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145 Cards in this Set
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Restrictive Lung Disease:
-microscopic strx clinical features, measurements radiographic, gross, microscopic findings |
• Reduction in lung compliance--> dyspnea
• Filling/total volume as measured by FVC decreased; FEV:FVC ratio is normal . • Alveolar epithelial, vasculature damage-->abnormal ventilation‐perfusion ratio; hypoxia ‐ Measured by dec. CO diffusing capacity • Symptoms: dyspnea, tachypnea, endinspiratory crackles progressing to cyanosis. No wheezing. • Chest radiograph features: diffuse infiltration by small nodules, irregular lines (reticulonodular pattern) or ground glass pattern. Advanced Disease: Honeycome lung on CT • Eventuate in secondary pulmonary hypertension; cor pulmonale. + Trichrome stain |
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Major Categories of Chronic Interstitial Lung Disease
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• Fibrosing:
‐ Idiopathic pulmonary fibrosis ‐ Associated with collagen vascular diseases ‐ Pneumoconeosis, Radiation, Drug reactions, others • Granulomatous: Sarcoidosis; Hypersensitivity pneumonitis • Eosinophilic • Smoking‐related: Desquamative interstitial pneumonia; Bronchiolitis associated interstitial disease • Other (no fibrosis): Pulmonary alveolar proteinosis |
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Wheezing
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by definition not restrictive lung disease
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Fibrosing Diseases
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Causes: Collagen vascular disease, asbestosis, radiation, chemotherapy, sarcoidosis, ARDS, idiopathic
Three morphologic patterns of interstitial fibrosis: ‐ Usual interstitial pneumonia ‐ Nonspecific interstitial pneumonia ‐ Cryptogenic organizing pneumonia (in order of severity of course prognosis:) |
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idiopathic pulmonary fibrosis:
Pathogenesis, Morphology, Course |
Unknown agent-->Repeated epithelial activation/injury--> Inflammation; TH2 response: eosinophils, mast cells, IL‐4; IL‐13
abnormal epithelial repair: type 1 pneumocytes release TGFBeta-1: fibroblastic foci Cobble stone pleural surface of retraction scars Cut surface is firm, rubbery and white from fibrosis Microscopic: usual interstitial pneumonia ‐ Fibroblastic foci ‐ Honeycomb fibrosis: cystic spaces formed of fibrous tissue; lined by type II pneumocytes ‐ Pulmonary hypertension vascular changes • Insiduous onset of dyspnea peak 40‐70 y/o, mean survival 3 years • “Dry” or “Velcro”‐like crackles on inspiration • Hypoxemia, cyanosis and clubbing occur late Dx: biopsy best; CT okay Tx: no effective drugs, must transplant lung dypsnea, ground glass infiltrates, Low pO2, lo2 O2sat |
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“Dry” or “Velcro”‐like crackles on inspiration
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idiopathic pulmonary fibrosis
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COP
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• Cryptogenic Organizing Pneumonia (COP)
• Clinical: cough, dyspnea; subpleural or peribronchial patchy airspace consolidation • Micro: plugs of organizing fibrous tissue w/in alveoli; bronchioles • Complete recovery with 6 mon. course steroids • Resembles organizing pneumonia of known cause |
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cough, dyspnea; subpleural or peribronchial patchy airspace consolidation
plugs of organizing fibrous tissue w/in alveoli; bronchioles |
• Cryptogenic Organizing Pneumonia (COP/BOP)
Organizing Interstitial Pneumonia • Clinical: cough, dyspnea; subpleural or peribronchial patchy airspace consolidation • Micro: plugs of organizing fibrous tissue w/in alveoli; bronchioles • Complete recovery with 6 mon. course steroids • Resembles organizing pneumonia of known cause |
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What 4 collagen vascular diseases are associated with pulmonary fibrosis?
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‐ SLE, RA, Scleroderma & Dermatomyositis
• Patterns may be UIP, NSIP or COP • Prognosis varies according to histology |
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Pulmonary Invovement of Rheumatoid arthritis
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30+%
‐ Chronic pleuritis, with or w/o effusions (fibrinous) ‐ Diffuse interstitial pneumonitis with fibrosis ‐ Intrapulmonary rheumatoid nodules ‐ Pulmonary hypertension |
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Pneumoconioses
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nonneoplastic lung reaction to inhalation of mineral dusts, organic particles; chemical fumes
Generally involve upper lobes of lung (exception: asbestosis) |
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Coal workers pneumoconiosis:
Pathogenesis, Spectrum, CA/TB risk |
• Anthracosis‐ asymptomatic
• Simple coal workers pneumoconiosis: coal dust macules/nodules w/ little-no dysfnx, <10% progress • Complicated coal workers pneumoconiosis: nodules up to 2 cm diameter in a background of simple CWP-->respiratory compromise • No associated risk for cancer, TB |
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Anthracosis
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Accumulation of black carbon pigment in the lungs
coal mining, smoking, urban air • Clinical: asymptomatic • Pathogenesis: macrophages engulf pigment,migrate to perilymphatic lung, pleura and hilar lymph nodes • ~Assoc w/dust emphysema |
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Caplan’s syndrome
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Coexistence of lung disease of RA & any pneumoconiosis
rapidly progressive |
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Silicosis:
pathogenesis, clinical, morphology, risks for TB/CA |
Most common chronic occupational disease in the world: foundry work, sand‐blasting, stone cutting and hard rock mining incl coal, iron ore
Fresh ground silica = rich in SiOH free radicals, inhalation--> bind & damage phospholipids • M0 ingest, activate, release mediators-->fibrosis • Hard collagenous scars • Coalescing nodules ~cavitating nodules in upper lobes (? Silicotuberculosis) • Massive fibrosis: scars up to 10 cm diameter • Calcification of LN • Polarized birefrigent material in nodules • Chronic debilitating pulmonary disease • Depressed CMI, M0 death--> Increased risk for tuberculosis • Not a predisposing factor for lung cancer • ~assoc w/ Caplan’s syndrome |
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Acute vs Progressive Silicosis
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Acute
• Heavy, acute, several month exposure • Lipoproteinaceous accumulation identical to pulmonary alveolar proteinosis • Sx: Dyspnea, Productive Cough of abundant gelatinous sputum Progressive • Initial disease: aSx nodules in upper lobes detected on X-ray, may coalesce into collagenous scars • Progressive massive fibrosis: dyspnea, progression in absence of exposure |
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List all asbestos‐related diseases. Which is most common?
