Pathology 310 PDF

# PATHOLOSIS ## RESPIRATORY TRACT ### ACUTE INFECTIONS OF UPPER RESPIRATORY TRACT #### RHINITIS - Manifesting as common cold - Causative organism: Rhinovirus, respiratory syncytial virus, para influenza and influenza virus - Manifestations: Nasal congestion and watery discharge, slight fever - M...

# PATHOLOSIS ## RESPIRATORY TRACT ### ACUTE INFECTIONS OF UPPER RESPIRATORY TRACT #### RHINITIS - Manifesting as common cold - Causative organism: Rhinovirus, respiratory syncytial virus, para influenza and influenza virus - Manifestations: Nasal congestion and watery discharge, slight fever - Morphology: Acute catarrhal inflammation with excess mucus #### ACUTE PHARYNGITIS - Mild: sore throat with common cold - Severe: β hemolytic streptococcus and adenovirus → marked hyperemia and exudate #### ACUTE TONSILLITIS - Common in children - Causative organism: β hemolytic streptococcus - Morphology: - Gross: swelling, redness with spots of pus (tonsillar crypts draining suppurating lymphoid follicles) - Microscopic: acute inflammatory cells with pus in lymphoid follicles - Complications: - Spread: - Direct: (Quinzy peritonsillar abscess, otitis media, pharyngitis, laryngitis) - Lymphatic: lymphadenitis (cervical lymph nodes) - Blood: bacteremia- toxemia- septicemia- pyaemia - Hypersensitivity: to streptococci → rheumatic fever - post streptococcal glomerulonephritis - Chronicity: chronic tonsillitis #### ACUTE SINUSITIS - Proceeded by acute or chronic rhinitis → edema → impairment of sinus drainage → retention of secretions → 2ry bacterial infection → periapical tooth infection → maxillary sinusitis ### OTITIS MEDIA - Causative organism: same as rhinitis - Morphology: - Starts as catarrhal inflammation → 2ry infection → purulent inflammation ### DIPHTHERIA - Life-threatening with pseudomembranous inflammation of throat and tonsils of children - Causative organism: droplet infection with corynebacterium diphtheria - Incubation period: 2- 5 days - Sites: tonsils, soft palate, larynx, trachea - Pathological features: - **Pseudomembranous inflammation:** - Gross: Multiple small yellow foci of necrosis → enlarge & fuse → continues membrane raised and adherent → bleeding ulcerating surface, reforms again if removed → yellow foci of necrosis, adherence & reforms again - Microscopic: dilated congested vessels, edema, fibrin, PMNL's (acute inflammatory cells) - Fibrin network with dead epithelia cells, PMNL's, pus cells and macrpohages - **Acute cervical lymphadenitis:** bilateral separate enlarged mobile soft, tender, painful severs acute toxemia - Complications: - Asphyxia by: edema, membrane, laryngeal spasm - Acute Toxemia: - toxic myocarditis, acute heart failure - cloudy swelling and focal necrosis of parenchymal organs - Hemorrhage and necrosis of supra renal cortex → acute insufficiency - Nerve affection → temporary paralysis of palatine, facial, pharyngeal, laryngeal muscles ## ALLERGIC INFLAMMATION OF UPPER RESPIRATORY ### ALLERGIC RHINITIS - Atopic IgE immune mediated reaction (type I hypersensitivity reaction) - Causes: pollen, dust.... type I hypersensitivity reaction - Gross: edema, erythema, of nasal mucosal membranes - Microscopic: acute allergic inflammation with eosinophils + submucous edema - Complications: - Repeated attacks → nasal polyp rich in plasma cells, lymphocytes, eosinophils ### NASAL POLYP - Recurrent allergic rhinitis → edematous mucosal protrusions rich in: plasma cells, lymphocytes, eosinophils → obstruct airway - Gross: - multiple soft pink polyps projecting from mucosa of nose and sinuses - Microscopic: - Respiratory epithelium: pseudo stratified columnar ciliated with chronic irritation → metaplasia → st. squamous epithelium - Hyperplasia of mucous glands - Thick pink basement membrane - With CT core: thick wide edematous infiltrated by plasma cells, lymphocytes, eosinophils - Complications: - nasal obstruction - 2ry infection - epistaxis ### ADENOIDS - Hyperplastic lymphoid tissue at posterior wall of nasopharynx - Due to chronic infections at children & infants - Effects & Manifestations: - Adenoid face: - Mouth breathing - Opened mouth - short upper lip - protruding upper incisors - narrow nasal openings - absent nasolabial folds - Complications: spread of infections - otitis media - pharyngitis ## CHRONIC SPECIFIC INFECTIONS OF UPPER RESPIRATORY TRACT ### RHINOSCLEROMA - Granulomatous inflammation of the nose may affect larynx, pharynx (laryngoscleroma) - Causative organism: Klebsiella rhinoscleromatis bacteria (endemic at Egypt) - Gross: - Small hard nodular mass or masses filling nasal cavity - Microscopic: - Chronic inflammatory infiltration involving submucosa - Mickulicz cells: predominant cells. Large Macrophages (bacteria multiplies inside macrophages) with foamy cytoplasm with small pyknotic nucleus - Russell bodies: plasma cells with hyaline change (accumulated IGs) - Late: Fibrosis - Complications: - 2ry infections - Ulceration - Nasal obstruction - deformity ## TUMORS OF NASOPHARYNX ### JUVENILE ANGIOFIBROMA: - Uncommon – exclusive At males – during adolescence - Benign mesenchymal tumor of nasopharynx - Extremely vascular → nasal bleeding (epistaxis) - Proliferating fibroblasts with wide blood vessels ## NASOPHARYNGEAL CARCINOMA - Incidence: Rare Common at Chinese, EBV - Histological Variants: - Keratinized squamous cell carcinoma - Non- keratinizing squamous cell carcinoma - Undifferentiated carcinoma: excess lymphocytes at stroma (lymphoepithelioma) The most commonly linked to EBV - Spread: - Direct, lymphatic to cervical LNs late to blood - Prognosis and treatment: - Radiosensitive - Lymphoepithelioma has better prognosis than squamous cell carcinoma with irradiation - Causes: - Trauma - FB - Tumors: angiofibroma - Nasal polyps - Rhinoscleroma - General causes: HTN, hemophilia, leukemia Vit C, K deficiency ### EPISTAXIS: Bleeding from nose ## LARYNX ### ACUTE LARYNGITIS: - Acute catarrhal inflammation - Causes: inhalation of irritant fumes or allergy - Causative organism: para influenza virus is the most common cause At children laryngobronchitis (croup) harsh persistent cough and inspiratory stridor ### TUBERCULOSIS OF LARYNX: - As complication of 2ry pulmonary TB - When sputum is coughed up - Ulcer: Undermined edges with caseous floor ## TUMORS ### SQUAMOUS CELL PAPILLOMA - Benign epithelial tumor - Cause: HPV 6,11 - at children: vertical transmission from infected mother during delivery - at adults or multiple, recurrent esp. at children - Gross: fine finger like surface protrusions - Microscopic: - Papillary thin fibrovascular core covered by hyperplastic stratified squamous epithelium with (hyperkertosis, parakeratosis, acanthosis) ### LARYNGEAL NODULE (SINGER NODULE) - Nodule at middle third of the vocal cords - Etiology: - heavy smoking (unilateral) - singers nodule excessive use of voice (bilateral) - Gross: - Smooth hemispheric protrusion less than 0.5 cm in diameter, firm, covered by mucosa - Microscopic: - Mucosa: covered by stratified squamous epithelium - Subepithelium: vascularized fibrous tissue with pink hyaliniosis - Clinical pic.: hoarseness of voice - Complications: - Hoarseness of voice - Recurrence after removal ### SQUAMOUS CELL CARCINOMA - > 95% of laryngeal cancers - Common in males > females 7:1 40 years old - Sites: Mostly On vocal cords but may arise above or below vocal cords (supraglottic- infraglottic) - Predisposing factors: - Chronic irritation: smoking, asbestos → dysplasia, carcinoma insitu → invasive carcinoma - Morphology: - Gross: ulcerative fungating mass - Microscopic: - squamous cell carcinomas - Glottic are keratinized and better differentiated than others - Clinically: - Smoker above 40 years old with hoarseness of voice - Complications: - Direct spread: esophagus, trachea, pharynx - Lymphatic to cervical LNs esp. supraglottic (area rich in lymphatics) ## LUNG DISEASES ### PULMONARY INFECTIONS #### ACUTE TRACHEOBRONCHITIS - Causes: - Viral infection: common cold, influenza, measles - Bacteria: streptococci, staphylococci, pneumococci - Pathology: - Chronic irritation: