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Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
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Pulmonary pathology
Pulmonary pathology
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Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
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Pulmonary pathology
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Pulmonary pathology
Pulmonary pathology
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Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
Pulmonary pathology
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Pulmonary pathology
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Pulmonary pathology
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Pulmonary pathology

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  • Typical normal 1000 gram lung (R550, L450), with lobes and bronchopulmonary segments, primary, secondary, tertiary bronchi, etc. Pleura “smooth and glistening”, arteries traveling with bronchi, veins being rather independent of bronchopulmonary segments and lobes. Why is weight important? Why is “smooth and glistening” important? What is “crepitance”? Why is crepitance important?
  • Classical classifications of diseases, degenerative, inflammatory, neoplastic. This classification still stands up today.
  • Typical normal 1000 gram lung (R550, L450), with lobes and bronchopulmonary segments, primary, secondary, tertiary bronchi, etc. Pleura “smooth and glistening”, arteries traveling with bronchi, veins being rather independent of bronchopulmonary segments and lobes. Why is weight important? Why is “smooth and glistening” important? What is “crepitance”? Why is crepitance important?
  • Know the microscopic criteria for all the items delineated on the right, especially the kinds of simple epithelium which line them.
  • The “space” between the endothelium and the type-1 pneumocyte, is the blood air interface
  • This simple embryology diagram may help explain most common congenital lung diseases. Why might this diagram be WRONG, especially the top figure?
  • “ NORMAL” chest X-Ray (CXR)
  • Resorption can be from a bronchial obstruction, such as a tumor. Compression can be from, say, a pleural effusion. Contraction can be from a diffuse lung fibrotic process.
  • FOUR main pathologic mechanisms of pulmonary edema
  • ARDS can be thought of as NON-cardiac pulmonary edema, or, more correctly, edema related to alveolar INJURY. It is NON-specific!!! It is also sometimes called “shock lung” as we will see in the section on shock. Is the alveolar “edema” of ARDS more likely to have more protein than cardiac pulmonary edema?
  • Two EXTREMELY important concepts of pulmonary pathology. OBSTRUCTION means SMALL AIRWAT EXPIRATIRY obstruction. RESTRICTION means REDUCED COMPLIACE, i.e., less sponginess!
  • Bullae, or “peripheral blebs” are hallmarks of chronic obstructive lung disease, COPD.
  • Note the heavy inflammatory cell infiltrate around bronchioles and small bronchi.
  • What are the 4 classic histologic findings in bronchial asthma? Answer: 1) Inflammation 2) Bronchial narrowing 3) Increased Mucous 4) Smooth muscle hyperplasia What is the 5 th finding if the etiology is allergy? Ans: Eosinophils
  • Bronchiectasis is not a specific disease, but simply a condition in which LARGE bronchi are damaged and DILATED due to a variety of causes.
  • How do you know these are not bullae?
  • If you “squeezed” a lung with restrictive lung disease, you would note it wasn’t as “spongy” as a normal lung. This is the definition of reduced compliance. It simply will not “comply” when squeezed (or moved by respiratory motion either)! In contract to the “obstructive” lung diseases, the chest x-ray shows diffuse INCREASE in density, NOT DECREASED, usually.
  • Would you see a lot of scar tissue here if you did a trichrome stain? Ans: yes
  • This image was “googled” from tumorboard.com, the internet’s FIRST diagnostic pathology image base. The fact that this is a mesenteric lymph node will remind you that sarcoidosis is NOT limited to the lungs.
  • The classical difference between a “caseating” and a “non-caseating” granuloma, is often the difference between TB and sarcoid. Which one might culture out acid-fast bacteria? Ans: The one on the LEFT (i.e., caseating)
  • Pulmonary edema on left, PAP (Pulmonary Alveolar Proteinosis) on the right.
  • A general rule with COPD is: As the alveoli become wider, the arterioles become narrower!
  • A common finding in most cases of pulmonary hypertension, no matter what the cause is. NORMAL thickness pulmonary arteriole on the LEFT.
  • Wegener's granulomatosis  is a form of  vasculitis  that affects the  lungs ,  kidneys  and other organs. Due to its end-organ damage, it can be a serious disease that requires long-term  immunosuppression . It is named after Dr.  Friedrich Wegener , who described the disease in 1936.
  • IPH has MUCH more hemosiderin in alveoli, usually, relative to chronic CHF. Acute CHF has NO hemosiderin. Why?
  • Why is the term “chronic” pneumonia here, kind of a misnomer, classically?
  • Viral pneumonias, generally interstitial, bacterial pneumonias generally alveolar!!!
  • Corona viruses are RNA, “enveloped”, i.e., “crowned” viruses
  • As soon as you step into a hospital, expect to be greeted by MRSA
  • An abscess can be thought of as a pneumonia in which all of the normal lung outline can no longer be seen, and there is 100% pus. Notice the increasing destruction of the alveolar framework as you progress closer to the center of the abscess.
  • “ Chronic” by classification, but “granulomatous” by histology.
  • Granulomatous reactions are commonly seen with mycobacteria, fungi, sarcoid, foreign bodies, and rarely with almost anything.
  • PCP is the most common pneumonia in AIDS patients. It is so prevalent, many rationales consist in giving treatment for it prophylactically. An interesting tidbit is that “cotton wool” or “wooly” exudates are described BOTH radiologically as well as histologically
  • Bronchiolitis obliterans, as seen with “COP”, occurs with chronic pulmonary transplant rejection
  • The NON-small cell cancers behave and are treated similarly, the SMALL cell carcinomas are WORSE than the non-small cell carcinomas, but respond better to chemotherapy, often drastically!
  • Once again, the best way to classify tumors of ANY organ or tissue is to simply remember the histology. Tumors are clonal proliferations of native cells.
  • Name the four most common histologic patterns of lung carcinoma and explain why! Squamous, adeno, large, small, going clockwise.
  • TNM ALWAYS relates to BIOLOGIC BEHAVIOR!
  • Once again, the best way to classify tumors of ANY organ or tissue is to simply remember the histology. Tumors are clonal proliferations of native cells.
  • Also recall that mesothelium does not only cover the lungs viscerally, as well as parietally, but also the pericardium and the peritoneum as well, so mesotheliomas and effusions of the pleura, and ALL diseases, are also have their corresponding counterparts in the pericardial space and peritoneal space as well.
