COPd Flashcards
Emphysema
Anatomically destruction of the lung alveoli with air space enlargement
Chronic bronchitis
Chronic cough and phlegm
Pathological halo mark of COPD
Small airways maybe narrowed by cells, mucus, and fibrosis and extensive small airway destruction
4 events of pathogens is of emphysema
- Chronic exposure to cigarette smoke 2. Inflammatory release proteinase 3. Structural cell death through oxidant induced damage 4. Disordered repair of elastin and other extracellular matrix components
genetic deficiency in α1 antitrypsin (α1AT), the inhibitor of the serine proteinase neutrophil elastase, were at increased risk of emphysema, and that instillation of elastases, including neutrophil elastase, into experimental animals, results in emphysema.
Elastase:Anti elastase hypothesis
key component of COPD pathobiology
Oxidative stress
Major regulator of oxidant-antioxidant balance
NRF2
Potent antioxidant
SOD3
Change in large airway cause
Cough and sputum production
Small airway
Responsible for physiologic alteration
Gold criteria
Stage I mild FEV1/FVC <0.7 and FEV1 >80% predicted II moderate FEV1 <0.7 and FEV1 >50% but 80% III severe FEV1/FVC <0.7 and FEV1 >30% but < 50% predicted IV very severe FEV1/FVC 0.7 and
Cellular changes
Goblet cell,etaplasia Mucus secreting cells replacing surfactant club cells Smooth muscle hypertrophic Luminal narrowing cause by fibrosis Reduced surfactant Mononuclear inflitration
Emphysema
Destruction of gas-exchanging air spaces, the respiratory bronchioles, alveolar ducts, and alveoli
Emphysema
Destruction of gas-exchanging air spaces, respiratory bronchioles, alveolar ducts and alveoli Dx: bronchioalveolar lavage: 5x as many macrophage as non smokers Neutrophils and T lymphocytes, particularly CD8
Centrilobolar emphysema
Type most frequently associated with cigarette smoking enlarged spaces found initially in respiratory bronchioles Most prominent in the upper lobes and superior segments of lower lobes and quite focal
Panlobular emphysema
Abnormally large air spaces evenly distributed within and across acinar units. Is commonly observed in patient with a1AT deficiency Predilection for the lower lobes
Partial pressure of oxygen in arterial blood pao2 usually remains near normal until
fFEV1 is decreased to 50% of predicted
Elevation of arterial carbon dioxide (PaCo2) is not expected unit
FEV1 is <25% of predicted
Pulmonary hypertension can cause
Cor pulmonary and right ventricular failure Occurs in individuals who have marked decrease in FEV1 (25%) and chronic hypoxemia (pao2 <55mmHg)
pack-years
average number of packs of ciga-rettes smoked per day multiplied by the total number of years of smok-ing
A1 antitrypsin deficiency
M allele- associated with normal a1AT levels S allele: associated with slightly reduced a1AT levels Z allele: associated with markedly reduced a1AT levels, also occur with frequencies of >1% in most populations.
Most common form of severe a1AT deficiency
Two Z allele And one null allele
Curve c : normal rate of decline after a reduced growth Curve B: early initiation of pulmonary function decline after normal growth Curve D: accelerate rates of lung function
The absolute annual loss in FEV1 tends to be highest in mild COPD and lowest in very severe COPD
three most common symptoms in COPD
cough, sputum production, and exertional dyspnea
independent poor prognostic factor in COPD
wasting
advanced disease have paradoxical inward movement of the rib cage with inspiration
Hoover’s sign result of alteration of the vector of diaphragmatic contraction on the rib cage as a result of chronic hyperinflation
most likely explanation for newly developed clubbing.
lung cancer
hallmark of COPD
airflow obstruction reduction in FEV1 and FEV1/FVC lung volumes may increase, resulting in an increase in total lung capacity, functional residual capacity, and residual volume
diffusing capacity may be reduced, reflecting the lung parenchymal destruction characteristic of this disease
emphysema
Arterial blood gases provide additional information about alveolar ventilation and acid-base status by measuring arterial Pco2 and pH.
The change in pH with Pco2 is 0.08 units/10 mmHg acutely 0.03 units/10 mmHg in the chronic state.
defined as Pco2 >45 mmHg
ventilatory failure,
chest x-ray findings that suggests the presence of emphysema Diagnostic test
Obvious bullae, paucity of parenchymal markings, or hyperlucency Diagnostic test: CT scan - to rule out lung ca -to evaluate possible surgical therapy
two main goals of therapy
provide symptomatic relief (reduce respiratory symptoms, improve exercise tolerance, improve health status) and reduce future risk (prevent disease progression, prevent and treat exacerbations, and reduce mortality)
three interventions have been demonstrated to improve survival of patients with COPD.
smoking cessation, oxygen therapy in chronically hypoxemic patients, and lung volume reduction surgery (LVRS)
are the primary treatment for almost all patients with COPD and are used for symptomatic benefit and to reduce exacerbations
bronchodilators
Anticholinergic Muscarinic Antagonists
Short-acting ipratropium bromide improves symptoms with acute improvement in FEV1. Long-acting muscarinic antagonists (LAMA, including aclidinium, glycopyrrolate, tiotropium, and umeclidinium) improve symptoms and reduce exacerbations
Beta Agonists
ease symptoms with acute improvements in lung function. Long-acting agents (LABA) provide symptomatic benefit and reduce exacerbations, though to a lesser extent than a LAMA. long-acting inhaled β agonists are arformoterol, formoterol, indacaterol, olodaterol, salmeterol, and vilanterol. The main side effects are tremor and tachycardia.
Inhaled Corticosteroids The main role of ICS
reduce exacerbations
frequent exacerbations, defined
two or more per year, and in patients with features of asthma, such as eosinophilia
chronic use of oral glucocorticoids is associated with significant side effects
osteoporosis, weight gain, cataracts, glucose intolerance, and increased risk of infection
Theophylline
modest improvements in airflow and vital capacity Nausea is a common side effect tachycardia and tremor have also been reported
the only pharmacologic therapy demonstrated to unequivocally decrease mortality rates in patients with COPD.
Supplemental O2 For patients with resting hypoxemia( <88%) And with signs of pulmonary hypertension (<89%)
Eligibility for α1AT augmentation therapy requires
Eligibility for α1AT augmentation therapy requires a serum α1AT level <11 μM (~50 mg/dL). Typically, PiZ individuals will qualify, although other rare types associated with severe deficiency (e.g., null-null) are also eligible
Centrilobular emphysema
Severe upper lobe involvement Smoker
Panlobular
Diffuse loss of lung parenchyma predominantly in the lower lobes Severe a1 deficiency
Paraseptal emphysema
Marked airway inflammation
Lung Volume Reduction Surgery important prognostic characteristics
anatomic distribution of emphysema and post-rehabilitation exercise capacity
most likely to benefit from LVRS
upper lobe–predominant emphysema and a low post-rehabilitation exercise capacity are most likely to benefit from LVRS.
not candidates for LVRS
FEV1 <20% of predicted and either diffusely distributed emphysema on CT scan or diffusing capacity of lung for carbon monoxide (DLCO) <20% of predicted have increased mortality after the procedure
Pulmonary function curve
Classification of COPD
Treatment for COPD
