RESPIRATORY SYSTEM Part 1 of 2

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 In the upper airways-
 Filtering mechanisms in the nasal cavity trap and
eliminate larger particles. Two reflexes: sneezing and
coughing.

 In conducting airways-
 Mucous and cilia

 In alveoli-
 Alveolar macrophages
 Interplay between the alveolar macrophages and T
and B lymphocytes

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 Ossification of ribs and stiffness of joints resulting
in increased work of breathing.
 Loss of elasticity in the chest
 Increased risk of sleep apnoea because of reduced
blood O2 levels
 Decreased efficiency of the respiratory system’s
protective mechanisms
 Ciliary activity of the mucosa decreases, and the
phagocytes in the lungs become sluggish

 Outcome??
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 Infections and inflammations:
 The Common Cold
 Sinusitis and Rhinitis
 Influenza
 Pneumonia/Legionnaire’s Disease
 Tuberculosis
 Lung cancer

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A.k.a. viral rhinitis (inflammation of the nasal mucosa)

Demographics:
 Most adults have 2 – 4 colds a year.
 The average school child may have up to 10.

Aetiology:
 Viral infection of the upper respiratory tract
associated with more than 200 viruses.

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Pathophysiology:
 Shedding of viruses usually picked up by the

fingers.
 Contamination through nasal mucosa and/or

conjunctiva.
 Highly contagious in the first three days from

onset of symptoms and incubation period is 5

days.
 Viruses invades mucous cells and reproduce

 Inflammation response ensues

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Symptoms:
 Feelings of dryness and stuffiness affect the

nasopharynx, accompanied by excessive

production of nasal secretions and tears.
 Usually the secretions remain clear and watery.

Also headaches and general malaise.

Treatment:
 Rest and antipyretic drugs

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 Sinusitis:
Inflammation of the paranasal sinuses

 Rhinitis:
Inflammation in the nasal mucosa.

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 Major causes of infections:
 Swelling obstructing sinus openings and impairing
mucociliary function
 Low oxygen content of the sinuses:
 Encourages opportunistic growth of micro-organisms
 Impairs local defense mechanisms
 Alters function of immune cells

 Inflammation promoted by:

 Upper respiratory tract infections
 Allergic rhinitis
 Nasal polyps
 Swimming and diving
 Airline travel
 Abuse of nasal decongestants
 Contagious dental infection
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 a. Sinusitis
 3 types
 Acute
 Sub-acute
 Chronic

 Symptoms of chronic
sinusitis include
– Same as common cold +
– Facial pain
– A sense of fullness in the ears
– Headache
– Postnasal drip
– Purulent nasal discharge
– Hoarseness
– Decreased sense of smell
– Chronic cough
– Fever
– Unpleasant breath
– Pain on bending

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 Treatment:
 Antibiotics
 Drainage of sinuses with topical and oral
decongestants or anti-histamines

 Allergic rhinitis – a.k.a. hay fever

 Similar symptoms to colds
 Aetiology: allergens
 An immunological reaction

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 Influenza spreads around
the world in seasonal
epidemics resulting in the
deaths of between 250,000
and 500,000 people every
year, up to millions in
some pandemic years. On
average 41,400 people
died each year in the
United States between
1979 and 2001 from
influenza.
 Predominantly an upper
respiratory tract infection
with the occasional spread
to the lower tract.

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 In April 2009 a novel flu strain
evolved that combined genes
from human, pig, and bird flu,
initially dubbed "swine flu" and
also known as influenza
A/H1N1, emerged in Mexico,
the United States, and several
other nations. The World Health
Organization officially declared
the outbreak to be a pandemic
on June 11, 2009 (see 2009 flu
pandemic).
 The WHO's declaration of a
pandemic level 6 was an
indication of spread, not
severity, the strain actually
having a lower mortality rate
than common flu outbreaks.

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 Although it is often confused with other influenza-like
illnesses, especially the common cold, influenza is a
more severe disease than the common cold and is
caused by a different type of virus.[
 Viral infection that can affect the upper and lower
respiratory tracts. Can cause:
 Rhinotracheitis
 Respiratory viral infection followed by bacterial infection
 Viral pneumonia

 Usually occurs in epidemics or pandemics.

 Two types of infection; types A and B.
 Incubation period is from 1 – 4 days, usually 2.
 People are infectious 1 day before their symptoms begin.
 Peaks in 3 – 5 days, finished in 7 – 10 days.

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Pathophysiology:
 Necrosis and shedding
of serous and ciliated
cells
 Seeping of extracellular
fluid
 Serous cells form quicker
than ciliated cells

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 Symptoms:
 Fever, chills, malaise,
muscle aching,
headache, nasal
discharge, non-
productive cough, and
sore throat.

