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Obstructive Pulmonary
Disease
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Characterized by airway obstruction that is increased
with expiration.
More force is required to expire a given volume of
air, or emptying of lungs is slowed, or both.
The most common obstructive diseases are asthma,
chronic bronchitis, and emphysema.
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COPD
Asthma Emphysema
ChronicBronchitis
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• Many people have both chronic bronchitis and
emphysema, and together these are often called
chronic obstructive pulmonary disease - COPD
• Major symptom of obstructive pulmonary disease
is dyspnea, and wheezing.
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COPD
Asthma Emphysema
ChronicBronchitis
Clinical Diagnosis
Physiologic Diagnosis PathologicDiagnosis
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1- Bronchial Asthma
• More intermittent and acute than COPD.
• It is a reversible disorder
• It occurs at all ages.
• Runs in families, so evidence genetics plays a role.
• Environmental factors interact with inherited
factors to increase the risk of asthma.
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• Childhood exposure to high levels of allergens,
smoking and/or respiratory viruses increases chances
of developing asthma.
• Major events in acute asthma attack are
–bronchiolar constriction,
–mucus hyper-secretion
– inflammatory swelling.
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Pathogenesis
• Smooth muscle spasm in bronchioles.
• Vascular congestion.
• Edema formation.
• Production of thick mucus.
• Impaired muco-ciliary function.
• Thickening of airway walls.
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• Untreated, this can lead to airway damage that is
irreversible.
• Obstruction increases resistance to air flow and
decreases flow rates
• Impaired expiration causes hyperinflation of
alveoli, and increases the work of breathing
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Clinical manifestations
• Dyspnea
• Sometimes, cough
• Wheezing
• Attacks may continue from few hours to days or
even weeks.
• During remission individual is asymptomatic and
pulmonary function tests are normal
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2- Chronic Bronchitis
• Hyper-secretion of mucus and chronic productive
cough for at least 3 months of the year for at least
two consecutive years.
• Incidence may be increased up to 20 times in
persons who smoke and more in persons exposed
to air pollution.
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Pathophysiology
• Inspired irritants result in inflammatory cell
infiltration into the bronchial wall.
• Causes bronchial edema and increases size and
number of mucus glands and goblet cells.
• Mucus is thick, and can’t be cleared because of
impaired ciliary function.
• Increases susceptibility to infection and injury
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• Initially affects only larger bronchi, but eventually all
airways involved.
• Airways collapse in early expiration, blocked by mucus
leads to hypo-ventilation
• Hypoxemia
• Air trapping prevents respiratory muscles from functioning
efficiently (barrel chest).
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Barrel Chest
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Treatment
• Best treatment is PREVENTION.
• Stop smoking ------ halts progression of the disease
• Bronchodilators, expectorants, and chest physical
therapy.
• Acute attacks may require antibiotics, and steroids.
• Oxygen therapy may be required
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3- Emphysema
• Abnormal, permanent enlargement of the gas-
exchange airways and destruction of the alveolar
walls.
• Obstruction results from changes in lung tissue
rather than mucus production and inflammation
(pathological changes).
• Major mechanism is loss of elastic recoil
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• Major cause is smoking
• Other causes are air pollution and recurrent
respiratory infections
• Primary emphysema linked to an inherited
deficiency of the enzyme alpha 1- antitrypsin
which can affect lung tissue.
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Normal Lung versus Emphysema
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Normal Lung versus Emphysema
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Pathophysiology
• Begins with the destruction of the alveolar septa, which
eliminates portions of the capillary bed, and increases
the volume of air in the alveolus.
• Continued alveolar loss and loss of elastic recoil
• Expiration becomes difficult, causing hyperexpansion
of the chest
• These are not effective in gas exchange and result in
hypoxia.
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Clinical manifestations
• Dyspnea at rest
• Barrel chest
• Minimal wheezing
• Prolonged expiration
• Hypoventilation and hypoxia
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Pursed Lip Breathing
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Atelectasis
• Collapse or incomplete expansion of part or
all of the lung
• Types:
– Resorption (obstruction of airway).
