15 lung
description
Transcript of 15 lung
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LUNGSLUNGS
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The LUNG• “Degenerative”
• Inflammatory
• Neoplastic and Pleura
• LAB: (Review, Cases, and/or Virtual Microscopy)
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OVERVIEW• 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
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OVERVIEW• INFECTIONS
• NEOPLASMS and PLEURA (effusions, pneumothorax, tumors)
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WEIGHT
LOBES
SEGMENTS
BRONCHI
ARTERIES, pulmonary
ARTERIES, bronchial
VEINS
PLEURA, visceral
PLEURA, parietal
NERVES
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Bronchi
Bronchioles
Terminal bronchioles
Alveolar ducts
Alveoli
Type 1 pneumocytes
Type 2 pneumocytes
Macrophages
Capillaries
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NORMAL
CXR
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OVERVIEW• Pathology
–CONGENITAL– Atalectasis– Acute Pulmonary Injury– Obstructive vs. Restrictive (infiltrative) concepts
–Obstructive Pulmonary Disease (COPD)
– Restrictive (Infiltrative) Pulmonary Disease– Vascular Pulmonary Diseases
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CONGENITAL• Agenesis/Hypoplasia
• Tracheal/bronchial anomalies, i.e., Tracheo-Esophageal (TE) fistula
• Vascular anomalies
• Congenital Emphysema
• Foregut cysts
• Pulmonary Artery Malformations (CPAM)
• Sequestration (no connection to airways)
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OVERVIEW• Pathology
– Congenital
–ATALECTASIS– Acute Pulmonary Injury– Obstructive vs. Restrictive (infiltrative) concepts
–Obstructive Pulmonary Disease (COPD)
– Restrictive Pulmonary Disease– Vascular Pulmonary Diseases
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ATALECTASIS• INCOMPLETE
EXPANSION
• COLLAPSE
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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
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PULMONARY EDEMA• IN-creased
venous pressure
• DE-creased oncotic pressure
• Lymphatic obstruction
• Alveolar injury
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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
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ARDS
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ACUTE INTERSTITIAL PNEUMONIA
• Think of it as ARDS with NO known etiology!
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OVERVIEW• Pathology
– Congenital– Atalectasis– Acute Pulmonary Injury
–OBSTRUCTION vs. RESTRICTION–Obstructive Pulmonary Disease (COPD)
– Restrictive (Infiltrative) Pulmonary Disease– Vascular Pulmonary Diseases
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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
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OVERVIEW• Pathology
– Congenital– Atalectasis– Acute Pulmonary Injury– Obstruction vs. Restriction
–OBSTRUCTIVE Pulmonary Diseases (COPD)
– Restrictive (Infiltrative) Pulmonary Disease– Vascular Pulmonary Diseases
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OBSTRUCTION (cOPD)• EMPHYSEMA (almost always
chronic)
• CHRONIC BRONCHITIS emphysema
• ASTHMA
• BRONCHIECTASIS
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EMPHYSEMA• COPD, or “END-STAGE” lung disease
• Centri-acinar, Pan-acinar, Paraseptal, Irregular
• Like cirrhosis, thought of as END-STAGE of multiple chronic small airway obstructive etiologies
• NON-specific• IN-creased crepitance, BULLAE (BLEBS)
• Clinically linked to recurrent pneumonias, and progressive failure
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CENTRO-acinar PAN-acinar
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1) HYPER-expansion 2) “flattened” diaphragms (blunted),
3) “bullae” 4) increased lucency* (why?)
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CHRONIC BRONCHITIS• INHALANTS, POLLUTION, CIGARETTES
• CHRONIC COUGH
• CAN OFTEN PROGRESS TO EMPHYSEMA
• MUCUS hypersecretion, early, i.e. goblet cell increase
• CHRONIC bronchial inflammatory infiltrate
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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
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What are the 4 classical histologic findings in bronchial asthma?
