Содержание

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Function of the Respiratory System

Slide 13.2

Oversees gas exchanges (oxygen and carbon dioxide)

Function of the Respiratory System Slide 13.2 Oversees gas exchanges (oxygen and
between the blood and external environment
Exchange of gasses takes place within the lungs in the alveoli(only site of gas exchange, other structures passageways
Passageways to the lungs purify, warm, and humidify the incoming air
Shares responsibility with cardiovascular system

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

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

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N O R M A L

C X R

N O R M A L C X R

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ATELECTASIS

INCOMPLETE EXPANSION
COLLAPSE

ATELECTASIS INCOMPLETE EXPANSION COLLAPSE

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PULMONARY EDEMA

IN-creased venous pressure
DE-creased oncotic pressure
Lymphatic obstruction
Alveolar injury

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

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ACUTE INTERSTITIAL PNEUMONIA

Think of it as ARDS with NO known etiology!

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

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OBSTRUCTION v. RESTRICTION

OBSTRUCTION
Air or blood?
Large or small?
Inspiration or Expiration?
Obstruction is SMALL AIRWAY

OBSTRUCTION v. RESTRICTION OBSTRUCTION Air or blood? Large or small? Inspiration or
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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OBSTRUCTION (cOPD)

EMPHYSEMA (almost always chronic)
CHRONIC BRONCHITIS? emphysema
ASTHMA
BRONCHIECTASIS

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

EMPHYSEMA COPD, or “END-STAGE” lung disease Centri-acinar, Pan-acinar, Paraseptal, Irregular Like cirrhosis,
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

EMPHYSEMA

CENTRO-acinar PAN-acinar EMPHYSEMA

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Bullae, or “peripheral blebs” are hallmarks of chronic obstructive lung disease, COPD.

Bullae, or “peripheral blebs” are hallmarks of chronic obstructive lung disease, COPD.

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CHRONIC BRONCHITIS

INHALANTS, POLLUTION, CIGARETTES
CHRONIC COUGH
CAN OFTEN PROGRESS TO EMPHYSEMA
MUCUS hypersecretion, early, i.e.

CHRONIC BRONCHITIS INHALANTS, POLLUTION, CIGARETTES CHRONIC COUGH CAN OFTEN PROGRESS TO EMPHYSEMA
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,

ASTHMA Similar to chronic bronchitis but: Wheezing is hallmark (bronchospasm, i.e. “wheezing”)
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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Bronchial Asthma

Chronic inflammatory disorder of the airways resulting in contraction of bronchial

Bronchial Asthma Chronic inflammatory disorder of the airways resulting in contraction of
muscle
Types
Extrinsic (atopic, allergic).
Allergens: food, pollen, dust, etc.
Intrinsic (non-atopic)
Initiated by infections, drugs, pollutants, chemical irritants

ATOPIC ASTHMA

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Note the heavy inflammatory cell infiltrate around bronchioles and small bronchi.

Note the heavy inflammatory cell infiltrate around bronchioles and small bronchi.

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What are the 4 classical histologic findings in bronchial asthma?

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,

BRONCHIECTASIS DILATATION of the BRONCHUS, associated with, often, necrotizing inflammation CONGENITAL TB,
many viruses
BRONCHIAL OBSTRUCTION (i.e., LARGE AIRWAY, NOT SMALL AIRWAY)
Rheumatoid Arthritis, SLE, IBD (Inflammatory Bowel Disease)

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BRONCHIECTASIS

BRONCHIECTASIS

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RESTRICTIVE (INFILTRATIVE)

REDUCED COMPLIANCE, reduced gas exchange)
Are also DIFFUSE
HETEROGENEOUS
FIBROSING
GRANULOMATOUS
EOSINOPHILIC
SMOKING RELATED
PAP (Pulmonary Alveolar Proteinosis

RESTRICTIVE (INFILTRATIVE) REDUCED COMPLIANCE, reduced gas exchange) Are also DIFFUSE HETEROGENEOUS FIBROSING

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FIBROSING

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

FIBROSING “IDIOPATHIC” PULMONARY FIBROSIS (IPF) NONSPECIFIC INTERSTITIAL FIBROSIS “CRYPTOGENIC” ORGANIZING PNEUMONIA “COLLAGEN”

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IPF (UIP)

IDIOPATHIC, i.e., not from any usual caused, like lupus, scleroderma
FIBROSIS

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

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

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CRYPTOGENIC ORGANIZING PNEUMONIA (COP)

IDIOPATHIC
“BRONCHIOLITIS OBLITERANS”

CRYPTOGENIC ORGANIZING PNEUMONIA (COP) IDIOPATHIC “BRONCHIOLITIS OBLITERANS”

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“COLLAGEN” VASCULAR DISEASES

Rheumatoid Arthritis
SLE (“Lupus”)
Progressive Systemic Sclerosis (Scleroderma)

“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,

PNEUMOCONIOSES “OCCUPATIONAL” “COAL MINERS LUNG” DUST OR CHEMICALS OR ORGANIC MATERIALS Coal
FLAX, BAGASSE, INSECTICIDES, etc.

