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RS Pathology
Respiratory System Pathology-Atelactasis, Acute lung injury, and ARDS
| Question | Answer |
|---|---|
| What is Alectasis? | The loss of lung volume caused by inadequate expansion of air spaces |
| What is the general consequence of atelactasis? | Shunting of inadequately oxygenated blood from pulmonary arteries into veins, thus giving rise to hypoxia |
| What are the three forms of atelactasis? | 1) Resorption 2) Compression 3) Contraction |
| When does resorption atelactasis occur? | In the case of obstruction. preventing air from reaching distal airways |
| Why is it called resorption atelactasis? | Because the air present gradually become absorbed and alveolar collapse follows |
| What part of the lung is affected by resorption atelactasis? | Either an entire lung, a complete lobe, or one or more segments. |
| What is the most common cause of resorption collapse? | Obstruction of a bronchus by a mucus or mucopurelent plug |
| In what cases can the bronchus be obstructed by a mucus or mucopurulent plug? | 1) Postoperatively 2) Complicated bronchial asthma, bronchiectasis, or bronchitis |
| How else may the bronchus be obstructed? | 1) Tumor 2) Foreign body aspiration (mainly in children) |
| What are some other names for compression atelactasis? | Passive/ Relaxation atelactasis |
| How does compression atelactasis occur? | Accumulation of fluid, blood, or air within the pleural cavity which mechanically collapses the adjacent lung |
| What is the most common cause of compression atelactasis? | Pleural effusion, caused by congestive heart failure |
| 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 |
| Basal atelactasis commonly occurs in: | 1) Bedridden patients 2) Ascites |
| What is another name for contraction atelactasis? | Cicatrization atelactasis |
| When does contraction atelactasis occur? | When either local or generalized fibrotic changes in the lung or pleura or prevents expansion of air spaces |
| Which type(s) of atelactasis is/are reversible? | Compression and Resorption |
| Which type(s) of atelactasis is/are irreversible? | Contraction |
| Treating atelactasis early on prevents: | Hypoxemia and superimposed infection of the collapsed lung |
| Acute lung injury includes: | A spectrum of bilateral pulmonary damage (endothelial and epithelial) which can be initiated by numerous conditions |
| 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 |
| 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 |
| Acute lung injury can progress to: | ARDS (Acute respiratory distress syndrome) |
| What is ARDS? | A clinical syndrome caused by diffuse alveolar capillary and epithelial damagage |
| 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) |
| The histologic manifestation of ARDS is known as: | DAD (Diffuse alveolar damage) |
| 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 |
| What are the common causes of direct lung injury? | Pneumonia Aspiration of gastric contents |
| What are the uncommon causes of direct lung injury? | Pulmonary contusion |
| What are the common causes of indirect lung injury? | Sepsis Severe trauma with shock |
| What are the uncommon causes of indirect lung injury? | Acute pancreatitis |
| What is the cause of ARDS in newborns? | Primary deficiency of surfactant |
| What are the two barriers of the alveolar capillary membrane? | 1) The microvascular endothelium 2) Alveolar epithelium |
| 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) |
| 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) |
| In, ARDS, lung injury is caused by an imbalance of? | Pro-inflammatory and anti-inflammatory mediators |
| 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 |
| Assault on the endothelium and epithelium increases: | Vascular leakiness and loss of sufactant The alveaolar unit is unable to expand |
| The destructive neutrophilic forces can be counteracted by: | Endogenous anti-Proteases, antioxidants, and inflammatory cytokines (IL-10) |
| The balance between the _____ and ______ factors determines the degree of tissue injury and clinical severity of ARDS | Destructive/ Protective |
| Which type of cells are thought to have an important role in the pathenogenesis of ARDS? | Neutrophils |
| Describe the general morphology of the lungs in acute ARDS | Red, Firm, Airless, and heavy |
| 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 |
| What is the most characteristic finding in ARDS? | Hyaline membranes in the alveolar ducts |
| What do these hyaline membranes consist of? | 1) Fibrin-rich edema fluid 2) Remnants of necrotic epithelial cells |
| In the organizing stage of ARDS, type 2 pneumocytes: | Vigorously proliferate and attempt to regenerate the alveolar lining |
| Resolution of the lungs after ARDS is: | Unusual |
| 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 |
| 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 |
| The mortality rate from ARDS has decreased from? | 60-40% |
| Predictors of poor prognosis include: | 1) Advanced age 2) Underlying bacteremia (sepsis) 3) Multi-system organ failure (especially cardiac, renal, or hepatic) |
| After the patient survives the acute stage: | Diffuse interstitial fibrosis may occur with continued compromise of respiratory function |
| In patients who survive the acute insult and are spared the chronic stage: | Normal respiratory function returns within 6-12 months |
Created by:
Ulaisl
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