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3. 2
Objectives • Overview
Obstructive Pulmonary Disorders
OBSTRUCTION FROM CONDITIONS IN THE WALL
OF THE LUMEN
• Asthma
• Acute Bronchitis
• Chronic Bronchitis
OBSTRUCTION RELATED TO LOSS OF LUNG
PARENCHYMA
• Emphysema
OBSTRUCTION OF THE AIRWAY LUMEN
• Bronchiectasis
• Bronchiolitis
• Cystic Fibrosis
• Acute Tracheobronchial Obstruction
• Epiglottitis
• Croup Syndrome

4. OBSTRUCTIVE
PULMONARY
DISORDERS
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5. Overview
• Obstructive lung diseases are manifested by increased resistance to airflow.
• Obstructive diseases of the lung can be classified into those involving
• 1.obstruction from conditions in the wall of the lumen (e.g., asthma, bronchitis)
• 2.obstruction resulting from increasing pressure around the outside of the airway lumen (e.g., emphysema
secondary to loss of lung tissue and elasticity, enlarged lymph node, or tumor)
• 3.obstruction of the airway lumen (e.g., presence of a foreign body, excessive secretions, aspiration of fluids).
These classifications are mainly terms of convenience because many respiratory disease
processes involve several areas of the pulmonary system.
Involvement of the airways produces narrowing of the passages so that airflow
obstruction occurs.
The major obstructive airway diseases are asthma, bronchitis, and emphysema.
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6.  OBSTRUCTIONFROMCONDITIONSINTHEW
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• Asthma
Etiology:
• Asthma is a lung disease characterized by
• (a) airway obstruction that is reversible (but not completely in some patients),
• (b) airway inflammation,and
• (c) increased airway reactivity to a variety of stimuli.
• Airway inflammation leads to epithelial denudation,collagen deposition beneath the
basement membrane,mast cell activation,mucosal edema,increased viscid secretions,and
smooth muscle contraction.
• The immunohistopathologic features of asthma include denudation of airway epithelium,
collagen deposition beneath the basement membrane,edema,mast cell activation,and
inflammatory cell infiltration by neutrophils,eosinophils,and lymphocytes.Inflammation of
the airway contributes to acute bronchospasm (bronchoconstriction),mucosal edema,
mucous plug formation,and airway wall remodeling.
Pathogenesis:
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7. Asthma
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8. •Asthma
(cont.) • Wheezing
• feelings of tightness of the chest
• dyspnea
• cough
• increased sputum production
Clinical manifestation:
Diagnosis:
• The diagnosis of asthma is based on history,physical findings,sputum
examination,pulmonary function tests,blood gas analysis,and chest radiography.
• Pharmacologic therapy for all three major obstructive disorders is similar and
focuses on decreasing inflammation and broncho constriction, including β2
agonists,corticosteroids, leukotriene modifiers,and mastcell inhibitors.
• Patients should be advised to avoid the objects in the environment thattrigger
asthma attacks.
Treatment:
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9. • AcuteBronchitis:
Etiology:
• Acute inflammation of the trachea and bronchi is produced most by a variety of viruses such
as influenza virusA or B, parainfluenza virus, respiratory syncytial virus, coronavirus,
rhinovirus, Coxsackievirus, and adenovirus. Nonviral causes include Streptococcus
pneumoniae, Haemophiles influenzae, mycoplasma, Moraxella, and Chlamydia pneumoniae.
Pathogenesis:
• The airways become inflamed and narrowed from capillary dilation, swelling from exudation
of fluid, infiltration with inflammatory cells, increased mucus production, loss of ciliary
function, and loss of portions of the ciliated epithelium.
Clinical Manifestation:
• Cough may be productive or non-productive
• low-grade fever
• Substernal chest discomfort
• sore throat
• postnasal drip
• fatigue
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10. AcuteBronchitis(cont.)
Diagnosis:
• Diagnosis of acute bronchitis is usually based on the clinical
presentation, with recent onset of cough being the distinctive
hallmark
Treatment:
• Acute bronchitis is predominantly caused by viruses Viral infections
do not respond to antimicrobial therapy
• Acute bronchitis caused by bacterial organisms responds well to
antibiotic therapy.
• The primary goal in management is symptom management with
antitussive agents,beta-2 agonists, and other classes of
bronchodilators in selective patients.
• Nonpharmacologic: recommendations are to increase fluid intake,
avoid smoke, and use a vaporizer in the bedroom.
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11. • ChronicBronchitis:
Etiology:
• The major causes of chronic bronchitis are
cigarette smoking repeated airway infections,
genetic predisposition, and inhalation of
physical or chemical irritants.
Pathogenesis:
• Pathologic changes in the airway include
chronic inflammation and swelling of the
bronchial mucosa resulting in scarring,
increased fibrosis of the mucous membrane,
hyperplasia of bronchial mucous glands and
goblet cells, hypertrophy of bronchial glands
and goblet cells, and increased bronchial wall
thickness, which potentiates obstruction to
airflow.

