Elderly Flashcards
when is end-of-life according to NICE guidelines
last year of someone’s life
what neurological changes occur when someone is dying
hypoactive delirium - reduced conscious, reduced response to verbal or visual stimuli
loss of pupillary reflex
changed breathing - Cheyennes stoke breathing (varying amplitude), apnoea (reduced O2)
fever
what neuromuscular changes occur when someone is dying
unable to close eyes
unable to swallow
neck hyper-extended
grunting sound when breathing (death rattle), using mandibular muscles to breathe
what cardiovascular changes occur when someone is dying
reduced blood pressure - can’t feel pulse
changed electrical activity of heart
reduced organ perfusion - skin mottling, low urine output
what are the 2 different types of ageing
chronological - measurement of age in years, constant rate for all
biological - progressive loss of function causing a decrease in physiological ability to meet demands of increasing chronological age
no standardised markers, not fixed rate
how do 2 people of the same age have different functional abilities
based on frailty
if old with high biological age = frail (when functionally dependent, so not Independent with ADL)
what occurs in IADL + PADL disability
IADL (independent ADL) disability = physical frailty, sarcopenia
PADL (personal activities of daily living) disability = disabled, loss of independence
how does inflammation cause biological ageing
with old age, immune response is mounted but not able to turn off
so there is low level inflammation (mild chronic elevation of IL6, TNF-a, CRP)
this low level inflammation can contribute to chronic diseases
what are 2 premature ageing syndromes
Werner = autosomal dominant, defective WRN gene (encodes DNA - so somatic DNA damage), onset in teens
more common
Hutchinson-gilford progeria = autosomal recessive, gene defect in lamina-A (abnormal nuclear structure/function), onset at 2yrs
summarise the different theories of ageing
1 - chronic, low-grade, sterile inflammation
2 - cellular senescence
3 - macromolecular dysfunction (accumulation of damaged DNA/proteins)
4 - stem-cell progenitor dysfunction
5 - non-genetic factors like nutrition/exercise affect rate of damage build-up
what is frailty
when no longer IADL
age related decline in multiple physiological symptoms
causing ‘at risk’ state, so - vulnerable to minor stresses, disproportionate change in health status
what abnormalities occur in __ system due to ageing
immune
endocrine
skeletal
immune - pro-inflammatory state as high IL6, CRP
endocrine - more catabolic state as high cortisol, but low GH/IGF1/sex hormones
skeletal - sarcopenia (loss of muscle mass/strength)
what is sarcopenia
progressive generalised skeletal muscle disorder, causing accelerated loss of muscle mass/function
muscle mass peaks in 40s then declines
if more catabolic than anabolic = overall loss of skeletal muscle (low mass + low strength = muscle failure)
does low muscle mass = sarcopenia (so frailty)
no sarcopenia (and frailty) = low muscle mass + low muscle strength
if low muscle mass alone = complex metabolic syndrome (malnutrition, cachexia)
what is deconditioning syndrome
prolonged bed rest and immobility causes syndrome of physical/psychological/functional decline
can affect any age but greater effect on old people as more rapid/severe and changes are irreversible
what are 2 frailty scoring systems
frailty phenotype by fried
- predefined set criteria with specific signs/symptoms
- clinical focus on sarcopenia and pre-disability
- categorical variable
- predetermined frailty cutoff
frailty index by rockall (clinical deficits out of 40, higher the score = more frail)
cut-off for frailty = 0.25 (upper threshold 0.67)
+ variable criteria according to pt comorbidities
+ multidimensional, including psychological/cognitive markers
+ continuous variable
- FI index too long (30 items) with varying cut-offs so unsure when to intervene
who is the clinical frailty score used for
65yr+
compare current state with baseline status (2wk prior to illness)
when is the clinical frailty score not useful
those with chronic disability
what is dementia
clinical syndrome
significant deterioration in cognition, causing functional impairment (measured by ADL functioning)
what are cognitive + behavioural symptoms of dementia
cognitive - poor memory, language difficulty, can’t plan or problem solve
behavioural - depressed/anxious, agitated, disinhibited, withdrawn
what are the 4 types of dementia
alzheimer (most common - ApoE4 gene)
B-amyloid plaques, abnormal tau protein, neurofibrillary tangles
progressive impaired memory loss (STM affected, can’t process new info)
vascular
abnormal cerebral vasculature - cerebral small vessel disease
stepwise progression, focal signs (stroke)
DLB/PD
alpha-synuclein plaque, reduced DA release from SN
parkinonism features - bradykinesia, unilateral tremor, rigidity)
Lewy body - visual hallucinations of small animals/people
frontotemporal dementia
atrophy of frontal/temporal lobes
personality change, disturbed behaviour
CJ disease - prion proteins
how is alzheimer diagnosed lab + imaging
B-amyloid deposition = low CSF AB, +ve amyloid on PET imaging
neuronal degeneration = high CSF tau, atrophy of medial temporal lobe, less FDG-PET uptake in temporoparietal cortices
what protects against dementia
high cognitive reserve = preserved cognitive function in later life
associated with:
education, socioeconomic factors
how is dementia investigated
clinical diagnosis with ICD10
cognitive assessment tools:
mini-cog at GP
AMTS, MMSE, ACE-III (addenbrokes cognitive assessment)
if ACE-III score 82-88 = mild cognitive impairment
if score 88+ = dementia
blood tests to exclude reversible cause:
FBC, UE, TFT, Ca, VitD, B12/B9, glucose
initial CT - tumour, stroke, chronic bleed
MRI gold standard - esp for prion disease CJD
how are different types of dementia managed
alzheimer = AChE inhibitor (donepezil, rivastigmine)
vascular = stop smoking, diet, aspirin/clopidogrel
PD = L-dopa with carbidopa (but less effective long term and risks motor symptoms - dystonia)
