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Mansoura University

Dr. M. Shalaby

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pathology respiratory system pneumonia lung abscess

Summary

These notes provide a comprehensive overview of pneumonia and lung abscess, covering definitions, etiology, and pathogenesis. The document also discusses different types of pneumonia and associated complications.

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pathology - respiratory pneumonia and lung abscess LECTURE (2) pneumonia and lung abscess Dr. M. Shalaby pathology - respiratory pneumonia and lung abscess DEFINITION  Inflammation of lung...

pathology - respiratory pneumonia and lung abscess LECTURE (2) pneumonia and lung abscess Dr. M. Shalaby pathology - respiratory pneumonia and lung abscess DEFINITION  Inflammation of lung tissue. ① BACTERIAL:  Lobar pneumonia.  Bronchopneumonia. ② PRIMARY ATYPICAL PNEUMONITIS:  Acute interstitial inflammation confined to alveolar septa without intra - alveolar exudate.  Caused by:  Viruses: as influenza, parainfluenza, mea sles chicken pox and small pox. ETIOLOGY  Mycoplasma pneumonia. ③ LOEFFLER'S PNUEUMONIA:  Pneumonia with eosinophilia.  Due to parasitic infestations e.g. ascaris, ankylostoma and Bi lharziasis ④ GRANULOMA:  T.B  Sarcoidosis  Leprosy  Actinomycosis Dr. M. Shalaby pathology - respiratory pneumonia and lung abscess  Acute sero fibrinous inflammation involving at least an entire lobe of lung DEFINITION caused by acute bacterial infection. CAUSE  Strept. pneumoniae in 95 % of cases. MOI  By inhalation (droplet infection). ① Pneumococci are inhaled to reach alveoli. ② In alveoli, it produces an inflammatory reaction with excess fluid exudate rich in fibrin (sero-fibrinous inflammation) ③ This fluid exudate pass from one alveolus to another through inter alveolar PATHOGENESIS pores to involve whole lobe & bacteria reach pleura. ④ The fluid together with the cellular exudate expel air away from the alveoli producing a firm airless lobe leading to consolidation (hepatization) of the affected lobe. RED HEPATIZATION GRAY HEPATIZATION Dr. M. Shalaby pathology - respiratory pneumonia and lung abscess STAGE OF RED STAGE OF CONGESTION STAGE OF GRAY HEPATIZATION STAGE OF RESOLUTION HEPATIZATION DURATION: 1st day 2nd - 4th day 5th - 8th day 9th day till 21 NE SIZE Enlarged COLOR Red Red Gray Wet sponge Consolidated CONSISTENCY Consolidated (Hepatized) (Hepatized)  Resolution occurs due to CUT SECTION Exudes frothy fluid Dry, Red Dry, Gray absence of necrosis with PLEURA - S.F Pleurisy S.F Pleurisy phagocytosis of cellular HILAR LN - Enlarged Enlarged debris by macrophages to ME restore normal aeration of ALVEOLAR alveoli & normal lung Congested Congested Less congested structure except pleurisy CAPILLARIES ALVEOLAR Thinned & compressed by which organizes to form Thickened Thickened adhesions. WALL distended alveolar spaces  Bacteria.  Bacteria  Dead bacteria  Fluid exudate  Fibrin  Shrunken fibrin ALVEOLAR  RBCs  Hemolyzed RBCs SPACES  Few neutrophils  Numerous PMNL  Macrophages Dr. M. Shalaby pathology - respiratory pneumonia and lung abscess Dr. M. Shalaby pathology - respiratory pneumonia and lung abscess RARE TO OCCUR AS RESOLUTION IS COMMON PULMONARY  Fibrosis: due to organization of alveolar exudate. A. Spread of infection: DIRECT  To pleura: Fibrous thickening and adhesion.  Pericarditis. LYMPHATIC  Mediastinitis. EXTRA  Osteomyelitis of chest wall bones. PULMONARY  Meningitis. BLOOD  Arthritis.  Bacteraemia and septicaemia. B. Due to toxaemia: Toxic myocarditis and acute heart failure.  The total clinical course of the disease will take 7-9 days.  The disease terminates by sudden improvement (i.e it ends by crisis = a turning point in the course of the disease).  Characterized by good prognosis because:  Resolution is common.  