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61 Cards in this Set
- Front
- Back
What are the characteristics of the R bronchus?
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- Wider
- Shorter - Steeper - 2 cm |
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What are the characteristics of the L bronchus?
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- Narrower
- Longer - More horizontal - 5 cm |
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Which bronchi is an inhaled foreign body more likely to enter? Why?
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Right Bronchus:
- Wider - Shorter - Steeper - 2 cm |
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Which part of the respiratory system is lined w/ respiratory epithelium? What kind of epithelium?
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- Lines airways proximal to the respiratory bronchioles
- Pseudostratified ciliated columnar epithelium |
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What is the acinus?
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Airway structures distal to the terminal bronchiole:
- Respiratory Bronchiole - Alveolar Duct - Alveolus |
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What are the L & R arrows pointing at?
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L: Normal Alveoli
R: Alveolar Septa |
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What kind of cells cover 95% of the alveolar surface
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Type 1 Pneumocytes
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What is the function of Type 2 Pneumocytes?
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- Produce surfactant
- Repair alveolar epithelium |
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Describe the continuity of the alveolar septum?
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- Fenestrated
- Pores of Kohn - Important for exchange of substances |
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What is Atelectasis?
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State in which the lung, in whole or in part, is COLLAPSED or without air; loss of lung volume d/t inadequate expansion of air-spaces
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What are the types of Atelectasis?
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1. Resorptive
2. Compressive 3. Loss of Surfactant (neonatal) 4. Contraction |
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What are the acquired forms of Atelectasis?
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- Resorptive
- Compressive - Contraction |
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What kind of Atelectasis is the consequence of COMPLETE airway obstruction?
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Resorption Atelectasis
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What causes Resorption Atelectasis?
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Complete Airway Obstruction:
- Mucus/mucopurulent plug following surgery - Aspiration of foreign materials - Bronchial asthma, bronchitis, bronchiectasis - Bronchial neoplasms (caveat - total obstruction) |
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Where does the obstruction occur in Resorption Atelectasis?
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Complete Airway Obstruction occurs in bronchi, subsegmental bronchi, or bronchioles
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What are the consequences of Resorption Atelectasis?
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- Prevents air from reaching the alveoli
- Resorption of air trapped in distal airspaces through the pores of Kohn - Lack of air in distal airspaces - Collapse |
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What are the clinical findings of Resorption Atelectasis?
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* Fever and dyspnea w/in 24-36 hours of collapse
- Ipsilateral deviation of trachea - Ipsilateral diaphragmatic elevation - Absent breath sounds and absent vocal vibratory sensation (tactile fremitus) - Collapsed lung does not expand on inspiration |
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What is the most common cause of fever 24-36 hours after surgery?
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Resorption Atelectasis
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What kind of Atelectasis is caused by air or fluid accumulation in the pleural cavity, causing collapse of the underlying lung?
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Compression Atelectasis
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What causes Compression Atelectasis?
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Air or fluid accumulation in pleural cavity, increases pressure and collapses underlying lung
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What are some examples of Compression Atelectasis?
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- Tension Pneumothorax
- Pleural Effusion |
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What are the clinical findings of Compression Atelectasis?
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- Trachea and mediastinum shift AWAY from atelectatic lung (contralateral side)
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What is happening in these lungs?
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Compression Atelectasis d/t Pneumothorax:
- Note that R lung has a darker / lucent appearance because of presence of air occupying almost entire pleural space - R lung is next to mediastinum - Deviation of trachea to contralateral side |
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What is happening in these lungs?
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Compression Atelectasis d/t Pleural Effusion
- Lung should be taking up entire space - Pleural Effusion filled entire space, but was drained before doing autopsy |
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What happens to the alveoli during Compression Atelectasis?
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Alveoli collapse into slit-like spaces
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What is the cause of Neonatal Atelectasis?
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Loss of Surfactant
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What are the components of Surfactant?
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Lipids:
- Phosphatidylcholine (Lecithin) - Phosphatidylglycerol Proteins: - Surfactant proteins A and D - Surfactant proteins B and C |
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What is the function of the proteins in Surfactant?
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- A and D: innate immunity
- B and C: reduces surface tension at air liquid barrier in alveoli |
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Where is Surfactant stored?
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Lamellar bodies
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What is the function of Surfactant?
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- Reduces surface tension in small airways
- Prevents collapse of airways on expiration |
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What modulates the synthesis of surfactant?
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- ↑ by cortisol and thyroxine
- ↓ by insulin |
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What can cause Neonatal Atelectasis?
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Decreased surfactant in fetal lungs:
- Prematurity - Maternal diabetes (fetal hyperglycemia stimulates insulin release) - C-section (labor and vaginal delivery ↑ stress related cortisol secretion which ↑ surfactant production) |
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What is happening in this image?
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Neonatal Atelectasis: collapsed alveoli are lined by hyaline membranes
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What happens to the alveoli during Neonatal Atelectasis?
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Collapsed alveoli are lined by hyaline membranes
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What are the clinical findings of Neonatal Atelectasis?
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- Respiratory distress w/in a few hours after birth
- Hypoxemia → Respiratory Acidosis - Ground glass appearance (opacified and pale) on chest x-ray |
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What are the complications of Neonatal Atelectasis?
