You are on page 1of 11

Disorders of the respiratory system 2.

viruses: the majority of upper respiratory


tract infections are caused by viruses as
Respiratory structures such as the airways,
rhinovirus and parainfluenza virus.
alveoli and pleural membranes may all be
affected by various disease processes. 3. fungi.
These respiratory diseases include: Depending on the organism and extent of
infection, the manifestations can range from
1. Infections such as pneumonia.
mild to severe and even life threatening.
2. Obstructive disorders that obstruct
airflow into and out of the lungs such as
asthma, bronchitis and emphysema. Upper respiratory tract Infections
3. Restrictive disorders are conditions that 1) The common cold
limit normal expansion of the lungs such
as pneumothorax, atelectasis, respiratory The most common viral pathogens for the
distress syndrome and cystic fibrosis. “common cold” are rhinovirus, parainfluenza
virus, respiratory syncytial virus, adenovirus and
4. Cancers or exposure to Inhaled particles
coronavirus.
alter the pulmonary function.
 These viruses tend to have seasonal
variations in their peak incidence.
General symptoms of respiratory disease
 They gain entry to the body through the
 Hypoxia : Decreased levels of oxygen in
nasal mucosa and the surfaces of the eye.
the tissues
They are readily spread from person to
 Hypoxemia : Decreased levels of oxygen person via respiratory secretions.
in arterial blood
 Manifestations of the common cold
 Hypercapnia : Increased levels of CO2 in include:
the blood
 Rhinitis: Inflammation of the
 Hypocapnia : Decreased levels of CO2 in
nasal mucosa
the blood
 Dyspnea : Difficulty breathing  Sinusitis :Inflammation of
the sinus mucosa
 Tachypnea : Rapid rate of breathing
 Pharyngitis : Inflammation
 Cyanosis : Bluish discoloration of skin
of the pharynx and throat
and mucous membranes due to poor
oxygenation of the blood
 Headache
 Hemoptysis : Blood in the sputum
 Nasal discharge and
congestion
Respiratory infections
2) Influenza
Infections of the respiratory tract can occur in:  Influenza is a viral infection that
can affect the upper or lower
1. The upper respiratory tract or respiratory tract.
2. The lower respiratory tract, or  Three distinct forms of influenza virus
have been identified: A, B and C, of
3. Both. these three variants, type A is the
most common and causes the most
Organisms capable of infecting respiratory
serious illness.
structures include:
 The influenza virus is a highly
1. bacteria. transmissible respiratory pathogen.
 Because the organism has a high
tendency for genetic mutation, new
variant of the virus are constantly  Inhibits the activity of viral
arising in different places around the neuraminidase enzyme that is
world. Serious pandemics (spread of necessary for spread of the
infection across a large region) of influenza virus
influenza are seen every 8 to 10 years
as a result of this genetic mutation
Symptoms of influenza infection:
 Headache Lower respiratory tract Infections
 Fever, chills
 Muscle aches  The respiratory tract is protected by a
 Nasal discharge number of very effective defense
 Unproductive cough mechanisms designed to keep infectious
 Sore throat organisms and particulates from reaching
 Influenza infection can cause marked the lungs.
inflammation of the respiratory
 For an organism to reach the lower
epithelium leading to acute tissue
respiratory tract, the organism must be
damage and a loss of ciliated cells
particularly virulent and present in very
that protect the respiratory passages
large number or the host defense
from other organisms.
barriers must be weakened.
 As a result, influenza infection may
lead to co-infection of the respiratory  Factor that might weaken the respiratory
passages with bacteria. defense barriers:
 It is also possible for the influenza
virus to infect the tissues of the lung  Cigarette smoking, which can
itself to cause a viral pneumonia. paralyze the cilia lining the cells of
 Treatment of influenza: the respiratory passages and
 Bed rest, fluids, warmth impair removal of secretions,
 Antiviral drugs particles and microorganisms.
 Influenza vaccine :
 Provides protection against certain A  The presence of a respiratory
and B influenza strains that are pathogen such as the cold or
expected to be prevalent in a certain influenza virus
year.
 The vaccine must be updated and Defenses of the Respiratory System
administered yearly to be effective but
will not be effective against influenza 1. Moist, mucus-covered surfaces :
strains not included in the vaccine. Trap particles and organisms
 The influenza vaccine is particularly
indicated in elderly people, in 2. Cell surface IgA, lysosomes
individuals weakened by other disease
and in health-care workers 3. Ciliated epithelium : Clears
 Drugs for Treating Influenza: trapped particles and organisms
 Amantidine from airway passages
 Used orally or by aerosol
4. Cough reflex and epiglottis :
administration
Prevents aspiration of particles
 Effective only against type A
and irritants into lower airways
influenza
 Inhibits viral fusion, assembly and
5. Pulmonary macrophages:
release from the infected host cell
Phagocytize foreign particles and
 Neuraminidase inhibitors (Zanamavir,
organisms in the alveolar spaces.
Oseltamivir)
 New drugs that can be used by 1) Pneumonia
inhalation (Zanamavir) or orally
(Oseltamivir)  Pneumonia is a condition that involves
 Effective against both type A and inflammation of lower lung structures
B influenza
such as the alveoli or interstitial  Klebsiella pneumoniae
spaces.
 Atypical
 It may be caused by bacteria or viruses
such as pneumocystis carinii.  Chlamydia pneumoniae

