Pathology of Respiratory System PDF

PATHOLOGY OF RESPIRATORY SYSTEM DR. PASSANT ESSAM SHIBEL LECTURER OF HISTOPATHOLOGY Upper Respiratory Tract Lower Respiratory Tract DISEASES OF THE RESPIRATORY TRACT INFLAMMATION. - Infective. - Allergic....

PATHOLOGY OF RESPIRATORY SYSTEM DR. PASSANT ESSAM SHIBEL LECTURER OF HISTOPATHOLOGY Upper Respiratory Tract Lower Respiratory Tract DISEASES OF THE RESPIRATORY TRACT INFLAMMATION. - Infective. - Allergic. TUMORS - Benign. - Malignant (primary or metastasis). + others in the lower respiratory tract DISEASES OF THE UPPER RESPIRATORY TRACT UPPER RESPIRATORY TRACT INFLAMMATION OF THE UPPER RESPIRATORY TRACT Infective: 1. Rhinitis (common cold) 2. Acute Sinusitis 3. Otitis Media 4. Acute pharyngitis ACUTE 5. Acute Tonsillitis 6. Diphtheria. 7. Acute laryngitis. 8. Adenoids. 9. Chronic specific (Rhinoscleroma). CHRONIC Allergic Rhinitis & nasal polyp  RHINITIS (COMMON COLD)  Etiology: Rhinovirus, respiratory syncytial virus, para- influenza and influenza virus.  Symptoms: Nasal congestion and watery or mucoidy discharge with slight fever.  Morphology: Acute catarrhal inflammation with excess mucus.  INFLAMMATION ACUTE CHRONIC NON- SUPPURATIVE SUPPURATIVE 1) Serous. 2) Fibrinous. 3) Catarrhal. 4) Membranous. 5) Allergic. 6) Hemorrhagic.  ACUTE SINUSITIS  Etiology: - Commonly preceded by acute or chronic rhinitis (edema impairs sinus drainage leading to retention of secretions and secondary infection). The same pathogens as rhinitis. - Maxillary sinusitis can occur by extension of a periapical tooth infection.  Morphology: It starts as a catarrhal inflammation and with secondary infection, it becomes purulent inflammation.  OTITIS MEDIA  Definition: Inflammaion of the middle ear.  Etiology: - Often associated with upper respiratory tract infection. - The Eustachean tube may become swollen and blocked, leading to trapping of exudate in the middle ear. Eardrum perforation may occur, following by draining of the exudate.  Complications 1) Mastoiditis, meningitis and brain abscess. 2) Inflammation may persist and become chronic with hear loss (due to damage of the ossicles).  ACUTE PHARYNGITIS - Mild pharyngitis manifesting as sore throat accompany common cold. - Severe pharyngitis: Associated with marked hyperemia and exudate occurs with B hemolytic streptococcal and adenovirus infection.  ACUTE TONSILITIS  Etiology: Infection with B hemolytic streptococci, common in children.  Gross: Tonsils are swollen, red with spots of pus on surface (pus in tonsillar crypts draining suppurating lymphoid follicles).  Microscopic: Acute Inflammation + pus in lymphoid follicles.  ACUTE TONSILLITIS  Complications: 1) Spread of infection: Direct: Peri-tonsillar abscess (Quinzy), otitis media, pharyngitis and laryngitis. Lymphatic: Cervical lymph nodes (lymphadenitis). Blood: Bacteremia, septicemia, toxemia and pyemia. 2) Hypersensitivity to streptococcal sore throat or URT infections may result in rheumatic fever or post streptococcal glomerulonephritis. 3) Chronicity: Chronic tonsillitis.  DIPHTHERIA  Definition: Life-threatening disease characterized by pseudo- membranous inflammation of throat and tonsils of young children.  Etiology: - Droplet infection by Corynebacterium diphtheria, - Incubation period is 2-5 days.  Sites: Throat, tonsils, soft palate, larynx & trachea.  DIPHTHERIA Pathological features: 1) Pseudo-membranous inflammation: Gross: - Multiple small yellowish foci of necrosis → gradually enlarge, fuse together and form a continuous membrane. - The membrane is slightly raised and adherent, but if removed by force it leaves bleeding ulcerating surface and re-forms again. Microscopic: - The membrane is formed of fibrin network entangling dead epithelial cells, polymorphs, pus cells and macrophages. - The submucosa shows dilated congested vessels, edema, fibrin and acute inflammatory cells.  DIPHTHERIA  Pathological features: 2. Acute cervical lymphadenitis: Cervical lymph nodes on both sides are enlarged, separate, mobile, soft, painful and tender. 3. Severe acute toxaemia.  Complications: TOXINS 1) Asphyxia: caused by the oedema, membrane & laryngeal spasm. 2) Temporary paralysis of muscles of palate, pharynx, larynx, eye, face, etc.. (nerve affection by bacterial toxins). 3) Acute toxemia may cause: - Toxic Myocarditis and acute heart failure. - Cloudy swelling & focal necrosis of parenchymal organs. - Haemorrhage & necrosis of supra-renal cortex resulting in acute insufficiency. INFLAMMATION OF THE UPPER RESPIRATORY TRACT Infective: 1. Rhinitis (common cold) 2. Acute Sinusitis 3. Otitis Media 4. Acute pharyngitis ACUTE 5. Acute Tonsillitis 6. Diphtheria. 7. Acute laryngitis. 8. Adenoids. 9. Chronic specific (Rhinoscleroma). CHRONIC Allergic Rhinitis & nasal polyp  ADENOIDS  Definition: Hyperplastic lymphoid tissue at the posterior wall of the nasopharynx, due to chronic infection in infants and children.  Effects: 1) Mouth breathing with characteristic ADENOID FACE: narrow nasal openings, opened mouth, short upper lip, protruding upper incisors, absent nasolabial folds. 2) Spread of infection leading to otitis media, pharyngitis.  RHINOSCLEROMA  Definition: A granulomatous inflammation of the nose. May affect other site as the larynx (laryngoscleroma), and pharynx.  Etiology: Klebsiella Rhinoscleromatis bacteria (endemic in Egypt).  Gross: Small hard nodular mass or masses filling the nasal cavity. Rhinoscleroma  RHINOSCLEROMA  Microscopic: - The bacteria multiplies in macrophages producing a foamy appearance of the cytoplasm. (Mickulicz cells). - There is a chronic inflammatory infiltrate involving the submucosa, including: Mickulicz cells: These are the predominant cells. They are macrophages with foamy cytoplasm. They are large with a small pyknotic nucleus. Plasma cells and Russell bodies (Plasma cells with hyaline change due to accumulated immunoglobulin)  RHINOSCLEROMA  Microscopic: - The bacteria multiplies in macrophages producing a foamy appearance of the cytoplasm. (Mickulicz cells). - There is a chronic inflammatory infiltrate involving the submucosa, including: Mickulicz cells: These are the predominant cells. They are macrophages with foamy cytoplasm. They are large with a small pyknotic nucleus. Plasma cells and Russell bodies (Plasma cells with hyaline change due to accumulated immunoglobulin) Later there is fibrosis.  