NUR 3850 Exam 2 | Med-Surg & Pathophysiology II |Correct Questions And Answers | Galen College of Nursing | 2026

Unit 3: Alterations in Oxygenation

Patho:
 Hypoventilation
o Air delivered to alveoli is insufficient to provide O2 and remove CO2
o Hypoventilation results in increased PACO2 and hypoxemia
o Etiology:
 Morphine, barbiturates
 Obesity
 Myasthenia gravis
 Obstructive sleep apnea
 Chest wall damage
 Paralysis of respiratory muscles
 Thorax/abdomen surgery
 Hyperventilation:
o Increase of air entering the alveoli
o Leads to hypocapnia (PACO2 <35 mm HG)
o Etiology:
 Pain
 Fever
 Anxiety
 Obstructive and restrictive lung diseases
 Sepsis
 High altitude
 Brainstem injury
 Hypoxemia
o Deficient levels of blood oxygen
 Hypoxia
o Decrease in tissue oxygenation
o Types:
 Hypoxic hypoxia: high altitude, hypoventilation, obstruction
 Anemic hypoxia (low HGB)
 Circulatory hypoxia (low cardiac output, shock, MI, heart failure)
 Histotoxic hypoxia: decreased O2 carrying capacity from toxic substance; cyanide poisoning
Med Surge:
 Drug therapy: Isoniazid, Rifampin, Pyrazinamide, Pseudoephedrine, Dextromethorphan, Guaifenesin, Acetylcysteine,
Albuterol, Budesonide, Prednisone, Ipratropium Bromide, Furosemide, Hydroxyzine, Morphine Sulfate, Naproxen

Acute Bronchitis
 Pathophysiology:
o Acute inflammation of the trachea and bronchi
 Etiology:
o Viral or non-viral
o Heat
o Inhalation of smoke and chemicals
o Allergic reactions
 Pathogenesis:
o Airways inflame and narrow from capillary dilation
o Swelling from fluid exudation
o Infiltration with inflammatory cells
o Increased mucus production
o Loss of ciliary function
o Loss of portions of the ciliated epithelium
 Clinical Manifestations:
o Usually mild and self-limiting
o Cough (productive and non-productive)
o Low-grade fever
o Substernal chest discomfort
o Sore throat
o Postnasal drip

, o Fatigue
 Diagnosis:
o Distinct hallmark of disease: recent onset of cough
o Chest x-ray to distinguish acute bronchitis from pneumonia

Chronic Bronchitis/ Type B COPD




 Pathophysiology:
o Damaged alveoli, boggy and cannot expel CO2
o Chronic inflammation and swelling of the bronchial mucosa resulting in scarring
 Extends into surrounding alveoli, preventing proper oxygenation and potentiating airway
obstruction
o Hyperplasia of bronchial mucous gland/goblet cells
 Increased mucus production with formation of mucus plugs
o Increased bronchial wall thickness
 Resistance increases work of breathing and O2 demands
 Ventilation-perfusion mismatch with hypoxemia and hypercarbia; increases pulmonary artery
resistance
o Pulmonary hypertension
 Inflammation in bronchial walls with vasoconstriction of pulmonary vessels and arteries
 Right-sided heart failure may occur r/t high pulmonary resistance
o Destruction of bronchial walls
 Etiology:
o Cigarette smoking (90%)
o Repeated airway infections
o Genetic predisposition
o Inhalation of physical or chemical irritants
o Chronic or recurrent productive cough >3 months > 2+ successive years
o Type B COPD, “blue bloater”
o Hypersecretion of bronchial mucus
o Persistent, irreversible when paired with emphysema
o 1:2 male to female ratio
o >30 to 40 years
 Clinical Manifestations:
o Overweight
o Easily fatigued
o Commonly associated with emphysema
o SOB on exertion
o Excessive sputum
o Chronic cough, severe in AM
o Evidence of excess body fluids (edema, hypervolemia)
o Cyanosis (late sign)
 Diagnosis:
o Chest x-ray
o Pulmonary function tests

, o ABGS
o ECG

Emphysema/ Type A COPD




 Pathophysiology:
o Type A COPD
o “Pink puffer”
o Destructive changes of the alveolar walls
 Damage is irreversible
 Etiology:
o Associated with chronic bronchitis
o Smoking >70 packs a year
o Air pollution
o Certain occupations (mining, welding, working with or near asbestos)
o A1-Antitrypsin deficiency
 Pathogenesis
o Group of genes
o Release of proteolytic enzymes from neutrophils and macrophages leading to alveolar damages
o Smoking causes alveolar damage
o Inflammation leads to release of proteolytic enzymes
o Inactive a1-antitrypsin (normally protects lung parenchyma)
o Reduction in pulmonary capillary bed
o Loss of elastic tissue in lung
o Air becomes trapped in distal alveoli
o Loss of alveolar wall and air trapping leads to bullae (large, thin-walled cysts in the lung) formation
o Loss of elastic tissue causes airways to close and trap air, which makes the chest round
 Clinical Manifestations:
o Progressive, exertional dyspnea
o Cough (minimal or absent)
o Use of accessory muscles
o Thin, wasted individual hunched forward
o Decreased breath sounds, lack of crackles and rhonchi
o Chronic morning cough
o Prolonged expiration
o Digital clubbing (clubbing of the fingers)
o Barrel chest
o Pursed-lip breathing
 Vital Sign Changes:
o Mild decrease in PaO2 and SpO2
 Breath Sounds:
o Wheezing
o Hyperresonance

, Type A and Type B COPD (Emphysema and Chronic Bronchitis)
 Diagnosis:
o Health History
o ABGs for O2, ventilation
o Sputum samples
o CBC
o Chest X-Ray
o Pulmonary Function Tests
 Pharmacologic/medication:
o Bronchodilators
o Corticosteroids
o Supplemental oxygen
o Mucolytics (to remove secretions)
 Surgical:
o Bullectomy
o Lung transplant
o Lung volume reduction surgery (remove diseased lung portions)
 Therapeutic/Nursing Management:
o Purse lip breathing (forces airway open)
o Weight loss prevention
o Nutrition, exercise promotion with assessment during exertion
o Teach: avoid heat and cold; heat increases body temp, raising O2 requirements; cold causes bronchospasm
 Complications:
o Hypoxemia/tissue anoxia
o Acidosis
o Respiratory infections
o Cardiac failure


Sarcoidosis




 Pathophysiology:
o Interstitial lung disease: progressive scarring of lung tissue
o Development of multiple, uniform, noncaseating epithelioid granulomas
o Affects multiple organs, most commonly lung tissue and lymph nodes
o Abnormal T cell function
o C4 K
 Etiology:
o Idiopathic
 Most likely an immunologic basis, immune mediated
o Hypersensitivity response (bacteria, fungi, virus): Fibrosis, loss of elasticity
o Activation of alveolar macrophage to unknown trigger
o First-degree relative increases risk 5-fold
 Clinical Manifestations:
o Noncaseating granuloma
o Malaise, fatigue
o Weight loss/Anorexia