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  • Typical normal 1000 gram lung (R550, L450), with lobes and bronchopulmonary segments, primary, secondary, tertiary bronchi, half billion alveoli, several hundred billion capillaries, 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? What is “compliance”? Why is compliance just as important as crepitance, in understanding lung diseases? <br />
  • Classical classifications of diseases, degenerative, inflammatory, neoplastic. This classification still stands up today. <br />
  • This is about a day’s (2-hour) job. <br /> NON PNEUMONIAS (caused by pathogens) <br /> NON TUMORS <br />
  • This is also about a day’s (2-hour) job. <br />
  • 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? Is crepitance the same as bubbliness? ANS: YES <br />
  • Know the microscopic criteria for all the items delineated on the right, especially the kinds of simple epithelium which line them. <br />
  • The “space” between the endothelium and the type-1 pneumocyte, is the blood air interface. <br /> Type-I pneumocyte, Type-2 pneumocyte, Endothelial cell, Alveolar macrophages, Interstitial fibroblasts. <br />
  • This simple embryology diagram may help explain most common congenital lung diseases. Why might this diagram be WRONG, especially the top figure? Ans: The RIGHT one is the main downward one, embryologically! <br />
  • “NORMAL” chest X-Ray (CXR). What features of “normal” are the most important? <br /> Infiltrates? Sharpness of costophrenic angles? Properly exposed? Hilar vasculature? Bronchi? <br /> Why is a CXR to a radiologist like pathologists fingers? <br />
  • By far, the most common scenario is for the baby to eat, and it comes back up WITHOUT food getting into the lungs. <br />
  • ATALECTASIS is strictly an anatomic/physiologic/geometric CONCEPT, NOT a disease by itself, but seen in many disease states. <br /> Reabsorption can be from a bronchial obstruction, such as a tumor. <br /> Compression can be from, say, a pleural effusion, or pneomothorax. <br /> Contraction can be from a diffuse lung fibrotic process. <br />
  • FOUR main pathologic mechanisms of pulmonary edema. <br /> In alveolar injury, the fluid is much more likely to be EXUDATE rather than TRANSUDATE, right? <br />
  • *…..as opposed to NEONATAL Respiratory Distress Syndrome <br /> 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?, i.e., exudate vs. transudate? <br />
  • Think of ARDS morphologically as NON-cardiogenic pulmonary edema where much more leaks into the alveoli than just transudative fluid, i.e., fibrin, protein, cells, etc. <br />
  • ARDS is generally SECONDARY to something else, when it ISN’T, we can call it ACUTE INTERSTITIAL PNEUMONIA. Histologically, they cannot be differentiated! <br />
  • O vs. R constitute the majority of pulmonary diseases which are not infectious pneumonias. <br />
  • Two EXTREMELY important concepts of pulmonary pathology. <br /> OBSTRUCTION means SMALL AIRWAY EXPIRATORY obstruction, air trapping , wheezing, more lucency, less density. <br /> RESTRICTION means REDUCED COMPLIACE, i.e., less sponginess, less gas transfer, more opacity, i.e., more density! <br />
  • Are thesese all related? Generally, YES. <br /> Sm,sm,sm,lg <br />
  • Which one would feel more “hypercrepitant” at autopsy? Which one would be more severe? Answer: the MORE hypercrepitant one, which involvs the WHOLE acinus, rather than just the central portion of the acinus. <br /> An acinus is NOT the same as an alveolus, the ACINUS is everything AFTER a terminal bronchiole. <br />
  • Bullae, or “peripheral blebs” are hallmarks of chronic obstructive lung disease, COPD. <br /> What would happen if a “bleb” was so paper-thin, that it ruptured? Ans: “Pneumo”-thorax <br />
  • Calling something “hyperlucent” to a radiologist is like calling something “understained” to a pathologist, i.e., many technical factors have to be taken into consideration before you diagnose disease <br />
  • Note the heavy inflammatory cell infiltrate around bronchioles and small bronchi. <br /> Would the presence of a small amount of cartilage in the wall tend to make us call this a small bronchus rather than a bronchiole? Ans: Yes Do you think you might already see some overexpanded alveoli here? <br />
  • What are the 4 classic histologic findings in bronchial asthma? <br /> Answer: 1) Inflammation 2) Bronchial (luminal) narrowing 3) Increased Mucous 4) Smooth muscle hyperplasia <br /> What is the 5th finding if the etiology is allergy? Ans: Increased eosinophils <br />
