12/7 COPD - Hussain Flashcards
COPD
chronic obstructive pulmonary disease
irreversible airflow obstruction and persistent inflammation
- bronchiectasis
- asthma (reversible)
- emphysema
- chronic bronchitis
- cystic fibrosis
chronic bronchitis
basics
- chronic cough and sputum production for at least 3 months per year for 2 conseutive years
- men more commonly affected
- primary risk factor: smoking
pathophysiology
- mucous metaplasia
- difficulty clearing secretions due to
- poor ciliary fx
- distal airway occlusion
- ineffective cough secondary to resp muscle weakness, reduced peak exp flow
-
airflow obstruction
- mucus hypersecretion → luminal occlusion
- epithelial layer thickens → luminal narrowing
- incr mucus alters airway surface tension → lumen predisposed to collapse
***diffuse disease : need to remember when trying to effect V/Q mismatch
what causes inflammation?
- inhaled noxious stimuli (cig smoke, etc)
- incr neutrophils in airway lumen
- macrophages in airway lumen, wall, parenchyma
- CD8 lymphocytes in airway wall and parenchyma
- contrast: asthmatics have more CD4 lymphocytes
causes of COPD
smoking
- nicotine stimulates SNS →
- incr HR
- peripheral vasoconstriction
- incr bp and cardiac work
infection
- major contributing factor to aggravation and progression of COPD
heredity
- alpha-antitrypsin deficiency
- accounts for < 1% of COPD cases
- AAT produced by liver, found in lungs
- deficiency → lysis of lung tissue by proteolytic enzymes from neutrophils and macrophages → emphysema
alpha1AT deficiency
two types/causes
result?
- alpha-antitrypsin deficiency accounts for < 1% of COPD cases
- AAT produced by liver, found in lungs
- deficiency → lysis of lung tissue by proteolytic enzymes from neutrophils and macrophages → emphysema
- functional AAT deficiency: smoking → ROS production → inactivation of antiproteases → incr neutrophil elastase
- congenital AAT deficiency: incr neutrophil elastase
emphysema
basics
pathophys: structural changes, later manifestations
- abnormal permanent enlargement of airspace distal to terminal bronchioles
- accompanied by destruction of bronchioles
pathophysiology
- structural changes
- hyperinflation of alveoli
- as more alveoli coalesce, blebs and bullae can develop
- destruction of alveolar cap walls
- reduced SA for oxygen diffusion
- compensation via incr RR to incr alveolar ventilation
- narrowed, tortuous small airways
- air that is trapped causes bronchioles to collapse
- loss of lung elasticity
- elastin and collagen destroyed
overall: air trapping (hyperinflation and overdistension)
- consequences of emphysema disease process
- hypoxemia develops late in disease
- small bronchioles become obstructed due to
- mucus
- sm muscle spasm
- infl process
- collapse of bronchiolar walls
- recurrent infection
- production/stimulation of neutrophils and macrophages
- release of proteolytic enzymes
- alveolar destruction
- infl, exudate, edema
two types of emphysema
-
centrilobular: central part of lobule destroyed
* most common -
panlobular: whole lobule destroyed
* usually assoc with AAT deficiency
emphysema
clinical manifestations
- dyspnea
* progresses in severity: fine for a long time → dyspnea on exertion → dyspnea interfering with ADLs and during rest - minimal cough, no to small sputum production
- overdistention of alveoli leading to flattening of diaphragm → incr AP diameter
- hypoxemia and hypercapnea
* results from hypoventilation and incr airway resistance, issues with gas exchange
complications of COPD
- pulmonary HTN (pulmo vessel constriction due to alveolar hypoxia and acidosis)
- cor pulmonale (R heart hypertrophy +/- RV failure)
- pneumonia
- acute resp failure
hypoxemia in COPD
V/Q mismatch in emphysema vs chronic bronchitis
emphysema:
- incr ventilation of poorly perfused lung units → high V/Q ratio
- incr physiological dead space
- body compensates by shunting blood to better ventilated areas until it can no longer do so → late hypoxemia
chronic bronchitis:
- perfusion of underventilated areas → low V/Q ratio
- subsequent physiological shunt
shunt
vs
dead space
how do you know if shunt-like hypoxia exists?
dead space is caused by ventilated alveoli NOT BEING PERFUSED
- nonuniform blood flow
- uniform ventilation
- (either bc there’s no means for perfusion as in conduction zone or bc there’s an obstruction to perfusion, ex. PE)
shunt is caused by failure of venous blood to reach ventilated alveoli
- nonuniform ventilation
- uniform blood flow
- shunt-like hypoxia test*
- if you put someone on FiO2 and still cant improve their PaO2, you’ve got a shunt
COPD diagnostic studies
CXR, PFTs, arterial blood gas
diff between chronic bronchitis and emphysema PFTs?
CXR:
- early in disease? may not show abnormalities
pulmo fx studies:
- reduced FEV1/FVC (has to be less than .7)
- incr residual volume
- incr total lung capacity
arterial blood gas
- decr PaO2
- emphysema late, chronic bronchitis early
- incr PaCO2 (esp CB)
- decr pH (esp CB)
- later stages of COPD, incr HCO3
diff between emphysema and chronic bronchitis PFTs:
- emphysema involves destruction of parenchyma → affects gas exchange and diffusion capacity
flow volume loops
COPD drug tx
- bronchodilators (maintenance tx)
- beta-adrenergic agonists (ex. ventolin)
- MDI or nebulizer preferred
- anticholinergics (ex. atrovent)
oxygen therapy
- raises PO2 in inspired air
respiratory therapy
- pursed lip breating: prolong exhalation, prevent bronchiolar collapse and air trapping
- diaphragmatic breathing: focuses on using diaphragm instead of accessory muscles → max inhalation, slow RR
chronic bronchitis vs emphysema
bronchiectasis
permanent, abnormal widening of bronchi caused by destruction of muscle and elastic tissue
- results from/assoc with chronic necrotizing infections
occurs in context of chronic airway infection and inflammation
- causes include postinfectious conditions like bacterial/viral/fungal necrotizing pneumonias,
- mild to moderate airflow obstruction
- in bronchiectasis, small airways become obstructed due to inflammatory infiltrate from wall
- airway dilates → cilia rendered ineffective → mucus can’t be cleared → organisms breed in it!
- inflammation/infectious process takes hold
