Med Surg 2 Exam 2 .
Med Surg 2 Exam
2 Oxygenation
Chapter 28: Chronic Obstructive Pulmonary Disease (COPD)
COPD Description
***COPD causes irreversible airway changes while asthma can change can
be reversed
• Airflow limitation not fully reversible
o Usually progressive
• Abnormal inflammatory response of lungs, primarily
caused by cigarette smoking and other noxious
particles or gases
***COPD exacerbations and other coexisting illnesses or co-morbidities
contribute to the overall severity of the disease.
Chronic bronchitis: the presence of cough and sputum production
for at least 3 months in each of 2 consecutive years.
o an independent disease that may precede or
follow the development of airflow limitation.
Emphysema: is the destruction of the alveoli, and is a pathologic
term that explains only one of several structural abnormalities in
COPD patients.
o Barrel chest= air trapping
o COPD is secondary to air trapping
COPD Significance
• Third leading cause of death in United States
• Kills more than 133,000 Americans each year
• An estimated 12.7 million adults in the United States older
than age 18 have COPD.
• The number of people with COPD is greatly underestimated
because
the disease usually is not diagnosed until it is moderately
advanced.
COPD Etiology
Risk factors
o Cigarette smoking
o Occupational chemicals and dust
▪ Landscapers and farmers
,Med Surg 2 Exam 2 .
o Air pollution
o Severe recurring respiratory infections
o α1-antitrypsin deficiency (autosomal recessive disorder)
,Med Surg 2 Exam 2 .
▪ enzyme deficiency that predisposes you to COPD
• Some degree of emphysema has been thought to occur as
a person ages.
o caused by changes in the lung structure and the respiratory
muscles, even in a nonsmoker.
***Spirometry: how to diagnosis COPD, tests airway/pulmonary function
***Packs per day times number of years smoking = 10 or more pack years
COPD Cigarette Smoking
• Clinically significant airway obstruction develops in 15% of smokers
• COPD should be considered in any person who is over
40 with a smoking history of 10 or more pack-years
Effects of nicotine
o Stimulates sympathetic nervous system
▪ Increases HR
▪ Causes peripheral vasoconstriction
▪ Increases BP and cardiac workload
o ↓ Amount of functional hemoglobin
o ↑ Platelet aggregation
o Compounds problems in CAD
Effects of Cigarette Smoking on respiratory tract
o Hyperplasia of goblet cells
▪ Increased production of mucus
o Lost or decreased ciliary activity
▪ Used to move bacteria/mucus out of the respiratory tract
o Abnormal distal dilation and destruction of alveoli
o Chronic, enhanced inflammation
o Cigarette smoking causes oxidative stress, as well as an
imbalance between proteases that break down
connective tissue in the lung and antiproteases that
protect the lungs.
▪ These changes resulting from cigarette smoking increase
with more severe disease and even persist after
smoking cessation.
▪ May be genetically related if COPD patient has never
smoked
Remodeling: Smoking causes chronic, enhanced inflammation of
various parts of the lung with structural changes and repair.
Effects of Carbon monoxide (CO) from Cigarette Smoking
, Med Surg 2 Exam 2 .
o ↓ O2-carrying capacity
▪ ↑ Heart rate
▪ Impaired psychomotor performance and judgment
Passive smoking (environmental tobacco smoke or secondhand
smoke)
o ↓ Pulmonary function
o ↑ Respiratory symptoms
o ↑ Risk of lung and nasal sinus cancer
COPD Occupational & Environmental
• COPD can develop with intense or prolonged exposure to:
o Dusts, vapors, irritants, or fumes
o High levels of air pollution
o Fumes/ biomass fuels from indoor heating or cooking
with fossil fuels
o Many women, particularly worldwide, who have never
smoked are developing COPD because of cooking
with these fuels in poorly ventilated areas.
o If a person has occupational exposure and smokes, the risk of
COPD increases.
COPD Infection
• Severe recurring respiratory tract infections in childhood
have been associated with reduced lung function and
increased respiratory symptoms in adulthood=
predisposes an individual to COPD
• Tuberculosis= increase risk for COPD
o Result= scarring of the lung tissue making it harder to breathe
• People who smoke and have HIV infection have an
accelerated development of COPD.
COPD Heredity
• α-Antitrypsin (AAT) deficiency (autosomal recessive genetic
risk factor for COPD)
o Severe AAT deficiency leads to premature bullous emphysema in
the lungs found on x-ray.
o Emphysema occurs because of AAT deficiency.
o Lower levels of AAT result in insufficient
inactivation and subsequent destruction of lung
tissue.
