Lobar pneumonia and bronciectasis.final.22 07-2013..pm.

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Lobar pneumonia and bronciectasis.final.22 07-2013..pm.

  1. 1. PATHOLOGY PRACTICAL 1
  2. 2. •LOBAR PNEUMONIA •BRONCHIECTASIS 2
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  7. 7. 1.COMMUNITY-ACQUIRED BACTERIAL ACUTE PNEUMONIAS (BACTERIAL) Streptococcus Pneumonia Haemophilus Influenzae Moraxella Catarrhalis Staphylococcus Aureus Klebsiella Pneumoniae Pseudomonas Aeruginosa Legionella Pneumophila 2.COMMUNITY-ACQUIRED ATYPICAL (VIRAL AND MYCOPLASMAL) PNEUMONIAS (NON-BACTERIAL) Influenza Infections Severe Acute Respiratory Syndrome (SARS) 3.NOSOCOMIAL PNEUMONIA 4.ASPIRATION PNEUMONIA 5.LUNG ABSCESS 6.CHRONIC PNEUMONIA Histoplasmosis, Morphology Blastomycosis, Morphology Coccidioidomycosis, Morphology 7.PNEUMONIA IN THE IMMUNOCOMPROMISED HOST 8.PULMONARY DISEASE IN HUMAN IMMUNODEFICIENCY VIRUS INFECTION PULMONARY INFECTIONS 7
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  13. 13. N O R M A L C X R 13
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  23. 23. • The specimen is a slice of the left lung. • The upper lobe is relatively normal, except for an old scar near the apex of the lung caused by tuberculosis. • The major abnormality is that the lower lobe is uniformly consolidated (airless and solid) due to lobar pneumonia, with inflammatory cells and exuded plasma filling the airspaces. • The shaggy material on the pleural surface is fibrin, a protein derived from fibrinogen in exuded plasma. 23
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  30. 30. • Microscopic Appearances: • Sections through the lower lobe show dilated, congested blood vessels in the alveolar walls. • The alveolar spaces are filled with inflammatory cells, mainly neutrophils, and inflammatory exudate, including fibrin. • There are large aggregates of fibrin on the pleural surface. 30
  31. 31. • Pneumonia is an acute inflammation of the airspaces of the lung, usually caused by bacterial infection. • This woman died of pneumonia affecting an entire lobe of the lung, before the advent of antibiotics. • Nowadays, it is uncommon to die in the acute stages of lobar pneumonia because Streptococcuspneumoniae ("the pneumococcal"), which is the bacterium that typically causes a lobar distribution of pneumonia, is sensitive to various antibiotics. • However, there is an increasing incidence of pneumococcal resistance to Penicillin - usually the most effective antibiotic in this situation. 31
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  33. 33. VIRAL PNEUMONIAS • Frequently “interstitial”, NOT alveolar 33
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  35. 35. BRONCHIECTASIS 35
  36. 36. Definition • Abnormal and irreversible dilatation of bronchi and bronchioles greater than 2.m.m. in diameter developing secondary to inflammatory weakening of the bronchial walls. • Persistent cough with expectoration of copious amounts of foul smelling purulent sputum. • Post infectious cases commonly develop in childhood and early adult life. 36
  37. 37. Aetiology • Hereditary and congenital factors • End bronchial obstruction • Infections. 37
  38. 38. Infections-Micro-organisms • Measles and Pertussis • Adeno & Influenza virus • Bacterial infection with virulent organisms: S.aureus, Klebsiella Anaerobes • Atypical mycobacteria • Mycoplasma • HIV • Tuberculosis • Fungi 38
  39. 39. IMPAIRED HOST DEFENCE • Local causes: End bronchial obstruction • Generalized impairment: 1. Immunoglobulin deficiency 2. Primary ciliary disorders 3. Cystic fibrosis 39
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  42. 42. • Persistent or recurrent cough with purulent sputum. • Hemoptysis • Initiating episode: Severe pneumonia, or insidious onset of symptoms or asymptomatic or non-productive cough – dry bronchiectasis in upper lobe, • Dyspnoea, wheezing – widespread bronchiectasis or underlying COPD. • Exacerbation of infection: Sputum volume increase, purulence or blood. 42
  43. 43. DIAGNOSIS • Clinical • Radiology: Chest XR: May be non-specific mild disease – normal XRC advanced disease – cysts + fluid levels peribronchial thickening, “tram tracks”, “ring shadows” CT Scan: Peribronchial thickening, dilated bronchioles. • Sputum culture: Pseudomonas aeuruginosa, H.influenzae. 43
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