Geriatric Flashcards
Major NCD prevalence
1-2% in 65yo (2/10)
30% in 85yo (1/3)
F > M
Global deterioration scale (1-7)
Mild = 3 Major = 4
Mild NCD prevalence
10-20% in 65yo (1-2/10)
Mild NCD conversion rates
5-10% / year to AD
75-80% / 10 years
BUT
25-30% RETURN TO NORMAL
Mild NCD treatment
ACEi not helpful
TREAT HYPERTENSION (target < 140mmHg systolic) Healthy lifestyle
Treat depression: SSRI tx > 4 years can delay progression to AD by 3 years
Major NCD distribution
AD 50-60% Vascular 15-30% Lewy body 10-25% Mixed 10% FTD 5%
Normal pressure hydrocephalus
WACKY, WOBBLY, WET
Cognitive decline, gait disturbance, urinary incontinence
Pseudodementia
Secondary DD, hospitalization, fecaloma, sensory deficit
NOT IMMOBILIZATION
Abrupt, symptoms progress rapidly Distressed about symptoms Worst in the morning Improves with sleep deprivation "I don't know" instead of confabulation
Ribot’s Law
Gradient to retrograde amnesia
recent > remote memories
Proteinopathies
AD = amyloid plaque, neurofibrillary tangles, TAU
Pugilistica (secondary TBI) = amyloid plaque, neurofibrillary tangles, TAU
LBD/PD = alpha synuclein
FTD (Pick) = TAU, TDP-34, ubiquitine
Which dementia aetiologies don’t have neurofibrillary tangles?
Those secondary to repeated cerebral insult
- vascular
- due to substance
- due to HIV
- due to other medical diagnosis (infection)
Cortical dementias
Alzheimer’s
FTD (Pick’s)
CJD
AMNESIA (recall + recog) AGNOSIA APRAXIA APHASIA SEIZURES COUNTING (EARLY)
Subcortical dementias
Parkinson's dementia Huntington's dementia Wilson's dementia HIV dementia NPH dementia
Depletion Depression Dysexecutive Delay Dysmnesia (recall only) Dysarthria Dystonia Chorea Slowing Counting (LATE)
Mixte dementias (cortical + subcortical)
Vascular dementia
LBD
Alcohol dementia
Indications for genetic testing
< 65 yo + family history
6-7% of cases
PSEN1 = ch 14 (30-70%)
PSEN2 = ch 1 (< 5%)
APP = ch 21 (10-15%)
Mini cog
Repeat 3 words
Clock
Recall 3 words
0/3 = positive 1-2/3 = positive only if abnormal clock
MMSE
Ceiling (not sensitive if high education) + floor (not specific if very low score) effect
Cutoff 24/30
Sensitivity 82%
Specificity 87%
MOCA
Extra point if schooling < 13 years
Cutoff 26/30
More SENSITIVE than MMSE
What does FMRI measure?
OXYGENATION
What does PET measure?
Glucose metabolism
NO DECREASE IN THALAMIC TUMOR
What is CT scan better for?
Acute bleed
Calcium
Bone
Test for frontal function?
LURIA SERIE
Major NCD due to AD criteria?
At least 2 cognitive domains
Mild NCD due to AD criteria?
At least 1 domain
Alzheimer’s dementia prevalence
10% in 70yo
20% in > 70yo
Risk factors for AD
Age Women Low education Depression Increased homocysteine Increased estrogen Trisomy 21
Protective factors for AD
Education (> 15 years)
APO-E2
Blood pressure (< 140mmHg systolic)
Genes involved in late AD
APO-E4 on CHROMOSOME 19
E4/E4 RR 8-11
E4/E3-2 RR 3
SORL1
Extracellular pathology in AD
AMYLOID PLAQUES (beta 42)
Intracellular pathology AD
NEUROFIBRILLARY TANGLES (tau)
Neurotransmitters in AD
LOW ACETYLCHOLINE (low AChE, high BuChe)
LOW NOREPINEPHRINE
LOW SOMATOSTATIN
LOW CORTICOTROPINE
Most common hallucination in AD?
