Care of the elderly - the ageing process in a nutshell
Is ageing a natural state to be borne, a disease to be cured where possible or a natural event that can be considered as a disease where steps may be taken to lessen its adverse effects?1 The debate remains unresolved, although the latter view seems to be the most relevant to practice today. Whatever the best description of ageing, it is a fact that ageing affects most, if not all, of the bodies organs and systems. Importantly, ageing does not necessarily lead to impairment, because the body often successfully compensates for the associated changes. Set out below is an overview of the main systems affected by ageing. It is, however, worth remembering that ageing processes interact with each other and should not be considered in isolation.
Most heart cells (myocytes) lack the capacity for regeneration (ie, they are terminally differentiated). Myocytes lost through ageing are therefore not replaced, leading to hypertrophy of the remaining cells. This causes characteristic changes in the cardiac architecture resulting in stiffer and less compliant ventricles. This is not a problem at rest, because compensatory reduced early diastolic filling allows cardiac output to be maintained. However at times of reduced ventricular loading (eg, dehydration, blood loss, diuretic or vasodilator use) the compensation may not be enough and the change in cardiac architecture can become symptomatic.
Loss of the pacemaker cells in the sinoatrial node and the calcification of the conduction system contribute to the common rhythm disturbances seen in old age (eg, atrial fibrillation, sick sinus syndrome and heart block). As arterial walls age, collagen and elastin crosslink. This reduces compliance and contributes to the development of isolated systolic hypertension and left ventricular hypertrophy.2
Blood levels of catecholamines also rise with age. This desensitises the heart to noradrenergic stimulation and thereby limits the maximum achievable heart rate. Sodium conservation is decreased and baroreceptor response changed, alterations which can predispose individuals to orthostatic and postprandial hypotension. There are age-related changes in the response of the endothelium to physical and chemical stimuli that limit its vasodilatory properties.
Changes in hormonal levels play a large part in the ageing process.1,3 For women, the loss of oestrogen at the menopause is accompanied by long-term effects of increased cardiovascular disease, loss of bone mass and cognitive impairment. In men, testosterone decline is less universal but has been associated with muscle weakness, anaemia, lower bone mass and mood disturbances. The decrease in oestrogen and testosterone levels results from a reduction in their universal precursor in peripheral tissues — dehydroepiandrosterone [DHEA] and its sulphate [DHEAS] — and has been termed the “adrenopause”. The use of DHEA supplements is controversial but has been linked with wide-ranging reversal of the signs of ageing.
The synthesis of other hormones is also affected. Levels of growth hormone (GH) and insulin-like growth factor I (IGF-I) reduce with age. This (termed the “somatopause”) is associated with a decrease in muscle and bone mass and an increase in fat mass. Insulin secretion is impaired with age (reducing to 50 per cent of normal levels in those aged over 80 years), affecting both the early and late responses to glucose load. Peripheral insulin resistance is increased with age and combined with poor diet, physical inactivity (eg, as a result of decreased skeletal muscle mass and frailty) and decreased lean body mass, puts the elderly at high-risk of all the complications associated with diabetes.
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Citation: Hospital Pharmacist URI: 10977330
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