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• Pleural plaques-- Most Common Manifestation
• Asbestosis: parenchymal interstitial fibrosis • Pleural effusions • Bronchogenic carcinoma • Mesotheliomas • Laryngeal and other carcinomas‐colon |
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Asbestos Exposures
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• Mining and milling
• Fabrication; ship building (World War II) • Installation/removal of insulation • Family member Risk of old insulation in public buildings is very slight |
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What is the pathogenesis of asbestos‐related fibrosis?
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• Stiff fibers penetrate airways at bifurcations; localize in distal lung
• Fibers generate free radicals; absorb and hold toxic chemicals • Macrophages attempt to ingest, become activated--> diffuse interstitial inflammation and fibrosis |
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Morphology of Asbestosis
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• Asbestos or ferruginous bodies: Golden‐brown, fusiform or beaded rods coated by iron‐containing protein, will stain + w/ Prussian blue
• Honeycomb pattern diffuse pulmonary fibrosis • Pleural plaque: Flat, well‐circumscribed rubbery on parietal pleura; often calcified Most common manifestation of asbestos |
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Clinical course of asbestosis
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• Starts in lower lobes with alveolar duct fibrosis appears as linear densities on radiographs
• Presenting symptom: exertional dyspnea >10 yrs,years after initial exposure -- progressive productive cough • May remain static or progress to cor pulmonale, death Asbestos is a tumor initiator and promotor: • Risk for developing bronchogenic carcinoma or mesothelioma, pleural and peritoneal |
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Asbestos and cigarettes
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• Bronchogenic carcinoma in asbestos workers: 5x general population
• Bronchogenic carcinoma in asbestos workers who smoke: 55X general population • Asbestos fibers absorb tobacco smoke carcinogens, hold them in lung |
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What therapies are associated with pulmonary fibrosis?
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• Drug induced interstitial pulmonary fibrosis
‐ Bleomycin, busulfan (cancer chemotherapy) ‐ Amiodarone (5‐15% of treated patients) • Chronic radiation pneumonitis : interstitial fibrosis that may arise from diffuse alveolar damage (DAD, morphology of ARDS) of acute radiation pneumonitis |
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Amiodarone
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Risk for Pulmonary Fibrosis
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Bleomycin
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Risk for Pulmonary Fibrosis
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Busulfan
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Risk for Pulmonary Fibrosis
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What is the pathogenesis and characteristic microscopic feature of sarcoidosis?
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noncaseating (hard) granulomas in many tissues and organs
deranged Type IV CMI vs unidentified antigen |
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Schaumann bodies
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concretions
Characteristic but not pathognomonic findings with in granulomas of sarcoidosis |
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Asteroid bodies
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stellate structures‐ w/in giant cells
Characteristic but not pathognomonic findings with in granulomas of sarcoidosis |
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What are the morphology of sarcoidosis with regard to the lungs‐chest radiographs?
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Lungs: Bronchial mucosal granulomas in various stages of healing
Pulmonary infiltrates with 1‐2 cm granulomas producing restrictive lung disease LN's enlarged, may calcify: Bilateral Hilar/Paratrachical "Potato" LN's Tonsils enlarged‐1/3 of cases |
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potato nodes
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bilateral hilar/paratracheal lymph node involvement in sarcoidosis
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What skin lesions are associated with sarcoidosis?
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• Skin plaques and nodules: sarcoid granulomas
• Lupus pernio: violaceous, scaling plaques • Erythema nodosum • Similar lesions involve mucous membranes |
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Describe the clinical features of pulmonary sarcoidosis.
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• Mikulicz’s syndrome: dry eyes, mouth
• Involvement of eye‐ iridocyclitis‐‐> corneal opacities, glaucoma, blindness • Hepatosplenomegaly‐ localized granulomas • Bone marrow; Bone lesions of hands, feet • Muscle: involvement common; usually asymptomatic. |
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Bilateral Hilar Lymphadenopathy
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Sarcoidosis
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Lab Findings in Sarcoidosis
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No test is sensitive or specific for sarcoidosis
• CBC: variable lymphocytopenia; anemia • Hypercalcemia • Polyclonal gammapathy • Serum ACE elevated |
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• CBC: variable lymphocytopenia; anemia
• Hypercalcemia • Polyclonal gammapathy • Serum ACE elevated |
Sarcoidosis
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Non-caseating granulomas
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Sarcoidosis
or Hypersensitivity Pneumonitis or Berylliosis |
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Hypersensitivity Pneumonitis
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• Immunologically mediated, predominantly interstitial lung disorders
• Abnormal Sensitivity to organic material in dust • Type III immune complex disease • Converts in 2/3 to type IV disease with interstitial noncaseating granulomas Remove exposure to prevent serious fibrosis |
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Morphology of Hypersensitivity Pneumonitis
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• Interstitial pneumonitis with lymphs, plasma cells, macrophages
• Interstitial fibrosis • Obliterative bronchiolitis • Noncaseating granulomas form in > 65% |
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Clinical of Hypersensitivity Pneumonitis
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• Acute attacks ~4 hrs after exposure
‐ Fever, dyspnea, cough and leukocytosis ‐ Diffuse and nodular infiltrates on x‐ray ‐ Restrictive pattern on pulmonary function test ‐ Resolves in 24+ hours unless re‐exposed • Chronic progressive respiratory failure with continued exposure: dyspnea, cyanosis • Treatment: early recognition and removal from antigen |
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Berylliosis
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hypersensitivity rxn in genetically predisposed individuals even with low duration/amt
‐ noncaseating granulomas in pleura, septa, bronchovascular tissue ‐ may progress to honeycomb lung, >15 yrs after exposure (restrictive) ‐ risk for lung cancer |
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Pulmonary Eosinophilias
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• Fever, night sweats, respiratory symptoms with abnormal chest x‐ray
• CBC: eosinophilia • Respond to corticosteroids: • Types: -- Acute and chronic eosinophilia -- Simple pulmonary eosinophilia/Loeffler’s syndrome=benign course |
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List smoking‐related interstitial lung diseases.