  • Bronchiectasis is not a specific disease, but simply a condition in which LARGE bronchi are damaged and DILATED due to a variety of causes. <br /> “-ectasis” is the root word for “dilatation”. <br />
  • How do you know these are not bullae? <br />
  • 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. Compliance is NOT crepitance. Another common denominator of the “restrictive” lung diseases is that they have anatomic/functional barriers to the classic gas exchange between an endothelial cell and a type-1 pneumocyte. <br />
  • “FIBROSING” is by far, the biggest category of restrictive lung diseases. <br /> Fibrosis follows inflammation, but there is an absence of infectious organisms. What does that sound like? Ans: Autoimmune? Perhaps. <br />
  • Would you see a lot of scar tissue here if you did a trichrome stain? Ans: yes <br />
  • Could this have been preceded by an unknown infectious pathogen? Yes. <br />
  • Often occurs in a transplanted lung. <br />
  • Because these are also classified as “irritants” which may produce a bronchitic component as well, there may also be “chronic obstructive” components to these diseases. <br />
  • Coal, “bagasse” (sugar cane leftovers), silica nodules, and asbestos (ferruginous bodies), going clockwise. <br />
  • Note that in this category, we do NOT include the systemic fungal diseases. <br />
  • This image was “googled” from tumorboard.com, the internet’s FIRST diagnostic pathology image base which started even BEFORE there was a world wide web, when it was only a BBS. <br /> The fact that this is a mesenteric lymph node will remind you that sarcoidosis is NOT limited to the lungs. <br />
  • 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) <br />
  • Why is it called “desquamative”? Ans: …because it looks like the alveolar wall “epithelium” is peeling off into the alveolus! <br />
  • Pulmonary edema on left, PAP (Pulmonary Alveolar Proteinosis) on the right. <br /> anti-GM-CSF autoantibodies in patients with PAP <br />
  • Three types of “vascular” lung diseases. <br />
  • Why would a PE usually NOT result in an infarct? <br />
  • Routine chest x-rays are the very LEAST helpful in diagnosing PE. Why? Ans: there is no radiologic “infiltrate” unless there is infarction which is rare for PE. Also…..the lung still VENTILATES! <br />
  • A general rule with COPD is: As the alveoli become wider, the arterioles become narrower! This is a totally non-scientific, but a TRUE observation. <br />
  • A common finding in most cases of pulmonary hypertension, no matter what the cause is. <br /> NORMAL thickness pulmonary arteriole on the LEFT. <br /> Vicious cycle: Pulmonary hypertension is destructive on the pulmonary arterioles and causes, eventually, fibrotic narrowing. PLUS, narrowing from ANY reason causes pulmonary hypertension! <br />
  • Wegener&apos;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, it often has ANCAs, i.e., Anti-Neutrophil Cytoplasmic Antibodies. <br /> Why do I LOVE “idiopathic” diseases? Because I don’t have to waste time talking about the etiology! <br /> What is probably the most COMMON cause of a hemorrhagic part of the lung? Ans: INFARCT? <br />
  • IPH has MUCH more hemosiderin in alveoli, usually, relative to chronic CHF. Acute CHF has NO hemosiderin. Why? <br />
  • Biggest killer? <br /> Biggest killer in hospitals? <br />
  • Why is the term “chronic” pneumonia here, kind of a misnomer, classically? <br />
  • PNEUMONIAS are also called LOWER respiratory infections, as opposed to UPPER. <br />
  • Logically speaking, would impairments at ANY of these levels set the stage for pneumonias? Ans: OFF COURSE <br />
  • I put this slide into my discussion of pneumonias 2-3 times. This is not enough times. <br />
  • Of course these are NOT mutually exclusive classifications, e.g., ANY pneumonia may result in an abscess. <br /> * Go back to the previous slide! <br />
  • COMMUNITY vs. HOSPITAL <br />
  • Know the gram staining properties of the common community acquired pneumonia organisms. <br />
  • Do the upper two images demonstrate the “lobar-ness” of the pneumonia? Ans: Yes <br />
  • H. Flu graphics <br />
  • * Go to slides 61 or 74 <br />
  • This is the reason why after you feel so good about curing your patients pneumonia with antibiotics, you wonder if he will be back again, due to the underlying REAL reason he got the pneumonia! <br />
  • Would a classical pneumonia produce more of a restrictive pattern or obstructive? Answer: Unfair question! (could be both). Functionally it might behave like a restrictive in the pulmonary blood gas lab, but it may be a complication of an obstructive. <br />
  • Viral pneumonias, generally interstitial, bacterial pneumonias generally alveolar!!! <br />