– Compressive (pleural effusion or pneumothorax)
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Bronchiectasis
Dilatation of bronchi and bronchioles secondary to
chronic inflammation
Associated conditions
Obstruction
Cystic fibrosis
Immotile cilia syndromes
Necrotizing pneumonia
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Respiratory Failure
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Respiratory Failure (RF)
• The inability of the lungs to adequately oxygenate the
blood and to clear it of carbon dioxide. RF could be :-
• Acute RF:
– Acute Respiratory Distress Syndrome (ARDS)
– Pulmonary embolism
– Direct injury to the lungs, airways or chest wall
– Indirect due to injury of another body system, as
brain.
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• Chronic respiratory failure
–Due to progressive hypoventilation from
airway obstruction or restrictive disease
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• Respiratory failure always presents with:-
– Dysnpea always present, but may be difficult to detect
a change in a chronic patient
– Since nervous tissue is highly oxygen-dependent ---
• Drowsiness, Memory and visual impairment,
• Headache due to increased intracranial
pressure due to cerebral vasodilatation
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1- Hypoxic Respiratory Failure
2- Hypoxic-Hypercapnic Respiratory Failure
Two principal patterns:
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1- Hypoxic Respiratory Failure:
Seen when pO2 {oxygen partial pressure} falls to
or below 60 mm Hg
Typically seen in:-
• chronic bronchitis and emphysema.
• lung consolidation due to bacterial infection (pneumonia).
• in lung collapse,
• pulmonary hypertension,
• pulmonary embolism and ARDS.
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• With a progressive lowering of pO2, more
widespread tissue damage and loss of
consciousness can occur.
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2- Hypoxic-Hypercapnic Respiratory Failure
• When arterial pCO2 {Carbon dioxide partial
pressure} (normally 40 mm Hg) exceeds 45 mm HG,
condition is called hypercapnia
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• Most often caused by airway obstructive conditions,
and hypoventilation from CNS problem, thoracic
cage or neuromuscular abnormalities.
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• Attempts to compensate include increased heart
rate and vasodilatation, which produces warm,
moist skin.
• CNS effects produce muscular tremors, drowsiness
and coma.
• Hypercapnia also produces acidosis.
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ARDS
• Mortality in persons < 60 is 40%
• Those over 65 and immunocompromised still have
mortality over 60 %
• Most survivors have almost normal lung function 1 year
after acute illness.
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Clinical manifestations:
• Symptoms developed progressively:
– Hyperventilation → respiratory alkalosis →
dyspnea and hypoxemia → metabolic acidosis →
respiratory acidosis → further hypoxemia →
hypotension, decreased cardiac output, death
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Evaluation and Treatment
• Diagnosis based on physical examination, blood gases
and imaging
• Treatment is based on early detection, supportive
therapy and prevention of complications, esp. infection
• Often requires mechanical ventilation.
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Tumors of the Lung
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Carcinoma of the Lung
• 7% of all deaths
• More common in males than females
Causes
85-95% smoking
1% asbestos + smoking (estimate)
Rare arsenic, chromium, nickel,
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Classification of Lung Carcinoma (Major Types)
• Squamous cell carcinoma 35%
• Adenocarcinoma 30%
• Small cell carcinoma 25%
• Large cell carcinoma 10%
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Squamous cell carcinoma
• Frequency: 35%
• Smoking: X 25 (increased risk)
• Males > females
• Survival (5 years): 15 - 20%
• Arises in bronchial squamous metaplasia
• Centrally located
• May cavitate
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Squamous cell carcinoma
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Adenocarcinoma
• Frequency: 30%
• Smoking: X 3
(increased risk)
• Males < females
• Survival (5 years): 15 -
20%
• Peripheral
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Bronchiolo-alveolar carcinoma
• Frequency: 2 %
• Smoking
• Males = females
• Survival (5 years): 25-40 %.
• Single or multiple tumor nodules
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Small cell carcinoma
• Frequency: 25 %
• Smoking: 95% of patients
• Males >> females
• Survival (5 years): 1 - 5 %.
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Small cell carcinoma
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Large Cell Carcinoma
• Frequency: 10 %
– Gross picture: Peripheral lesion
• Microscopic
–Wastebasket group of tumors that do not fit the
criteria of a squamous cell carcinoma,
adenocarcinoma, or small cell carcinoma
– Prognosis: Similar to adenocarcinoma
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Large Cell Carcinoma
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Mesothelioma–Malignant tumor of mesothelial cells
– Highly malignant neoplasm with short survival
–Most patients (70%) have an asbestos exposure
history
• Asbestos exposure also increases the risk of
pulmonary cancer
• Smoking is not related to mesothelioma
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