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• Types:
‐ Respiratory bronchiolitis‐assoc. interstitial dis. ‐ Desquamative interstitial pneumonia, DIP [• Prognosis good with cessation of smoking ‐ DIP responds to corticosteroids • Characterized by smoker’s macrophages in alveoli • Occur after some years of smoking] |
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What are causes and clinical findings of pulmonary alveolar proteinosis?
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• Inability of macrophages to clear surfactant: accumulation: Patchy asymmetric pulmonary opacification:
• Acquired PAP: Antibody to GM‐CSF (Most common form) • Congenital PAP‐ Rare. Fatal age 3‐6 mon. ‐ Insidious onset cough; production of abundant, (sometime chunky) gelatinous material; ‐ Dyspnea, cyanosis, respiratory insufficiency ‐ Consolidated lung: amorphous granular, PAS+ material ‐ No inflammation or fibrosis (Does not progress to fibrosis) ‐ Risk of secondary infections • Treatment: whole lung lavage; GM‐CSF in research |
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Secondary PAP
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‐ inhalation syndromes: silicosis;
‐ immunodeficiencies ‐ hematopoietic disorders, others |
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Alveoli filled with amorphous granular, PAS positive material.
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PAP
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List fetal consequences of maternal smoking
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• Fetal hypoxia; high CO levels
• Increased risk congenital heart disease; cleft palate • Increased spontaneous abortion • Low birth weight infants • Increased premature birth • Increased complications of delivery • Increased risk of suddent infant death |
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List lab test results related to smoking
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• Increased plasma glucose
• Increased catecholamines and cortisol • Increased free fatty acids • Increased WBC with neutrophilia • Increased CEA‐Carcinoembryonic antigen • Increased carboxyhemoglobin (carbon monoxide content) • Increased hemoglobin; polycythemia |
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What are all the listed risk factors for lung
cancer? |
• Radiation: Therapeutic, Radon gas/uranium miners
• Air pollutants: radon gas indoors, benzopyrenes and hydrocarbons from exhaust • Heavy metal exposures: nickel, chromate, beryllium, iron, arsenic • Mustard gas • Newspaper and haloether exposure • Asbestos: esp carcinoma, 10+ yrs. after exposure |
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Molecular Genetics of Lung Cancers
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Some nicotine and CYP polymorphisms= familial
10+ mutations in transformed cells 3p- is early, found in benign epithlium of smokers • Oncogenes associated with lung CA c‐myc: small cell K‐ras: adenocarcinoma EGFR –cancer in nonsmokers • Recessive gene mutations in lung CA p53 mutation: benzopyrene exposure p16INK4A |
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Histogenesis of Lung Carcinoma
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Bronchogenic
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Small vs non-small cell carcinomas
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Small: often met at Dx, Tx w/ radiation, chemotherapy
Nonsmall cell carcinoma: localized at dx, Tx w/ Sx |
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Squamous cell carcinoma:
primary tumor location, growth rate metastases, paraneoplastic sx, genetics, premalignant histologies, microscopic morphologies |
primary tumor location: central
primary tumor growth rate: slow, become large, caviatate metastases: late genetics: premalignant histologies: keratin microscopic morphologies: eosinophilic cells w/ sqamous pearls paraneoplastic sx: hypercalcemia Patient: smoking ++, M>F |
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Adenocarcinoma of the Lung
primary tumor location, growth rate metastases, paraneoplastic sx, genetics, premalignant histologies, microscopic morphologies |
primary tumor location: periheral pleural based
primary tumor growth rate: small, slow metastases: early, widespread genetics: EGFR, KRAS premalignant histologies: TTF-1, CEA, cytokeratins microscopic morphologies: glandular differentiaton/mucin prodxn paraneoplastic sx: none Patient: F?M, smoking+/- |
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Broncioalverolar Carcinoma
primary tumor location, growth rate metastases, paraneoplastic sx, genetics, premalignant histologies, microscopic morphologies |
primary tumor location: terminal broncioles, arises from atypical adenomatous hyperplasia
primary tumor growth rate: metastases: airborne seeding, genetics: premalignant histologies: cyokeratines microscopic morphologies: tall columnar growing along septum w/o invasion, lepidic growth (butterflies) paraneoplastic sx: none prgoression: may invade to become invasive adenocarcinoma, death from suffocation Patient: non smokers>20 yo |
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Small cell carcinoma
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primary tumor location: central
primary tumor growth rate: rapid metastases: early, widespread genetics: MYC premalignant histologies: neuoendocrine cells, dense core granules, chromogranin, synaptophysin, CD56 microscopic morphologies: small cells with dark nuclei little cytoplasm below intact epithelium, "crush" artifact paraneoplastic sx: ACTH: Cushings, SIADH, Gastrin- releasing peptice, calcitonin, Lambert-Eating myathenic syndrome Patient: +++++Smoker, most agressive, chemo for mets, rad for spread |
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Large cell carcinoma
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highly undifferentiated forms of sqamous cell and adenocarcinoma
large nuclei, prominent nuclei, little cytoplasm early mets |
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What are the manifestations of bronchial obstruction by lung cancer? Which is most common?
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• Pneumonia behind obstructing tumor: common presenting symptom
• Lung abscess • Bronchiectasis • Focal emphysema • Total obstruction: atelectasis Superior Vena Cava Obstrxn |
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What are vascular manifestations of local extension by lung cancer?
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Superior vena cava syndrome: dusky cyanosis and edema in upper body, death via rupture, inoperable
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Arms fail to empty on elevation
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superior vena caval syndrome
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Know additional locations of direct extension
of lung cancer and consequences of each. |
• Into pleura: malignant pleural effusion
• Chest wall/rib invasion: pathologic fracture • Pericarditis; cardiac tamponade • Esophageal extension: dysphagia • Recurrent laryngeal nerve extension: hoarseness • Phrenic nerve : paralysis of diaphragm |
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Define Horner syndrome. Describe associated
lung tumor. |
Unilateral enopthalmos, ptosis, miosis, and facial anhidrosis due to cervical sympathetic disease
if lung cancer: Pancoast'stumor of the superior sulcus/apex of the lung |
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What are typical sites of lung cancer metastases?