 The prevalence and severity of  Legionella pneumophila


pneumonia have been heightened in
recent years due to the emergence of HIV  Mycoplasma pneumoniae.
as well as antibiotic resistance.
 • Viruses
 Pneumonia may be classified according
to the pathogen that is responsible for the  • Fungi
infection.
 • Less Common pathogens
 There tend to be distinct organisms that
 – N. meningitidis
cause pneumonia in the hospital setting
vs. the community setting.  – Chlamydia psittaci
Individuals Most at Risk for Pneumonia  – B. anthracis
 Elderly  – Y. pestis
 Those with viral infection

 Chronically ill

 AIDS or immunosuppressed
patients

 Smokers

 Patients with chronic respiratory


disease e.g. bronchial asthma.

 • Community acquired pneumonia


(CAP)

 • Aspiration pneumonia

 • Hospital

 –Hospital acquired pneumonia (HAP)

 –Ventilator associated pneumonia


(VAP)

 –Healthcare associated pneumonia


(HCAP)

Potential Pathogens

 Typical

 Streptococcus pneumoniae
A second classification scheme for pneumonia is
based on the specific structures of the lung that
 Hemophilus influenzae
the organisms infect and includes typical and
 Mycobacterium catarrhalis atypical pneumonia.
Typical pneumonia Treatment of pneumonia:

• Usually bacterial in origin. • Antibiotics if bacterial in origin. The


health-care provider should consider the
• Organisms replicate in the spaces of the alveoli. possibility that antibiotic-resistant
organisms are present.
Manifestations:
• Oxygen therapy for hypoxemia.
• Inflammation and fluid accumulation are seen in
the alveoli. • A vaccine for pneumococcal pneumonia
is currently available and highly effective.
• White cell infiltration and exudation can been This vaccine should be considered in
seen on chest radiographs. high-risk individuals.