12. ChronicBronchitis(cont.)
Clinical manifestation:
• Shortness of breath on exertion
• excessive amounts of sputum
• chronic cough
• excess body fluids (edema, hypervolemia),
• Chills
• malaise
• muscle aches
• fatigue
• loss of libido
• Insomnia.
• By the time dyspnea on exertion is present
• In the end-stage disease process, the
patient presents with signs of right-sided
heart failure (distended neck veins, right
ventricular heave,right ventricular gallop,
and peripheral edema).
• Hypoxia leads to pulmonary hypertension.
• Cyanosis is a late sign

13. ChronicBronchitis(cont.)
Diagnosis:
• Measures used to confirm the diagnosis include chest radiography,
congested lung fields, an enlarged horizontal cardiac silhouette, and
evidence of previous pulmonary infection.
• Arterial blood gas (ABG)↑ PaCO2,↓ Pao2 (often below 65 mm Hg);
abnormal ABGs develop early in the disease process.
• The electrocardiogram may reveal atrial dysrhythmias and evidence of
right ventricular hypertrophy.
• Secondary polycythemia related to continuous or nocturnal hypoxemia is
common.
Treatment:
• Pharmacologic treatment involves the use of inhaled short-acting β
2
agonists and inhaled anticholinergic bronchodilators, cough suppressants
• antimicrobial agents for infections.
• Inhaled or oral corticosteroids may also be used in the treatment of some
patients for acute exacerbations.

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Emphysema
Etiology:
• Emphysema (also referred to as type A COPD) is defined pathologically
by destructive changes of the alveolar walls and abnormal enlargement
of the distal air sacs.
• Smoking is commonly associated with emphysema
Pathogenesis:
• The pathologic changes leading to alveolar destruction are associated
with the release of proteolytic enzymes from inflammatory cells such
as neutrophils and macrophages
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15. E
m
p
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a(cont.)
Clinical manifestation:
• Cough
• difficulty in breathing
• progressive dyspnea
• Increasing shortness of breath
• Digital clubbing
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16. E
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a(cont.)
Diagnosis:
• The diagnosis of emphysema is based on the
patient’s history and physicalfindings,
pulmonary function tests, chest radiographs,
ABGs, andelectrocardiogram.
Treatment:
• Poor prognosis is associated with weight loss,
so treatment is focused on maintaining proper
nutrition.
• Pharmacologic treatment involves the use of
inhaled short-acting β2 agonists and inhaled
anticholinergic bronchodilators, cough
suppressants, and antimicrobial agents for
infections. Inhaled or oral corticosteroids may
also be used in the treatment of some patients
for acute exacerbations.
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17.  OBSTRUCTIONOFTHEAIRW
A
YLUMEN
• Bronchiectasis
shape: saccular (with cavity-like dilatations) or cylindrical
and with widening of the bronchial walls. A fusiform shape
is a combination of saccular and cylindrical changes.
Bronchiectasis
Etiology:
• Bronchiectasis means dilation of bronchi. It is either
acquired or congenital and is classified as both an
obstructive and a suppurative(pus-forming) disorder.
• bronchiectasis can be classified according to bronchial
Pathogenesis:
• Bronchiectasis is characterized by recurrent infection and
inflammation of bronchial walls, which leads to persistent
dilatation of the medium sized bronchi and bronchioles.
H. influenzae is the most common cause of
bacterial infections.

