Respiratory System Pathology-Atelactasis, Acute lung injury, and ARDS
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| What is Alectasis? | The loss of lung volume caused by inadequate expansion of air spaces
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| What is the general consequence of atelactasis? | Shunting of inadequately oxygenated blood from pulmonary arteries into veins, thus giving rise to hypoxia
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| What are the three forms of atelactasis? | 1) Resorption
2) Compression
3) Contraction
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| When does resorption atelactasis occur? | In the case of obstruction. preventing air from reaching distal airways
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| Why is it called resorption atelactasis? | Because the air present gradually become absorbed and alveolar collapse follows
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| What part of the lung is affected by resorption atelactasis? | Either an entire lung, a complete lobe, or one or more segments.
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| What is the most common cause of resorption collapse? | Obstruction of a bronchus by a mucus or mucopurelent plug
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| In what cases can the bronchus be obstructed by a mucus or mucopurulent plug? | 1) Postoperatively
2) Complicated bronchial asthma, bronchiectasis, or bronchitis
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| How else may the bronchus be obstructed? | 1) Tumor
2) Foreign body aspiration (mainly in children)
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| What are some other names for compression atelactasis? | Passive/ Relaxation atelactasis
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| How does compression atelactasis occur? | Accumulation of fluid, blood, or air within the pleural cavity which mechanically collapses the adjacent lung
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| What is the most common cause of compression atelactasis? | Pleural effusion, caused by congestive heart failure
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| What are some other causes of compression atelactasis? | 1) Leakage of air into the pleural cavity (pneumothorax)
2) Hemothorax
3) Basal atelactasis resulting from the elevated position of the diaphragm
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| Basal atelactasis commonly occurs in: | 1) Bedridden patients
2) Ascites
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| What is another name for contraction atelactasis? | Cicatrization atelactasis
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| When does contraction atelactasis occur? | When either local or generalized fibrotic changes in the lung or pleura or prevents expansion of air spaces
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| Which type(s) of atelactasis is/are reversible? | Compression and Resorption
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| Which type(s) of atelactasis is/are irreversible? | Contraction
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| Treating atelactasis early on prevents: | Hypoxemia and superimposed infection of the collapsed lung
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| Acute lung injury includes: | A spectrum of bilateral pulmonary damage (endothelial and epithelial) which can be initiated by numerous conditions
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| What are the clinical manifestations of Acute lung injury? | 1) Acute onset of dyspnea
2) Decreased arterial oxygen pressure (hypoxemia)
3) Bilateral pulmonary infiltrates on the chest radiograph
4) Absence of clinical evidence of left sided heart failure
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| Accumulations in this type of injury are considered noncardiogenic pulmonary edema because: | The pulmonary infiltrates in acute lung injury are caused by damage to the alveolar capillary membrane rather than by left sided heart failure
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| Acute lung injury can progress to: | ARDS (Acute respiratory distress syndrome)
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| What is ARDS? | A clinical syndrome caused by diffuse alveolar capillary and epithelial damagage
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| ARDS is usually characterized by: | 1) Rapid onset of respiratory insufficiency (possibly fatal)
2) Severe arterial hypoxemia which is refractory to oxygen therapy and may progress to organ failure (multisystemic)
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| The histologic manifestation of ARDS is known as: | DAD (Diffuse alveolar damage)
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| ARDS is associated with two types of lung injury. What are they? | 1) Direct injury to the lung
2) Indirect injury in the setting of a systemic process
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| What are the common causes of direct lung injury? | Pneumonia
Aspiration of gastric contents
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| What are the uncommon causes of direct lung injury? | Pulmonary contusion
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| What are the common causes of indirect lung injury? | Sepsis
Severe trauma with shock
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| What are the uncommon causes of indirect lung injury? | Acute pancreatitis
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| What is the cause of ARDS in newborns? | Primary deficiency of surfactant
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| What are the two barriers of the alveolar capillary membrane? | 1) The microvascular endothelium
2) Alveolar epithelium
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| IN ARDS, what occurs to these barriers? | The integrity of these barriers is compromised by either endothelial or epithelial injury, or both (the most common)
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| The acute consequences of damage to the alveolar capillary membrane include: | 1) Increased vascular permeability and alveolar flooding
2) Loss of diffusion capacity
3) Widespread surfactant abnormalities (damage to type 2 pneumocytes)
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| In, ARDS, lung injury is caused by an imbalance of? | Pro-inflammatory and anti-inflammatory mediators
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| As early as 30 minutes after an acute insult: | 1) IL-8 synthesis increases (a neutrophil chemotactic and activating agent) by pulmonary macrophages
2) IL-1, TNF, and manily neutrophils released --> endothelial activation and damage
3) Neutrophils release oxidants, proteases, leukotrienes
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| Assault on the endothelium and epithelium increases: | Vascular leakiness and loss of sufactant
The alveaolar unit is unable to expand
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| The destructive neutrophilic forces can be counteracted by: | Endogenous anti-Proteases, antioxidants, and inflammatory cytokines (IL-10)
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| The balance between the _____ and ______ factors determines the degree of tissue injury and clinical severity of ARDS | Destructive/ Protective
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| Which type of cells are thought to have an important role in the pathenogenesis of ARDS? | Neutrophils
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| Describe the general morphology of the lungs in acute ARDS | Red, Firm, Airless, and heavy
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| Microscopic findings of ARDS affected lung: | 1) Capillary congestion
2) Necrosis of alveolar epithelial cells
3) Interstitial and intra alveolar edema and hemorrhage
4) Increased neutrophils in vascular space, interstitium, and the alveoli
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| What is the most characteristic finding in ARDS? | Hyaline membranes in the alveolar ducts
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| What do these hyaline membranes consist of? | 1) Fibrin-rich edema fluid
2) Remnants of necrotic epithelial cells
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| In the organizing stage of ARDS, type 2 pneumocytes: | Vigorously proliferate and attempt to regenerate the alveolar lining
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| Resolution of the lungs after ARDS is: | Unusual
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| What happens instead of resolution? | 1) Organization of fibrin exudates, with resultant intra alveolar fibrosis
2) Marked thickening of the alveolar septa, caused by proliferation of interstitial cells and deposition of collagen
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| How long does it take most patients to develop the clinical syndrome of acute lung injury or ARDS? | (85%) Within 72 hours of the initiating insult
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| The mortality rate from ARDS has decreased from? | 60-40%
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| Predictors of poor prognosis include: | 1) Advanced age
2) Underlying bacteremia (sepsis)
3) Multi-system organ failure (especially cardiac, renal, or hepatic)
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| After the patient survives the acute stage: | Diffuse interstitial fibrosis may occur with continued compromise of respiratory function
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| In patients who survive the acute insult and are spared the chronic stage: | Normal respiratory function returns within 6-12 months
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