Pulmonary Diseases
Part 2
Eman Almaamari
MSN student
Objectives
• Discuss the Definition ,types, causes of asthma
• Discuss the early wearing signs and Symptoms of asthma.
• Explain the pathophysiology of asthma
• Explain the diagnostic management and intervention related to
asthma
• Discuss the Definition ,types, causes of COPD
• Discuss the signs and Symptoms of COPD.
• Explain the treatment of COPD
• Differentiate between ASTHMA and COPD.
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Pulmonary disease
Asthma
is a chronic lung disease (no cure) that causes narrowing and inflammation
of the airways (bronchi and bronchioles) that leads to difficulty breathing.
• 6.3 m in children 17.7adults
• Familial more than 100 genes
• Phenotype: not linked to specific pathological process
• Allergic: eosinophil
• Viral RTI: neurophilic asthma
• Exercise induce asthma
• Aspirin sensitive asthma
• Comorbidities: obesity, Gasteroesophageal reflux, allergic rhinitis
• Endotype: specific pathophysiology
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Types of asthma
Type I
Atopic allergic
asthma
Type II
Non atopic
• Most common
• It is type 1 IgE reaction resulting
from an exposure to allergen
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Results from a variety of triggers
Drugs (aspirin , NSAIDS)
Airborne pollutants
Hormonal change
Respiratory tract infection
patho
• Innate and adaptive immune response
• Persistent Inflammation of the mucosa membrane and
hyperresponsiveness of the airway
• Dendric cells (antigen presenting macrophages), T helper 2
lymphocytes, B lymphocytes, mast cells, neutrophile, and basophils
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Early phase:
• bronchoconstriction. Maximum in 30 minutes and resolve in
1-3 hours
• Antigens affect mast cells and produce mediators: mucus
secretion, vascular leak, airway smooth muscle constriction
and neutrophile activation.
• Another pathway: Antigens Dendric cells see pic
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Late phase
• 4-6 hours
• Chemotactic recruitment of lymphocyte, eosin,
neutron, baso
• Again more bronchospasm and mucus secretion
• Eosinophile: tissue injury and fibrosis
• Damage to ciliated epithelial cells impaired mucous
removal
• Nitric oxide: oxidative injury and chronic
inflammation
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Consequences
• Airway obstruction…. Increase resistance to airflow especially
expiratory flow…… air trapping…………. Hyperinflation distal to
obstruction………… increased workload………….. Increase intrapleural
and alveolar pressure……………decreased perfusion of the alveoli
• Increase alveolar pressure decreased ventilation and decreased
perfusion within different lung segments (constriction and trapping
not even in all areas)
• Hypoxemia and co2 retention
• Hypoxemia: stimulation of respiratory center (increase
ventilation)…… decrease paco2 (alkalosis)
• Due to continues trapping…………. Expanded lungs …..muscle
failure…………resp. acidosis and respiratory failure
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• Between attacks are asymptomatic and PFT normal
• Early attack: chest constriction, expiratory wheezing, dysp,
nonproductive cough, prolonged expiration,
• Severe attack (use of accessory muscles): wheezing inspiration and
expiration
• Pulsus paradoxus: decrease in systolic BP during inspiration
• ABGs hypoxemia and resp. alkalosis (early)
• If not treated, severe bronchospasm, hypoxemia will not able to
stimulated resp. center to increase ventilation acidosis and resp. fail
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What can trigger asthma?
Environment: smoke, pollen, pollution, perfumes,
dander, dust mites, pests (cockroaches), cold and
dry air, mold
Body Issue: respiratory infection, hormonal shifts
Intake of Certain Substances: drugs (beta adrenergic
blockers that are nonselective), NSAIDS, aspirin
Early S/S
SOB
easily fatigued with physical
activity
Frequent cough (night)
sleep issues
Wheezing
Active S/S
Chest tightening
Expiratory wheezing
Coughing
Dispense
 RP
Diagnosis
• History (recurrent wheezing, cough and exercise
intolerance)
• Physical examination
• Laboratory Findings (ABGs)
• Expiratory flow rate
• Chest X-ray
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Treatment
Oxygen
Beta-2 adrenergic receptor agonists
Bronchodilators: opens the airways to increase air flow – Theophylline
inhaler or nebulizer: used as the fast acting relief during an asthma attack or
prior to
For persistent Asthma; anti inflame and and inhaled (corticosteroid) are the
main treatment.
Anti-inflammatories: decreases swelling and mucus production…used as longterm treatment to control asthma not an acute attack.
• Iv magnesium
• Antibiotic for acute asthma (bacterial infection)
• Allergy control
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Nursing intervention
• Assess history of allergic reactions to medications before
administering medications.
