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)
25
Q
What are key indicators for a COPD dx?
A
- chronic cough: present intermittently or every day, often present throughout the day, seldom only nocturnal
- chronic sputum production: present for many years, worst in winters, initially mucoid, becomes purulent with exacerbation
- dyspnea that is progressive, and persistent, worse on exercise and worse during respiratory infections
- acute bronchitis: repeating episodes
- Hx of exposure to RFs: smoking, occupational dusts and chemical smoke from home cooking and heating fuel
26
Q
What does COPD look like on a CXR?
A
- hyperinflation
- flattening of diaphragm
- increased retrosternal air space
- long narrow heart shadow
27
Q
What are some sig. changes in a CXR that would indicate emphysema?
A
- hyperinflated - a lot of airspace, looks blacked out
- diaphragm is flattened
- heart is narrow
28
Q
What will the ABGs be in COPD?
A
- will show mild to moderate hypoxia without hypercapnia in early states
- with progression of disease, hypercapnia becomes more prominent, lower pH with renal compensation
ABGs:
pH - 7.35
PCO2 - 75
PO2 - 60
HCO3 - 32
29
Q
WHat will the PFTs look like in COPD?
A
- FEV1 decreased
- TLC, FVC and RV increased
- CO2 diffusing capacity is decreased
- no reversibility with bronchodilators like asthma
- EKG may show RVH
30
Q
What are the complications of COPD?
A
- Cor Pulmonale:
Pulm. HTN and R sided Heart failure
poor gas exchange
Lower O2 level in blood
constriction of blood vessels
RVH
loss of contractile efficacy - Pneumonia: strep pneumo most common
- pneumothorax: bullae, weakened lung structure
- secondary polycythemia: body increases production of O2 carrying RBCs to compensate
- end stage lung disease: resp failure, decline in lung fxn, rising levels of CO2 in blood, eventually leads to slow LOC and cessation of breathing
31
Q
COPD tx?
A
- smoking cessation
- pulmonary rehab: respiratory muscle conditioning, whole body conditioning and strengthening, breathing training
- immunizations: pneumo and flu
- meds: tx of choice: bronchodilator: SABA at first or ipratropium (quick acting relief) can add on anticholinergic Tiotropium for persistent, or can add LABA + SABA or anticholinergic for rescue combo - frequent exacerbations LABA + Tiotropium, when in respiratory failure: add on ICS (supp O2)
32
Q
What is a part of the pharmacotherapy for COPD?
A
- bronchodilators: SABA: albuterol LABA: salmeterol Anticholinergics: Ipratropium (quick relief), Tiotropium Methylxanthines: theophylline - steroids: oral: prednisolone ihaled: fluticasone or Budesonide
33
Q
What are the SA inhaled bronchodilators?
A
- beta 2 agonists: albuterol
anticholinergics: ipratropium (atrovent)
impt that pt knows how to use properly and when to use - give both bronchodilators together (combo therapy)
34
Q
What are the LA inhaled bronchodilators?
A
- salmerterol (serevent) LABA
- tiotropium (spiriva: anticholinergic)
- or theophylline (not to be used much because of SE and narrow therapeautic window
35
Q
Use of steroids?
A
- inhaled first: advair - pts need to rinse out mouth after (otherwise will get thrush)
- use systemic for severe exacerbations
36
Q
What tx is more effective for stable COPD tx - LA bronchodilators or short acting?
A
- regular tx with long acting is more effective and more convenient
37
Q
What has been found with combined tx of LABA+ICS for COPD?
A
- reduced exacerbation rates
- no significant difference in rate of hospitalizations
- mortality was also lower with combined tx
- improved quality of life, lung function improvement and better compliance
38
Q
Use of Mucolytics in COPD?
A
- Mucolytics: mucomyst
- in pts with chronic bronchitis or COPD: tx with mucolytics was associated with a small reduction in acute exacerbations and a reduction in total number of days of disability
- benefit may be greater in individuals who have frequent or prolonged exacerbations or those who are repeatedly admtted to hospital with exacerbations with COPD
- they should be considered for use especially during winter months, in pts with moderate or severe COPD in whome ICS are not Rx
- they aren’t considered std therapy
39
Q
What is the non-pharm therapy used in COPD pts? what pts should be on this therapy?
A
- long term O2 therapy is the only tx that has been shown to prolong survival
- pts with the following should have long term continuous O2 therapy:
O2 sats of less than 90%, this will decrease the risk of:
R sided heart failure
polycythemia
impaired mental status
40
Q
Why is supp O2 controversial?
