NU 545 PATHOPHYSIOLOGY UNIT 5, RESPIRATORY AND
RENAL EXAM QUESTIONS AND ANSWERS WIT
COMPLETE SOLUTIONS VERIFIED
Alveoli
Alveoli: Primary gas exchange units (cont.)
• Oxygen enters the blood, and carbon dioxide (CO2) is
removed.
• Pores of Kohn
• Epithelial cells
-Type I alveolar cells (Alveolar structure)
-Type II alveolar cells (Surfactant production: Prevents lung collapse)
• Contain alveolar macrophages: Ingest foreign material,
and remove it through the lymphatic system.
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Surfactant
1. Lipid/PRO mix
2. Produced by Alveolar type II cells
3. Maintains alveolar expansion (decreases surface tension)
Bronchiolitis
,Bronchiolitis
1. Diffuse inflammation of small airways or bronchioles
2. Most common in children
3. Occurs in adults with chronic bronchitis or those with a
viral infection or who have inhaled toxic gases
4. Clinical manifestations
• Rapid ventilatory rate; significant use of accessory muscles;
low grade fever; dry, nonproductive cough; and hyperinflated
chest
5. Treatment
• Antibiotics, steroids, immunosuppressive agents, and chest
physical therapy (humidified air, coughing and deep breathing, physical therapy (humidified air, coughing
and deep breathing,
postural drainage)
Bronchiolitis Obliterans
1. Fibrotic Dz of airways
2. Can occur with all causes of bronchiolitis
3. Tx:
-Corticosteroids
How is alveolar ventilation measured?
-ABG.
Asthma Patho
,Chronic inflammatory disorder of the bronchial mucosa.
Causes bronchial hyperresponsiveness, constriction of the
airways and variable airflow obstruction that is reversible.
1. Episodic attacks of bronchospasm, bronchial inflammation,
mucosal edema , and increased mucous production
2. Early asthmatic response
•Vasodilation
•Increased capillary permeability
•Mucosal edema
•Bronchial smooth muscle contraction (bronchospasm)
•Tenacious mucous secretion
3. Late asthmatic response
•Begins 4 8 hours after the early response.
•Chemotactic recruitment of lymphocytes, eosinophils,
basophils, neutrophils, and lymphocytes occurs.
-Airway scarring
-Increased bronchial hyper-responsiveness
-Impaired mucociliary function with accumulation of mucous and
cellular debris, forming plugs in the airways
-Decreased Treg cells
, -Leads to airway remodeling if left untreated
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Asthma CM's:
1. Asymptomatic between attacks
2.General S/S: Chest constriction, expiratory wheezing, dyspnea, nonprod. coughing, prolonged
expiration, tachycardia, tachypnea
3. Pulsus Paradoxus
4. Status asthmaticus
-Bronchospasm not reversed by usual measures
-Life threatening!
5. Ominous signs of impending death
-SIlent chest (no audible air movement)
-PaCO2 > 70mmHg
Asthma Tx
1. O2
2. Inhaled beta-agonist bronchodilators
3. Inhaled corticosteroids
4. Leukotriene agonists
5. Immunotherapy
-Monoclonal antibodies to IgE
6. Education about allergens and irritants and peak flowmeters
Aging and the pulmonary system
RENAL EXAM QUESTIONS AND ANSWERS WIT
COMPLETE SOLUTIONS VERIFIED
Alveoli
Alveoli: Primary gas exchange units (cont.)
• Oxygen enters the blood, and carbon dioxide (CO2) is
removed.
• Pores of Kohn
• Epithelial cells
-Type I alveolar cells (Alveolar structure)
-Type II alveolar cells (Surfactant production: Prevents lung collapse)
• Contain alveolar macrophages: Ingest foreign material,
and remove it through the lymphatic system.
Copyright
Surfactant
1. Lipid/PRO mix
2. Produced by Alveolar type II cells
3. Maintains alveolar expansion (decreases surface tension)
Bronchiolitis
,Bronchiolitis
1. Diffuse inflammation of small airways or bronchioles
2. Most common in children
3. Occurs in adults with chronic bronchitis or those with a
viral infection or who have inhaled toxic gases
4. Clinical manifestations
• Rapid ventilatory rate; significant use of accessory muscles;
low grade fever; dry, nonproductive cough; and hyperinflated
chest
5. Treatment
• Antibiotics, steroids, immunosuppressive agents, and chest
physical therapy (humidified air, coughing and deep breathing, physical therapy (humidified air, coughing
and deep breathing,
postural drainage)
Bronchiolitis Obliterans
1. Fibrotic Dz of airways
2. Can occur with all causes of bronchiolitis
3. Tx:
-Corticosteroids
How is alveolar ventilation measured?
-ABG.
Asthma Patho
,Chronic inflammatory disorder of the bronchial mucosa.
Causes bronchial hyperresponsiveness, constriction of the
airways and variable airflow obstruction that is reversible.
1. Episodic attacks of bronchospasm, bronchial inflammation,
mucosal edema , and increased mucous production
2. Early asthmatic response
•Vasodilation
•Increased capillary permeability
•Mucosal edema
•Bronchial smooth muscle contraction (bronchospasm)
•Tenacious mucous secretion
3. Late asthmatic response
•Begins 4 8 hours after the early response.
•Chemotactic recruitment of lymphocytes, eosinophils,
basophils, neutrophils, and lymphocytes occurs.
-Airway scarring
-Increased bronchial hyper-responsiveness
-Impaired mucociliary function with accumulation of mucous and
cellular debris, forming plugs in the airways
-Decreased Treg cells
, -Leads to airway remodeling if left untreated
Copyright ©
Asthma CM's:
1. Asymptomatic between attacks
2.General S/S: Chest constriction, expiratory wheezing, dyspnea, nonprod. coughing, prolonged
expiration, tachycardia, tachypnea
3. Pulsus Paradoxus
4. Status asthmaticus
-Bronchospasm not reversed by usual measures
-Life threatening!
5. Ominous signs of impending death
-SIlent chest (no audible air movement)
-PaCO2 > 70mmHg
Asthma Tx
1. O2
2. Inhaled beta-agonist bronchodilators
3. Inhaled corticosteroids
4. Leukotriene agonists
5. Immunotherapy
-Monoclonal antibodies to IgE
6. Education about allergens and irritants and peak flowmeters
Aging and the pulmonary system
