COPD- Prager Flashcards
COPD Definition
Characterized by airflow limitation
that is not fully reversible. Airflow limitation is
both progressive and associated with an abnormal
inflammatory response of the lungs to noxious
particles or gases.
2 compartments: bronchi: bronchitis/bronchiolitis, parenchyma/alveoli: Emphysema
Pathophysiolgoy of chronic bronchitis
Cigarette smoke and other irritants causing mucous gland hyperplasia and inflammatory cellular infiltrate
• Pathology: hyperplasia of bronchial submucosal mucous glands, mucosal edema, and inflammatory cell infiltrate (but not lots of mast cells/eosinophils)
Emphysema definition
Permanent enlargement of air spaces distal to the
terminal bronchioles with wall destruction, reduction in elastic recoil
- Excessive airways collapse upon expiration
- Irreversible obstruction on PFT’
What are the main causes of COPD?
• Cigarettes: 15-20% of pack-a-day smokers
develop significant COPD
• Alpha 1-antitrypsin deficiency: a very
uncommon cause of genetically determined
emphysema (from proteased matrix proteins in interalveolar space)
• Chronic asthma with airway remodeling
Biomass smoke
Pathology of Emphysema vs Chronic Bronchitis
• EMPHYSEMA
– 1. alveolar wall destruction, fewer in number alveoli, loss of elasticity and disrupted alveolar attachments
– 2. enlarged air spaces (cysts, bulla)
• CHRONIC BRONCHITIS
– 1. narrowing of airways due to inflammation
– 2. edema of airway walls, and
– 3. excessive mucous production
What are they physiologic consequences of COPD?
• Hyperinflation of lung
• Overdistension of the Chest Wall (d/t effort)
• Flattening of diaphragm - shortening of muscles of
inspiration-respiratory muscle fatigue and hypoventilation
• V/Q mismatch-hypoxemia, hypercapnea in severe cases (Respiratory acidosis with compensating metabolic alkalosis)
• Loss of elastic recoil w/ emphysema - airways
obstruction
• Airway narrowing due to airway inflammation with
mucous hypersecretion, hypertrophic airway
epithelium, airway edema
• Slowing of forced maximal expiratory flow
(Vmax)-lower FEV1
• High airway resistance
• Reduced lung elastic recoil
• Excessive airways collapsibility (―floppy
airways
Retained air-air trapping, increased RV d/t premature airway closure, decreased DLCO
Mechanism of pulmonary hypertension in COPD
• Alveolar hypoxia leads to pulmonary vascular
constriction
• Pulmonary hypertension due to vasoconstriction
(reversible); vascular intimal thickening
(irreversible); loss of vascular cross-sectional area
(irreversible)
• Right heart failure (cor pulmonale)
Causes of Hypoxemia
• Ventilation/perfusion mismatch (COPD, asthma-increased A-a gradient)
• Hypoventilation (Resp Ms fatigue, drugs,
scoliosis, neuropathy)
• Shunt (alveoli filled with fluid: pulmonary edema,
pneumonia; atelectasis)
• Diffusion defect (interstitial disease)
• Decreased FI O2 (altitude
What is the difference in oxygen consumption devoted to respiratory muscles in a healthy patient vs an obese or emphysematous patient?
Normal can get up to 140 L/min, obese up to 40, Emphysema up to 30. Of that in emphysema 25% of O2 consumption needs to be used for respiratory muscles.
Pink Puffers Vs. Blue bloaters: difference in types of COPD
Pink puffers are pure emphysema, blue bloaters are bronchitic
What medications can be given for COPD?
• Bronchodilators (inhaled or pills): beta-agonists
(albuterol); anticholinergics [ipra(short)/tio(long) tropium],
theophylline (phosphodiesterase inhibitor, raises cAMP,
causing bronchodilitation, some anti inflammatory
effects)
– decrease airway resistance by increasing airway diameter
• Antibiotics for bronchial infections
• Corticosteroids (inhaled, oral)
– Potent anti-inflammatory agent: decrease airway edema,
mucous production, bronchospasm
Not so helpful for emphysema- just O2