  • Pleuritis = Pleurisy
  • How would you differentiate a pleural transudate from an exudate? Ans: SPGR, cells, protein, LDH
  • Typical growth appearance of a malignant mesothelioma, it compresses the lung from the OUTSIDE.
  • Mesothelial cells have MANY more microvilli than most epithelial cells and express a protein called CALRETININ. The differentiation between mesothelioma and carcinoma may be crucially important!
  • Transcript

    • 1. LUNGS www.freelivedoctor.com
    • 2. LUNG <ul><li>“ Degenerative” </li></ul><ul><li>Inflammatory </li></ul><ul><li>Neoplastic and Pleura </li></ul><ul><li>LAB: (Review, Cases, and/or Virtual Microscopy) </li></ul>www.freelivedoctor.com
    • 3. OVERVIEW <ul><li>Normal Anatomy and Histology </li></ul><ul><li>Pathology </li></ul><ul><ul><li>Congenital </li></ul></ul><ul><ul><li>Atalectasis </li></ul></ul><ul><ul><li>Acute Pulmonary Injury </li></ul></ul><ul><ul><li>Obstructive vs. Restrictive (infiltrative) concepts </li></ul></ul><ul><ul><li>O bstructive P ulmonary D isease (C OPD ) </li></ul></ul><ul><ul><li>Restrictive (Infiltrative) Pulmonary Disease </li></ul></ul><ul><ul><li>Vascular Pulmonary Diseases </li></ul></ul>www.freelivedoctor.com
    • 4. OVERVIEW <ul><li>INFECTIONS </li></ul><ul><li>NEOPLASMS and PLEURA (effusions, pneumothorax, tumors) </li></ul>www.freelivedoctor.com
    • 5. WEIGHT LOBES SEGMENTS BRONCHI ARTERIES, pulmonary ARTERIES, bronchial VEINS PLEURA, visceral PLEURA, parietal NERVES www.freelivedoctor.com
    • 6. Bronchi Bronchioles Terminal bronchioles Alveolar ducts Alveoli Type 1 pneumocytes Type 2 pneumocytes Macrophages Capillaries www.freelivedoctor.com
    • 7. www.freelivedoctor.com
    • 8. www.freelivedoctor.com
    • 9. www.freelivedoctor.com NORMAL” chest X-Ray [CXR]
    • 10. <ul><li>Pathology </li></ul><ul><ul><li>CONGENITAL </li></ul></ul><ul><ul><li>Atalectasis </li></ul></ul><ul><ul><li>Acute Pulmonary Injury </li></ul></ul><ul><ul><li>Obstructive vs. Restrictive (infiltrative) concepts </li></ul></ul><ul><ul><li>O bstructive P ulmonary D isease (C OPD ) </li></ul></ul><ul><ul><li>Restrictive (Infiltrative) Pulmonary Disease </li></ul></ul><ul><ul><li>Vascular Pulmonary Diseases </li></ul></ul>www.freelivedoctor.com
    • 11. CONGENITAL <ul><li>Agenesis/Hypoplasia </li></ul><ul><li>Tracheal/bronchial anomalies, i.e., Tracheo-Esophageal (TE) fistula </li></ul><ul><li>Vascular anomalies </li></ul><ul><li>Congenital Emphysema </li></ul><ul><li>Foregut cysts </li></ul><ul><li>Pulmonary Artery Malformations (CPAM) </li></ul><ul><li>Sequestration (no connection to airways) </li></ul>www.freelivedoctor.com
    • 12. www.freelivedoctor.com
    • 13. OVERVIEW <ul><li>Pathology </li></ul><ul><ul><li>Congenital </li></ul></ul><ul><ul><li>ATALECTASIS </li></ul></ul><ul><ul><li>Acute Pulmonary Injury </li></ul></ul><ul><ul><li>Obstructive vs. Restrictive (infiltrative) concepts </li></ul></ul><ul><ul><li>O bstructive P ulmonary D isease (C OPD ) </li></ul></ul><ul><ul><li>Restrictive Pulmonary Disease </li></ul></ul><ul><ul><li>Vascular Pulmonary Diseases </li></ul></ul>www.freelivedoctor.com
    • 14. ATALECTASIS <ul><li>INCOMPLETE EXPANSION </li></ul><ul><li>COLLAPSE </li></ul>www.freelivedoctor.com
    • 15. OVERVIEW <ul><li>Pathology </li></ul><ul><ul><li>Congenital </li></ul></ul><ul><ul><li>Atalectasis </li></ul></ul><ul><ul><li>ACUTE PULMONARY INJURY </li></ul></ul><ul><ul><ul><li>Pulmonary Edema </li></ul></ul></ul><ul><ul><ul><li>ARDS ( D iffuse A lveolar D amage) </li></ul></ul></ul><ul><ul><ul><li>Acute Interstitial Pneumonia </li></ul></ul></ul><ul><ul><li>Obstructive vs. Restrictive (infiltrative) concepts </li></ul></ul><ul><ul><li>O bstructive P ulmonary D isease (C OPD ) </li></ul></ul><ul><ul><li>Restrictive (Infiltrative) Pulmonary Disease </li></ul></ul><ul><ul><li>Vascular Pulmonary Diseases </li></ul></ul>www.freelivedoctor.com
    • 16. PULMONARY EDEMA <ul><li>IN-creased venous pressure </li></ul><ul><li>DE-creased oncotic pressure </li></ul><ul><li>Lymphatic obstruction </li></ul><ul><li>Alveolar injury </li></ul>www.freelivedoctor.com
