Give 3 reasons for the “squaring of the rectangle” ie. death almost exclusively in old age now vs. premature death
- less infant mortality
- better standard of living
- improved public health/sanitation
- improved diet
- modern medicine
Suggest why there is higher disability prevalence in old age.
- physiological ageing bring illness threshold closer
- acute illness has larger impact
- isolation/poverty
- increased burden of chronic illness
What does Frie’s Compression of Morbidity state for the years we add on to life expectancy…
-The years we add on to life expectancy…
…the period of suffering gets shorter
What is frailty?..the result of which leads to increased vulnerability to adverse outcomes
A physiological syndrome characterised by decreased reserve and resistance to stressors due to cumulative decline
Strehler’s concepts for a true ageing process vs. disease are universal, intrinsic, progressive and deleterious, explain each.
Universal: in all members of species
Intrinsic: changes of endogenous skin
Progressive: change continues with time
Deleterious: eventually harmful
The fact that the older age reached without disabiility = shorter period of dependency before death, should mean what clinically should we strive to do?
- postpone age of onset of disability as much as poss
- as this will prevent suffering
A healthy old age is possible. How should we manage disease vs death?
- postpone disease onset as much as poss
- do not postpone death in this way
Explain the Mutation Accumulation Theory of ageing (non-adaptive evolution)? “miscellaneous collection of late acting deleterious genes that accumulate over millenia…->ageing”
- powers of natural selection decline as we age
- early expressed genes effect most of population
- those expressed after repro are lost from evolutionary control
Explain the Antagonistic Pleiotropic Genes Theory of ageing (non-adaptive evolution)?
- gene has an early good effect so is retained
- but has a bad late effect that contributes to ageing
What is the “Disposable Soma” Theory of Ageing (builds on non-adaptive evolution)? Includes species specific longevity due to varying ecological niche/priorities
- organism as machine that takes free energy and makes progeny
- success is to ensure survival of genes in most efficient way
How can the 2nd law of Thermodynamics be applied to ageing?
-entropy increases, we should age and decay over time
What does the “Neuroendocrine Theory” say about HOW we age?
- functional decrease in neurones &hormones -> ageing
- HPA controls growth maybe controls ageing too
What does “cross link formation” mean as a cellular explanation of how we age?
-collagen cross-link formation alters the physical and chemical properties of cells
HSP are produced at times of cell stress, how are they implicated in how we age?
- they disassemble proteins and transport in new ones
- we have less HSP as we age
- we have a decreased ability to cope with stressors ->ageing
What was Haflick’s phenomena? Discovered by looking at fibroblasts grown in culture..aim to explain how we age..?
- showed the fibroblasts undergo a set no. of divisions then stop
- younger sources do more divisions
What are Geronto-Genes and Assurance-Genes in relation to ageing?
-Geronto-Genes: age quicker
-Assurance-Genes: slow ageing
Genetics play large role in life expectancy
How may Telomeres have a role in how/why we age?
- they stabilise chrsm in cell division
- they shorten with each division
- reach a critical limit when no more divisions can occur -> ageing
If Telomeres have a role in how we age by effecting cell division, how to cancer cells continue replicating? What other cell group have this ability?
Produce telomerase to re-expand the teleomeres
Germ cells
What does “error catastrophe” refer to as a genetic theory of how we age?
- transcrip/translation errors are corrected by replacing abnormal protein
- if abnormal protein is in the DNA repair chain -> cascade and cell death
- accumulation of the errors here -> ageing
Explain the Free Radical Theory of ageing (genetic)?
- free radicals from reactions damage cellular DNA
- whilst we have some protective enzymes, they decrease with age e.g. superoxide dismutase, vit E..
Explain the Mitochondrial Theory of ageing (genetic)?
ageing due to mt DNA damage via high exposure to O2 radicals as mt has no protein coat more damage
-mt dysfunction syndromes mimic ageing
What 2 methods have been tested to stop ageing?
- calorie restriction in rats (but delays puberty and more infections)
- moderate excercise, sexual activity (overcrowding bad)
What may older patients disadv. have with healthcare? Deferential? Support? Needs?
- accept Dr more, dont make own choice (deferential)
- impaired/fluctuating capacity
- more dependent of social/fam. support
- discriminated against
Where a patient lacks capacity what 2 questions should be asked?
- is there a valid LPA (lasting power of attourney)
- is there a valid AD (advance decision)