• AAT, a α1-protease inhibitor, is a serum protein produced
by the liver and normally found in the lungs.
o Function: to protect normal lung tissue from attack by proteases
Med Surg 2 Exam
2 Oxygenation
Chapter 28: Chronic Obstructive Pulmonary Disease (COPD)
COPD Description
***COPD causes irreversible airway changes while asthma can change can
be reversed
• Airflow limitation not fully reversible
o Usually progressive
• Abnormal inflammatory response of lungs, primarily
caused by cigarette smoking and other noxious
particles or gases
***COPD exacerbations and other coexisting illnesses or co-morbidities
contribute to the overall severity of the disease.
Chronic bronchitis: the presence of cough and sputum production
for at least 3 months in each of 2 consecutive years.
o an independent disease that may precede or
follow the development of airflow limitation.
Emphysema: is the destruction of the alveoli, and is a pathologic
term that explains only one of several structural abnormalities in
COPD patients.
o Barrel chest= air trapping
o COPD is secondary to air trapping
COPD Significance
• Third leading cause of death in United States
• Kills more than 133,000 Americans each year
• An estimated 12.7 million adults in the United States older
than age 18 have COPD.
• The number of people with COPD is greatly underestimated
because
the disease usually is not diagnosed until it is moderately
advanced.
COPD Etiology
Risk factors
o Cigarette smoking
o Occupational chemicals and dust
▪ Landscapers and farmers
,Med Surg 2 Exam 2 .
o Air pollution
o Severe recurring respiratory infections
o α1-antitrypsin deficiency (autosomal recessive disorder)
,Med Surg 2 Exam 2 .
▪ enzyme deficiency that predisposes you to COPD
• Some degree of emphysema has been thought to occur as
a person ages.
o caused by changes in the lung structure and the respiratory
muscles, even in a nonsmoker.
***Spirometry: how to diagnosis COPD, tests airway/pulmonary function
***Packs per day times number of years smoking = 10 or more pack years
COPD Cigarette Smoking
• Clinically significant airway obstruction develops in 15% of smokers
• COPD should be considered in any person who is over
40 with a smoking history of 10 or more pack-years
Effects of nicotine
o Stimulates sympathetic nervous system
▪ Increases HR
▪ Causes peripheral vasoconstriction
▪ Increases BP and cardiac workload
o ↓ Amount of functional hemoglobin
o ↑ Platelet aggregation
o Compounds problems in CAD
Effects of Cigarette Smoking on respiratory tract
o Hyperplasia of goblet cells
▪ Increased production of mucus
o Lost or decreased ciliary activity
▪ Used to move bacteria/mucus out of the respiratory tract
o Abnormal distal dilation and destruction of alveoli
o Chronic, enhanced inflammation
o Cigarette smoking causes oxidative stress, as well as an
imbalance between proteases that break down
connective tissue in the lung and antiproteases that
protect the lungs.
▪ These changes resulting from cigarette smoking increase
with more severe disease and even persist after
smoking cessation.
▪ May be genetically related if COPD patient has never
smoked
Remodeling: Smoking causes chronic, enhanced inflammation of
various parts of the lung with structural changes and repair.
Effects of Carbon monoxide (CO) from Cigarette Smoking
, Med Surg 2 Exam 2 .
o ↓ O2-carrying capacity
▪ ↑ Heart rate
▪ Impaired psychomotor performance and judgment
Passive smoking (environmental tobacco smoke or secondhand
smoke)
o ↓ Pulmonary function
o ↑ Respiratory symptoms
o ↑ Risk of lung and nasal sinus cancer
COPD Occupational & Environmental
• COPD can develop with intense or prolonged exposure to:
o Dusts, vapors, irritants, or fumes
o High levels of air pollution
o Fumes/ biomass fuels from indoor heating or cooking
with fossil fuels
o Many women, particularly worldwide, who have never
smoked are developing COPD because of cooking
with these fuels in poorly ventilated areas.
o If a person has occupational exposure and smokes, the risk of
COPD increases.
COPD Infection
• Severe recurring respiratory tract infections in childhood
have been associated with reduced lung function and
increased respiratory symptoms in adulthood=
predisposes an individual to COPD
• Tuberculosis= increase risk for COPD
o Result= scarring of the lung tissue making it harder to breathe
• People who smoke and have HIV infection have an
accelerated development of COPD.
COPD Heredity
• α-Antitrypsin (AAT) deficiency (autosomal recessive genetic
risk factor for COPD)
o Severe AAT deficiency leads to premature bullous emphysema in
the lungs found on x-ray.
o Emphysema occurs because of AAT deficiency.
o Lower levels of AAT result in insufficient
inactivation and subsequent destruction of lung
tissue.
• AAT, a α1-protease inhibitor, is a serum protein produced
by the liver and normally found in the lungs.
o Function: to protect normal lung tissue from attack by proteases
