Lung Disease Flashcards
1
Q
Cancer number 2 cause of death in US
A
lung CA
*More deaths than breast, colon, prostate, pancreatic cancers combined
~30% of cancer deaths
2
Q
what is CA screening and what is its purpose?
A
-Asymptomatic disease in a large population with low incidence of that disease and must have growth pattern that allows intervention
Goals
- Reduction of cancer specific mortality
- Stage shift—fewer advanced cancers
3
Q
Risks and pitfalls to CA screening
A
- Lead time bias
- Length time bias
- Overdiagnosis
- Additional testing and work up (radiation, more invasive procedures, and FP)
4
Q
Who do we screen for lung CA and how
A
high risk patients by low dose CT
- ages 55-80 y/o who have a 30 pack-yr smoking hx
- currently smoke OR
- have quit smoking in past 15 years
*screening should be DCed once a person has not smoked for 15 yrs or develops a health problem that substantially limits life expectancy or the ability or willingness to have curative lung surgery
5
Q
Should you screen for Lung CA?
59 WF with DOE and cough: DOE walking 200ft has regular frequent cough productive of clear sputum
Cough is quite bothersome, treated multiple times for exacerbations
60 pack years of tobacco, quit a year ago
GOLD stage IV COPD, FEV1 = 0.8L (29%pred)
Chronically on oxygen
A
Screening candidate: NO- bc has sx
DO diagnostic CT !
6
Q
what is a solitary pulmonary nodule
A
- Focal rounded opacities less than or equal to 3cm
- Majority are less than one centimeter
- More high resolution imaging, dramatic increase in the number of nodules detected
7
Q
Nodule frequency on screening CT
- over 45y/o, 85% smokers:
- over 60y/o, over 10pky:
- 50 y/o, over 20pky:
- 55-75y/o, greater/equal 30pky:
A
- over 45y/o, 85% smokers: 13%
- over 60y/o, over 10pky: 23%
- 50 y/o, over 20pky: 69%
- 55-75y/o, greater/equal 30pky: 24%
*39% of participants at least 1 positive CT
8
Q
Minority of nodules found on screening CT scans are___
A
malignant, 2-12%
*dependent on a variety of factors
9
Q
clinical features to consider for solitary pulmonary nodule
A
- Patient age**
- Female gender
- Family or personal history of cancer (1.5 fold risk)
- Smoking history*
- COPD
10
Q
Lung CA relative risks
A
- Age
- Smoking 20-fold at 1ppd
- Passive ~2-5x
- Pipes/Cigars 4-5x
- THC ? - COPD 2-5x (despite correction for smoking)
- Family History 1.3-3.5x
- Race
- AA ~2x
- Latino 0.5x - Exposures
- Asbestos (10x),
- Radon (dose dependent)
- Pollution
- Industry
11
Q
describe the risk of lung CA with tobacco use
A
1-14 cig/day–> 7.7 RR of Lung CA
15-24 cigs/day–> 13.7
over 25–> 24.5
12
Q
radiographic features of solitary pulmonary nodule
A
- Size
- Border–Smooth vs spiculated
- “Popcorn” lesion with calcification, fat density–>hamartoma
- Benign calcification
- Solid vs ground glass
- Upper lobe vs non-upper lobe
- Radiographic emphysema
*Interval change on serial imaging
13
Q
describe the relationship between nodule size at detection and chance of malignancy
A
larger in size= greater chance of malignancy at detection
14
Q
Goals of SPN evaluation
A
- Expedite resection of potentially curable lung cancer
2. Minimize resection of benign nodules
15
Q
ACCP Evidence-Based Guidelines for SPN
A
- All previous CXRs should be reviewed
- Stable imaging for > 2 years does not need evaluation
- Benign, central calcification – no further eval
- Spiral chest CT with contrast
- For SPN less than 1 cm – PET NOT recommended
- SPN in marginal candidates, PET, if negative repeat CT in 3 months
- All resections must include a lymph node dissection
- Lobectomy is preferred over wedge or segmentectomy
16
Q
describe the Fleischner Society Guidelines for F/U and management of nodules smaller than 8mm detected incidentally at nonscreening CT
A
If less/equal to 4mm:
- LR: no F/u needed
- HR: F/u CT at 12 months, if unchanged, no further f/u
if greater 4-6mm:
- LR: f/u CT at 12 months , if unchanged, no further f/u
- HR: Initial f/u CT at 6-12 months then at 18-24 month if no change
greater 6-8mm:
- LR: Initial f/u CT at 6-12 months then at 18-24 month if no change
- HR: Initial f/u CT at 3-6 mo then at 9-12 and 24 mo if no change
Greater 8mm:
-LR and HR: F/u CT at 3, 9, and 24 mo, dynamic contrast-enhanced CT, PET, and/or biopsy
17
Q
what is COPD
A
- Airflow limitation that is not fully reversible
- Usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases.
