RESPIRATORY SYSTEM Part 2 of 2

 Obstructive airway disorders:

 Asthma

 Chronic obstructive pulmonary diseases:

 Chronic bronchitis
 Emphysema
 Cystic Fibrosis (genetic)

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 The ANS controls the contraction or
relaxation of the smooth muscles by adjusting
the diameter of the airways.
 The parasympathetic nervous system produces
bronchial constriction (via the vagus nerve)
 The sympathetic nervous system increases
bronchodilation.

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 Normal:
 Bronchodilation effects by stimulation of the
sympathetic nervous system.
 Slight bronchoconstriction effect because of inhibition of
the parasympathetic nervous system (especially during
exercise).

 Pathological:
 The binding of an antigen on sensitised mast cells
promotes the release of inflammatory mediators
(mostly histamine) in the airways.
 These inflammatory mediators act on smooth muscles
of the airways and promote bronchoconstriction.

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 Asthma is Australia's most
widespread chronic (long-
term and persistent) health
problem.

 It affects over 2 million

Australians: 1 in 7 primary
school-aged children, 1 in 8
teenagers and 1 in 9 adults.
At present the cause of
asthma is not known and
there is no cure.

 www.asthmaaustralia.org.au/
 www.nationalasthma.org.au/
 www.asthma.org.au/

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 Prevalence:
 In 2004-05, 10% of people (about 2 million) in
Australia reported that they had asthma.

http://www.abs.gov.au/Ausstats/abs@.nsf/39433889d406eeb9ca2570610019e9a5/0b8f928452bc9647ca256e7a
0080829b!OpenDocument#In%202004-05%2C%20after%20adjusting%20for%20a 6
 Definition:
 A chronic inflammatory disorder of the airways
promoted by certain cells such as mast cells,
eosinophils, T lymphocytes, and epithelial cells.

 The inflammatory process produces airway

obstruction with wheezing, breathlessness, chest
tightness, and a cough that often is worse at night
than in the early morning.

 Although most symptoms are reversible

spontaneously or with treatment, sensitivity of the
bronchi is enhanced.

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Aetiology:
Allergens
Respiratory tract infections
Hyperventilation
Cold air
Exercise
Airborne pollutants
Drugs and chemicals
Hormonal changes
Emotional upsets
Gastroesophageal reflux

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 Pathophysiology:
 Trigger: either bronchospastic or inflammatory
 Acute/early response (within 10-20 minutes)
Immediate bronchoconstriction of airways on exposure
of irritant
 Antigen binds to IgE coated mast cells on mucosal
surface of airways promoting release of chemical
mediators from mast cells.
 This results in
 Increased mucus secretions
 Mucosal oedema from increased vascular permeability
 Bronchoconstriction

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Path 2 - Naturopathy - 2008 - Véronique
Gouneau 10
 Pathophysiology:
 Late phase response (4-8 hours post exposure)
 May last for several hours/days/weeks
Involves inflammation and increased airway
responsiveness.
 Release of chemical mediators from mast cells,
macrophages and epithelial cells promote migration and
activation of basophils, oesinophils, neutrophils
producing:
 Epithelial injury and oedema
 Changes in mucociliary function
 Reduced clearance of respiratory tract secretions
 Increased airway responsiveness (narrowing of airways)
 Chronic inflammation can lead to airway
remodelling limiting the movement of air within
the airways.
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 Hygiene hypothesis:
 Two types of T helper cells have been found:
 TH1 and TH2
 TH1 is produced in response to microbes
 TH2 is produced in response to allergens and
intestinal parasites
 An infant who does not come in contact with
many diseases has an immune system skewed
towards TH2
 Children who have childhood diseases have
higher levels of TH1 and have a lower incidence of
asthma.
 The absence of these diseases in genetically
predisposed individuals may favour the
production of TH2 in response to environmental
allergens.
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 Symptoms:
 Are wide and range from episodic wheezing, Feelings
of chest tightness, to acute immobilising attack
 May occur spontaneously
 Often worse at night

 During an asthma attack:

 Mild: chest tightness, slight increase in respiratory rate with
prolonged expiration , and mild wheezing + cough
 More severe: use of accessory muscles, distant breath sounds
due to air trapping, and loud wheezing
 If condition progresses: fatigue, moist skin, anxiety and
apprehension, severe dyspnea, unable to speak more than 1
or 2 words before taking a breath.

If airflow markedly decreases: breath sounds inaudible, diminished

wheezing , cough ineffective, respiratory failure

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 Treatment:
 Management of asthma is through
minimizing the factors that trigger an
attack and pharmacological
treatment.
 Minimising the factors:
 Avoiding irritants
 Influenza vaccine recommended for
people with persistent asthma
 Relaxation techniques and controlled
breathing
 Desensitisation

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 Treatment:
 Pharmacological treatment:
 Quick relief: bronchodilators and systemic
corticosteroids
 The acute response can be inhibited or reversed by
bronchodilators but not the anti-inflammatory
response.
 Long-term: On a daily basis: anti-inflammatories,
long-acting bronchodilators, and leukotriene
modifiers.
 Deaths occur outside of hospitals mainly due to a lack
of understanding as to the degree of dyspnea being
suffered.
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 A.k.a. COPD
 Chronic obstruction of air flow in the
pulmonary airways
 Mainly due to smoking
 Progressively worsen unless stimulus is
removed, but damage is permanent and
cannot be reversed.