  • Can you see the RLL “subtle” infiltrate? Or do you want to call the radiologist? <br />
  • Corona viruses are RNA, “enveloped”, i.e., “crowned” viruses <br />
  • As soon as you step into a hospital, expect to be greeted by MRSA. <br /> Two things live in hospitals: 1) bugs resistant to antibiotics 2) sick people <br />
  • STREP, STAPH, H.FLU, PSEUDOMONAS are the most frequent secondary complicators. <br />
  • This is not a TYPE of pneumonia, but a complication of ANY pneumonia! <br />
  • 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. <br />
  • The word “chronic” pneumonia classification may be a misnomer because most show a “granulomatous” pattern of inflammation, rather than pure “chronic”. i.e., monos. They are chronic CLINICALLY, however, if not strictly pathologically. <br />
  • In this case CHRONIC means CLINICALLY CHRONIC, not PATHOLOGICALLY CHRONIC. <br />
  • “Chronic” by classification, but “granulomatous” by histology. <br />
  • Granulomatous reactions are commonly seen with mycobacteria, fungi, sarcoid, foreign bodies, and rarely with almost anything. <br />
  • * Really jiroveci, not carinii any more. <br />
  • PCP is the most common pneumonia in AIDS patients. It is so prevalent, many rationales consist in giving treatment for it prophylactically. <br /> An interesting tidbit is that “cotton wool” or “wooly” exudates are described BOTH radiologically as well as histologically <br />
  • *really “jiroveci” <br /> Protozoan vs. Fungi? <br />
  • Bronchiolitis obliterans, as seen with “COP”, occurs with chronic pulmonary transplant rejection <br />
  • Different mutations may be occurring at different steps of this cascade! <br />
  • 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! <br />
  • 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. <br />
  • The classical squamous cell carcinoma starting in a large bronchus centrally, with bronchial obstruction. <br /> Adenocarcinomas tend to be more peripheral. Note the features of malignant cells on sputum cytology. <br />
  • Name the four most common histologic patterns of lung carcinoma and explain why! <br /> Squamous, adeno, large, small, going clockwise. <br />
  • TNM ALWAYS relates to BIOLOGIC BEHAVIOR! <br />
  • 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. <br />
  • NB: OFTEN, the very first distant metastasis for a lung carcinoma is the adrenal! <br /> LIVER:PORTAL DRAINED ORGANS::LUNG:SARCOMAS <br />
  • 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. 12 possibilities ? Pneumo, hydro, hemo, chylo X pleura, pericardial, peritoneal <br />
  • Pleuritis = Pleurisy <br />
  • How would you differentiate a pleural transudate from an exudate? Ans: SPGR, cells, protein, LDH <br />
  • The diagnosis of “MESOTHELIOMA” is RARELY preceded by the word benign or malignant on histology alone! <br />
  • Typical growth appearance of a malignant mesothelioma, it compresses the lung from the OUTSIDE. <br />
  • Mesothelial cells have MANY more microvilli than most epithelial cells and express a protein called CALRETININ, which epithelial cells do NOT. <br /> The differentiation between mesothelioma and carcinoma may be crucially important! <br />

Minarcik robbins 2013_ch15-lung Minarcik robbins 2013_ch15-lung Presentation Transcript

  • LUNGS
  • The LUNG • “Degenerative” • Inflammatory • Neoplastic and Pleura • LAB: (Review, Cases, and/or Virtual Microscopy)
  • OVERVIEW I • Normal Anatomy and Histology • Pathology – Congenital – Atalectasis – Acute Pulmonary Injury – Obstructive vs. Restrictive (infiltrative) concepts –Obstructive Pulmonary Disease (COPD) – Restrictive (Infiltrative) Pulmonary Disease – Vascular Pulmonary Diseases
  • OVERVIEW II • INFECTIONS • NEOPLASMS and PLEURA (effusions, pneumothorax, tumors)
  • WEIGHT LOBES SEGMENTS BRONCHI ARTERIES, pulmonary ARTERIES, bronchial VEINS PLEURA, visceral PLEURA, parietal NERVES
  • Bronchi Bronchioles Terminal bronchioles Alveolar ducts Alveoli Type 1 pneumocytes Type 2 pneumocytes Macrophages Capillaries
  • N O R M A L C X R
  • OVERVIEW • Pathology –CONGENITAL – Atalectasis – Acute Pulmonary Injury – Obstructive vs. Restrictive (infiltrative) concepts –Obstructive Pulmonary Disease (COPD) – Restrictive (Infiltrative) Pulmonary Disease – Vascular Pulmonary Diseases
  • CONGENITAL • Agenesis/Hypoplasia • Tracheal/bronchial anomalies, i.e., Tracheo-Esophageal (TE) fistula • • • • • Vascular anomalies Congenital Emphysema (idiopathic usually) Foregut cysts Pulmonary Artery Malformations (CPAM) Sequestration (no connection to airways or pulmonary arteries, but systemic!)
