Download Free Medical Lung PowerPoint Presentation

Lung PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : All about Lung powerpoint ppt presentation slides

Tags : Lung,about lung,body parts

Published on : Sep 28, 2021 | Views : 175 | Downloads : 0

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

LUNGS
Slide 2-

The LUNG “Degenerative” Inflammatory Neoplastic and Pleura LAB: (Review, Cases, and/or Virtual Microscopy)
Slide 3-

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
Slide 4-

OVERVIEW II INFECTIONS NEOPLASMS and PLEURA (effusions, pneumothorax, tumors)
Slide 5-

WEIGHT LOBES SEGMENTS BRONCHI ARTERIES, pulmonary ARTERIES, bronchial VEINS PLEURA, visceral PLEURA, parietal NERVES
Slide 6-

Bronchi Bronchioles Terminal bronchioles Alveolar ducts Alveoli Type 1 pneumocytes Type 2 pneumocytes Macrophages Capillaries
Slide 7-

ppt slide no 7 content not found
Slide 8-

ppt slide no 8 content not found
Slide 9-

N O R M A L C X R
Slide 10-

OVERVIEW Pathology CONGENITAL Atalectasis Acute Pulmonary Injury Obstructive vs. Restrictive (infiltrative) concepts Obstructive Pulmonary Disease (COPD) Restrictive (Infiltrative) Pulmonary Disease Vascular Pulmonary Diseases
Slide 11-

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!)
Slide 12-

ppt slide no 12 content not found
Slide 13-

OVERVIEW Pathology Congenital ATALECTASIS Acute Pulmonary Injury Obstructive vs. Restrictive (infiltrative) concepts Obstructive Pulmonary Disease (COPD) Restrictive Pulmonary Disease Vascular Pulmonary Diseases
Slide 14-

ATALECTASIS INCOMPLETE EXPANSION COLLAPSE
Slide 15-

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
Slide 16-

PULMONARY EDEMA IN-creased venous pressure DE-creased oncotic pressure Lymphatic obstruction Alveolar injury
Slide 17-

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
Slide 18-

ARDS
Slide 19-

ACUTE INTERSTITIAL PNEUMONIA Think of it as ARDS with NO known etiology!
Slide 20-

OVERVIEW Pathology Congenital Atalectasis Acute Pulmonary Injury OBSTRUCTION vs. RESTRICTION Obstructive Pulmonary Disease (COPD) Restrictive (Infiltrative) Pulmonary Disease Vascular Pulmonary Diseases
Slide 21-

OBSTRUCTION v. RESTRICTION OBSTRUCTION Air or blood? Large or small? Inspiration or Expiration? Obstruction is SMALL AIRWAY EXPIRATION obstruction, i.e., wheezing HYPEREXPANSION on CXR RESTRICTION “Compliance” “Infiltrative” REDUCED lung VOLUME, DYSPNEA, CYANOSIS REDUCED GAS TRANSFER “GROUND GLASS” on CXR
Slide 22-

OVERVIEW Pathology Congenital Atalectasis Acute Pulmonary Injury Obstruction vs. Restriction OBSTRUCTIVE Pulmonary Diseases (COPD) Restrictive (Infiltrative) Pulmonary Disease Vascular Pulmonary Diseases
Slide 23-

OBSTRUCTION (cOPD) EMPHYSEMA (almost always chronic) CHRONIC BRONCHITIS emphysema ASTHMA BRONCHIECTASIS
Slide 24-

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
Slide 25-

CENTRO-acinar PAN-acinar ACINUS vs. ALVEOLUS
Slide 26-

ppt slide no 26 content not found
Slide 27-

HYPER-expansion 2) “flattened” diaphragms (blunted), 3) “bullae” 4) increased lucency* (why?)
Slide 28-

CHRONIC BRONCHITIS INHALANTS, POLLUTION, CIGARETTES CHRONIC COUGH CAN OFTEN PROGRESS TO EMPHYSEMA MUCUS hypersecretion, early, i.e. goblet cell increase CHRONIC bronchial inflammatory infiltrate
Slide 29-

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
Slide 30-

ppt slide no 30 content not found
Slide 31-

What are the 4 classical histologic findings in bronchial asthma?
Slide 32-

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)
Slide 33-

BRONCHIECTASIS
Slide 34-

OVERVIEW Pathology Congenital Atalectasis Acute Pulmonary Injury Obstruction vs. Restriction Obstructive Pulmonary Diseases (COPD) RESTRICTIVE (INFILTRATIVE) PULMONARY DISEASES Vascular Pulmonary Diseases
Slide 35-