• High fever, chest pain, chills, and malaise are Obstructive Respiratory Disorders
present.
1) Bronchial asthma
• Purulent sputum is present.
 Asthma is a condition characterized by
• Some degree of hypoxemia is present. reversible bronchospasm and chronic
inflammation of airway passages.
Atypical pneumonia
 The incidence of asthma has been
• Usually viral in origin. steadily increasing in recent years.
 Although the exact etiology is still
• Organisms replicate in the spaces around the uncertain, there appears to be a definite
alveoli. genetic predisposition to the development
of asthma.
Manifestations:  A key component of asthma appears to be
airway “hyper reactivity” in affected
• Milder symptoms than typical pneumonia. individuals. Exposure to certain “triggers”
can induce marked bronchospasm and
• Lack of white cell infiltration in alveoli. airway inflammation in susceptible
patients
• Lack of fluid accumulation in the alveoli.
 Individuals with asthma appear to produce
• Not usually evident on radiographs. large amounts of the antibody IgE that
attach to the mast cells present in many
• May make the patient susceptible to bacterial
tissues.
pneumonia.
 Exposure to a trigger such as pollen
will result in the allergen-binding mast cell-
Opportunistic organisms
bound IgE, which in turn causes the
 A number of organisms not commonly release of inflammatory mediators such as
associated with respiratory illness in Histamine , Leukotrienes and Eosinophilic
otherwise healthy individuals can cause Chemotactic factor.
severe respiratory infections and  The response of a patient with asthma to
pneumonia in patients with HIV or those these triggers can be divided into an “early
who are immunocompromised as a result phase” and a “late phase.”
of immune suppressive therapy.
**Some Potential Asthma Triggers**
 These organisms include mycobacteria,
 Allergens — Pollen, pet dander, fungi,
fungus (Histoplasma) and protozoa
dust mites
(Pneumocystis carinii).
 Cold air
 Treatment of these organisms requires
specific drug therapy, and, in the case of
 Pollutants
protozoa and fungi, the organisms are
very difficult to kill.
 Cigarette smoke The bronchospasm that occurs may be the
result of the increased release of certain
 Strong emotions inflammatory mediators such as histamine,
prostaglandins and bradykinin that, in the
 Exercise early stages of asthmatic response, promote
bronchoconstriction rather than inflammation.
 Respiratory tract infections

Late phase of asthma:


Clinical Classification of Asthma
 The late phase of asthma can occur
 Mild intermittent : Attacks occur 2 times several hours after the initial onset of
per week or less symptoms and manifests mainly as an
inflammatory response.
 Mild persistent : Attacks occur more than
2 times per week  The primary mediators of inflammation
during the asthmatic response are the
 Moderate persistent : Attacks occur daily
white blood cells Eosinophils that
or almost daily and are severe enough to
stimulate mast cell degranulation and
affect activity
release substances that attract other white
cells to the area.
 Severe persistent : Attacks are very
frequent and persist for a long period of
 Subsequent infiltration of the airway
time; attacks severely limit activity
tissues with white blood cells such as
Neutrophils and lymphocytes also
Early phase of asthma:
contributes to the overall inflammatory
The early phase of asthma is characterized response of the late phase of asthma.
by:
Manifestations of asthma :
a. marked constriction of bronchial
 Coughing, wheezing
airways (bronchospasm)
 Difficulty breathing
b. edema of the airways
 Rapid, shallow breathing
c. production of excess mucus.
 Increased respiratory rate
 Excess mucus production severity of the asthma attacks and may
include the following:
 Significant anxiety
 1. Avoidance of triggers, and allergens.
Staging of the Severity of an Acute Asthma Improved ventilation of the living spaces,
Attack use of air conditioning.

 Stage I (mild)  2. Bronchodilators (examples: albuterol,


terbutaline):
 Mild Dyspnea
 Short acting β-Adrenergic receptor
 Diffuse wheezing activators. May be administered as
needed in the form of a nebulizer
 Adequate air exchange solution using a metered dispenser
or may be given subcutaneously.
 Stage II (moderate)
These drugs block
 Respiratory distress at rest bronchoconstriction but do not
prevent the inflammatory
 Marked wheezing response.

 Stage III (severe)  3.Xanthine drugs (example: theophylline) :

 Marked respiratory distress  Cause bronchodilation and also inhibit


the late phase of asthma.
 Cyanosis
 These drugs are often used orally as
 Marked wheezing or second-line agents in combination with
absence of breath sounds other asthma therapies such as
steroids.
 Stage IV (respiratory failure)
 Drug like theophylline can have
 Severe respiratory distress, significant central nervous system,
lethargy, confusion, cardiovascular and gastrointestinal
prominent pulsus side effects that limit their overall
paradoxus usefulness.

