Sensory enhancement/relaxation

2. Social contact

3. Structured activities (recreational, physical)

4. Environmental modifications (reduced stimulation)

5. Training of staff, family/caregivers

(BC Best Practices for accommodating and managing BPSD in residential care, 2012)

Psychotic features - use atypical antipsychotics

Without psychotic features - can use atypical antipsychotics, trazodone, citalopram, or sertraline

Sexual disinhibition - hormone therapy in men, SSRI, atypical antipsychotics

FTD - trazodone, SSRI

PDD or DLB - cholinesterase inhibitors as first line, and quetiapine if needed

(CCSMH 2006 LTC guidelines)

1. Executive dysfunction

2. Psychomotor slowing

3. Apathy

30-50 ml
Reassess 30-60 minutes after procedure
Objective measurements:
-Gait speed
-Stride length
-Number of steps to turn 180 or 360 degrees

(Up-to-date)

In order of increasing absorbance

Films

Gauze

Hydrogel

Hydrocolloid

Foam

Alginate

If infected, use silver

1. Wide based

2. Decreased step height and stride length

3. Feet turned outwards

4. Diminished cadence

5. Slow turn with several steps

6. No response to visual or verbal cues

(Up-to-date)

1. Improvement with CSF tap test

2. Known secondary cause (SAH, meningitis, aqueductal stenosis)

3. Mild amount of cognitive impairment

4. Gait disturbance preceded mental impairment

5. Short history of mental impairment

6. Absence of substantial white matter lesions

7. B-waves during > 50% of recording time on continuous ICP monitoring

1. Overdrainage causing headache

2. Shunt failure (blockage)

3. Bleed

4. Seizure

5. Shunt infection, meningitis

6. Arrhythmia from incorrect placement or systemic emboli (particularly for ventriculoatrial shunt)

Stage 1: Skin intact. Non-blanchable erythema

Stage 2: Partial thickness loss of dermis. Shallow open ulcer with a red/pink wound bed. May blister. No slough.

Stage 3: Full thickness skin loss. No bone, tendon or muscle visible or directly palpable. May have undermining/tunneling.

Stage 4: Full thickness tissue loss. Exposed bone, tendon or muscle. + slough or eschar. Often undermining/tunnelling.

Unstageable: Full thickness tissue loss in which the base of the ulcer is covered by slough and/or eschar in the wound bed.

Suspected deep tissue injury: purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying tissue from pressure and/or shear.

1. Odds of death at final follow-up (OR 0.81)

2. Odds of death or institutionalized care (OR 0.78)

3. Odds of death or dependency (OR 0.79)

Cochrane 2013: Organised inpatient (stroke unit) care for stroke

1. CSF flow void sign, especially in the aqueduct

2. White matter lesions, due to transependymal egress of fluid

3. Corpus callosum impingement

1. Cognition

2. Demonstration of carry-over

3. Ability to sit

4. Ability to transfer

5. Ability to perform ADLs

6. Medical stability

7. Urinary and bowel continence

(HFH admission guidelines)

University of California, San Francisco Criteria (UCSF, 2007)

1. Rapid cognitive decline

2. Two of the following six signs/symptoms

a. Myoclonus

b. Pyramidal/extrapyramidal dysfunction

c. Visual dysfunction

d. Cerebellar dysfunction

e. Akinetic mutism

f. Focal cortical signs (e.g. neglect, aphasia, acalculia, apraxia)

3. Typical EEG and/or MRI

4. Other investigations should not suggest an alternate diagnosis

Geshwind 2015. Continuum. Prion Diseases.

1. Tau-immunoreactive degenerative changes, distinct from other tauopathies such as AD, with preferential involvement of superficial cortical layers

2. Astrocytic tangles

3. Spindle-shaped and thread-like neurites

4. In 40% of causes, diffuse senile plaques (β-amyloid)

(McKee A. J Neuropathol Exp Neurol 2009;68(7):709-735)

1. Exercise

2. Nutrition interventions

3. Anxiety reduction

RPD defined as a dementia that develops within 12 months after first cognitive symptoms.

For individuals with AD, a decline of 3 or more points on MMSE in 6 months identifies a group with worse prognosis, and is a signal to explore co-morbid conditions and review pharmacological management.