Complications: 1) Nasal obstruction and deformity 2)Ulceration and secondary infection. INFLAMMATION OF THE UPPER RESPIRATORY TRACT Infective: 1. Rhinitis (common cold) 2. Acute Sinusitis 3. Otitis Media 4. Acute pharyngitis ACUTE 5. Acute Tonsillitis 6. Diphtheria. 7. Acute laryngitis. 8. Adenoids. 9. Chronic specific (Rhinoscleroma). CHRONIC Allergic Rhinitis & nasal polyp  Allergic Rhinitis  Definition: Atopic disease, immunoglobulin E (IgE)-mediated immune reaction caused by different antigens.  Etiology: Pollen/grass/dust etc.. produce Type I hypersensitivity.  Gross: Marked mucosal edema and erythema of the nasal mucosal membranes  Microscopic: Acute allergic inflammation rich in eosinophils & increased submucosal edema.  Complications: Repeated attacks result in nasal polyp rich in plasma cells, lymphocytes & eosinophils.  Nasal Polyp  Nasal polyps occur with recurrent allergic rhinitis.  Edematous mucosal protrusions infiltrated by esinophils, and plasma cells. When multiple or large, they obstruct the airway.  Gross: Multiple, soft, pink polyps projecting from mucosa of nose & sinuses.  Nasal Polyp  Microscopic: - Pseudostratified columnar ciliated (respiratory) epithelial cover, but with chronic irritation it may changes to squamous (metaplasia). - Thickened, pink basement membrane  Nasal Polyp  Microscopic: - Pseudostratified columnar ciliated (respiratory) epithelial cover, but with chronic irritation it may changes to squamous (metaplasia). - Thickened, pink basement membrane - Thick, very wide edematous core with many eosinophils, lymphocytes and plasma cells. - Increased number of mucous glands (hyperplasia).  Complications: Nasal obstruction leading to 2ry infection & spread of the infection, & epistaxis. INFLAMMATION OF THE UPPER RESPIRATORY TRACT Infective: 1. Rhinitis (common cold) 2. Acute Sinusitis 3. Otitis Media 4. Acute pharyngitis ACUTE 5. Acute Tonsillitis 6. Diphtheria. 7. Acute laryngitis. 8. Adenoids. 9. Chronic specific (Rhinoscleroma). CHRONIC Allergic Rhinitis & nasal polyp  TUMORS OF THE NASOPHARYNX JUVENILE ANGIOFIBROMA  An uncommon benign mesenchymal tumor of the nasopharynx.  It occurs exclusively in males, usually during adolescence (ANDROGEN RECEPTORS).  It is formed of proliferating fibroblasts with wide blood vessels.  They are extremely vascular and lead to nasal bleeding (epistaxis).  TUMORS OF THE NASOPHARYNX NASOPHARYNGEAL CARCINOMA  Nasopharyngeal carcinoma is a rare neoplasm linked to EBV  It is common among the Chinese.  Microscopic: It may take one of three histological variants: 1) Keratinizing squamous cell carcinoma. 2) Non-keratinizing squamous cell carcinoma. 3) Undifferentiated carcinoma with excess lymphocytes in the stroma [lymphoepithelioma]. It is the most common and the one most commonly linked to EBV.  TUMORS OF THE NASOPHARYNX NASOPHARYNGEAL CARCINOMA  Spread: 1) Directly. 2) Lymphatics to cervical lymph nodes. 3) Blood: late.  Treatment & prognosis: - They tend to be radiosensitive. - Lymphoepithelioma gives better results than squamous cell carcinoma with irradiation.  EPISTAXIS Definition: Bleeding through the nose Causes:  Local causes: - Trauma - Foreign bodies. - Rhinoscleroma. - Nasal polyp - Tumors: angiofibroma or carcinoma  General causes: Hypertension, hemophilia, leukemia, Vit C & K deficiency.  LARYNX LARYNGITIS ACUTE LARYNGITIS:  Definition: Acute catarrhal inflammation of laryngeal mucosa.  Etiology: - It can result from inhalation of irritant fumes or allergy. - In children, para-influenzae virus is the most common cause of laryngotracheobronchitis, known as croup.  It is characterized by harsh persistent cough, and inspiratory stridor. TUBERCULOSIS OF THE LARYNX:  It is a complication of secondary pulmonary tuberculosis. Infection of the larynx occurs as sputum is coughed up.  The result is a laryngeal ulcer with undermined edges and caseous floor.  Tumors of the larynx SQUAMOUS CELL PAPILLOMA OF LARYNX  A benign epithelial tumor.  Caused by human papilloma virus (HPV 6 & 11).  They may be multiple and recurrent especially in children, but are usually single in adults. The most likely cause of their occurrence in children is vertical transmission from infected mothers during delivery.  Gross: Fine finger-like surface protrusions.  Microscopic: Papillary thin fibrovascular core covered by hyperplastic stratified squamous epithelium, showing hyperkerotosis, parakeratosis and acanthosis.  LARYNGEAL NODULE  Definition: Nodule in middle third of vocal cords.  Etiology: Caused by heavy smoking (unilateral) or excessive use of voice (bilateral) as in singers “singers nodule”  Clinical picture: Hoarseness of voice  Gross: Smooth, hemispheric protrusions less than 0.5 cm in diameter. It is firm & covered by mucosa.  Microscopic: Surface is covered by stratified squamous epithelium. The subepithelium shows vascularized fibrous tissue with pink HYALINOSIS.  Complications: 1) Hoarseness of voice. 2) Recurs after removal.  Tumors of the larynx SQUAMOUS CELL CARCINOMA  Incidence: - >95% of laryngeal cancer - Common in males > females (7:1). - 40 years of age  Predisposing factors: Chronic irritation e.g. smoking or exposure to asbestos may have a role. Cancer larynx is preceded by dysplasia & carcinoma insitu, which later develops into invasive carcinoma.  Site: MCQ - Most of laryngeal carcinomas arise on the vocal cords, however it may arise above the vocal cords (supraglottic) or below (subglottic).  Tumors of the larynx SQUAMOUS CELL CARCINOMA  Gross: Ulcerating or fungating tumors.  Tumors of the larynx SQUAMOUS CELL CARCINOMA  Microscopic: Squamous cell carcinoma. Glottic tumors are usually keratinizing and better differentiated than others.  Clinical Picture: Hoarseness of voice. This should raise suspicion of malignancy in smoker males over 40.  