RESTRICTIVE (INFILTRATIVE) REDUCED COMPLIANCE, reduced gas exchange) Are also DIFFUSE, ↑ density, ↓ crepitance HETEROGENEOUS ETIOLOGIES FIBROSING GRANULOMATOUS EOSINOPHILIC SMOKING RELATED PAP (Pulmonary Alveolar Proteinosis
Slide 36-

FIBROSING “IDIOPATHIC” PULMONARY FIBROSIS (IPF) NONSPECIFIC INTERSTITIAL FIBROSIS “CRYPTOGENIC” ORGANIZING PNEUMONIA “COLLAGEN” VASCULAR DISEASES PNEUMOCONIOSES DRUG REACTIONS RADIATION CHANGES
Slide 37-

IPF (UIP) IDIOPATHIC, i.e., not from any usual caused, like lupus, scleroderma FIBROSIS
Slide 38-

NON-SPECIFIC INTERSTITIAL PNEUMONIA WASTEBASKET DIAGNOSIS, of ANY pneumonia (pneumonitis) of any known or unknown etiology FIBROSIS CELLULAR INFILTRATE (LYMPHS & PLASMA CELLS)
Slide 39-

CRYPTOGENIC ORGANIZING PNEUMONIA (COP) IDIOPATHIC “BRONCHIOLITIS OBLITERANS”
Slide 40-

“COLLAGEN” VASCULAR DISEASES Rheumatoid Arthritis SLE (“Lupus”) Progressive Systemic Sclerosis (Scleroderma)
Slide 41-

PNEUMOCONIOSES “OCCUPATIONAL” “COAL MINERS LUNG” DUST OR CHEMICALS OR ORGANIC MATERIALS Coal (anthracosis) Silica Asbestos Be, FeO, BaSO4, CHEMO HAY, FLAX, BAGASSE, INSECTICIDES, etc.
Slide 42-

ppt slide no 42 content not found
Slide 43-

GRANULOMATOUS SARCOIDOSIS, i.e., NON-caseating granulomas (IDIOPATHIC) HYPERSENSITIVITY (DUSTS, bacteria, fungi, Farmer’s Lung, Pigeon Breeder’s Lung)
Slide 44-

SARCOIDOSIS Mainly LUNG, but eye, skin or ANYWHERE UNKNOWN ETIOLOGY IMMUNE, GENETIC factors F>>M B>>W YOUNG ADULT BLACK WOMEN
Slide 45-

NON-Caseating Granulomas are the RULE “Asteroid” bodies within these granulomas are virtually diagnostic, but hard to find
Slide 46-

ppt slide no 46 content not found
Slide 47-

SMOKING RELATED DIP (Desquamative Interstitial Pneumonia) M>>F CIGARETTES 100% Survival Alveolar Macrophages
Slide 48-

PAP (Pulmonary Alveolar Proteinosis) Very RARE, usually acquired Proteinaceous Material in Alveoli MINIMAL cellular inflammatory infiltrate Like Pulmonary Edema, but MUCH Protein
Slide 49-

OVERVIEW Pathology Congenital Atalectasis Acute Pulmonary Injury Obstruction vs. Restriction Obstructive Pulmonary Diseases (COPD) Restrictive (Infiltrative) Pulmonary Diseases VASCULAR PULMONARY DISEASES
Slide 50-

VASCULAR PULMONARY DISEASES PULMONARY EMBOLISM (with or usually WITHOUT infarction) PULMONARY HYPERTENSION, leading to cor pulmonale HEMORRHAGIC SYNDROMES GOODPASTURE SYNDROME HEMOSIDEROSIS, idiopathic WEGENER GRANULOMATOSIS
Slide 51-

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
Slide 52-

VQ scan CT CXR GROSS “saddle” embolism
Slide 53-

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
Slide 54-

VERY thickened arteriole in pulmonary hypertension NORMAL pulmonary arteriole Narrowing causes HTN, and HTN causes narrowing! (vicious cycle)
Slide 55-

