Chronic obstructive pulmonary disease (COPD see the first part) is a
nosological framework characterized by progressive airflow obstruction, not
fully reversible. This reduction of flow is usually associated with an abnormal
inflammatory response following inhalation of cigarette smoke and noxious gases
or particles. All patients with chronic cough and sputum with a history of
exposure to risk factors should be tested for the presence of bronchial
obstruction, even in the absence of dyspnea.
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Chronic obstructive pulmonary disease is a preventable and treatable disease
characterized by airflow limitation, not quite reversibile.Tale limitation is
usually progressive and associated with abnormal inflammatory response of the
lungs to noxious particles and gases, primarily cigarette smoke.
COPD affects the lungs as well as has important systemic consequences
It can distinguish the following clinical pictures (in fact we speak of bronchus
COPD:
Simple chronic bronchitis with excessive sputum from large airways, chronic
productive cough> 3 months / year> 2 years, if no obstruction: Stage 0
Chronic obstructive bronchiolitis, small airway obstruction with evident
inflammation;
Emphysema, ie destruction of alveolar walls with abnormal flaring of the air
spaces, loss of elasticity and airway obstruction.
...... From the clinical and pathophysiological bronchitis patients are
classically divided them:
type "pink puffer" dyspnoeic stress, thin, pulmonary hyperinflation, with
increased lung capacity and normal pulmonary artery pressure, hematocrit limits,
pan lobular emphysema.
type "blue bloater" Less dyspnoeic, obese, edematous lung capacity with normal
or slight increase, modest increase in pulmonary arterial pressure, hematocrit
increased in smokers in general, centrilobular emphysema is
Smoking is a major risk factor for the etiology of chronic bronchitis. There are
defense mechanisms that are represented by the activity of cilia of the
epithelium lining the airways, the physiological mechanism of bronchospasm and
activity scavengers made by cells called macrophages. But when such moments that
are causative turn to the clinical COPD, then become pigmented macrophages and
bronchiolar implement changes: edema, epithelial changes, fibrosis, mucus
hypersecretion and thus overlap with stagnation of mucus and bacterial infection,
and hypertrophy of mucous glands themselves and basal cells. The activity is
accentuated antielastica (inactivation of antiprotease inhibitor and mucus
dell'alfa1-antitrypsin). You can even arrive at the framework neoplastic process
hindered by cellular repair and inhibition of oxidative deamination of amino
groups.
.
Surely the basis of chronic bronchitis we have the manifestation of the
inflammatory process, which at one point, after repeated acute exacerbation of
COPD, it becomes irreversible.
Those were the facts, we can safely say that there are stages, ie clinical,
during which the patient gradually you start to complete disability, which is
the job of the specialist physician and pulmonologist, prevent, slow down and
treat different phases:
Impairment: namely the loss of normal respiratory function but also
psychological, physiological and anatomical structure of the individual harm
that can be quantized through instrumental measurements (spirometry) that are
reflected in a decrease of FEV1 and nell'intrappolamento air and loss of
peripheral muscle function, particularly in respiratory muscle chest and back.
Disability: refers to the inability to performa a respiratory activity in the
range of normality. This disability includes the reduction of dynamic function,
its restriction and physical performance. This phase is often characterized by
functional tests such as the walk up to 6 minutes or as the baseline and
transitional dyspnea Indexes.
Handicap: the disadvantage is that results from a "impariment or" disability "in
the sense that a business result disability if you can not change the
performance means it has developed a disability, ie a permanent reduction in
performance.
Natural history of COPD
Recognize the disease in terms of its natural history, although a long-term
variable and the resulting individual exposure to known risk factors and the
ability to genetically determined personal response, recognizing that
estrisencano different stages in the clinical manifestation through specific
signs and symptoms and a decline in lung function that is slow but inexorable,
determined by a chronic inflammation of the lung tissue that becomes, ultimately,
systemic disease, monitor through the markers of inflammation: polymorphonuclear
and PCR.
In this context, the exacerbations of the disease are sudden events that are
recognized and treated early because very damaging the economy overall
functional disease. This path is therefore characterized by clinical and
functional changes that must be recognized early in order to search through
un'approccio integrated therapeutic, to avoid the onset of the patient under
respiratory disability which constitutes a real handicap was respiratory
How to deal?
In the final stages overt respiratory disability, resulting from exacerbations
of COPD, it is still possible treatment with NIV, ie Non-Invasive Positive
Pressure Ventilation.
>>>see first page
>>>see also RICERCA