Complications: Spread 1) Direct: nearby structures (esophagus, trachea & pharynx) 2) Lymphatic: Cervical lymph nodes, especially supraglottic tumors because this area is rich in lymphatics. MCQ 3) BLOOD. LOWER RESPIRATORY TRACT DISEASES OF THE LOWER RESPIRATORY TRACT  INFLAMMATION (MAINLY INFECTIONS).  OBSTRUCTIVE AND RESTRICTIVE LUNG DISEASES.  TUMORS.  PULMONARY INFECTIONS BRONCHITIS AND TRACHEOBRONCHITIS. PNEUMONIA. LUNG ABSCESS. GRANULOMATOUS  ACUTE BRONCHITIS (ACUTE TRACHEO-BRONCHITIS)  Etiology Same as laryngitis - Infections: ▪ Viral : common cold, influenza and measles. ▪ Bacterial : Streptococci, Staphylococci & Pneumococci. - Chronic Irritation (allergic reaction): by dust, smoke or irritant gases.  Pathology: Catarrhal inflammation: Congested mucosal lining with mucoid exudate or suppurative inflammation (mucopurulent exudate).  Definition: PNEUMONIA Inflammation of the lung parenchyma. BACTERIAL VIRAL Lobar pneumonia Bronchopneumonia Interstitial Pneumonia Involves part or all of a lobe. Involves more than one lobe, results Confined to the alveolar septa from initial infection of the bronchi and and interstitium bronchioles and with extension into lung alveoli.  PNEUMONIA  Clinical picture - Commonly follows a viral upper respiratory tract infection. - Abrupt onset with high fever, chills, pleuritic chest pain and a productive cough with muco-purulent sputum, occasionally there is hemoptysis.  LOBAR PNEUMONIA  Definition: ACUTE NON-SUPPURATIVE DIFFUSE FIBRINOUS INFLAMMATION of the alveoli, occurring in one or more lobes of the lung.  Etiology: Organism: Streptococcus pneumoniae (pneumococci) in more than 90% of lobar pneumonias. Route: airborne by droplet infection.  Occurs in previously healthy young individuals & middle aged people (organism is highly virulent). STAGES OF LOBAR PNEUMONIA Day 8-10  STAGES OF LOBAR PNEUMONIA STAGE DURATION PATHOLOGICAL CHANGES GROSS PICTURE 1) 24 hours The capillaries show hyperemia and the The lung is heavy CONGESTION lung alveoli are filled with a protein rich edematous and red. exudate 2) RED Few days The alveoli show fibrin with massive The lung is red, solid HEPATIZATION accumulation of polymorphs with some and airless, and lymphocytes and macrophages. Many red consistency resembles cells are extravasated. fresh liver. 3) GREY Few days Lysis of the red blood cells occurs. The The lung is grey, and HEPATIZATION alveoli show more accumulation of fibrin solid. which shrinks away from the alveolar wall. 4) 8-10 days in Liquefaction and absorption of the exudate, The lung returns to RESOLUTION untreated and enzymatic digestion of inflammatory normal. cases debris  LOBAR PNEUMONIA  Fate: Most cases end by resolution.  Complications (NOT COMMON): 1) Failure of resolution results in Carnification (organization of the alveolar exudate and the lung becomes like a piece of flesh). 2) Post pneumonic lung abscess & gangrene: focal tissue necrosis and suppuration in a consolidated area produces an abscess & gangrene can follow under the effect of putrefactive organisms. 3) Spread: - Direct: pleurisy, empyema (if suppuration occurred), pericarditis & mediastinitis - Blood: Toxemia: Occurs on 9th day may lead to acute heart failure due to toxic myocarditis Septicemia leading to meningitis, arthritis and infective endocarditis (if suppuration occurred).  BRONCHOPNEUMONIA (SEPTIC BRONCHOPNEUMONIA):  Definition: SUPPURATIVE Lung inflammation characterized by patchy areas of consolidation centered on inflamed bronchioles. These areas are distributed in one or several lobes, commonly basal and bilateral. Etiology: Causative Organisms: - Streptococcus pneumoniae, Hemophilus influenza, staphylococcus aureus. - In Hospital-Acquired pneumonias: Methicillin resistant staphylococcus aureus (MERSA), Pseudomonas and Klebsiella Predisposing factors: WEAK IMMUNITY - It occurs most commonly in extreme of age: infants and old age. - Commonly in patients with debilitating diseases such as diabetes, cancer and cardiac failure. - It may complicate viral infections as viral bronchitis.  BRONCHOPNEUMONIA (SEPTIC BRONCHO-PNEUMONIA):  Morphology: Gross: Usually bilateral lower lobe affection - Bronchioles: contain pus - Patchy areas of yellow consolidation (purulent exudate in alveoli), some areas may become confluent. - Pleurisy. - Enlarged hilar lymph nodes (lymphadenitis). Microscopic Suppurative (neutrophilic) exudation filling bronchi, bronchioles, and alveoli (patchy areas of consolidation). BRONCHOPNEUMONIA (SEPTIC BRONCHO-PNEUMONIA):  Complications: VERY COMMON 1. Post pneumonic lung ABSCESS & gangrene. 2. FIBROSIS is common, due to tissue destruction by suppuration. 3. Bronchiectasis: healing of bronchial walls by fibrosis, results in weakened walls and permanent dilatation of the lumen due to traction on wall by peribronchial fibrosis. 4. SPREAD: Direct: pleura causing empyema, pericarditis, mediastinitis. Blood: - Toxemia causing toxic myocarditis. - Septicemia causing meningitis, arthritis, osteomyelitis and infective endocarditis. 5. Death, especially in debilitated patients.  LOBAR PNEUMONIA BRONCHOPNEUMONIA ETIOLOGY Healthy individuals BACTERIA Weak immunity Middle age Extremes of age DISTRIBUTION Diffuse Patchy (basal and bilateral) TYPE OF Acute Non-Suppurative Fibrinous Acute Suppurative INFLAMMATION COMPLICATIONS Uncommon Common - POST-PNEUMONIC ABSCESS & GANGRENE. - FIBROSIS. - SPREAD  ATYPICAL (INTERSTITIAL) PNEUMONIA (VIRAL OR MYCOPLASMA PNEUMONIA):  Inflammation confined to the alveolar septa and interstitium.  It was called atypical due to absence of consolidation on physical examination and lack of alveolar exudates on radiology.  Etiology: - Mycoplasma pneumoniae. - Viruses such as influenza viruses, adenoviruses, syncytial viruses, COVID 19  Pathogenesis: A common mechanism is attachment of the organism to the respiratory epithelium, followed by necrosis of the cells and inflammatory response. ATYPICAL PNEUMONIA (VIRAL OR MYCOPLASMA PNEUMONIA)  Pathology: - The process may be patchy or involve whole lobes bilaterally or unilaterally. - The inflammatory infiltrate (mononuclear cells: lymphocytes, macrophages and few plasma cells) is confined to the interstitium with little or no alveolar exudates. - In severe cases there is diffuse alveolar cell damage with formation of a HYALINE MEMBRANE of fibrin (adult respiratory distress syndrome ARDS)  ATYPICAL PNEUMONIA (VIRAL OR MYCOPLASMA PNEUMONIA)  Clinical picture: - May simulate severe upper respiratory tract infection,(fever, headache, malaise, cough) - There may be respiratory distress out of proportion to physical or radiological findings because the inflammatory infiltrate in the alveolar wall blocks the gas exchange. - Superimposed bacterial infection can occur.  