(CCCDTD4, 2012)

EEG:

1-2 Hz period sharp-wave (often biphasic or triphasic) complexes in about two-thirds of cases

MRI DWI and ADC showing restricted diffusion in the cortical or deep nuclei gray matter.

-Cortical ribboning: abnormal hyperintensity on FLAIR and especially DWI in the cortical gyri

-Abnormal hyperintensity also in the caudate, putamen or thalamus. When striatum is involved, there is an anterior to posterior gradient of decreasing hyperintensity

1. Alcohol-Related Problems Survey (ARPS), specifically for geriatric population.

2. Alcohol Use Disorders Identification Test (AUDIT)

3. Self-Administed Michigan Alcoholism Screening Test (SMAST)

Men: < 2 drinks/day, < 7 drinks/week, < 4 drinks/occasion.

Women: < 1 drink/day, < 5 drinks/week, < 3 drinks/occasion.

(BCMJ 2011 Geriatric drinkers - evaluation and treatment foralcohol overuse)

1. Cognition

2. Acute or fluctuating illness

3. Neuromuscular disease or neurological affects

4. Drugs

5. Record (of accidents/violations)

6. In-car experiences (near accidents, unexplained car damage, change in driving skills, self-restriction, becoming lost, needing a copilot, etc)

7. Vision

8. Ethanol use

In general, a capable adult must be able to understand information and appreciate the consequences of decisions.

(Elder abuse practical guide 2011)

In other words, the 4Cs: need to understand the context, choices, consequences, and express their wishes with consistency.

1. The nature and effect of making a will.

2. The extent of the testator’s property that may be disposed by a will.

3. The persons who are to receive the property under the will, and the moral claims of persons (such as family members and others who are close to the testator) who should receive a share of that property.

4. The way in which the assets are to be distributed under the will.

(BCLI Consultation Paper on Common Law Tests of Capacity, Feb 2013, Page 25)

1. Condition for which health care needs to be provided to the adult

2. Nature of the health care that needs to be provided

3. Risks and benefits of receiving or not receiving the health care

4. That the information about the health care and the need for such health care applies to the situation of the adult

(Martha Donnelly's slides on Incapability assessments)

1. Dementia type (DLB or FTD are red flags)

2. Functional impact of the dementia/MCI

3. Family concerns (granddaughter question)

4. Visuospatial function (intersecting pentagons, clock drawing numbers)

5.Physical inability (neck turn, use of steering wheel/pedals, cardiac/neurologic issues)

6. Vision/visual fields

7. Drugs

8. Trailmaking A&B tests (>3 minutes or ≥ 3 errors on the Trails B test is unsafe)

9. Ruler drop reaction time test (12” ruler, normal is catch at 6-9”)

10. Judgment/insight

Pooled survival to discharge after in-hospital CPR was

70-79 yo: 18.7%

80-89 yo: 15.4%

90+: 11.6%

Of those who survive and are older than 80, only 20% were able to return to independent functioning outside institutionalized care.

At 1 year follow-up, the survival rate is somewhere between 7 - 21%

(Myke S. Age Ageing 2014;43:456-463)

1. The research question can be addressed only with participants within the identified group; and

2. The research does not expose the participants to more than minimal risk without the prospect of direct benefits for them; or

3. Where the research entails only minimal risk, it should at least have the prospect of providing benefits to participants or to a group that is the focus of the research and to which the participants belong.

Source: http://www.pre.ethics.gc.ca/eng/policy-politique/initiatives/tcps2-eptc2/chapter4-chapitre4/, article 4.6

Bruises, black eyes

Welts, rope marks

Swelling

Broken assistive devices

Lacerations

Punctures

Untreated injuries in various stages of healing

Fractures, sprains, dislocations

Unpaid bills

Sudden change in lifestyle and living conditions

No money for basic necessities

Absence of aids, medications, services

Refusing to spend money without permission of caregiver

Sudden appearance of previously uninvolved relatives

Abrupt changes in wills/accounts

Forged signature

Sudden sale or change in property title

1. Urge to move legs with/without uncomfortable and unpleasant sensation in the legs

2. Worse with inactivity

3. Better with activity

4. Worse towards the evening/night

5. Not accounted for by symptoms of another medical or behavioural condition

Anticholinergics, amantadine, DA, MAO-B and COMT inhibitors, and lastly, reduce levodopa.

