Obstructive Pulmonary Diseases Flashcards
1
Q
How is COPD characterized?
A
- by decreased airflow rate during expiration
- often accompanied by elevated functional residual capacity resulting from trapped air
2
Q
What are the major COPD disorders?
A
- COPD:
chronic bronchitis: barrel chested, yellow sputum, chronic productive cough for 3 months in each of 2 successive years
emphysema: pink puffers, skinny, on supp O2, pursed lip breathing, abnormal and permanent enlargement of the airspaces that are distal to the terminal bronchioles. THis is accompanied by destruction of airspace walls, without obvious fibrosis - Bronchiectasis: outpocketing - mucus and bacteria build up, mucus plugging, and bronchioles will become dilated, maybe even necrotized, caused by infection
- irreversible, supp O2 is only tx that helps with longevity
3
Q
WHO definition of COPD?
A
- preventable and tx disease with some significant extrapulmonary effects that may contribute to its severity in individual pts. Its pulmonary component is characterized by airflow limitation that isn’t fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases
4
Q
Stats on COPD?
A
- 3rd leading COD in US
- approx 14.2 mill people have COPD
- 8-17% men
- 10-19% women
- prevalence rates have increased in women
- mortality rates: 200/100000 in men
80/100000 in women - COPD causes high utilization of resources of health care system: frequent office visits, frequent hospitalizations due to exacerbateions, chronic therapy: meds and O2
5
Q
How is COPD characterized?
A
- slow, progressive irreversible airway obstruction due to chronic bronchitis and or emphysema
- periodic exacerbations with:
increased dyspnea (stop exercising, become sedentary) - increased sputum (usually colorless)
- occasionally respiratory failure
- takes years to become clinically significant
- dx usually made in middle aged or older persons
- cigarette smoking is most frequent cause, although 1/5 smokers develop the disease
- signs of airflow obstruction on PFTs can ID susceptible patients
6
Q
What are known RFs for COPD? Possible RFs?
A
known:
- agents: cigarette smoke, enviro/occupational dusts and gases
- host: AAT deficiency
Possible:
- agents: air pollution, passive smoking, resp. viruses, socioeconomic factors, living conditions, alcohol
Host: age, gender, familial/genetic, airway hyper responsiveness
7
Q
Where is the site of airway obstruction in COPD? what does this result in?
A
- in smaller conducting airways ( less than 2 mm in diameter) this results in peripheral airway resistance due to: destruction of alveolar support loss of elastic recoil structural narrowing due to inflammation
8
Q
How are lung volumes affected by COPD?
A
- RV and Functional residual capacity are increased
- TLC may remain normal but is often increased
- vital capacity is reduced due to:
air trapping
decrease in lung elastic recoil (fibrosis and mucus destruction of alveoli tissue)
demands for increased minute volume may not allow lungs to empty completely during the time available for expiration
9
Q
How else are the lungs destructed in COPD?
A
- loss of surface area along with bronchial obstruction and altered distribution of ventilated air results in V/Q mismatch
- Hyperinflation of lungs in which alveolar pressure exceeds pulmonary artery pressure - this stops perfusion and creates physiologic dead space
- metabolic costs of breathing become excessive and respiratory muscles fatigue
- structural changes increase the work of breathing
- larger lung volumes put inspiratory muscles at mechanical disadvantage
- diaphragm is flattened, decreasing its ability to change intrathoracic volume: see this on CXR
- destruction of alveoli decreases surface area for gas exchange
10
Q
Definition of asthma, how does it differ from COPD?
A
- a complex disorder characterized by variable and recurring sxs, airflow obstruction, bronchial hyerresponsiveness and an underlying inflammation
- airflow limitations:
bronchoconstriction: bronchial smooth muscle contraction in response to exposure to a variety of stimuli
airway hyper-responsiveness: exaggerated bronchoconstrictore response to stimuli
airway edema: edema, mucus hypersecretion, formation of thickened mucus plugs
11
Q
Cell involvement in COPD and asthma?
A
- Asthma: (sensitizing agent) asthmatic airway inflammation, CD4 T cells, and eosinophils, completely reversible
- COPD: (noxious agent) COPD airway inflammation, CD8 T cells, macrophages, and neutrophils, this is completely irreversible
12
Q
Pts with chronic bronchitis are referred to as?
A
- blue bloaters
13
Q
Chronic bronchitis pathology and presentation?