PULMONARY INFECTIONS BRONCHITIS AND TRACHEOBRONCHITIS. PNEUMONIA. LUNG ABSCESS. GRANULOMATOUS  LUNG ABSCESS  Definition: Localized suppurative inflammation of the lung tissue, resulting in the formation of one or more cavities containing pus.  Organisms: PYOGENIC BACTERIA Staphylococci, pneumococci , Klebsiella pneumoniae, streptococcus pyogenes.  Causes and types: 1) Aspiration lung abscess 2) Post-pneumonic abscess. 3) Bronchial obstruction with bronchogenic carcinoma. 4) Pyemic abscess. 5) Direct traumatic punctures or spread of infection from adjacent Organs.  LUNG ABSCESS CAUSES AND TYPES 1) Aspiration Lung Abscess  Etiology: Aspiration of: cough reflex a) Blood clots or infected material during oral surgery b) Vomitus during anesthesia c) Foreign body or food in comatosed patients or patients with depressed cough reflex  Pathology: - Single abscess develops, more common on the right side. It is usually in the posterior segment of upper lobe or apical segment of lower lobe. These locations represent the more direct course for the aspirated material from the trachea when the patient is recumbent. - The abscess wall is irregular and congested. The lining is shreddy yellow (pyogenic membrane) and the contents of cavity is yellow pus. Overlying pleura shows pleurisy.  LUNG ABSCESS CAUSES AND TYPES 2) Post Pneumonic Abscess:  A complication of pneumonia.  Pathology: One or more abscesses in a background of lobar or bronchopneumonia. 3) Bronchial obstruction with bronchogenic carcinoma:  Distal atelactasis and aspiration of blood and tumor fragments contribute to the development of lung abscess.  LUNG ABSCESS CAUSES AND TYPES 4) Pyemic Abscess:  Etiology: - Septic emboli from septic thrombophlebitis of systemic veins. - Infective endocarditis of the right side of the heart.  Pathology: Multiple, very small and always next to a blood vessel. Yellow spots surrounded by a zone of congestion (usually too small to form cavities). 5) Direct traumatic punctures or spread of infection from adjacent Organs.  LUNG ABSCESS FATE AND COMPLICATIONS 1) Small size: Resolve with proper treatment 2) Rupture into a bronchus results in hemoptysis & cough of purulent sputum 3) Rupture into a pleural cavity results in empyema and pyopneumothorax.  LUNG ABSCESS FATE AND COMPLICATIONS 4) Lung gangrene (the cavity is irregular with a necrotic black lining & has a foul odor). 5) Embolization of septic material to the brain results in meningitis and brain abscess. 6) Chronic lung abscess. Well- defined cavity with a thick fibrous wall. The lining is smooth & the contents are inspissiated (thick pus). Secondary amyloidosis may complicate long standing cases. GRANULOMATOUS INFLAMMATION OF THE LUNG  Causes - Tuberculosis (see module 103). - Fungal diseases: Cryptococcosis, aspergillosis. - Sarcoidosis (non-infectious).  PULMONARY INFECTIONS BRONCHITIS AND TRACHEOBRONCHITIS. PNEUMONIA. - Lobar pneumonia. - Bronchopneumonia - Interstitial (viral). LUNG ABSCESS. - Aspiration - Post-pneumonic. - Bronchogenic carcinoma: - Pyemic. - Traumatic punctures or spread of infection from adjacent Organs. GRANULOMATOUS  OBSTRUCTIVE VERSUS RESTRICTIVE LUNG DISEASES Impaired Respiratory Functions Tests 1) OBSTRUCTIVE LUNG DISEASE 2) RESTRICTIVE LUNG DISEASES  Characterized by an increase in  Characterized by reduced lung resistance to air flow due to expansion. partial or complete obstruction at any level (excluding tumors and foreign body).  Difficulty in EXHALING the air  Difficulty in INHALING the air  The major diffuse obstructive  It occurs in two general categories: airway diseases are: - Chest wall disorders in the presence of - Emphysema. normal lungs. Examples are severe obesity, diseases of the pleura, - Chronic bronchitis. neuromuscular disorders. - Bronchiectasis. - Chronic interstitial lung diseases e.g. - Bronchial asthma. pneumoconiosis and interstitial fibrosis. OBSTRUCTIVE LUNG DISEASE - Emphysema. - Chronic bronchitis. - Bronchiectasis. - Bronchial asthma.  EMPHYSEMA  Definition: Permanent OVER-DISTENTION of air spaces distal to the terminal bronchioles, with DESTRUCTION of their walls.  PROTEASES EMPHYSEMA  Pathogenesis: PROTEASE ALVEOLAR WALL DESTRUCTION in emphysema likely INHIBITORS results from IMBALANCES between pulmonary PROTEASES and their INHIBITORS. 1) Tobacco smoke and air pollutants 1) Recruit neutrophils and macrophages. 2) Enhance elastase release from macrophages and neutrophils 3) Inhibit alpha 1 anti-trypsin. - The elastases unless checked by anti-elastases (e.g. alpha 1 antitrypsin), degrade the extracellular matrix and elastic tissue of the alveoli thus preventing alveoli from returning to normal size after their inflation with air during inspiration. 2) Congenital alpha 1 anti-trypsin deficiency - Develop panacinar emphysema at a young age if they smoke. ❖ There is marked individual variation in susceptibility to the development of emphysema. Multiple genetic factors control the response to injury after smoking.  EMPHYSEMA  Types - Emphysema is classified according to its anatomic distribution within the lobule. - The cluster of three to five acini are called a lobule The acinus is the structure distal to the terminal bronchioles, formed of respiratory bronchiole, alveolar duct and alveoli. 1) Centri-acinar (bronchiolar emphysema) 2) Distal acinar (Paraseptal). 3) Pan-acinar (panlobular).  