(Canadian consensus guidelines 2012)

Presentation: bone pain, bone deformity, warmth over bone. Rarer presentations include deafness, hydrocephalus, high output HF, osteosarcoma.

Disease markers: ALP, P1NP

Indications for treatment: symptomatic. In asymptomatic patients, if skull, spine or long bone affected, or disease close to a major joint.

Treatment: alendronate 40 mg daily x 6 months, risedronate 30 mg daily x 2 months, or zoledronate 5 mg IV x 1

Resting tremor (PD)
Kinetic tremor (cerebellar)
Postural tremor (ET)

Propanolol

Primidone

Botox injection

Benzodiazepines

Shifting weight
Wider turns
Concentrating on taking a bigger step forward
Laser or L-shaped cane
Auditory cue (e.g. singing to a beat)

Motor symptoms (tremor, difficulty turning over)

Nocturia

Pain

Depression

Daytime somnolence

RLS

PLMS

Hallucinations

Nightmares

Constipation

OH

Urinary incontinence

Pain

Dementia

Depression

Psychosis

REMSBD

RLS

Fatigue

Olfactory dysfunction

Immobilization in sling

Ice

Analgesics

Iron-deficiency
Pregnancy
CKD
Alpha-synucleinopathies (MSA, PD, DLB)
MDD, GAD, panic disorder, ADHD

Recurrent fractures despite pharmacologic therapy.

Bone loss despite osteoporosis treatment.

Comorbid conditions that affect vitamin D absorption or action.

Periodontitis

Smoking

Glucocorticoid use

Diabetes

Bisphosphonates (used in oncology settings)

1. Compliance

2. Taking properly?

3. 25-OH-D levels

4. Calcium untake

5. Secondary causes - SPEP, pathological fracture?

Hypercalcemia

Primary or secondary hyperparathyroidism

Increased risk of osteosarcoma (Paget's disease of bone, history of prior RT)

Severe renal insufficiency

Prolonged mineralization lag time

Widened osteoid seams

Increased osteoid volume

Hypometric saccades

Impaired vestibuloocular reflex

Impaired upward gaze and convergence

Eyelid opening apraxia

Major RF:

i. Age ≥ 65

ii. Vertebral compression fracture

iii. Fragility fracture after age 40

iv. Family history of osteoporotic fracture

v. Systemic steroids > 3 months

vi. Malabsorption syndrome

vii. Primary hyperparathyroidism

viii. Propensity to fall

ix. Osteopenia on x-ray

x. Hypogonadism

xi. Early menopause (before age 45)

Minor RF:

i. RA

ii. Past history of clinical hyperthyroidism

iii. Chronic anticonvulsant use

iv. Low dietary calcium intake

v. Smoker

vi. Excess alcohol intake

vii. Excess caffeine

viii. Weight < 57 kg

ix. Weight loss 10% of weight at age 25

x. Chronic heparin use

Insomnia

Excessive daytime somnolence

REMSBD

RLS

Vascular parkinsonism:

1. Presents with postural instability and falls

2. Wider base of stance

3. Absence of festination

4. Pyramidal signs

5. Early subcortical dementia

6. Poor or non-sustained response to levodopa

7. Greater involvement of legs

1. Additional vertebral fracture(s) (>25% height loss with end-­plate disruption).

2. Previous wrist fracture in individuals older than age 65 or those with T-score ≤ -2.5.

3. Lumbar spine T-score much lower than femoral neck T-score.

4. Rapid bone loss.

5. Men on androgen deprivation therapy for prostate cancer.

6. Women on aromatase inhibitor therapy for breast cancer.

7. Long-term or repeated systemic glucocorticoid use (oral or parenteral) that does not meet the conventional criteria for recent prolonged systemic glucocorticoid use.

8. Recurrent falls defined as falling 2 or more times in the past 12 months.

9. Other disorders strongly associated with osteoporosis, rapid bone loss or fractures.

Benefits:

1. Blood pressure improvements

2. Reduced pain from OA

3. COPD symptoms and functional capacity

4. Cognition

5. Decreases falls

6. Decreases cardiovascular disease

7. Decreases depressive symptoms

Contraindications:

