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PNEUMONIA & other patterns of acute lung injury
DIFFUSE ALVEOLAR DAMAGE
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PNEUMONIA Nasal clearance Tracheobronchial clearance
Inflammatory consolidation of the lung parenchyma NORMAL DEFENCES MECHANISMS Nasal clearance Tracheobronchial clearance Alveolar clearance
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PNEUMONIA – why? Local Factors Impaired Host Resistance
Loss / impairment of cough reflex Impaired mucociliary elevator Impaired function of alveolar macrophages Accumulated / stagnant secretions Impaired Host Resistance Chronic Disease Malignancy Immune Defficiency Iatrogenic – immunosuppressive Rx
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PNEUMONIA Classification Anatomic Distribution Aetiology
Nature of host inflammatory reaction
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PNEUMONIA - Anatomic Distribution
Lobar vs. Bronchopneumonia Lobar (less frequent) - widespread fibrinosuppurative consolidation of a large portion of a lobe or an entire lobe Bronchopneumonia - patchy consolidation, usually extension of pre-existing bronchitis / bronchiolitis
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PNEUMONIA - Aetiology INFECTIOUS ASPIRATION
Acute Bacterial Pneumonia NB Streptococcus pneumoniae = pneumococcus The others: Staphyllococcus aureus Streptococcus pyogenes Haemophilius Influenza Klebsiella pneumoniae Legionella pneumoniae Viral, Mycobacterial, Fungal, Parasitic (NB in an immunocompromised population) ASPIRATION LIPID – endogenous vs. exogenous
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PNEUMONIA - Nature of Host Response
Acute fibrinous Granulomatous Organizing Interstitial Eosinophilic
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LOBAR PNEUMONIA Abrupt onset Pleuritic chest pain, rusty sputum
High fever, rapid & shallow resps, Leucocytosis Healing “by crisis”
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LOBAR PNEUMONIA Structural Changes: uniform 4 Stages: Congestion
Red Hepatization Grey Hepatization Resolution
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BRONCHOPNEUMONIA Successive infection of conductive airways
Infants, debilitated young children, elderly, post-operative Insidious onset Peripheral hypoxia Slow healing, resolution “by lysis”
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BRONCHOPNEUMONIA Widespread patchy areas of inflammation spreading from bronchitis and bronchiolitis Lower lobes – larger and more numerous foci Pale areas raised above the surface of the surrounding lung parenchyma Recovery – liquefaction – but also by fibrosis
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Acute Pneumonia Alveolar Spaces filled by acute inflammatory cells (neutrophils)
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Acute Pneumonia Acute Inflammatory cells within alveolar spaces
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PNEUMONIA - Complications
Abscess Formation Organization Empyema – suppurative pericarditis Bronchiectasis Bacteraemic dissemination to other organs (metastatic abscesses) – endocarditis meningitis peritonitis suppurative arthritis
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LUNG ABSCESS Localized focus of suppuration consisting of a collection of pus that is walled off by chronic inflammatory / granulation tissue and fibrous tissue Formation of an abscess entails necrosis and destruction of lung tissue Causes – preceding pneumonia, bronchial obstruction – tumour, foreign body, aspiration, septic embolism
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BRONCHIECTASIS Permanent dilatation of the bronchi accompanied by inflammatory changes in their walls and surrounding parenchyma Recurrent inflammation of bronchial walls & fibrosis in the surrounding parenchyma – traction on bronchi – dilatation Divided into post-inflammatory, post-obstructive, and congenital / hereditary conditions Cough, fever, foul sputum
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BRONCHIECTASIS Localized vs. widespread
Basal segments of LLs, RML & lingula Gross: dilated bronchi exending to pleural surface, surrounding scarring Microscopy: mucosal ulceration, submucosal CI & granulation tissue, adjacent OP Complications: Cor pulmonale Brain abscess Amyloid
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DIFFUSE ALVEOLAR DAMAGE (DAD)
Pathologic manifestation of Adult Respiratory Distress Syndrome (ARDS) Sequence of events that follows acute lung injury caused by a variety of toxic insults Diffuse = damage to all parts of the alveolus: epithelium, endothelium and interstitium
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DAD - Clinical Syndrome
Acute onset of dyspnoea Diffuse pulmonary infiltrates Rapid development of respiratory failure High mortality ~ 50%
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DAD - Pathology Two Discrete but Overlapping Stages: Early and Late
Acute and Organizing Exudative and proliferative
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DAD Early / Acute / Exudative Phase:
Day 1: Interstitial / alveolar haemorrhage & fibrin Day 3-7: Hyaline membranes Type II pneumocyte hyperplasia Week 1: Interstitial inflammation Late / Organizing / Proliferative Phase: 1-2 weeks: Fibroblast proliferation Organization & fibrosis
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DAD has many Aetiolgies
Infection Inhalants Ingestants Drugs Shock Sepsis Radiation Misc. Idiopathic
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