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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)
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BRONCHIECTASIS
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OVERVIEW• Pathology
– Congenital– Atalectasis– Acute Pulmonary Injury– Obstruction vs. Restriction– Obstructive Pulmonary Diseases (COPD)
–RESTRICTIVE (INFILTRATIVE) PULMONARY DISEASES
– Vascular Pulmonary Diseases
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RESTRICTIVE (INFILTRATIVE)
• REDUCED COMPLIANCE, reduced gas exchange)• Are also DIFFUSE• HETEROGENEOUS
• FIBROSING• GRANULOMATOUS• EOSINOPHILIC• SMOKING RELATED• PAP (Pulmonary Alveolar
Proteinosis
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FIBROSING• “IDIOPATHIC” PULMONARY FIBROSIS (IPF)
• NONSPECIFIC INTERSTITIAL FIBROSIS
• “CRYPTOGENIC” ORGANIZING PNEUMONIA
• “COLLAGEN” VASCULAR DISEASES
• PNEUMOCONIOSES
• DRUG REACTIONS
• RADIATION CHANGES
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IPF (UIP)• IDIOPATHIC, i.e., not from any usual
caused, like lupus, scleroderma• FIBROSIS
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NON-SPECIFIC INTERSTITIAL PNEUMONIA
• WASTEBASKET DIAGNOSIS, of ANY pneumonia (pneumonitis) of any known or unknown etiology– FIBROSIS– CELLULAR
INFILTRATE (LYMPHS & PLASMA CELLS)
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CRYPTOGENIC ORGANIZING PNEUMONIA (COP)
• IDIOPATHIC
• “BRONCHIOLITIS OBLITERANS”
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“COLLAGEN” VASCULAR DISEASES
• Rheumatoid Arthritis
• SLE (“Lupus”)
• Progressive Systemic Sclerosis (Scleroderma)
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PNEUMOCONIOSES• “OCCUPATIONAL”
• “COAL MINERS LUNG”
• DUST OR CHEMICALS OR ORGANIC MATERIALS– Coal (anthracosis)– Silica– Asbestos
– Be, FeO, BaSO4, CHEMO– HAY, FLAX, BAGASSE, INSECTICIDES, etc.
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GRANULOMATOUS• SARCOIDOSIS, i.e., NON-caseating
granulomas (IDIOPATHIC)
• HYPERSENSITIVITY (DUSTS,
bacteria, fungi, Farmer’s Lung,
Pigeon Breeder’s Lung)
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SARCOIDOSIS• Mainly LUNG, but eye, skin or
ANYWHERE
• UNKNOWN ETIOLOGY
• IMMUNE, GENETIC factors
• F>>M
• B>>W
• YOUNG ADULT BLACK WOMEN
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NON-Caseating Granulomas are the RULE
“Asteroid” bodies within these granulomas are virtually diagnostic
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SMOKING RELATED• DIP
(Desquamative Interstitial Pneumonia)
– M>>F– CIGARETTES– 100% Survival
Alveolar Macrophages
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PAP (Pulmonary Alveolar Proteinosis)
• Very RARE, usually acquired
• Proteinaceous Material in Alveoli
• MINIMAL cellular infiltrate
• Like Pulmonary Edema, but MUCH Protein
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OVERVIEW• Pathology
– Congenital– Atalectasis– Acute Pulmonary Injury– Obstruction vs. Restriction– Obstructive Pulmonary Diseases (COPD)– Restrictive (Infiltrative) Pulmonary Diseases
–VASCULAR PULMONARY DISEASES
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VASCULAR PULMONARY DISEASES
• PULMONARY EMBOLISM (with or usually WITHOUT infarction)
• PULMONARY HYPERTENSION, leading to cor pulmonale
• HEMORRHAGIC SYNDROMES– GOODPASTURE SYNDROME
– HEMOSIDEROSIS, idiopathic
– WEGENER GRANULOMATOSIS
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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
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VQ scan
CT
CXR
GROSS “saddle” embolism
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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
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VERY thickened arteriole in pulmonary hypertension
NORMAL pulmonary arteriole
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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
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CHF, CHRONICIDIOPATHIC
PULMONARY
HEMOSIDEROSIS
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PNEUMONIA
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COMMUNITY-ACQUIRED BACTERIAL ACUTE PNEUMONIASStreptococcus PneumoniaeHaemophilus InfluenzaeMoraxella CatarrhalisStaphylococcus AureusKlebsiella PneumoniaePseudomonas AeruginosaLegionella Pneumophila
COMMUNITY-ACQUIRED ATYPICAL (VIRAL AND MYCOPLASMAL) PNEUMONIASMorphology.Clinical Course.Influenza InfectionsSevere Acute Respiratory Syndrome (SARS)
NOSOCOMIAL PNEUMONIAASPIRATION PNEUMONIALUNG ABSCESS
Etiology and Pathogenesis.CHRONIC PNEUMONIA
Histoplasmosis, MorphologyBlastomycosis, MorphologyCoccidioidomycosis, Morphology
PNEUMONIA IN THE IMMUNOCOMPROMISED HOSTPULMONARY DISEASE IN HUMAN IMMUNODEFICIENCY VIRUS INFECTION
PULMONARY INFECTIONS
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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 • 2 DIAGNOSTIC METHODS• ANY ORGANISM CAN CAUSE PNEUMONIA!!!