EMPHYSEMA TYPE OF CENTRI-ACINAR PAN-ACINAR DISTAL ACINAR EMPHYSEMA (BRONCHIOLAR) (PANLOBULAR) (PARA-SEPTAL) DISTENDED - Central part of the acinus All air spaces distal to the Distal part of the acinus. Proximal part PART OF (respiratory bronchioles). terminal bronchiole i.e. of the acinus is normal ACINUS Distal alveoli are spared. the whole lobular unit SITE More common and severe in More commonly in the - Usually sub-pleural, or along the lobular the UPPER lobes, LOWER lung zones. connective tissue septae. particularly the upper - Usually in the UPPER half of the lung, segments. - It is a cause of spontaneous pneumothorax in young adults Forms multiple adjacent dilated air spaces, some forming cystic structures called bullae. COMMON Cigarette smokers & coal Alpha 1 antitrypsin Occurs adjacent to areas of pulmonary CAUSE workers’ pneumoconiosis deficiency. scarring or atelectasis.  EMPHYSEMA  Morphology: Gross: - Pan-acinar emphysema produce pale, dry, voluminous lungs that obscure the heart in x- ray. - In centri-acinar emphysema the lungs are less pale and less voluminous. The upper two thirds of the lung are more severely affected.  EMPHYSEMA  Morphology: Microscopic: - There is marked enlargement and dilatation of the air spaces with thinning and destruction of the alveolar wall. - The number of alveolar capillaries is diminished.  EMPHYSEMA  Conditions related to emphysema Compensatory emphysema: Compensatory dilatation of alveoli in response to loss of lung substance nearby. E.g. next to fibrosis or atelectasis. Commonly asymptomatic Bullous emphysema: It is not a separate type of emphysema. It is a localized accentuation of any form of emphysema. There are large cystic spaces (bullae) greater than 1 cm. Senile or atrophic emphysema: Occurs as a result of senile loss of elasticity of tissues accompanying the atrophic changes of aging. Asymptomatic  EMPHYSEMA  Conditions related to emphysema Interstitial emphysema: - Air collects out of the air spaces in the connective tissue septa of the lung and track into the connective tissue of the mediastinum and the neck. - It may occur spontaneously with sudden increase in intra-alveolar pressure (as violent coughing in children with whooping cough), or from perforating injuries of the lung. - There is marked swelling of the neck with crepitus under the skin. Air is absorbed spontaneously.  EMPHYSEMA  Clinical picture - Dyspnea, starts insidiously and is steadily progressive. - Finger clubbing due to hypoxia. - If associated with chronic bronchitis (in smokers), there is coughing and wheezing. - Barrel chest (increased antero-posterior diameter) due to lung overinflation.  Complications: 1) Pulmonary hypertension and right sided heart failure (cor pulmonale) 2) Respiratory failure from defective ventilation, perfusion & diffusion of gases with increased CO2 in blood, respiratory acidosis & death. 3) Rupture bullae containing air into pleura producing pneumothorax (air in pleural cavity).  CHRONIC BRONCHITIS  Definition: - Chronic bronchitis is defined clinically as PERSISTENT PRODUCTIVE COUGH for at least 3 consecutive months, for 2 consecutive years. - A subset of these patients, especially heavy smokers, develop chronic outflow obstruction, usually with associated emphysema. - Chronic bronchitis and emphysema are clinically grouped together under the name chronic obstructive pulmonary disease (COPD). Previously bronchial asthma was included in this group but not anymore.  Etiology: - The most important causative factor is CIGARETTE SMOKING. - Clinical episodes are associated with low grade bronchial infections by Hemophilus influenzae and streptococcus pneumonia.  CHRONIC BRONCHITIS  Pathology: The most important feature of chronic bronchitis is hypersecretion of mucus in trachea and large bronchi due to hypertrophy of submucosal mucous glands at these sites.  Bronchiolitis (small airway disease): Affection of the bronchioles is in the form of goblet cell metaplasia in the lining epithelium with formation of mucus plugs, inflammation and bronchiolar wall fibrosis. It is the submucosal fibrosis that leads to luminal narrowing and outflow obstruction.  BRONCHIAL ASTHMA  Definition: Chronic inflammatory disorder of the airways, characterized by paroxysmal reversible bronchospasm due to smooth muscle hyper-reactivity and increased mucus production.  Types: 1) Atopic (allergic) asthma: - Most common type. - Type I hypersensitivity reaction (IgE-mediated) triggered by environmental antigens (e.g. pollen, certain foods). - Positive family history of atopy is common with high serum IgE level. 2) Non-atopic asthma: - Hyper-reactivity of airways can be triggered by respiratory tract infections and chemical irritants. - No family history and serum IgE level is not elevated. 3) Aspirin induced asthma: Exact mechanism not known.  BRONCHIAL ASTHMA  Pathology The pathology in the lung has been described from autopsy of patients who died of prolonged severe attack of asthma (status asthmaticus). Gross: - Lungs are overinflated - Bronchial lumen contains large amounts of thick mucus plugs. - Bronchial wall is thick, swollen & red.  BRONCHIAL ASTHMA  Pathology Microscopic: - Occlusion of bronchi and bronchioles by MUCUS PLUGS which contain whorls of shed epithelium known as Curschmann spirals, numerous eosinophils and Charcot-Leyden crystals derived from eosinophils. - BRONCHIAL WALL  BRONCHIAL ASTHMA  Pathology Microscopic: - MUCUS PLUGS - The BRONCHIAL WALL shows: 1) Thickening of basement membrane 2) Smooth muscle hypertrophy. 1 3) Mucous gland hyperplasia. 2 3  BRONCHIAL ASTHMA  Clinical Picture: Wheezing (due to bronchospasm) & cough with scanty, tenacious mucus.  Complications: 1) Repeated attacks and bronchiolar inflammation can cause outflow obstruction and centri-acinar emphysema. 2) An acute prolonged attack is termed status asthmaticus which may end in death from respiratory failure.  BRONCHIECTASIS  Definition: Abnormal permanent dilatation of medium sized bronchi and bronchioles associated with chronic suppurative infection.  Mechanism (pathogenesis): Two processes are involved: OBSTRUCTION AND CHRONIC PERSISTENT SUPPURATIVE INFECTION. Either of them may come first.  Etiology 1) Congenital or hereditary conditions (e.g., cystic fibrosis, Kartagener syndrome) ▪ Kartagener’s syndrome: a rare hereditary disorder associated with bronchiectasis. Structural abnormalities of the cilia impair mucus clearance in the airways resulting in persistent infections. ▪ Mucoviscidosis (cystic fibrosis): A hereditary disease associated with thick mucus in exocrine glands, respiratory, gastrointestinal and reproductive tracts. Abnormally thick mucus secretions predisposes to obstruction & 2ry infection. 