9/21- COPD Flashcards
(51 cards)
1
Q
Spectrum of Obstructive Lung Diseases (picture)
A
2
Q
What is COPD (definition)
- Onset
A
Preventable and treatable disorder of the airways characterized by airflow limitation that is not fully reversible
- Onset in midlife
- Airflow limitation usually progressive and associated with abnormal inflammatory response to particles or gases primarily caused by cigarette smoking
3
Q
Epidemiology of COPD
- Affected
- Diagnosed
- Deaths
- Disability
A
- 24 million affected in US
- Only 50% diagnosed (12 million)
- Estimated 130,000 deaths, being the #3 COD in the US (2012)
- #2 cause of disability (prob most common by 2020)
4
Q
Affected populations in COPD
- Age
- Gender
A
Age: 70% are under 65 yo
- COPD > diabetes and asthma in pts 45-64
Gender: women > men (5x)
- Deaths in women > men as well
5
Q
What is chronic bronchitis?
A
A clinical disorder
- Chronic cough on most days for at least 3 mo/year
- At least two consecutive years
- Cough and sputum production not due to any other specific causes
6
Q
What is emphysema?
A
A disease in which airspaces distal to the terminal bronchioles are enlarged with destruction of alveolar walls.
(defined in anatomic-pathologic terms)
7
Q
What are risk factors for COPD?
- Host factors
- Exposures
- Other
A
Host factors:
- Genetics (not all smokers get COPD)
- Gender
- Airway hyperreactivity
Exposures:
- Smoking
- Environmental pollution
- Perinatal events and childhood infection
- Recurrent infections
- Occupational and environmental exposure (e.g. coal dust, silica)
- Socio-economic status and (poor) diet
Others:
- Preexisting bronchial hyperreactivity (Dutch hypothesis)
8
Q
What is the relationship between smoking and COPD?
A
- Smoking is the predominant risk factor for development of COPD (>90% of pts with COPD)
- Dose-response relationship of FEV1 to the intensity of cigarette smoking
9
Q
What is the most important genetic risk factor for COPD?
- Mechanism (chrom)
- Alleles
- Inheritance
- Normal function
A
Alpha-1 anti-trypsin deficiency
- Deficiency of the protein from deficiency alleles of the AAT gene on chrom 14
Alleles:
- Normal = M, causes production of normal AAT
- S allele: slightly reduced levels
- Z allele: markedly reduced levels
- Null alleles may rarely be present
Inheritance:
- Autosomal recessive
- 1/3000 inherit, but only minority recognized - Not all pts with PiZZ develop COPD
- AAT def accounts for under 1% of COPD in US
Function:
- AAT-protein has potent protease inhibitor activity; protects normal lung tissue from proteolytic attack during inflammation
- Normal levels are 120-200 mg/dL
10
Q
When should you screen for AAT deficiency?
A
- COPD in a never-smoker
- Premature onset of COPD (moderate to severe impairment, by/before age 50)
- A predominance of basilar (lower lobe) emphysema
- Family Hx of AAT def or COPD onset before age 50
- Cirrhosis without apparent risk factors
- Bronchiectasis, esp. w/o risk factors for the disease
11
Q
What is the pathophysiology of COPD?
- What are the 2 main components of COPD?
A
- Environment/occupational exposures and childhood respiratory infections (and other risk factors) act on genetic susceptibility
- CD8 lymphocyte and neutrophil activation (MCP-1) and release of proteases
- Protease activation and tissue destruction (protease inhibitors knocked out)
- Airway inflammation and remodeling
Overall result = airflow limitation
2 main components of COPD:
- Airway wall thickening and inflammation (presentation = chronic bronchitis)
- Destruction of lung tissue (presentation = emphysema)
12
Q
How many COPD patients have never smoked?
A
~10%
13
Q
What cell types play a big role in COPD? Asthma?
A
COPD
- Macrophages
- Neutrophils
- CD8 lymphocytes
(elevated inflammatory mediators: IL-8, TNF-a, LTB-4, oxidants and imbalance in protease/anti-proteases)
Asthma
- CD4 lymphocytes
- Eosinophils
14
Q
How does cigarette smoking predispose people to COPD?
