Chapter 15

Chapter 15The Respiratory System

Respiratory/Circulatory A Cooperative Effort

• Oxygen delivery to the tissues and waste product removal requires a cooperative effort of the respiratory and circulatory systems

• The respiratory system oxygenates the blood and removes carbon dioxide

• The circulatory system transports these gases in the bloodstream

Lung Components• System of tubes to conduct air into and out of the lungs• Bronchi: largest conducting tube• Bronchioles (little bronchi): next in size• Terminal Bronchioles: smallest• Respiratory Bronchioles: tubes distal to terminal

bronchioles; they have alveoli projecting from their walls. Transport air but also participate in gas exchange

• Alveoli where oxygen and carbon dioxide exchange between air and pulmonary capillaries

• Lung divided into large segments called lobes, each one consisting of smaller units, lobules

Structure Terminal Air Passages

Respiration: Function• Acinus or respiratory unit: functional unit of the

lung• Respiration has two functions1. Ventilation

– Air movement caused by movement of ribs and diaphragm

2. Gas exchange– Gases diffuse between blood, tissues, and

pulmonary alveoli due to differences in their partial pressures

Pulmonary Function Tests

• Vital capacity• One-second forced expiratory volume (FEV1)• Arterial PO2 and PCO2

The Pleural Cavity• Lungs are covered by a thin membrane called pleura,

which also extends over the internal surface of the chest wall

• The potential space between the lungs and the chest wall is called pleural cavity

• Intrapleural pressure is less than the intrapulmonary pressure

• The negative intrapleural pressure is caused by the tendency of the stretched lung to pull away from the chest wall

• A release of the vacuum in the pleural cavity leads to a collapse of the lung - Atelectasis

How Does the Vacuum get released?• A hole is created in the pleura – known as a

pneumothorax • The hole can be one from the outside of the

body “traumatic pneumothorax” – example – knife wound – this allows higher pressure outside air to enter the pleural space

• The hole can be one from the inside where an surface alveoli bursts “spontaneous pneumothorax”– this allows higher pressure lung air to enter the pleural space

• The air in the pleural space can cause a collapse of the lung “atelectasis”

Pneumothorax Pathogenesis/Manifestations

Pathogenesis• Lung injury or pulmonary disease that allows air to

escape into the pleural space• Stab wound or penetrating injury to the chest wall• Spontaneous – generally in young healthy personsManifestations• Chest pain• Shortness of breath• Air in pleural cavity• Tension pneumothorax

Tension Pneumothorax• Development of a higher than atmospheric

pressure in the pleural cavity – creating a tension

• Can accompany any type of pneumothorax • Upon inhalation air enters pleural space – due to

drop in intrapleural pressure• On exhalation – air gets trapped due to the

edges of the tear compressing as a result of the increased intrapleural pressure – thus the pressure in the intrapleural space is getting greater and greater

• Heart and Mediastinal structures shifted away from pneumothorax

Pneumothorax Treatment

• A chest tube is inserted into the pleural cavity and left in place until tear in lung heals– Prevents accumulation of air in pleural cavity– Aids reexpansion of lung

Atelectasis An incomplete expansion of the lung, a collapse of a

part of the lungThere are two types1. Obstructive atelectasis: complete bronchial

obstruction by • Mucous secretions, tumor, foreign object• Resulting in collapse of the part of the lung

supplied by the blocked bronchus• Can also develop as a postoperative

complication, where because of the pain, the patient does not cough or breathe deeply, accumulating mucous secretions

Atelectasis2. Compression atelectasis

– External compression on the lung • Fluid, air, or blood in the pleural cavity,

reducing its volume and preventing lung expansion

Pneumonia

An inflammation of the lung• The exudate spreads unimpeded through the lung• Filling the alveoli• The affected portions of the lung become relatively

solid (consolidation)• At times, the exudate reaches the pleural surface

Pneumonia Classification

Classification 1. Etiology: most important because it serves as a

guide for treatment– Bacteria, chlamydia, mycoplasmas, rickettsiae,

viruses, fungi2. Anatomic distribution of the inflammatory process-

describes what part of the lung is involved– Lobar: entire lung (bacteria, neutrophil

infiltration)– Bronchopneumonia (bacteria, neutrophil

infiltration): parts of one or more lobes adjacent to the bronchi – bronchopulmonary segments

