Why is chronic bronchitis blue bloater

Antismoking measures are a major aim in management. A bronchodilator regimen combining a slow-release oral theophylline with an inhaled beta 2-agonist, ipratropium, and high-dose inhaled steroids is proposed because even modest improvement in obstruction can help these patients.

In acute exacerbations with purulent sputum, antimicrobials against Streptococcus pneumoniae and Hemophilus influenzae are used with controlled oxygen therapy aiming to keep the arterial PO2 over 50 mm Hg without the pH falling below 7.

Influenza prophylaxis is recommended, but pneumococcal vaccination remains debatable. Clinical signs at the fingers include cigarette stains although actually tar and asterixis metabolic flap at the wrist if they are carbon dioxide retainers NOTE: finger clubbing is NOT a general feature of emphysema. Examination of the face reveals a plethoric complexion if there is a secondary polycythemia , pursed-lipped breathing, and central cyanosis.

Examination of the chest reveals increased percussion notes particularly over the liver and a difficult to palpate apex beat all due to hyperinflation , decreased breath sounds, audible expiratory wheeze, as well as signs of fluid overload seen in advanced disease such as pitting peripheral edema. Classically,clinical examination of an emphysematic patient reveals no overt crackles, however, in some patients the fine opening of airway 'popping' dissimilar to the fine crackles of pulmonary fibrosis or coarse crackles of mucinous or oedematous fluid can be auscultated.

Diagnosis is by spirometry lung function testing , including diffusion testing. Diffusion tests such as DLCO will show a decreased diffusion capacity. Other investigations might include X-rays, high resolution spiral chest CT-scan, bronchoscopy when other lung disease is suspected, including malignancy , blood tests, pulse.

A way to help AAT is to put more into the blood flow and eat more protein. In normal breathing, air is drawn in through the bronchial passages and down into the increasingly fine network of tubing in the lungs called the alveoli , which are many millions of tiny sacs surrounded by capillaries. These absorb the oxygen and transfer it into the blood. When toxins such as smoke are breathed into the lungs, the particles are trapped and cause a localized inflammatory response.

Chemicals released during the inflammatory response e. This leads to significant modifications of lung architecture[1], characterized mainly by intrapulmonary air collections and confining parenchyma collapse [1] ; as far as the process proceeds expiratory bronchial obstruction and thoracic cage expansion also occur, with the clinical picture of COPD.

Mainly decreased is the ability to exude carbon dioxide due to ventilation deficit and, in the more serious cases, oxygen uptake is also impaired. The activity of another molecule called alpha 1-antitrypsin normally neutralizes the destructive action of one of these damaging molecules.

After a prolonged period, hyperventilation becomes inadequate to maintain high enough oxygen levels in the blood. The body compensates by vasoconstricting appropriate vessels. This leads to pulmonary hypertension, which places increased strain on the right side of the heart, the one that pumps deoxygenated blood to the lungs, and it often fails.

The failure causes the heart muscle to thicken to pump more blood. Eventually, as the heart continues to fail, it becomes larger and blood backs up in the liver. Emphysema occurs in a higher proportion in patients with decreased alpha 1-antitrypsin A1AT levels alpha 1-antitrypsin deficiency , A1AD. In A1AD, inflammatory enzymes such as elastase are able to destroy the alveolar tissue the elastin fibre, for example.

The pattern of emphysema in A1AD is described as panacinar involving the entire acinus as opposed to the centrilobular pattern seen with smoking; the former typically affects the lower lungs, and the former affects the upper lungs.

However, smokers with A1AD are in the highest risk category for emphysema. Patients with chronic bronchitis will have symptoms such as shortness of breath, chronic cough, excessive mucus production and wheezing which can lead to pulmonary hypertension.

Patients with emphysema have symptoms such as a barrel chest, enlarged lungs, shortness of breath, and weight loss. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Two is because most people with cyanosis are treated with supplemental oxygen. So, this makes sure their oxygen levels stay up and their skin stays pink. So, it has been phased out as an acceptable medical term. You will rarely see it used in modern medical literature.

Pink puffer is a generalized term for a person who is thin, breathing fast and is pink. They usually present with shortness of breath and pursed lip breathing. By pink, we mean the color of their skin. Like blue bloaters, they have trouble oxygenating. But, their bodies compensate for this by increasing respiratory rate. This assures that tissues are adequately oxygenated. But, because they are breathing so fast, this makes their skin look pink. They usually have large chests. This used to be called a barrel chest.

Take in a deep breath and hold it. This is what a barrel chest looks like. It gives the appearance of a barrel, hence the name. It happens when air gets trapped inside your lungs. Air gets in but some of this air cannot get back out. So, this is a common feature of severe emphysema. They also use pursed lips. This is an effort to slow down their expiratory phase.