NSG 3850 EXAM 2 REVIEW | PATHOPHYSIOLOGY II ACTUAL
QUESTIONS AND ANSWERS LATEST UPDATED 2026/2027
(GRADED A+)- GALEN COLLEGE OF NURSING
AT GALEN COLLEGE OF NURSING
Patho Exam Review #2
Ch. 21: Respiratory Function and Alterations in Gas Exchange
HYPOventilation
Occurs when the delivery of air to the alveoli is insufficient to meet the need to
provide oxygen and remove carbon dioxide
Influenced by decreased rate and depth of respiration
Results in increased PaCO2 (>45) and resultant hypoxemia due to increased
alveolar carbon dioxide which displaces oxygen
Causes
o Drugs: Morphine or barbiturates (depress the central respiratory drive)
o Disorders: Obesity, Myasthenia gravis, Obstructive Sleep Apnea, chest
wall damage, or paralysis of respiratory muscles
o Pain r/t surgery of the thorax or abdomen
HYPERventilation
Is an increase in the amount of air entering the alveoli, leading to hypocapnia
PaCO2 (< 35).
Increased risk of rate and depth of respiration
Causes: hypoxic stimulation of peripheral chemoreceptors
o Pain
o Fever
o Anxiety
o Less common
▪ Obstructive and restrictive lung disease
▪ Sepsis
▪ Brainstem injury
mechanism
, o Normal physiologic response to high altitude as a compensatory
Hypoxemia
Deficient levels of blood oxygen
o Measured by ABGs or pulse ox
Hypoxia
Decrease in tissue oxygenation
, Decrease in blood flow leads to a decrease in oxygen delivery
Types of Hypoxias
o Hypoxic hypoxia
▪ PaO2 is decreased despite normal O2 carrying capacity
▪ Causes: high altitude,
hypoventilation, and airway obstruction
Oxygen therapy
o Anemic hypoxi a
▪ Results from a decrease in O2 carrying capacity
▪ Causes: any disorder resulting in low hemoglobin concentration
o Circulatory hypoxia
▪ Results from a low cardiac output state in which the O2 carrying
capacity is normal but the blood flow is reduce d
▪ Examples: shock, cardiac arrest, severe blood loss, thyrotoxicosis, and
CHF
o Histotoxic hypoxia
▪ Occurs when interference of a toxic substance leads to the inability of
tissues to utilize available oxygen
▪ Example: cyanide poisoning
Obstructive Pulmonary Disorders: Acute Bronchitis
Acute inflammation of the trachea and bronchi
Etiology
o Viruses (influenza)
o Non-viral (Strep)
o Heat, smoke inhalation, inhalation or irritant chemicals (sulfur dioxide,
chlorine, bromine, or fluorine gases)
o Allergic rxns
o *Highest incidence noted in: smokers, young children, and elderly in the
winter months
Pathogenesis
o Airways become inflamed and narrowed from capillary dilation
o Swelling from exudation of fluid
o Infiltration with inflammatory cells
o Increased mucus production
o Loss of ciliary function
o Loss portion of the ciliated epithelium
Clinical Manifestations
, o Usually mild and self-limited
o Cough may be productive or non-productive
o Low grade fever
o Substernal chest discomfort
o Sore throat
o Postnasal drip
o Fatigue
Diagnosis
o Usually based on the clinical presentation with recent onset of cough being
t he distinctive hallma
rk
o Chest radiograph may be help to distinguis h acute bronchitis (normal
radiograph) from (pulmonary infiltrates on radiograph)
pneumoniaChronic Bronchitis
Obstructive Pulmonary Disorders:
Etiology (Major causes)
o Cigarette smoking (90% of cases)
o Repeated airway infx
o Genetic predisposition
o Inhalation of physical or chemical irritants
o Type B COPD “Blue Bloater”
▪ Diagnosed symptomatically by hypersecretion of bronchial mucus
and a chronic or recurrent productive cough of more than 3 months
duration and occurring each year for 2 or more successive years
o Airway obstruction is persistent and irreversible when paired with
emphysema
Pathogenesis
o Chronic inflammation and swelling of the bronchial mucosa resulting in
scarring
▪ Extend into surrounding alveoli prevents proper oxygenation and
potentiates airway obstruction
o Hyperplasia of bronchial mucous gland/goblet cells
▪ Increased m uc us prod ucti on 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
QUESTIONS AND ANSWERS LATEST UPDATED 2026/2027
(GRADED A+)- GALEN COLLEGE OF NURSING
AT GALEN COLLEGE OF NURSING
Patho Exam Review #2
Ch. 21: Respiratory Function and Alterations in Gas Exchange
HYPOventilation
Occurs when the delivery of air to the alveoli is insufficient to meet the need to
provide oxygen and remove carbon dioxide
Influenced by decreased rate and depth of respiration
Results in increased PaCO2 (>45) and resultant hypoxemia due to increased
alveolar carbon dioxide which displaces oxygen
Causes
o Drugs: Morphine or barbiturates (depress the central respiratory drive)
o Disorders: Obesity, Myasthenia gravis, Obstructive Sleep Apnea, chest
wall damage, or paralysis of respiratory muscles
o Pain r/t surgery of the thorax or abdomen
HYPERventilation
Is an increase in the amount of air entering the alveoli, leading to hypocapnia
PaCO2 (< 35).