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- Intraventricular hemorrhage
- PDA (persistent hypoxemia) - Necrotizing enterocolitis (intestinal ischemia) - Hypoglycemia (excessive insulin release) - O2 therapy damages lungs (bronchopulmonary dysplasia) and may cause cataracts (blindness) |
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What are the complications of O2 therapy in Neonatal Atelectasis?
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- Damages lungs (bronchopulmonary dysplasia)
- Cataracts (blindness) |
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Why does Neonatal Atelectasis cause Hyaline Membranes to form on the alveoli?
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- Prematurity leads to reduced surfactant synthesis, storage, and release
- Causes increased alveolar surface tension - Leads to atelectasis: uneven perfusion and hypoventilation - Causes hypoxemia and CO2 retention - Leads to acidosis, pulmonary vasoconstriction, and pulmonary hypoperfusion - Leads to endothelial and epithelial damage which causes plasma to leak into alveoli - Causes fibrin and necrotic cells to accumulate within alveoli forming a Hyaline Membrane |
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What type of Atelectasis is caused by fibrotic changes in lung or pleura, which prevents full expansion?
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Contraction Atelectasis
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What happens in Contraction Atelectasis?
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- Fibrotic changes in lung parenchyma or pleura
- Prevents full expansion - Not reversible |
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What part of the lung is damaged in Acute Lung injury?
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Endothelium or Epithelium
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Is there a genetic predisposition to Acute Lung injury?
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- There are both non-heritable and heritable forms
- The response and survival of heritable forms depends on multiple loci on different chromosomes |
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What are the chemical mediators of Acute Lung injury?
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- Cytokines, oxidants, growth factors
- TNF; IL-1, -6, -10; TGF-β |
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What are the manifestations of Acute Lung injury?
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- Mild form: pulmonary edema
- Severe form: diffuse alveolar damage (acute respiratory distress syndrome) |
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What are the features of the mild form of Acute Lung Injury?
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* Pulmonary Edema
- Microvascular or alveolar injury → increase in capillary permeability |
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What causes pulmonary edema in acute lung injury?
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Alterations in Starling forces:
- ↑ Hydrostatic P in pulmonary capillaries - ↓ Oncotic P |
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What can cause increased hydrostatic pressure in pulmonary capillaries? Outcome?
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- L sided heart failure
- Volume overload - Mitral stenosis - Hemodynamic disturbances - cardiogenic pulmonary edema Leads to pulmonary edema |
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What can cause decreased oncotic pressure in pulmonary capillaries? Outcome?
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- Nephrotic syndrome
- Liver cirrhosis Leads to pulmonary edema |
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What are the features of pulmonary edema in acute lung injury?
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- Transudate (low in proteins)
- Edema fluid accumulation in alveoli w/ heart failure cells and brown induration |
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What can cause increased capillary permeability / pulmonary edema in acute lung injury?
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Microvascular or Alveolar Injury:
- Infections - Aspiration - Drugs, shock, trauma - High altitude |
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What causes Acute Respiratory Distress Syndrome?
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Non-cardiogenic pulmonary edema resulting from acute alveolar-capillary damage:
- Direct lung injury - Indirect lung injury (systemic diseases) |
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What are the risks for Acute Respiratory Distress Syndrome?
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* Gram negative sepsis (40%)
* Gastric Aspiration (30%) * Severe trauma (10%) * Pulmonary infections (diffuse) (these account for >50% of causes) - Heroin - Smoke inhalation |
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What are the clinical findings of Acute Respiratory Distress Syndrome?
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- Dyspnea
- Severe hypoxemia NOT responsive to O2 therapy - Respiratory acidosis |
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What does this x-ray show?
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- White-out appearance (like a snow storm)
- Represents severe and advanced Acute Respiratory Distress Syndrome (ARDS) |
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What is the pathogenesis of Acute Respiratory Distress Syndrome?
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- Acute injury to alveolar epithelium or endothelium
- Alveolar macrophages and other cells release cytokines → neutrophil chemotaxis → transmigration of neutrophils into alveoli → leakage of protein (fibrin) rich exudate → form hyaline membrane - Damage to pneumocytes causes surfactant deficiency leading to atelectasis - Progressive interstitial fibrosis |
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What tries to repair damage in Acute Respiratory Distress Syndrome?
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Type 2 Pneumocytes
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What is the prognosis for Acute Respiratory Distress Syndrome?
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Poor ~60% mortality rate
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What is seen in this image?
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Hyaline Membrane in Acute Respiratory Distress Syndrome
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What is seen in this image?
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Hyperplastic Type 2 Pneumocytes, trying to repair damage
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What are the stages of Acute Respiratory Distress Syndrome? What happens in each stage? Timeline?
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Exudative Stage (days 0-7)
- Edema (peaks day 1) - Hyaline Membrane formation (peaks day 4) Proliferative Stage (days 7-14) - Interstitial Inflammation (peaks day 11) - Interstitial Fibrosis (peaks day 14) - Interstitial inflammation and fibrosis begin during exudative stage |
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Case: 60 yo woman develops pneumonia complicated by septicemia. 3 wks later develops multiple organ failure. Abx led to sputum and blood cultures lacking growth of organisms. Requires intubation w/ mechanical ventilation and becomes more difficult to maintain SaO2. Chest x-ray shows increasing opacifications of all lung fields.
What is the pathologic process most likely to be present in her lungs? |
Diffuse hyaline membrane formation
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