Possible complications of asthma can  4.Cromolyn sodium :


include :
 Anti-inflammatory agent that blocks
 Severe acute Asthma (status asthmatics), both the early and late phase of
which is a life-threatening condition of asthma. The mechanism of action is
prolonged bronchospasm that is often not unclear but may involve mast cell
responsive to drug therapy. function or responsiveness to
allergens.
 Pneumothorax : is also a possible
consequence as a result of lung pressure  5. Anti-inflammatory drugs
increases that can result from the extreme (corticosteroids) :
difficulty involved in expiration during a
prolonged asthma attack.  Used orally or by inhalation to blunt
the inflammatory response of
 Respiratory failure: marked hypoxemia asthma.
and acidosis might occur.  The most significant unwanted
effects occur with long-term oral
Treatment of asthma: use of corticosteroids and may
include immunosuppression ,
The appropriate drug treatment regimen for increased susceptibility to
asthma is based on the frequency and infection, osteoporosis and effects
on other hormones such as the • Dyspnea
glucocorticoids.
• Hypoxia, cyanosis
 6. Leukotrienes modifiers (example:
Zafirlukast) : New class of agents that • Symptoms of cor pulmonale
blocks the synthesis of the key
inflammatory mediators, leukotrienes. • Fluid accumulation (edema) in later
stages

Treatment of chronic bronchitis:


2) Bronchitis
1. Cessation of smoking or exposure to
 Bronchitis is an obstructive respiratory irritants
disease that may occur in both acute and
chronic forms. 2. Bronchodilators to open airway passages
 Acute bronchitis: Inflammation of the
3. Expectorants to loosen mucus
bronchial passages most commonly
caused by infection with bacteria or 4. Anti - inflammatory to relieve airway
viruses. inflammation and reduce mucus secretion
 Acute bronchitis is generally a self-limiting
condition in healthy individuals but can 5. Prophylactic antibiotics for respiratory
have much more severe consequences in infections
individuals who are weakened with other
illness or who are immunocompromised. 6. Oxygen therapy
 Symptoms of acute bronchitis often
include productive cough, Dyspnea and
possible fever.
 Chronic bronchitis: Chronic bronchitis is a 3) Emphysema
chronic obstructive pulmonary disease
that is most frequently associated with  Emphysema is a respiratory disease that
cigarette smoking (approximately 90% of is characterized by destruction and
cases). permanent enlargement of terminal
 Chronic bronchitis may also be caused by bronchioles and alveolar air sacs
prolonged exposure to inhaled particulates
such as coal dust or other pollutants.
 The disease is characterized by excess
mucus production in the lower respiratory
tract. This mucus accumulation can impair
function of the ciliated epithelium and
lining of the respiratory tract and prevent
the clearing of debris and organisms. As a
result, patients with chronic bronchitis  Well over 95% of all patients with
often suffer repeated bouts of acute emphysema were chronic cigarette
respiratory infection. smokers. Although the exact etiology of
 Chronic bronchitis sufferers are often emphysema is still uncertain,
referred to as “blue bloaters” as a result of
the cyanosis and peripheral edema that is  Chronic exposure to cigarette smoke
often present. causes chronic inflammation of the
alveolar airways, which results in
Manifestations of chronic bronchitis: infiltration by lymphocytes and
macrophages.
• Productive, chronic cough
 Excess release of protease enzymes such
• Production of purulent sputum as trypsin from lung tissues and
leukocytes can digest and destroy the
• Frequent acute respiratory infections elastic walls of the alveoli.
 Levels of a protective enzyme α-1- o Pneumothorax is the entry of air into the
antitrypsin have been shown to be lacking pleural cavity in which the lungs
in certain individuals who are chronic reside.
cigarette smokers. This enzyme o In order for normal lung expansion to
inactivates destructive protease enzymes occur, there must be a negative pressure
(trypsin) in lung tissue. within the pleural cavity with respect to
atmospheric pressure outside the pleural
 In fact, a rare form of emphysema occurs cavity. The inside of the pleural cavity is
in individuals who are not cigarette essentially a vacuum and when air enters
smokers but who have a genetic lack of the pleural cavity the negative pressure is
α-1-antitrypsin. lost and the lungs collapse.
o Because each lung sits in a separate
Mainly caused by: Loss of alveolar (lung) pleural cavity, pneumothorax of one plural
elasticity and a decrease in the overall surface cavity will not cause collapse of the other
area for gas exchange within the lungs. lung.