dust, smoking irritant gases - Catarrhal inflammation, congested mucosa with mucoid or mucopurulent exudate #### PNEUMONIA ##### Bacterial pneumonia - Definition: Inflammation of lung parenchyma - Anatomic patterns: two - **LOBAR PNEUMONIA:** - Part or all of a lobe is filled with exudate - By radiograph: consolidation - **BRONCHOPNEUMONIA:** - Patchy distribution of inflammation involves more than one lobe - Cause: initial infection of bronchi and bronchioles + extension into lung alveoli - Clinical picture of pneumonia: - Common Follow viral upper respiratory tract infection - Abrupt onset: high fever, chills, pleuritic chest pain - Muco-purulent sputum - Occasional hemoptysis - **LOBAR PNEUMONIA:** - Acute diffuse fibrinous inflammation of alveoli affects part or all of one or more lobes are homogeneous filled with exudate on radiographs as a lobar consolidation - Causative organism: *Streptococcus pneumoniae (pneumococci) > 90%* - Highly virulent affects previously healthy young individuals (middle aged). - Route: airborne by droplet - Pathology (morphology): classic example of acute inflammation - Site: lower lobes or right middle lobe is most involved - Four stages: - Congestion: lasts for 24 hrs - lobe is heavy, red, edema - *Microscopic:* lung alveoli are filled with protein rich exudate, capillaries show hyperemia - Red hepatization: lasts for few days - lung is red solid airless, lobe, liver-like consistency - *Microscopic:* the alveolar spaces are uniformly filled with neutrophils, some lymphocytes and macrophages, red cells, and fibrin - Grey hepatization: lasts for few days - the lung is dry, grey, firm, solid - *Microscopic:* - Lysis of RBC's - accumulation of fibrin → shrinks away from alveoli - **Resolution:** on 8-10 days in untreated cases - liquefaction and absorption of Exudates - enzymatic digestion of inflammatory debris macrophages, coughed up - the lung returns to normal - **Fate:** most cases resolution (not common) - **Complications (not common).** - **1- failure of resolution → Carnification (organization of exudate -> lung becomes like piece of flesh)** - **2- Toxemia: on 9th day acute heart failure due to toxic myocarditis** - **3- Spread:** - **Direct: empyema, pericarditis, mediastinitis** - **Blood:** toxemia, septicemia, meningitis, arthritis, infective endocarditis - **4- Post pneumatic lung abscess & gangrene:** focal necrosis and suppuration, putrefactive organisms - **N.B:** - **Consolidation:** solidification of lung tissue due to inflammatory exudate replacing air in alveolar spaces - When affects whole lobe → solid (liver like = hepatization) #### BRONCHOPNEUMONIA (SEPTIC BRONCHOPNEUMONIA) - ✓ patchy areas of consolidation centered on inflamed bronchioles - ✓ infection of bronchi and bronchioles then extension into lung alveoli - ✓ one or several lobes, basal and bilateral - ✓ nature: Suppurative inflammation - **Etiology:** - **Predisposing factors:** - In extreme of ages: infants, old age - With debilitating diseases: diabetes, cancer, heart failure - Complication of viral bronchitis - **Causative organism:** - Streptococcus pneumoniae. H influenza, staph. Aureus, Klebsiella - Hospital acquired pneumonia: MERSA, pseudomonas, Morophology - **Gross:** - bilateral and basal (lower lobe) - patchy yellow consolidation (purulent) (bronchioles contain pus) - **Microscopic:** - Suppurative (neutrophilic) exudate filling bronchi, bronchioles, alveoli - Alveoli are filled with pus (patchy areas of consolidations) - **Complications (very common):** - Death if debilitated patient - Post pneumatic abscess & spread: empyema, pericarditis, mediastinitis - toxemia: toxic myocarditis - septicemia → meningitis, arthritis, infective endocarditis - Fibrosis: common due to tissue destruction by suppuration - Bronchiectasis: healing of bronchial wall by fibrosis → weak walls → permanent dilatation of lumen by traction on wall by peribronchial fibrosis ### ATYPICAL PNEUMONIA - Viral or mycoplasma pneumonia - Definition: inflammation Confined to alveolar septa and interstitium - Atypical due to absence of consolidation on physical examination and lack of alveolar exudate on radiology - Cause: - Mycoplasma pneumoniae - Virus: influenza virus, adenovirus, syncytial viruses - Pathogenesis: - Attachment of organism to respiratory epithelium then necrosis and inflammatory response - Pathology: - Gross: - Patchy or involve whole lobes - Unilateral or bilateral - Microscopic: - Infiltration by mononuclear lymphocytes, macrophages, few plasma cells confined to interstitium with little or without alveolar exudate - In severe cases: diffuse alveolar damage → formation of hyaline membrane of fibrin (adult respiratory distress syndrome (ARDS)) ### LUNG ABSCESS - Definition: localized suppurative inflammation → cavity containing pus - Causative organism: staph. aureus, pneumococci, klebsiella streptococcus pyogenous - Causes and types: 1ry on healthy lung or 2ry on diseased lung - Aspiration lung abscess: - Aspiration of infected materials during oral surgery - Vomitus during anesthesia - FB or food: Comatose patients or with depressed cough reflex (alcoholic intoxication, debilitated patients) - Morphology: - Single - On right side - Posterior segment of upper lobe or apex of lower lobe - More direct course for aspirated material from trachea when the patient is recumbent - Wall: Irregular congested thin wall - Shreddy yellow pyogenic membrane containing yellow pus - Overlying pleura: pleurisy - **Post pneumatic abscess:** - One or more in background of bronchopneumonia or pneumonias as a complication - **Bronchial obstruction with bronchogenic carcinoma:** - Distal atelectasis and aspiration of blood and tumor fragments - **Pyemic abscess:** - Septic embolism from septic thrombophlebitis of systemic veins or from infective endocarditis of the right side of the heart - Morphology: - Multiple small next to blood vessels. - Yellow spots surrounded by zone of congestion(too small to form cavities) - Direct traumatic puncture or spread from adjacent organ: - Direct spread: from mediastinum - Fate and complications: - Small: resolve with treatment - Rupture into bronchus: hemoptysis & cough of purulent sputum - Rupture into pleural cavity: empyema and pyopneumothorax - Lung Gangrene: irregular cavity with necrotic lining + black color, foul odor - Embolization of septic emboli to brain: meningitis and brain abscess - Chronic lung abscess: well defined thick fibrous wall with smooth wall contains thick inspissated thick pus - 2ry amyloidosis with long standing cases ## GRANULOMATOUS INFLAMMATION OF THE LUNG - 1- tuberculosis - 2- sarcoidosis (autoimmune noninfectious) - 3- fungal: aspergillosis, cryptococcoisis ## OBSTRUCTIVE VS RESTRICTIVE PULMONARY DISEASES ### Diffuse pulmonary diseases #### Obstructive (airway) disease: the ratio of FEV1/ FVC is decreased - limitation of air outflow - increase in resistance due to partial or complete obstruction (excluding tumors and FB) - major diffuse obstructive airway diseases: - emphysema - chronic bronchitis - bronchiectasis - bronchial asthma #### Restrictive disease: Ratio of FEV1 / FVC is near normal. - reduced expansion - (-) total lung capacity. - Causes (two categories): - chest wall disorders in normal lungs: - severe obesity, diseases of the pleura, neuromuscular disorders - Chronic interstitial lung diseases: - pneumoconiosis - interstitial fibrosis, sarcoidosis ## OBSTRUCTIVE LUNG (AIRWAY) DISEASES ### EMPHYSEMA - Permanent over distension of the air spaces distal to the terminal bronchioles + destruction of their walls without fibrosis - Types of Emphysema - **CENTRIACINAR (CENTRILOBULAR) (BRONCHIOLAR) EMPHYSEMA:** - The central or proximal parts of the acini (respiratory bronchioles) are affected, while distal alveoli are spared. - More common and sever In the upper lobes (apical segments). - At cigarette smokers, coal worker pneumoconiosis - **PANACINAR (PANLOBULAR) EMPHYSEMA:** - The whole lobular unit, acini are enlarged, distal to terminal bronchioles from the level of the respiratory bronchiole to the terminal alveoli