Cell Damage and Repair in Alveolar Region

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10 Questions

What is the effect of bronchoconstriction on airway diameter and resistance to airflow?

Decrease in airway diameter and increase in resistance to airflow

What is the result of stimulating nerve endings in the nose with certain gases and vapors?

Holding of the breath or changes in breathing patterns

What is the effect of acidic or alkaline irritants on alveolar walls?

Increased permeability and cell necrosis

What is the characteristic of ozone lesions?

Propagated by a cascade of secondary reaction products

What is the role of glutathione S-transferases and glutathione peroxidase in lung xenobiotic metabolism?

Involved in the pathogenesis of lung injury

What is the result of inhalation of HCl, NO2, NH3, or phosgene?

No apparent damage in the respiratory tract

What is the characteristic of bronchoconstriction-associated symptoms?

Wheezing, coughing, and chest tightness

What is the effect of exercise on bronchoconstriction-associated problems?

Potentiates the problems

What is the result of damage to the lung parenchyma?

Capable of repairing itself

What is the mechanism of ozone-induced lung injury?

Cascade of secondary reaction products and reactive oxygen species

Study Notes

Lung Injury and Repair

  • Type I cell damage triggers the proliferation of type II epithelial cells, which eventually transform into new type I cells.
  • Clara cells in the airways proliferate and divide after injury.
  • Leukocytes migrating across pulmonary capillaries into the alveolar lumen may trigger a mitotic response.

Chronic Responses of the Lung to Injury

Fibrosis

  • Fibrotic lungs contain increased amounts of collagen, particularly type I and type III collagen in a 2:1 ratio.
  • Excess collagen is observed in the alveolar interstitium, alveolar ducts, and respiratory bronchioles.
  • Changes in collagen cross-linking may contribute to increased lung stiffness.

Emphysema

  • Emphysema results in lungs becoming larger and overly compliant, with a distended, hyperinflated lung that no longer effectively exchanges oxygen and carbon dioxide.
  • Destruction of the gas-exchanging surface area occurs due to loss of tissue and air trapping.
  • Cigarette smoke is the major cause of human emphysema, but other toxicants can also elicit this response.

Toxic Inhalants, Gases, and Dosimetry

  • The site of deposition of toxicants in the respiratory tract defines the pattern of toxicity.
  • Water solubility determines how deeply a gas penetrates into the lung.
  • Highly soluble gases like SO2 do not penetrate beyond the nose, while relatively insoluble gases like ozone and NO2 penetrate deeply into the lung.

Particle Size and Clearance

  • Larger particles are distributed to the upper air passages, while smaller particles are transported to the alveoli.
  • Particle shape and density may also play a role in distribution.
  • Particle clearance is an important aspect of lung defense, with rapid removal lessening the time available to cause damage.

Mechanisms of Respiratory Tract Injury

Airway Reactivity

  • Bronchial smooth muscle tone is regulated by the autonomic nervous system.
  • Bronchoconstriction can be provoked by irritants, cholinergic drugs, and other substances, leading to a decrease in airway diameter and increased resistance to airflow.

Pulmonary Edema

  • Certain gases and vapors stimulate nerve endings in the nose, causing breath-holding or changes in breathing patterns.
  • Acidic or alkaline irritants can produce cell necrosis and increased permeability of the alveolar walls, leading to pulmonary edema.
  • Inhalation of certain agents can produce delayed pulmonary edema, which can be fatal.

This quiz covers the processes of cell damage and repair in the alveolar region, including the proliferation of type II epithelial cells, migration of leukocytes, and role of other cells in the alveolar zone.

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