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1. Pathology: inflammation and fibrosis of the bronchial wall, hypertrophy of the
submucosal glands and hypersecretion of mucus, and loss of elastic lung fibers and
alveolar tissue. This airflow obstruction causes a mismatch in ventilation and perfusion.
Alveolar tissue destruction leads to a decreased surface area for gas exchange.
2. Clinical presentation:
- fatigue, exercise intolerance, cough, sputum
-Viral or bacterial infections, respiratory infections and chronic respiratory failure
3. diagnosis:
1. history, physical exam, PFTs, chest xray, lab tests
,4. treatment
- stop smoking to slow disease progression
- pneumonia and flu vax
- inhaled short and long acting bronchodilators, to relax airway smooth muscle
- oxygen therapy when PCO2 levels drop below 55 mmHg
Give this one a go later!
Be familiar with the disease pathology, clinical presentation, diagnosis, and
treatment of COPD.
Type 1 and II alveolar cells, macrophages
Give this one a go later!
What cells are in the alveolar epithelium?
As dissolved carbon dioxide, attached to hemoglobin, becomes bicarbonate
Give this one a go later!
How is carbon dioxide transported in the blood?
measures respiratory response during rapid maximal inspiration
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, Forced inspiratory vital flow (FIF)
Trachea, bronchi, bronchioles, alveoli
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What are the levels of branching?
-Chronic bronchitis is a clinical diagnosis: chronic cough productive of sputum for at
least 3 months per year for at least 2 consecutive years.
-Emphysema is a pathologic diagnosis: permanent enlargement of air spaces distal to
terminal bronchioles due to destruction of alveolar walls
Give this one a go later!
chronic bronchitis and emphysema
1. Risk factors:
- spontaneous: tall boys between 10 and 30 due to difference in pleural pressure
from top to bottom of lung. Lung disease, especially emphysema.
2. Disease pathology:
Tension occurs when air enters pleural space but cant exit, such as penetrating
chest wound. It can collapse the lung on affected side and compress mediastinal
structures.
4. clinical presentation:
-chest pain on affected side, increased rest rate and difficulty
breathing.
1. Pathology: inflammation and fibrosis of the bronchial wall, hypertrophy of the
submucosal glands and hypersecretion of mucus, and loss of elastic lung fibers and
alveolar tissue. This airflow obstruction causes a mismatch in ventilation and perfusion.
Alveolar tissue destruction leads to a decreased surface area for gas exchange.
2. Clinical presentation:
- fatigue, exercise intolerance, cough, sputum
-Viral or bacterial infections, respiratory infections and chronic respiratory failure
3. diagnosis:
1. history, physical exam, PFTs, chest xray, lab tests
,4. treatment
- stop smoking to slow disease progression
- pneumonia and flu vax
- inhaled short and long acting bronchodilators, to relax airway smooth muscle
- oxygen therapy when PCO2 levels drop below 55 mmHg
Give this one a go later!
Be familiar with the disease pathology, clinical presentation, diagnosis, and
treatment of COPD.
Type 1 and II alveolar cells, macrophages
Give this one a go later!
What cells are in the alveolar epithelium?
As dissolved carbon dioxide, attached to hemoglobin, becomes bicarbonate
Give this one a go later!
How is carbon dioxide transported in the blood?
measures respiratory response during rapid maximal inspiration
Give this one a go later!
, Forced inspiratory vital flow (FIF)
Trachea, bronchi, bronchioles, alveoli
Give this one a go later!
What are the levels of branching?
-Chronic bronchitis is a clinical diagnosis: chronic cough productive of sputum for at
least 3 months per year for at least 2 consecutive years.
-Emphysema is a pathologic diagnosis: permanent enlargement of air spaces distal to
terminal bronchioles due to destruction of alveolar walls
Give this one a go later!
chronic bronchitis and emphysema
1. Risk factors:
- spontaneous: tall boys between 10 and 30 due to difference in pleural pressure
from top to bottom of lung. Lung disease, especially emphysema.
2. Disease pathology:
Tension occurs when air enters pleural space but cant exit, such as penetrating
chest wound. It can collapse the lung on affected side and compress mediastinal
structures.
4. clinical presentation:
-chest pain on affected side, increased rest rate and difficulty
breathing.