-asthma, emphysema, and chronic bronchitis
18
Q
Most common (exposed) risk factor for COPD in the US and worldwide?
A
- smoking- most common exposure in US
- worldwide burning of biomass fuels (cooking indoors, burning organic matter)
**NOT dependent on SX
19
Q
compare asthma, emphysema, and chronic bronchitis
A
Asthma: reversible obstruction
Emphysema: enlarged airspace, “pink puffers” thin– dont require a lot of O2
-obstruction of alveolar air sacs
Chronic bronchitis: airway inflammation, cough and suptum, “blue bloaters” stocky, cor pulmonale
-desaturate more easily and need more O2)
20
Q
Cigarette smoking and exposure results in an estimated ___ deaths annually
A
443,000
*In 2007, smoking rates in the US finally dropped to below 20% (19.8%) but changes in smoking rates take decades to affect COPD rates
21
Q
how many smokers are there in the US and worldwide?
A
US: 48 million
Worldwide: 1.1 billion
22
Q
COPD is the __ leading cause of death in the U.S.
A
third
23
Q
describe the burden of COPD exacerbation on total health care
A
- 8 million office visits
- 1.5 million emergency department visits
- 715,000 hospitalizations
- 133,965 deaths in the United States
24
Q
how do you diagnose COPD
A
- Spirometry: A post-bronchodilator FEV1/FVC less than 0.70 confirms the presence of airflow limitation that is not fully reversible.
- also use spirometry to monitor its progression
25
who should you consider COPD dx in?
any pt who has cough, sputum production, dyspnea, and/or hx of exposure to risk factors
*To help ID individuals earlier in the course of disease, spirometry should be performed for patients who have chronic cough and sputum production even if they do not have dyspnea.
26
describe the grades of COPD
Grade 1: Mild
FEV1/FVC < 0.70
FEV1 > 80% predicted
Grade 2: Moderate
FEV1/FVC < 0.70
50% < FEV1 < 80% predicted
Grade 3: Severe
FEV1/FVC < 0.70
30% < FEV1 < 50% predicted
Grade 4: Very Severe
FEV1/FVC < 0.70
FEV1 < 30% predicted
27
Severity of FEV1 ___ correlate with mortality as well as exacerbations
does not
28
COPD tx is now aimed at:
- reducing symptoms,
- improving quality of life and
- trying to avoid exacerbations
29
when do you do spirometry
Sx: cough, suptum, SOB
| Exposure to RF: tobacco, occupation, indoor/outdoor pollution
30
Risk factors for COPD
1. cig smoke
2. occupational dust/chemicals
3. environmental tobaccos smoke
4. indoor and outdoor air pollution
5. nutrition
6. Genetics (ex. alpha1 AT-- think in young ppl)
7. infections (HIV)
8. socio-econiomic status
9. aging population
31
describe the pathogenesis of COPD
RF are amplifying mechanisms for lung inflammation--> lung inflammation prevents oxidative and proteinases/ repair mechanisms to take place
32
describe small airway disease
- airway inflammation
- airway fibrosis, luminal plugs
- increased airway resistance
33
How does COPD affect the entire body
1. Heart and vascular disease
2. Lung cancer (6-8 fold)
3. Osteoporosis
4. Poor nutrition/weight loss
5. Muscle dysfunction
6. Depression/Anxiety
7. Poor mental acuity
34
Goals of management of COPD
Determine the severity of the disease, its impact on the patient’s health status and the risk of exacerbations to guide therapy.