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
Slide 56-

CHF, CHRONIC IDIOPATHIC PULMONARY HEMOSIDEROSIS
Slide 57-

PNEUMONIA
Slide 58-

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 PULMONARY INFECTIONS
Slide 59-

BASIC CONSIDERATIONS PNEUMONIA vs. PNEUMONITIS DIFFERENTIATION from INJURIES, OBSTRUCTIVE DISEASES, RESTRICTIVE DISEASES, VASCULAR DISEASES DIFFERENTIATION FROM NEOPLASMS CLASSICAL STAGES of INFLAMMATION LOBAR- vs. 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!!!
Slide 60-

PREDISPOSING FACTORS LOSS OF COUGH REFLEX DIMINISHED MUCIN or CILIA FUNCTION ALVEOLAR MACROPHAGE INTERFERENCE VASCULAR FLOW IMPAIRMENTS BRONCHIAL FLOW IMPAIRMENTS
Slide 61-

Although pneumonia is one of the most common causes of death, it usually does NOT occur in healthy people spontaneously
Slide 62-

Classifications of PNEUMONIAS COMMUNITY ACQUIRED COMMUNITY ACQUIRED, ATYPICAL NOSOCOMIAL ASPIRATION CHRONIC NECROTIZING/ABSCESS FORMATION PNEUMONIAS in IMMUNOCOMPROMISED HOSTS*
Slide 63-

Classifications of PNEUMONIAS COMMUNITY ACQUIRED COMMUNITY ACQUIRED, ATYPICAL NOSOCOMIAL ASPIRATION CHRONIC NECROTIZING/ABSCESS FORMATION PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
Slide 64-

COMMUNITY ACQUIRED STREPTOCOCCUS PNEUMONIAE (i.e., “diplococcus”) HAEMOPHILUS INFLUENZAE (“H-Flu”) MORAXELLA STAPHYLOCOCCUS (STAPH) KLEBSIELLA PNEUMONIAE PSEUDOMONAS AERUGINOSA LEGIONELLA PNEUMOPHILIA
Slide 65-

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
Slide 66-

ppt slide no 66 content not found
Slide 67-

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
Slide 68-

ppt slide no 68 content not found
Slide 69-

MORAXELLA CATARRHALIS 2nd most common COPD pneumonia, after haemophilus Gram NEGATIVE coccobacillus, like H. Flu
Slide 70-

STAPH aureus Most common pneumonia following viral pneumonias M.R.S.A., of course, is usually NOT “community” acquired
Slide 71-

KLEBSIELLA PNEUMONIAE DEBILITATED MALNOURISHED PEOPLE ALCOHOLICS with pneumonia are often thought of as having Klebsiella until proven otherwise
Slide 72-

PSEUDOMONAS Aeruginosa Usually NOT community acquired but nosocomial CYSTIC FIBROSIS patients with pneumonia are presumed to have PSEUDOMONAS until proven otherwise
Slide 73-

LEGIONELLA (pneumophila) Often in OUTBREAKS Often LOBAR Spread by water “droplets” Often immunosuppressed patients, but remember………..*
Slide 74-

Although pneumonia is one of the most common causes of death, it usually does NOT occur in healthy people spontaneously
Slide 75-

MORPHOLOGY ACUTE ORGANIZING CHRONIC FIBROSIS vs. FULL RESOLUTION “HEPATIZATION”, RED vs. GREY CONSOLIDATION “INFILTRATE”, XRAY vs. HISTOPATH Loss of “CREPITANCE”
Slide 76-

Classifications of PNEUMONIAS COMMUNITY ACQUIRED COMMUNITY ACQUIRED, ATYPICAL NOSOCOMIAL ASPIRATION CHRONIC NECROTIZING/ABSCESS FORMATION PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
Slide 77-

COMMUNITY ACQUIRED, (atypical) VIRAL (INFLUENZA) MYCOPLASMAL (MYCOPLASMA PNEUMONIAE (obligate intracellular)) NOT BACTERIAL CULTURES NOT HELPFUL
Slide 78-

VIRAL PNEUMONIAS Frequently “interstitial”, NOT alveolar
Slide 79-

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
Slide 80-

ppt slide no 80 content not found
Slide 81-

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
Slide 82-

S A R S
Slide 83-

Classifications of PNEUMONIAS COMMUNITY ACQUIRED COMMUNITY ACQUIRED, ATYPICAL NOSOCOMIAL ASPIRATION CHRONIC NECROTIZING/ABSCESS FORMATION PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
Slide 84-

