L1: Pathology of upper respiratory tract

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L1: Pathology of upper respiratory tract. Assistant prof.Marwa Mosaad Department of Pathology BUC/ASU.

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ILOs. Identify clinicopathologic features of rhinosinusitis Explain pathogenesis and pathologic features of different types of pulmonary infections List causes, clinical presentations and pathologic features of vascular disorders of the lung.

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Paranasal sinuses. Hollow, airfilled cavities surrounding the nose lined with mucus and drain into the nasal cavity. They serve to humidify inspired air. The four groups of paranasal sinuses are the frontal, sphenoid, ethmoid , and maxillary sinuses.

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Rhinosinusitis. Inflammation of the paranasal sinuses. When sinus drainage into the nasal cavity becomes obstructed (typically by mucus), the sinuses can become infected..

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Rhinosinusitis. Causes: viral upper respiratory tract infections (URIs). Viral with secondary bacterial infections, Streptococcus pneumoniae (40%), Haemophilus influenzae (35%), and Moraxella catarrhalis (5 %)..

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Rhinosinisitis. Presentation Sinus inflammation presents with tenderness to palpation , A sensation of “ fullness” in the affected paranasal regions (may mimic toothache), and, rarely, earache. When rhinosinusitis is superimposed by bacterial infections, patients present with fever and purulent nasal discharge, Bacterial infections can also be suspected when viral URI symptoms persist or worsen after 1–2 weeks. Antibiotics are generally not indicated for sinusitis, unless symptoms have persisted longer than 10 days,.

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Rhinosinisitis. Diagnosis Primarily clinical suspicion based on patient history and physical examination. CT scan can show air-fluid levels. Treatment ■ Rhinosinusitis due to viral URI is typically self-limiting. ■ If complicated by bacterial infections, antibiotics are indicated..

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Pulmonary infections. MM.shakweer. BADR N.

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Def: consolidation of lung tissue by the presence of an intra alveolar inflammatory exudate of infective origin Classification: - lobar pneumonia, bronchopneumonia - bacterial, viral, fungal, rickettsial , chlamydial and protozoal.

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http://www.google.com.eg/url?sa=i&source=images&cd=&ved=0CAUQjBw4Qw&url=http%3A%2F%2Fupload.wikimedia.org%2Fwikipedia%2Fcommons%2F5%2F52%2FLobar_Pneumonia_and_bronchopneumonia_illustrated.jpg&ei=1ApWVIOJEtDmarGMgMAL&psig=AFQjCNGPJqkjqs2LWClpCd4lIE7OLymJ2A&ust=1415011412386850.

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Case 35: Bronchopneumonia the areas of consolidation are related to the air passages alveolar spaces filled with viable and degenerate polymorphs.

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Patchy consolidation With suppurative inflammation of the bronchi and surrounding alveoli Occurs in extremes of life (infancy and old age) In children it usually complicates measels , whooping cough and gastroentritis Causative organism: staphylococci, streptococci, pneumococci and H influenza.

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Multiple patches of consolidation Multilobar bilateral basal Microscopic: the bronchi, bronchioles and adjacent alveoli are filled by suppurative exudate.

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1- lung abscess 2- spread: pleura ( empyema ), pericardium ( suppurative pericarditis ) 3- healing by fibrosis ( lung fibrosis) 4- blood spread ( pyeamic abscess) in other organs.

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Lobar pneumonia. http://www.google.com.eg/url?sa=i&source=images&cd=&ved=0CAUQjBw4Cg&url=http%3A%2F%2Fweb.med.unsw.edu.au%2Fpathmus%2F1338071.jpg&ei=1w1WVIDCMsblaMqHgbAB&psig=AFQjCNH4cnT_LQvV6c701x1wNi-fqysGbA&ust=1415012183947653.

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Def: fibrinous inflammation affecting an entire lobe of the lung Organism: pneumococci , staph, strept , H.influenza Pathologic features: congestion, red hepatization (consolidation), grey hepatization , resolution Microscopic: alveoli filled with fibrin and neutrophils.

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Stage Of congestion • Active hyperernia and ede Stage Of red hepatization Neutrophils • Congest ion • Fibrin Stage Of grey hepatization • Degradation Of red blood cells Stage Of resolution.

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Bacterial pneumonia. Acute inflammation and consolidation (solidification) of the lung are due to a bacterial agent. Clinical signs and symptoms include fever and chills; productive cough with yellow-green (pus) or rusty (bloody) sputum; tachypnea ; pleuritic chest pain; and decreased breath sounds, rales, and dullness to percussion ..

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Bacterial pneumonia. Investigations : elevated white blood cell count Chest x-ray typically shows lobar consolidation (opacification), and for bronchopneumonia typically shows patchy opacification. In general, the keys to effective therapy are identification of the organism and early treatment with antibiotics..

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Age: early childhood Organism: respiratory syncitial virus, adenovirus, Influenza A and B, Herpes virus Gross : hemorrhagic consolidation of both lungs Microscopic: marked congestion and diffuse alveolar damage Interstitial inflammation -necrotizing bronchitis and bronchiolitis Secondary infection with pyogenic bacteria transforms the disease into severe suppurative bronchopneumonia.

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Diffuse alveolar damage (DAD) is manifested by injury to alveolar lining and endothelial cells, pulmonary edema, hyaline membrane formation and later by proliferative changes involving alveolar and bronchiolar lining cells and interstitial cells.

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Pathogenesis. Exudative (acute) phase: 1 - 7 days Proliferative / organizing (subacute) phase: 1 - 3 weeks Fibrotic (chronic) phase: after 3 weeks.

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Exudative phase. Exudative (acute) phase: 1 - 7 days Neutrophil mediated inflammation damages the alveolar capillary barrier (alveolar epithelium and endothelium), increases its permeability and causes intra-alveolar hemorrhage and edema Protein rich edema interacts with alveolar surfactants, resulting in decreased pulmonary compliance Hyaline membranes are developed on alveolar wall where epithelium is denudated and disrupted.

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Proliferative phase. Proliferative / organizing (subacute) phase: 1 - 3 weeksRestoration of type II pneumocytes and subsequent differentiation into type I pneumocytes Proliferation of myofibroblasts Drainage of alveolar edema by restored type II pneumocytes.

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Fibrotic phase. Fibrotic (chronic) phase: after 3 weeks: Collagenous fibrosis in alveolar spaces and interstitium Refractory rigidity of alveoli due to architectural remodeling.

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Lung abscess. A localized collection of neutrophils (pus) and necrotic pulmonary parenchyma . Etiology : Aspiration is the most common cause: It tends to involve right lower lobe and typically has mixed oral flora (often both anaerobic and aerobic) for infecting organisms. Following pneumonia Airway obstruction Complications of lung abscess include empyema, pulmonary hemorrhage, and secondary amyloidosis..

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Thank you.