  • OVERVIEW • Pathology – Congenital –ATALECTASIS – Acute Pulmonary Injury – Obstructive vs. Restrictive (infiltrative) concepts –Obstructive Pulmonary Disease (COPD) – Restrictive Pulmonary Disease – Vascular Pulmonary Diseases
  • ATALECTASIS • INCOMPLETE EXPANSION • COLLAPSE
  • OVERVIEW • Pathology – Congenital – Atalectasis – ACUTE PULMONARY INJURY • Pulmonary Edema • ARDS (DiffuseAlveolarDamage) • Acute Interstitial Pneumonia – Obstructive vs. Restrictive (infiltrative) concepts – Obstructive Pulmonary Disease (COPD) – Restrictive (Infiltrative) Pulmonary Disease – Vascular Pulmonary Diseases
  • PULMONARY EDEMA • IN-creased venous pressure • DE-creased oncotic pressure • Lymphatic obstruction • Alveolar injury
  • ACUTE* RESPIRATORY DISTRESS SYNDROME (ARDS or D.A.D., i.e., Diffuse Alveolar Damage) (aka, “SHOCK” lung) • NON-specific pattern of lung injury • • • • • • INFECTION PHYSICAL INJURY TOXIC CHEMICAL DIC ETC
  • ARDS
  • ACUTE INTERSTITIAL PNEUMONIA • Think of it as ARDS with NO known etiology!
  • OVERVIEW • Pathology – Congenital – Atalectasis – Acute Pulmonary Injury –OBSTRUCTION vs. RESTRICTION –Obstructive Pulmonary Disease (COPD) – Restrictive (Infiltrative) Pulmonary Disease – Vascular Pulmonary Diseases
  • OBSTRUCTION v. RESTRICTION • OBSTRUCTION • RESTRICTION • Air or blood? • Large or small? • Inspiration or Expiration? • “Compliance” • “Infiltrative” • Obstruction is SMALL AIRWAY EXPIRATION • REDUCED lung VOLUME, DYSPNEA, CYANOSIS • REDUCED GAS TRANSFER obstruction, i.e., wheezing • “GROUND GLASS” on CXR • HYPEREXPANSION on CXR
  • OVERVIEW • Pathology – Congenital – Atalectasis – Acute Pulmonary Injury – Obstruction vs. Restriction –OBSTRUCTIVE Pulmonary Diseases (COPD) – Restrictive (Infiltrative) Pulmonary Disease – Vascular Pulmonary Diseases
  • OBSTRUCTION (cOPD) • EMPHYSEMA (almost always chronic) • CHRONIC BRONCHITIS emphysema • ASTHMA • BRONCHIECTASIS
  • EMPHYSEMA • COPD, or “END-STAGE” lung disease • Centri-acinar, Pan-acinar, Paraseptal, Irregular • (PROGRESSIVE) EXPIRATORY AIR TRAPPING, i.e., WHEEZING • Like cirrhosis, thought of as END-STAGE of multiple chronic small airway obstructive etiologies • NON-specific • IN-creased crepitance, BULLAE (BLEBS) • Clinically likely to produce recurrent pneumonias, and progressive failure
  • ACINUS vs. ALVEOLUS CENTRO-acinar PAN-acinar
  • 1) HYPER-expansion 3) “bullae” 2) “flattened” diaphragms (blunted), 4) increased lucency* (why?)
  • CHRONIC BRONCHITIS • INHALANTS, POLLUTION, CIGARETTES • CHRONIC COUGH • CAN OFTEN PROGRESS TO EMPHYSEMA • MUCUS hypersecretion, early, i.e. goblet cell increase • CHRONIC bronchial inflammatory infiltrate
  • ASTHMA • Similar to chronic bronchitis but: – Wheezing is hallmark (bronchospasm, i.e. “wheezing”) – STRONG allergic role, i.e., eosinophils, IgE, allergens – Often starting in CHILDHOOD – ATOPIC (allergic) or NON-ATOPIC (infection) – Chronic small airway obstruction and infection – 1) Mucus hypersecretion with plugging, 2) lymphocytes/eosinophils, 3) lumen narrowing, 4) smooth muscle hypertrophy
  • What are the 4 classical histologic findings in bronchial asthma?