Complications as fibrosis are rare. Dr. M. Shalaby pathology - respiratory pneumonia and lung abscess  Acute suppurative inflammation of the bronchioles and the surrounding DEFINITION alveoli with patchy consolidation due to bacterial infection. CAUSATIVE ① Staphylococcus aureus ORGANISMS ② Streptococcus pyogenes MOI  Inhalation (Droplet Infection). PRIMARY SECONDARY  Due to 1ry exogenous  Due to 2ry endogenous invaders which invaders. complicate other diseases. A. Post infective:  Complicates respiratory tract infection as influenza.  Occur In extremes of age B. Inhalation: of infected material. ① Infancy C. Hypostatic: ② Children  Complicates pulmonary edema of heart failure. ③ Old age. D. Terminal:  Complicates severe diseases as cancer or coma & usually fatal. Dr. M. Shalaby pathology - respiratory pneumonia and lung abscess  Acute suppurative inflammation. ① Multiple patches of consolidation ± suppuration centered around bronchioles. ② Areas between the patches are normal. ③ Pleurisy is not a marked feature, as the patches do not usually contact pleura ④ Suppurative patches heal by fibrosis. N/E A. AFFECTED BRONCHIOLES & ATTACHED ALVEOLI :  Show picture of acute suppurative inflammation: ① The lumen is filled with pus and shedded epithelium. ② Epithelial lining is ulcerated. ③ Wall infiltrated by excessive number of neutrophils & pus cells. B. PATCHES  Early non suppurative patches,  Late suppurative patches, or  Healed fibrotic patches. M/E C. LUNG TISSUE IN BETWEEN:  Patches appear normal. Dr. M. Shalaby pathology - respiratory pneumonia and lung abscess COMMON TO OCCUR AS RESOLUTION IS RARE.  Pulmonary Fibrosis “secondary to extensive suppuration” → PULMONARY compression on pulmonary capillaries → pulmonary hypertension → right-sided heart failure.  Spread of infection: DIRECT  To surroundings.  Pericarditis. LYMPHATIC  Mediastinitis. EXTRA  Osteomyelitis of chest wall bones. PULMONARY  Meningitis. BLOOD  Arthritis.  Bacteraemia and septicaemia.  Due to toxaemia: Toxic myocarditis and acute heart failure.  The total clinical course of the disease will take 2-3 weeks.  The disease terminates by severe complications or even death (i.e it ends by lysis = gradual bad course without abrupt change).  Characterized by poor prognosis because:  Resolution is rare.  Complications as fibrosis are common. Dr. M. Shalaby pathology - respiratory pneumonia and lung abscess LOBAR PNEUMONIA BRONCHOPNEUMONIA  Acute sero-fibrinous  Acute suppurative inflammation DEF: inflammation AETIOLOGY: ORGANISM Pneumococci (95%). Staph, Strept, H influenza ROUTE Primary exogenous infection. 1ry & 2ry infections.  4 stages.  No stages.  Diffuse lesion not related to  Patchy lesion related to N/E: bronchiole bronchiole  No pus on pressure.  pus exudes on pressure.  Fibrinous pleurisy is marked.  Usually absent.  Diffuse lesion.  Patchy around bronchioles  Alveolar spaces contain fibrin,  Contains pus cells, RBCs & neutrophils, RBCs & macrophages. M/E: macrophages.  Bronchiolitis occurs.  No bronchiolitis.  No pleurisy.  Pleurisy.  Resolution is common.  Resolution is rare. FATE:  Fibrosis is rare.  Fibrosis is common.  7-9 days.  2-3 weeks. COURSE:  Ends by crisis.  Ends by lysis. Dr. M. Shalaby pathology - respiratory pneumonia and lung abscess DEFINITION  Localized suppurative inflammation due to pyogenic organisms. ① Inhalation (aspiration) abscess. ② Pyaemic abscess. CAUSES & ③ Post-pneumonic abscess: may complicate lobar pneumonia or TYPES bronchopneumonia. ④ Secondary infected lung lesions. INHALATION LUNG ABSCESS PYAEMIC LUNG ABSCESS INCIDENCE More common Less common CAUSE Inhalation of infected material Pulmonary pyaemia ① Site: ① Site  Right Lung  Both lungs  Upper and lower lobar are equally  All lobes are affected especially affected subpleural PATHOLOGY  Related to a small peripheral  Not related to bronchi, but bronchus related to blood vessels ② Single. ② Multiple. ③ Variable sizes ③ Small and uniform. ④ Associated with serofibrinous pleurisy ④ No pleurisy as it is rapidly fatal Dr. M. Shalaby

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