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• Hilar lymph nodes, first for most lung cancers
• Supraclavicular lymph nodes • Bone/bone marrow • Brain • Liver • Adrenal gland |
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The T of Lung Cancer TNM Staging
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T1= localized, < 3cm diameter
T2= > 3cm diameter or a smaller tumor that involves pleura, mainstem bronchus (> 2cm from carina) or lobar atelectasis present • T3, T4: Invasion of chest wall, diaphragm, carina, heart, great vessels, esophagus or a malignant effusion (T4). Surgery generally not attempted. N1, N2 lymph nodes on ipsilateral side generally considered operable N3 = contralateral hilar; scalene nodes; usually inoperable M0= no metastases M1 = metastases present Mx = metastases not evaluated |
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Lung Cancer Stage Grouping
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• Stage 1a: tumor < 3cm in size, > 2 cm distal to carina, no nodes, no mets (T1, N0, M0)
• Stage 2: tumor > 2 cm distal to carina, any involved nodes are on same side as tumor, no hematogenous metastases • Stage 1, 2 are curable by surgery but are infrequent stages at time of presentation Stage 4 Lung Cancer: any distant mets, common presenation |
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Compare prognosis for the various types of lung cancer
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~25% are resectable at time of discovery
• Squamous, adenocarcinomas generally the most likely to be operablesurvival 50% for stage 1, 2 tumors • Large cell carcinoma likely to be metastatic • Small cell carcinoma considered inoperable ‐ survival w/o treatment: 6‐17 weeks ‐ median survival with treatment: 1 year ‐ potential cure with radiation, chemotherapy:15+% • All lung cancer: 16% survive 5 years |
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SIADH
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hyponatremia; small cell carcinoma
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Cushing syndrome
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ACTH: Weight gain, ruddy complexion, impaired glucose tolerance hypertension, hypokalemia, osteoporosis
Small cell carcinoma |
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Hypercalcemia:
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PTH‐like PTH‐RP Associated with squamous cell CA
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Hypocalcemia
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calcitonin (small cell ca)
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Lambert‐Eaton myasthenia‐like syndrome
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Muscle weakness, esp of pelvis, thighs (small cell ca)
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Pulmonary osteoarthropathy
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Painful periostitis of long bones with
characteristic x‐ray • Humoral/neurogenic factors increase blood flow to affected extremity • Pain relieved by successful excision of the tumor; clubbing disappears |
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Define and list causes with associations of pneumothorax. What are the signs / symptoms What is tension pneumothorax and its consequence?
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air in the pleural cavity
• Types of pneumothorax Therapeutic: (formerly) treatment of TB Traumatic; due to perforating injury of the chest wall Spontaneous |
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Spontanous Pneumothorax
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Rupture of alveolar wall into pleural space
• Secondary to commonly related conditions: ‐ Emphysema‐ruptured bleb or bulla ‐ Asthma ‐ Cavities and bronchopleural fistula: TB, Cocci • Idiopathic spontaneous pneumothorax: Recurrent in young adults; due to rupture of subpleural blebs (paraseptal emphysema) |
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Sequelae of Pneumothorax
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• Small pneumothorax: Slow resorption
• Large volume pneumothorax: Requires chest tube therapy • Tension pneumothorax |
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Clinical presentation of pneumothorax
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• Chest pain
• Dyspnea • Cough • Decreased breath sounds on side of pneumothorax |
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Describe pleural plaque, including associations.
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Benign; not a precursor for malignant mesothelioma
Associated with asbestos exposure Involves parietal pleura |
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Describe the clinical, gross and microscopic morphology and etiology of mesothelioma
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~10% of asbestos workers 25+ years after exposure
Smoking does not increase risk, SV40 may May involve any serosa, generally starts in parietal pleura Histology: ‐ Sarcomatoid pattern: spindle cells, resembles fibrosarcoma ‐ Epithelial type: resembles adenocarcinoma ‐ Mixed or biphasic type • Symptoms: chest pain, dyspnea, recurrent pleural effusion • May begin as localized mass • Often encases and invades lung; metastases to lymph nodes • 50% mortality at 1 yr., few survive >2 yrs. • Peritoneal mesothelioma: heavy asbestos exposure, 50% have asbestosis, obstructs or produces inanition. |
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What are the consequences of pulmonary
emboli? |
• Nonperfusion causes respiratory compromise
• Hemodynamic compromise ‐ pulmonary artery obstructed; resistance increased ‐‐ > pulmonary hypertension ‐‐ > acute cor pulmonale • Sudden death: saddle or massive emboli • Pulmonary hemorrhages; hemoptysis • Pulmonary infarction ‐ uncommon in young; 10% of all emboli ‐ wedge‐shaped, hemorrhagic • Pleural effusion, serosanguinous • Pulmonary hypertension occurs with recurrent emboli or extensive embolization • Most are small, silent; 30% are recurrent |
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Pulmonary hypertension
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• Normal pulmonary pressure <1/8 of systemic
• Pulmonary hypertension is present when pressure increases to 1/4 of systemic Causes: • Chronic obstructive or interstitial lung diseases: fewer capillaries • Left to right shunts : increased flow ‐ Mitral stenosis: pulmonary venous back pressure • Obstructive sleep apnea • Recurrent thromboemboli; chronic PE: capilaries • Autoimmune vascular disorders: especially systemic sclerosis • Appetite suppressant drugs: aminorex, fenfluramine and phentermin, action via serotonin transporter |
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Describe the pathogenesis and clinical findings of idiopathic pulmonary arterial hypertension
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young women, age 20‐40
fatigue, dyspnea on exertion, syncope with exercise; may have angina mutation of bone morphogenic protein receptor type 2 (BMPR2) signaling pathway BMPR2 is a member of TGF‐ß family normally inhibits proliferation of smm, and favors apoptosis Autosomal dominant with incomplete penetrance (2hit) 80% mortality w/in 5 years |
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Describe and recognize the morphology of
pulmonary arterial hypertension. |
• Atheroma‐large pulmonary arteries
• Medial hypertrophy of arteries • Plexiform lesion of small, medium arteries ‐ more common in idiopathic pulmonary hypertension; congenital heart disease, HIV and drugs |
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List causes of diffuse pulmonary hemorrhage.