1. UA

2. Severe VHD

3. End stage CHF

4. Severe AS

5. BP > 200/110

6. Large or expanding aortic aneurysm

7. Known cerebral aneurysm or recent intracranial bleed

8. Uncontrolled or end-stage systemic disease

9. Acute retinal hemorrhage or recent ophthalmologic surgery

10. Acute or unstable MSK injury

11. Severe dementia or behavioural disturbance

Falls

Institutionalization

Mortality

Poor post-operative function

1. Weight loss (≥ 5% of body weight in last year)

2. Exhaustion (positive response to questions)

3. Weakness (decreased grip strength)

4. Slow walking speed (> 6-7 seconds to walk 15 feet)

5. Decreased physical activity (Kcals spent per week: males expending <383 Kcals and females < 270 Kcals)

ACE principles:

1. Early rehabilitation

2. Enhanced discharge planning

3. Frequent medical review

4. Patient-centred care

5. Prepared environment

Outcomes:

1. Decreased hospital cost

2. Decreased LOS

3. Increased discharge home

4. Decreased functional decline

5. Decreased delirium

6. Decreased falls

Healthy living with these behaviours can add 14 years of life:

1. Not smoking

2. Exercising

3. Eating fruits and vegetables

4. Drinking alcohol moderately

Triage Risk Screening Tool (TRST)

Oral phase

1. Chewing

2. Food retained in cheek pouches

3. Tongue movement

4. Saliva

5. Bolus formation

6. Drooling

Pharyngeal phase

1. Soft palate elevation

2. Vocal folds close

3. Hyoid bone and larynx pull upward and forward

4. Epiglottis tilts backward

5. Coughing

6. Change in voice quality

7. Pharyngeal clearance

1. Malnutrition

2. Dehydration

3. Aspiration

4. Social interaction

5. Airway obstruction

1. Patient has severe mobility disability

2. High risk of falls where environment assessment required

3. Severe and disruptive behaviour problem making clinic visit problematic

4. End-stage terminal illness

5. No access to transportation

6. Refuse to come into clinic but willing to be seen in home

1. At risk of losing independence

2. Few supports at home (social frailty)

3. Caregivers with caregiver burnout

4. Need for multidisciplinary support

5. Motivated to participate

1. Less likely to live in LTC
2. Lower mortality

3. Cognition

(BMJ 2011)

1. Favourable physical environment

2. Zero tolerance for ageism throughout the organization

3. ACE unit for patients above a certain age

4. Informed and shared decision-making

5. Fostering links between the hospital and the community

6. Focus on delirium management

7. Comanagement for patients in ortho, oncology, cardiac surgery

8. Comprehensive nutrition support program

9. Elder-assist program to navigate hospital services and appointments

10. Specialized unit for management of patients with BPSD

(CGJ “Moving Towards the Age-friendly Hosptial” by Huang 2011)

1. Orthopedics

2. Oncology

3. Stroke

Gait speed

Grip speed

1. Only looks at recorded time, not the patient's movements

2. Can't be performed in small areas

3. Footwear and assistive devices may alter test results unpredictably

4. Chair may alter test results unpredictably

5. Three meters may not be long enough

Financial
Physical
Psychological

1. Advanced age

2. Female

3. African American / Hispanic

4. Social isolation

5. Cognitive impairment

6. Physical impairment

7. Poor mental health of caregiver

8. Substance abuse

1. Does not prevent aspiration

2. Does not prevent complications of malnutrition

3. Does not prolong survival

4. Does not reduce risk of pressure sores or infx

5. Does not improve function

6. Does not improve comfort

7. Adverse effects of tube feeding including aspiration pneumonia, leaking, tube occlusion, and infection

Falls, institutionalization, death, disability.

Risk of death by 21.2% within 70 months, and entry into institution by 23.9%

Agitation

Fearfulness (especially in presence of caregiver)

Low self-esteem

Sleep disturbance

Withdrawal

Deference to caregiver

1. Transfer of patients from acute care to LTC

2. Excess use of antibiotics

3. Inadequate infection control precautions, facilitating spread

4. Risk factors for colonization/infection (percutaneous gastrostomy tubes, pressure ulcers, malnutrition, immunosuppression)

Acute: paresthesia, poikilothermia, paralysis, pulselessness, pallor, pain.

Chronic: lack of hair, thickened nails, shiny atrophic skin, ulcers, bruits/pulseless.