    • 17. ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS or D.A.D., i.e., Diffuse Alveolar damage) (aka, “SHOCK” lung) <ul><li>NON-specific pattern of lung injury </li></ul><ul><li>INFECTION </li></ul><ul><li>PHYSICAL INJURY </li></ul><ul><li>TOXIC </li></ul><ul><li>CHEMICAL </li></ul><ul><li>DIC </li></ul><ul><li>ETC </li></ul>www.freelivedoctor.com
    • 18. ARDS www.freelivedoctor.com
    • 19. ACUTE INTERSTITIAL PNEUMONIA <ul><li>Think of it as ARDS with NO known etiology! </li></ul>www.freelivedoctor.com
    • 20. OVERVIEW <ul><li>Pathology </li></ul><ul><ul><li>Congenital </li></ul></ul><ul><ul><li>Atalectasis </li></ul></ul><ul><ul><li>Acute Pulmonary Injury </li></ul></ul><ul><ul><li>OBSTRUCTION vs. RESTRICTION </li></ul></ul><ul><ul><li>O bstructive P ulmonary D isease (C OPD ) </li></ul></ul><ul><ul><li>Restrictive (Infiltrative) Pulmonary Disease </li></ul></ul><ul><ul><li>Vascular Pulmonary Diseases </li></ul></ul>www.freelivedoctor.com
    • 21. OBSTRUCTION v. RESTRICTION <ul><li>OBSTRUCTION </li></ul><ul><li>Air or blood? </li></ul><ul><li>Large or small? </li></ul><ul><li>Inspiration or Expiration? </li></ul><ul><li>Obstruction is SMALL AIRWAY EXPIRATION obstruction, i.e., wheezing </li></ul><ul><li>HYPEREXPANSION on CXR </li></ul><ul><li>RESTRICTION </li></ul><ul><li>“ Compliance” </li></ul><ul><li>“ Infiltrative” </li></ul><ul><li>REDUCED lung VOLUME, DYSPNEA, CYANOSIS </li></ul><ul><li>REDUCED GAS TRANSFER </li></ul><ul><li>“ GROUND GLASS” on CXR </li></ul>www.freelivedoctor.com
    • 22. OVERVIEW <ul><li>Pathology </li></ul><ul><ul><li>Congenital </li></ul></ul><ul><ul><li>Atalectasis </li></ul></ul><ul><ul><li>Acute Pulmonary Injury </li></ul></ul><ul><ul><li>Obstruction vs. Restriction </li></ul></ul><ul><ul><li>OBSTRUCTIVE Pulmonary Diseases (COPD) </li></ul></ul><ul><ul><li>Restrictive (Infiltrative) Pulmonary Disease </li></ul></ul><ul><ul><li>Vascular Pulmonary Diseases </li></ul></ul>www.freelivedoctor.com
    • 23. OBSTRUCTION (cOPD) <ul><li>EMPHYSEMA (almost always chronic) </li></ul><ul><li>CHRONIC BRONCHITIS  emphysema </li></ul><ul><li>ASTHMA </li></ul><ul><li>BRONCHIECTASIS </li></ul>www.freelivedoctor.com
    • 24. EMPHYSEMA <ul><li>COPD, or “END-STAGE” lung disease </li></ul><ul><li>Centri-acinar, Pan-acinar, Paraseptal, Irregular </li></ul><ul><li>Like cirrhosis, thought of as END-STAGE of multiple chronic small airway obstructive etiologies </li></ul><ul><li>NON-specific </li></ul><ul><li>IN-creased crepitance, BULLAE (BLEBS) </li></ul><ul><li>Clinically linked to recurrent pneumonias, and progressive failure </li></ul>www.freelivedoctor.com
    • 25. CENTRO-acinar PAN-acinar www.freelivedoctor.com
    • 26. www.freelivedoctor.com Bullae, or “peripheral blebs” are hallmarks of chronic obstructive lung disease, COPD.
    • 27. <ul><li>HYPER-expansion 2) “flattened” diaphragms (blunted), </li></ul><ul><li>3) “bullae” 4) increased lucency </li></ul>www.freelivedoctor.com
    • 28. CHRONIC BRONCHITIS <ul><li>INHALANTS, POLLUTION, CIGARETTES </li></ul><ul><li>CHRONIC COUGH </li></ul><ul><li>CAN OFTEN PROGRESS TO EMPHYSEMA </li></ul><ul><li>MUCUS hypersecretion, early, i.e. goblet cell increase </li></ul><ul><li>CHRONIC bronchial inflammatory infiltrate </li></ul>www.freelivedoctor.com
    • 29. ASTHMA <ul><li>Similar to chronic bronchitis but: </li></ul><ul><ul><li>Wheezing is hallmark (bronchospasm, i.e. “wheezing”) </li></ul></ul><ul><ul><li>STRONG allergic role, i.e., eosinophils, IgE, allergens </li></ul></ul><ul><ul><li>Often starting in CHILDHOOD </li></ul></ul><ul><ul><li>ATOPIC (allergic) or NON-ATOPIC (infection) </li></ul></ul><ul><ul><li>Chronic small airway obstruction and infection </li></ul></ul><ul><ul><li>1) Mucus hypersecretion with plugging, 2) lymphocytes/eosinophils, 3) lumen narrowing, 4) smooth muscle hypertrophy </li></ul></ul>www.freelivedoctor.com
    • 30. www.freelivedoctor.com Note the heavy inflammatory cell infiltrate around bronchioles and small bronchi.