A
- Smooth muscle hypertrophy
- Replacement of Clara cells with mucus-secreting cells; less surfactant and more mucus
- Small airway, goblet cell metaplasia
- Neutrophil activation; elastases destroy walls of terminal bronchioles and alveolar ducts
All result in airway narrowing -> dyspnea
15
Q
What are the structural changes in COPD (histological/micro-anatomical)?
A
- Goblet cell hyperplasia/metaplasia
- Mucus gland hypertrophy
- Increased smooth muscle mass
- Airway fibrosis
- Alveolar destruction
Mucociliary dysfunction:
- Mucus hypersecretion
- Reduced mucociliary transport
- Mucosal damage
16
Q
Airflow limitation in COPD is caused by what?
A
- Loss of alveolar attachments
- Loss of elastic recoil
- Increased smooth muscle contraction
17
Q
What are the end results of the pathologic changes seen in COPD?
A
- Airflow obstruction
- Hyperinflation
- Impaired gas exchange
18
Q
What factor of COPD correlates more directly with patient-reported outcomes?
A
Hyperinflation (increased airway resistance)
19
Q
What are the clinical features expected in a COPD patient’s history?
A
- Smoking history
- Cough with sputum production
- Exertional dyspnea: usually gradual and progressive, constant
- RV failure (cor pulmonale) symptoms like pedal edema
20
Q
What is expected upon inspection of COPD patient? Palpation? Percussion?
A
Inspection
- Thin, asthenic (more in emphysema)
- Tachypnea
- Use of accessory muscles
- Tripod position
- Barrel chest
- Cyanosis rare
- Nicotine stained fingernails
- Hoover’s sign-inward movement of rib cage with inspiration
- Elevated JVD (if RHF)
Palpation:
- Barrel chest
Percussion:
- Enlarged lung volumes
21
Q
T/F: Clubbing is a common sign in COPD
A
False!
- Clubbing is not seen in pure COPD and it’s presence should alert you to look for alternate/additional diagnosis
22
Q
What is Hoover’s sign?
A
Sign of inspiratory muscle fatigue
- Inward movement of rib cage with inspiration
23
Q
What is expected upon auscultation of COPD patient?
A
- Decreased breath sounds,
- Prolonged expiration
- Wheezing, usually during exacerbations
24
Q
What is seen here?
A
Left: pink puffer
- Muscle wasting
- Use of intercostals/accessory neck muscles
- Pursed lips
Right: blue bloater
- Cyanosis seen in lips
25
Various patterns of disease seen in COPD?
26
What do flow volume loops look like in COPD?
- Scooped/spooned expiratory portion (obstructive disease)
- Hyperinflation indicated by increased RV and TLC
- Lower peak and slower flow
27
What x-ray view is best to diagnose COPD? What will be seen?
Lateral
- Can see air trapping and flattened diaphragm
28
Differences between COPD/asthma
- Onset
- Symptom progression
- Reversibility
- Smoking hx
- Cells involved
- Cytokines involved
- _Onset_: midlife for COPD; early in asthma
- Progressive sx in COPD but varied in asthma
- COPD is irreversible/poorly reversible airflow limitation while asthma is largely reversible
- COPD involves smoking Hx commonly (asthma hx could include allergic rhinitis and eczema)
- _Cells_: macrophages/neutrophils in COPD vs. eosinophils/mast cells in asthma
- CD8 T cells (COPD) vs. CD4 T cells (asthma)
- LTB4 (COPD) vs. LTD4 (asthma)
- _Cytokines_: COPD has IL-8, TNF while asthma has IL-4, 5, and 13
29
What is seen here?
Asthma
30
What is seen here?
Chronic bronchitis
31
What is seen here?
Emphysema
32
What is the global strategy for diagnosis, mgmt, and prevention of COPD?
Assessment:
- Assess symptoms
- Assess degree of airflow limitation using spirometry
- Assess risk of exacerbations
- Assess co-morbidities
33
How is COPD assessed?
