obstructive pulmonary conditions Flashcards
obstructive pulmonary conditions
emphysema
chronic bronchitis
asthma
asthma
chronic inflammation of bronchial airways (NOT alveoli)
asthma risk factors
-genetic
-level of exposure to allergens
-urban residency
-exposure to pollution
-tobacco exposure/smoker
-recurrent respiratory viral infections & GERD
patho of ashtma
- exposure to trigger/antigen 2. airway inflammation
- hyper secretion of mucus, airway muscle constriction, swelling bronchioles
- narrow breathing passage
- wheezing, cough, SOB, tightness in chest
patho of ashtma
- exposure to trigger/antigen 2. airway inflammation
- hyper secretion of mucus, airway muscle constriction, swelling bronchioles
- narrow breathing passage
- wheezing, cough, SOB, tightness in chest
what immune cells are involved in asthma process?
dendritic
T helper
B lymphocytes
mast cells
neutrophils
basophils
eosinophils
early asthmatic response
responses activated immediately and release of inflammatory mediators occurs within minutes
-vasodilation
-increased capillary permeability
-mucosal edema
-bronchoconstriction
-mucus secretion
late asthmatic response
4-8 hours after early
-eosinophils, neutrophils, lymphocytes gather
-another release of inflammatory mediators again –> causing same process
airway remodeling
untreated inflammation
long-term airway damage - IRREVERSIBLE
1 sign of asthma attack
bronchoconstriction
what is the biggest problem r/t asthma?
inflammation
long-term problem that causes seriousness of disease
how is asthma diagnosed? gold standard
pulmonary functions test: measures lung function with respect to time
*decreased FEV-1
*decreased flow rate
classic asthma symptoms
wheezing, SOB, cough, chest tightness
severe asthma symptoms (attack)
use of accessory muscles, distant breath sounds, diaphoresis, inability to speak, RESPIRATORY FAILURE (inaudible breath sounds, repetitive hacking cough, pCO2 >70)
management of asthma
avoid triggers
*peak flow meter (measures FEV1 @ home)
*lose-dose corticosteroids
*SABA (mild)
*anti-inflammatory, inhaled corticosteroids, LABA, leukotriene antagonist (severe)
*immunotherapy
treatment for asthma attack
bronchodilators, corticosteroids, oxygen
chronic bronchitis
hyper secretion of mucus and chronic productive cough for at least 3 months of the year for 2 years
acute bronchitis
inflammation of bronchi and bronchioles
*caused by bacterial or viral infection - NO obstruction
*mild and self-limiting - usually better in 3-4 weeks
chronic bronchitis
bronchitis for 3 months of of the year for 2 years
caused by SMOKING and OBSTRUCTION of airway
*may have acute exacerbation
what is the prognosis of acute exacerbation?
premature morbidity and mortality
chronic bronchitis: S/S
*persistent productive cough (purulent)
*frequent resp infections
as disease progresses…
increased cough, congestion, SOA
chronic bronchitis: diagnosis
based on hx of symptoms, exam, chest imaging, PFTs
low FEV1
*typically disease is progressed and irreversible by the time pt seeks treatment
patho chronic bronchitis
- inhaled irritants = airway inflammation
- infiltration of neutrophils, macrophages, lymphocytes into bronchial wall
- continual bronchial inflammation –> bronchial edema increase number and size of GOBLET cells and mucus glands
- causes thick mucus and can’t be cleared bc impaired ciliary fxn
late clinical manifestations of chronic bronchitis
pulmonary HTN: increase in pulmonary artery pressure d/t elevated pulmonary venous pressure, increased pulmonary blood flow, pulmonary vascular obstruction or hypoxemia
^may result in right-sided heart failure (cor pulmonale)
S/S: DOE, syncope, fatigue
treatment of chronic bronchitis
IRREVERSIBLE
stop smoking: halt progression
TEACH: if stopped before s/s occur, risk for bronchitis decreases considerably
*bronchodilators
*expectorants
*CPT
*steroids (late disease or acute exacerbations)
*O2 therapy
emphysema
chronic, irreversible, progressive lung disease characterized by:
-loss of elastic recoil
-abnormal, permanent enlargement of air sacs distal to bronchioles –> destruction of alveolar walls and capillaries
*AIRWAY REMODELING
-lung hyperinflation
destruction in emphysema results from
tissue changes NOT mucus production
loss of elastic recoil in emphysema - caused by
SMOKING
air pollution
childhood resp infections
genetic emphysema (alpha-antitrypsin
clinical manifestations of emphysema
*DOE
*SOA at rest (prolonged expiratory phase + O2 dependent)
*wheezing
*malnourished
*decrease muscle mass
*barrel chest
*pursed lip breathing
*decreased breath sounds !!!!!
diagnosis of emphysema
PFT’s: FEV1 decreased
CXR: hyperinfiltration
ABG’s: respiratory acidosis (high CO2, decreased pH)
check alpha1-antitrypsin (AAT)
treatment of emphysema
stop smoking
bronchodilators and anti-inflammatories
O2 therapy
breathing retraining
relaxation techniques
ATB for acute infections