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
Slide 85-

Classifications of PNEUMONIAS COMMUNITY ACQUIRED COMMUNITY ACQUIRED, ATYPICAL NOSOCOMIAL ASPIRATION CHRONIC (often granulomatous) NECROTIZING/ABSCESS FORMATION PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
Slide 86-

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
Slide 87-

ppt slide no 87 content not found
Slide 88-

LUNG ABSCESSES ASPIRATION SEPTIC EMBOLIZATION NEOPLASIA From NEIGHBORING structures: ESOPHAGUS SPINE PLEURA DIAPHRAGM ANY pneumonia which is severe and destructive, and UN-treated enough
Slide 89-

ppt slide no 89 content not found
Slide 90-

Classifications of PNEUMONIAS COMMUNITY ACQUIRED COMMUNITY ACQUIRED, ATYPICAL NOSOCOMIAL ASPIRATION CHRONIC NECROTIZING/ABSCESS FORMATION PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
Slide 91-

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
Slide 92-

CHRONIC Pneumonias TB HISTO-PLASMOSIS BLASTO-MYCOSIS COCCIDIO-MYCOSIS
Slide 93-

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
Slide 94-

ppt slide no 94 content not found
Slide 95-

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
Slide 96-

ppt slide no 96 content not found
Slide 97-

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
Slide 98-

GRANULOMA
Slide 99-

COMPROMISED HOSTS PNEUMOCYSTIS CARINII* CYTOMEGALOVIRUS (CMV) FUNGI
Slide 100-

PCP
Slide 101-

Methenamine SILVER stain for Pneumocystis carinii* WOOLY?
Slide 102-

LUNG TRANSPLANTATION EMPHYSEMA Pulmonary Fibrosis Cystic Fibrosis Pulmonary Hypertension Any end-stage lung disease in which the patient can tolerate long term immunosuppression, and often just ONE lung is enough, donors very SCARCE!
Slide 103-

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)
Slide 104-

ppt slide no 104 content not found
Slide 105-

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
Slide 106-

PATHOGENESIS NORMAL BRONCHIAL MUCOSA METAPLASTIC/DYSPLASTIC MUCOSA CARCINOMA-IN-SITU (squamous, adeno) INFILTRATING (i.e., “INVASIVE”) cancer
Slide 107-

TWO TYPES NON-SMALL CELL SQUAMOUS CELL CARCINOMA ADENOCARCINOMA LARGE CELL CARCINOMA SMALL CELL CARCINOMA
Slide 108-

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
Slide 109-

OTHER TUMORS
Slide 110-

ppt slide no 110 content not found
Slide 111-

ppt slide no 111 content not found
Slide 112-

TNM, Lung
Slide 113-

LOCAL effects of LUNG CANCER
Slide 114-

SYSTEMIC effects of LUNG CANCER (PARA-NEOPLASTIC SYNDROMES)~ 5% ADH (hyponatremia) ACTH (Cushing) PTH (Hyper-CA) CALCITONIN (Hypo-CA) GONADOTROPINS SEROTONIN/BRADYKININ
Slide 115-

OTHER TUMORS
Slide 116-

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!
Slide 117-

PLEURA PLEURITIS (pleurisy) PNEUMOTHORAX EFFUSIONS HYDRO-THORAX (Peric-, Perito-) HEMO-THORAX (Peric-, Perito-) CHYLO-THORAX (Peric-, Perito-) MESOTHELIOMAS
Slide 118-

PLEURITIS Usual bacteria, viruses, etc. Infarcts Lung abscesses, empyema TB “Collagen” diseases, e.g., RA, SLE Uremia Metastatic
Slide 119-

PNEUMOTHORAX SPONTANEOUS, TRAUMATIC, THERAPEUTIC OPEN or CLOSED “TENSION” pneumothorax, “valvular” effect “Bleb” (bulla) rupture Perforating injuries Post needle biopsy
Slide 120-

EFFUSIONS TRANSUDATE (HYDROTHORAX) EXUDATE (HYDROTHORAX) BLOOD (HEMOTHORAX) LYMPH (CHYLOTHORAX)
Slide 121-

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”
Slide 122-

ppt slide no 122 content not found
Slide 123-

 EM H&E, IMMUNOCHEMISTRY (CALRETININ)