Question

Performance criteria
Q1	In your own words, explain the pathophysiology of COPD and how it affects Jim.
Chronic obstructive pulmonary disease, or COPD, refer to chronic lung diseases that makes breathing difficulty. It is a progressive condition, meaning that it gets worse over the passage of time. COPD has a several of effects on the lungs that reduce their capability to take in oxygen and distribute it to organs in the bloodstream. COPD normally causes coughing that produces large amounts of mucus, shortness of breath, and other symptoms. This is a good definition but we need pathophysiology – whats happening to the alveoli ? why does it make breathing difficult?

Answer 1

Chronic obstructive pulmonary disease

Alveoli are the very small air sacs where the exchange of oxygen and carbon dioxide takes place. Capillaries are blood vessels in the walls of the alveoli. Blood passes through the capillaries.

Pathology

Chronic obstructive pulmonary disease (COPD) is characterised by poorly reversible airflow obstruction and an peculiar inflammatory response in the lungs. The latter represents the innate and adaptive immune responses to long time period exposure to noxious particles and gases, specially cigarette smoke. All cigarette smokers have some inflammation in their lungs,however those who develop COPD have an enhanced or unusual response to inhaling toxic agents. This amplified response may additionally result in mucous hypersecretion (chronic bronchitis), tissue destruction (emphysema), and disruption of normal repair and defence mechanisms inflicting small airway inflammation and fibrosis (bronchiolitis).These patpathologi changes end result in expanded resistance to airflow in the small conducting airways, multiplied compliance of the lungs, air trapping, and modern characterstic elements of COPD. We have appropriate perception of the Cell and molecular mechanisms underlying the pathological adjustments.

Psthophysiology

The above pathogenic mechanisms end result in the  changes discovered in COPD. These in flip result in physiological abnormalities—mucous hypersecretion and ciliary dysfunction, airflow obstruction and hyperinflation, gasoline alternate abnormalities, pulmonary hypertension, and systemic effects.​

Airflow obstruction and air trapping (hyperinflation)

The main site of airflow obstruction takes place in the small conducting airways that are < two mm in diameter. This is due to the inflammation and narrowing (airway remodelling) and inflammatory exudates in the small airways. Other elements contributing to airflow obstruction encompass loss of the lung elastic decrease returned (due to destruction of alveolar walls) and destruction of alveolar guide (from alveolar attachments).The airway obstruction regularly traps air throughout expiration, ensuing in hyperinflation at relaxation and dynamic hyperinflation in the course of exercise. Hyperinflation reduces the inspiratory capacity and consequently the functional residual capability at some point of exercise. These points end result in breathlessness and restrained exercise capacity usual of COPD. The airflow obstruction in COPD is great measured by means of spirometry and is a prerequisite for its diagnosis.

Gas exchange abnormalities

These take place in superior disorder and are characterised with the aid of arterial hypoxaemia with or without hypercapnia.A peculiar distribution of ventilation:perfusion ratios—due to the anatomical modifications discovered in COPD—is the predominant mechanism for abnormal gas exchange. The extent of impairment of diffusing ability for carbon monoxide per litre of alveolar extent correlates well with the severity of emphysema.

Psthophysiology of exacerbations

Exacerbations are often associated with increased neutrophilic inflammation and, in some mild exacerbations, increased numbers of eosinophils. Exacerbations can be caused by infection (bacterial or viral), air pollution, and changes in ambient temperature.

In mild exacerbations, airflow obstruction is unchanged or only slightly increased. Severe exacerbations are associated with worsening of pulmonary gas exchange due to increased inequality between ventilation and perfusion and subsequent respiratory muscle fatigue. The worsening ventilation-perfusion relation results from airway inflammation, oedema, mucous hypersecretion, and bronchoconstriction. These reduce ventilation and cause hypoxic vasoconstriction of pulmonary arterioles, which in turn impairs perfusion.

Respiratory muscle fatigue and alveolar hypoventilation can contribute to hypoxaemia, hypercapnia, and respiratory acidosis, and lead to severe respiratory failure and death. Hypoxia and respiratory acidosis can induce pulmonary vasoconstriction, which increases the load on the right ventricle and, together with renal and hormonal changes, results in peripheral oedema.

* In people with COPD, the air sacs no longer jump back to their authentic shape. The airways can additionally grow to be swollen or thicker than normal  and mucous production may increase. The floppy airways are in part blocked, or obstructed, making it even more difficult to get air out of the lungs.