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• Goodpasture’s syndrome
• Idiopathic pulmonary hemorrhage • Vasculitis‐associated hemorrhage ‐ Wegener’s granulomatosis ‐ Systemic lupus erythematosis and other collagen vascular diseases • Hemorrhagic diathesis |
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Describe the pathogenesis, clinical and lab
findings of Goodpasture syndrome. |
toxic injury to lungs exposes basement membrane antigen+ genetic HLA-DR presipostion: anti-alpha3 chain Type IV collagen antibody mediates type 2 destrx of glomerular basemetn membrane
rapidly progressive glomerulonephritis and necrotizing hemorrhagic interstitial pneumonitis • Lungs heavy; areas of red‐brown consolidation, focal pneumonia on X ray • Intra‐alveolar hemorrhages: hemoptysis • Hemosiderin laden macrophages in alveoli (Prussian) • Necrosis of alveolar walls proceeds to fibrous thickening of alveoli • Kidneys: rapidly evolving glomerulonephritis • Linear immunofluorescent staining for Ig • Progression to renal failure and death without treatment (Plasmapheresis & Immunosuppression) • Diagnosis by kidney biopsy |
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What are the symptoms and morphology of Wegener’s granulomatosis?
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• 80% of patients with WG develop upper resp. or pulmonary disease
• Disease may be limited to lung • Symptoms: sinusitis, epistaxis, cough, hemoptysis, chest pain • Micro: Necrotizing vasculitis, capillaritis with poorly formed granulomas and pulmonary hemorrhages • C‐ANCA positive in serum |
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Community Acquired Bacterial Pneumonias
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H. influenza
S. pneumoniae K. pneumoniae S. aureus P. aeruginosia Legionella pneumophila |
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Streptococcus pneumoniae
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• Gram positive, lancet‐shaped diplococci
• Most common cause of community acquired pneumonia • Most common causes of lobar pneumonia • Type 3 (uncommon) assoc. with abscess of lung • Patients with splenectomy; sickle cell disease at increased risk of infection; increased risk of death from infection • Children more vulnerable to infection |
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Klebsiella pneumoniae
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• Gram negative bacillus
• Most common cause of gram negative pneumonia • Chronic alcoholics are at significant risk • Thick, gelatinous sputum is difficult to expectorate • Risk for complication of lung abscess |
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Staphylococcus aureus
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• Gram positive cocci
• Secondary bacterial pneumonia, complicating: ‐ Measles in children ‐ Viral influenza in adults and children • Common in IV drug users; associated with infective endocarditis • Often hospital‐acquired pneumonia • High incidence of complications: >>abscess; empyema<< |
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Pseudomonas aeruginosa
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• Community acquired in cystic fibrosis
• Acquired infection in antibiotic treated COPD; hospitalized patients with burns, mechanical ventilation; neutropenia (chemotherapy, etc) • Invades blood vessels at site of infection resulting in vasculitis with necrosis • Septicemia is fulminant; death w/in days |
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Legionella pneumophila
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Legionnaires disease
• Source: aspiration of contaminated aerosols (water) • Predisposing conditions: ‐ chronic illnesses: cardiac, renal, hematologic ‐ organ transplant recipients at high risk • Morphology: Neutrophil‐macrophage lobular infiltrates of multiple lobes ‐ Necrosis may be marked; may cause fibrosis • Fatality rates in immunosuppressed: 50% |
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Compare/contrast bronchopneumonia with lobar
pneumonia. Compare morphology and clinical risks for each. |
classic, overlapping patterns:
• Bronchopneumonia: patchy consolidation; may evolve into lobar pneumonia • Lobar pneumonia: fibrinosuppurative confluent consolidation of most or all of an entire lobe • Micro‐organism virulence factors and host factors determine pattern of pneumonia |
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Bronchopneumonia
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• Patchy consolidation; extends from bronchitis or bronchiolitis
• Commonly occurs following: ‐ Aspiration, congestion; edema ‐ Viral/ influenza pneumonia ‐ Lipid pneumonia; foreign body • More commonly seen in elderly, very young • Foci of consolidation with neutrophilic infiltrate approximately 3‐4cm diameter • Usually multilobar and bilateral • Most frequent in basal regions of lower lobes |
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Lobar pneumonia
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• Acute bacterial infection of a large portion of a lobe or of an entire lobe
• Etiology/ agents ‐ Large dose of virulent micro‐organisms in healthy person ‐ community acquired ‐ Dysfunction of barriers to infection‐ smoking, alcohol, etc: community acquired & nosocomial ‐ May be due to agents of bronchopneumonia in persons with low resistance • Stages of pneumonia: Congestion, Red hepatization, Gray hepatization, Resolution or organization • Outcomes: ‐ Resolution by enzymic digestion: granular debris; macrophages in alveoli OR: ‐ Organization: fibroblasts form scar • Fibrinous pleuritis occurs when consolidation extends to surface (symptom: pleurisy) ‐ Pleuritis organizes to fibrosis or adhesions |
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Congestion Stage of Lobar Pneumonia
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• Vascular engorgement
• Intra‐alveolar serous fluid with few neutrophils • Infection spreads through pores of Kohn • Cough; typically nonproductive of sputum |
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Red Hepatization Stage of Lobar Pneumonia
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• Red cells and neutrophils fill alveoli
• Lobe has consistency of liver • Productive of “rusty” and tenacious sputum |
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Gray Hepatization Stage of Lobar Pneumonia
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• RBCs disentegrated
• Macrophage phagocytosis • Fibrinous exudate fills alveoli |
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Acute Bacterial Pneumonia: Clinical
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• Abrupt onset of high fever, shaking chills and cough, productive of mucopurulent sputum
• Hemoptysis may occur • Pleuritic pain: pain with respirations, Friction rub • Radiographs of pneumonia ‐ Lobar: radio‐opaque well‐circumscribed lobe ‐ Bronchopneumonia: focal opacities • Ab Tx: resolution 48 - 72 hrs. • Published criteria exist for hospitalization age is an important factor • Fatality rate in hospitalized patients <10% ‐ death due to complications of pneumonia, underlying debilitating disease or chronic alcoholism |
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Complications of Acute Bacterial Pneumonia
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• Abscess formation‐ localized necrosis of lung