Complications:
 include; sinusitis, otitis
media, bronchitis, and
bacterial pneumonia
(post-infection).

It can be difficult to distinguish between the common cold and influenza in the early
stages of these infections, but a flu can be identified by a high fever with a sudden
onset and extreme fatigue. Diarrhea is not normally a symptom of influenza in adults.

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Treatment:
 Rest, keeping warm, drinking lots of water- avoid
alcohol and tobacco.
 Anti-viral drugs (Tamiflu) if taken early (slight
reduction)
 Immunisation recommended for high risk groups
 Efficacy depends on age, immuno-competency, and match b/n
virus strains in vaccine and those in circulation
 The Centre’s for Disease Control and Prevention update the
composition of the vaccine yearly, to compensate for mutations
occurring in the viruses.

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 The term pneumonia describes the inflammation of the
parenchymal structures of the lungs (lower respiratory
tract) such as the alveoli and the bronchioles.

 Infectious and non-infectious causes (fumes or

gastric contents).
 Pneumonia is an important cause of death within
the elderly population, even with the use of
antibiotics.

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 Typical (bacterial) pneumonia is characterised
by chills and fevers, severe malaise, purulent
sputum, elevated white blood count, and patchy
or lobar infiltrates seen on the chest radiograph.

 Atypical (non bacterial) pneumonia is less severe

 Pneumonia is being classified as either

community acquired or hospital acquired (must
be diagnosed within 48 hours of hospitalisation.)

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 Legionnaires' disease acquired
its name in July 1976 when an
outbreak of pneumonia
occurred among people
attending a convention of the
American Legion in
Philadelphia. On January 18,
1977 the causative agent was
identified as a previously
unknown bacterium,
subsequently named Legionella.

 The fatality rate of Legionnaires'

disease has ranged from 5% to
30% during various outbreaks.
According to the journal,
hospital-acquired Legionella
pneumonia has a fatality rate of
28%.

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 In April 2000, an outbreak of Legionella pnemophila
serogroup 1 occurred in Melbourne, Australia.

 The outbreak resulted in 125 confirmed cases of

Legionnaire's disease, with 95 (76%) hospitalised.
It is reported that 4 died from the outbreak. The
investigation traced the source of the infection to
the cooling tower at the newly opened aquarium.

 Since this outbreak, legionella infection statistics are

required to be reported by the state government as
a notifiable disease.

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 Legionellosis infection normally occurs after inhaling an aerosol
(suspension of fine particles in air) containing Legionella bacteria.
Such particles could originate from any infected water source.

 When mechanical action breaks the surface of the water, small

water droplets are formed, which evaporate very quickly. If these
droplets contain bacteria, the bacteria cells remain suspended in
the air, invisible to the naked eye and small enough to be inhaled
into the lungs.

 This often occurs in poorly ventilated areas such as prisons where

a condensating air conditioner can spread it throughout the entire
room, infecting anyone not immune to the strain of bacteria.

 Potential sources of such contaminated water include cooling

towers used in industrial cooling water systems as well as in large
central air conditioning systems, evaporative coolers, hot water
systems, showers, windshield washers, whirlpool spas,
architectural fountains, room-air humidifiers, ice making
machines, misting equipment, and similar disseminators that
draw upon a public water supply.
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 Patients with Legionnaires' disease usually have
fever, chills, and a cough, which may be dry or
may produce sputum.

 Some patients also have muscle aches, headache,

tiredness, loss of appetite, loss of coordination
(ataxia), and occasionally diarrhea and vomiting.
Laboratory tests may show that patients’ renal
functions, liver functions and electrolytes are
deranged, including hyponatremia. Chest X-rays
often show pneumonia with bi-basal consolidation.
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 Risk of catching Legionnaires rises with:
 Smoking
 Chronic diseases
 Impaired cell-mediated immunity
 Symptoms appear 2 – 10 days after infection.
 As well as the lungs being involved, there is
CNS and GIT involvement.
 Treated with antibiotics.

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 One third of the world's
population is thought to
be infected with M.
tuberculosis,[ and new
infections occur at a rate
of about one per second.
 In the past, tuberculosis
has been called
consumption, because it
seemed to consume
people from within,
with a bloody cough,
fever, pallor, and long
relentless wasting.

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 The foremost cause of death from a single infectious agent.