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Coal, “bagasse”, asbestos, silica nodules, and asbestos, going clockwise.

Coal, “bagasse”, asbestos, silica nodules, and asbestos, going clockwise.

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GRANULOMATOUS

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

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

SARCOIDOSIS Mainly LUNG, but eye, skin or ANYWHERE UNKNOWN ETIOLOGY IMMUNE, GENETIC
WOMEN

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NON-Caseating Granulomas are the RULE
“Asteroid” bodies within these granulomas are virtually diagnostic

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

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

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Pulmonary tuberculosis

Caused by Mycobacterium tuberculosis.
Transmitted through inhalation of infected droplets
Primary
Single granuloma within

Pulmonary tuberculosis Caused by Mycobacterium tuberculosis. Transmitted through inhalation of infected droplets
parenchyma and hilar lymph nodes (Ghon complex).
Infection does not progress (most common).
Progressive primary pneumonia
Miliary dissemination (blood stream).

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Pulmonary tuberculosis

Secondary
Infection (mostly through reactivation) in a previously sensitized individual.
Pathology
Cavitary fibrocaseous lesions
Bronchopneumonia
Miliary

Pulmonary tuberculosis Secondary Infection (mostly through reactivation) in a previously sensitized individual.
TB

Miliary

Granuloma

Fibrocaseous

Mycobacterium

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VASCULAR PULMONARY DISEASES

PULMONARY EMBOLISM (with or usually WITHOUT infarction)
PULMONARY HYPERTENSION, leading to

VASCULAR PULMONARY DISEASES PULMONARY EMBOLISM (with or usually WITHOUT infarction) PULMONARY HYPERTENSION,
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

P.E. Usually secondary to debilitated states with immobilization, or following surgery Usually
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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GROSS “saddle” embolism

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,

PULMONARY HYPERTENSION COPD, C”I”PD (vicious cycle) CHD (Congenital HD, increased left atrial
e.g., PSS (Scleroderma), i.e., fibrotic pulmonary vasculature

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VERY thickened arteriole in pulmonary hypertension

NORMAL pulmonary arteriole

VERY thickened arteriole in pulmonary hypertension NORMAL pulmonary arteriole

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CHF, CHRONIC

IDIOPATHIC
PULMONARY
HEMOSIDEROSIS

CHF, CHRONIC IDIOPATHIC PULMONARY HEMOSIDEROSIS

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PNEUMONIA

PNEUMONIA

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PULMONARY INFECTIONS

COMMUNITY-ACQUIRED BACTERIAL ACUTE PNEUMONIAS
Streptococcus Pneumoniae
Haemophilus Influenzae
Moraxella Catarrhalis
Staphylococcus Aureus
Klebsiella Pneumoniae
Pseudomonas Aeruginosa
Legionella Pneumophila
COMMUNITY-ACQUIRED

PULMONARY INFECTIONS COMMUNITY-ACQUIRED BACTERIAL ACUTE PNEUMONIAS Streptococcus Pneumoniae Haemophilus Influenzae Moraxella Catarrhalis
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

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BASIC CONSIDERATIONS

PNEUMONIA vs. PNEUMONITIS
DIFFERENTIATION from INJURIES, OBSTRUCTIVE DISEASES, RESTRICTIVE DISEASES, VASCULAR DISEASES
DIFFERENTIATION

BASIC CONSIDERATIONS PNEUMONIA vs. PNEUMONITIS DIFFERENTIATION from INJURIES, OBSTRUCTIVE DISEASES, RESTRICTIVE DISEASES,
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

PREDISPOSING FACTORS LOSS OF COUGH REFLEX DIMINISHED MUCIN or CILIA FUNCTION ALVEOLAR
IMPAIRMENTS
BRONCHIAL FLOW IMPAIRMENTS

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Although pneumonia is one of the most common causes of death, it

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

Classifications of PNEUMONIAS COMMUNITY ACQUIRED COMMUNITY ACQUIRED, ATYPICAL NOSOCOMIAL ASPIRATION CHRONIC NECROTIZING/ABSCESS