Infection

Bleeding

VTE

Delirium

Dislocation

Non-union

Chronic pain

1. Women are equally represented

2. Polyarticular

3. Upper extremities more often

4. Increased tophi

1. Severe hepatic impairment

2. Severe renal impairment

3. Concurrent use of CYP 3A4 inhibitor, in setting of hepatic or renal impairment

1. Increased collagen and structural changes in elastin

2. Prolonged availability of intracellular calcium causes persistent activation of contractile filaments

3. Increased vascular stiffness causes prolonged contraction time

4. Increased afterload leads to LVH

5. CAD

Age

Smoking

Diabetes

HTN

Dyslipidemia

1. Fractures secondary to tumour or infection

2. Loss of integrity of posterior vertebral cortex

3. Coagulopathy

4. Complete vertebral collapse

1. Handwashing protocol

2. Patient, family and staff education

3. Immunization program for staff and residents

4. Rapid confirmation of suspected cases

5. Isolation of suspected and confirmed cases

1. Patellofemoral instability

2. Patellar component loosening

3. Patella fracture

4. Extensor mechanism rupture (quadriceps or patellar tendon)

5. Periprosthetic fracture

6. Polyethylene wear

Determining an outbreak has occurred
1. Assess suspected cases, including obtaining specimens.
2. Establish a case description.
3. Begin a line-list.

Managing outbreak:
1. General infection control measures
2. Declare outbreak and notify local Medical Officer of Health
3. Notify other appropriate individuals
4. Identify new cases by surveillance of symptoms, obtaining specimens
5. Treatment and prophylaxis (antiviral)
6. Communications to residents, family, staff, volunteers

Index of elasticity of the arterial wall.

1. Debridement

2. Total joint arthroplasty

3. Joint resurfacing

1. Postural BP

2. Telemetry

3. ECG

4. Echocardiogram

5. Cardiac stress test

1. Decreased erythropoietin level (from decline in renal function)

2. Proinflammatory cytokines with age (IL-6)

3. Decrease in androgens

1. Absence of pain while seated

2. Improvement of pain when bending forward

3. Presence of bilateral buttock or leg pain

4. Wide-based gait

5. Abnormal Romberg

(JAMA 2010 RCE on lumbar spinal stenosis)

If patient never received pneumovax before, then give prevnar 13 followed by pnuemovax 23 8 weeks later.

If patient has already received pneumovax, then prevnar 13 should be given 1 year later.

Remove offending agents

Sedation with benzodiazepines

Supportive care (fluids, O2, monitoring)

Anti-serotonergic agent (cyproheptadine)

Adversedrug reaction (ADR) = noxious response to drugs used in usual doses for treatment/prevention.

Adverse drug event (ADE) = any injury that occurs from a drug, including noxious responses but also drug administration error.

Valacyclovir 1 g TID x 7 days

Validity: The extent to which an observation reflects the “truth” of the phenomenon being measured.

Three types of validity

1. Content validity: does a test measure all dimensions of a particular problem?

2. Construct validity: is the measure affirmed by an external established indicator?

3. Criterion validity: does the test predict an observable phenomenon. That is, does the test relate to the real world?

(Uptodate: Glossary of common biostatistical and epidemiological terms)

Strong, sustained and easily repeatable contraction.

Can be elicited by stimulation of areas other than the palm.

Whispered voice test.
Tone-emitting otoscope.

Average number of years that an individual is expected to live in a healthy state

1. Decreased diurnal variation in ADH

2. Redistribution of peripheral edema due to diastolic dysfunction

3. Autonomic neuropathy

4. Chronic kidney disease

5. Obstructive sleep apnea

Neovascularization

Growth into subretinal space, as opposed to drusen in the RPE

Age-related hearing loss. It is a true sensorineural hearing loss.

Three main types:

1. Sensory, characterized by loss of hair cells and a high-frequency hearing deficit.

2. Metabolic, characterized by loss of stria vascularis, and a low-frequency hearing deficit.

3. Neural, characterized by loss of ganglion cells and a variable pattern of hearing loss.

1. In QA, a cut‐off point is set that demarcates the border between acceptable and unacceptable quality whereas in QI the aim is to improve quality overall by reducing unnecessary variation and focusing on what happens most often rather than what happens relatively rarely.

2. In QA, outliers, that fall below the cut‐off point (and thus are deemed undesirable) are removed but QI strives to improve the system and its processes rather than trying to eliminate an outlier event and therefore thrives in learning environments.