Increased risk of rate and depth of respiration
Causes: hypoxic stimulation of peripheral chemoreceptors
o Pain
o Fever
o Anxiety
o Less common
▪ Obstructive and restrictive lung disease
▪ Sepsis
▪ Brainstem injury
mechanism
, o Normal physiologic response to high altitude as a compensatory
Hypoxemia
Deficient levels of blood oxygen
o Measured by ABGs or pulse ox
Hypoxia
Decrease in tissue oxygenation
, Decrease in blood flow leads to a decrease in oxygen delivery
Types of Hypoxias
o Hypoxic hypoxia
▪ PaO2 is decreased despite normal O2 carrying capacity
▪ Causes: high altitude,
hypoventilation, and airway obstruction
Oxygen therapy
o Anemic hypoxi a
▪ Results from a decrease in O2 carrying capacity
▪ Causes: any disorder resulting in low hemoglobin concentration
o Circulatory hypoxia
▪ Results from a low cardiac output state in which the O2 carrying
capacity is normal but the blood flow is reduce d
▪ Examples: shock, cardiac arrest, severe blood loss, thyrotoxicosis, and
CHF
o Histotoxic hypoxia
▪ Occurs when interference of a toxic substance leads to the inability of
tissues to utilize available oxygen
▪ Example: cyanide poisoning
Obstructive Pulmonary Disorders: Acute Bronchitis
Acute inflammation of the trachea and bronchi
Etiology
o Viruses (influenza)
o Non-viral (Strep)
o Heat, smoke inhalation, inhalation or irritant chemicals (sulfur dioxide,
chlorine, bromine, or fluorine gases)
o Allergic rxns
o *Highest incidence noted in: smokers, young children, and elderly in the
winter months
Pathogenesis
o Airways become inflamed and narrowed from capillary dilation
o Swelling from exudation of fluid
o Infiltration with inflammatory cells
o Increased mucus production
o Loss of ciliary function
o Loss portion of the ciliated epithelium
Clinical Manifestations
, o Usually mild and self-limited
o Cough may be productive or non-productive
o Low grade fever
o Substernal chest discomfort
o Sore throat
o Postnasal drip
o Fatigue
Diagnosis
o Usually based on the clinical presentation with recent onset of cough being
t he distinctive hallma
rk
o Chest radiograph may be help to distinguis h acute bronchitis (normal
radiograph) from (pulmonary infiltrates on radiograph)
pneumoniaChronic Bronchitis
Obstructive Pulmonary Disorders:
Etiology (Major causes)
o Cigarette smoking (90% of cases)
o Repeated airway infx
o Genetic predisposition
o Inhalation of physical or chemical irritants
o Type B COPD “Blue Bloater”
▪ Diagnosed symptomatically by hypersecretion of bronchial mucus
and a chronic or recurrent productive cough of more than 3 months
duration and occurring each year for 2 or more successive years
o Airway obstruction is persistent and irreversible when paired with
emphysema
Pathogenesis
o Chronic inflammation and swelling of the bronchial mucosa resulting in
scarring
▪ Extend into surrounding alveoli prevents proper oxygenation and
potentiates airway obstruction
o Hyperplasia of bronchial mucous gland/goblet cells
▪ Increased m uc us prod ucti on 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
