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38 Cards in this Set
- Front
- Back
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COPD
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-smoking associated
-Emphysema and chronic bronchitis make up the disease |
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Asthma
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-obstructive airway disorder
-impacts the conducting airways -episodic -chronic inflamm process -hyper-responsive to triggers -broncho-constriction -edema and inflamm -mucus secretion |
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Risk factors for asthma
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-hype I hypersensitivity allergy
-genetic susceptibility -maternal smoking during preg -smoke exposure -childhood disease predicts adult disease -persistent disease--> persistent obstruction with airway remodeling |
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Childhood asthma
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-wheezing before age 3 does not always lead to astham
-may outgrow -approx 80% adult asthmatics had childhood asthma |
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Occupational asthma
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-adult onset
-need to get occupational hx -involves both immune-mediated and irritant mechanisms -includes pre-existing asthma becoming worse and new asthma |
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Symptoms of asthma
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-episodic: wheezing, SOB, chest tightness, cough
-nightime and early morning ssx -tiggered by AEROALLERGENS, particles, exercise, VIRAL INFECTIONS (RSV, Rhinovirus) -can present with only cough |
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Late phase asthmatic response
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-delayed ssx and fall in FEV1 hrs after stimulu
-hyperresponsiveness and inflamm -IgE mediated |
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Diagnosis of asthma
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1. Hx: observe over time
2. PE: upper resp tract (stridor), skin (eczema, hives?), lungs (wheezes on expiration, dec breath sounds) 3. CXR- hyperinflation 4. Spirometry with reduced airflow (scooped appearance) 5. Biomarkers |
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PE
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Between attacks: hyperinflated and hyper-resonant; nml lungs
During attack: hyperventilating, wheezing or quiet chest w/dec air movement; using accessory muscles |
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DDX
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1. COPD
2. CHF 3. Pulmonary embolism 4. pulmonary infiltration w/eosinophilia 5. cough due to drugs 6. Vocal cord dysfunction |
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COPD
|
-smoking associated
-Emphysema and chronic bronchitis make up the disease |
|
|
Asthma
|
-obstructive airway disorder
-impacts the conducting airways -episodic -chronic inflamm process -hyper-responsive to triggers -broncho-constriction -edema and inflamm -mucus secretion |
|
|
Risk factors for asthma
|
-hype I hypersensitivity allergy
-genetic susceptibility -maternal smoking during preg -smoke exposure -childhood disease predicts adult disease -persistent disease--> persistent obstruction with airway remodeling |
|
|
Childhood asthma
|
-wheezing before age 3 does not always lead to astham
-may outgrow -approx 80% adult asthmatics had childhood asthma |
|
|
Occupational asthma
|
-adult onset
-need to get occupational hx -involves both immune-mediated and irritant mechanisms -includes pre-existing asthma becoming worse and new asthma |
|
|
Symptoms of asthma
|
-episodic: wheezing, SOB, chest tightness, cough
-nightime and early morning ssx -tiggered by AEROALLERGENS, particles, exercise, VIRAL INFECTIONS (RSV, Rhinovirus) -can present with only cough |
|
|
Late phase asthmatic response
|
-delayed ssx and fall in FEV1 hrs after stimulu
-hyperresponsiveness and inflamm -IgE mediated |
|
|
Diagnosis of asthma
|
1. Hx: observe over time
2. PE: upper resp tract (stridor), skin (eczema, hives?), lungs (wheezes on expiration, dec breath sounds) 3. CXR- hyperinflation 4. Spirometry with reduced airflow (scooped appearance) 5. Biomarkers |
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PE
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Between attacks: hyperinflated and hyper-resonant; nml lungs
During attack: hyperventilating, wheezing or quiet chest w/dec air movement; using accessory muscles |
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DDX
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1. COPD
2. CHF 3. Pulmonary embolism 4. pulmonary infiltration w/eosinophilia 5. cough due to drugs 6. Vocal cord dysfunction |
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Severity classification of asthma
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1. intermittent: sx <2x/wk, asymp b/t attacks
2. Persistant: -Mild: Sx >2x/wk but not daily; night sx: >2x/month -Mod: Daily sx and B-agonist use; >1wk/night-time sx -Severe: limited by continuous sx; frequent nightime sx |
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Bronchial Hyperresponsiveness
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-sensitive to triggers and stimuli
-respond with bronchial constriction -histology shows inflamm: eosinophils, lymphocytes, airway remodeling (thickening of muscular layer) -mediates result in further cell injury and inflamm amplification |
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Cells and cell products
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-mediators: histamines, tryptase, leukotriense, cytokines
-neropeptides: modulate airway tone |
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Changes in airway morphology in asthma
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1. mucous gland hypertrophy
2. edema 3. mucus 4. thickening of basement membrane 5. 6. 7. |
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physiology of asthma
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-narrowed airways --> inc airway resistance
-inc work of breathing -reduced FEV1 ration -high volumes with air trapping -FRC increased -oxygenation defect much less common -respiratory alkalosis |
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Exercised induced bronchospasm
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-provokes bronchoconstriction
-cool dry air on epithelial surface -also seen in winter months -take bronchodilator 10-15 min before |
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Tx of asthma
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1. Quick relief: SABA, anticholinergics (atrovent, ipatropium), systemic steroids (prednisone)
2. Long term: ICS, Cromolyn Na and nedocromil, Anti-IgE, Leukotriene modifiers, LABA, Methylxanthines (many SI) |
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Pt education for asthma
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1. Self monitoring with peak flow or symptom diary
2. Written asthma action plan 3. Medication technique 4. Avoid enviornmental triggers, smoking 5. Take into account educational level and cultural issues |
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asthma- Treat co-morbidities
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1. GE reflux
2. Obestiy 3. Sleep apnea 4. Rhinitis 5. Sinusitis 6. Stres 7. Depression 8. Allergic BronchoPulmonary Aspergillosis (thick mucous plugs in airways) -tx is steroids |
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Chronic bronchitis
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-chronic cough and sputum production
-airflow obstruction: reduced FEV1 and ratio |
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Emphysema
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-irreversible enlargement of air spaces distal to terminal bronchioles
-alveolar wal destruction -airflow obstruction |
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mechanisms of airflow limitation in COPD
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-mucus
-hypersecretion- constant (luminal obstruction) -disrupted alveolar attachments (emphysema) -mucosal and peribronchial inflammation and fibrosis |
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The pink puffer
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-emphysema pt
-at end stage: -very skinny -pursed lip breathing -tipoding |
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Blue bloater
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-chronic bronchitis pt
-slightly cyanotic (not guarantee) -constantly coughing and bringing up sputum |
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CXR for COPD pts
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-Low, flattened diaphragm
-increased A-P diameter - hyperinflation (huge lung volumes) |
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Natual hx of COPD
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-normal decline in FEV1: 25-30 mL/yr from peak at age 25
-FEV1 decline in smokers: 45-60 mL/yr -more cigarettes smoked = stepper rate of decline -quitting at ANY age: better pulmonary function, slower rate of decline than those who continue to smoke |
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a1 Anti-trypsin deficiency in the pathogenesis of Emphysema
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-a1AT is an antiprotease and an inhibitor of neutrophil elastase
-the Z variant of a1 AT has deficient anti-proteolytic function and causes the most clinically sig manifestations -the ZZ genotype shows early onset of COPD |
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COPD management
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Mild: stop smoking, exercise, SABAs
Mod: LABAs (spireva), pulmonary rehabilitation (multi-disicplinary approach-breath training, diet), ICS Severe: O2 (decreased mortality), surgery (lung vol reduction) |
