18.06.2019 - Safir Şehir Portalı & Firma Rehberi Teması

Diseases of the cardiovascular system

Diseases of the cardiovascular system
Reklam

n Hypertension
Hypertension is a condition in which resting blood pressure is significantly
above normal levels (see Table 8.2).
Two broad causes of hypertension have been identified:

  1. Secondary hypertension: here, hypertension is the result of a disease process,
    usually involving the kidneys, adrenal glands or aorta. This type of
    hypertension accounts for about 5 percent of cases.
    THE CARDIOVASCULAR SYSTEM 231
  2. Essential (primary) hypertension: in the majority of cases, there is no
    known disease process that causes the problem. It seems to be the ‘normal’
    consequence of a number of risk factors, such as obesity, lack of exercise
    and a high salt intake. It is a progressive condition, and people with the
    condition usually experience a gradual rise in blood pressure over a period
    of years.
    Psychological stress may also contribute to the development of essential
    hypertension (e.g. Ming, Adler, Kessler et al. 2004). At times of stress, sympathetic
    activity increases muscle tone in the arteries and the strength of the
    heart’s contractions – both of which contribute to short-term increases in
    blood pressure, which then falls as parasympathetic activity follows a period
    of stress. If the stress is sustained or frequent, however, the activity of the
    sympathetic nervous system begins to dominate and gradually pushes blood
    pressure up for longer periods until the individual develops chronically raised
    blood pressure.
    Hypertension may be present and remain unnoticed for many years, or
    even decades. It is usually considered to be a syndrome with few if any symptoms,
    and many cases of hypertension are detected during routine screening
    (see Chapter 6). If high blood pressure has no symptoms, why bother treating
    it? At low levels of high blood pressure – mild hypertension – some have
    argued that medical treatment may actually be of little benefit, and that the
    side-effects of treatment may outweigh its benefits (although this position is
    now being challenged as new drugs are used to treat the condition: see Weber
    and Julius 1998). However, as blood pressure rises, so too does the amount
    of damage it can do. High blood pressure increases the risk of a heart attack
    (myocardial infarction; MI – see below), stroke, kidney failure, eye damage
    and heart failure. It also contributes to the development of atheroma,
    described below.
    Table 8.2 Typical blood pressure readings in normal and hypertensive individuals
    Diastolic (mmHg) Systolic (mmHg)
    Normal <90 <140 Mild hypertension 90–99 140–159 Hypertension >100 >160
    IN THE SPOTLIGHT
    The life and (heroic) death of John Henry
    John Henry was born a slave in the USA in the 1840s or 1850s. So what has he got to do with
    modern-day psychology? Well, legend has it that he was a giant of a man, who rose to any
    challenge he faced – a characteristic that eventually resulted in his death. He died while working
    as a labourer on the railroad tunnelling through a mountain in West Virginia. One of his
    jobs was to pound holes into rock, which were then filled with explosives and used to blast
    heart failure
    a state in which the
    heart muscle is
    damaged or weakened
    and is unable to
    generate a cardiac
    output sufficient to
    meet the demands of
    the body.
    continued
    232 CHAPTER 8 • THE BODY IN HEALTH AND ILLNESS
    n Coronary heart disease
    Like hypertension, coronary heart disease (CHD) is often a silent disease in
    that it may develop over many years before becoming evident. Indeed, people
    may have quite significant CHD and never be aware of their condition.
    The long-term, and silent, element of CHD is the development of atheroma
    in the blood vessels. This may result in more obvious manifestations of CHD,
    including an MI and angina (see below).
    Atheroma
    Atheroma is now understood to be the result of the process of damage and
    repair of artery walls and inflammatory processes involving the immune
    system. One of the key constituents of atheroma is cholesterol. This is a waxy
    substance that is present in blood plasma and in all animal tissues. It is also
    a key chemical in the body. Without it, cells throughout the body could not
    maintain the integrity of their walls, and we would become seriously ill or
    die. Too much cholesterol, on the other hand, may be harmful.