3. In QA, statistically the remaining points tend to automatically redistribute into a bell‐shaped curve over time and thus outlying points reappear below the cut‐off point.

Process measures = what a provider does to maintain or improve health. E.g. the percentage of people with diabetes who had their blood sugar tested and controlled.

Outcome measures = the impact of the intervention on the health status of the patients. E.g. rate of surgical complications or hospital-acquired infections.

Likely to have complications, such as dysphagia due to strictures, Barrett's, hemorrhagic esophagitis, recurrent aspiration.

May also mimic angina.

1. Virus enters via monocytes that go across BBB.

2. Macrophages and microglial cells are key in pathogenesis.

3. HIV infects astrocytes.

4. Macrophage/microglial cells and altered cytokine/chemokine production lead to abnormal neuronal pruning.

1. NSAIDs including aspirin

2. Diuretics

3. Warfarin

(STOPP and START)

1. Simplified Nutritional Assessment Questionnaire (SNAQ)

2. Mini-nutritional assessment (MNA)

3. Malnutrition universal screening tool (MUST)

1. Dryness – pruritus

2. Reduced response of eccrine sweat glands – overheating

3. Loss of melanin – increased susceptibility to damage and cancer

1. Don’t use antimicrobials to treat bacteriuria unless specific symptoms are present

2. Don’t use benzodiazepines or other sedative-hypnotics as first choice for insomnia, agitation, or delirium

3. Don’t recommend percutaneous feeding tubes in advanced dementia

4. Don’t use antipsychotics as first choice for BPSD

5. Avoid medications known to cause hypoglycemia to achieve A1C < 7.5%. Moderate control is generally better.

1. Sedation

2. Headache

3. Dizziness

4. Dry mouth

(Lexicomp)

Diagnostic:

1. Dix-Hallpike

2. Side-lying test

3. Supine Head Roll test

Repositioning maneuvers

1. Epley

2. Semont

3. Brandt-Daroff

1. Repeated ≥2 HF hospitalizations in the last year

2. Progressive deterioration in renal function

3. Weight loss (cardiac cachexia)

4. Intolerance of ACEi because of hypotension or renal function

5. Intolerance of BB because of HF, hypotension

6. Persistent dyspnea with activities such as dressing, or bathing

7. Inability to walk one block on level ground

8. Need to escalate diuretics to maintain volume status; often furosemide > 160 mg, and/or need metolazone

9. Progressive decline in sodium < 133

10. Frequent ICD shocks

1 year mortality of 75%, no survival at 2 years

(J of Cardiac Failure 2015)

Multicomponent exercise program

1. Strength and balance training twice weekly

2. 150 mins or more of moderate intensity aerobic exercise weekly, in bouts of 10 minutes or more

(CGS CME Journal 2016)

1. International Physical Activity Questionnaire (IPAQ)

2. Rapid Assessment of Physical Activity (RAPA)

(CGS CME Journal 2016)

4D (causes associated with compensatory tachycardia)

1. Drugs (6 anti's - hypertensives, anginals, parkinson, depressants, psychotics, BPH)

2. Dehydration

3. Deconditioning

4. Dysfunctional heart (low EF, aortic stenosis)

AID (causes associated with lack of compensatory tachycardia)

1. Autonomic dysfunction (B12, thyroid, DM, amyloidosis, EtOH abuse, parkinsonism)

2. Idiopathic (Bradbury-Eggleston)

3. Drugs (beta-blockers)

(CGS CME Journal 2016)

Step 1: sleep log x 2-3 weeks

Step 2: calculate total sleep time average (TST)

Step 3: prescribe time in bed (TIB) = TST average

Step 4: qweekly, increased TIB by 15-20 minutes when sleep efficiency > 85%. Wake-up time is fixed. Bedtime should be no later than 2 am.

(CGS CME Journal 2016)

4 "izes or ises"

1. Temporize. Don't rush. R/o delirium. Ask caregiver to keep a diary of behaviours.

2. Optimize. Try ChEI and memantine.

3. Improvise. Try non-pharmacological strategies. Try antidepressants.

4. Compromise. If all else fails, try low dose risperidone, olanzapine, or aripiprazole.

(CGS CME Journal 2016)

1. Cognitive impairment

2. Peripheral neuropathy

3. Glossitis

4. Macrocytic anemia

5. Subacute combined degeneration

6. Depression

Romosozumab study.