A
- persistent cough resulting in sputum production for more than 3 months in each of the past 2 years
- pathologic findings: goblet cell hyperplasia, mucus plugging, excess mucus secretion, and fibrosis, loss of supporting alveolar, cause airflow limitation due to airway wall deformities thus narrowing the airway lumen. Excessive bronchial secretions and airway obstruction cause a ventilation/perfusion mismatch
- blue bloaters unable to maintain normal blood gases by increasing their breathing effort
- hypoxemia, hypercapnia, and cyanosis develop earlier than emphysema: when hypoxemia - pulmonary vessels are going to constrict - further impairs gas exchange and contributes to pulm HTN - leads to R ventricular hypertrophy (can’t relax) - have a greater chance of developing Cor Pulmonale
14
Q
What are the classic sxs of chronic bronchitis?
A
- increasingly productive cough - a lot of mucus production
- 1st sx: dyspnea with a progressive decrease in exercise tolerance
- frequent and recurrent pulmonary infections
- weight gain (early on)
15
Q
What are emphysema pts known as?
A
- pink puffers
16
Q
What is occurring in Emphysema?
A
- abnormal enlargement of the airspaces distal to the terminal bronchioles with destruction of the alveolar walls and capillary beds
- abnormal airspaces called bullae compress surrounding area of more normal lung
- loss of lung elasticity
17
Q
What are the most common causes of Emphysema? Presentation of emphysema?-
A
- most common causes: cigarette smoking, and AAT deficiency
- long hx of progressive dyspnea with late onset of nonproductive cough. Pts don’t realize they have it until well into later stages of disease
- initially they are able to overventilate and maintain relatively normal blood gas levels until late in the disease
- the work of breathing makes eating difficult. Pts are usually cachetic
- pursed lip breathing is helpful for:
increases resistance to outflow of air - helps to pervent airway collapse by increase airway pressure
18
Q
What are the 2 types of pathology of emphysema?
A
- centrilobar emphysema (CLE): most common, characterized by focal destruction, seen predominately in male smokers, most severe in the upper lobes
- panlobuar emphysema (PLE): involves the entire alveolus distal to the terminal bronchiole, most severe in lower lung zones, generally develops in pts with homozygous alpha 1 antitrypsin deficiency
19
Q
When should alpha-1 antitrypsin be considered?
A
- congenital
- should be considered in younger pts who show signs of emphysema, whether they have smoked or not
- pts with AAT deficiency frequently develop dyspnea 20-30 years earlier (at age 30-45 yo) than do smokers with emphysema and normal AAT levels
- cigarette smoking accelerates the progression of emphysema in pts with AAT deficiency. Sxs develop about 10 years earlier in AAT deficient individuals who smoke regularly.
20
Q
What is alpha-1 antitrypsin?
A
- in healthy persons, alpha 1 antiprotease serves as a protective screen that prevents alveolar wall destruction
- individuals with the AAT genetic defect don’t release alpha1 antiprotease from the liver, and serum and alveolar levels of the protein are low. Consequently alveoli lack antiprotease protection
- the imbalance of proteases - antiproteases in alveolus leads to unimpeded neutrophil elastase digestion of elastin and collagen in the alveolar walls and progressive emphysema
21
Q
What lab studies are done to test for emphysema?
A
- serum alpha 1 antitrypsin levels: used to ID disease and determine serum alpha1 antitrypsin levels, phenotyping is required to confirm AAT deficiency. DOn’t initiate AAT replacement therapy without testing
- chest radiography: AAT deficiency emphysema produces a hyperlucent appearance because healthy tissue has been destroyed,
Chest CT: demonstrates widespread abnormally hypoattenuating areas resulting from a lack of lung tissue
22
Q
Tx for AAT deficiency emphysema?
A
- AAT deficient individuals who have or show signs of developing significant emphysema can be tx with prolastin, a pooled, purified, human plasma protein concentrate replacement for the missing enzyme. Th US FDA has approved 2 other AAT protein concentrates, Aralast and Zemaira for augmentation therapy
- weekly IV infusions of AAT protein concentrates restore serum and alveolar AAT concentrations to protective levels. Although other dosing regimens have been used, only the weekly infusion schedule has US FDA approval
- once tx pts do pretty well
23
Q
What are the physical signs of COPD?
A
- increased anteroposterior chest diameter (barrel chest)
- use of accessory muscles to breathe
- peripheral cyanosis
- clubbing of the fingernails (a sign of chronic hypoxia)
- decreased breath sounds
- hyperresonance on percussion
- wheezing on expiration
- prolonged expiratory phase
- low flat diaphragm
24
Q
WHat are findings in advanced COPD disease?
A
- intervals between exacerbations become shorter
- cyanosis
- significant hypoxia and hypercapnea
- polycythemia - erythocytosis (red in the cheeks)
- pulmonary HTN
- R ventricular hypertrophy
- R sided Heart failure (cor pulmonale): JVD, peripheral edema, hepatojugular reflex (push on liver and jugular vein engorges)