Pneumonia Classification

– Interstitial pneumonia or primary atypical pneumonia (virus or mycoplasma; lymphocyte, monocyte, and plasma cell infiltration): alveolar septa affected

3. Predisposing factors that lead to its development• Any condition associated with poor lung ventilation

and retention of bronchial secretions– Postoperative – atelectasis and secondary

bacterial infection– Aspiration– Obstruction

– Clinical features of pneumonia• Manifestations of systemic infection

– Feeling ill – Elevated temperature– Increased white blood cell count

• Manifestations of lung inflammation – Cough– Purulent sputum– Pain on respiration if involves pleura– Shortness of breath

Legionnaires’ Disease

• First known occurrence 1976 at American Legion Convention in Philadelphia

• Gram-negative rod shaped bacteria called Legionella pneumophila

• Found in moist environments • Airborne infection – not spread from

human to human• Treated by appropriate antibiotics

SARSSevere Acute Respiratory Syndrome

• A highly communicable serious pulmonary infection, caused by an unusual coronavirus that has spread rapidly through several countries since it was first identified in late 2002

• In 2003 a Chinese Physician became ill while staying in a hotel in Hong Kong along with 12 other hotel occupants – they flew out to other countries and it spread

• Many become seriously ill and some die (5% of patients –higher rate in patients with other diseases like diabetes) from Respiratory Distress Syndrome

• The SARS-associated virus is a unique RNA virus not closely related to other coronaviruses and the first one to cause severe disease in people. The virus has crown like (corona) spikes projecting from its surface

• The virus probably was an animal virus that mutated and was able to infect humans

• Virus present in the blood during early stages then in feces later

• Can survive in the environment for up to 3 hours. • Incubation period 2 to 7 days but may be up to 10 days.• Illness begins with chills, fever and sometimes mild

respiratory symptoms and occasionally diarrhea. After 3 -7 days it manifests as a lower respiratory tract infection with varying severity.

• The most infected need mechanical ventilation• Can be transmitted from person to person through coughing,

sneezing, by hands, towels, and other items contaminated with the virus

• There are no effective antiviral drugs that can influence the course of the disease

Swine Flu• Swine influenza (also swine flu) refers to

influenza caused by any virus of the family Orthomyxoviridae, that is endemic to pig (swine) populations. Strains endemic in swine are called swine influenza virus (SIV), and all known strains of SIV are classified as Influenza virus A (common) or Influenza virus C (rare).

Influenzavirus B has not been reported in swine. All three classes, Influenzavirus A, B, and C, are endemic in humans

• People who work with poultry and swine, especially people with intense exposures, are at risk of infection from these animals if the animals carry a strain that is also able to infect humans. SIV can mutate into a form that allows it to pass from human to human. The strain responsible for the 2009 swine flu outbreak is believed to have undergone this mutation.

• In humans, the symptoms of swine flu are similar to those of influenza and of influenza-like illness in general

Signs and Symptoms• Main symptoms of swine flu in humans.• According to the

Centers for Disease Control and Prevention (CDC), in humans the symptoms of swine flu are similar to those of influenza and of influenza-like illness in general. Symptoms include fever, cough, sore throat, body aches, headache, chills and fatigue. A few more patients than usual have also reported diarrhea and vomiting.