• Empyema ‐ intrapleural fibrinosuppuration; often requires surgical removal; leads to pleural adhesions • Organization– permanent scarring • Bacterial dissemination to: ‐ heart valves; pericardium; meningitis ‐ metastatic abscesses: brain, kidneys, spleen ‐ joints: suppurative arthritis |
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What are the causes, clinical findings and
morphology of atypical pneumonias? |
moderate sputum production; no physical findings of consolidation, moderate leukocytosis and no alveolar exudate
• Causes: Mycoplasma pneumoniae, Chlamydia pneumoniae, Coxiella burnetti (Q fever), Viruses: Influenza A and B, RSV and others • Interstitial inflammation w/in walls of septae: septae widened; edematous • Lymphocytic infiltrate predominates after initial acute neutrophilic response • Alveoli ‐ free of exudate or: may have proteinaceous material present with hyaline membrane (DAD) formation • May cause severe upper respiratory infection‐ “ chest cold” • Few localizing symptoms ‐ Cough + Fever, headache, myalgias, pains in legs ‐ Respiratory symptoms out of proportion to physical findings due to edema, fibrin exudates in lungs • Usually mild; mortality very low; Usually heals w/o scarring • Secondary bacterial infections common |
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What are signs, symptoms and complications of
common cold (viral URI)? |
• Eustachian tube block may lead to
suppurative bacterial ear infection • Bronchitis; bronchiolitis, laryngotracheitis ‐ vocal cord swelling; plugging of small airways |
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Why does aspiration pneumonia occur? What are
the potential outcomes? |
• Predisposition: Debilitation : Dec. consciousness, gag reflex (anesthesia, drugs, ETOH and stroke); vomiting
• Pneumonia combination of chemical injury (gastric acid) and polymicrobic oral flora with mixed aerobes and anaerobes • Tends to necrosis, fulminant course, death • Abscess common in survivors • Aspiration of oil (used for laxative) causes more indolent course |
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Describe the morphology of lung abscess. What
are causes, common organisms, clinical features? |
suppurative destruction/liquefactive necrosis of the lung parenchyma forming a central area of cavitation ‐ peripheral granulation tissue / fibrous proliferation
• Chest x‐ray: Cavity air filled or with fluid level • Early symptoms: Fever Cough production of copious foul‐smelling purulent or sanguinous sputum • Chest pain, weight loss • Diagnosis must be confirmed by chest radiographs • R/O lung cancer (cause of up to 15%) • Many resolve with antibiotics • May require surgery |
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Complications of Lung Abscess
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• Pneumatocele formation (Staphyloccocal
abscess): abscess breaks into airway ‐ thin‐walled sac lined by resp. tissue ‐ rapid expansion p p causes compression/rupture • Septic embolization: brain abscess or meningitis • Bronchopleural fistula • Empyema • Hemorrhage • Secondary amyloidosis, type AA |
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How is immunity to TB achieved
What is the morphology of TB Infection |
• TH1 response to antigen presenting cells:
lymphs produce interferon gamma, INF‐γ ‐ stimulated by IL12 • INF‐γ activates macrophages to: ‐ kill Mycobacteria via nitric oxide synthetase production of NO ‐ Formation of granulomas; kill/clear infection ‐ Macrophage secretion of: ‐‐ TNF‐a: recruits additional monocytes; produces fever, weight loss, tissue damage |
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Morphology of caseating
granuloma/soft tubercle |
Small, hard granulomas (tubercle) formed
initially • Central caseation follows (soft granuloma) ‐ grossly cheesy ‐ micro: amorphous (formless) eosinophilic material Surrounded by epithelioid (activated, epitheliallike appearance) histiocytes (macrophages) with Langhans giant cell Surrounding lymphocyte infiltrates; fibrous tsu |
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What are two outcomes of primary TB? Correlate
progressive with risk factors. What is The morphology of each? |
Whatever man
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Secondary (reactivation) pulmonary TB
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• Multiple fibrocavitary lesions
‐ typically superior‐posterior ‐ may be anywhere in the lung Caseous material in cavities contains AFB |
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Describe the distribution of progressive, extra‐
Pulmonary TB. |
• Dissemination via hematogenous route:
‐ Miliary TB (see organs commonly involved) ‐ Seeding, extension of local infection • Isolated TB ‐ may involved a single locale w/o evidence of active pulmonary disease ‐ distribution: see miliary Lymphatic: mediastinum; cervical lymph nodes (scrofula) |
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Miliary pulmonary tuberculosis
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• Lymphohematogenous involvement
• Return of infected macrophages to lungs via venules from lymph nodes • Small yellow white foci, 2 mm, evenly spread throughout lung ‐ size of a millet seed • May expand; coalesce • Disseminate to systemic infection: any organ |
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List diseases attributable to cigarette smoking
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CA's:
• Lung and bronchus; trachea, larynx ‐ Lung cancer risk in life‐long smokers: 1 in 6 • Lip, oral cavity, pharynx ‐strongly associated with chewing tobacco and snuff • Esophagus • Bladder and urinary tract • Uterine cervix • Pancreas • Stomach Ischemic Heart Disease • Promotes hypertension • Promotes hypercholesterolemia • Increases atherosclerosis • Promotes arrhythmias • Increases platelet adhesion, aggregation, endothelial dysfunction‐‐> thrombosis • Hypoxia; carbon monoxide inc.; lung disease • Use with oral contraceptives: increased risk for MI, stroke in women Additional diseases • Peptic ulcer disease increased ‐ Recurrence increased: poor healing • Increased rate of progression of HIV disease • Increased rate of abdominal aortic aneurysm • Risk factor for macular degenerationa cause of blindness • Poor wound healing • Children of smokers are more likely to smoke Chronic Respiratory Disease• Chronic obstructive pulmonary disease(COPD) ‐ Emphysema, chronic bronchitis‐ major factor ‐ Exacerbates ALL lung disease except sarcoidosis • Increased morbidity from respiratory infections ‐ Colds, influenza ‐ Increased acute and chronic sinusitis ‐ Mechanism: impaired ciliary activity and bronchial irritation Sidestream smoke related disease • Synonym: environmental tobacco smoke • Increased rates of sudden infant death in infants of smoking mothers • Children of smoking parents ‐ Increased respiratory and ear infection ‐ Exacerbation of asthma • Nonsmoking adult members of household ‐ Increased risk of lung cancer, ischemic heart disease and MI Work‐related injury & Smoking • On the job injuries increased in smokers ‐ Inattention ‐ Vector of other hazardous materials: radon, asbestos • Exacerbates bronchitis and asthma associated with industrial and farm exposures • Promotes lung injury from pneumoconioses |
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List, define and describe associations of anomalies of the lung.