    To get to body cell walls in order to repair and maintain them, cholesterol
    must be transported through the body – via the bloodstream. However, it
    is insoluble in the blood. To allow such transport, it is therefore attached
    to groups of proteins called lipoproteins. Low-density lipoproteins (LDLs)
    transport cholesterol to the various tissues and body cells, where it is
    separated from the lipoprotein and is used by the cell. It can also be absorbed
    into atheroma on the inner surface of the blood vessels. High-density lipoproteins
    (HDLs) transport excess or unused cholesterol from the tissues back
    to the liver, where it is broken down to bile acids and is then excreted. LDLs
    are therefore characterised as ‘harmful’ cholesterol: HDLs are considered to
    be health-protective. Although some cholesterol is absorbed from our food
    through the gut, about 80 percent of cholesterol in our bodies is produced by
    the liver.
    The development of atherosclerosis:
    through tunnels. When the railroad owners brought in steam drills to do the same job more
    quickly and cheaply, he challenged the steam drill to a contest. He won the contest but died
    of exhaustion soon after. His name has now become synonymous with a process, initially at
    least, thought to drive hypertension in black males – John Henryism.
    Hypertension is particularly prevalent in African Americans. Black people in the USA are
    up to four times more likely than whites to develop hypertension by the age of 50 (Roberts
    and Rowland 1981). One of the reasons for this is thought to be that black people are more
    frequently placed in situations of high effort coping with difficult psychological stressors –
    poverty, racism, and so on – than their white counterparts. This chronic high effort coping
    results in chronic and sustained increases in heart rate and blood pressure. This, in turn, overcomes
    the body’s homeostatic processes and pushes the resting blood pressure increasingly up
    until they develop long-term hypertension. Although initially viewed as an issue for black
    men, the process is increasingly being seen as the outcome of the stresses associated with low
    socio-economic position – and may account for some of the health inequalities considered in
    Chapter 2.
    low-density lipoprotein
    (LDL)
    the main function of
    LDLs seems to be to
    carry cholesterol to
    various tissues
    throughout the body.
    LDLs are sometimes
    referred to as ‘bad’
    cholesterol because
    elevated levels of LDL
    correlate most directly
    with coronary heart
    disease.
    high-density lipoprotein
    (HDL)
    lipoproteins are fat
    protein complexes in
    the blood that transport
    cholesterol, triglycerides
    and other lipids to
    various tissues. The
    main function of HDL
    appears to be to carry
    excess cholesterol to the
    liver for ‘re-packaging’
    or excretion in the bile.
    Higher levels of HDL
    seem to be protective
    against CHD, so HDL is
    sometimes referred to
    as ‘good’ cholesterol.
    THE CARDIOVASCULAR SYSTEM 233
  3. Early atherosclerosis: fatty streaks are laid down in artery walls. These
    usually occur at sites of disturbed blood flow, such as bifurcations of
    arteries. They occur as part of a repair process to damage of the artery wall
    caused by the disturbed blood flow and increases in pressure associated
    with high blood pressure linked to sympathetic activation. In this process,
    inflammatory monocytes, which are precursors to macrophages (see the
    section on the immune system earlier in the chapter), absorb LDL cholesterol
    from the circulating blood to become what are known as foam cells.
    These form a coat over the lining of the damaged artery. As the foam cells
    die, they lose their contents of LDL, resulting in pools of cholesterol forming
    between the foam cells and the artery wall. The presence of foam cells
    may trigger the growth of smooth muscle cells from the artery wall to
    cover them. In this way, the walls of the artery are lined with lipids, foam
    cells and finally a wall of smooth muscle. This process results in a gradual
    reduction of the diameter of the artery.
  4. Later atherosclerosis: the progress of atherosclerosis is determined by the
    relative influence of the inflammatory monocytes and development of
    smooth muscle. Monocytes and their subsequent foam cells add to the
    development of atherosclerosis; the building of smooth muscle repairs the
    artery and provides a smooth artery wall – albeit of decreasing diameter.
    At times, clots of cholesterol and foam cells may be pulled out of the artery
    wall, resulting in two potential outcomes:
    n A clot blocks an artery in a key organ such as the heart, resulting in a
    myocardial infarcation (MI) (see below).
    n The damage to the artery wall initiates acute repair processes, including
    the deposition of platelets around the damage site, before more smooth
    muscle cells build over the damage – dramatically increasing the degree
    of occlusion of the artery.
