Study Set Content:
can change the site of deposition of a particle of a given size. The size of a particle may change during inspiration before deposition in the respiratory tract.
Patterns of breathing
Lung defense is dependent on (), wherein rapid removal lessens the time available to cause damage to the pulmonary tissues or permit local absorption o Nasal clearance o Tracheobronchial clearance o Mucociliary clearance o Alveolar clearance
particle clearance
– occurs in the upper respiratory tract and large proximal airways where the airflow is faster than in the small distal airways.
Impaction
In humans, most > () particles are deposited in the nose or oral pharynx and cannot penetrate tissues distal to the larynx.
10 μm
For 2.5 to 10 μm particles, impaction continues to be the mechanism of deposition in the first generations of the () region.
Tracheobronchial region
occurs when the trajectory of a particle brings it near enough to a surface so that an edge of the particle contacts the airway surface.
Interception
– controls deposition in the smaller bronchi, the bronchioles, and the alveolar spaces, where the airways are small and the velocity of airflow is low.
Sedimentation
Difusion – diffusion of a particle within the air is an important factor in the deposition of submicrometer particles. It is an important deposition mechanism in the nose, airways, and alveoli or particles
≤ 0.5 μm
– is a minor deposition mechanism or positively charged particles. The surface of the airways is negatively charged and attracts positively charged particles
Electrostatic deposition
certain gases and vapors stimulate nerve endings in the nose, particularly those of the trigeminal nerve. • The result is () or(), to avoid or reduce further exposure. Transient receptor potential channel receptors may be activated by many irritants causing tickling, itching, and painful nasal sensations.
holding of the breath, changes in breathing patterns
are activated by several irritants including acrolein, allyl isothiocyanate (wasabi), allicin (garlic), cinnamaldehyde, chlorine, ozone, and hydrogen peroxide.
Subfamily A receptors
can be provoked by irritants (acrolein), cigarette smoke, air pollutants, cholinomimetic drugs(acetylcholine), histamine, various prostaglandins and leukotrienes, substance P, and nitric oxide
Bronchoconstriction
– causes a decrease in airway diameter and a corresponding increase in resistance to airflow. Characteristic symptoms include wheezing, coughing, chest tightness, and dyspnea.
Bronchoconstriction
is marked by alveolar epithelial and endothelial cell perturbation and inflammatory cell influx that leads to surfactant disruption, pulmonary edema, and atelectasis.
Adult/Infant respiratory Distress Syndrome)
represents an acute, exudative phase of lung injury that alters ventilation– perfusion relationships and limits diffusive transfer of O2 and CO2 even in otherwise structurally normal alveoli. • Example: Acrolein, HCl, NO2, NH3, or phosgene – may compromise alveolar barrier function
Toxic pulmonary edema
is defined by the presence of sputum production and cough or at least three months
Chronic bronchitis
destruction of the gas-exchanging surface area results in a distended, hyperinflated lung that no longer effectively exchanges oxygen and carbon dioxide as a result of both loss of tissue and air trapping.
Emphysema
The potential mechanisms of lung carcinogenesis center on damage to
DNA
There is an increased airway reactivity of the bronchial smooth muscle in response to exposure to irritants. • Characterized clinically by attacks of shortness of breath, which is caused by narrowing of the large conducting airways (bronchi).
Asthma
– from humans with acute or chronic pulmonary fibrosis contain increased amounts of collagen. In lungs damaged by toxicants, the response resembles adult or infant respiratory distress syndrome.
Fibrotic lungs