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• Pulmonary hypoplasia
• Cystic adenomatoid malformation • Bronchogenic cyst • Sequestration: Extralobar or Intralobar • Bronchial atresia • Bronchopulmonary dysplasia Path-27-15 |
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Pulmonary Hypoplasia
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Congenital Anomaly>>pulmonary hypertension
Common finding of neonatal autopsy Involves both lungs • Associations: ‐ Oligohydramnios (inadequate volume of amniotic fluid, often due to fetal renal disease) ‐ Pleural effusion (fetal hydrops) ‐ Other anomalies of thorax ‐ Trisomies 13, 18, 21 ‐ congenital diaphragmatic hernia -----stomach/intestines occupy hemithorax, most commonly left side Path-27-16 |
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Bronchogenic Cysts
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Respiratory epithelium lined cyst adjacent to, but not communicating with bronchi;
Congenital Anomaly from abnormal detachment of primitive foregut aSx, mass effect, Infx/abscess, or Rupture Path-27-19 |
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Adenomatoid Malformation
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aka CPAM: Congenital Pulmonary Airway Malformation
• Hamartomatous dilated bronchiolar structures, multiple types, usually limited to one lobe of lung [• Prognosis varies from good to poor related to size of cysts • 1: 5000 births • Most seen before age 2: respiratory distress] Path-27-22 |
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Bronchopulmonary Sequestration
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Congenital Anomaly: Segment of lung tissue not connected to bronchial tree
Blood supply arises from aorta or its branches • Extralobar: external to lung, discovered as an abnormal thoracic mass • Intralobar: within lung, sublpleural, acquired due to repeated infections Path-27-24 |
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Bronchopulmonary Dysplasia
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Number of alveoli decreased; other, inconsistent changes
Occurs in infants born extremely premature as ventilatory support and oxygen therapy arrest pulmonary development Path-27-26 |
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atelectasis
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Incomplete expansion (neonatal) or collapse of previously inflated lung:
Ventilation‐perfusion imbalance results in hypoxia; fever may occur • Acquired types – Absorption/resorption due to obstruction – Compression (relaxation?) – Contraction is due to scarring • Increases risk for bacterial pneumonia • Potentially reversible (except contraction type) Path-27-31 |
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Absorption/resorption atelectasis
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complete airway obstruction from mucous plug or exudates in small airways
from: postop complication (common cause of PO fever in first 24‐36h) asthma, bronchitis, bronchiectasis Foreign body Tumors (least common) • Trapped oxygen is reabsorbed • Mediastinum shifts toward atelectasis Path-27-33 Path-RC-679 |
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Pulmonary Edema
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Causes
‐ Hemodynamic: High hydrostatic pressure, low oncotic pressure (albumin) ‐ Microvascular injury: to injury to alveolar septal capillary endotherlium Morphology • Acute: heavy, wet lungs alveolar siderophages; heart failure cells • Longstanding: brown induration fibrosis with accumulation of siderophages Sx: weak, groggy, and short of breath, delirious, coughing up blood‐laced froth. Path-27-39 |
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Acute Respiratory Distress Syndrome
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Continuum of progressive respiratory failure
• Common cause: pulmonary edema after heart failure • Defined by: ‐ Acute onset of dyspnea ‐ Hypoxemia/decreased arterial O2 pressure; refractory to O2 therapy ‐ Bilateral pulmonary infiltrate development‐ x‐ray ‐ No clinical evidence of 1o left heart failure Path-27-48 |
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Etiology of ARDS: Most common causes
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Greater than 50% are due to 4 causes:
‐ Sepsis ‐ Diffuse pulmonary infections ‐ Trauma including head injury ‐ Aspiration of gastric contents |
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Local injuries as causes of ARDS
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• Diffuse pulmonary infection
• Oxygen toxicity • Inhalation of irritants‐ smoke, chemicals • Aspiration of gastric contents • Near drowning • Radiation – acute radiation pneumonitis 1‐6 mon. following radiation therapy • Fat embolism secondary to fractures Path-27-52 |
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Systemic causes of ARDS Shock
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• Septic shock
• Pancreatitis • Surgery‐abdominal, cardiac • Cancer chemotherapy: bleomycin, busulfan • Narcotic overdose • Hypersensitivity to drugs • Transfusion related lung injury (TRALI) • Disseminated intravascular coagulation (DIC) Path-27-57 |
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ARDS
Pathogenensis, Morphology, Clinical Findings |
• Diffuse damage to alveolar capillaries induces a proinflammatory shift
• M0 Cytokines (eg IL‐8, TNF, IL‐1) recruit and sequester PMN's (alveolitis) • Neutrophils products damage epithelium • Increased capillary permeability leads to to fibrin exudation---> hyaline membranes • Pneumocytes destroyed; surfactant lost • Resolution phase: ---Exudate resorption; dead cells removed ---Type II pneumocytes proliferate, repopulate Type I's • Gross: Patchy‐ normal regions mixed with dark red, firm, airless, heavy, consolidated, collapsed areas • Microscopically – Congestion, edema, hemorrhage, alveolar cell necrosis, neutrophils, hyaline membranes (fibrinous intraalveolar exudates) Clincial: Severe dyspnea with hypoxia w/in hours of insult • Hypoxia leads to respiratory acidosis; • High O2 therapy causes further injury • Outcome ~= severity, multisystem hypoxic injury, fatal in 40% • Interstitial Fibrosis risk in survivors Path-27-61 |
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Obstructive Pulmonary Disease
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Airway narrowing or loss of airway elastic recoil
• Asthma • Emphysema • Chronic bronchitis • Bronchiectasis • Bronchiolitis, small‐airway disease Path-27-85 |
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Restrictive pulmonary diseases
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• FVC reduced; FEV1 normal to proportionally reduced: FEV1: FVC normal
• Pulmonary and extrapulmonary causes • Extrapulmonary causes ‐ Obesity ‐ Kyphoscoliosis ‐ Neuromuscular disorders‐polio; Gullian‐Barre Path-27-87 |
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Emphysema
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Permanent enlargement of air spaces distal to the terminal bronchioles with destruction of alveolar walls w/o obvious fibrosis; caused by decreased alpha1-antitrypsin &/or increased elastase prodxn (both by smoking), often coexists with chronic bronchitis