• Assess respiratory status.
• Assess medications.
• Pharmacologic therapy
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Pulmonary disease
COPD
Chronic obstructive pulmonary disease
chronic obstruction of airflow from the lungs
• Preventable, airflow limitation
• Not fully reversible
• Progressive
• 3rd leading cause of death
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TWO Types Of COPD
chronic bronchitis
emphysema
Risk factor :
• Cigarette smoking
• Air pollution
• Occupational Irritants
• Hyper reactive airways
• Alpha-1 antitrypsin deficiency
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• Chronic bronchitis: hypersecretion of mucus, chronic productive
cough for 3 month, 2 years
• Emphysema: permanent enlargement of gas-exchange airway
accompanied by destruction of alveolar wall without fibrosis and loss
of recoil of bronchial wall.
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Pathophysiology
• Irritant recruit lymphocytes, neutrophil, macrophages to the lung
• Damage to lung: inflammation, oxidative stress
• Oxidative stress is a phenomenon caused by an imbalance between
production and accumulation of oxygen reactive species (ROS) in cells and
tissues and the ability of a biological system to detoxify these reactive
products.
• Irritant…….. Bronchial inflam……edema…………….increase no. and size of mucus
gland…………. and goblet cells……….smooth muscle hypertrophy……. With fibrosis
and narrowing airway.
• Mucus increase infection ……….injury and ineffective repair
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• Emphysema: breakdown of alveoli wall due to breakdown of elastin
• Imbalance between protease and ant protease (effect of neutrophil).
• Macrophages: pro-inflammatory
• Significant ventilation-perfusion mismatch and hypoxemia
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Signs and symptoms
Remember: Lung Damage
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Lack of energy
Unable to tolerate activity (shortness of breath)
Nutrition poor (weight loss) due to energy used breathing especially with
emphysema
Gases abnormal (high PCO2 >45 and low PO2 <90)..respiratory acidosis
Dry or productive cough constant (productive with chronic bronchitis)
Accessory muscle usage during breathing, Abnormal lung sounds: diminished, coarse crackles
(chronic bronchitis) or wheezing
Modification of skin color from pink to cyanosis in lips, mucous membranes, nail beds (“blue
bloaters”)
Anteroposterior diameter increased (barrel chest)….emphysema “pink puffers”
Gets in the Tripod Position during dyspnea (stands leaning forward while supporting body with
hands on knees or an object)
Extreme dyspnea
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How is COPD Diagnosed?
• Spirometry: A test where a patient breathes into a tube that measure
how much volume the lungs can hold during inhalation and how
much and fast air volume is exhaled.
• Measuring the FVC (Forced Vital Capacity): a low reading shows
restrictive breathing….it measures the largest amount of air a person
exhales after breathing in deeply in one second.
• Forced Expiratory Volume: measures how much air a person can
exhale within one second. A low reading shows the severity of the
disease.
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Treatment
Remember: Chronic Pulmonary Medications Save Lungs
Corticosteroids: inflammation and mucous production used in combination with
bronchodilator like:Symbicort
Methylxanthines: Theophylline type of bronchodilator
Phosphodiestrace-4 inhibitors: “Roflumilast”
Short-acting bronchodilators: relaxes the smooth muscle of the bronchial tubes and are
used in emergency situations where quick relief is needed
Albuterol (beta 2 agonist) and Atrovent
Long-acting Bronchodilators: relaxes the smooth muscle of the bronchial tubes (same
as short-acting bronchodilators BUT their effects last longer) used over a longer period
of time
Beta 2 agonist: salmeterol,
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Asthma ………COPD
• Both are chronic inflammatory diseases that involve the small
airways and cause airflow limitation
• COPD affects both the airways and the parenchyma, whilst asthma
affects only the airways
• The most important difference between asthma and COPD is the
nature of inflammation, which is primarily eosinophilic and CD4driven in asthma, and neutrophilic and CD8-driven in COPD. This is a
very important distinction because the nature of the inflammation
affects the response to pharmacological agents. There is now ample
evidence that inhaled corticosteroids are effective against the
eosinophilic inflammation in asthma but largely ineffective against
the primarily neutrophilic inflammation seen in COPD
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SO, IT’S Same OR Different
• < 40 y
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asthma
allergy
acute
upper airways
Little production
Focus on allergy
• >40 y
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COPD
Inflammation
Chronic
Lower airways
Sputum production
Focus on decreasing
inflammation
Nursing consideration :
To stop smoking
Avoid Expose to known allergy
Encourage diaphragmatic
breathing /pursed lip
Avoid high pleases
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References
• Pathophysiology eighth edition (2015), Kathryn L. Mccance and Sue E.
Huether.
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