Obstructive Airway Conditions Flashcards
Air trapping results in:
HYPOventilation and HYPERcapnia
Chronic LOW O2 and HIGH CO2
What does obstructive mean?
Narrowed airways
-Casues airway obstruction worse on EXPIRATIONS
Causes increased work of breathing
-emptying of the lungs is slowed
-FEV1
-Use or accessory muscles
All obstructive diseases cause V/Q mismatch and hypoxemia
Dyspnea and wheezing are present in ALL obstructive diseases
Define air trapping
A person not able to fully EXHALE (cannot get out) = HIGH CO2
Air is trapped in the alveoli(a person works harder to breathe, and lungs are hyperinflated
Asthma
Chronic inflammation of the bronchial airways (NOT aveoli)
-causes bronchial HYPERRESPNSIVENESS, constriction of the airways and variable airflow obstruction that is reversible
Chronic disease state with exacerbations
Risk factors for Asthma
-Usually starts in childhood (highly associated with ALLERGIES)
-Familial link (1000 genes identified)
-Levels of allergen exposure
-Urban residency
-Exposure to indoor and outdoor air pollution
-Tobacco exposure/smoke
-Recurrent respiratory tract viral infections, and GERD
Pathophysiology of Asthma
-Exposure to antigen (trigger factor)
-Lots of immune cells involved in these processes (dendritic cells, T-helper 2 cells, B lymphocytes, mast cells, neutrophils, basophils, EOSINOPHILS
Common Asthma Triggers
-Activity
-Secondhand smoke
-Climate conditions
-Exposure to dust mites
-Pet dander
-Pollen
Early vs. Late Responses
Asthma
Early: initial response cascade of release of inflammatory mediators occurs within minutes
-Vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction and mucus secretion
Late: 4-8 hours later
-Recruitment of eosinophils, neutrophils, and lymphocytes during the acute response, causes another release of inflammatory mediators inciting the same process
Airway Remodeling
Chronic Asthma
Untreated inflammation can lead to long-term airway damage that is IRREVERSIBLE
Two responses of Asthma
Bronchoconstriction
#1 symptom of asthma attack
Inflammation
-The biggest problem and causes the seriousness of the disease
How do we diagnose Asthma?
History of allergies, recurrent episodes of wheezing, dyspnea, and course/exercise intolerance
PFTs (Pulmonary Function Tests)
-Measures lung function with respect to time
-GOLD STANDARD for diagnosing
-Decreased expiratory flow rate
-Decreased forced expiratory volume in 1 second
Symptoms with Asthma
Classic
-Wheezing
-SOA (breathlessness, dyspnea)
-Cough
-Chest tightness
Severe Attacks
-Use of accessory muscles
-Distant breath sounds
-Diaphoresis
-Inability to speak one or two words before taking a breath
RESPIRATORY FAILURE
-inaudible breath sounds
-repetitive hacking cough
Asthma Management
-Avoid asthma irritants
-Use peak flow meters
-Low-dose corticosteroids (mainstay for exacerbations), short-acting beta-agonist inhalers for milder forms
More severe
-Antiinflammatory medications are essential and INHALED corticosteroids, long-acting beta-agonist inhalers, or leukotriene antagonists
Status Asthmaticus
SEVERE SYMPTOMS
Unrelenting asthma attack
-Silent chest
-pCO2 >70 mmhg
LIFE-THREATENING EMERGENCY
May have epi pen for potential episode
treatment of status asthmaticus
-avoidance of precipitating factors and prophylactic
-bronchodilators, corticosteroids, and oxygen therapy are mainstays of treatment for an acute attack
-asthma meds are classified as either; 1.) preventors, 2.) relievers or rescue meds
chronic bronchitis
hypersecretion of mucus and chronic productive cough for at least 3 months of the year for at least 2 consecutive years
what are the 2 major types of bronchitis?
-simple (acute)
-chronic
simple (acute) bronchitis
-inflammation of the bronchioles and bronchi
-etiology: bacterial or viral- no airflow obstruction
-presentation: usually mild and self limited/requires only supportive care
-prognosis: good, usually better in 3-4 weeks
chronic bronchitis
-bronchitis for 3 months out of the year for at least 2 years
-etiology: cigarettes- positive airflow obstruction
-presentation: may have acute exacerbation of chronic bronchitis
-prognosis: premature morbidity and mortality
chronic bronchitis: clinical manifestations
-persistent productive cough- purulent if superimposed respiratory infection
-as disease progresses: increased cough, congestion and SOA
chronic bronchitis diagnosis
-based on history of symptoms, physical exam, chest imaging, PFT’s
-typically by the time people seek treatment, disease is in a progressive state and the pathological changes that have occurred are IRREVERSIBLE
-who gets chronic bronchitis?- SMOKERS
chronic bronchitis: patho
-inhaled irritants result in airway inflammation-infiltration occurs with neutrophils, macrophages, lymphocytes into the bronchial walls
-continual bronchial inflammation-bronchial edema, increase number and size of the GOBLET cell and mucus glands
-thick tenacious mucus produced and cannot be cleared because of impaired ciliary function
-initially process only affect larger bronchi- but eventually all airways involved
-obstruction of airway results, particularly during expiration when airways are narrowed
chronic bronchitis: LATE clinical manifestations
-pulmonary hypertension-advanced disease: increase in pulmonary artery pressure d/t elevated pulmonary venous pressure, increased pulmonary blood flow, pulmonary vascular obstruction, or hypoxemia
-symptoms: syncope, dyspnea on exertion, and fatigue
-right sided heart failure= cor pulmonale
chronic bronchitis: treatment
-prevention: irreversible- if patient stops smoking, disease process can be halted but not cured
-bronchodilators
-expectorants
-chest physiotherapy
-steroids late in disease
-home O2 therapy
emphysema
-abnormal, permanent enlargement of gas exchange airways, accompanied by DESTRUCTION of alveolar walls
-obstruction results from inflammatory and destructive changes in lung tissues
-major mechanism of airflow limitation is loss of elastic recoil with collapse of the airways during expiration
-lung hyperinflation
-destruction results from tissue changes and not mucus production
-2 degree change in lung tissue
emphysema causes
-major mechanism of airflow limitation is loss of elastic recoil caused by:
-SMOKING- including second hand
-air pollution
-childhood respiratory infections
-genetic emphysema-inherited deficiency of enzyme- antitrypsin
emphysema clinical manifestations
-gradual increase in BREATHLESSNESS- particularly with exertion
-eventually SOA at rest-with prolonged expiratory phase
-wheezing
-malnourished
-decreased muscle mass
-barrel chest
-pursed lip breathing
-decreased breath sounds- hallmark of emphysema
emphysema diagnosis:
-PFT’s- FEV1 decreased
-chest xray- hyperinflation
-ABG’s- respiratory acidosis
-alpha1-antitrypsin
emphysema treatment
-SMOKING CESSATION
-bronchodilators and anti-inflammatory agents- mainstay of treatment
-O2 supplementation
-breathing retraining
-relaxation techniques
-antibiotics for acute infections
Chronic Bronchitis (from picture slide)
-clinical diagnosis: daily productive cough for 3 months or more, in at least 2 consecutive years
-overweight and cyanotic
-elevated hgb
-peripheral edema
-rhonchi and wheezing
emphysema (from picture slide)
-pathologic diagnosis: permanent enlargement and destruction of airspaces distal to the terminal bronchiole
-older and thin
-severe dyspnea
-quiet chest
-x ray: hyperinflation with flattened diaphragms