  • BRONCHIECTASIS • DILATATION of the BRONCHUS, associated with, often, necrotizing inflammation – CONGENITAL –TB, other bacteria, many viruses – BRONCHIAL OBSTRUCTION (i.e., LARGE AIRWAY, NOT SMALL AIRWAY) – Rheumatoid Arthritis, SLE, IBD (Inflammatory Bowel Disease)
  • BRONCHIECTASIS
  • OVERVIEW • Pathology – Congenital – Atalectasis – Acute Pulmonary Injury – Obstruction vs. Restriction – Obstructive Pulmonary Diseases (COPD) –RESTRICTIVE (INFILTRATIVE) PULMONARY DISEASES – Vascular Pulmonary Diseases
  • RESTRICTIVE (INFILTRATIVE) • REDUCED COMPLIANCE, reduced gas exchange) • Are also DIFFUSE, ↑ density, ↓ crepitance • HETEROGENEOUS ETIOLOGIES • • • • • FIBROSING GRANULOMATOUS EOSINOPHILIC SMOKING RELATED PAP (Pulmonary Alveolar Proteinosis
  • FIBROSING • “IDIOPATHIC” PULMONARY FIBROSIS (IPF) • NONSPECIFIC INTERSTITIAL FIBROSIS • “CRYPTOGENIC” ORGANIZING PNEUMONIA • “COLLAGEN” VASCULAR DISEASES • PNEUMOCONIOSES • DRUG REACTIONS • RADIATION CHANGES
  • IPF (UIP) • IDIOPATHIC, i.e., not from any usual caused, like lupus, scleroderma • FIBROSIS
  • NON-SPECIFIC INTERSTITIAL PNEUMONIA • WASTEBASKET DIAGNOSIS, of ANY pneumonia (pneumonitis) of any known or unknown etiology – FIBROSIS – CELLULAR INFILTRATE (LYMPHS & PLASMA CELLS)
  • CRYPTOGENIC ORGANIZING PNEUMONIA (COP) • IDIOPATHIC • “BRONCHIOLITIS OBLITERANS”
  • “COLLAGEN” VASCULAR DISEASES • Rheumatoid Arthritis • SLE (“Lupus”) • Progressive Systemic Sclerosis (Scleroderma)
  • PNEUMOCONIOSES • “OCCUPATIONAL” • “COAL MINERS LUNG” • DUST OR CHEMICALS OR ORGANIC MATERIALS – Coal (anthracosis) – Silica – Asbestos – Be, FeO, BaSO4, CHEMO – HAY, FLAX, BAGASSE, INSECTICIDES, etc.
  • GRANULOMATOUS • SARCOIDOSIS, i.e., NON-caseating granulomas (IDIOPATHIC) • HYPERSENSITIVITY (DUSTS, bacteria, fungi, Farmer’s Lung, Pigeon Breeder’s Lung)
  • SARCOIDOSIS • Mainly LUNG, but eye, skin or ANYWHERE • UNKNOWN ETIOLOGY • IMMUNE, GENETIC factors • F>>M • B>>W • YOUNG ADULT BLACK WOMEN
  • NON-Caseating Granulomas are the RULE “Asteroid” bodies within these granulomas are virtually diagnostic, but hard to find
  • SMOKING RELATED • DIP (Desquamative Interstitial Pneumonia) – M>>F – CIGARETTES – 100% Survival Alveolar Macrophages
  • • • • • PAP (Pulmonary Alveolar Proteinosis) Very RARE, usually acquired Proteinaceous Material in Alveoli MINIMAL cellular inflammatory infiltrate Like Pulmonary Edema, but MUCH Protein
  • OVERVIEW • Pathology – Congenital – Atalectasis – Acute Pulmonary Injury – Obstruction vs. Restriction – Obstructive Pulmonary Diseases (COPD) – Restrictive (Infiltrative) Pulmonary Diseases –VASCULAR PULMONARY DISEASES
  • VASCULAR PULMONARY DISEASES • PULMONARY EMBOLISM (with or usually WITHOUT infarction) • PULMONARY HYPERTENSION, leading to cor pulmonale • HEMORRHAGIC SYNDROMES – GOODPASTURE SYNDROME – HEMOSIDEROSIS, idiopathic – WEGENER GRANULOMATOSIS
  • P.E. • Usually secondary to debilitated states with immobilization, or following surgery • Usually deep leg and deep pelvic veins (DVT), NOT superficial veins • Follows Virchow’s triad, i.e., 1) flow problems, 2) endothelial disruption, 3) hypercoagulabilty • Usually do NOT infarct, usually ventilate • When they DO infarct, the infarct is hemorrhagic • Decreased PO2, acute chest pain, V/Q MIS-match • DX: Chest CT, V/Q scan, angiogram • RX: short term heparin, then long term coumadin
  • VQ scan CT CXR GROSS “saddle” embolism
  • PULMONARY HYPERTENSION • COPD, C”I”PD (vicious cycle) • CHD (Congenital HD, increased left atrial pressure) • Recurrent PEs • Autoimmune, e.g., PSS (Scleroderma), i.e., fibrotic pulmonary vasculature
