Obstructive Pulmonary Conditions (Exam 1b) Flashcards
What does obstructive mean?
Narrowed airways (causes airway obstruction worse on EXPIRATION) (Air trapped in the lungs)
Obstructive airway causes
Increase work of breathing
With obstruction the emptying of lungs is slowed and this is measured by
Forced expiratory volume in 1 second (FEV1)
All obstructive disease cause
V/Q mismatch and hypoxemia (watch video)
Air trapping results in
Hypoventilation and hypercapnia
Build up CO2 and decrease O2
Obstructive Pathophysiology: Air Trapping
Occurs when person is not able to fully exhale so air cannot get out
Build up of CO2 in blood
Air trapped in the alveoli –> person works harder to breathe, lungs are Hyperinflated
Therefore: Normal exhalation is obstructed
Air trapping causes
Chronically HIGH CO2 and Low O@
Asthma
Chronic inflammation of bronchial airways
(not alveoli like other Obstructive conditions)
Chronic inflammation causes bronchial HYPERRESPONSIVENESS, constriction of the airways and variable airflow obstruction that is reversible
Asthma is a chronic disease (not curable) state with
Acute exacerbations
Risk factors for Asthma
Usually starts in childhood –> highly associated with allergies
Familial link
Levels of allergen exposure
Urban residency
Exposure to indoor and outdoor air pollution
Tobacco exposure and smoke
RI and GERD
Pathophysiology of Asthma
Exposure to antigen (trigger factor)
Lots of immune cells involved in these process –> dendritic cells-T helper-B lymphocytes-mast cells-neutrohphils-basophils-EOSINOPHILS
Trigger factors (antigen) causes
Bronchial airway inflammation which causes
- Hypersecretion of Mucus
- Airway Muscle Constriction
- Swelling Bronchial Membranes
Causes
Narrow Breathing Passages
Wheezing, cough, SOB, Tightness in chest
Common Asthma Triggers
Exercise (most common)
Second Hand Smoke (2nd)
Climate (3rd)
Dust mite
Pets
Pollen
Early Response Asthma
These cellular responses are activate immediately and the cascade of release of inflammatory mediators
Vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction and mucus secretion
Late Asthmatic Response
4-8 hours after early response
Recruitment of WBC causes another realse of inflammatory mediators inciting same process
Untreated Asthma Inflammation
Can lead to long term airway damage that is IRREVERSIBLE and is known as airway remodeling (CHRONIC ASTHMA)
Two Responses of Asthma
Bronchoconstriction = 1# symptoms of asthma attack
Inflammation: Biggest problem and causes the seriousness of the disease (airway remodeling)
How do we diagnose Asthma
History of allergies, recurrent episodes of wheezing, dyspnea, and exercise intolerance
What is the gold standard for diagnosing Asthma?
PFT’s
Measures lung function with respect to time (seconds)
-Decreased expiratory flow rate
-Decreased FEV1 (how much air can a patient blow out in one second)
Symptoms of asthma
Wheezing
SOA
Cough
Chest tightness
Severe Asthma Attacks
-Use of accessory muscles
-Distant breath sounds
-Diaphoresis
-Can not speak
-Respiratory failure (Silent chest)
-Repetitive hacking cough
Asthma Management
-Avoidance of irritants
-Use peak flow meter
-Low does corticosteroids (mainstay for exacerbations), short acting beta-agonist inhaler for milder forms
-Immunotherapy (allergy shots)
Severe asthma managment
Add anti inflammatory medications that are inhaled corticosteroid, long acting beta agonist inhalers, or leukotriene antagonists
How to monitor treatment
Use peak flow meter and keep an action plan
Status Asthmaticus
Severe symptoms = pCO2> 70 mm hg
Unrelenting asthma attack and silent chest because no air movement
Life Threatening Emergency
Chronic Bronchitis
Hypersecretion of mucus and chronic productive cough for at least 3 months of the year for at least 2 consecutive years
Chronic Bronchitis: Etiology
90% smoke cigs
Form of COPD
Chronic Bronchitis: Presentation
May have acute exacerbation of chronic bronchitis = AECB
Prognosis of Chronic Bronchitis
Premature morbidity and mortality
Chronic Bronchitis: Clinical Manifestations
Persistent Productive Cough
Purulent if superimposed respiratory infection (mucus becomes a favorable breeding ground for infections)
Chronic Bronchitis: Diagnosis
Based on history of symptoms, physical exam, chest imagining, pulmonary function test
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 AND VAPERS
Chronic Bronchitis: Pathophysiology
Inhaled irritants result in airway inflammation –> infiltration occurs with neutrophils, 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
Accumulation of inflammatory cells
Leads to thickened smooth muscles secondary to chronic bronchospasm (fibrosis)
Initially the process of chronic bronchitis
only affects 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 (syncope-DOE-Fatigue)
Right sided heart failure = cor pulmonale
cor pulmonale
right sided heart failure cause by pulmonary hypertension
Chronic Bronchitis: Treatment
Prevent if you can :/
If smoking is stopped before symptoms occurs, the risk for bronchitis decreases considerably and eventually reaches that of a person who have never smoked
Chronic Bronchitis Treatment Cont
Bronchodilators
Expectorants
CPT
Steroids late in disease ( or with acute exacerbations)
Emphysema
Abnormal, PERMANENT enlargement of gas exchange airways, accompanied by DESTRUCTION of alveolar walls
Obstruction results from inflammatory and dexctruces changes in lung tissues
Major mechanism of airflow limitation in Emphysema
Loss of elastic recoil with collapse of the airways during expiration
Emphysema
Disease of alveoli
Permanently enlarger
Emphysema is defined by
Chronic, Irreversible, Progressive, and Destructive lung disease characterized by:
Loss of elastic recoil = Decrease Recoil
Abnormal PERMANENT enlargement of air spaces distal to terminal bronchioles
Lung hyperinflation
Destruction results from tissue changes and not mucus production
What causes Emphysema and loss of Elastic recoil
SMOKING SMOKING SMOKING
Air pollution
Childhood Respiratory Infections
Genetic Emphysema
Primary emphysema
Inherited deficiency of enzyme –> alpha antitrypsin protein
Emphysema: Clinical Manifestations
-Gradual increase in breathlessness with any exceptions. = DOE
-Eventually SOA at REST (With prolonged expriartory phase) (May become oxygen dependent)
-Wheezing
-Malnourished (r/t increased WOB)
-Decrease Muscle Mass
-Barrel Chest
-Pursed lip breathing
-Decreased Breath Sounds Throughout
Emphysema: Diagnosis
PFT’s FEVI decreased
CXR - Hyperinflation of lungs
ABGS - Respiratory Acidosis ( really high CO2 causing low ph)
Emphysema: Treatment
Smoking cessation
Bronchodilators and Anti Inflammatory agent
O2 supplementation
Breathing retraining
Relaxation techniques
Antibiotics for acute infections
Blue Bloaters and Pink Puffers
SLIDE
COPD Umbrella
Term that can be used to describe a range of pulmonary conditions, including:
Chronic Bronchitis
Emphysema
Irreversible or refractory asthma
Hallmark sign of emphysema
Decrease breath sounds throughout