Consider:
1. current level of patient’s symptoms
2. severity of the spirometric abnormality
3. frequency of exacerbations
4. presence of comorbidities
35
Non-medical COPD therapies
1. smoking cessation
2. pulmonary rehab
3. O2 /NIV
36
The single most effective—and cost effective—intervention to reduce the risk of developing COPD and/or stop its progression
smoking cessation
* Counseling by health professionals significantly increases quit rates over self-initiated strategies
* Even a brief (3-minute) period of counseling to urge a smoker to quit results in smoking cessation rates of 5-10%.
37
Nicotine replacement therapies
1. Patches (slow onset, use for basal nicotine level)
2. Lozenges
3. Gum
4. Nasal Spray (most rapid onset)
5. Inhaled
*Recommended when counseling is not sufficient
38
Pharmacotherapy for smoking cessation
1. nicotine replacements (patches, gum, sprays, etc.)
2. Buproprion (Zyban)
3. Varenicline (Chantix)
39
what is Buproprion (Zyban) and describe its use
- Atypical antidepressant with unrelated anti-smoking activity
- Long-term abstinence rates similar to NRT (~19%)
- Start 1-2 weeks before quit date and 7-12 weeks after
40
what is Varenicline (Chantix) and describe its use
- Partial nicotine receptor agonist/antagonist
- Short-term quit rates higher than NRT, but long-term probably similar (~19%)
- Start week before quitting, 3months of treatment
- Concerns regarding depression?
41
describe the use of oxygen therapy for COPD
-Increases survival > 15h/day
Improves:
1. Hemodynamics
2. Polycythemia
3. Exercise capacity
4. Mental state
42
what are medicare qualifications for oxygen therapy?
1. PaO2 less/equal 55mmHg
2. SpO2 less/equal 88%
OR
PaO2 55-60mmHg
SpO2 less/equal 89%
-PHTN
-Peripheral edema
-Polycythemia (HCT over 55%)
Sleep:
30-45% desat.
SaO2 less/equal 93% predictive
SaO2 over 95% -safe
43
Why is nocturnal non-invasive ventilation (NIV) for patients good?
1. Clear benefits for hospitalized patient with acute hypercarbic respiratory failure
2. Improves acidosis, pCO2
3. Reduces need for intubations and mortality
*unclear benefits in chronic stable COPD
44
what is pulmonary rehab
Formalized program consisting of exercise training, nutritional counseling and disease education
-Inhaler use, oxygen titration, preventing infections
*All COPD patients benefit from regular physical activity and should be encouraged to remain active
45
benefits of pulmonary rehab
1. Improves exercise capacity and QOL
2. Reduces SOB
3. Reduces hospitalizations for exacerbations seen within 4 weeks of exacerbation
*Not widely available, not always covered by insurance
46
Medical therapies for COPD
1. vx
2. SABA / LABA
3. ICS
47
Pharmacotherapy for COPD is used to ____
| Not used to ____
decrease symptoms and complications (i.e. reduce exacerbations)
modify the long-term decline in lung function
48
vaccinations important for COPD
1. flu-- annually, reduces serous illness and death by 50%
2. Pneumovax 23 (pneumococcal polysaccharide vx)- Recommended for COPD patients over 65 years and for COPD patients less than 65 with an FEV1 less than 40% predicted
Reduces disseminated pneumococcal infections in COPD patients by 35%
3. Prevnar 13 (pneumococcal conjugate vx)-- Recommended for patients over 65 years
49
short acting bronchodilators for COPD
Albuterol (ProAir, Proventil, Ventolin)
Levalbuterol (Xopenex)
Ipratropium (Atrovent)
Ipratropium/Albuterol (Combivent)
50
Long acting bronchodilators for COPD
```
Tiotropium (Spiriva)
Aclidinium (Tudorza)
Salmeterol (Serevent)
Formoterol/Arformoterol (Foradil/Brovana)
Indacaterol (Arcapta)
Vilanterol
```
51
Pros and Cons of inhaled glucocorticoids
Pros
1. decrease sx
2. decrease exacerbations
3. Combined with a long-acting ß2-agonist is more effective than the individual components
Cons:
1. Increased risk of pneumonia
2. Chronic treatment with systemic glucocorticosteroids should be avoided because of an unfavorable benefit-to-risk ratio
52
inhaled glucocorticoids are best used in
-appropriate for symptomatic COPD patients with an FEV1 less than 50% predicted (Grade 3 or 4) and repeated exacerbations
53
___ is better than either component alone (TORCH trial)
LABA/ICS combination