  • NORMAL pulmonary arteriole VERY thickened arteriole in pulmonary hypertension Narrowing causes HTN, and HTN causes narrowing! (vicious cycle)
  • HEMORRHAGIC SYNDROMES • GOODPASTURE Syndrome: Ab’s to the alpha-3 chains of collagen IV, GBM deposits too! • IDIOPATHIC PULMONARY HEMOSIDEROSIS, to be differentiated from chronic CHF • WEGENER GRANULOMATOSIS
  • CHF, CHRONIC IDIOPATHIC PULMONARY HEMOSIDEROSIS
  • PNEUMONIA
  • PULMONARY INFECTIONS COMMUNITY-ACQUIRED BACTERIAL ACUTE PNEUMONIAS (BACTERIAL) Streptococcus Pneumoniae Haemophilus Influenzae Moraxella Catarrhalis Staphylococcus Aureus Klebsiella Pneumoniae Pseudomonas Aeruginosa Legionella Pneumophila COMMUNITY-ACQUIRED ATYPICAL (VIRAL AND MYCOPLASMAL) PNEUMONIAS (NON-BACTERIAL) 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
  • BASIC CONSIDERATIONS • PNEUMONIA vs. PNEUMONITIS • DIFFERENTIATION from INJURIES, OBSTRUCTIVE DISEASES, RESTRICTIVE DISEASES, VASCULAR DISEASES • DIFFERENTIATION FROM NEOPLASMS • CLASSICAL STAGES of INFLAMMATION • LOBARvs. BRONCHO• INTERSTITIAL vs. ALVEOLAR • COMMUNITY vs. NOSOCOMIAL • ETIOLOGIC AGENTS vs. HOST IMMUNITY • 2 PRESENTING SYMPTOMS: What are they? • 2 DIAGNOSTIC METHODS: What are they? • ANY ORGANISM CAN CAUSE PNEUMONIA!!!
  • PREDISPOSING FACTORS • LOSS OF COUGH REFLEX • DIMINISHED MUCIN or CILIA FUNCTION • ALVEOLAR MACROPHAGE INTERFERENCE • VASCULAR FLOW IMPAIRMENTS • BRONCHIAL FLOW IMPAIRMENTS
  • Although pneumonia is one of the most common causes of death, it usually does NOT occur in healthy people spontaneously
  • Classifications of PNEUMONIAS • • • • • • • COMMUNITY ACQUIRED COMMUNITY ACQUIRED, ATYPICAL NOSOCOMIAL ASPIRATION CHRONIC NECROTIZING/ABSCESS FORMATION PNEUMONIAS in IMMUNOCOMPROMISED HOSTS*
  • Classifications of PNEUMONIAS • COMMUNITY ACQUIRED • • • • • • COMMUNITY ACQUIRED, ATYPICAL NOSOCOMIAL ASPIRATION CHRONIC NECROTIZING/ABSCESS FORMATION PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
  • COMMUNITY ACQUIRED • STREPTOCOCCUS PNEUMONIAE (i.e., “diplococcus”) • HAEMOPHILUS INFLUENZAE (“H-Flu”) • MORAXELLA • STAPHYLOCOCCUS (STAPH) • KLEBSIELLA PNEUMONIAE • PSEUDOMONAS AERUGINOSA • LEGIONELLA PNEUMOPHILIA
  • STREPTOCOCCUS • The classic LOBAR pneumonia • Normal flora in 20% of adults • Only 20% of victims have + blood cultures • “Penicillins” are often 100% curative • Vaccines are often 100% preventive
  • HAEMOPHILUS PNEUMONIA • Commonest in CHILDREN <2, with otitis, URI, meningitis, cellulitis, osteomyelitis • PNEUMONIAS in CHILDREN <2 are often thought of as being H Flu until proven otherwise, otitis, meningitis too • Most common pneumonia from COPD in adults • BACTRIM (Trimethoprim-Sulfa) most common treatment
  • MORAXELLA CATARRHALIS • 2nd most common COPD pneumonia, after haemophilus • Gram NEGATIVE coccobacillus, like H. Flu
  • STAPH aureus • Most common pneumonia following viral pneumonias • M.R.S.A., of course, is usually NOT “community” acquired
  • KLEBSIELLA PNEUMONIAE • DEBILITATED MALNOURISHED PEOPLE • ALCOHOLICS with pneumonia are often thought of as having Klebsiella until proven otherwise
  • PSEUDOMONAS Aeruginosa • Usually NOT community acquired but nosocomial • CYSTIC FIBROSIS patients with pneumonia are presumed to have PSEUDOMONAS until proven otherwise
  • LEGIONELLA (pneumophila) • • • • Often in OUTBREAKS Often LOBAR Spread by water “droplets” Often immunosuppressed patients, but remember………..*
  • Although pneumonia is one of the most common causes of death, it usually does NOT occur in healthy people spontaneously