Visual
Mechanisms of vascular dementia
- Multiple cortical strokes
- Strategic stroke (anterior cerebral artery, thalamus, parietal lobe, singular gyrus)
- Lacunar strokes (small vessel disease)
Vascular dementia
Decreased complex attention
Decreased executive functioning
STEPWISE DECLINE rather than insidious
Risk factors:
Cerebral amyloid antipathy
CADASIL
Binswanger
Type of VASCULAR dementia Slowly progressing SUBCORTICAL vascular encephalopathy Chronic hypertension Pseudobulbar, parkinsonian, pyramidal sx
Lewy body dementia symptoms
CORE SX
- fluctuating cognition
- repeated visual hallucinations
- spontaneous Parkinsonism (more often symmetrical)
SUGGESTIVE SX
- REM sleep trouble
- Severe hypersensitivity to antipsychotics
Lewy body dementia criteria
Probable = 2 core OR 1 core + 1 suggestive
Possible = 1 core OR many suggestive
Other diagnostic elements of Lewy body dementia
Fall/syncope
Autonomic dysfunction
Delusions
Depression
Decreased dopamine in the basal ganglia
OCCIPITAL HYPOMETABOLISM ON PET
Fully formed “little” people or animals (lilliputian)
Parkinson Plus syndromes
- Corticobasal degenerescence
- Supranuclear progressive paralysis
- Multi-system atrophy
- Lewy body dementia
Corticobasal degenerescence
Strange limb
Fronto-parietal symptoms
Resistant to L-dopa
Asymmetrical rigidity
Supranuclear progressive paralysis
Symmetric Parkinson Supranuclear paralysis (can't look up) Postural problems Moderate response to L-dopa TAU disease
HUMMINGBIRD SIGN on imaging
Multi-system atrophy
Autonomic dysfunction Urinary incontinence Orthostatic hypotension Cerebella syndrome Decreased sensitivity to L-dopa
Frontotemporal dementia
Suspect if young (average age 56 yo)
Life expectancy 3-14 years after diagnosis
POST-SYNAPTIC SEROTONIN DEFICIT
Genes = TAU/TDP34
Chromosomes 9 & 17
Early personality & language changes
Preserved memory and visuospatial function
Frontotemporal dementia genes?
10-15% autosomal DOMINANT
MAPT
Granulin
C9orf72
Frontotemporal dementia types?
Behavioural variant (50%)
Language variant aka primary progressive aphasia (50%)
a) semantic
b) agrammatical/non-fluent
c) logopenic
FTD behavioral variant
M»_space;
BILATERAL ORBITOFRONTAL
At least 3 criteria
- disinhibition
- apathy
- lack of empathy
- stereotyped movements
- hyperorality
Pick’s disease - 40% familial
FTD language variant
a) Semantic
- M»_space;
- LEFT TEMPORAL LOBE atrophy
- trouble with naming + understanding
b) Agrammatical/non-fluent
- F >
- LEFT POSTERIOR FRONTOTEMPORAL
- trouble with naming + understanding
- lacks spontaneity in speech
c) Logopenic
- associated with Alzheimer’s
NCD secondary TBI treatment
Apathy: modafinil, psychostimulants, ADs that increase NE
Aggressivity: propranolol, pindolol, epival, tegretol
NOT ENOUGH EVIDENCE FOR NEUROLEPTICS
Risk factors for psych issues following TBI
Long period unconscious
Long period amnesia
Older age
CJD
CORTICAL
Prion disease
Classical pathology triad
- Spongiform vacuolisation
- Neuronal loss
- Astrocyte proliferation
Predominant cerebellar and motor symptoms
- myoclonus
- choreoathetoid movements
- ataxia
- ballistic movements
Anomaly in FLAIR/DWI MRI = multifocal hyper intensities of cortical grey matter (“cortical ribbon” sign)
Protein TAU or 14-3-3 in CSF
EEG = diffuse slowing, typical periodic sharp wave complexes (triphasic waves)
Huntington Chorea
Mutation on CHROMOSOME 4
Gene = IT15
Trinucleotide repetition CAG (cytosine-adenosine-guanine) > 36-40
of repeats correlates with cognitive symptoms but NOT WITH PSYCHIATRIC SYMPTOMS
Triad = MOTOR, PSYCHIATRIC, COGNITIVE
Atrophy of CAUDATE & lenticular nuclei (especially putamen then globus pallidus
NNT for ACEi?
4-13
2 types of cholinesterase?
Acetylcholinesterase (in synaptic cleft)
Butyrylcholinesterase
ACEi not indicated for?
Mild NCD
FTD
Being in a CHSLD is NOT a reason to stop treatment
RAMQ coverage for ACEi?
For MMSE 10-26
Stops if decrease of > 3 points in 6 months of tx
Contra-indications for ACEi?
Bundle branch block
Fascicular block
Interaction with OXYBUTYRIN (decreased efficacy)
DO ECG BEFORE STARTING
ACEi side effects?
GI (increased ulcer risk) Insomnia NIGHTMARES (especially Donepezil) Bradycardia (via VAGAL nerve stimulation) Syncope Urinary incontinence Neuromuscular
Aricept (Donepezil)
Selective inh. acetylcholinesterase
LIVER (2D6/3A4)
Half life = 70 hours
10mg DIE
Galantamine (Reminyl)
Inh. acetylcholinesterase + STIMULATES NICOTINIC
Liver + kidney
Half-life = 7-8 hours
16-24mg (DIE or BID dosing)
Rivastigmine (Exelon)
Inh. BOTH acetylcholinesterase + butyrylcholinesterase
Oral or transdermal
3-6mg BID
5-10mg patch
TAKE WITH FOOD
KIDNEYS
First choice for Lewy body dementia
Memantine (Ebixa)
ANTAGONIST NMDA RECEPTORS
(glutamate in excess in Alzheimer’s)
10mg BID
Side effects
Dizziness, headache, constipation
Contraindicated in RENAL FAILURE
RAMQ covers if MMSE 2-14 and NOT in CHSLD
RAMQ does NOT cover combination with ACEi
FTD treatment
NOT ACEi
Trazodone (irritability)
Paxil
Lewy body dementia treatment
RIVASTIGMINE which can decrease hallucinations
Avoid APs but if need SEROQUEL or CLOZAPINE
Parkinson’d dementia treatment
CLOZAPINE
Vascular dementia treatment
Not enough evidence for ACEi but if yes then Donepezil or Galantamine
BPSD
in > 90% patient with dementia
Only APs approved to treat are:
Risperdal
Abilify
Zyprexa
PRNs:
Trazodone
Ativan
Symptoms that don’t respond well to Rx:
- apathy (anterior cingulate)
- disinhibition
- wandering (“errance”)
- verbal
Try to decrease or stop Rx every 3-6 months
What is the #1 cause of psychotic symptoms in elderly?