in the lower lung zones - in a1-antitrypsin deficiency. - **DISTAL ACINAR (PARASEPTAL) EMPHYSEMA:** - proximal portion of the acinus is normal but the distal part is affected. - adjacent to the pleura, at the margins of the lobules (subpleural). Along lobular connective tissue septa - It occurs adjacent to areas of fibrosis, scarring, or atelectasis ### PATHOGENESIS - Imbalance between pulmonary protease and inhibitors - Exposure to toxic substances: tobacco smoke and air pollutants → inflammation → recruit neutrophils, macrophages and neutrophils at same time (--) a1-antitrypsin. - Smoking → (++) elastase release from macrophages and neutrophils at same time (--) a1-antitrypsin - Elastase is checked by antielastases (a1-antitrypsin) - Elastases → degrade extracellular matrix (ECM) and elastic tissue of alveoli - prevent alveoli from returning to normal size after inflation during inspiration - congenital al-antitrypsin deficiency → panacinar emphysema at young age - marked individual variation in susceptibility to emphysema because multiple genetic factors control the response to injury after smoking. ### MORPHOLOGY - **Gross:** - **Panacinar emphysema:** pale, dry, voluminous lungs that obscure the heart. - **centriacinar emphysema:** less voluminous and less pale. the upper two thirds of the lungs are more severely affected. - **Microscopic:** - thinning and destruction of alveolar walls without fibrosis → marked enlarged air spaces - loss of septa → (-) number of alveolar capillaries ### CLINICAL FEATURES - Dyspnea: starts insidious and steady progressive - In patients with chronic bronchitis, cough and wheezing - Barrel chest (++ AP diameter) overinflation - Finger clubbing due to hypoxia - **Complications:** - Pulmonary HTN → RHF → corpulmonale - Respiratory failure: (--) ventilation (--) perfusion - (++) Co2 in blood → acidosis & death - Rupture of bulla → pneumothorax ### Conditions Related to Emphysema: SIBK - **Compensatory emphysema:** Asymptomatic - Loss of lung substance nearby → next to fibrosis or atelectasis → compensatory dilation of alveoli & after surgical removal of a diseased lung or lobe - **Bullous emphysema:** - Not separate type of emphysema - Localized accentuation of any form of emphysema → large subpleural blebs or bullae (large cystic spaces greater than 1 cm in diameter) they may rupture → pneumothorax. - **Senile atrophic emphysema:** asymptomatic - senile loss of elasticity accompanying the atrophic changes at old age - **Interstitial (Medial) emphysema:** - Air collect out of the air spaces in the connective tissue septa of the lung → track into connective tissue of the mediastinum and the neck ### CAUSES: - Spontaneous with a sudden increase in intra alveolar pressure (violent coughing in children with whooping cough). - from perforating injuries of the lung. - Clinical pic: - marked swelling of the head and neck - crepitation under skin - air is absorbed spontaneously ### CHRONIC BRONCHITIS - The diagnosis is clinical: persistent productive cough for at least 3 consecutive months in at least 2 consecutive years - Heavy smokers develop chronic outflow obstruction with associated emphysema ### COPD: chronic bronchitis + emphysema (bronchial asthma is not involved any more in this group) - Etiology: - Heavy smokers - Clinical episodes are associated with low grade bronchial infections H influenza, streptococcus pneumonia ### PATHOLOGY: - hypersecretion of mucus, in the large airways (trachea and large bronchi). - hypertrophy of mucous glands in the trachea and main bronchi → marked increase in mucin-secreting goblet cells - In contrast with asthma, there are no eosinophils in chronic bronchitis. ### BRONCHIAL ASTHMA - Definition: chronic inflammatory disorder of airways with paroxysmal recurrent reversible episodes of bronchospasm due to smooth muscle hyper reactivity + increase mucous production - Types: - **ATOPIC (ALLERGIC): the most common type** - type I IgE-mediated hypersensitivity reaction - is triggered by environmental antigens: dusts, pollen, foods - A positive family history of atopy and/or asthma - Asthmatic attacks are preceded by allergic rhinitis, urticaria, or eczema. - A skin test: + ve - **NONATOPIC:** hyper reactivity of airway can be triggered by respiratory infections (viral) + chemical irritation - no family history - serum Ig E is not elevated - **ASPIRIN INDUCED:** - present with triad rhinitis, sinusitis and asthma after exposure to aspirin ### MORPHOLOGY: from autopsy of prolonged sever attack (status asthmaticus) - Gross: - lungs are overinflated - bronchial wall: Thick swollen red - Bronchial lumen: Occlusion by large amount of thick, mucous plugs. - Histologically: - Mucous plugs contain whorls of shed epithelium (Curschmann spirals). - Numerous eosinophils - Charcot-Leyden crystals (derived from eosinophils) - Bronchial wall shows: - Thickening of basement membrane - hypertrophy of the submucosal glands - Hypertrophy and/or hyperplasia of the bronchial smooth muscles ### CLINICAL FEATURES - Wheezing - Cough with scanty tenacious mucous - Repeated attacks of bronchial inflammation → central airway obstruction due to airflow obstruction. - Prolonged emphysema → Status asthmaticus → death from respiratory failure ### BRONCHIECTASIS - permanent dilation of medium sized bronchi and bronchioles associated with chronic suppurative infection - caused by destruction of the muscle and the supporting elastic tissue - Etiology: - **Congenital or hereditary conditions:** - **KARTAGENER SYNDROME:** - Rare hereditary disorder associated with bronchiectasis. ### PATHOGENESIS - Two processes any one of them can come first: Obstruction + chronic persistent infection. - Septic bronchopneumonia: sever persistent suppurative necrotizing inflammation in the bronchi or bronchioles - loss of cough reflex - accumulation of secretions - inflammation of wall → weakening of wall by fibrosis - superimposed infection → damage of weak walls → dilatation - peribronchial fibrosis → traction (-) clearance and accumulation of secretions → obstruction by FB or cancer (--) bronchial wall → Collapsed lung parenchyma with weak bronchial wall - Intrathoracic negative pressure with each inspiration → irreversible dilation. - **MORPHOLOGY** - Gross: bilateral & sever at peripheral lower lobes - Lower lobes bilaterally more usual diameter and bronchioles. - Airways are dilated four times their distal bronchi - bronchi appear thickened with suppuration - Pleura: Thickening and fibrosis with adhesions (subpleural ectatic bronchi) - Dilated bronchi could be seen From hilum to the pleura - Types: - Saccular bronchiectasis: apart of circumference of a segment → sac like dilatation - Fusiform bronchiectasis: the whole circumference of segment of the bronchus - Cylindrical bronchiectasis: the whole circumference of the whole length of bronchus - Microscopic: - Bronchi: - lumen filled with pus & blood - epithelial lining → shows areas of ulceration. - Intense acute and chronic inflammatory exudate - Alveoli: adjacent → fibrosis. Others → compensatory emphysema - pleura: fibrosis and adhesions - Clinical Features - episodic and precipitated by upper respiratory tract infections. - severe, persistent cough with mucopurulent sputum - cough can be associated with morning rising, positional changes → drain collected pus and secretions into bronchi. - Culture: mixed flora: staph. Aureus, strept. Cocci, pneumococci, H. influenza, pseudomonas aeruginosa. - **Complications:** - frank hemoptysis with foul smelling, yellow red sputum - lung abscess - lung gangrene - spread: empyema, pericarditis, mediastinitis, Metastatic brain abscesses - bilateral lung fibrosis → PHT → RHF → cor pulmonale - Secondary reactive amyloidosis - Squamous metaplasia → squamous lung carcinoma ## (RESTRICTIVE, INFILTRATIVE) LUNG DISEASES ### CHRONIC INTERSTITIAL LUNG DISEASES (CILDS) - reduced expansion of the lung - Reduction in total lung capacity. - Chronic interstitial diseases: heterogeneous group of disorders (many are unknown causes) - Bilateral - Patchy - chronic involvement of interstitium