  • MORPHOLOGY • • • • ACUTE ORGANIZING CHRONIC FIBROSIS vs. FULL RESOLUTION • • • • “HEPATIZATION”, RED vs. GREY CONSOLIDATION “INFILTRATE”, XRAY vs. HISTOPATH Loss of “CREPITANCE”
  • Classifications of PNEUMONIAS • COMMUNITY ACQUIRED • COMMUNITY ACQUIRED, ATYPICAL • • • • • NOSOCOMIAL ASPIRATION CHRONIC NECROTIZING/ABSCESS FORMATION PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
  • COMMUNITY ACQUIRED, (atypical) • VIRAL (INFLUENZA) • MYCOPLASMAL (MYCOPLASMA PNEUMONIAE (obligate intracellular)) • NOT BACTERIAL • CULTURES NOT HELPFUL
  • VIRAL PNEUMONIAS • Frequently “interstitial”, NOT alveolar
  • INFLUENZA VIRUS • A,B,C • 1915, 1918, PAN-demics, type A • Has MUTATED throughout history, many STRAINS, avian swine, etc. • B and C in children • Exact strains can be ID’s by PCR
  • SARS (Severe Acute Respiratry Syndrome) • • • • CORONA-VIRUS 2002 China outbreak Spread CHIEFLY in Asia Like most other NON-bacterial pneumonias confirmed by PCR • Like most viral pneumonias, interstitium infiltrated, some giant cells often present
  • S A R S
  • Classifications of PNEUMONIAS • COMMUNITY ACQUIRED • COMMUNITY ACQUIRED, ATYPICAL • NOSOCOMIAL • • • • ASPIRATION CHRONIC NECROTIZING/ABSCESS FORMATION PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
  • NOSOCOMIAL • Acquired in HOSPITALS, also called “hospital acquired”, versus “community acquired” pneumonias. – DEBILITATION – CATHETERS, VENTILATORS – ENTEROBACTER, PSEUDOMONAS – STAPH (MRSA) – MRSA (MR=Methicillin Resistant) • OTHER Common causes of Noso. Pneum. P. aeruginosa Klebsiella E. coli S. pneumoniae H. influenzae
  • Classifications of PNEUMONIAS • COMMUNITY ACQUIRED • COMMUNITY ACQUIRED, ATYPICAL • NOSOCOMIAL • ASPIRATION • CHRONIC (often granulomatous) • NECROTIZING/ABSCESS FORMATION • PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
  • ASPIRATION PNEUMONIAS • • • • UNCONSCIOUS PATIENTS PATIENTS IN PROLONGED BEDREST LACK OF ABILITY TO SWALLOW OR GAG USUALLY CAUSED BY ASPIRATION OF GASTRIC CONTENTS • POSTERIOR LOBES (gravity dependent) MOST COMMONLY INVOLVED, ESPECIALLY THE SUPERIOR SEGMENTS of the LOWER LOBES • Often lead to ABSCESSES
  • • • • • LUNG ABSCESSES ASPIRATION SEPTIC EMBOLIZATION NEOPLASIA From NEIGHBORING structures: – ESOPHAGUS – SPINE – PLEURA – DIAPHRAGM • ANY pneumonia which is severe and destructive, and UN-treated enough
  • Classifications of PNEUMONIAS • • • • COMMUNITY ACQUIRED COMMUNITY ACQUIRED, ATYPICAL NOSOCOMIAL ASPIRATION • CHRONIC • NECROTIZING/ABSCESS FORMATION • PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
  • CHRONIC Pneumonias • USUALLY NOT persistences of the community or nosocomial bacterial infections, but CAN BE, at least histologically • Often SYNONYMOUS with the 4 classic systemic fungal or granulomatous pulmonary infections infections, i.e., TB, Histo-, Blasto-, Coccidio• If you see pulmonary granulomas, think of a CHRONIC process, often years
  • CHRONIC Pneumonias • TB • HISTO-PLASMOSIS • BLASTO-MYCOSIS • COCCIDIO-MYCOSIS
  • • • • • HISTOPLASMOSIS Spores in bird or bat droppings Mimics TB Histoplasma CAPSULATUM Pulmonary granulomas, often large and calcified • Tiny organisms live in macrophages • Ohio, Mississippi valley • MANY other organs can be affected
  • BLASTOMYCOSIS • Spores in soil • Mimics TB, like ALL the granulomatous lung dideases do. • Blastomyces DERMATIDIS • Pulmonary granulomas, often large and calcified • Large distinct SPHERULES (larger than coccidio) • Ohio, Mississippi valley, Great Lakes, WORLDWIDE • MANY other organs can be affected, especially SKIN