A
- possibility that with supp O2 the hypoxic ventilatory drive in COPD pt may be decreased resulting in worsening hypercarbia (hypercapnia)
- arterial O2 must be maintained in a range that is compatible with life even at the expense of precipitating respiratory failure requiring mechanical ventilation
- O2 delivery must be as low of a dose as possible to maintain hemodynamic stability
41
Q
Pros of supp O2? How much is needed?
A
- less dyspnea
- improved functional capacity and quality of life
- improvement in pulmonary htn
- prolonged survival
- but to benefit must use close to 24 hours/day, or at least more than 15 hours per day, no beneft if O2 sat isnt low to begin with
- can use stationary system for home and ambulatory system for mobility
42
Q
Other tx for COPD other than O2 and Rx?
A
- whole body conditioning: shown that when increased exercise, tolerance improves pulmonary sx and quality of life
- nutrition: COPD pts often protein malnourished need to work with dietician to improve protein status and gain and maintain weight
- Pulmonary rehab: relieves dyspnea and fatigue.
improves emotional function and enhances pts sense of control over their condition, these improvements are moderately large and clinically significant, rehab forms an impt component of the management of COPD
43
Q
What is tx for severe COPD?
A
- lung reduction surgery for emphysema: 5-20% mortality, 86% mean improvement in FEV1 at 6 months, benefits may be lost by 5 years (limited group - take out most distended area of lungs and reshape)
- or lung transplant
44
Q
Explain lung volume reduction surgery?
A
- not a cure for COPD but can improve quality of life
- goal of surgery is to reduce the size of lungs by removing about 20-30% of most of diseased lung tissues so that the remaining healthier portio can perform better
- also allows diaphragm to return to its normal shape allowing pt to breathe more efficiently
- surgery has been shown to help improve breathing ability, lung capacity and overall quality of life among those who qualify for it
45
Q
guidelines for the LVRS?
A
- BODE index exceeding 5
- takes into account BMI, airway obstruction (FEV1), dyspnea (MMRC dyspnea scale), and exercise tolerance (hall walk test). In addition researchers say the BODE index is better predictore of COPD mortality than FEV1 alone
46
Q
What are the guidelines for transplantation?
A
- pts with BODE index of 7-10 and at least one of the following:
hx of hospitalization for exacerbation assocd with acute hypercapnia (CO2 exceeding 50 mm Hg)
pulm HTN or cor pulmonale, or both despite O2 therapy
FEV1 of less than 20% and either DLCO of less than 20% or homogenous distribution of emphysema
47
Q
What is a COPD acute exacerbation
A
commonly considered to be episodes of increasing dyspnea and cough and change in amt and character of sputum
- it may or may not be accompanied by fever, myalgias, and sore throat
- approach to the pt includes assessment of severity, ID of precipitating factor and institution of therapy
48
Q
What are precipitating causes of COPD exacerbation?
A
- bacterial infections play role in many episodes: H influenzae. S. pneumo (Most common), M. cat and mycoplasma
- viral infections are involved in 1/3 of cases
- in 20-30% no specific precipitant can be Idd
49
Q
Pt assessment of COPD exacerbation?
A
- hx should include questions in regard to:
dyspnea during activities and at rest, fever, change in character of sputum, associated sxs as nausea, vomiting, diarrhea, myalgias, and chills - inquire about frequency and severity of previous exacerbations
- CXR, CBC, and possibly ABGs (hosp pts)
50
Q
What therapy should be instituted?
A
- O2 to achieve and maintain PAO2 of greater than 55-60 mm Hg and to keep arterial sats above 90%, hypoxic respiratory drive plays small role in pts of COPD
- inhaled bronchodilators: SABA first line agents (albuterol reduces duration of action in acute exacerbation allowing tx frequency of every 30-60 min as tolerated)
- anticholinergic agents equally effective, combo therapy: synergistic bronchodilation, rapid onset of action and few SEs
- glucocorticoids: 30-40 mg of oral prednisolone over 10-14 days. Reduce hosp stay, and improve recovery and reduce the chance of subsequent exacerbation or relapse for a period up to 6 months
- Abx: first line: septra, amoxicillin, doxy (don’t tx with same abx 2x in a row)
- for allergies or recurrent exacerbations: azithro, clarithro (Biaxin), levofloxacin (gram -)
51
Q
What are indications for ICU admission?
A
- severe dyspnea
- mental status changes
- persistent worsening hypoxemia
- hypercapnia
- respiratory acidosis
52
Q
D/C criteria?