    • 31. What are the 4 classical histologic findings in bronchial asthma? www.freelivedoctor.com
    • 32. BRONCHIECTASIS <ul><li>DILATATION of the BRONCHUS, associated with, often, necrotizing inflammation </li></ul><ul><ul><li>CONGENITAL </li></ul></ul><ul><ul><li>TB , other bacteria, many viruses </li></ul></ul><ul><ul><li>BRONCHIAL OBSTRUCTION (i.e., LARGE AIRWAY, NOT SMALL AIRWAY) </li></ul></ul><ul><ul><li>Rheumatoid Arthritis, SLE, IBD (Inflammatory Bowel Disease) </li></ul></ul>www.freelivedoctor.com
    • 33. BRONCHIECTASIS www.freelivedoctor.com
    • 34. OVERVIEW <ul><li>Pathology </li></ul><ul><ul><li>Congenital </li></ul></ul><ul><ul><li>Atalectasis </li></ul></ul><ul><ul><li>Acute Pulmonary Injury </li></ul></ul><ul><ul><li>Obstruction vs. Restriction </li></ul></ul><ul><ul><li>Obstructive Pulmonary Diseases (COPD) </li></ul></ul><ul><ul><li>RESTRICTIVE (INFILTRATIVE) PULMONARY DISEASES </li></ul></ul><ul><ul><li>Vascular Pulmonary Diseases </li></ul></ul>www.freelivedoctor.com
    • 35. RESTRICTIVE (INFILTRATIVE) <ul><li>REDUCED COMPLIANCE, reduced gas exchange) </li></ul><ul><li>Are also DIFFUSE </li></ul><ul><li>HETEROGENEOUS </li></ul><ul><li>FIBROSING </li></ul><ul><li>GRANULOMATOUS </li></ul><ul><li>EOSINOPHILIC </li></ul><ul><li>SMOKING RELATED </li></ul><ul><li>PAP [Pulmonary Alveolar Proteinosis] </li></ul>www.freelivedoctor.com
    • 36. FIBROSING <ul><li>“ IDIOPATHIC” PULMONARY FIBROSIS (IPF) </li></ul><ul><li>NONSPECIFIC INTERSTITIAL FIBROSIS </li></ul><ul><li>“ CRYPTOGENIC” ORGANIZING PNEUMONIA </li></ul><ul><li>“ COLLAGEN” VASCULAR DISEASES </li></ul><ul><li>PNEUMOCONIOSES </li></ul><ul><li>DRUG REACTIONS </li></ul><ul><li>RADIATION CHANGES </li></ul>www.freelivedoctor.com
    • 37. IPF (UIP) <ul><li>IDIOPATHIC, i.e., not from any usual caused, like lupus, scleroderma </li></ul><ul><li>FIBROSIS </li></ul>www.freelivedoctor.com
    • 38. NON-SPECIFIC INTERSTITIAL PNEUMONIA <ul><li>WASTEBASKET DIAGNOSIS, of ANY pneumonia (pneumonitis) of any known or unknown etiology </li></ul><ul><ul><li>FIBROSIS </li></ul></ul><ul><ul><li>CELLULAR INFILTRATE (LYMPHS & PLASMA CELLS) </li></ul></ul>www.freelivedoctor.com
    • 39. CRYPTOGENIC ORGANIZING PNEUMONIA (COP) <ul><li>IDIOPATHIC </li></ul><ul><li>“ BRONCHIOLITIS OBLITERANS” </li></ul>www.freelivedoctor.com
    • 40. “ COLLAGEN” VASCULAR DISEASES <ul><li>Rheumatoid Arthritis </li></ul><ul><li>SLE (“Lupus”) </li></ul><ul><li>Progressive Systemic Sclerosis (Scleroderma) </li></ul>www.freelivedoctor.com
    • 41. PNEUMOCONIOSES <ul><li>“ OCCUPATIONAL” </li></ul><ul><li>“ COAL MINERS LUNG” </li></ul><ul><li>DUST OR CHEMICALS OR ORGANIC MATERIALS </li></ul><ul><ul><li>Coal (anthracosis) </li></ul></ul><ul><ul><li>Silica </li></ul></ul><ul><ul><li>Asbestos </li></ul></ul><ul><ul><li>Be, FeO, BaSO4, CHEMO </li></ul></ul><ul><ul><li>HAY, FLAX, BAGASSE, INSECTICIDES, etc. </li></ul></ul>www.freelivedoctor.com
    • 42. GRANULOMATOUS <ul><li>SARCOIDOSIS , i.e., NON-caseating granulomas (IDIOPATHIC) </li></ul><ul><li>HYPERSENSITIVITY (DUSTS, bacteria, fungi, Farmer’s Lung, Pigeon Breeder’s Lung) </li></ul>www.freelivedoctor.com
    • 43. SARCOIDOSIS <ul><li>Mainly LUNG, but eye, skin or ANYWHERE </li></ul><ul><li>UNKNOWN ETIOLOGY </li></ul><ul><li>IMMUNE, GENETIC factors </li></ul><ul><li>F>>M </li></ul><ul><li>B>>W </li></ul><ul><li>YOUNG ADULT BLACK WOMEN </li></ul>www.freelivedoctor.com
    • 44. NON-Caseating Granulomas are the RULE “ Asteroid” bodies within these granulomas are virtually diagnostic www.freelivedoctor.com
    • 45. www.freelivedoctor.com
    • 46. SMOKING RELATED <ul><li>DIP (Desquamative Interstitial Pneumonia) </li></ul><ul><ul><li>M>>F </li></ul></ul><ul><ul><li>CIGARETTES </li></ul></ul><ul><ul><li>100% Survival </li></ul></ul>Alveolar Macrophages www.freelivedoctor.com
    • 47. PAP (Pulmonary Alveolar Proteinosis) <ul><li>Very RARE, usually acquired </li></ul><ul><li>Proteinaceous Material in Alveoli </li></ul><ul><li>MINIMAL cellular infiltrate </li></ul><ul><li>Like Pulmonary Edema, but MUCH Protein </li></ul>www.freelivedoctor.com
    • 48. OVERVIEW <ul><li>Pathology </li></ul><ul><ul><li>Congenital </li></ul></ul><ul><ul><li>Atalectasis </li></ul></ul><ul><ul><li>Acute Pulmonary Injury </li></ul></ul><ul><ul><li>Obstruction vs. Restriction </li></ul></ul><ul><ul><li>Obstructive Pulmonary Diseases (COPD) </li></ul></ul><ul><ul><li>Restrictive (Infiltrative) Pulmonary Diseases </li></ul></ul><ul><ul><li>VASCULAR PULMONARY DISEASES </li></ul></ul>www.freelivedoctor.com