* Trend towards reduced mortality
* LABA solo therapy OK for COPD (black box warning for asthma)
54
Effects of Tiotropium
1. reduces symptoms,
2. exacerbations and
3. hospitalizations (UPLIFT trial)
* may be additive to LABA/ICS combo
- concern for increased mortality w/ anticholinergic inhalers
55
describe the use of Macrolide Abx for COPD
1. azithromycin 250 mg daily
2. increases time to next exacerbation
3. Beware CV effects/QT prolongation
4. Increased bacterial resistance but less likely to become colonized
56
describe the use of phosphdiesterase- 4 inhibitors for COPD
1. roflumilast 500 mcg daily
2. reduces exacerbations in GOLD 3 - 4 patients with a history of exacerbations and chronic bronchitis
3. GI symptoms particularly diarrhea and weight loss may lead to intolerance of medication
57
what is the treatment for mild, stage I COPD
1. active reduction of RF (give flu vx)
| 2. SABA prn or SAMA prn
58
what is the treatment for moderate, stage II COPD
1. active reduction of RF (give flu vx)
2. SABA or SAMA prn
3. Add regular tx w/ one or more LABA or LAMA
4. Add pulm. rehab
59
what is the treatment for severe, stage III COPD
1. active reduction of RF (give flu vx)
2. SABA or SAMAprn
3. Add regular tx w/ one or more LABA or LAMA
4. Add pulm. rehab
5. Add inhaled glucocorticosertoids if repeated exacerbations
60
what is the treatment for very severe, stage IV COPD
1. active reduction of RF (give flu vx)
2. SABA or SAMA prn
3. ICS + LABA and/or LAMA
4. Add pulm. rehab
5. Add long term oxygen if chronic respiratory failure
6. Consider surgical tx
61
what is an exacerbation of COPD (AECOPD)
“An event in the natural course of the disease characterized by a change in the patient’s baseline dyspnea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patient with underlying COPD.”
62
Consequences of COPD exacerbations
1. Neg. impact on quality of life
2. accelerated lung fx decline
3. increased mortality
4. increased economic costs
5. impact on symptoms and lung fx
63
Consequences of AECOPD
1. Risk of re-hospitalization after hospitalization for AECOPD
- 25% at 1 year
- 44% at 5 years
2. Risk of death after hospitalization for AECOPD
- 21% at 1 year
- 55% at 5 years
3. Increased age and prior hospitalizations independent predictors for both
4. Up to 2/3 of exacerbations go unreported
64
Causes of AECOPD
1. Infections: Bacterial and Viral
2. Air Pollution
3. Unknown cause (1/3 of cases)
4. Pneumonia, PE, CHF, 5. Pneumothorax may mimic or aggravate COPD symptoms
65
Management of AECOPD
Mainstay of therapy:
- Short acting bronchodilators
- Systemic glucocorticoids
- Antibiotics
66
describe the use systemic steroids for AECOPD
1. shorter recovery time and hospital stay,
2. Improved lung function and hypoxemia
3. Reduced risk of treatment failure, early relapse
44. Prednisone 20-60 mg per day probably adequate but optimal duration is unclear (5 days? 7-14 days?)
67
describe the use of antibiotics for AECOPD
1. Reduce the likelihood of treatment failure
| 2. Length of treatment 5-10 days, specific therapy determined by local resistance patterns
68
describe the benefits of lung volume reduction surgery (LVRS)
20-30% of the diseased portions of the lungs are removed so that there is more space for the good lung tissue to expand. This allows the lungs to oxygenate blood more effectively and also allows more room for the diaphragm to take its normal shape and function.
69
describe the outcome of lung transplantation
5 Year Survival
Single lung transplants ~ 50%
Double lung transplants ~ 75%
70
2 mechanism that limit airflow
1. Small airway disease:
- airway inflammation
- airway fibrosis, luminal plugs
- increased airway resistance
2. Parenchymal destruction:
- loss of alveolar attachments
- decrease of elastic recoil leads to decreased expiratory airflow
71
What should you do if:
a lung nodule HAS benign calcification pattern or 2yr radiographic stability
what is if doesn't
Has: no further testing
doesn't have: asses probability of CA and surgical risk
72
Surgical risk factors for a lung nodule
1. projected post-op FEV1 less than 40% of predicted
2. VO2 max less than 15ml/kg/min
3. other comorbidities