    The distribution of atheroma within the circulatory system is not uniform
    throughout the body. It may be most developed around the junctions of
    arteries because disturbances in blood flow at such points can facilitate these
    processes, but the heart arteries are also one of the areas most likely to be
    affected.
    n Acute manifestations of CHD
    Myocardial infarction
    As we noted earlier in the chapter, an important end-point of CHD is when
    a clot is pulled off an artery wall and enters the circulating blood. This may
    prove a harmless event, with no health implications for the individual.
    However, if the circulating clot has a greater diameter than the blood vessels
    it is passing through, it will inevitably block such blood vessels and prevent
    the flow of blood beyond them. This blockage (occlusion) may result in
    significant health problems if it occurs in the arteries supplying oxygen and
    nutrients to the heart. Unless rapidly treated, the cells of the heart muscle no
    longer receive their nutrients and oxygen will die – a process known as an
    MI. The severity of damage that will occur as a consequence of this is determined
    by how large a blood vessel is affected (larger is worse) and which
    parts of the heart are damaged.
    234 CHAPTER 8 • THE BODY IN HEALTH AND ILLNESS
    The classic symptoms of an MI include what is often called a ‘crushing
    chest pain’. The affected individual may feel like their chest is trapped in a
    vice. Other symptoms include shortness of breath, coughing, pain radiating
    down the left arm, dizziness and or collapse, nausea or vomiting, and
    sweating. An MI may also be much less dramatic. Indeed, many people delay
    seeking help for an MI as their symptoms are vague, may be confused with
    heartburn or indigestion, and the affected individual hopes that the symptoms
    will go away without treatment. Perhaps the strangest symptom that
    can rarely be indicative of an MI is toothache – although we would not recommend
    you visit your local hospital complaining of a heart attack should you
    be unfortunate enough to develop this problem! Approximately 45 percent
    of people will die of their MI immediately or in the week or so following the
    event. The majority of people go on to make a good recovery. This may be
    aided by treatment with drugs known as ‘clot busters’. These drugs dissolve
    the clot causing the blocked artery and, if given within an hour or so of the
    infarction, can prevent the permanent muscle damage that will occur if they
    are not given.
    IN THE SPOTLIGHT
    According to the Royal College of Physicians, giving clot-busting drugs saves about thirty
    lives per 1,000 patients treated. They estimate that this proportion could be increased,
    perhaps up to sixty-five per 1,000, if treatment is started within the first hour after onset of
    symptoms. The problem is that only about 55 percent of patients with an MI are admitted
    into hospital – where they can receive medical treatment – within one hour of its onset,
    rendering such drugs of little benefit.
    We know that one of the most important reasons for delay is because patients are not sure
    their symptoms are serious – and that they are more likely to seek medical help if there is
    someone with them at the time of their onset. Most of us are aware of the acute and dramatic
    symptoms that may signal a myocardial infarction. However, we may be less aware of the
    potentially rather vague symptoms that may accompany one. Of course, over-responding to
    such symptoms may result in health services being overwhelmed by the ‘worried well’. So the
    health services have a clear dilemma: educate the public that a myocardial infarction may be
    associated with vague symptoms, including feeling nauseous, weak, vague discomfort in the
    chest, and there is the potential for overuse of health services. Don’t warn the public, and
    many people may delay seeking treatment until it is too late. Appropriate education of the
    public is not easy.
    However, there is another way in which treatment speed can be increased. Delay can be
    broken into two components. Patient delay in contacting the health service, and the delay
    between the ambulance call and them actually receiving treatment – usually in hospital. An
    alternative and potentially more attractive way of minimising the delay between onset and
    this specific treatment is to allow emergency ambulance personnel to treat patients using clot
    busters. While it has its obvious benefits, and this issue is now being considered within the
    emergency services, this also has a number of problems. In particular, treatment requires
    ambulance personnel to make a diagnosis, and to give a drug with potentially negative sideeffects.
    These responsibilities usually lie with medical staff, who cannot go to all emergencies.
    Whether they will eventually come within the remit of ambulance personnel – and potentially
    save lives – is a topic of hot debate.
Reklam
BU KONUYU SOSYAL MEDYA HESAPLARINDA PAYLAŞ
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