• Because these symptoms are not specific to swine flu, a differential diagnosis of probable swine flu requires not only symptoms but also a high likelihood of swine flu due to the person's recent history. For example, during this 2009 swine flu outbreak in the United States, CDC advised physicians to "consider swine influenza infection in the differential diagnosis of patients with acute febrile respiratory illness who have either been in contact with persons with confirmed swine flu, or who were in one of the five U.S. states that have reported swine flu cases or in Mexico during the 7 days preceding their illness onset.“[A diagnosis of confirmed swine flu requires laboratory testing of a respiratory sample (a simple nose and throat swab).

Pathophysiology• Influenza viruses bind through hemagglutinin

onto sialic acid sugars on the surfaces of epithelial cells; typically in the nose, throat and lungs of mammals and intestines of birds (Stage 1 in infection figure).[17]

Swine flu in humans• People who work with poultry and swine,

especially people with intense exposures, are at increased risk of zoonotic infection with influenza virus endemic in these animals, and constitute a population of human hosts in which zoonosis and re-assortment can co-occur.

• Transmission of influenza from swine to humans who work with swine was documented in a small surveillance study performed in 2004 at the University of Iowa. This study among others forms the basis of a recommendation that people whose jobs involve handling poultry and swine be the focus of increased public health surveillance.

• The 2009 swine flu outbreak is an apparent re-assortment of several strains of influenza A virus subtype H1N1, including a strain endemic in humans and two strains endemic in pigs, as well as an avian influenza.

• The CDC reports that the symptoms and transmission of the swine flu from human to human is much like that of seasonal flu.

• Common symptoms include fever, lethargy, lack of appetite and coughing, while runny nose, sore throat, nausea, vomiting and diarrhea have also been reported.

• It is believed to be spread between humans through coughing or sneezing of infected people and touching something with the virus on it and then touching their own nose or mouth. Swine flu cannot be spread by pork products, since the virus is not transmitted through food.

• The swine flu in humans is most contagious during the first five days of the illness although some people, most commonly children, can remain contagious for up to ten days.

Diagnosis • made by sending a specimen, collected during the first

five days, to the CDC for analysis.Treatment• The swine flu is susceptible to four drugs licensed in the

United States, amantadine, rimantadine, oseltamivir and zanamivir, however, for the 2009 outbreak it is recommended it be treated under medical advice only with oseltamivir and zanamivir to avoid drug resistance.

• The vaccine for the human seasonal H1N1 flu does not protect against the swine H1N1 flu, even if the virus strains are the same specific variety, as they are antigenically very different.

Prevention• Recommendations to prevent infection by the virus

consist of the standard personal precautions against influenza. This includes frequent washing of hands with soap and water or with alcohol-based hand sanitizers, especially after being out in public. People should avoid touching their mouth, nose or eyes with their hands unless they've washed their hands. If people do cough, they should either cough into a tissue and throw it in the garbage immediately, cough into their elbow, or, if they cough in their hand, they should wash their hands immediately.

• Vaccines that are effective against the current strain are being developed.

Pneumocystis Pneumonia• Humans and many animals harbor this

microorganism – Pneumocystis carinii• Caused by protozoan parasite of low pathogenicity• Does not affect normal persons

• Affects immunocompromised persons– Persons with AIDS – Persons receiving immunosuppressive drugs– Premature infants whose immune defenses are poorly

developed• Organisms injure alveoli, leading to exudation of protein-

rich material into alveoli– Dyspnea– Cough– Pulmonary consolidation

• Cysts demonstrated by special stains• Within the cysts are sporozoites- when released

from the cysts these organisms mature and enlarge into trophozoites. Some trophozoites give rise to more cysts, repeating the cycle but some attack the lining of the alveoli (destruction).

• Evidence of pulmonary consolidation visualized on chest radiograph

• Diagnosis established by biopsy of lung tissue obtained by bronchoscopy

• Treatment – Drugs that inhibit growth of organism– Infection has high mortality

Tuberculosis• It is a special type of pneumonia caused by

Mycobacterium tuberculosis – an acid – fast bacteria• Because the tubercle bacillus has a capsule composed

of waxes and fatty substances, it is more resistant to destruction than others – thick cell wall

• As a result of this organism’s resistance – monocytes accumulate around the bacteria – many fuse with the bacteria attempting phagocytosis – but the fusion produces a large multinucleated “giant cell”. Lymphocytes and plasma cells surround the area – followed by fibrous tissue proliferation. The central portion becomes necrotic – thus a granuloma is formed. TB is termed a granulomatous disease.

