• Asthma is a disease in which the smooth muscles of the bronchioles contract suddenly (spasm).
• This partially narrows the bronchioles, making breathing very difficult.
• Asthma is becoming more common.
• It affects about 7%–8% of people in the United States.
• The World Health Organization (WHO) estimates that more than 262 million people worldwide have asthma.
• The usual cause of asthma is excessive contraction (hypersensitivity) of the bronchiolar smooth muscle in response to foreign substances in the air.
• In about 70% of patients younger than 30 years, asthma is caused by allergic hypersensitivity, especially to plant pollens.
• In older people, asthma is usually caused by hypersensitivity to non-allergic airborne irritants, such as smog.
• People with allergic asthma produce unusually large amounts of immunoglobulin E (IgE) antibodies.
• These IgE antibodies attach to mast cells present in the lung interstitium near the bronchioles and small bronchi.
• When the person inhales an allergen (such as pollen) to which they are sensitive:
  • The allergen binds to IgE antibodies on the mast cells.
  • This activates the mast cells.
• Activated mast cells release several substances, including:
  • Histamine
  • Slow-reacting substance of anaphylaxis (a mixture of leukotrienes)
  • Eosinophilic chemotactic factor
  • Bradykinin
• The combined effects of these substances, especially the slow-reacting substance of anaphylaxis, cause:
  • Edema (swelling) of the walls of the small bronchioles
  • Secretion of thick mucus into the bronchioles
  • Spasm of the bronchiolar smooth muscle
• These changes greatly increase airway resistance.
• During expiration, the bronchioles become narrower than during inspiration because they collapse more easily during expiratory effort.
• Since the bronchioles are already partially blocked in asthma, this additional narrowing causes severe airway obstruction during expiration.
• Therefore, a person with asthma can usually inhale fairly well but has great difficulty exhaling.
• Clinical findings include:
  • Greatly reduced maximum expiratory flow rate
  • Reduced timed expiratory volume
• These changes produce dyspnea (air hunger).
• During an acute asthma attack, the functional residual capacity (FRC) and residual volume (RV) increase because air cannot be expelled completely from the lungs.
• After many years of asthma, the chest becomes permanently enlarged, producing a barrel chest.
• In long-standing asthma, the functional residual capacity and residual volume remain permanently increased.

KEY CONCEPT

• Asthma is caused by spasm of bronchiolar smooth muscle, leading to partial airway obstruction and difficult breathing.
• The most common cause is hypersensitivity of the bronchioles to allergens or airborne irritants.
• In allergic asthma, IgE antibodies activate mast cells, which release histamine, leukotrienes, eosinophilic chemotactic factor, and bradykinin.
• These mediators cause bronchiolar edema, thick mucus secretion, and smooth muscle spasm, greatly increasing airway resistance.
• Airway obstruction is more severe during expiration, making exhalation more difficult than inhalation.
• Clinical findings include reduced expiratory flow rate, reduced timed expiratory volume, and dyspnea.
• Acute asthma increases FRC and RV, while long-standing asthma may cause a permanent barrel chest with persistently increased FRC and RV.

TUBERCULOSIS

• In tuberculosis (TB), tubercle bacilli infect the lungs and produce a characteristic tissue reaction.
• This tissue reaction includes:
  • Invasion of the infected area by macrophages.
  • Formation of a fibrous wall around the infected area, creating a tubercle.
• The fibrous wall helps prevent the spread of tubercle bacilli within the lungs.
• Therefore, walling off the infection is a protective mechanism that limits the extension of tuberculosis.
• If tuberculosis is not treated, the walling-off process fails in about 3% of affected people.
• When this happens, tubercle bacilli spread throughout the lungs.
• The infection may destroy large areas of lung tissue.
• This destruction can lead to the formation of large abscess cavities in the lungs.
• In the late stages of tuberculosis, the lungs contain many areas of fibrosis (scar tissue).
• There is also a reduction in the amount of functional lung tissue.
• These changes produce the following effects:
  • The respiratory muscles must work harder to ventilate the lungs.
  • Vital capacity and breathing capacity decrease.
  • The total surface area of the respiratory membrane decreases.
  • The respiratory membrane becomes thicker.
  • Pulmonary diffusing capacity progressively decreases.
  • The ventilation-perfusion (V/Q) ratio becomes abnormal.
  • Diffusion of both O₂ and CO₂ across the lungs decreases further.

KEY CONCEPT

• Tuberculosis is caused by tubercle bacilli, which produce macrophage infiltration and fibrous walling-off of the infected area to form a tubercle.
• The fibrous wall limits the spread of infection within the lungs.
• If untreated, walling off fails in about 3% of patients, allowing widespread spread of bacilli, severe lung destruction, and formation of large abscess cavities.
• Late-stage tuberculosis causes extensive fibrosis and loss of functional lung tissue.
• These changes increase the work of breathing, reduce vital capacity, decrease respiratory membrane surface area, increase membrane thickness, reduce pulmonary diffusing capacity, produce an abnormal ventilation-perfusion ratio, and impair O₂ and CO₂ diffusion.

MADE BY SELF LEARNING CEO AND FOUNDER DR SHEEN