    • 49. VASCULAR PULMONARY DISEASES <ul><li>PULMONARY EMBOLISM (with or usually WITHOUT infarction) </li></ul><ul><li>PULMONARY HYPERTENSION , leading to cor pulmonale </li></ul><ul><li>HEMORRHAGIC SYNDROMES </li></ul><ul><ul><li>GOODPASTURE SYNDROME </li></ul></ul><ul><ul><li>HEMOSIDEROSIS , idiopathic </li></ul></ul><ul><ul><li>WEGENER GRANULOMATOSIS </li></ul></ul>www.freelivedoctor.com
    • 50. P.E. <ul><li>Usually secondary to debilitated states with immobilization, or following surgery </li></ul><ul><li>Usually deep leg and deep pelvic veins (DVT), NOT superficial veins </li></ul><ul><li>Follows Virchow’s triad, i.e., 1) flow problems, 2) endothelial disruption, 3) hypercoagulabilty </li></ul><ul><li>Usually do NOT infarct, usually ventilate </li></ul><ul><li>When they DO infarct, the infarct is hemorrhagic </li></ul><ul><li>Decreased PO2, acute chest pain, V/Q MIS-match </li></ul><ul><li>DX: Chest CT, V/Q scan, angiogram </li></ul><ul><li>RX: short term heparin, then long term coumadin </li></ul>www.freelivedoctor.com
    • 51. PULMONARY HYPERTENSION <ul><li>COPD, C”I”PD (vicious cycle) </li></ul><ul><li>CHD (Congenital HD, increased left atrial pressure) </li></ul><ul><li>Recurrent PEs </li></ul><ul><li>Autoimmune, e.g., PSS (Scleroderma), i.e., fibrotic pulmonary vasculature </li></ul>www.freelivedoctor.com
    • 52. VERY thickened arteriole in pulmonary hypertension NORMAL pulmonary arteriole www.freelivedoctor.com
    • 53. HEMORRHAGIC SYNDROMES <ul><li>GOODPASTURE Syndrome: Ab’s to the alpha-3 chains of collagen IV, GBM deposits too! </li></ul><ul><li>IDIOPATHIC PULMONARY HEMOSIDEROSIS, to be differentiated from chronic CHF </li></ul><ul><li>WEGENER GRANULOMATOSIS </li></ul>www.freelivedoctor.com
    • 54. CHF, CHRONIC IDIOPATHIC PULMONARY HEMOSIDEROSIS www.freelivedoctor.com
    • 55. PNEUMONIA www.freelivedoctor.com
    • 56.   COMM UNITY-ACQUIRED BACTERIAL ACUTE PNEUMONIAS Streptococcus Pneumoniae Haemophilus Influenzae Moraxella Catarrhalis Staphylococcus Aureus Klebsiella Pneumoniae Pseudomonas Aeruginosa Legionella Pneumophila COMMUNITY-ACQUIRED ATYPICAL (VIRAL AND MYCOPLASMAL) PNEUMONIAS Morphology. Clinical Course. Influenza Infections Severe Acute Respiratory Syndrome (SARS) NOSOCOMIAL PNEUMONIA ASPIRATION PNEUMONIA LUNG ABSCESS Etiology and Pathogenesis. CHRONIC PNEUMONIA Histoplasmosis, Morphology Blastomycosis, Morphology Coccidioidomycosis, Morphology PNEUMONIA IN THE IMMUNOCOMPROMISED HOST PULMONARY DISEASE IN HUMAN IMMUNODEFICIENCY VIRUS INFECTION PULMONARY INFECTIONS www.freelivedoctor.com
    • 57. BASIC CONSIDERATIONS <ul><li>PNEUMONIA vs. PNEUMONITIS </li></ul><ul><li>DIFFERENTIATION from INJURIES, OBSTRUCTIVE DISEASES, RESTRICTIVE DISEASES, VASCULAR DISEASES </li></ul><ul><li>DIFFERENTIATION FROM NEOPLASMS </li></ul><ul><li>CLASSICAL STAGES of INFLAMMATION </li></ul><ul><li>LOBAR- vs. BRONCHO- </li></ul><ul><li>INTERSTITIAL vs. ALVEOLAR </li></ul><ul><li>COMMUNITY vs. NOSOCOMIAL </li></ul><ul><li>ETIOLOGIC AGENTS vs. HOST IMMUNITY </li></ul><ul><li>2 PRESENTING SYMPTOMS </li></ul><ul><li>2 DIAGNOSTIC METHODS </li></ul><ul><li>ANY ORGANISM CAN CAUSE PNEUMONIA!!! </li></ul>www.freelivedoctor.com
    • 58. PREDISPOSING FACTORS <ul><li>LOSS OF COUGH REFLEX </li></ul><ul><li>DIMINISHED MUCIN or CILIA FUNCTION </li></ul><ul><li>ALVEOLAR MACROPHAGE INTERFERENCE </li></ul><ul><li>VASCULAR FLOW IMPAIRMENTS </li></ul><ul><li>BRONCHIAL FLOW IMPAIRMENTS </li></ul>www.freelivedoctor.com
    • 59. Although pneumonia is one of the most common causes of death, it usually does NOT occur in healthy people spontaneously www.freelivedoctor.com
    • 60. Classifications of PNEUMONIAS <ul><li>COMMUNITY ACQUIRED </li></ul><ul><li>COMMUNITY ACQUIRED, ATYPICAL </li></ul><ul><li>NOSOCOMIAL </li></ul><ul><li>ASPIRATION </li></ul><ul><li>CHRONIC </li></ul><ul><li>NECROTIZING/ABSCESS FORMATION </li></ul><ul><li>PNEUMONIAS in IMMUNOCOMPROMISED HOSTS </li></ul>www.freelivedoctor.com
    • 61. Classifications of PNEUMONIAS <ul><li>COMMUNITY ACQUIRED </li></ul><ul><li>COMMUNITY ACQUIRED, ATYPICAL </li></ul><ul><li>NOSOCOMIAL </li></ul><ul><li>ASPIRATION </li></ul><ul><li>CHRONIC </li></ul><ul><li>NECROTIZING/ABSCESS FORMATION </li></ul><ul><li>PNEUMONIAS in IMMUNOCOMPROMISED HOSTS </li></ul>www.freelivedoctor.com
    • 62. COMMUNITY ACQUIRED <ul><li>STREPTOCOCCUS PNEUMONIAE (i.e., “diplococcus”) </li></ul><ul><li>HAEMOPHILUS INFLUENZAE (“H-Flu”) </li></ul><ul><li>MORAXELLA </li></ul><ul><li>STAPHYLOCOCCUS (STAPH) </li></ul><ul><li>KLEBSIELLA PNEUMONIAE </li></ul><ul><li>PSEUDOMONAS AERUGINOSA </li></ul><ul><li>LEGIONELLA PNEUMOPHILIA </li></ul>www.freelivedoctor.com
    • 63. STREPTOCOCCUS <ul><li>The classic LOBAR pneumonia </li></ul><ul><li>Normal flora in 20% of adults </li></ul><ul><li>Only 20% of victims have + blood cultures </li></ul><ul><li>“ Penicillins” are often 100% curative </li></ul><ul><li>Vaccines are often 100% preventive </li></ul>www.freelivedoctor.com