– Manifestations• Course of infection

– Acquired from organisms inhaled in airborne droplets– Organisms lodge within pulmonary alveoli where they

proceed to multiply– Initially the organisms do not elicit a marked

inflammatory reaction because they do not produce any toxins or destructive enzymes

– Macrophage phagocytose the bacteria but are unable to destroy them – they may even carry the organisms to other parts of the lung and into regional lymph nodes.

– After several weeks cell-mediated immunity develops– Sensitized T- cytotoxic lymphocytes attract and activate

macrophages – the activated macrophages attack and destroy many of the organisms forming the characteristic granulomas formed

– In the majority of cases the person is unaware they have been infected – no symptoms

– Infection arrested in majority of cases• Outcome depends

– Number of organisms inhaled– State of body’s defenses– May heal by scarring or progress to cavitation

• Sometimes the granuloma is large enough to be seen on X-ray but most of the times it is too small

• The positive skin test reveals the infection• Cell-mediated immunity generally controls the infection• The healed granuloma may contain small numbers of

viable organisms and the infection may become reactivated when the immune system drops

• In some individuals the primary infection does not respond favorably to the immune system fight

• The granuloma may extend into a nearby bronchus and necrotic inflammatory tissue is discharged into it

• A cavity may form• If the person gets reactivation of the bacteria (becomes

active) and they have cavitation (into bronchus) their sputum can be infectious to others

• Most cases of active TB do not result from the initial infection – but rather by a reactivation – however some are due to a reinfection (new case)

• How does reactivation occur- it is due to a drop in the immune system action as a result of AIDS, other debilitating diseases, treatment with corticosteroids, treatment with immunosuppressive therapy

Miliary and tuberculous pneumonia are two uncommon but extremely serious forms of TB

• Miliary Tuberculosis – Mass of tuberculous inflammatory tissue erodes into a

large blood vessel thus dissemination of organisms by bloodstream

– Miliary is derived from the resemblance of multiple foci of disseminated TB (seen in liver, spleen, kidney and other tissues) to millet seeds. These are foci of small white nodules from about 1 – 2 mm in diameter (like millet seeds)

• TB pneumonia is an overwhelming infection characterized by extensive TB consolidation on one or more lobes of the lung. Persons with AIDs and other immunocompromised persons are prone to this type of rapidly progressive infection

• Extrapulmonary tuberculosis– Result of hematogenous spread of tubercle

bacilli – thus a secondary infection– Sites

» Kidneys » Bone » Uterus» Fallopian tubes

Sometimes the secondary infection may progress even though the pulmonary infection has healed leading to an active extrapulmonary TB without clinically apparent pulmonary TB

TuberculosisDiagnosis

– Skin test (Mantoux): a positive test reveals recent infection

– chest x-ray: when the granuloma is large enough to be detected – or see pulmonary infiltrates

– sputum culture – acid fast bacteria

• The tuberculosis skin test (also known as the tuberculin test or PPD test) is a test used to determine if someone has developed an immune response to the bacterium that causes tuberculosis (TB). This response can occur if someone currently has TB, if they were exposed to it in the past, or if they received the BCG vaccine against TB (which is not performed in the U.S.).

• The tuberculin skin test is based on the fact that infection with M. tuberculosis produces a delayed-type hypersensitivity skin reaction to certain components of the bacterium.