Manifestations include the following: Types of pneumothorax:

 Tachypnea (increased respiratory rate): 1. Open or communicating pneumothorax


Because that is effective in maintaining
arterial blood gases, one does not usually • Usually involves a traumatic chest
see hypoxia or cyanosis until the end wound.
stages of the disease.
• Air enters the pleural cavity from the
 Barrel chest from prolonged expiration. atmosphere.

 Lack of purulent sputum. • The lung collapses due to equilibration of


pressure within the pleural cavity with
 Possible long-term consequences, atmospheric pressure.
including cor pulmonale , respiratory
failure.

Comparison of Symptoms for Chronic


Bronchitis and Emphysema

2. Closed or spontaneous pneumothorax

• Occurs when air “leaks” from the lungs


into the pleural cavity.

• May be caused by lung cancer, rupture,


pulmonary disease.

• The increased plural pressure prevents


lung expansion during inspiration and the
lung remains collapsed.
Restrictive Pulmonary Disorders
3. Tension pneumothorax
1) Pneumothorax
• A condition in which there is a one-way due to blockage of the airways or
movement of air into but not out of the compression of the alveolar sacs.
pleural cavity.
 Types of atelectasis:
• May involve a hole or wound to the
pleural cavity that allows air to enter and 1. Absorption atelectasis
the lung to collapse. Upon expiration, the
hole or opening closes, which prevents the • Results when the bronchial passages are
movement of air back out of the pleural blocked with mucus, tumors or edema
cavity.
• May occur with conditions such as chronic
• A life-threatening condition because bronchitis or cystic fibrosis in which there is the
pressure in the pleural cavity continues to accumulation of excess mucus in the respiratory
increase and may result in further lung passages
compression or compression of large
blood vessels in the thorax or the heart. 2. Compression atelectasis

• Occurs when lung tissue is compressed


externally by air, blood, fluids or a tumor

 Manifestations of atelectasis:

• Dyspnea, cough.

• Reduced gas exchange.

• Shunting of blood to areas of the lungs that are


inflated. The ventilation– perfusion coupling ability
of the lungs will help ensure that blood is directed
to areas of the lungs where gas exchange can
 Manifestations of pneumothorax: still occur.

• Tachypnea, Dyspnea Treatment of atelectasis:

• Chest pain • Removal of airway blockage

• Possible compression of thoracic blood vessels • Removal of air, blood, fluids, tumors, etc. that
and heart, especially with tension pneumothorax are compressing lung tissues

 Treatment of pneumothorax:

• Removal of air from the pleural cavity with a 3) Bronchiectasis


needle or chest tube
 It is a condition that results from prolonged
• Repair of trauma and closure of opening into injury or inflammation of respiratory
pleural cavity airways and bronchioles.

 It is characterized by abnormal dilation of


the bronchus or bronchi. It is most
frequently associated with chronic
respiratory disease, infections, cystic
fibrosis, tumor growth or exposure to
respiratory toxins.
2) Atelectasis
 The major manifestations of
 Atelectasis is a condition in which there is bronchiectasis are impaired ventilation of
incomplete expansion of lung tissues the alveoli, chronic inflammation and
possible fibrosis of the areas.
 • Diuretics to reduce edema

Adult respiratory distress syndrome (ARDS)  • Correction of acid–base balance

 ARDS is a syndrome associated with


destruction of alveolar membranes and
their related capillaries. It may occur as a
result of direct injury to the lungs or as a
result of dramatic decreases in blood flow Respiratory distress syndrome of the
to the lung (“shock lung,”. newborn

Possible Causes of ARDS  The etiology of newborn respiratory


distress syndrome differs considerably
 Septicemia, uremia from that of the adult disorder.