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COMMUNITY ACQUIRED

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

COMMUNITY ACQUIRED STREPTOCOCCUS PNEUMONIAE (i.e., “diplococcus”) HAEMOPHILUS INFLUENZAE (“H-Flu”) MORAXELLA STAPHYLOCOCCUS (STAPH)

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STREPTOCOCCUS

The classic LOBAR pneumonia
Normal flora in 20% of adults
Only 20% of victims

STREPTOCOCCUS The classic LOBAR pneumonia Normal flora in 20% of adults Only
have + blood cultures
“Penicillins” are often 100% curative
Vaccines are often 100% preventive

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MORPHOLOGY

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

MORPHOLOGY ACUTE ORGANIZING CHRONIC FIBROSIS vs. FULL RESOLUTION “HEPATIZATION”, RED vs. GREY

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VIRAL PNEUMONIAS

Frequently “interstitial”, NOT alveolar

VIRAL PNEUMONIAS Frequently “interstitial”, NOT alveolar

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ASPIRATION PNEUMONIAS

UNCONSCIOUS PATIENTS
PATIENTS IN PROLONGED BEDREST
LACK OF ABILITY TO SWALLOW OR GAG
USUALLY

ASPIRATION PNEUMONIAS UNCONSCIOUS PATIENTS PATIENTS IN PROLONGED BEDREST LACK OF ABILITY TO
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

LUNG ABSCESSES ASPIRATION SEPTIC EMBOLIZATION NEOPLASIA From NEIGHBORING structures: ESOPHAGUS SPINE PLEURA
UN-treated enough

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Lung abscess

Localized suppurative necrosis
Organisms commonly cultured:
Staphylococci
Streptococci
Gram-negative
Anaerobes
Frequent mixed infections
Pathogenesis:
Aspiration
Pneumonia
Septic emboli
Tumors
Direct infection

Lung abscess Localized suppurative necrosis Organisms commonly cultured: Staphylococci Streptococci Gram-negative Anaerobes

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An abscess can be thought of as a pneumonia in which all

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.

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CHRONIC Pneumonias

USUALLY NOT persistences of the community or nosocomial bacterial infections, but

CHRONIC Pneumonias USUALLY NOT persistences of the community or nosocomial bacterial infections,
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

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

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GRANULOMA

GRANULOMA

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LUNG TUMORS

Benign, malignant, epithelial, mesenchymal, but 90% are CARCINOMAS
BIGGEST USA killer. Why?

LUNG TUMORS Benign, malignant, epithelial, mesenchymal, but 90% are CARCINOMAS BIGGEST USA
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

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

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,

The BIG list Squamous cell carcinoma Small cell carcinoma Combined small cell
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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The classical squamous cell carcinoma starting in a large bronchus centrally, with

The classical squamous cell carcinoma starting in a large bronchus centrally, with
bronchial obstruction.
Adenocarcinomas tend to be more peripheral. Note the features of malignant cells on sputum cytology.

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Name the four most common histologic patterns of lung carcinoma and explain

Name the four most common histologic patterns of lung carcinoma and explain
why!
Squamous, adeno, large, small.

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LOCAL effects of LUNG CANCER

LOCAL effects of LUNG CANCER

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METASTATIC TUMORS

LUNG is the MOST COMMON site for all metastatic tumors, regardless

METASTATIC TUMORS LUNG is the MOST COMMON site for all metastatic tumors,
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

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

PLEURITIS Usual bacteria, viruses, etc. Infarcts Lung abscesses, empyema TB “Collagen” diseases,

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PNEUMOTHORAX

SPONTANEOUS, TRAUMATIC, THERAPEUTIC
OPEN or CLOSED
“TENSION” pneumothorax, “valvular” effect
“Bleb” rupture
Perforating injuries
Post needle biopsy

PNEUMOTHORAX SPONTANEOUS, TRAUMATIC, THERAPEUTIC OPEN or CLOSED “TENSION” pneumothorax, “valvular” effect “Bleb”

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EFFUSIONS

TRANSUDATE (HYDROTHORAX)
EXUDATE (HYDROTHORAX)
BLOOD (HEMOTHORAX)
LYMPH (CHYLOTHORAX)

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

MESOTHELIOMAS “Benign” vs. “Malignant” differentiation does not matter, but a self limited
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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Typical growth appearance of a malignant mesothelioma, it compresses the lung from

Typical growth appearance of a malignant mesothelioma, it compresses the lung from the OUTSIDE.
the OUTSIDE.
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