A
- use of inhaled bronchodilators less freq. than q 4 hrs
- clinical and ABG stability for at least 12-24 hrs
- acceptable ability to eat, sleep and ambulate
53
Q
Prevalence of bronchiectasis?
A
- 110,000 individuals in US
- increases with age
- more common in women
- decrease in prevalence because of abx and vaccine
54
Q
What happens to bronchioles in bronchiectasis?
A
- loss of cilia
- increased mucus
- destruction of wall which leads to permanent dilation
55
Q
Differences b/t bronchiectasis and COPD?
A
- etiology: Bronchiectasis - infection or genetic or immune defect, COPD: smoking
- role of infection: B - primary, and COPD: secondary
- predominant organism: B- H flu, COPD: Strep pneumo
- both have airflow obstruction and hyperresponsiveness
- findings on chest imaging: B: airway dilation and thickening, mucus plugging, COPD: hyperlucency, hyperinflation, and airway dilation
Quality of sputum: B: purulent, 3 layered, COPD: clear and mucoid
56
Q
What 2 factors does bronchiectasis require?
A
- infectious insult
- impaired drainage, airway obstruction or defect in host defense
- host response to insult or blockage results in release of immune effector cells, neutrophilic proteases, and inflammatory cytokines
- these cause transmural inflammation, mucosal edema, ulceration, and neovascularization in airways
- result is perm. abnormal dilation and destruction of major bronchi and bronchiole walls
- recurrent infection is common which feeds into the cycle of further scarring, obstruction and distortion of airways along with temporary or perm. damage to lung parenchyma
57
Q
Pathogenesis of bronchiectasis?
A
- abnormal destruction and dilation of large airways
- congenital or acquired
- in bronchiectasis, the diameter of the bronchi is unusually large
- exam of walls of bronchial tubes reveals destruction of normal structural elements with replacement by scar tissue (remodeling)
- pus collects within the bronchi and the normal flow of O2 into the lungs, and CO2 out of lungs is impaired
58
Q
Etiologies of bronchiectasis?
A
- often caused by recurrent inflammation or infection of the airways
- it may be present at birth, but most often begins in childhood as a complication from infection or inhaling a foreign object
- defective host defenses
- cystic fibrosis causes about 50% of all cases of bronchiectasis in US today
- recurrent severe lung infections (pneumonia, TB, fungal infections)
- obstruction of airway by FB or tumor (CXR)
- can also be caused by routinely breathing in food particles while eating (aspiration)
59
Q
Presentation of bronchiectasis?
A
- sxs often develop gradually and may occur months or years after the event that causes the bronchiectasis sxs: chronic cough with LARGE amts of foul smelling sputum production hemoptysis cough worsened by lying on one side SOB worsened by exercise wt loss fatigue clubbing of fingers wheezing cyanosis paleness haitosis
60
Q
Dx of bronchiectasis?
A
- may hear small clicking, bubbling, wheezing, rattling or other sounds usually in lower lobes
- work up:
CXR
Chest CT: good at revealing thick dilated bronchial walls - sputum culture
- CBC: reveal anemia and diff may show evidence of left shift or fungal infection
- sweat test or ofther CF testing (newborns)
- serum immunoglobin analysis for CF or immune dysfunction in host
- serum precipitins (testing for abs to fungus aspergillus)
- A PPD skin test for prior TB infection
61
Q
Tx of bronchiectasis?
A
- should invovle efforts to reolve underlying disorder and improving bronchial hygeine
- abx therapy for approp. organism
- obstruction may require removal of fb or tumor
- mucolytics indicated to help thin sputum - so it can be more effectively expectorated and to tx infections approp
- physiotherapy: percussion and postural drainage may help lungs drain more effectively
- surgery indicated when particular area of lung constantly and severely infected
- Pneumococcal and influenza vaccination
- ICS: fluticasone BID: decreases H flu from sticking to walls of bronchioles
- NSAIDS: sig slowed progression of disease in CF bronchiectasis
- pulm rehab improved exercise
- tolerance by simulataneous inspiratory muscle training offtered but no additional benefit
62
Q
Abx therapy for bronchiectasis?
A
- used to tx acute exacerbations, to prevent infection or reduce bacterial burden
- 3 strategies:
1 - high oral dose for prolonged time of zithromax 500 mg 2/weeks for 6 months
2 - aerosolized abx: gentamycin
3 - regular pulsed dose of IV abx 2-3 week courses with 1-2 months in b/t