• The components of the organism are contained in extracts of culture filtrates and are the core elements of the classic tuberculin PPD (also known as purified protein derivative). This PPD material is used for skin testing for tuberculosis. Reaction in the skin to tuberculin PPD begins when specialized immune cells, called T cells, which have been sensitized by prior infection, are recruited by the immune system to the skin site where they release chemical messengers called lymphokines. These lymphokines induce induration (a hard, raised area with clearly defined margins at and around the injection site) through local vasodilation (expansion of the diameter of blood vessels) leading to fluid deposition known as edema, fibrin deposition, and recruitment of other types of inflammatory cells to the area.

• An incubation period of two to 12 weeks is usually necessary after exposure to the TB bacteria in order for the PPD test to be positive.

TuberculosisTreatment• Cell-mediated immunity generally controls the

infection• The healed granulomas, however, may contain small

numbers of viable organisms, and the infection may become reactivated

• Not all primary infections respond as favorably– If a large number of organisms are inhaled or if

the host is compromised (body’s defenses are inadequate), the inflammation will progress, causing more destruction of lung tissue

Tuberculosis– People who have active progressive tuberculosis with a

tuberculous cavity can infect others because they can discharge large numbers of tubercle bacilli in the sputum

– Treatment• Antibiotics and Chemotherapeutic agents• Drug-resistant tuberculosis treatment

– More prolonged – Results less satisfactory

• Drugs recommended– Following conversion of a negative into positive skin test

reaction– Patients with inactive tuberculosis who have increased

risk

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Bronchitis

An inflammation of the tracheobronchial mucosa• Acute bronchitis

– Common and self-limiting• Chronic bronchitis – often associated with

emphysema in COPD– Secondary to chronic irritation by smoking or

atmospheric pollution

• Bronchiectasis – Walls weakened by inflammation and dilate– Distended bronchi retain secretions

» Chronic cough» Production of large amounts of purulent sputum

– Diagnosed with bronchogram– A specialized X-ray which consists of taking films after

instilling a radiopaque oil into the trachea and bronchi. The oil covers the mucosa of the bronchi, and the abnormal bronchi can be recognized as dilated

– Only effective treatment is surgical resection of affected segments of lung

• Upper Respiratory System – From nose and mouth down to Lungs – (includes nose, mouth, pharynx, larynx, and trachea

• Lower Respiratory System – Mainstem bronchus to Alveoli

• Upper Airway – From nose and mouth to and inclusive of larynx (voice box)

• Lower Airway – Trachea down to alveoli

Chronic Obstructive Pulmonary DiseaseCOPD

Chronic Obstructive Pulmonary Disease• Emphysema and chronic bronchitis occur together so frequently

that they are usually considered a single entity, designated COPD

• Emphysema is characterized by loss of elasticity (increased pulmonary compliance) of the lung tissue caused by destruction of structures feeding the alveoli

• Chronic bronchitis – Secondary to chronic irritation by smoking or atmospheric pollution

Clinical manifestations• Dyspnea• Cyanosis

Chronic Obstructive Pulmonary Disease

The chief clinical manifestations of any type of chronic pulmonary disease are

• Dyspnea: sensation of shortness of breath• Cyanosis: blue tinge of skin and mucous membrane

from an excessive amount of reduced hemoglobin in the blood

The three main anatomic derangements in COPD are

1. Inflammation and narrowing of the terminal bronchioles

2. Dilatation and coalescence of pulmonary air spaces

3. Loss of lung elasticity

– Derangements of pulmonary structure and function

1. Inflammation and narrowing of terminal bronchioles– Causes swelling of bronchial mucosal– Reduces caliber of bronchi and bronchioles – Stimulates increased bronchial secretions– Air can enter lungs more readily than it can be expelled –

leads to trapped air– Nonuniform ventilation of alveoli reduces efficiency of

ventilation

2. Dilation and coalescence of pulmonary air spaces– Enlargement of air spaces and reduction of capillary bed

reduces efficiency of gas exchange– Movement of air into and out of enlarged spaces is

impeded by bronchiolar obstruction

3. Loss of lung elasticity– Expiration requires active expiratory effort– Pressure required to force air out of lungs raises

intrapleural pressure and compresses the lungs– Bronchi and bronchioles tend to collapse during

expiration» Obstructs air flow» Traps more air in lungs

Emphysema• The air spaces distal to the terminal

bronchioles are enlarged and their walls are destroyed

• The normally fine alveolar structure of the lung is destroyed

• The large cystic air spaces form throughout the lung

• The destructive process usually begins in the upper lobes but eventually may affect all lobes

