chapter 28: obstructive pulmonary disease Flashcards
COPD: what it is and what it isn’t
-preventable, but usually progressive disease
-limits airflow
-inflammation of airways and lungs and pulmonary blood vessels
NOT
-chronic bronchitis = cough + sputum for 3 months; 2 yrs in a row
-Emphysema = destruction of alveoli w/o fibrosis
*more men get it, but its worse for women
Risk factors for COPD: cigarettes
-Hyperplasia of cells, reducing airway diameter
-fucks with cilia
-dilates distal airway, messing up alveoli
-precancerous cells
-“remodeling” = chronic inflammation in lungs
-oxidative stress + protease imbalance (even after you’ve quit)
*secondhand smoke causes damage too
Risk for COPD: infections
-recurring respiratory infections from childhood
-HIV ppl get it faster
-TB is risk
Risk for COPD: asthma, air pollution, occupational chems
-lots of overlap bt asthma and COPD
-air pollution MIGHT be a risk factor
-coal and biomass fuels are deffinitely risk factors
-occupational exposure to smoke/chems is bad
Risk for COPD: aging and genetics
unclear whether aging is a factor
effects of aging:
-loss of elasticity/recoil
-stiffening of chest wall and rib mobility
-rounding of rib cage due to increased residual volume
-less alveoli as peripheral airways lose supporting tissue
-genes are a maybe –> some smokers get COPD, others don’t
Risk for COPD: Alpha-1 Antitrypsin Deficiency (AATD)
-autosomal recessive disorder that affects lungs and liver
-AAT is made by liver and found in lungs and inhibits alpha proteases during inflammation
-severe AATD causes premature bullous emphysema in lungs –> smoking makes it worse
What even is COPD?
airflow restriction bc loss of recoil and obstruction –> mucus, edema, bronchospasms
-progresses to pulmonary hypertension and systemic manifestations
-Inability to expire air
Inflammation process of COPD
-neutrophils, macrophages, and lymphocytes attract leukotrienes and proinflammatory cytokines
-oxidants make it worse –> increase protease activity (breakdown CT) and decrease antiprotease activity (protection)
Explain barrel chestedness/emphysema of COPD
alveolar attachments to small airways are destroyed, trapping air in lungs and increasing functional residual capacity
makes passive respiration difficult –> becomes dyspneic with little exercise
hypoxemia in COPD
-doesn’t happen at rest until late stages
-often issues during excercise –> give O2
As disease worsens, air trappings increase, alveolar walls get destroyed, and bullae/blebs form –> poor gas exchange
**Bullae not a/w capillaries
**hypercapnia is major issue
COPD mucus
-only present if predominant chronic bronchitis
caused by
-more goblet cells
-bigger submucosal glands
-cilia dysfunc
-stimulation f/ inflammatory mediators
systemic changes w/ COPD
-osteoporosis, diabetes, metabolic syndrome, and CV disease
pulmonary vascular issues
-arteries constrict bc of hypoxia
-smooth muscle thickens
-more pressure on vessels due to expansion of dysfunctional alveoli
-Right ventricle hypertroohy and possibly right HF
Classification of COPD
GOLD 1 = mild = FEV > 80%
GOLD 2 = moderate = FEV 50-80%
GOLD 3 = severe = FEV 30-50%
GOLD 4 = very severe = FEV <30%
Manifestations/Progression of COPD
cough (productive or not)
difficulty getting full breaths
dyspnea (constant) –> starts affecting ADLS
-lungs overinflate (emphysema), diaphragm flattens –> chest breather (inefficient)
-wheezing and chest tightness
-fatigue, anorexia, weight loss
-hypoxemia, hypercapnia, polycythemia, cyanosis
-high Hemoglobin, but low other stuff
Complications of COPD: pulmonary HTN and Cor Pulmonale
-erythropoiesis causes polycythemia, increasing blood viscosity
-Right hypertrophy and failure
-S3, S4, murmurs, big liver, and water retension
Give O2, maybe diuretics, and anticoagulants