of alveolar walls - The hallmark features: - (--) compliance → stiff lung so more pressure to expand the lungs → main clinical presentation is dyspnea, cyanosis - Damage to the alveolar epithelium and interstitial vasculature → (--) ventilation perfusion ratio → hypoxia. - Scarring → "honeycomb" lung. - Chest radiographs X rays: diffuse small tiny nodules, "ground glass shadows." - End with respiratory failure, pulmonary hypertension and cor pulmonale - Types: - PS CIN - 1- idiopathic pulmonary fibrosis - 2-Non-specific chronic interstitial pneumonia - 3-Cryptogenic organizing pneumonia - 4-Pulmonary involvement in collagen disease as RA, SLE - 5-Sarcoidosis - 6-Pneumoconiosis ### PNEUMOCONIOSIS - ✓ Lung disease that is caused by Inhalation of dust (organic and inorganic (minerals)). - **COAL WORKERS' PNEUMOCONIOSIS:** - Was common at coal workers Now is reduced - **Simple Anthracosis:** - Coal dust pigments are taken by alveolar macrophages - carbon-carrying macrophages: dust cells - **Macules and nodules:** - coal dust laden macrophages with delicate collagen fibers - centrilobular emphysema - **Progressive massive fibrosis:** - Complicated stage - Fibrotic nodules filled with necrotic black fluid. - SILICOSIS silica pesent in sand - the most prevalent chronic occupational lung disease - exposure to free silica dust - in rock mining, sand blasting glass manufacturers, stone cutters - silica is engulfed by alveolar macrophages → die & release their proteolytic enzymes → damage of lung tissue followed by fibrosis - *Silicotic nodules:* whorling fibrosis in which silica can be detected by polarized light - Finally → honey comb pattern - Silicosis is associated with increased susceptibility to tuberculosis silicotuberculosis. - ASBESTOSIS: used for insulation, At brake linings and other friction materials - inhalation of asbestos fibers → Dyspnea and dry cough - Microscopic: - Diffuse pulmonary fibrosis and honey comb appearance - *asbestos bodies (ferruginous bodies):* - golden yellow-brown, beaded rod-shaped bodies with clubbed ends - Predisposition to bronchogenic carcinoma and relative risk to malignant mesothelioma (which is rare tumor) of the pleura (>1000 times greater) ### ATELECTASIS (COLLAPSE) - Failure of expansion Or collapse of previously inflated lung, Affecting part or all of one lung - **Resorption atelectasis:** - Complete airway obstruction prevents air from reaching alveoli - The air already present becomes absorbed → Alveolar collapse. - Cause: obstruction of a bronchus by a mucous plug, postoperative or bronchial asthma, tumor or foreign body in children - **Compression atelectasis:** - Accumulation of fluid, blood, air within the pleural cavity → compress the lung - **Effect of atelectasis:** - Hypoxia - peridispose to bronchiectasis ## LUNG TUMORS - Malignant tumors: - Malignant tumors are more common than benign tumors of lung - The most common lung tumor is metastases (secondary) - Primary lung carcinomas: - 95% carcinoma of lung - the most important Iry malignant tumor - 5%: - carcinoid tumor - fibrosarcoma - leiomyosarcoma - lymphoma - BENIGN TUMORS: - The most common benign tumor is HAMARTOMA: - Gross: spherical 3-4cm, coin like shadow on X ray - Microscopic: mature cartilage, with fat, fibrous tissue and blood vessels ## CARCINOMA OF THE LUNG (BRONCHOGENIC CARCINOMA) LUNG CANCER - incidence: - With the worst prognosis - Lung carcinoma is the leading cause of death from cancer in the world - Age around 50 years - Male > female with increasing incidence in females with cigarette smoking. - (85% to 90%) of lung cancers in smokers: the most common tumors in smokers are adenocarcinoma. - Lung cancers in non-smokers are adenocarcinoma. - Predisposing factors: - Cigarette smoking - Air pollution - Pneumoconiosis (inorganic dust): silicosis, asbestosis - Bronchiectasis - Types: - Squamous cell carcinoma - Adenocarcinoma - Large cell carcinoma - Small cell carcinoma - **SMALL CELL CARCINOMAS (SCLC) (OAT CELL CARCINOMAS)** - rapid growing early metastasizes - smokers - Gross: - in perihilar region central mass - Microscopic: - Cells are twice the size of lymphocytes with scanty cytoplasm. - Extensive Necrosis - Secrete polypeptide hormones (paraneoplastic syndrome) - cells with neuroendocrine features: stained by chromogranin A (marker for neuroendocrine cells) - **NON-SMALL CELL CARCINOMAS (NSCLC) SQUAMOUS CELL CARCINOMAS:** - arise central - males > females - closely related to smokers - preceded by squamous metaplasis, dysplasia, CIS (may last several years) - Gross: ill-defined greyish white hilar mass - central mass 85% arise in major bronchi: - 1. endobronchial growth - 2. infiltrative tumor invade the bronchial wall and surrounding lung tissue - Microscopic: - cell nests and keratin pearls - various grades of differentiation - **ADENOCARCINOMAS** - arise peripheral, may be multiple - Most common primary lung cancers in women. - Most common lung cancers in non-smokers. - Precursor: atypical adenomatous hyperplasia with adenocarcinoma insitu - Gross: - Peripheral and may be multiple - If at males it is central - Early seeding of the pleura - **LARGE CELL CARCINOMAS:** - undifferentiated tumors with no glandular or keratin formation - May represent undifferentiated SCC or adenocarcinoma. - Diagnosis by exclusion. Can no longer be recognized by light microscope - **Clinical manifestations of lung cancer:** - Cough - Cachexia - Hemoptysis - Dyspnea - Chest pain (pleuritic pain) - **Complications and spread of lung carcinoma:** - bronchial obstruction → collapse - 2ry bacterial infection: bronchiectasis or lung abscess - Hemoptysis - Spread: - Direct: pericardium, mediastinum, esophagus or pancreas - **Pancoast tumor (superior sulcus tumor):** - Apical neoplasm → involvement of the apex of the lung - invade brachial plexus → pain at distribution of ulnar nerve - invade cervical sympathetic chain → Horner syndrome ipsilateral (ptosis, miosis, and anhydrosis) - Pleural seeding: adenocarcinoma - Lymphatic spread: hilar LNs or supraclavicular LN (virchow's LN) may be the first presentation - Blood spread: brain, bone, liver, suprarenal glands, other lung, - **Paraneoplastic endocrine syndromes:** 3-10%, secretion of polypeptide hormones - (ACTH) or ACTH-like activity, hyponatremia with small cell carcinoma (SIADH) with small cell carcinoma of the lung (++ADH) - hypercalcemia and parathyroid-like activity with squamous cell carcinoma. - Myasthenia gravis - Cushing syndrome ## SECONDARY LUNG TUMORS - More common than 1ry - Reach lung through lymphatics or blood - discrete nodules Scattered throughout the lung - From both carcinoma and sarcoma - Carcinoma and sarcoma can metastasize to lung (breast, kidney. GIT) are common ## PULMONARY DISEASES OF VASCULAR ORIGIN ### PULMONARY HYPERTENSION - Causes: - 1- Chronic obstructive or interstitial lung diseases - 2-Recurrent pulmonary emboli - 3-Mitral stenosis - 4-Congenital left to right shunt due to increase pulmonary blood flow - 5-Idiopathic or primary pulmonary hypertension - Pathology: (similar to changes with systemic hypertension) - main elastic artery: Atheroma - Medium sized arteries: cellular and smooth muscles hyperplasia → thick wall narrow lumen - Small arterioles: hyalinosis, elastosis and narrow lumen ## DISEASES OF PLEURA ### INFLAMMATORY PLEURAL EFFUSION - accumulation of fluid in pleural cavity - 1. transudate: HF, liver cirrhosis (hydrothorax) - 2. exudate: serofibrinous (bread and butter) inflammation - Causes: TIC - infections: TB, lung abscess, pneumonia - metastatic tumors to pleura (hemorrhagic) - pulmonary infarction - viral pleurisy - collagen diseases: RA, SLE ### EMPYEMA - Suppurative inflammation of pleura with pus at pleural cavity - Causes: pyogenic organism (staph.) - Direct spread from lung infection, abscess, bronchiectasis, pneumonia - penetrating infected trauma - blood spread: septicemia - Pathology: - diffuse: total: (acute): purulent effusion filling pleura → collapse of lung tissue - localized in pockets (more common) - Complications: - chest sinus draining pus - spread to