RMD 575 Vital Gases Summative Review Notes (PDF)

RMD 575 Vital Gases Summative Review Notes 1) ARDS a) Noncardiogenic pulmonary edema caused from pulmonary capillary-alveolar damage b) Common causes: pulmonary infections, gram-negative sepsis, gastric aspiration, inhaled irritants, chemical injury, traumatic shock c) Clinical find...

RMD 575 Vital Gases Summative Review Notes 1) ARDS a) Noncardiogenic pulmonary edema caused from pulmonary capillary-alveolar damage b) Common causes: pulmonary infections, gram-negative sepsis, gastric aspiration, inhaled irritants, chemical injury, traumatic shock c) Clinical findings: acute dyspnea, tachypnea, severe hypoxemia in addition to underlying cause d) Chest radiography: bilateral interstitial infiltrates, then progression to diffuse consolidation with air bronchograms e) Pathology i) Acute exudative stage: congestion, interstitial and intra-alveolar edema, inflammation, fibrin deposition, and diffuse alveolar damage. The alveolar walls become lined with waxy hyaline membranes ii) Proliferative or organizing stage: type II pneumocytes proliferate, and granulation tissue forms in the alveolar walls and spaces 2) Pulmonary Infections a) Pneumonia—Clinical types: lobar pneumonia, bronchopneumonia, interstitial pneumonia i) Community-acquired pneumonia (1) Lobar pneumonia: a complete or near-complete consolidation of a lobe of lung (2) Bronchopneumonia: begins as an acute bronchitis, then infection extends into surrounding alveoli (the lobule that the involved bronchus feeds into) leading to patchy areas of consolidation (a) Epidemiology: majority caused by bacterial pathogens, S. pneumoniae most common (b) Clinical findings (i) Sudden onset of high fever with productive cough (ii) Chest pain (iii) Late inspiratory crackles (c) Chest radiography/CT scan: Consolidation involving a lobe (lobar pneumonia) or patchy infiltrates (bronchopneumonia) (d) Pathology (i) Congestion stage: capillary congestion, intra-alveolar edema fluid containing a few neutrophils, and the presence of bacteria (ii) Red hepatization stage: massive confluent exudation fills alveolar spaces—numerous neutrophils, red cells, and fibrin (iii) Gray hepatization stage: progressive disintegration of inflammatory and red cells and the persistence of a mononuclear cell exudate (macrophages and lymphocytes) (iv) Organizing stage: exudates are converted to fibromyxoid masses rich in macrophages and fibroblasts (3) Interstitial pneumonia (“atypical” pneumonia): inflammatory cells are in interstitium rather than in alveoli (a) Epidemiology: Mycoplasma pneumoniae, Chlamydia pneumoniae, viruses (influenza, coronaviruses) (b) Clinical findings (i) Insidious onset of low-grade fever (ii) Nonproductive cough (iii) Chest pain (iv) “Flulike” symptoms: pharyngitis, laryngitis, myalgias, headache (v) No signs of consolidation on physical exam (c) Chest radiography/CT scans: diffuse bilateral interstitial infiltrates (d) Pathology (i) Mononuclear infiltrates (lymphocytes, plasma cells, macrophages) in interstitium rather than alveoli b) Lung abscess i) Liquefactive necrosis of lung tissue secondary to a microbial infection ii) Epidemiology (1) Most often caused by aspiration of oropharyngeal or gastric material (a) Risk factors: alcoholism, loss of consciousness, recent dental work (2) May occur as a complication of bacterial pneumonia (especially S. aureus and Klebsiella pneumoniae iii) Clinical findings (1) Spiking fever and productive cough, usually of foul-smelling sputum iv) Chest radiograph: area with cavitation and air-fluid level  v) Pathology (1) Primarily located on the right side, especially superior segment of right lower lobe; cavity filled with necrotic material containing pus (neutrophils and liquefied cellular material) c) Pneumocystis jiroveci pneumonia i) A yeastlike fungus that primarily causes lung infections and is a significant opportunistic infection in AIDS patients ii) Pathology (1) Alveolar interstitial thickening and eosinophilic honeycombed exudate in the lumen of the lung (2) Cysts are found in the alveolar exudate and have a characteristic cup-shaped appearance, or they are oval with a central dot d) Tuberculosis i) Clinical (1) Screening test: PPD/tuberculin skin test does not distinguish active from inactive disease (2) HIV infection is a risk factor for progression to active tuberculosis and for reactivation of TB (3) Fever, drenching night sweats, weight loss (4) Pathology (a) Primary TB (i) Subpleural location in upper part of lower lobes or lower part of upper lobes 1. Area of granulomatous inflammation with caseous necrosis (Ghon focus) 2. Involvement of lung as well as regional (hilar, mediastinal) lymph nodes (“Ghon complex”) 3. Either or both areas undergo calcification, detected radiographically and called “Ranke complex” (b) Secondary (reactivation) TB (i) Involves one or both lung apices (ii) Gray-white areas of consolidation with and without cavitation and necrosis (c) Miliary TB (i) Caused by hematogenous or lymphatic dissemination of infection (ii) Multiple small nodules diffusely scattered through lungs and other organs e) Aspergillosis i) Narrow-angle (