    • 64. HAEMOPHILUS PNEUMONIA <ul><li>Commonest in CHILDREN <2, with otitis, URI, meningitis, cellulitis, osteomyelitis </li></ul><ul><li>PNEUMONIAS in CHILDREN <2 are often thought of as being H Flu until proven otherwise, otitis, meningitis too </li></ul><ul><li>Most common pneumonia from COPD in adults </li></ul><ul><li>BACTRIM (Trimethoprim-Sulfa) most common treatment </li></ul>www.freelivedoctor.com
    • 65. MORAXELLA CATARRHALIS <ul><li>2nd most common COPD pneumonia, after haemophilus </li></ul><ul><li>Gram NEGATIVE coccobacillus </li></ul>www.freelivedoctor.com
    • 66. STAPH aureus <ul><li>Most common pneumonia following viral pneumonias </li></ul><ul><li>M.R.S.A., of course, is usually NOT “community” acquired </li></ul>www.freelivedoctor.com
    • 67. KLEBSIELLA PNEUMONIAE <ul><li>DEBILITATED MALNOURISHED PEOPLE </li></ul><ul><li>ALCOHOLICS with pneumonia are often thought of as having Klebsiella until proven otherwise </li></ul>www.freelivedoctor.com
    • 68. PSEUDOMONAS Aeruginosa <ul><li>Usually NOT community acquired but nosocomial </li></ul><ul><li>CYSTIC FIBROSIS patients with pneumonia are presumed to have PSEUDOMONAS until proven otherwise </li></ul>www.freelivedoctor.com
    • 69. LEGIONELLA (pneumophila) <ul><li>Often in OUTBREAKS </li></ul><ul><li>Often LOBAR </li></ul><ul><li>Spread by water “droplets” </li></ul><ul><li>Often immunosuppressed patients, but remember……….. </li></ul>www.freelivedoctor.com
    • 70. Although pneumonia is one of the most common causes of death, it usually does NOT occur in healthy people spontaneously www.freelivedoctor.com
    • 71. MORPHOLOGY <ul><li>ACUTE </li></ul><ul><li>ORGANIZING </li></ul><ul><li>CHRONIC </li></ul><ul><li>FIBROSIS vs. FULL RESOLUTION </li></ul><ul><li>“ HEPATIZATION”, RED vs. GREY </li></ul><ul><li>CONSOLIDATION </li></ul><ul><li>“ INFILTRATE ”, XRAY vs. HISTOPATH </li></ul><ul><li>Loss of “CREPITANCE” </li></ul>www.freelivedoctor.com
    • 72. Classifications of PNEUMONIAS <ul><li>COMMUNITY ACQUIRED </li></ul><ul><li>COMMUNITY ACQUIRED, ATYPICAL </li></ul><ul><li>NOSOCOMIAL </li></ul><ul><li>ASPIRATION </li></ul><ul><li>CHRONIC </li></ul><ul><li>NECROTIZING/ABSCESS FORMATION </li></ul><ul><li>PNEUMONIAS in IMMUNOCOMPROMISED HOSTS </li></ul>www.freelivedoctor.com
    • 73. COMMUNITY ACQUIRED , (atypical) <ul><li>VIRAL (INFLUENZA) </li></ul><ul><li>MYCOPLASMAL (MYCOPLASMA PNEUMONIAE (obligate intracellular)) </li></ul><ul><li>NOT BACTERIAL </li></ul><ul><li>CULTURES NOT HELPFUL </li></ul>www.freelivedoctor.com
    • 74. VIRAL PNEUMONIAS <ul><li>Frequently “interstitial”, NOT alveolar </li></ul>www.freelivedoctor.com
    • 75. INFLUENZA VIRUS <ul><li>A,B,C </li></ul><ul><li>1915, 1918, PAN-demics, type A </li></ul><ul><li>Has MUTATED throughout history, many STRAINS, avian swine, etc. </li></ul><ul><li>B and C in children </li></ul><ul><li>Exact strains can be ID’s by PCR </li></ul>www.freelivedoctor.com
    • 76. www.freelivedoctor.com
    • 77. SARS (Severe Acute Respiratry Syndrome) <ul><li>CORONA-VIRUS </li></ul><ul><li>2002 China outbreak </li></ul><ul><li>Spread CHIEFLY in Asia </li></ul><ul><li>Like most other NON-bacterial pneumonias confirmed by PCR </li></ul><ul><li>Like most viral pneumonias, interstitium infiltrated, some giant cells often present </li></ul>www.freelivedoctor.com
    • 78. S A R S www.freelivedoctor.com
    • 79. Classifications of PNEUMONIAS <ul><li>COMMUNITY ACQUIRED </li></ul><ul><li>COMMUNITY ACQUIRED, ATYPICAL </li></ul><ul><li>NOSOCOMIAL </li></ul><ul><li>ASPIRATION </li></ul><ul><li>CHRONIC </li></ul><ul><li>NECROTIZING/ABSCESS FORMATION </li></ul><ul><li>PNEUMONIAS in IMMUNOCOMPROMISED HOSTS </li></ul>www.freelivedoctor.com
    • 80. NOSOCOMIAL <ul><li>Acquired in HOSPITALS, also called “hospital acquired”, versus “community acquired” pneumonias. </li></ul><ul><ul><li>DEBILITATION </li></ul></ul><ul><ul><li>CATHETERS, VENTILATORS </li></ul></ul><ul><ul><li>ENTEROBACTER, PSEUDOMONAS </li></ul></ul><ul><ul><li>STAPH (MRSA) </li></ul></ul><ul><ul><li>MRSA (MR=Methicillin R esistant) </li></ul></ul><ul><li>OTHER Common causes of Noso. Pneum. P. aeruginosa Klebsiella E. coli S. pneumoniae H. influenzae </li></ul>www.freelivedoctor.com
    • 81. Classifications of PNEUMONIAS <ul><li>COMMUNITY ACQUIRED </li></ul><ul><li>COMMUNITY ACQUIRED, ATYPICAL </li></ul><ul><li>NOSOCOMIAL </li></ul><ul><li>ASPIRATION </li></ul><ul><li>CHRONIC (often granulomatous) </li></ul><ul><li>NECROTIZING/ABSCESS FORMATION </li></ul><ul><li>PNEUMONIAS in IMMUNOCOMPROMISED HOSTS </li></ul>www.freelivedoctor.com