18. • Bronchiectasis

19. •Bronchiectasis(cont.)
Clinical manifestation:
• Use of accessory muscles to breathe
• Pursed-lip breathing
• Minimal or absent cough
• Leaning forward to breathe
• Barrel chest
• Digital clubbing
• Dyspnea on exertion
Diagnosis:
• The diagnosis of bronchiectasis is based on a history of chronic productive
cough. The patient complains about producing copious amounts of foul-
smelling, purulent sputum. Radiographic abnormalities may reveal small
cysts, thickening of bronchial walls, and increased bronchial markings
Treatment:
• Antibiotic therapy accompanied by inhalation of bronchodilators followed
by vigorous chest percussion and postural drainage is the mainstay of
treatment. 18

20. Bronchiectasis

21. • Bronchiolitis
Etiology:
Bronchiolitis is characterized by widespread
inflammation of bronchioles attributable to
infectious agents such as respiratory syncytial
virus(RSV) (50% of cases), influenza virus (type
A, B, or C), or bacteria (H. influenzae,
pneumococci, or hemolytic streptococci) and
occasionally is produced by allergic reactions.
Pathogenesis:
Once initiated by the causal agent,
proliferation and necrosis of
bronchiolar epithelium occur, producing
obstruction and increased mucus production

22. Bronchiolitis
(cont.)
Clinical manifestation:
• wheezing attributable to bronchospasm
• crackles
• decreased breath sounds
• retractions
• Increased sputum
• Dyspnea
• tachypnea (rapid, shallow respirations)
• low-grade fever
Diagnosis:
• Patients commonly have an elevated WBC count. The chest
radiograph may show enlarged air sacs, interstitial infiltrates,
atelectasis, or severe hyperinflation.
Treatment:
• Adequate oxygenation is maintained by providing humidified
oxygen; monitoring blood gases or oxygen saturation; and
administering oral, inhaled, or intravenous bronchodilator agents
and, in selected cases, corticosteroids.

23. • Cystic Fibrosis
Etiology:
• Cystic fibrosis (mucoviscidosis) is an autosomal-recessive disorder of the
exocrine glands. Cystic fibrosis can be classified either as an airflow
obstructive disorder or as a suppurative (pus-forming) disorder.
Hypersecretion of abnormal, thick mucus that obstructs exocrine glands and
ducts isa characteristic finding in the disease.
Pathogenesis:
• Cystic fibrosis is classified as an autosomal-recessive disorder. One genetic
defect associated with cystic fibrosis involves deletion of three base pairs in
codon 508 (AF508) that code for phenylalanine on chromosome 7 (band
q31).This is the most common genetic mutation causing cystic fibrosis and
occurs in 60% to 75%of cystic fibrosis patients tested.
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24. • Cystic Fibrosis (cont.)
Clinical manifestation:
• history of cough in a young adult or child
• thick, tenacious sputum; recurrent pulmonary infections (commonly Pseudomonas
aeruginosa)
• recurrent episodes of bronchitis.
Diagnosis:
• The diagnosis of cystic fibrosis is based on clinical and laboratory findings.Diagnostic studies
that are routinely performed include ABG measurements, pulmonary function tests, sputum
culture and sensitivity with Gram stain, and chest radiography. Specific diagnostic tests for
cystic fibrosis include stool examination for fat, pilocarpine iontophoresis (sweat test), and
genetic testing.
Treatment:
• Treatment includes the use of bronchodilators, and mobilization of the thick mucus by
postural drainage and chest physiotherapy (percussion and vibration) is a priority. Alternative
methods for mucus removal include the forced expiratory technique, which involves
coughing(huffing) with an open glottis.
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25. • Acute Tracheobronchial Obstruction
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Etiology:
• Acute tracheobronchial obstruction requires immediate treatment. Causes
frequently include aspiration of a foreign body, mispositioned endotracheal
tube, laryngospasm,epiglottitis, trauma, swelling from smoke inhalation,
postsurgical blood clot, and compression of the bronchus or trachea by tumors
or enlarged lymph nodes.
Pathogenesis:
• Obstruction by one of the etiologic agents can be partialor complete. The
health care worker must be prepared to assess thesituation rapidly and act
immediately to clear the airway