 Trauma  Respiratory distress in the newborn is


most commonly caused by a lack of
 Near drowning surfactant in the lungs.

 Inhalation of toxic gases or agents  Pulmonary surfactant is a mixture of lipids


and proteins produced by Type II cells of
 Aspiration of gastric contents the alveoli.

 Widespread pneumonia  A thin layer of surfactant covers the


surfaces of the alveoli and provides
 Drug overdose surface tension that prevents the thin-
walled alveoli from collapsing.
 Systemic shock
 Surfactant also moistens the alveolar
Manifestations of ARDS surfaces to facilitate gas exchange.
 • Dyspnea, tachypnea.  Respiratory distress syndrome of the
newborn occurs most commonly in infants
 • Hypoxemia: CO2 is significantly more
who are born prematurely and whose
water soluble than O2 and can still be
lungs have not developed to the point
eliminated from the lungs via diffusion; as
where they are producing adequate
a result blood levels of oxygen are more
surfactant.
affected by ARDS than CO2. Hypocapnia
may result.  Clinical manifestations become evident
immediately at birth and can be rapidly
 • Infiltration of lung tissues with immune
fatal if not treated.
cells that release inflammatory mediators.
Manifestations of respiratory distress
 • Accumulation of fluids in alveoli and
syndrome in the newborn
around alveolar spaces.
 • Rapid, shallow breathing
 • Changes in blood pH due to altered
blood levels of CO2.  • Lung collapse
 • Pulmonary fibrosis.  • Lung inflammation and damage
 • Respiratory failure.  • Hypoxemia
Treatment of ARDS  • Nasal flaring, grunting upon inspiration
 • Oxygen therapy Treatment of respiratory distress syndrome in
the newborn
 • Anti-inflammatory drugs
 • Delay or prevention of premature A) Acute
delivery of infant if possible.
 Pneumothorax
 • Treatment of premature newborn with
synthetic surfactant delivered directly into  Drug overdose (opioids, sedatives)
the lower respiratory tract. Exogenous
surfactant will need to be supplied until the  Pleural effusion — Accumulation of fluids
infant’s lungs have matured to the point in the pleural cavity
where they are producing their own
surfactant.  Airway obstruction

 • Mechanical ventilation.  Status asthmaticus

 • Injection of cortisol in the mother prior to  Inhalation of toxins or noxious gases.


delivery may significantly reduce the
B) Chronic
incidence of respiratory distress syndrome
in premature infants.  Emphysema
 Cortisol has also been shown to stimulate  Interstitial lung diseases
activity of Type II cells.
 Cystic fibrosis

 Spinal cord or brain injury


Respiratory Failure
 Congestive heart failure
 Respiratory failure is a condition that
results when the lungs are no longer able  Neuromuscular disorders: Muscular
to oxygenate the blood sufficiently or dystrophy, myasthenia gravis, amyotrophic
remove CO2 from it. lateral sclerosis
 It may occur as:  Pulmonary emboli
 the end result of chronic respiratory  Diffuse pneumonia
diseases, or it may be an acute event
caused by factors such as neumothorax or  Pulmonary edema
Opioid drug overdose
Treatment of respiratory failure:
Manifestations of respiratory failure
• Bronchodilators
 • Hypoxemia.
• Correction of blood pH
 • Hypercapnia
• Oxygen therapy
 • Cyanosis, possible but not always
present. • Mechanical ventilation

 • Central nervous system symptoms:


Slurred speech, confusion, impaired motor
function

 • Altered blood pH

 • Initial tachycardia and increased cardiac


output followed by bradycardia and
decreased cardiac output

Causes of Respiratory Failure

You might also like