- Description of breathlessness
- Lung function (mild to very severe on GOLD scale)
34
What are the treatment goals for COPD?
**Reduce symptoms**
- Relieve Sx
- Improve exercise tolerance
- Improve health status
**Reduce risk:**
- Prevent disease progression
- Prevent and treat exacerbations
- Reduce mortality
35
What are nonpharmacologic approaches to COPD management?
All stages of disease
- Smoking cessation
- Avoidance of indoor and outdoor occupational exposures
**Vaccinations**
- Influenza
- Pneumococcal – no documented evidence
**Optimizing nutrition**
**Oxygen Pulmonary rehabilitation**
**Surgical interventions** (LVRS, transplantation)
36
What is the most effective way to improve clinical outcomes in pts at all stages of COPD?
Smoking cessation
37
What effects does smoking cessation have in COPD patients?
- Rate of FEV1 decline can return to that seen in nonsmokers (with early smoking cessation)
- Decreased smoking slows the decline in FEV1
38
What are smoking cessation strategies?
**Advice from MD** (most imp motivator)
**Pharmacologic interventions:**
- Antidepressants (Buproprion), Chantix
- Nicotine replacement therapy
- Combo pharmacotherapy
- Clonidine patch
Behavior modification + pharmacologic intervention is better than either alone
39
What are the criteria for long-term Oxygen therapy?
- PaO2 under 55 mmHg or SaO2 under 885
- PaO2 under 59 mmHg and evidence of at least one of the following:
* Pulmonary HTN (P wave \> 3mm in LII, III or avF)
* Cor pulmonale (dependent edema)
* Erythrocytosis (Hct \> 56%)
40
What are common indications for pulmonary rehabilitation?
- Anxiety with activity
- Breathlessness
- Limitations with activity
- Loss of independence
41
What are essential components of pulmonary rehab?
**Education**
**Exercise training**
- upper-extremity
- lower-extremity
- strength
- respiratory-muscle
**Psychosocial/behavioral**
42
What are the main classes of bronchodilators available for the treatment of obstructive lung diseases?
- Anticholinergics
- Beta-2 agonists
- Methyl-xanthines
43
What are surgical therapies for COPD?
**Bullectomy**
- For patients with bulla \>1/3 of hemithorax
**Lung volume reduction surgery**
- LVRS offers a mortality and symptomatic benefit in selected patients with emphysema (upper lobe predominant and low post rehab. exercise capacity)
**Lung transplantation**
- Currently COPD is leading indication for transplant
44
What are novel treatment options for COPD?
Non-surgical bronchoscopic lung volume reduction (still under investigation)
45
What is COPD exacerbation? What should be done in these cases?
Marked worsening of symptoms from baseline
- Need to assess severity and try to identify precipitant
- May need CXR to rule out pneumonia and ABG to assess severity of hypoxemia and hypercarbia
46
How to treat COPD exacerbation?
- Aggressive bronchodilators
- Antibiotics
- Systemic corticosteroids
- Oxygen if needed
- Non-invasive mechanical ventilation
- Mechanical ventilation
47
What can cause bronchiectasis?
- Infection-most common
* Virulent bacterial, influenza, Pertussis childhood infection and Tuberculosis
* ABPA
- Slow growing endobronchial tumors, foreign body aspiration, stenosis
- Impaired pulmonary defense: immunoglobulin deficiency, primary ciliary disorder, cystic fibrosis
- Toxic inhalation, yellow-nail syndrome
48
What is the inheritance pattern of cystic fibrosis?
Autosomal recessive
49
What systems are affected in cystic fibrosis?
- Respiratory (bronchiectasis)
- Gastrointestinal
- GU symptoms
50
What are clinical findings in cystic fibrosis?
- Abnormal sweat chloride test (increased Na and Cl)
- Obstructive disorder symptoms
51
What is seen here?
Classic for **bronchiectasis**
- "**Signet ring**" sign
- Can see thickening of airway wall (not here)
