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27 Cards in this Set
- Front
- Back
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2 distinct processes that make up COPD:
Definition of Emphysema? Definition of Chronic Bronchitis? |
Emphysema: permanent destruction and dilatation of alveolar airspace (due to loss of normal architecture). no fibrosis.
Chronic Bronchitis: presence of productive cough (sputum produced on most days for at least 3 months over 2 consecutive years) |
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How does an airway of a person with COPD differ from a normal airway (3 main features)?
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1. Destruction of septa and alveolar attachments (emphysema)
2. Mucus hypersecretion, causing airway narrowing 3. Inflammation of mucosa and fibrosis (brochiolitis) |
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What 2 pathways leading from inflammation are responsible for AIRFLOW LIMITATION?
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Inflammation -->
1. small airway disease, inflammation, remodeling 2. parenchymal destruction, loss of alveolar attachments and elastic recoil |
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What is the primary cause of COPD?
Describe the pathogenesis of this... |
Cigarette smoking! (in 90% of all COPD patients!).
1. Damage Airways (mucous hypersecretion, inflammatory cell response to oxygen free radicals) 2. Parenchymal destruction of CT matrix (neutrophils release elastase, matrix metalloproteinases) |
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What is a genetic abnormality linked to COPD? When does it typically present and what are some aggravating factors if any?
What is the Rx? |
a1-AT deficiency (deficiency of molecule that protects against lung destruction). Seen in 30s-40s (accelerated by smoking).
Rx= enzyme replacement therapy. Prevents progression (not cure). |
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Why do airwways become small in COPD?
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- goblet cell hyperplasia, edema, fibrosis, mucous plugs, increased smooth muscle
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Difference between Panacinar (panlobular) and Centriacinar (centrilobular) emphysema?
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- Panacinar: uniform involvement of acinus beyond terminal bronchiole, (seen in a1-AT deficiency)
- Centriacinar: affects proximal acinus and respiratory bronchiole (seen in smokers) |
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What happens to vasculature in patients with COPD?
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- thickening of pulm vessels
- vasoconstriction (in presence of hypoxia) - can lead to endothelial remodelling (thickened vessels) |
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What is the hallmark end-effect of airflow obstruction in COPD?
How does this manifest? |
Hyperinflation- due to increased obstruction (small airways) and airway collapse upon exhalation
Can flatten diaphragm (mechanical disadvantage). Manifests as DYSNEA (worsen with activity), limited inspiratory capacity |
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How does Inspiratory capacity during exercise differ between a normal person and someone with COPD?
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Normal: can exercise and will dip into some EELV (end expiratory lung volume), so will never fully reach IC.
COPD: Their EELV is building up (from air trapping and obstruction) so they will become ventilatory limited (hit up against IC) |
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What is the major mechanism of hypoxemia in patients with COPD?
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V/Q mismatch!
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Why do we see Pulmonary Hypertension with COPD?
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- Hypoxic vasoconstriction (chronic hypoxia)
- remodelling of pulm arteries - destruction of pulm capillary bed by emphysema * Remember, pulm HTN is associated with cor pulmonale (Right side heart failure) |
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Distinguish between the Pink Puffer and Blue Bloater types of COPD patients?
What would you do for each of them if they had a PCO2 of 50? |
Pink Puffer: emphysema associated, dyspnea, high Ve, using accessory muscles to breathe, poor response (will need to intubate), less V/Q mismatch.
Blue Bloater: associated with chronic bronchitis, overweight, brings up sputum, peripheral edema, more V/Q mismatch. |
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What kind of clincal history is suspicious for COPD?
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- >20 pack year smoking hx
- tends to present in mid-life (5th decade) with cough and frequent sputum - wheezing may be heard - dypsnea upon exertion in later stages *always check PFTs in patient who have smoked with cough |
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What is the Dyspnea Spiral?
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Breathlessness --> inactivity --> reduced exercise capacit --> deconditioning of muscles --> exacerabation of COPD and air trapping and dyspnea
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What happens to the FEV1 of patients with COPD?
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FEV1 decreases by ~50-100 ml per year
(need severe drop in FEV1 to exhibit DoE, dyspnea at rest, and cor pulmonale) |
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Physical appearance of Type A vs Type B patients?
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Type A (Pink puffer): Looks skinny, barrel chested, pursed lips, dyspneic. Patient is leaning forward- uncomfortable.
Type B (Blue bloater): Looks fat, edematous, cyanotic. Appears in less respiratory distress. |
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Risk factors for COPD?
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- smoking
- age >40 - exposure to dust/chemicals - Socioeconomic status - dyspnea/exercise intolerence/ fatigue |
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What would you expect to see on the chest xray of a patient with COPD?
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Chest X-ray:
1. Emphysema- increased lucency, bullae Hyperinflation (increased AP diameter, flattened diaphragm, narrow heart shadow) 2. Chronic Bronchitis- increased markings may be seen |
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What PFT value is essential for the diagnosis of COPD?
What other PFT values are consistent with COPD? |
Reduced FEV1/FVC (<70)
* remember- degree of reduction determines severity Hyperinflation: TLC increases Air trapping: RV increases * With emphysema, DLCO falls with disease progress |
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Severity of COPD, as determined by GOLD guidelines
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FEV1/FVC:
Mild 80-100 Moderate 50-80 Severe 30-50 Very Severe 0-30 |
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What is the BODE Index?
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Measure that classifies patients with COPD on prognosis/survivial.
B= BMI O= Obstruction D= Dyspnea E= Exercise capacity |
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Four components of COPD managemet?
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- assess severity, monitor disease
- Reduce risk factors! - Manage stable COPD (drugs, patient education, etc.) - Manage exacerbations |
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What is the only COPD treatment that both changes the TRAJECTORY of the disease and REDUCES MORTALITY?
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Smoking cessation (only 6% are successful). It can provide survival benefit and revert FEV1 levels back to that of a non-smoker
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What pharmacologic treatments could you consider giving a patient with COPD?
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Combination Therapy is ideal
B2 agonists Anticholinergics Methylxanthines (PDEi) ICS Oral CS *combined treatments will change the status of the disease (turn the clock back) but NOT the outcome/trajectory |
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When is it appropriate to give antibiotics to patients with COPD?
What about long term oxygen therapy? |
Abx- if infection or exacerbation (typically protecting against pneumococcus and H. Flu). Also give flu and pneumococcus vaccines!!
Long term O2 therapy increases survival in those with Pulm HTN or right heart failure and low pO2. |
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What surgical treatments would you consider in patients with COPD?
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- Lung volume reduction surgery (less tissue, less hyperinflation --> improves elastic recoil)
- Lung transplant (esp. for ATT deficient patients) |