2) Septic bronchopneumonia particularly in children. 3) Bronchial obstruction (e.g., by tumor or foreign body).  BRONCHIECTASIS  Mechanism (pathogenesis): - Two processes are involved: OBSTRUCTION AND CHRONIC PERSISTENT SUPPURATIVE INFECTION. Either of them may come first. 1) IN SEPTIC BRONCHOPNEUMONIA: Severe persistent suppurative inflammation in bronchi or bronchioles causes: a) Loss of cough reflex and accumulation of secretions. b) Inflammation of the wall and weakening of the wall by fibrosis c) Peribronchial fibrosis and traction on the weak bronchial walls, leading to their dilatation. 2) IN CASE OF OBSTRUCTION as in foreign body and tumors a) There is accumulation of secretions which favor INFECTION. Infection damages the bronchial walls leading to their weakening b) The COMPLETE obstruction causes COLLAPSE of lung parenchyma, and the weak bronchial wall are exposed to the negative intrathoracic pressure with each inspiration leading to its dilatation.  Pathology: BRONCHIECTASIS Gross: - The disease is mostly bilateral; Most severe changes occur in peripheral lower lobes. - Airways can be dilated up to four times the normal size. - The dilated bronchi could be seen from hilum till the pleura (In the normal lung only the bronchi around hilum are seen, but the smaller bronchi towards the pleura are not seen by the naked eye due to their small diameter)  BRONCHIECTASIS  Pathology: Gross: - There are 3 types of dilatation: ▪ Saccular: dilatation involves a part of the circumference of a segment → sac like dilatation ▪ Fusiform: dilatation involves the whole circumference of a segment of the bronchus ▪ Cylindrical: dilatation involves the whole circumference of the whole length of the bronchus. - The bronchi appear thickened, with suppuration of their lining. - The pleura is thickened and fibrotic with adhesions  BRONCHIECTASIS  Pathology: Microscopic: ▪ Bronchi: - Lumen: filled with pus & blood. - Lining respiratory epithelium shows areas of ulceration and may show squamous metaplasia. - Wall shows intense acute and chronic inflammatory cells and fibrosis. ▪ Alveoli - Adjacent alveoli undergo fibrosis. - Patches of compensatory emphysema (to compensate for non- functioning alveoli). ▪ Pleura: Fibrosis and adhesions. BRONCHECTASIS BRONCHIAL ASTHMA  BRONCHIECTASIS  Clinical Presentation: - Persistent, severe cough, fever, and abundant purulent sputum. - Coughing can be associated with morning rising and positional changes that drain collected pus and secretions into the bronchi. - Symptoms may be episodic and precipitated by upper respiratory tract infection - Culture reveals mixed flora: staphylococci, streptococci, pneumococci, enteric organisms, Hemophilus influenza and pseudomonas aeruginosa.  BRONCHIECTASIS  Complications: 1)Hemoptysis with abundant foul smelling, yellowish red sputum (pus + blood). 2) Lung abscess – gangrene. 3) Spread of infection. as septic bronchopneumonia 4) Bilateral lung fibrosis , pulmonary hypertension & right sided heart failure (cor pulmonale). 5) Secondary amyloidosis (chronic destructive condition). 6) Squamous metaplasia (due to chronic irritation) which may lead to squamous cell carcinoma.  OBSTRUCTIVE LUNG DISEASES WHY OBSTRUCTIVE? MAIN SYMPTOM Loss of elastic recoil (functional obstruction) MUCOUS + CHRONIC BRONCHIOLITIS EMPHYSEMA Dyspnea fibrosis BRONCHITIS COUGH Spasm + mucous BRONCHIAL ASTHMA Cough with scanty tenacious sputum Pus in lumen + wall weakening BRONCHECTASIS Cough with excess purulent sputum RESTRICTIVE LUNG DISEASE  RESTRICTIVE LUNG DISEASES CHRONIC INTERSTITIAL LUNG DISEASES (CILDS)  Heterogeneous group of disorders characterized by bilateral, patchy, chronic involvement of the interstitium of the lung.  Many are of unknown cause.  The hallmark of these diseases is reduced compliance. More pressure is required to expand the lungs because they are stiff.  Clinical Manifestation: 1) Dyspnea. 2) Affection of the ventilation and perfusion causes hypoxia. 3) Patients may finally end with respiratory failure often with pulmonary hypertension and cor pulmonale.  RESTRICTIVE LUNG DISEASES normal CHRONIC INTERSTITIAL LUNG DISEASES  Clinical Manifestation: (CILDS)  Chest X-rays in many conditions show diffuse infiltration by tiny nodules (ground glass shadows).  Advanced forms of disease end in scarring and honey-comb lung appearance.  RESTRICTIVE LUNG DISEASES CHRONIC INTERSTITIAL LUNG DISEASES (CILDS)  Types: Idiopathic Pulmonary Fibrosis Cryptogenic Organizing pneumonia 1) Idiopathic pulmonary fibrosis. 2) Non- specific chronic interstitial pneumonia 3) Cryptogenic organizing pneumonia 4) Pulmonary involvement in collagen diseases as rheumatoid arthritis and systemic lupus erythematosus). 5) Sarcoidosis. 6) Pneumoconiosis  RESTRICTIVE LUNG DISEASES CHRONIC INTERSTITIAL LUNG DISEASES (CILDS) PNEUMOCONIOSIS  Definition: Lung disease caused by inhaled dust. Dust may be inorganic (mineral) or organic.  Include: SAME MECHANISM 1) Coal-worker’s pneumoconiosis (CARBON) Macrophage uptake…proteases 2) Silicosis (SILICA) release….Inflammatory 3) Asbestosis (ASBESTOS) reaction….Interstitial Fibrosis….Honey comb  RESTRICTIVE LUNG DISEASES CHRONIC INTERSTITIAL LUNG DISEASES (CILDS) PNEUMOCONIOSIS 1) Coal-Worker’s Pneumoconiosis - Used to be common among coal workers. Now much reduced. - The disease has several stages: Simple anthracosis: Presence of coal dust pigments which are taken by alveolar macrophages. Macules and nodules of dust –laden macrophages with delicate collagen fibers. Can lead to centri-lobular emphysema. Complicated stage: Progressive massive fibrosis with black pigment.  RESTRICTIVE LUNG DISEASES CHRONIC INTERSTITIAL LUNG DISEASES (CILDS) PNEUMOCONIOSIS 2) Silicosis  Silicosis is the most prevalent occupational disease. Silica is present in sand.  Workers involved in sand blasting or rock mining are affected.  