Periods of naturally increased susceptibility

There are times within a healthy lifespan when these barriers to disease are less effective. These can be seen as periods of naturally increased susceptibility to disease (see Q2.1a-4).

The three periods when a healthy person is more than usually susceptible to disease are during infancy, pregnancy and old age. In infancy, the barriers to disease, such as the immune system or the ability to maintain a steady body temperature, are not fully mature. In pregnancy, the vitality required to maintain the healthy barriers to disease is diverted to the growing fetus (e.g. calcium is diverted to the fetus and the mother’s teeth become more vulnerable to decay). In old age, all barriers to disease are in a state of degeneration (e.g. the skin and bones become less strong and are more vulnerable to damage by trauma).

Moreover, in ill-health susceptibility is increased because one or more of these barriers will not be functioning as they should be. The susceptibility that results from ill-health can be categorised as either congenital (dating from the time of birth) or acquired (developing at a later stage in life as a result of deficiency, disease or injury).

Congenital susceptibility

Congenital susceptibility means that one or more of the barriers to disease are not functioning well from birth (see Q2.1a-5). Examples of congenital disease conferring susceptibility include albinism, haemophilia and congenital heart disease. In albinism an inability to produce the skin pigment melanin leads to vulnerability to sunburn and skin cancer. In haemophilia an inability to produce sufficient blood-clotting proteins leads to vulnerability to bleeding into joints and muscles. In congenital heart disease poorly formed heart valves and gaps in the internal muscle wall of the heart lead to a vulnerability to poor heart pumping action, breathlessness and, over time, lung damage. The important congenital diseases are described in detail in Chapter 5.4c.

Some forms of congenital susceptibility are more subtle. Although a named inherited condition, such as cystic fibrosis, may not be present, it is clear that some people fall ill more often than others, and for some, this has been the case since infancy. The term ‘weak constitution’ might be applied in such a situation. This is because the inherited barriers to disease are not as strong as they could be, but are not so damaged as to constitute a named disease.

Acquired susceptibility

Acquired susceptibility is the consequence of a weakening of the barriers to disease after birth. Any one of the conventionally accepted causes of disease (Chapter 1.1e), such as poor diet, lack of exercise, obesity and smoking, is understood to contribute to increased susceptibility before disease is seen to occur.

For example, a long-term smoker may appear to be very fit but in fact is very likely to have sustained damage to a number of the barriers to disease, thus meaning that he or she has a higher risk of succumbing to disease. Reasons for this include the fact that smoking damages the protective lining of the lungs, so lung infections are more likely to take hold, and also that it impairs the free circulation of blood and increases the tendency of the blood to clot, which mean that diseases of the cardiovascular system such as heart attack are more likely to occur. However, the fact that some smokers do not develop smoking smoking-related diseases tells us that susceptibility is not the same as disease (see Q2.1a-6).

A smoker will always increase his or her risk of developing smoking-related disease by smoking because cigarette smoke invariably damages the lungs and circulation to some degree. If the smoker’s constitution is strong, the damage from smoking may not be so severe as to lead to a very high risk of disease, although his or her personal risk of disease has undoubtedly increased. A smoker with a poor constitution manifesting in weakness in the lungs or circulation (e.g. someone with asthma or diabetes) already has an increased risk of developing lung and heart disease. The risk of these diseases therefore becomes even higher if such a person smokes.

Nevertheless, both types of smoker may avoid disease, because other factors may be present that reduce susceptibility. For example, in the case of smokers, living in a warm, dry climate may reduce the risk of bronchitis, and eating a healthy, low-fat diet may reduce the risk of circulatory problems. Such factors are known as ‘protective factors’. Some protective factors may be far less easy to assess clinically than others. For example, personality traits such as a generally positive attitude or a calm approach to the vicissitudes of life may well be protective against illness.

Primary wound healing

Primary wound healing can take place when the edges of a cut or puncture are in close opposition. Figure 2.1b-I illustrates the three stages of primary wound healing. The edges of the wound ooze blood from the broken capillaries, and the blood rapidly forms into a clot in the confined space. The blood clot releases chemicals that stimulate the process of ‘chemotaxis’, i.e. the attraction of the cells of the immune system (the leukocytes) and the fibroblasts (the connective tissue repair cells) into the region of the clot. The phagocytic (‘engulfing’) leukocytes move into the clot and absorb and remove cell debris, dirt and bacteria. Fibroblasts lay down a delicate network of fibrous strands that begin to bridge the gap formed by the wound. Into this meshwork the broken ends of the capillaries start to re-grow a new network of tiny vessels so that this developing scar tissue has a rich blood supply. At the same time, the deepest layer of the epithelium of the broken skin grows through the upper regions of the blood clot to close the breach formed by the injury. This stage is one of proliferation, and when the fibrous and capillary network is sufficiently strong it causes the scab, the dried blood clot overlying the wound, to drop away, leaving the pink and delicate scar tissue protected by a layer of new epithelium beneath. The proliferative stage takes 5–30 days. Over the next few days to weeks the maturation phase involves the delicate scar tissue becoming strengthened and more organised due to increasing amounts of fibrous tissue. The initially complex network of tiny capillaries is simplified in this phase. At the end of this phase what remains is a stronger, more densely structured and paler tissue than the newly formed scar.

Figure 2.1b-I • The stages of primary wound healing (healing by first intention).

Secondary wound healing

Secondary wound healing is the process that takes place when the wound leaves a gap in both the skin and the underlying connective tissue. Figure 2.1b-II illustrates the three stages of secondary wound healing. As is the case with primary wound healing, the first stage is the lining of this breach with a blood clot originating from blood that has oozed from the remaining damaged tissue. The clot encourages the ingrowth of new fibrous tissue and capillaries and the appearance of phagocytic cells to remove debris and bacteria. This delicate new tissue is known as ‘granulation tissue’. This proliferative stage takes longer than the corresponding stage in primary wound healing, the time to healing being dependent on the size of the breach in the tissue, and the health and quality of blood supply to the underlying tissue. If foreign bodies (dirt) and bacteria are present they can be the focus for ongoing damage, and will further slow this stage of the healing process. The initially shallow layer of proliferating new tissue cannot yet be lined by epithelium and, once the scab drops away, it is instead covered by a moist yellowing layer of dead cells called ‘slough’. Like the old blood clot, slough continues to be a stimulus for the chemotaxis of fibroblasts, leukocytes and new capillaries. Once the new scar tissue reaches the level of the edges of the broken skin epithelium, the new epithelium can grow inwards, closing the breach by degrees. Any breach in an epithelium is called an ‘ulcer’, which means that secondary wound healing always involves the formation of an ulcer. Ideally, the ulcer is gradually reduced in size until it is has been closed over entirely by new epithelium. Following the closure of the ulcer the maturation phase continues to strengthen and organise the new fibrous tissue until the healed wound eventually appears as a pale, shiny patch of tough new scar (see Q2.1b-1 and Q2.1b-2).

Figure 2.1b-II • The stages of secondary wound healing (healing by second intention).

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