Ch. 22 Flashcards

1
Q

Etiology of Asthma:

A

Airway obstruction that is reversible (not completely in some patients). Airway inflammation: Acute bronchospasm (bronchoconstriction) and Mucosal edema, mucous plug formation

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2
Q

Extrinsic Asthma

A

1/3 to ½ of asthma cases
An IgE-mediated response is common
Intermittent vs persistent

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3
Q

Non-Allergic Asthma

A

Develops in middle age with less favorable prognosis
No history of allergies
Respiratory infections or psychological factors appear to be contributory
Allergen-specific immunotherapy and environmental control not helpful

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4
Q

Exercised Induced Asthma

A

Common in children and adolescents
Bronchospasm often occurs within 3 minutes after the end of exercise; usually resolves in 60 minutes
Running, jogging, and tennis are the most common stimulators

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5
Q

Occupational Asthma

A

Often have positive skin test reactions to protein allergens in the work environment
Tends to have progressively more severe attacks with subsequent exposures

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6
Q

Drug Induced Asthma

A

Can produce symptoms ranging from mild rhinorrhea to respiratory arrest requiring mechanical ventilation
Aspirin, NSAIDs can trigger attacks

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7
Q

Pathogenesis: Allergic Asthma

A

Manifested by elevated IgE levels
Associated with allergic rhinitis, eczema, a positive family history of allergy
Chemical mediators are released in response to allergen

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8
Q

Clinical Manifestations of Asthma

A
Wheezing
Feeling of tightness of chest
Dyspnea
Cough (dry or productive)
Increased sputum production (thick, tenacious, scant, and viscid) 
Hyperinflated chest
Decreased breath sounds
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9
Q

Clinical Manifestations of SEVERE Asthma Attack

A
Use of accessory muscles of respiration
sternocleidomastoid, scalenes
Intercostal retractions
Distant breath sounds with inspiratory wheezing
Orthopnea
Agitation
Tachypnea: >30 breaths/min
Tachycardia: >120 beats/min
Wheezing is NOT a good indicator of air flow
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10
Q

Asthma Treatment

A

Avoid triggers
Environmental control
Dust control, removal of allergens, air purifiers, air conditioners
Preventive therapy
Stop smoking, avoid second-hand smoke, aerosols, odors, early treatment for respiratory infections
Desensitization (allergen specific immunotherapy)
Medications

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11
Q

Acute Bronchitis Etiology

A
Acute inflammation of the trachea and bronchi
Causes
Viral or nonviral
Heat
Smoke inhalation
Inhalation of irritant chemicals
Allergic reactions
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12
Q

Acute Bronchitis Pathogenesis

A

Airways become inflamed and narrowed
Swelling
Increased mucus production
Loss of ciliary function

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13
Q

Acute Bronchitis Clinical Manifestations

A
Usually mild and self limiting
Cough (productive or nonproductive)
Low-grade fever
Substernal chest discomfort
Sore throat
Postnasal drip
Fatigue
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14
Q

Acute Bronchitis Treatment

A
Usually no treatment needed for viral 
Antibiotic therapy (bacterial)
Codeine-containing medications (for cough)
Increase fluid intake
Avoid smoke
Use a vaporizer in bedroom
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15
Q

Chronic Bronchitis Etiology

A

Type B COPD, “blue bloater”
Hypersecretion of bronchial mucus
Chronic or recurrent productive cough >3 months >2+ successive years
Persistent, irreversible when paired with emphysema
1:2 male to female ratio
>30 to 40 years

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16
Q

Chronic Bronchitis Pathogenesis

A

Chronic inflammation and swelling of bronchial mucosa scarring
Hyperplasia of bronchial mucous gland/goblet cells  mucus
Increased bronchial wall thickness
Resistance increases work of breathing and O2 demands
Pulmonary hypertension
Inflammation in bronchial walls with vasoconstriction of pulmonary vessels and arteries
Right-sided heart failure may occur due to high pulmonary resistance
Destruction of bronchial walls
Results in dilation of airway sacs
Dilated sacs contain pools of infected secretion that do not clear themselves  further infection

17
Q

Chronic Bronchitis Treatment

A
Goals
Block the progression of the disease
Return to optimal respiratory function
Return to usual activities of daily living
Medications
Inhaled short-acting B2 agonists
Inhaled anticholinergic bronchodilators
Cough suppressants
Antimicrobial agents (bacterial infections)
Inhaled/oral corticosteroids

Low-dose O2 therapy
Smoking cessation

18
Q

Emphysema Etiology

A

Type A COPD
“Pink puffer”
Destructive changes of the alveolar walls
Abnormal enlargement of the distal air sacs
Damage is irreversible
Associated with chronic bronchitis

19
Q

Emphysema Pathogenesis

A

Smoking causes alveolar damage
Inflammation leads to release of enzymes that inactivate a substance that normally protects lung tissue
Exchange of O2 and CO2 between alveolar and capillary blood impaired
Loss of elastic tissue in lung
Air becomes trapped in distal alveoli
Loss of alveolar wall and air trapping leads to bullae (large, thin-walled cysts in the lung) formation

20
Q

Emphysema Clinical Manifestations

A
Progressive, exertional dyspnea
Thin 
Due increased respiratory effect, increased caloric expenditure, and decreased ability to consume adequate calories
Use of accessory muscles
Pursed-lip breathing
Cough (minimal or absent)
Digital clubbing
Barrel chest
21
Q

Emphysema Treatment

A
O2 therapy
Smoking cessation
Medications
Inhaled short-acting B2 agonists
Inhaled anticholinergic bronchodilators
Cough suppressants
Antimicrobial agents (infections)
Inhaled/oral corticosteroids
Theophylline products
22
Q

Pulmonary Function Test (PFT)

A

Demonstrates obstruction of airflow in lungs
Spirometry
Determines severity and diagnosis of COPD
Patient inhales deeply and exhales as quickly as possible until maximal air is exhaled
Forced vital capacity (FVC)
Total volume of air exhaled
Time required for exhaling the air is also measured
Forced expiratory volume in 1 second (FEV1)
Volume exhaled in 1st second is reliable index of obstructive airway disease

23
Q

Bronchial Provocation Test

A

Controlled induction of bronchospasm by inhalation of various agents; then ventilations measured