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PREDISPOSING FACTORS• LOSS OF COUGH REFLEX
• DIMINISHED MUCIN or CILIA FUNCTION
• ALVEOLAR MACROPHAGE INTERFERENCE
• VASCULAR FLOW IMPAIRMENTS
• BRONCHIAL FLOW IMPAIRMENTS
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Although pneumonia is one of the most common causes of death, it usually does
NOT occur in healthy people spontaneously
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Classifications of PNEUMONIAS
• COMMUNITY ACQUIRED
• COMMUNITY ACQUIRED, ATYPICAL
• NOSOCOMIAL
• ASPIRATION
• CHRONIC
• NECROTIZING/ABSCESS FORMATION
• PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
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Classifications of PNEUMONIAS
• COMMUNITY ACQUIRED• COMMUNITY ACQUIRED, ATYPICAL
• NOSOCOMIAL
• ASPIRATION
• CHRONIC
• NECROTIZING/ABSCESS FORMATION
• PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
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COMMUNITY ACQUIRED• STREPTOCOCCUS PNEUMONIAE (i.e.,
“diplococcus”)• HAEMOPHILUS INFLUENZAE (“H-Flu”)• MORAXELLA• STAPHYLOCOCCUS (STAPH)• KLEBSIELLA PNEUMONIAE • PSEUDOMONAS AERUGINOSA• LEGIONELLA PNEUMOPHILIA
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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
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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
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MORAXELLA CATARRHALIS• 2nd most common COPD pneumonia, after haemophilus• Gram NEGATIVE coccobacillus
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STAPH aureus• Most common pneumonia
following viral pneumonias
• M.R.S.A., of course, is usually NOT “community” acquired
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KLEBSIELLA PNEUMONIAE
• DEBILITATED MALNOURISHED PEOPLE
•ALCOHOLICS with pneumonia are often thought of as having Klebsiella until proven otherwise
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PSEUDOMONAS Aeruginosa
• Usually NOT community acquired but nosocomial
• CYSTIC FIBROSIS patients with pneumonia are presumed to have PSEUDOMONAS until proven otherwise
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LEGIONELLA (pneumophila)
• Often in OUTBREAKS
• Often LOBAR
• Spread by water “droplets”
• Often immunosuppressed patients, but remember………..
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Although pneumonia is one of the most common causes of death, it usually does
NOT occur in healthy people spontaneously
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MORPHOLOGY• ACUTE• ORGANIZING• CHRONIC• FIBROSIS vs. FULL RESOLUTION
• “HEPATIZATION”, RED vs. GREY• CONSOLIDATION• “INFILTRATE”, XRAY vs. HISTOPATH• Loss of “CREPITANCE”
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Classifications of PNEUMONIAS
• COMMUNITY ACQUIRED
• COMMUNITY ACQUIRED, ATYPICAL
• NOSOCOMIAL
• ASPIRATION
• CHRONIC
• NECROTIZING/ABSCESS FORMATION
• PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
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COMMUNITY ACQUIRED, (atypical)
• VIRAL (INFLUENZA)
• MYCOPLASMAL (MYCOPLASMA PNEUMONIAE (obligate intracellular))
• NOT BACTERIAL
• CULTURES NOT HELPFUL
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VIRAL PNEUMONIAS• Frequently “interstitial”, NOT alveolar
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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
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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
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S
A
R
S
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Classifications of PNEUMONIAS
• COMMUNITY ACQUIRED
• COMMUNITY ACQUIRED, ATYPICAL
• NOSOCOMIAL• ASPIRATION
• CHRONIC
• NECROTIZING/ABSCESS FORMATION
• PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
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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. aeruginosaKlebsiellaE. coliS. pneumoniaeH. influenzae
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Classifications of PNEUMONIAS
• COMMUNITY ACQUIRED
• COMMUNITY ACQUIRED, ATYPICAL
• NOSOCOMIAL
• ASPIRATION• CHRONIC (often granulomatous)
• NECROTIZING/ABSCESS FORMATION
• PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
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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
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LUNG ABSCESSES• ASPIRATION
• SEPTIC EMBOLIZATION
• NEOPLASIA