    • 82. ASPIRATION PNEUMONIAS <ul><li>UNCONSCIOUS PATIENTS </li></ul><ul><li>PATIENTS IN PROLONGED BEDREST </li></ul><ul><li>LACK OF ABILITY TO SWALLOW OR GAG </li></ul><ul><li>USUALLY CAUSED BY ASPIRATION OF GASTRIC CONTENTS </li></ul><ul><li>POSTERIOR LOBES (gravity dependent) MOST COMMONLY INVOLVED, ESPECIALLY THE SUPERIOR SEGMENTS of the LOWER LOBES </li></ul><ul><li>Often lead to ABSCESSES </li></ul>www.freelivedoctor.com
    • 83. www.freelivedoctor.com
    • 84. LUNG ABSCESSES <ul><li>ASPIRATION </li></ul><ul><li>SEPTIC EMBOLIZATION </li></ul><ul><li>NEOPLASIA </li></ul><ul><li>From NEIGHBORING structures: </li></ul><ul><ul><li>ESOPHAGUS </li></ul></ul><ul><ul><li>SPINE </li></ul></ul><ul><ul><li>PLEURA </li></ul></ul><ul><ul><li>DIAPHRAGM </li></ul></ul><ul><li>ANY pneumonia which is severe and destructive, and UN-treated enough </li></ul>www.freelivedoctor.com
    • 85. www.freelivedoctor.com
    • 86. Classifications of PNEUMONIAS <ul><li>COMMUNITY ACQUIRED </li></ul><ul><li>COMMUNITY ACQUIRED, ATYPICAL </li></ul><ul><li>NOSOCOMIAL </li></ul><ul><li>ASPIRATION </li></ul><ul><li>CHRONIC </li></ul><ul><li>NECROTIZING/ABSCESS FORMATION </li></ul><ul><li>PNEUMONIAS in IMMUNOCOMPROMISED HOSTS </li></ul>www.freelivedoctor.com
    • 87. CHRONIC Pneumonias <ul><li>USUALLY NOT persistences of the community or nosocomial bacterial infections, but CAN BE, at least histologically </li></ul><ul><li>Often SYNONYMOUS with the 4 classic fungal or granulomatous pulmonary infections infections, i.e., TB, Histo-, Blasto-, Coccidio- </li></ul><ul><li>If you see pulmonary granulomas, think of a CHRONIC process, often years </li></ul>www.freelivedoctor.com
    • 88. CHRONIC Pneumonias <ul><li>TB </li></ul><ul><li>HISTO-PLASMOSIS </li></ul><ul><li>BLASTO-MYCOSIS </li></ul><ul><li>COCCIDIO-MYCOSIS </li></ul>www.freelivedoctor.com
    • 89. HISTOPLASMOSIS <ul><li>Spores in bird or bat droppings </li></ul><ul><li>Mimics TB </li></ul><ul><li>Histoplasma CAPSULATUM </li></ul><ul><li>Pulmonary granulomas, often large and calcified </li></ul><ul><li>Tiny organisms live in macrophages </li></ul><ul><li>Ohio, Mississippi valley </li></ul><ul><li>MANY other organs can be affected </li></ul>www.freelivedoctor.com
    • 90. www.freelivedoctor.com
    • 91. BLASTOMYCOSIS <ul><li>Spores in soil </li></ul><ul><li>Mimics TB, like ALL the granulomatous lung dideases do. </li></ul><ul><li>Blastomyces DERMATIDIS </li></ul><ul><li>Pulmonary granulomas, often large and calcified </li></ul><ul><li>Large distinct SPHERULES </li></ul><ul><li>Ohio, Mississippi valley, Great Lakes, WORLDWIDE </li></ul><ul><li>MANY other organs can be affected, especially SKIN </li></ul>www.freelivedoctor.com
    • 92. COCCIDIOMYCOSIS <ul><li>Spores in soil </li></ul><ul><li>Mimics TB </li></ul><ul><li>Coccidioides IMMITIS </li></ul><ul><li>Pulmonary granulomas, often large and calcified </li></ul><ul><li>Tiny organisms live in macrophages </li></ul><ul><li>American SOUTHWEST </li></ul><ul><li>MANY other organs can be affected </li></ul>www.freelivedoctor.com
    • 93. GRANULOMA www.freelivedoctor.com
    • 94. COMPROMISED HOSTS <ul><li>PNEUMOCYSTIS CARINII </li></ul><ul><li>CYTOMEGALOVIRUS (CMV) </li></ul><ul><li>FUNGI </li></ul>www.freelivedoctor.com
    • 95. PCP www.freelivedoctor.com
    • 96. Methenamine SILVER stain for Pneumocystis Carinii www.freelivedoctor.com
    • 97. LUNG TRANSPLANTATION <ul><li>EMPHYSEMA </li></ul><ul><li>Pulmonary Fibrosis </li></ul><ul><li>Cystic Fibrosis </li></ul><ul><li>Pulmonary Hypertension </li></ul>Any end-stage lung disease in which the patient can tolerate long term immunosuppression, and often just ONE lung is enough, donors very SCARCE! www.freelivedoctor.com
    • 98. Lung Transplant Pathology <ul><li>Infections (immunocompromised patients) </li></ul><ul><ul><li>Bacterial </li></ul></ul><ul><ul><li>Viral (CMV) </li></ul></ul><ul><ul><li>Fungal </li></ul></ul><ul><ul><li>PCP </li></ul></ul><ul><li>ACUTE rejection, pneumonias, usually weeks to months </li></ul><ul><li>CHRONIC rejection, HALF of all patients by 3-5 years, “bronchiolitis obliterans” </li></ul>www.freelivedoctor.com
    • 99. www.freelivedoctor.com
    • 100. LUNG TUMORS <ul><li>Benign, malignant, epithelial, mesenchymal, but 90% are CARCINOMAS </li></ul><ul><li>BIGGEST USA killer. Why? Ans: Prevalence not as high as prostate or breast but mortality higher. Only 15% 5 year survival. </li></ul><ul><li>TOBACCO has polycyclic aromatic hydrocarbons, such as benzopyrene, anthracenes, radioactive isotopes </li></ul><ul><li>Radiation, asbestos, radon </li></ul><ul><li>C-MYC, K-RAS, EGFR, HER-2/neu </li></ul>www.freelivedoctor.com
    • 101. PATHOGENESIS <ul><li>NORMAL BRONCHIAL MUCOSA </li></ul><ul><li>METAPLASTIC/DYSPLASTIC MUCOSA </li></ul><ul><li>CARCINOMA-IN-SITU (squamous, adeno) </li></ul><ul><li>INFILTRATING (i.e., “INVASIVE”) cancer </li></ul>www.freelivedoctor.com
