Managing Chronic Disease Exam questions and
answers
What is COPD characterized by?
Airflow limitation that is not fully reversible and is usually progressive
What causes the inflammation in COPD?
Long term exposure to noxious particles and gases
What are the consequences of the amplified inflammatory response in COPD?
Hypersecretion of mucus (chronic bronchitis), parenchymal destruction (emphysema), and fibrosis
(bronchiolitis)
What are the characteristic physiologic abnormalities associated with COPD?
Mucus hypersecretion, Ciliary dysfunction, Airflow obstruction and hyperinflation, Gas exchange
abnormalities, Pulmonary hypertension
How does air-trapping and decreased ventilation affect gas exchange in COPD?
It leads to hypoxemia with or without hypercapnia
What is the main mechanism for abnormal gas exchange in COPD?
Abnormal V/Q ratios due to anatomical changes
How does airway obstruction in COPD impact gas exchange?
It leads to a decrease in forced expiratory volume (FEV1) and air trapping
What happens to CO2 levels in COPD due to inability to fully exhale?
They elevate
How does a reduction in ventilation or an increase in physiologic dead space affect gas exchange in
COPD?
It leads to decreased gas exchange
Spirometry results include:
•Forced vital capacity (FCV)
•Forced expiratory volume (FEV-1)
Treating Stable COPD
•Bronchodilators
•Beta-2 agonists, antimuscarinics, methylxanthines
•Inhaled corticosteroids
, •Systemic glucocorticoids
•Phosphodiesterase inhibitors (Viagra)
Treating Acute Exacerbations
•Controlled oxygen therapy
•Increased dose/frequency of bronchodilators
•IV glucocorticoids
•Antibiotics if indicated
•Monitor fluid balance, nutritional status, coagulation
Spontaneous Pneumothorax
Damage to lung tissue can result in leakage of air into the pleural spaces, which can cause lungs to
collapse
What is pulmonary hypertension?
Remodeling of the pulmonary vasculature in later stage COPD due to severe gas exchange abnormalities
What happens to the medial layers in pulmonary hypertension?
Medial layers hypertrophy to support ongoing vasoconstriction (think V/Q shunting)
How do endothelial cells change in pulmonary hypertension?
Remodeled endothelial cells do not release vasodilating agents (NO) but do release vasoconstricting
agents such as endothelin
nitric oxide (NO)
Vasodilating agent
Endothelin
vasoconstrictor agent
Ongoing vasoconstriction of the pulmonary arteries leads to
pulmonary hypertension
Severe pulmonary hypertension increases
right ventricular afterload, eventually leading to right-sided heart failure (cor pulmonale)
Chronic hypoxia results in
long-term SNS activity associated with increased blood pressure
•This increases workload of the heart, leading to hypertrophy and dilation
poor oxygenation triggers
ectopic areas, which can lead to atrial fibrillation and other dysrhythmias
Osteoporosis
answers
What is COPD characterized by?
Airflow limitation that is not fully reversible and is usually progressive
What causes the inflammation in COPD?
Long term exposure to noxious particles and gases
What are the consequences of the amplified inflammatory response in COPD?
Hypersecretion of mucus (chronic bronchitis), parenchymal destruction (emphysema), and fibrosis
(bronchiolitis)
What are the characteristic physiologic abnormalities associated with COPD?
Mucus hypersecretion, Ciliary dysfunction, Airflow obstruction and hyperinflation, Gas exchange
abnormalities, Pulmonary hypertension
How does air-trapping and decreased ventilation affect gas exchange in COPD?
It leads to hypoxemia with or without hypercapnia
What is the main mechanism for abnormal gas exchange in COPD?
Abnormal V/Q ratios due to anatomical changes
How does airway obstruction in COPD impact gas exchange?
It leads to a decrease in forced expiratory volume (FEV1) and air trapping
What happens to CO2 levels in COPD due to inability to fully exhale?
They elevate
How does a reduction in ventilation or an increase in physiologic dead space affect gas exchange in
COPD?
It leads to decreased gas exchange
Spirometry results include:
•Forced vital capacity (FCV)
•Forced expiratory volume (FEV-1)
Treating Stable COPD
•Bronchodilators
•Beta-2 agonists, antimuscarinics, methylxanthines
•Inhaled corticosteroids
, •Systemic glucocorticoids
•Phosphodiesterase inhibitors (Viagra)
Treating Acute Exacerbations
•Controlled oxygen therapy
•Increased dose/frequency of bronchodilators
•IV glucocorticoids
•Antibiotics if indicated
•Monitor fluid balance, nutritional status, coagulation
Spontaneous Pneumothorax
Damage to lung tissue can result in leakage of air into the pleural spaces, which can cause lungs to
collapse
What is pulmonary hypertension?
Remodeling of the pulmonary vasculature in later stage COPD due to severe gas exchange abnormalities
What happens to the medial layers in pulmonary hypertension?
Medial layers hypertrophy to support ongoing vasoconstriction (think V/Q shunting)
How do endothelial cells change in pulmonary hypertension?
Remodeled endothelial cells do not release vasodilating agents (NO) but do release vasoconstricting
agents such as endothelin
nitric oxide (NO)
Vasodilating agent
Endothelin
vasoconstrictor agent
Ongoing vasoconstriction of the pulmonary arteries leads to
pulmonary hypertension
Severe pulmonary hypertension increases
right ventricular afterload, eventually leading to right-sided heart failure (cor pulmonale)
Chronic hypoxia results in
long-term SNS activity associated with increased blood pressure
•This increases workload of the heart, leading to hypertrophy and dilation
poor oxygenation triggers
ectopic areas, which can lead to atrial fibrillation and other dysrhythmias
Osteoporosis
