Elderly Flashcards

1
Q

when is end-of-life according to NICE guidelines

A

last year of someone’s life

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2
Q

what neurological changes occur when someone is dying

A

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

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3
Q

what neuromuscular changes occur when someone is dying

A

unable to close eyes
unable to swallow
neck hyper-extended
grunting sound when breathing (death rattle), using mandibular muscles to breathe

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4
Q

what cardiovascular changes occur when someone is dying

A

reduced blood pressure - can’t feel pulse
changed electrical activity of heart
reduced organ perfusion - skin mottling, low urine output

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5
Q

what are the 2 different types of ageing

A

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

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6
Q

how do 2 people of the same age have different functional abilities

A

based on frailty
if old with high biological age = frail (when functionally dependent, so not Independent with ADL)

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7
Q

what occurs in IADL + PADL disability

A

IADL (independent ADL) disability = physical frailty, sarcopenia
PADL (personal activities of daily living) disability = disabled, loss of independence

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8
Q

how does inflammation cause biological ageing

A

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

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9
Q

what are 2 premature ageing syndromes

A

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

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10
Q

summarise the different theories of ageing

A

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

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11
Q

what is frailty

A

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

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12
Q

what abnormalities occur in __ system due to ageing
immune
endocrine
skeletal

A

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)

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13
Q

what is sarcopenia

A

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)

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14
Q

does low muscle mass = sarcopenia (so frailty)

A

no sarcopenia (and frailty) = low muscle mass + low muscle strength

if low muscle mass alone = complex metabolic syndrome (malnutrition, cachexia)

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15
Q

what is deconditioning syndrome

A

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

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16
Q

what are 2 frailty scoring systems

A

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

17
Q

who is the clinical frailty score used for

A

65yr+
compare current state with baseline status (2wk prior to illness)

18
Q

when is the clinical frailty score not useful

A

those with chronic disability

19
Q

what is dementia

A

clinical syndrome
significant deterioration in cognition, causing functional impairment (measured by ADL functioning)

20
Q

what are cognitive + behavioural symptoms of dementia

A

cognitive - poor memory, language difficulty, can’t plan or problem solve

behavioural - depressed/anxious, agitated, disinhibited, withdrawn

21
Q

what are the 4 types of dementia

A

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

22
Q

how is alzheimer diagnosed lab + imaging

A

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

23
Q

what protects against dementia

A

high cognitive reserve = preserved cognitive function in later life

associated with:
education, socioeconomic factors

24
Q

how is dementia investigated

A

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

25
Q

how are different types of dementia managed

A

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)