Silica is engulfed by macrophages which then die and release their proteolytic enzymes which damage lung tissue followed by fibrosis.  The lung shows characteristic nodules of whorling fibrosis, in which silica particles can be detected by polarized light. And finally a honeycomb pattern may develop.  Silicosis increase the susceptibility to tuberculous infection.  RESTRICTIVE LUNG DISEASES CHRONIC INTERSTITIAL LUNG DISEASES (CILDS) PNEUMOCONIOSIS 3) Asbestosis  Asbestosis is used for insulation and manufacture of brake- linings and other friction materials.  Asbestosis manifests with dyspnea and dry cough.  Histologically, there is diffuse pulmonary fibrosis and honey- comb lung. Asbestos bodies may be recognized in the alveoli as golden brown beaded rods  Both cancer lung and mesothelioma (cancer of the pleura) occur in asbestos workers, but the relative risk for mesothelioma (which is normally a very rare tumor) is more than 1000 times greater.  ATELECTASIS & COLLAPSE  Definition: Failure of expansion of the lung or collapse of previously inflated lung, affecting part or all of one lung.  Types: Resorption atelectasis: - Occurs with COMPLETE airway obstruction e.g. mucus plugs post-operatively or with bronchial asthma, and foreign bodies in children. - Obstruction prevents air from reaching the alveoli, and the air already present becomes absorbed and the corresponding alveoli collapse. Compression atelectasis: - Associated with accumulation of fluid, blood or air in the pleural cavity, which compress and collapse the lung.  Effect: Atelectasis causes hypoxia and predisposes to bronchiectasis.  LUNG TUMORS ❖ MALIGNANT - SECONDARY (METASTASIS). - PRIMARY. ❖ BENIGN  TUMORS OF THE LUNG  MALIGNANT TUMORS - Malignant tumors of the lung are more common than benign tumors - These include: 1) Metastases (more common). 2) Primary malignant tumors. - The most important primary malignant tumor is carcinoma of the lung (95% of primary malignant tumors). - The remaining 5% include carcinoid tumor, fibrosarcoma, leiomyosarcoma and lymphoma.  BENIGN TUMORS The most commom benign tumor is HAMARTOMA which is a spherical (3-4cm) coin- like shadow on X ray. It consists mainly of mature cartilage admixed with fat, fibrous tissue and blood vessels.  CARCINOMA OF THE LUNG (BRONCHOGENIC CARCINOMA, LUNG CANCER)  Incidence: - Lung cancer is the leading cause of death from cancer in the world, with the worst overall prognosis. - The peak incidence is around the age of 50. - More male affection, but incidence in females is increasing.  Predisposing factors 1) Cigarette smoking. 2) Air pollution. 3) Pneumoconiosis (inorganic dusts) e.g. Silicosis, asbestosis… 4) Bronchiectasis.  Types: The most common types of carcinoma of the lung are: 1) Squamous cell carcinoma. 2) Adenocarcinoma. 3) Large cell carcinoma. 4) Small cell carcinoma.  CARCINOMA OF THE LUNG (BRONCHOGENIC CARCINOMA, LUNG CANCER) 1. Squamous Cell Carcinoma: - More common in men than women, closely related to smoking. - They are preceded by squamous metaplasia, dysplasia and carcinoma insitu which may last several years. Gross: - Centrally located mass: 85% of tumors arise in major bronchi and present as: ❑ An endobronchial growth. ❑ An infiltrative tumor that invade the bronchial wall and surrounding lung tissue. Microscopic: Squamous cell carcinoma with various grades of differentiation and keratin pearl formation.  CARCINOMA OF THE LUNG (BRONCHOGENIC CARCINOMA, LUNG CANCER) 2) Adenocarcinoma: - Most common type of lung cancer in women. Gross: - Most are peripherally located and may be multiple. - Can occur centrally in men. - Seeding of the pleura occur early. - The precursor of adenocarcinoma is thought to be atypical adenomatous hyperplasia which progresses to adenocarcinoma in situ (previously called bronchiolo- alveolar carcinoma).  CARCINOMA OF THE LUNG (BRONCHOGENIC CARCINOMA, LUNG CANCER) 3) Large cell carcinoma: Large cell undifferentiated carcinoma that have no glandular or keratin formation (probably represents squamous cell carcinoma or adenocarcinoma that are so undifferentiated that they can no longer be recognized by light microscopy).  CARCINOMA OF THE LUNG (BRONCHOGENIC CARCINOMA, LUNG CANCER) 4) Small cell carcinoma: - A rapidly growing and early metastasizing tumor. Gross: A central mass. Microscopic:  Cells are twice the size of small lymphocytes with scant cytoplasm.  Necrosis is always present and may be extensive.  The tumor cells can be stained by anti chromogranin which is a marker of neuroendocrine cells. - These tumors often secrete a variety of polypeptide hormones that may result in paraneoplastic syndromes.  CARCINOMA OF THE LUNG (BRONCHOGENIC CARCINOMA, LUNG CANCER)  Clinical Presentation: Cough, hemoptysis, dyspnea, chest pain (pleuritic pain) and cachexia.  Spread and complications: 1. Spread: - Direct: 1) Pleural seeding especially in adenocarcinoma. 2) Pericardium, mediastinum and esophagus. 3) Pancoast tumors: Apical neoplasms may invade the brachial or cervical sympathetic plexusus to cause pain in the distribution of ulnar nerve, Horner syndrome (ipsilateral miosis, ptosis and anhydrosis). - Lymphatic: To the hilar and mediastinal lymph node. The supraclavicular node affection (Virchow’s node) may be the first presentation. - Blood: To the brain, bones, liver, adrenals or other lung.  CARCINOMA OF THE LUNG (BRONCHOGENIC CARCINOMA, LUNG CANCER)  Spread and complications: 1. Spread. 2. Hemoptysis. 3. Obstruction leading to collapse, secondary infection, bronchiectasis or lung abscess. 4. Paraneoplastic syndrome: 3-10% of patients with lung cancer develop clinical paraneoplastic syndrome due to secretion of polypeptide hormones. It presents in one or more of the following forms: Hypercalcemia. Cushing syndrome. Myasthenia gravis. Excess ADH.  SECONDARY LUNG TUMORS - More common than primary tumors. - Reach the lung by blood or lymphatic spread. - The secondaries appear as discrete nodules scattered throughout the lung. - Both carcinoma and sarcoma can metastasize to the lung. - Carcinomas that commonly give rise to secondaries in the lung are those of the breast, kidney, and GIT.  PULMONARY DISEASES OF VASCULAR ORIGIN PULMONARY HYPERTENSION  Causes: 1. Chronic obstructive or interstitial lung disease. 