3850 Pathophysiology Exam 2 -
Comprehensive Review Notes 2026
, UNIT 3- OXYGENATION
ALTERATIONS IN PULMONARY FUNCTION- HYPOVENTILATION
• Patho
o Air delivered to alveoli is insufficient to provide O2 and remove CO2 o
Hypoventilation results in increased PaCO2 and hypoxemia
• Etiology o Drugs
Morphine and barbiturates (any drugs that cause respiratory depression)
o Obesity
o Myasthenia gravis (neuromuscular condition, that doesn’t allow person to take
deep breath)
o Obstructive sleep apnea (something occludes patient airway and prevents
normal exchange)
o Chest wall damage (broken ribs) o Paralysis of respiratory muscles o Surgery
of the thorax or abdomen
HYPERVENTILATION
• Pathos
o Increase of air entering the alveoli leads to hypocapnia (PaCO2 <35 mm Hg)
• Etiology
o Pain, fever, obstructive and restrictive lung diseases, sepsis, high altitude, and
brainstem injury
HYPOXIA
• Patho
o Decrease in tissue oxygenation
• Types
o Hypoxic hypoxia (high altitude, hypoventilation, obstruction)
o Anemic hypoxia (low Hg)
o Circulatory hypoxia (low cardiac output; shock)
o Histotoxic hypoxia (decreased O2 carrying capacity from a toxic substance;
cyanide poisoning)
,ACUTE BRONCHITITS
• Pathos
o Acute inflammation of the trachea and bronchi
• Etiology
o Viral or non-viral
o Heat
o Inhalation of smoke or chemicals o Allergic reactions
• Pathogenesis o **Airways become inflamed and narrowed 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
• Diagnostic test o Distinct hallmark of disease: recent onset of cough o
Chest x-ray to distinguish acute bronchitis from pneumonia
• Clinical manifestations o Cough (productive or non-productive)
o Low-grade fever o Substernal chest discomfort
o Sore throat o Postnasal drip Fatigue
CHRONIC BRONCHITIS
• Patho/etiology/pathogenesis o Etiology
Cigarette smoking (90%)
Repeated airway infections
Genetic predisposition
, Inhalation of physical or chemical irritants
Chronic or recurrent productive cough greater than 3 months, greater
than 2+ years
Type B COPD, **“blue bloater”
Hypersecretion of bronchial mucus
Persistent, irreversible when paired with emphysema
1:2 male to female ratio
>30 to 40 years o Pathogenesis
**Chronic inflammation and swelling of the bronchial mucosa resulting
in scarring
• Elevated IL8 levels recruit neutrophil activation
• Elevated CD8 T-lymphocytes
• Extend into surrounding alveoli prevents proper oxygenation and
potentiates airway obstruction
Hyperplasia of bronchial mucous gland/goblet cells
• Increased mucus production with formation of mucus plugs
Increased bronchial wall thickness
• Resistance increases work of breathing and O2 demands
• Ventilation-perfusion mismatch with hypoxemia and
hypercapnia; increases pulmonary artery resistance
Pulmonary hypertension
• Inflammation in bronchial walls with vasoconstriction of
pulmonary vessels and arteries
• Right-sided heart failure may occur r/t high pulmonary resistance
Destruction of bronchial walls
• Results in dilation of airway sacs: bronchiectasis
• Dilated contain pools of infected secretions that do not clear
themselves; can cause further infection that can spread to
adjacent lung fields by the lymphatics or venous drainage to
other areas of the body, commonly the brain
o Diagnostic tests
Chest x-ray
Pulmonary function test
Arterial blood gas
ECG
Secondary polycythemia
Comprehensive Review Notes 2026
, UNIT 3- OXYGENATION
ALTERATIONS IN PULMONARY FUNCTION- HYPOVENTILATION
• Patho
o Air delivered to alveoli is insufficient to provide O2 and remove CO2 o
Hypoventilation results in increased PaCO2 and hypoxemia
• Etiology o Drugs
Morphine and barbiturates (any drugs that cause respiratory depression)
o Obesity
o Myasthenia gravis (neuromuscular condition, that doesn’t allow person to take
deep breath)
o Obstructive sleep apnea (something occludes patient airway and prevents
normal exchange)
o Chest wall damage (broken ribs) o Paralysis of respiratory muscles o Surgery
of the thorax or abdomen
HYPERVENTILATION
• Pathos
o Increase of air entering the alveoli leads to hypocapnia (PaCO2 <35 mm Hg)
• Etiology
o Pain, fever, obstructive and restrictive lung diseases, sepsis, high altitude, and
brainstem injury
HYPOXIA
• Patho
o Decrease in tissue oxygenation
• Types
o Hypoxic hypoxia (high altitude, hypoventilation, obstruction)
o Anemic hypoxia (low Hg)
o Circulatory hypoxia (low cardiac output; shock)
o Histotoxic hypoxia (decreased O2 carrying capacity from a toxic substance;
cyanide poisoning)
,ACUTE BRONCHITITS
• Pathos
o Acute inflammation of the trachea and bronchi
• Etiology
o Viral or non-viral
o Heat
o Inhalation of smoke or chemicals o Allergic reactions
• Pathogenesis o **Airways become inflamed and narrowed 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
• Diagnostic test o Distinct hallmark of disease: recent onset of cough o
Chest x-ray to distinguish acute bronchitis from pneumonia
• Clinical manifestations o Cough (productive or non-productive)
o Low-grade fever o Substernal chest discomfort
o Sore throat o Postnasal drip Fatigue
CHRONIC BRONCHITIS
• Patho/etiology/pathogenesis o Etiology
Cigarette smoking (90%)
Repeated airway infections
Genetic predisposition
, Inhalation of physical or chemical irritants
Chronic or recurrent productive cough greater than 3 months, greater
than 2+ years
Type B COPD, **“blue bloater”
Hypersecretion of bronchial mucus
Persistent, irreversible when paired with emphysema
1:2 male to female ratio
>30 to 40 years o Pathogenesis
**Chronic inflammation and swelling of the bronchial mucosa resulting
in scarring
• Elevated IL8 levels recruit neutrophil activation
• Elevated CD8 T-lymphocytes
• Extend into surrounding alveoli prevents proper oxygenation and
potentiates airway obstruction
Hyperplasia of bronchial mucous gland/goblet cells
• Increased mucus production with formation of mucus plugs
Increased bronchial wall thickness
• Resistance increases work of breathing and O2 demands
• Ventilation-perfusion mismatch with hypoxemia and
hypercapnia; increases pulmonary artery resistance
Pulmonary hypertension
• Inflammation in bronchial walls with vasoconstriction of
pulmonary vessels and arteries
• Right-sided heart failure may occur r/t high pulmonary resistance
Destruction of bronchial walls
• Results in dilation of airway sacs: bronchiectasis
• Dilated contain pools of infected secretions that do not clear
themselves; can cause further infection that can spread to
adjacent lung fields by the lymphatics or venous drainage to
other areas of the body, commonly the brain
o Diagnostic tests
Chest x-ray
Pulmonary function test
Arterial blood gas
ECG
Secondary polycythemia
