module 11 obstructive lung disease Flashcards
PFT
spirometry
pt takes deep inhalation and then exhales as quickly as possible until maximal air exhaled
- differentiates between obstructive and restrictive lung disease
normal PFT; FEV1, FVC
FEV1: forced expiratory volume in 1 second
- provides index for obstructive diseases
- 3.0L
FVC: forced vital capacity: total air exhaled
- 4.0L
FEV1/FVC = 75%
time of exhale determines flow
FEV1/FVC ratio
75% or > : no obstruction
50-60% : moderate obstruction
< 50%: severe obstruction
obstructive disease PFT
FEV1: less in 1st second than normal - 1.0L FVC: can exhale same amount, but it takes longer - 4.0L FEV1/FVC: 25% : severe obstruction
obstructive lung diseases
increased resistance to air flow within bronchi and bronchioles Wall lumen conditions: - asthma - acute/ chronic bronchitis Loss of lung parenchyma - Emphysema/COPD Obstruction of airway lumen - bronchiectasis - cystic fibrosis - acute trachobronchial obstructin - epiglottitis - croup syndrome
asthma
obstructive lung disease associated with trigger characterized by - reversible airway obstruction - airway inflammation - inc. airway reactivity to a variety of stimuli
asthma pathogenesis
airway inflammation -> loss od epithelial tissue
- > collagen deposition under basement membrane
- > mast cell activation/ IgE mediated
- > mucosal edema
- > inc. secretions
- > smooth muscle contraction
- > PSNS: bronchial constriction
intrinsic/nonallergic asthma
no history of allergies
- usually develops in middle age
- r/t resp. tract infections or psychological factors
- attacks severe
- variable response to therapy
extrinsic/allergic asthma
history of allergies
exercise induced asthma
bronchospasm occurs within 3 min after end of exercise, resolves around 60 min.
- heat loss, water, los, inc. osmolarity of lower resp. mucosa -> mediator release from basophil and mast cell -> smooth muscle contraction
asthma s/s
wheezing tightness of chest dyspnea cough inc. sputum SEVERE - retractions - dec. breath sounds - orthopnea - agitation - inc. RR - inc. HR - cyanotic
bronchitis
obstructive disease acute inflammation of trachea and bronchi - mucus accumulation - inflammation of epithelium - mucous plug - hyperinflation of alveoli - enlarge submucosal gland
acute bronchitis
inflammation of trachea and bronchi - mild and self- limiting - capillary dilation - swlling from exudation of fluid - infiltration w/ inflammatory cells - inc. mucus production - loss of ciliary funtion - loss of ciliated epithelium commonly causes by a virus, sometimes bacteria highest incidence in smokers, young children, elderly inc. prevalence in winter months
acute bronchitis s/s
cough low fever substernal chest discomfort ST postnasal drip fatigue
chronic bronchitis
Type B COPD "Blue bloater" dx symptomatically - hypersecretion of bronchial mucus and - productive cough of -- >3 mo. duration annually, x2 or more successive years Bacterial colonization common
chronic bronchitis s/s
males > females excess body fluids chronic cough SOB on exertion inc. sputum cyanosis (late sign) chills malaise muscle aches fatigue dec. libido insomnia
causes of chronic bronchitis
smoking repeated infections genetic predisposition inhalation of physical or chemical irritants inc. neutrophils inc. CD8 lymphocytes inc. eosinophils often extends into alveoli - narrowed airway - mucus plugs
chronic bronchitis pathogenesis
chronic inflammation and swelling of bronchial mucosa -> scarring, inc. fibrosis, hyperplasia of mucous glands and goblet cells, inc. wall thickness
-> worsened obstruction of airflow
emphysema
obstructive disease
Type A COPD
destructive changes of alveolar walls and abnormal enlargement of distal air sacs
- develops over long period of time
emphysema etiologies
smoking
air pollution
occupational exposure
a1-antitrypsin deficiency
antitrypsin
protective enzyme that inhibits proteolytic breakdown of alveolar tissue
emphysema pathogenesis
neutrophils release proteolytic enzymes -> alveolar destruction
smoking -> inflammation of parenchyma -> release of proteolytic enzymes -> damage to alveoli
– smoking inactivates antitrypsin
loss of alveolar walls and dec. pulmonary capillary bed -> dec. gas exchange
loss of elastic tissue -> dec. size of smaller bronchioles
-> loss of radial traction (nmlly holds airway open)
-> inc. pressure around outside of airway lumen
-> inc. resistance and dec. airflow
inhalation: air moves in
exhalation: bronchial walls collapse: air trapping -> Bullae
bullae
large, thin called cysts in lungs
3 classifications of emphysema
centriacinar (centrilobular) - smoking and chronic bronchitis -> destroyed bronchioles Panacinar (panlobular) - destroys alveoli Paraseptal - affects peripheral lobules
emphysema s/s
thin: inc. effort -> caloric expenditure use of accessory muscles pursed- lip breathing minimal or absent cough leaning forward to breath barrel chest digital clubbing dyspnea on exertion (late sign) bullae risk of pneumothorax