Aetiology:
 Mycobacterium tuberculosis, a slender, rod shaped,
aerobic bacteria that do not form spores.
 Mycobacterium tuberculosis hominis: airborne
 Mycobacterium tuberculosis bovis: from milk
 Its waxy outer capsule makes it more resistant to
destruction. It can survive in old necrotic tissue and
calcified lesions, capable of reinitiating growth.
Pathophysiology:
 The tubercle bacillus has no known antigens to stimulate an
early immunoglobulin response (B cell); instead the host mounts
a delayed-type cell-mediated immune response (T cell).

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Two types: primary or reactivated-
Primary:
 In people with no previous contact to tubercle bacillus
 Inhalation of droplet nuclei that has implanted on
respiratory bronchiole or alveolus then engulfed by
macrophages where it multiplies
 Growth of organisms for 2-12 weeks before eliciting
immune response
 Degradation of some mycobacteria by macrophage and
presentation of antigens to T-cells which initiates a cell-
mediated immune response.

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 Formation of Ghon’s foci (circumscribed
granulomatous lesion containing tubercle bacilli,
modified macrophages, and other immune cells.)
 Scar tissue formation and encapsulation of
primary lesion, then calcification visible on X-
rays.
 Occasionally, primary tuberculosis may progress
to other parts of the respiratory system or the
body.

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Reactivated Tuberculosis:
 Reactivation of a previously healed primary
lesion often from impaired immunity
 Hypersensitivity reaction occurs leading to
cavitation and bronchial dissemination.
 Cavities may coalesce to 10-15 cm in
diameter, pleural effusion and tuberculous
empyema are common as disease progresses

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Symptoms:
Mostly asymptomatic because of no immediate
immunology defense from the the body and the
fact that TB grows slowly.
 Primary: asymptomatic
 Progressive primary or reactivation: mild fever,
night sweats, easy fatigability, anorexia, and
weight loss. Dry cough becoming productive
and purulent, may contain blood. Then dyspnea
and orthopnea.

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Diagnostic:
 Tuberculin skin test positive with Mantoux
test
 Calcified regions on X-rays

Treatment:
 Drugs (often multiple) for long periods of
time.
 Vaccine: BCG (Bacillus Calmette-Guérin)

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Pathophysiology 2 - Naturopathy -
Véronique Gouneau - 2008 33
Lung cancer is the leading cause of cancer
death in Australia.
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It is estimated that 80% of lung cancers are associated to
smoking. One in ten smokers will contract lung
cancer.

 Because cancer of the lung is usually far

advanced before it is discovered, the prognosis is
generally poor.
 The overall 5 year survival rate is 13 – 15%, a
dismal statistic that has not changed since the
late 1960s.
 Bronchogenic carcinoma, constitutes 90 – 95% of
all lung cancers.

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 Bronchogenic carcinomas can be divided into
four major categories:
 squamous cell lung carcinoma
 Adenocarcinoma
 small cell carcinoma
 and large cell carcinoma.

 Aetiology:
 Smoking
 Industrial hazards (radiation/ gases etc)
 Genetics
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Manifestations of lung cancer can be divided into
three categories.
 Those due to lung involvement & adjacent structures.
 The effects of local spread and metastasis.
 Involvement of endocrine, neurologic and connective
tissue function.

Diagnosis:
Chest x-ray and biopsy.
 As with other cancers, weight loss occurs.

Treatment:
 Depends on type of cancer and age of patient.
 Combinations of surgery, irradiation and chemotherapy
are used.

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Symptoms:
The main symptoms are:
 Chronic cough/ a new cough

 Breathlessness/ wheezing

 chest pain due to tissue invasion (retrosternal)

 coughing up blood (hemoptysis)

Other symptoms include fatigue, weight loss, shortness

of breath, hoarseness, and difficulty swallowing, but
there are often seen in people with advanced cancer.
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 A paraneoplastic syndrome is a disease or symptom that
is the consequence of the presence of cancer in the body,
but is not due to the local presence of cancer cells. These
phenomena are mediated by humoral factors (by
hormones or cytokines) excreted by tumor cells or by an
immune response against the tumor.

 Paraneoplastic syndromes are typical among middle

aged to older patients, and they most commonly present
with cancers of the lung, breast, ovaries or lymphatic
system (a lymphoma).

 Sometimes the symptoms of paraneoplastic syndromes

show even before the diagnosis of a malignancy.

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 Among most commonly seen Paraneoplastic Syndromes
are:

 Blood clot formation in cancer of pancreas

 Low Sodium Level in Small Cell Lung Cancer
 High Calcium Levels in various cancers
 Fever
 Eaton Lambert Syndrome
 Myasthenia Gravis due to Thymoma
 Nerve Dysfunctions due to various cancers
 Anemia

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 The most common
sites for metastases
are the brain bone and
liver.

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