Restrictive Respiratory Diseases
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| Restrictive diseases are characterized by ______________________ of the lungs due to changes in ____________________________. | Decreased expansion (expansionability?) of the lungs due to changes in lung parenchyma, pleura, chest wall, or muscles (or some combination)
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| Are restrictive diseases chronic or acute? | Can be either chronic or acute.
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| What is pneumonia? | The inflammation of lung parenchyma - the alveoli.
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| The inflammation in pneumonia results in what? | Lots of fluid being secreted into the alveoli (consolidation). This occurs because the capillaries become very "leaky."
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| Pneumonia is almost always due to some kind of _________________. | Infection (almost always viral. bacteria are 2nd most common, but other things can infect and cause pneumonia).
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| What is our fear when it comes to pneumonia? | That alveoli will fill with our own juices.
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| Treatment for pneumonia | Antibiotics.
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| What are 2 classifications (that we care about) for pneumonia? | 1) Community-acquired pneumonia. 2) hospital-acquired pneumonia.
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| What is interstitial lung disease also referred to as? | Interstitial pneumonia, or diffuse interstitial lung disease.
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| What is interstitial lung disease? | Infiltration of alveolar walls by cells, fluid and connective tissue.
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| Interstitial lung disease can lead to what? | Fibrosis. (irreversible)
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| What is fibrosis of the lung? | Excessive scarring of lung tissue. (extra cellular proteins make up scar tissue)
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| Sometimes lung damage can lead to ____________________________ instead of emphysema. | Pulmonary fibrosis.
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| What is pulmonary fibrosis characterized by? | Characterized by accumulation of fibrous connective tissue.
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| What does pulmonary fibrosis occur from? | Inhalation of particles less than 6 micrometers in size, such as in black lung disease (anthracosis) from coal dust.
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| Interstitial disease = thickening of ____________________. | Alveolar interstitium.
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| In interstitial lung disease, there is buildup of __________ in the interstitium. There is also infiltration by ________________. This is followed by what? | There is buildup of collagen in the interstitium. Infiltration of white blood cells - this inflammatory response can be followed y fibrosis (lots of fibroblasts are produced) and tissue destruction.
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| What is the end result of all the collagen deposition in the alveolar walls in interstitial lung disease? | They essentially go away and you end up with a few large sacs where before you had lots of small ones, which of coure decreases surface area for the exchange.
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| What is hypersensitivity pneumonitis? | An occupational disease. Organic dusts are inhaled and cause inflammation (happens in non-smokers).
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| Hypersensitivity pneumonitis leads to what? | Alveolar wall thickening, exudate appearance in the lumen of bronchioles, lots of immune cells; can lead to fibrosis.
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| 2 examples of how to get hypersensitivity pneumonitis? | Wheat workers - drop flour bag (small particles). Inhaling organic chemicals.
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| What is pneumoconiosis? | Parenchymal lung disease caused by inhaled inorganic dust particles.
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| Examples of things inhaled in pneumoconiosis: | Anthracosis - black lung (from coal mining). Sillicosis (sand blasting - sand has silicon). Asbestos.
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| What cancer is caused by asbestos? | Mesothelioma - cancer of the lining of thoracic and abdominal cavities. Even acute exposure to asbestos can cause mesothelioma.
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| What is "Acute Adult" Respiratory Distress Syndrome? (ARDS) | primary problem is damage to alveolar-capillary membrane. Partial pressure of oxygen drops and oxygen therapy doesn't help.
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| Damage in ARDS occurs as a result of what? | An increase in pulmonary blood vessel permeability, leading to an increase in alveolar fluid rich in protein (edema, but without an increase in pulmonary blood pressure).
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| Four reasons ARDS is bad: | 1) alveolar tissue gets damaged. 2) alveolar diameter changes (some collapse, some get bigger). 3) pulmonary blood vessels are damaged. 4) oxygen transport/exchange is impaired.
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| Treatment for ARDS: | Ventilation with oxygen therapy - keeps the alveoli open, which increases functional residual capacity, decreases atelectasis, and also may preserve surfactant.
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| What is Infant Respiratory Distress Syndrome? | Found in premies, who have pulmonary edema, and some atelectasis.
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| What is the primary cause of infant RDS? | lack of sufficient surfactant. Baby has to pump (the bellows) lots harder, but babys chest is really soft and pliable, so babys work is less efficient.
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| What is given to baby with RDS? | Oxygen therapy doesn't help the hypoxemia. Steroids help reduce incidence (maybe bump surfactant production into gear). Mechanical ventilation is done. (high O2 delivery can be bad for baby). Administering surfactant helps.
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| A secondary cause of IRDS is _________________________. | Immaturity of capillary blood supply, which screws up ventilation/perfusion ratios and makes baby's breathing job that much harder.
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