Lower vertebral fractures at 12 months, RR 0.27, and after transition to denosumab, at 24 months.

Lower clinical fractures (clinical vertebral and non-vertebral), HR 0.64

No significant difference in non-vertebral fractures, but this may have been due to inclusion of Latin American geographical region, that had lower than expected rates of non-vertebral fractures.

295 patients, moderate to severe dementia, with donepezil for at least 3 months were randomized to:

Continue donepezil

Discontinue donepezil

Discontinue donepezil and start memantine

Continue donepezil and add memantine

Both donepezil and memantine were associated with cognitive and functional benefits at 1 year, but there was no additive benefit of combined therapy.

1. Decreased fast-twitch (type II) fibres

2. Decrease in GH levels

3. Decrease in IGF-1 levels

4. Change in sex hormones

5. Increase in cytokine levels (IL-6, TNF-alpha)

Advantages

1. Well tolerated

2. Few drug interactions

3. No monitoring

Disadvantages

1. Slow titration

2. Risk of SJS

3. Frequent rash

Complex attention

-Sustained attention

-Divided attention

Executive function

-Decision making

-Planning

Learning and memory

-immediate memory span

-recent memory

Language

-expressive language

-receptive language

Perceptual-motor

-visual perception

-praxis

-gnosis

Social cognition

-recognition of emotions

-theory of mind

1. Physical - pain and physical conditions.

2. Intellectual - understand losses from dementia (amnesia, aphasia, apathy, agnosia, apraxia, anosognosia, altered perception).

3. Emotional - consider adjustment disorder, depression, personality disorder, delusions.

4. Capabilities - ADL/IADLs.

5. Environment - consider over/understimulation.

6. Social - consider social network, life story, culture.

Fluid intelligence is the ability to solve new problems without any previous training.

-declines in normal aging

-due to decreased processing speed, attention, executive function

Crystallized intelligence is the amount of knowledge and information that one brings to the testing situation

-stable, or increases through life

-e.g. school-based knowledge, vocabulary, reading

1. Delayed colonic transit time.

2. Decreased number of high amplitude propagated contractions.

3. Higher sensory threshold to rectal distention.

1. Healthy elderly should target same glycemic, BP and lipid targets as younger people.

2. In the frail elderly, target A1C < or = 8.5%, and FPG 5-12.

3. Elderly with T2DM should do exercise

4. Caution with sulphonylureas. Start at half the dose.

5. Caution with thiazolidinediones, due to fracture and HF.

6. Clock draw test may be done to predict who will have trouble with insulin management.

1. Older age

2. Rigidity/hypokinesia as initial symptom

3. Comorbid stroke, auditory deficits, visual impairments

4. Postural instability/gait difficulty (PIGD)

5. Male

CROMP

1. Test-retest

2. Inter-rater

3. Parallel forms (administering different versions of an assessment tool to same group of individuals)

Pain

Gait and balance disorder

Reduced muscle strength

Neurological entrapment

1. Individualized, goal-oriented care plan based on person's preferences

2. Ongoing review of the person's goals and care plan

3. Support by an interprofessional team

4. One primary or lead point of contact on the healthcare team

5. Continual information sharing and integrated communication

JAGS 2016; 64(1)

Apraxia: inability to carry out purposeful, voluntary movements in the absence of motor and sensory deficit.

Agnosia: inability to process sensory information.

10% (Canada Public Health website)

1. Look for triggers for wandering (pain, toileting needs)

2. Keep objects associated with outdoors (keys, jackets, shoes) out of view

3. Re-locate door locks above eye level

4. Door alarm

5. Door mats that set off alarm

6. Review medications

7. Physical activity

8. Tell neighbors, nearby businesses, local police about the situation

9. Identification bracelet

10. Disguise the doors

1. Poor effort

2. Cognitive impairment

3. Predicted values may be based on younger patients

4. Decline in height may affect predicted values

5. Can't hear instructions

6. Can't form tight seal with lips

Asymmetric presentation of 2 of:

1. Limb rigidity or akinesia

2. Limb dystonia

3. Limb myoclonus

Plus 2 of:

1. Orobuccal or limb apraxia

2. Cortical sensory deficit

3. Alien limb phenomenon

OR 0.78, 95% CI 0.64-0.92

1,25-hydroxy-D binds to highly specific nuclear receptor in muscle, leading to improved muscle function.