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 Chronic bronchitis is a
chronic inflammation of the
bronchi (medium-size
airways) in the lungs. It is
generally considered one of
the two forms of chronic
obstructive pulmonary
disease (COPD).
 Chronic bronchitis is
common among smokers. In
Western countries it is
estimated that chronic
bronchitis occurs in
approximately 18% of male
and 14% of female smokers
compared to 7% and 6% of
non-smokers, respectively.

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Pathogenesis:
 Irritants (cigarette smoke) damage the
bronchial wall.
 Inflammation and fibrosis of the bronchial

wall.
 Hyperplasia of submucosal glands and
hypersecretion of mucus.
 Loss of elastic lung fibres and alveolar tissue.

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Diagnosis:
 A history of a chronic productive
cough of more than three months
duration, for more than 2
consecutive years is necessary for a
diagnosis.
 Presence of symptoms indicate that
the disease is very advanced.

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Symptoms:
 Chronic cough with gradual increase of purulent sputum
 Shortness of breath with decreased exercise tolerance
 High vulnerability to lung infections.
 As diseases progresses, breathing becomes difficult even at rest.
 In late stage: oxygen deprivation, cyanosis and peripheral oedema
because of heart failure (right-side)
 Clubbing of fingers in chronic obstructive bronchitis

Patients with chronic bronchitis are classically described as "blue bloaters"

due to the presence of cyanosis and oedema. They have reduced levels of
ventilation and are not very breathless. There are low levels of oxygen in
the blood and high levels of carbon dioxide which can cause other signs
such as bounding pulse, asterixis (flapping of the hands), and in severe
cases, confusion and progressive drowsiness.

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Treatment:
 Removal of the stimulus (smoking)
 Treatment of infections
 Oxygen may be needed or bronchodilators
 Vaccination recommended (flu and pneumonia)

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 A loss of lung elasticity and abnormal
enlargement of the air spaces distal to the
terminal bronchioles, with destruction of the
alveolar walls and capillary beds.

 Aetiology:
 Genetics: deficiency of 1-anti-trypsin, an anti-
protease enzyme that protects the lung from
injury.
 Cigarette smoke and other stimulants causing
movement of inflammatory cells into lungs

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 Pathogenesis:
 Breakdown of elastin and other alveolar wall by
enzymes “proteases” that digest proteins.
 Proteases are released by macrophages and
neutrophils.
 In normal condition 1-anti-trypsin prevents
proteolysis but inflammation increases the
presence of proteases.

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 Symptoms:
 May take years to be noticed: dry cough, pain when
breathing, shortness of breath, wheezing
 Hyperventilation
 Weight loss
 Barrel chest

Patients with predominantly emphysema on the other hand are

described as "pink puffers" as they are very breathless and
hyperventilating (with pursed lips) but have near normal levels
of oxygen and carbon dioxide in the blood. However, these
clinical signs aren't always reliable and do not always correlate
with pathology.

 Treatment:
 Human anti-trypsin is available for replacement therapy in
persons with a hereditary deficiency of the enzyme.

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 Cystic Fibrosis (CF) is a
genetic disease that
affects approximately 1
in 2,500 babies born in
the United States and
about 1 in 25 Caucasian
people are carriers of
the CF gene.

 www.cysticfibrosis.org.a
u/
 www.cysticfibrosis.org.au

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 A.k.a. mucoviscidosis or mucoviscoidosis.
 Definition:
 A multisystem disease causing recurrent chest
infections and pancreatic exocrine dysfunction.
 It affects the body epithelial cells which line the
lungs, the pancreas, the liver, the sweat glands, the
digestive tract and the reproductive organs.
 The disease is caused by the production of an
abnormally viscid mucus that cannot be cleared
from the lungs and causes blockage of the main
pancreatic ducts.

 Aetiology:
 Autosomal recessive disorder of chromosome 7.

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 Pathogenesis:
 In affected individuals, a defective protein is produced
in the membrane of their epithelial cells.
 This protein affects the permeability of chloride ions
and prevents them from leaving the cell.
 The presence of chloride ions in the cell prevents water
and sodium from leaving the cell.
 No or little excretion of water is possible outside the
cells which renders the mucus viscid (thick).

A viscid mucus increases the risk of infections, obstruction of

the airways causing atelectasis (collapse of the lung).

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Symptoms:
 Dyspnea
 Coughing and wheezing
 Fatigue
 Bulky stools
 Steatorrhea
 Salty skin
 Respiratory infections

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 Diagnosis:
 Respiratory and gastrointestinal manifestations
typical of cystic fibrosis:
 Chronic lung disease (cough, dyspnea, etc.)
 Pancreatic exocrine deficiency (steatorrhoea,diarrhoea,
abdominal pain and discomfort)
 Elevated sodium chloride in sweat

 Treatment:
 Replacement of pancreatic enzymes
 Physical measures (percussion) to clear lung
secretions
 Bronchodilator therapy
 Prompt treatment of respiratory tract infection

 Prognosis:
 Median age of survival is 30 years.

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