Types of emphysema: Centriacinar, Panacinar, Distal acinar (paraseptal), Irregular (common at autopsy; due to scarring, aSx/insignificant) Path-27-97 |
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Centriacinar (centrilobular) Emphysema
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• Central parts of acini affected
• Emphysema/normal alveoli same acinus • Location: starts in apical segments lung • Associations ‐ Heavy cigarette smoking (in persons w/o congenital α‐1 antitrypsin deficiency) ‐ Coal workers pneumoconiosis ‐ May be associated with bronchitis and bronchiolitis Path-27-99 |
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Panacinar (panlobular) Emphysema
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• Entire (pan) acinus involved
• Location of most disease: lower lung, anterior margins • Associated with a1‐antirypsin deficiency ‐ Protease inhibitor, Pi ‐ Codominant inheritance: multiple phenotypes ‐ PiMM type: most normal people ‐ PiZZ associated with emphysema at young age; with or w/o smoking Path-27-80 |
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Distal acinar –paraseptal –localized emphysema
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• Distal part of acinus involved
• Tends to occur in smokers • Location: ‐ SUBPLEURAL ‐ adjacent to areas of fibrosis, atelectasis ‐ most severe upper half of lungs ‐ multiple, continuous enlarged airspaces up to 2 cm • Associated with spontaneous pneumothorax of young adults |
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Pathogenesis of centri‐ and panacinar emphysema
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Protease‐antiprotease and oxidant‐antioxidant imbalances
• Excess inflammation due to smoking; excess elastase (protease) activity • Initiating event: bronchiolitis w/ obstruction--> goblet cell metaplasia with mucous plugging, influx of inflam cells/PMN's, B's & T's--> thickening of wall of bronchiole • Nicotine and free radicals chemotactic for inflammatory cells • Neutrophils and macrophages accumulate in alveoli of smokers • Neutrophils, macrophages release elastase, matrix metalloproteinases • Enzymes digest alveolar connective tissue Path-27-118 |
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Emphysema in patient < 40
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suspect a1 AT deficiency
Path-27-121 |
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Interstitial emphysema
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Air in connective tissue of lung, mediastinum, subcutaneous tissue caused by
• Alveolar wall tear in emphysema • Whooping cough, bronchitis in children • Rib fracture • Artificial ventilation (barotrauma) • Inhalation of irritant gases Coughing + bronchiolar obstruction--> pressure tears ts, dissects CT of lungs, mediastinum, out to periphery Clinical: Crepitant swelling head/neck Resorbs when leak is sealed Path-27-136 |
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Blue bloater
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COPD: predominantly Bronchitis
• Age of onset: 40‐45 • Dyspnea: late • Copious sputum; constant cough • Infections common • Repeated respiratory insufficiency • Cor pulmonale common and early • Airway resistance increased; recoil normal • x‐ray: prominant pulmonary vessels; large heart • Blood gases: hypercapnea Path-27-155 |
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Bronchial Asthma
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Chronic inflammatory disorder of airways
causes recurrent episodes of wheezing, dyspnea, chest tightness, particularly at night and/or in the early morning . Usually assoc. with widespread but variable bronchoconstriction and airflow limitation that is at least partly reversible Inflammation causes an increase in airway responsiveness, bronchospasm. Path-27-115 |
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Types of Asthma
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• Atopic (Extrinsic) : type I hypersensitivity
• Intrinsic (nonatopic): Rhinovirus, parainfluenza virus, others lower threshold of vagal receptors to irritants • Drug induced asthma: (genetic predisposition) Aspirin/NSAID: inhibition of COX but not LOX: asthma; nasal polyps • Occupation: type I reaction to fumes, dust • Allergic bronchopulmonary aspergillosis: from colonization by Aspergillus Path-27-159 |
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Pathogenesis of Extrinsic Asthma
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• Genetic predisposition to type I hypersensitivity
---CD4's secrete more IL-4 than 2, strong TH2 rxns. ---Lymphs cannot secrete IFNy, would block TH2 • Initial sensitization of TH2 type CD4+ cells to inhaled antigen • Cells release cytokines IL‐4, [IL‐5]--> ---synthesis of IgE by B cells ---growth of mast cells in the mucosal surface ---growth/activation of eosinophils • Bronchial hyperresponsiveness, Re‐exposure = 2 phase response • Acute and chronic airway inflammation Path-27-162 |
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Asthma: immediate response to allergen exposure
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• Onset 30‐60 minutes; followed by remission
• Mast cell release of histamine, proteases ‐ Bronchoconstriction via histamine, subepithelial vagal receptor stimulation ‐ Edema of bronchi ‐ Mucous secretion • Mast cells release chemotactic factors to recruit eosinophils, neutrophils Path-27-167 |
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Protracted late phase of asthma
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Onset 4‐8 hrs. after allergen exposure; may persist 24+h
Recruited basophils, eosinophils (via MPB), neutrophils cause epithelial damage, bronchoconstriction, intensification of response Repeated episodes favor airway remodeling Path-27-169 |
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Leukotrienes and asthma
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vasospasm, vascular permeability, bronchoconstriction
Path-27-171 |
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ACh & Asthma
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Controls Motor Nerves
Path-27-171 |
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Genetics of Asthma
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Multifactoral, environmental
• Gene cluster for cytokine regulation, IL‐4R & IL13 (strongest assoc.) • Class II HLA alleles associated with tendency to produce p IgE in response to some antigens • ADAM‐33 polymorphisms = MMP; accelerates proliferation in bronchial wall (correlates with hyperresponsiveness) Path-27-172 |
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Morphology of Asthma
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• Mucous plugs; Curschmann’s spirals (micro)
• Charcot‐Leyden crystals (eos. remnants) • Changes in bronchial mucosa ‐ Overall thickening ‐ Edema bronchial mucosa ‐ Inflammation; up to 50% eosinophils ‐ Increased mucous glands; goblet cells ‐ Smooth muscle hypertrophy/hyperplasia ‐ Sub‐basement membrane fibrosis • Hyperinflation of the lungs |
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Status Asthmaticus
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• Severe paroxysm unresponsive to usual therapy which may last days to weeks and may be fatal
• Labs ‐ hypercapnia ‐ acidosis ‐ hypoxia • Autopsy: hyperinflated lungs Path-27-136 |