• Once emphysema has developed, the damaged lungs cannot be restored to normal

Pathogenesis of emphysema – secondary to bronchitis• Chronic irritation from cigarette smoking or

inhalation of injurious agents produces chronic bronchitis

• Inflammatory swelling of mucosa – Narrows bronchioles– Increases bronchioles resistance to expiration– Causes air to be trapped in the lung

• Leukocytes that accumulate in bronchioles and alveoli may contribute to damage

– Release proteolytic enzymes– Enzymes attack elastic fibers

– Emphysema as a result of alpha, antitrypsin deficiency• Antitrypsin

– Prevents lung damage from lysosomal enzymes– Released from leukocytes in lung

• Deficiency permits enzymes to damage lung tissue– Develop progressive pulmonary emphysema– Manifest in adolescence or early adulthood– Tends to affect lower lobes of lungs– Less common type of emphysema

– Prevention and treatment• Refrain from smoking • Avoid inhalation of injurious agents

– Treatment • Will not restore damaged lung• Will prevent further progression• May improve pulmonary function

Bronchial Asthma• Spasmodic contraction of smooth muscles in the walls

of the smaller bronchi and bronchioles• It causes shortness of breath and wheezing respiration• Exerts a greater effect on expiration than on inspiration• Attacks are precipitated by allergens: inhalation of

dust, pollens, animal dander, or other allergens• Treated with drugs such as epinephrine or theophylline

that relax bronchospasms and block the release of mediators from mast cells

• Bronchial Asthma– Pathogenesis

• Spasmodic contraction of smooth muscles in walls of smaller bronchi and bronchioles

• Associated with increased secretions from bronchial mucous glands

– Clinical manifestations• Shortness of breath• Wheezing respirations• Air flow impeded more on expiration than on

inspiration– Air trapped in lungs– Lungs become overinflated

– Attacks precipitated by allergens• Interact with mast cells coated with IgE antibody • Release chemical mediators that induce

bronchospasm– Treatment

• Drugs that relax bronchospasm– Epinephrine– Theophylline

• Drugs that block release of mediators from mast cells

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Neonate Respiratory Distress Syndrome

• It occurs soon after birth• Due to inadequate surfactant in the lungs, which

cause the alveoli not to expand normally during inspiration and tend to collapse during expiration

• Predisposed groups– Premature infants– Infants born by cesarean section– Infants with diabetic mothers

– Neonatal respiratory distress syndrome• Pathogenesis

– Inadequate surfactant» Alveoli do not expand normally during inspiration» Promotes collapse

• Groups predisposed to syndrome– Premature infants– Infants born by cesarean section– Infants with diabetic mothers

• Treatment– Adrenal corticosteroid hormones administered to mother

within twenty-four hours before delivery– Infants who develop respiratory distress after delivery

treated by instillation of surfactant-type material

Adult Respiratory Distress Syndrome

• Pathogenesis1. Conditions that cause shock, causing fall in blood

pressure, and reduced blood flow to lungs• The shock may result from any type of severe injury

(traumatic shock) or from a serious systemic infection (septic shock)

2. Direct lung damage: caused by aspiration of acid gastric contents, inhalation of irritant or toxic gases, of damage caused by SARS

• Damaged alveolar capillaries leak fluid and protein • Impaired surfactant production from damaged alveolar

lining cells

– Adult respiratory distress syndrome / ARDS / shock lung• Pathogenesis

– Conditions that cause shock which leads to» Fall in blood pressure» Reduced blood flow to lungs» Impaired lung perfusion