    • 102. TWO TYPES <ul><li>NON-SMALL CELL </li></ul><ul><ul><li>SQUAMOUS CELL CARCINOMA </li></ul></ul><ul><ul><li>ADENOCARCINOMA </li></ul></ul><ul><ul><li>LARGE CELL CARCINOMA </li></ul></ul><ul><li>SMALL CELL CARCINOMA </li></ul>www.freelivedoctor.com
    • 103. The BIG list <ul><li>Squamous cell carcinoma </li></ul><ul><li>Small cell carcinoma </li></ul><ul><li>Combined small cell carcinoma   </li></ul><ul><li>Adenocarcinoma: Acinar, papillary, bronchioloalveolar, solid, mixed subtypes </li></ul><ul><li>Large cell carcinoma </li></ul><ul><li>Large cell neuroendocrine carcinoma </li></ul><ul><li>Adenosquamous carcinoma </li></ul><ul><li>Carcinomas with pleomorphic, sarcomatoid, or sarcomatous elements </li></ul><ul><li>Carcinoid tumor: Typical, atypical   </li></ul><ul><li>Carcinomas of salivary gland type </li></ul><ul><li>Unclassified carcinoma </li></ul>www.freelivedoctor.com
    • 104. OTHER TUMORS www.freelivedoctor.com
    • 105. www.freelivedoctor.com
    • 106. TNM, Lung www.freelivedoctor.com T1 Tumor <3 cm without pleural or main stem bronchus involvement T2 Tumor >3 cm or involvement of main stem bronchus 2 cm from carina, visceral pleural involvement, or lobar atelectasis T3 Tumor with involvement of chest wall (including superior sulcus tumors), diaphragm, mediastinal pleura, pericardium, main stem bronchus 2 cm from carina, or entire lung atelectasis T4 Tumor with invasion of mediastinum, heart, great vessels, trachea, esophagus, vertebral body, or carina or with a malignant pleural effusion N0 No demonstrable metastasis to regional lymph nodes N1 Ipsilateral hilar or peribronchial nodal involvement N2 Metastasis to ipsilateral mediastinal or subcarinal lymph nodes N3 Metastasis to contralateral mediastinal or hilar lymph nodes, ipsilateral or contralateral scalene, or supraclavicular lymph nodes M0 No (known) distant metastasis M1 Distant metastasis present
    • 107. LOCAL effects of LUNG CANCER www.freelivedoctor.com Clinical Feature Pathologic Basis Pneumonia, abscess, lobar collapse Tumor obstruction of airway Lipid pneumonia Tumor obstruction; accumulation of cellular lipid in foamy macrophages Pleural effusion Tumor spread into pleura Hoarseness Recurrent laryngeal nerve invasion Dysphagia Esophageal invasion Diaphragm paralysis Phrenic nerve invasion Rib destruction Chest wall invasion SVC syndrome SVC compression by tumor Horner syndrome Sympathetic ganglia invasion Pericarditis, tamponade Pericardial involvement SVC, superior vena cava.
    • 108. SYSTEMIC effects of LUNG CANCER (PARA-NEOPLASTIC SYNDROMES)~ 5% ADH (hyponatremia) ACTH (Cushing) PTH (Hyper-CA) CALCITONIN (Hypo-CA) GONADOTROPINS SEROTONIN/BRADYKININ www.freelivedoctor.com
    • 109. OTHER TUMORS www.freelivedoctor.com
    • 110. METASTATIC TUMORS <ul><li>LUNG is the MOST COMMON site for all metastatic tumors, regardless of site of origin </li></ul><ul><li>It is the site of FIRST CHOICE for metastatic sarcomas for purely anatomic reasons! </li></ul>www.freelivedoctor.com
    • 111. PLEURA <ul><li>PLEURITIS </li></ul><ul><li>PNEUMOTHORAX </li></ul><ul><li>EFFUSIONS </li></ul><ul><ul><li>HYDRO-THORAX (Peric-, Perito-) </li></ul></ul><ul><ul><li>HEMO-THORAX (Peric-, Perito-) </li></ul></ul><ul><ul><li>CHYLO-THORAX (Peric-, Perito-) </li></ul></ul><ul><li>MESOTHELIOMAS </li></ul>www.freelivedoctor.com
    • 112. PLEURITIS <ul><li>Usual bacteria, viruses, etc. </li></ul><ul><li>Infarcts </li></ul><ul><li>Lung abscesses, empyema </li></ul><ul><li>TB </li></ul><ul><li>“ Collagen” diseases, e.g., RA, SLE </li></ul><ul><li>Uremia </li></ul><ul><li>Metastatic </li></ul>www.freelivedoctor.com
    • 113. PNEUMOTHORAX <ul><li>SPONTANEOUS, TRAUMATIC, THERAPEUTIC </li></ul><ul><li>OPEN or CLOSED </li></ul><ul><li>“ TENSION” pneumothorax, “valvular” effect </li></ul><ul><li>“ Bleb” rupture </li></ul><ul><li>Perforating injuries </li></ul><ul><li>Post needle biopsy </li></ul>www.freelivedoctor.com
    • 114. EFFUSIONS <ul><li>TRANSUDATE (HYDROTHORAX) </li></ul><ul><li>EXUDATE (HYDROTHORAX) </li></ul><ul><li>BLOOD (HEMOTHORAX) </li></ul><ul><li>LYMPH (CHYLOTHORAX) </li></ul>www.freelivedoctor.com
    • 115. MESOTHELIOMAS <ul><li>“ Benign” vs. “Malignant” differentiation does not matter, but a self limited localized nodule can be regarded as benign, and a spreading tumor can be regarded as malignant </li></ul><ul><li>Visceral or parietal pleura, pericardium, or peritoneum </li></ul><ul><li>Most are regarded as asbestos caused or asbestos “related” </li></ul>www.freelivedoctor.com
    • 116. www.freelivedoctor.com
    • 117.  EM H&E, IMMUNOCHEMISTRY www.freelivedoctor.com

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