Transcript Document

Chapter 15
The 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 functions
1. 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 persons
Manifestations
• 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 lung
There are two types
1. 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
Atelectasis
2. 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, fungi
2. Anatomic distribution of the inflammatory processdescribes 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
SARS
Severe 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 reassortment 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 proteinrich 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
• 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
Tuberculosis
Diagnosis
– 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.
Tuberculosis
Treatment
• 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
•
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 Disease
COPD
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
•
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
• Pathogenesis
1. 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
•
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
Lung Cancer
• 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 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
– 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