• From NEIGHBORING structures:– ESOPHAGUS– SPINE– PLEURA– DIAPHRAGM
• ANY pneumonia which is severe and destructive, and UN-treated enough
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Classifications of PNEUMONIAS
• COMMUNITY ACQUIRED
• COMMUNITY ACQUIRED, ATYPICAL
• NOSOCOMIAL
• ASPIRATION
• CHRONIC• NECROTIZING/ABSCESS FORMATION
• PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
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CHRONIC Pneumonias• USUALLY NOT persistences of the
community or nosocomial bacterial infections, but CAN BE, at least histologically
• Often SYNONYMOUS with the 4 classic
fungal or granulomatous pulmonary infections infections, i.e., TB, Histo-, Blasto-, Coccidio-
• If you see pulmonary granulomas, think of a CHRONIC process, often years
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CHRONIC Pneumonias
• TB
• HISTO-PLASMOSIS
• BLASTO-MYCOSIS
• COCCIDIO-MYCOSIS
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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
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BLASTOMYCOSIS• Spores in soil• Mimics TB • Blastomyces DERMATIDIS• Pulmonary granulomas, often large and
calcified• Large distinct SPHERULES• Ohio, Mississippi valley, Great Lakes,
WORLDWIDE• MANY other organs can be affected,
especially SKIN
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COCCIDIOMYCOSIS• Spores in soil
• Mimics TB
• Coccidioides IMMITIS
• Pulmonary granulomas, often large and calcified
• Tiny organisms live in macrophages
• American SOUTHWEST
• MANY other organs can be affected
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GRANULOMA
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COMPROMISED HOSTS
• PNEUMOCYSTIS CARINII
• CYTOMEGALOVIRUS (CMV)
• FUNGI
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PCP
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Methenamine SILVER stain for
Pneumocystis Carinii
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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!
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Lung Transplant Pathology • Infections (immunocompromised patients)
– Bacterial– Viral (CMV)– Fungal– PCP
• ACUTE rejection, pneumonias, usually weeks to months
• CHRONIC rejection, HALF of all patients by 3-5 years, “bronchiolitis obliterans”
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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
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PATHOGENESIS• NORMAL BRONCHIAL MUCOSA• METAPLASTIC/DYSPLASTIC
MUCOSA• CARCINOMA-IN-SITU
(squamous, adeno)• INFILTRATING (i.e.,
“INVASIVE”) cancer
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TWO TYPES• NON-SMALL CELL
–SQUAMOUS CELL CARCINOMA
–ADENOCARCINOMA
–LARGE CELL CARCINOMA
• SMALL CELL CARCINOMA
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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
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OTHER TUMORS
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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
TNM, Lung
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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.
LOCAL effects of LUNG CANCER
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SYSTEMIC effects of LUNG CANCER
(PARA-NEOPLASTIC SYNDROMES)~ 5%ADH (hyponatremia)
ACTH (Cushing)
PTH (Hyper-CA)
CALCITONIN (Hypo-CA)
GONADOTROPINS
SEROTONIN/BRADYKININ
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OTHER TUMORS
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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!
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PLEURA• PLEURITIS• PNEUMOTHORAX• EFFUSIONS
–HYDROTHORAX–HEMOTHORAX–CHYLOTHORAX
• MESOTHELIOMAS
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PLEURITIS• Usual bacteria, viruses, etc.
• Infarcts
• Lung abscesses, empyema
• TB
• “Collagen” diseases, e.g., RA, SLE
• Uremia
• Metastatic
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PNEUMOTHORAX• SPONTANEOUS, TRAUMATIC,
THERAPEUTIC
• OPEN or CLOSED
• “TENSION” pneumothorax, “valvular” effect
• “Bleb” rupture
• Perforating injuries
• Post needle biopsy
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EFFUSIONS• TRANSUDATE (HYDROTHORAX)
• EXUDATE (HYDROTHORAX)
• BLOOD (HEMOTHORAX)
• LYMPH (CHYLOTHORAX)
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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”
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EM
H&E, IMMUNOCHEMISTRY