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Acute Tracheobronchial Obstruction (cont.)
• Clinical manifestation:
•inability to talk,
•tachycardia
•cyanosis
•rapid progression to unconsciousness unlessthe problem is quickly
reversed
Diagnosis:
• The diagnosis of airway obstruction is based on clinical features andABG
analyses.ABG values frequently show hypoxemia and hypercarbia.Chest
radiographs may reveal the location of the obstruction
Treatment:
• Treatment involves opening the obstructed airway as quickly as possible.Blows
to the patient’s back or use of abdominal thrusts (previouslycalled the
Heimlich maneuver) may be necessary for the foreign body to be expelled.

27. •Epiglottitis
• Epiglottitis is a rapidly progressive cellulitis of the epiglottis and adjacent
soft tissues. Acute epiglottitis is suspected when odynophagia (pain with
swallowing) seems out of proportion to pharyngeal findings
Etiology:
Pathogenesis:
• The infecting agent localizes in the supraglottic area in the epiglottis
and pharyngeal structures, causing rapid and potentially fatal inflammation
with swelling and airway obstruction.
Clinical manifestation:
• Drooling,
• Dysphagia,
• Rapid Onset of Fever
• Dysphonia
• Inspiratory Stridor
• Inspiratory Retractions
Diagnosis:
• Definitive diagnosis is obtained by direct or fiberoptic visualization of
the epiglottis.
Treatment:
• Antibiotic therapy should be started immediately

28. • Etiology: Viral croup affects the larynx, trachea, and bronchi. It is often caused by
parainfluenza virus type 1.Other potential infecting organisms include parainfluenza types 2
and3, RSV, influenza virus, adenovirus, and Mycoplasma pneumoniae.
• Pathogenesis: The infectious agent causes inflammation along the entire airway, leading to
edema formation in the subglottic area
• Clinical Manifestation:
• Upper respiratory tract infection or cold that has developed into a barking cough with
stridor.
• Fever is low grade or absent.
• Diagnosis: Diagnosis is based on clinical manifestations and lateral neck films to rule out
epiglottitis. Direct laryngoscopy is also used to confirm the presence of epiglottitis because
the clinical presentation is similar to that of croup.
• Treatment: Supportive treatment is used for viral croup. Mist therapy, oral hydration, and
avoidance of stimulation are used in outpatient therapy.
• Croup Syndrome

29. • Obstructive pulmonary disorders are characterized by increased resistance to airflow.
• With bronchiectasis, obstruction is due to inflammation, infection, and dilatation of the bronchioles.
• Similarly, bronchiolitis is associated with inflammation; inflammation leads to mucosal edema and
excessive mucus production.
Airway obstruction from cystic fibrosis is related to production of excessive, thick secretions.
•
• Obstruction of the airway in croup is the result of edema and increased secretions caused by viral
infection.
• Similarly, epiglottitis is an infectious process requiring emergency treatment.
• The inflammation is associated with increased mucus production and edema of the tracheal
bronchial mucosa in asthma and bronchitis.
• Bronchospasm of the tracheobronchial tree attributable to exposure to allergens, pulmonary
irritants, stress, and exercise may result in hypoxemia.
• Obstruction to airflow in emphysema is due to loss of alveoli and small airways. The most common
cause is cigarette smoking.
SUMMARY
• Obstructive pulmonary diseases include
• airway obstruction,
• obstruction from conditions affecting the tracheobronchial walls
• loss of lung parenchyma (emphysema).

30. Banasik,J
.L.(2019).P
athophysiology
.ElsevierHealthSciences.
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