2. Recurrent pulmonary emboli. 3. Mitral stenosis. 4. Congenital left to right shunt due to increased pulmonary blood flow 5. Idiopathic or primary pulmonary hypertension.  Pathology: Vascular changes similar to those seen in systemic hypertension: 1. Main elastic artery show atheroma. 2. Medium sized arteries: cellular and smooth muscle hyperplasia leading to thick wall vessels and narrow lumen. 3. Small arteries and arterioles: hyalinosis, elastosis and narrow lumen. DISEASES OF THE PLEURA INFLAMMATORY DISORDERS TUMORS  DISEASES OF THE PLEURA INFLAMMATORY DISORDERS  PLEURAL EFFUSION  EMPYEMA  HEMOTHORAX  CHYLOTHORAX  PNEUMOTHORAX  DISEASES OF THE PLEURA INFLAMMATORY DISORDERS PLEURAL EFFUSION  Definition: Accumulation of fluid in the pleural cavity. This fluid may be - Transudate (as in heart failure and liver cirrhosis) and is then called hydrothorax. - Exudate ▪ Causes of exudative pleural effusion 1) Infections as TB, lung abscess, pneumonia. 2) Viral pleurisy 3) Collagen diseases as rheumatoid arthritis and systemic lupus erythematosus. 4) Pulmonary infarction IRRITATION 5) Metastatic tumors to the pleura (frequently hemorrhagic). Pathology of exudative pleural effusion: Serofibrinous inflammation (see general)  DISEASES OF THE PLEURA INFLAMMATORY DISORDERS EMPYEMA  Definition: Suppurative inflammation of the pleura with pus in the pleural cavity,  Etiology: pyogenic organisms: Staph, strept, pneumococci…… - Direct spread from lung infection, abscess, bronchiectasis, pneumonia. - Trauma e.g. penetrating infected stab wounds - Blood spread in septicemia  Pathology: - Diffuse or total empyema (usually acute): pleural cavity is filled with purulent effusion resulting in collapse of underlying lung tissue - Localized pus in pockets, as a result of fibrous adhesions (more common)  DISEASES OF THE PLEURA INFLAMMATORY DISORDERS EMPYEMA  Complications 1) Spread: - Direct: Chest sinuses discharging pus. Pericardium and mediastinum. - Blood: Toxemia, septicemia, pyemia. 2) Chronic empyema resulting in secondary amyloidosis.  DISEASES OF THE PLEURA INFLAMMATORY DISORDERS HEMOTHORAX  Accumulation of blood in the pleural cavity due to rupture of aneurysm or trauma. CHYLOTHORAX:  Accumulation of milky white fluid (lymph).  It is usually left sided.  Caused by thoracic duct obstruction due to malignancy.  DISEASES OF THE PLEURA INFLAMMATORY DISORDERS PNEUMOTHORAX  Definition: Air in pleural cavity.  Etiology 1-Trauma: air is sucked through a chest wall defect or enters the pleura from laceration of the lung by a broken rib. 2-Spontaneous pneumothorax as a complication of rupture of an emphysematous bulla or after a bout of severe coughing  Clinical Picture: - Sudden onset of severe chest pain & dyspnea - Physical examination reveals hyper-resonace over one lung with decreased breath sounds by auscultation.  Complications: Lung collapse.  DISEASES OF THE PLEURA INFLAMMATORY DISORDERS  PLEURAL EFFUSION  EMPYEMA  HEMOTHORAX  CHYLOTHORAX  PNEUMOTHORAX  PLEURAL TUMORS MALIGNANT MESOTHELIOMA  Incidence: - Occurs in patients with asbestos exposure (miners, insulator factories or living in nearby areas). There is also increased incidence of mesothelioma in family members of asbestos workers. (Asbestos exposure through contaminated clothes). - Usually above 50 years, but may occur in younger ages.  Gross: Mesothelioma is usually unilateral, starting as small nodules on the visceral pleura and extends to cover the whole lung and obliterate the pleural cavity. The tumor is yellowish white.  PLEURAL TUMORS MALIGNANT MESOTHELIOMA  Microscopic: Epithelioid type: Cuboidal cells forming papillae and acini (looks like adenocarcinoma) Sarcomatoid type: sheets of spindle malignant cells (looks like sarcoma) Mixed type (biphasic): Epithelial + sarcomatous  Prognosis: Poor  Complications 1) Spread: direct spread to pericardium, mediastinum, aorta and esophagus. 2) Compression collapse of the lung.  PLEURAL METASTASIS  This a very common condition.  Metastasis from any malignant tumor in the body.  The most common primary tumors are breast and lung reaching pleura through blood spread or lymphatic spread.  HEMOPTYSIS  Definition: Coughing of blood  Causes: - Local causes: 1) Bronchitis, bronchiectasis, pneumonia, lung abscess 2) Chronic fibrocaseous tuberculosis 3) Carcinoid tumor, carcinoma of the lung and secondaries of the lung. 4) Chronic venous congestion of the lung - General causes: leukemia, hemophilia, purpura, vitamin C and K deficiency.  TRUE OR FALSE  Fibrosis is more extensive following septic bronchopneumonia than in lobar pneumonia.  Diphtheria is a chronic suppurative inflammation.  Most common site of laryngeal squamous cell carcinoma is the glottic region.  Non-atopic asthma is commonly hereditary.  Septic bronchopneumonia usually occurs in healthy middle aged individuals  The most common causative organism in lobar pneumonia is Streptococcus pneumonia.  Singer’s node is commonly unilateral.  TRUE OR FALSE  Laryngeal squamous cell papilloma is usually single in children.  Pyemic lung abscesses are commonly multiple and near the blood vessels.  Bronchogenic squamous cell carcinoma is most commonly peripheral.  Laryngeal squamous cell papilloma is commonly caused by HPV type 16.  Aspiration lung abscess is more common in left lung.  Among types of emphysema, spontaneous pneumothorax is most common in distal acinar.  Bronchogenic carcinoma is more common then lung metastasis.  ENUMERATE  Types of pneumonia.  Types of emphysema.  Types of lung abscess.  Stages of lobar pneumonia.  Complications of bronchiectasis.  Complications of lung abscess. DEFINE  Bronchectasis.  Emphysema.  Match  Rhinoscleroma.  Pan-acinar emphysema.  Smoking  Thickened basement membrane.  Allergic nasal polyp.  Thoracic duct obstruction.  Lung adenocarcinoma  Acute diffuse non-suppurative fibrinous  Asbestosis. inflammation  Apical lung tumors  Chromogranin.  Alpha 1 anti-trypsin  Mickulikz cells deficiency.  Centri-acinar emphysema.  Small cell carcinoma.  Mesothelioma.  Chylothorax  Atypical adenomatous hyperplasia.  Lobar pneumonia  Horner syndrome