DEMENTIA
What medication is NOT RECOMMENDED in BPSD
EPIVAL
Black box warning in elderly patients with dementia-related psychosis treated with atypical antipsychotic drugs
NNH = 100 (1 extra death per 100 patients)
RR death 1.6-1.7 (1% higher than placebo over 10 weeks)
RR stroke 10 (@ 1 week)
RR fall 1.7
RR pneumonia 4.5
DICE approach to non-pharmacological interventions
Describe
Investigate
Create a plan
Evaluate if working
Delirium criteria
ATTENTION AWARENESS \+ 1 OTHER COGNITIVE DOMAIN \+ Direct physiological consequence of illness/substance
Delirium types
Hyperactive 30%
Hypoactive 24%
Mixed 46%
What medication to give ventilated patients to prevent delirium?
PRECEDEX
dexmedetomidine
Risk factors for delirium?
>65yo Male Cognitive deficit Delirium hx Sensory deficit Immobilization Malnutrition Medical co-morbidity
Delirium prevalence?
1-2% in general population
10-30% in hospitalized population
Most implicated neurotransmitter in delirium?
ACETYLCHOLINE (decreased)
Most implicated brain region in delirium?
RETICULAR FORMATION (regulates attention and arousal)
Main pathway = dorsal tegmental (reticular formation and thalamus)
EEG in delirium
Generalized slowing (theta & delta)
Increased mortality in the year following delirium dx by how much?
40-50%
Pharmacokinetic changes in elderly
NO CHANGE IN ABSORPTION
Decreased gastric motility
Increased gastric pH
Increased fat stores (less liposoluble Rx)
Increased volume of distribution (increased 1/2 life)
Decreased CYP metabolism by 2-3x (linear with age, down first pass)
GLYCUROCONJUGAISON SAME (2nd pass)
Decreased albumin so increased free Rx
Decreased body water volume (more hypo soluble Rx)
Neurobiology changes in elderly
Decreased processing speed & motor speed
Decreased norepinephrine in CNS
Increased serotonin & MAO in brain
Suicide in the elderly
High res despite low rates of depression, due to solitude
DEMENTIA IS NOT A RISK FACTOR
Less explicit signs
Higher lethality (less history of past attempts)
Less contact with services
Emotions in the elderly
MORE POSITIVE EMOTIONS
Less negative emotions
Geriatric depression scale
30 Y or N questions about how they feel THAT DAY/OVER THE LAST WEEK
Target: healthy, medically ill, mild to moderate cognitive impairment
92% sensitivity
89% specificity
Cutoff is 10/30
(20 = severe)
Anticholinergic toxicity
Flushing, dry skin Mydriasis Loss of accommodation Tachycardia Hypertension Fever Urinary retention Functional ileus Tremor Myoclonic jerking Altered mental status
Rx causing delirium
Psychoactive medications Anticholinergic medications (MOST COMMON as per K&S) Sedative/hypnotics Meperidine (opioids) Corticosteroids
Which opioid is worst for delirium?
MEPERIDINE (demerol)
Delirium treatment
PHARMACOTHERAPY IS OFF-LABEL
Haldol (least anti-cholinergic)
Second-generation antipsychotic
Which genetic syndrome common in FTD?
KLUVER-BUCY
no hypersomnia unlike Kleine-Levin…think they have inappropriate sexual behaviour so they are UP ALL NIGHT
Which BPSD symptom responds best to antipsychotics?
AGGRESSION/agitation
Most common BPSD?
APATHY (72%)
Which dementia has NO TANGLES?
VASCULAR dementia
What percentage of dementias are reversible?
15%!
Hypothyroid, tumor, NPH, B12
Memory centres in brain?
Medial temporal lobe:
- hippocampus
- amygdala
Most commonly reported elder abuse in Canada
FINANCIAL (according to K&S)
Late-onset schizophrenia
Good response to antipsychotics, use lower doses
Generally negative symptoms are rarer in late-onset
Paranoid most common
Schizophrenia in >65yo
20% have no active symptoms by 65
Pharmacokinetics in elderly
Absorption largely unchanged No change in LFTs (reflect damage, not liver function) Unchanged conjugation (phase 2) Decreased phase 1 (oxidation, reduction, hydrolysis)