  • • • • • • • • • COCCIDIOMYCOSIS Spores in soil Mimics TB Coccidioides IMMITIS Pulmonary granulomas, often large and calcified Smaller spherules than blasto. Tiny organisms live in macrophages American SOUTHWEST MANY other organs can be affected
  • GRANULOMA
  • COMPROMISED HOSTS • PNEUMOCYSTIS CARINII* • CYTOMEGALOVIRUS (CMV) • FUNGI
  • PCP
  • WOOLY? Methenamine SILVER stain for Pneumocystis carinii*
  • LUNG TRANSPLANTATION Any end-stage lung disease in which the patient can tolerate long term immunosuppression, and often just ONE lung is enough, donors very SCARCE! • • • • EMPHYSEMA Pulmonary Fibrosis Cystic Fibrosis Pulmonary Hypertension
  • Lung Transplant Pathology • Infections (patients are on immunosuppressives ) – Bacterial – Viral (CMV) – Fungal – PCP • ACUTE rejection, pneumonias, usually weeks to months • CHRONIC rejection, HALF of all patients by 3-5 years, “bronchiolitis obliterans” (COP)
  • LUNG TUMORS • Benign, malignant, epithelial, mesenchymal, but 90% are CARCINOMAS • BIGGEST USA killer. Why? Ans: Prevalence not as high as prostate or breast but mortality higher. Only 15% 5 year survival. • TOBACCO has polycyclic aromatic hydrocarbons, such as benzopyrene, anthracenes, radioactive isotopes • Radiation, asbestos, radon • C-MYC, K-RAS, EGFR, HER-2/neu
  • PATHOGENESIS • NORMAL BRONCHIAL MUCOSA • METAPLASTIC/DYSPLASTIC MUCOSA • CARCINOMA-IN-SITU (squamous, adeno) • INFILTRATING (i.e., “INVASIVE”) cancer
  • TWO TYPES • NON-SMALL CELL – SQUAMOUS CELL CARCINOMA – ADENOCARCINOMA – LARGE CELL CARCINOMA • SMALL CELL CARCINOMA
  • • • • • • • • • • • • The BIG list Squamous cell carcinoma Small cell carcinoma Combined small cell carcinoma   Adenocarcinoma: Acinar, papillary, bronchioloalveolar, solid, mixed subtypes Large cell carcinoma Large cell neuroendocrine carcinoma Adenosquamous carcinoma Carcinomas with pleomorphic, sarcomatoid, or sarcomatous elements Carcinoid tumor: Typical, atypical   Carcinomas of salivary gland type Unclassified carcinoma
  • OTHER TUMORS
  • TNM, Lung 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 Ipsi-lateral hilar or peribronchial nodal involvement Metastasis to ipsilateral mediastinal or subcarinal lymph nodes Metastasis to contra-lateral mediastinal or hilar lymph nodes, ipsilateral N2 N3 or contralateral scalene, or supraclavicular lymph nodes M0 No (known) distant metastasis M1 Distant metastasis present
  • LOCAL effects of LUNG CANCER 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
  • SYSTEMIC effects of LUNG CANCER (PARA-NEOPLASTIC SYNDROMES)~ 5% ADH (hyponatremia) ACTH (Cushing) PTH (Hyper-CA) CALCITONIN (Hypo-CA) GONADOTROPINS SEROTONIN/BRADYKININ
  • OTHER TUMORS
  • METASTATIC TUMORS • LUNG is the MOST COMMON site for all metastatic tumors, regardless of site of origin • It is the site of FIRST CHOICE for metastatic sarcomas for purely anatomic reasons!
  • PLEURA • PLEURITIS (pleurisy) • PNEUMOTHORAX • EFFUSIONS – HYDRO-THORAX (Peric-, Perito-) – HEMO-THORAX (Peric-, Perito-) – CHYLO-THORAX (Peric-, Perito-) • MESOTHELIOMAS
  • PLEURITIS • • • • • • • Usual bacteria, viruses, etc. Infarcts Lung abscesses, empyema TB “Collagen” diseases, e.g., RA, SLE Uremia Metastatic
  • PNEUMOTHORAX • SPONTANEOUS, TRAUMATIC, THERAPEUTIC • OPEN or CLOSED • “TENSION” pneumothorax, “valvular” effect • “Bleb” (bulla) rupture • Perforating injuries • Post needle biopsy
  • • • • • EFFUSIONS TRANSUDATE (HYDROTHORAX) EXUDATE (HYDROTHORAX) BLOOD (HEMOTHORAX) LYMPH (CHYLOTHORAX)
  • MESOTHELIOMAS • “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 • Visceral or parietal pleura, pericardium, or peritoneum • Most are regarded as asbestos caused or asbestos “related”
  • H&E, IMMUNOCHEMISTRY (CALRETININ)  EM