COPD Flashcards
1
Q
Chronic Bronchitis Basics
A
- CLINICAL dx - productive cough for 3+ mo for 2 successive yrs
- Histo - airway inflammation, airway edema, mucus gland hypertrophy and excessive bronchial secretions
- Source of Resistance - narrowing of lumen from inflammation. edema and secretions
2
Q
Emphysema Basics
A
- HISTO/ANATOMIC dx - destruction of alveolar walls –> permanent airspace enlargement AND destruction of pulmonary capillary bed (distal to terminal bronchioles)
- Source of Resistance - loss of tethering effect of pulm parenchyma on the small airways –> lose patency during expiration AND pleural p becomes more pos –> airways collapse
3
Q
How are lung volumes affected in emphysema?
A
-Dec elastic recoil of lungs so get to FRC at higher pressure (inc FRC)
- Dec elastic recoil also means lungs can stretch to great max vol in inspiration (inc TLC)
- *Inc in TLC is less than inc FRC (so less inspiratory capacity)
-Also inc RV
4
Q
Exercise Induced Hypoxemia in Emphysema
A
- capillary destruction –> inc blood velocity even at rest (same CO must go thru smaller + caps)
- SO w/ exercise CO inc even more –> insufficient time for equilibrations at cap interface –> dec PaO2
- Emphysema is only obstructive disease w/ dec diffusion capacity due to cap destruction
5
Q
COPD Risk Factors
A
- Exposure to toxic fumes and gases - SMOKING, air pollution (dec max lung funct normally attained in young adulthood; quicker plateau then more rapid dec in function w/ age)
- Mucus hypersecretion and inc # acute exacerbations
- Strong correlation b/n childhood resp infections and COPD
6
Q
COPD Pathophysiology
A
- Smoking –> recruit neutrophils –> inflammation
- Both smoke and neutrophils inc the oxidant burden
- How inflammation is sustained in UNKNOWN
- Hypo - imbalance b/n proteinases (destroy lung tissue) and anti-proteinases –> ECM destruction and cells not attached to matrix are more susceptible to death + impairment of repair –> enlarged air space/depleted parenchymal elastic fibers/abnormal collagen arrangement
- Ex) dec in alpha-1 antitrypsin which normally inhibits neutrophil elastase (now more elastic destruction by neutrophils)
7
Q
Signs/Symptoms
A
- Cough (mucoid but maybe purulent in acute infections), dyspnea (why ppl present)
- PE - prolonged expiratory time (>4 sec), maybe some rhonchi or wheezing (level of wheezing does not relate
to severity) - Later - barrel chest, pursed lips during breathing, emaciation
- “Tripodding” - sit forward and support upper body w/ extended arms
8
Q
COPD Imaging
A
- X-ray used to r/o other causes NOT SPECIFIC; but may see inc lung markings and inc thickness of bronchial walls
- May see hyperinflation - flattened or concave diaphragm
- CT - better for pulm parenchyma; can quantify severity and anatomic extent; can see bullae
- Not diagnostic; must do functional tests
9
Q
COPD Complications (3)
A
- Pneumothorax - if sudden worsening of dysnpea; can be life-threatening
- Cor Pulmonale - results from alveolar hypoxia –> vasoconstriction
- Systemic - CVD, skeletal muscle weakness, bone disease, weight loss (all due to metabolic alterations and maybe inc circulating inflammatory cytokines - TNF-alpha and IL-6)
10
Q
Smoking Cessation Strategies (4)
A
- Nicotine replacement
- Buproprion - inhibits NE, serotonin and dopamine reuptake; reduces urge by more neuroTs available and dec reward
- Varinicline Tartrate (Chantix) - partial nicotine agonist; can also antagonize nicotine to blunt reward when ppl do smoke
- E-cigs release propylene glycol vapor w/o CO, carcinogens or hydrocarbons; 10% as much nicotine
11
Q
Meds and Therapies for COPD
A
-Smoking cessation
- Meds -
- Bronchodilators improve quality of life, dec exacerbation freq, maintain function
- Steroids do not improve function but dec exacerbation freq and improve quality
- Azithromycin / PDE4 inhibitor (roflumilast) - dec exacerbation freq in more severe COPD patients w/ very - Oxygen
- Pulmonary Rehab (education, exercise, psychosocial/behavioral support groups)
- Surgery - lung vol reduction in upper lobe dominant emphysema (allows healthy lung tissue to take up that space –> inc elastic recoil and dec hyperinflation to return diaphragm to normal shape) OR transplant (inc quality of life but not survival benefit)