– Direct lung damage» Trauma» Gastric aspiration inhalation of irritants or toxic gases

• Derangement– Damaged alveolar capillaries leak fluid and protein– Impaired surfactant production from damaged alveolar

lining cells– Formation of hyaline membranes

• Treatment– Correct shock– Treat underlying condition that initiated respiratory

distress– Improve oxygenation by administering oxygen under

positive pressure

Pulmonary Fibrosis• May be caused by lungs continually exposed to

injurious substances such as irritant gases discharged into the atmosphere and many kinds of airborne organic and inorganic particles

• Fibrous thickening of alveolar septa make the lungs increasingly rigid, restricting normal respiratory excursions

• Causes progressive respiratory disability similar to that in emphysema

• Collagen diseases- may lead to pulmonary fibrosis

Pulmonary Fibrosis• Pneumoconoisis: lung injury produced by inhalation

of injurious dust or other particulate material• The best known are

– Silicosis: a type of progressive nodular pulmonary fibrosis caused by inhalation of rock dust

– Asbestosis: a diffuse pulmonary fibrosis caused by inhalation of asbestos fibers

– Inhalation of coal dust, cotton fibers, certain types of fungus spores, and many other substances attending certain occupations also may cause pulmonary fibrosis

• Pulmonary Fibrosis– Fibrous thickening of alveolar septa

• Lungs become rigid• Respiratory excursions restricted• Diffusion of oxygen and carbon dioxide between

alveolar air and pulmonary capillaries hampered– Pathogenesis

• Collagen diseases• Pneumoconoisis

– Silicosis» Inhalation of rock dust» Progressive nodular pulmonary fibrosis

– Asbestosis» Inhalation of asbestos fibers» Diffuse pulmonary fibrosis» Increased incidence of other diseases

» Lung carcinoma » Pleural malignant mesothelioma

– Other substances inhaled in course of occupations

– Treatment• No specific treatment• Prevent occupational exposure

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Lung Carcinoma

• Usually smoking-related neoplasm• Common malignant tumor in both men and women• Mortality from lung cancer in women exceeds breast

cancer• Arises from mucosa of bronchi and bronchioles

Lung Carcinoma Classification

• Because the neoplasm of lung cancer usually arises from the bronchial mucosa, the term bronchogenic carcinoma, is often used

Classification • Squamous cell carcinoma: very common• Adenocarcinoma: very common• Large cell carcinoma: large, bizarre epithelial cells• Small cell carcinoma: very poor prognosis

• Accounts for 1/3 of all cancer deaths in the U.S.

• 90% of all patients with lung cancer were smokers

• The three most common types are:– Squamous cell carcinoma (20-40% of cases)

arises in bronchial epithelium– Adenocarcinoma (25-35% of cases) originates

in peripheral lung area– Small cell carcinoma (20-25% of cases)

contains lymphocyte-like cells that originate in the primary bronchi and subsequently metastasize

Lung Cancer

Lung Carcinoma• Because of the rich lymphatic and vascular network

in the lung, the neoplasm readily gains access to lymphatic channels and pulmonary blood vessels and soon spreads to regional lymph nodes and distant sites

• Treatment usually consists of surgical resection of one or more lobes of the lung

• Radiation and anticancer chemotherapy rather than surgery are used to treat small cell carcinoma and tumors that are too far advanced for surgical resection

• Lung Carcinoma– Pathogenesis

• Smoking-related neoplasm• Most common malignant tumor in men• Mortality from lung cancer in women exceeds

breast cancer • Arises from mucosa of bronchi and bronchioles

– Classification • Squamous cell carcinoma• Adenocarcinoma• Large cell carcinoma• Small cell carcinoma

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– Prognosis• Differs due to several histologic types • Poor prognosis due to early spread to distant sites

– Treatment• Surgical resection of one or more lobes• Small cell carcinoma treated by chemotherapy and

radiation