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94 Cards in this Set
- Front
- Back
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define asthma
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1. Reversible airway obstruction
2. Airway inflammation 3. Increased bronchial hyperresponsiveness |
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Status Asthmaticus
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1. Severe airway obstruction developing over day - weeks
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Hallmark of Asthma:
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Bronchial wall hyperresponsiveness
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Early Phase Asthma Reaction:
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Bronchoconstriction
1. Antigenic stimulation of bronchial wall 2. Mast cell degranulation releases A. histamine B. chemotactics C. proteolytics D. heparin 3. Smooth muscle bronchoconstriction |
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2. Mast cell degranulation releases what in early phase asthma attack?
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A. histamine
B. chemotactics C. proteolytics D. heparin |
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Late phase asthma reaction
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Bronchial inflammation
1. Inflammatory cells A. Neutrophils B. Monocytes C. Eosinophils 2. Release cytokines, vasoactives, arachidonic acid 3. Epithelial and endothelial cell inflammation 4. Release of interleukin 3-6, TNF, interferon-gamma |
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. Inflammatory cells release what in late phase asthma reactions?
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A. Neutrophils
B. Monocytes C. Eosinophils |
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FH of asthma?
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1. One parent with asthma:
Up to 25% risk for child 2. Two parents with asthma: Up to 50% risk for child |
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Risks for asthma?
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Family history
1. One parent with asthma: Up to 25% risk for child 2. Two parents with asthma: Up to 50% risk for child Parental tobacco abuse Associated aspirin or NSAID allergy 1. Classic Triad: Asthma, nasal polyps, aspirin allergy RSV bronchiolitis history 1. Strongly associated with later development of asthma |
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1. Classic Triad of asthma associated with what? Name the triad
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Associated aspirin or NSAID allergy
asthma, aspirin allergy and nasal polyp |
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Types of asthmas
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Extrinsic asthma (allergic)
Intrinsic asthma (non- allergic) Mixed asthma (extrinsic and intrinsic asthma) Occupational asthma 1. Toluene di-isocyanate 2. Platinum 3. Nickel Drug induced asthma 1. Aspirin or NSAID allergy Cough variant asthma 1. Very common!!!! (especially in children) |
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Occupational asthma
associated with what? |
1. Toluene di-isocyanate
2. Platinum 3. Nickel |
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Extrinsic Asthma
pathophys, epi, causes |
Pathophysiology
A. IgE medicated response to allergens Causes A. Airborne allergen B. Animal dander C. Foods D. Most common extrinsic Allergan: 1. House dust or mites Epidemiology A. Much more common in children than adults B. Age onset under 40 years old |
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Intrinsic Asthma
pathophys, epi, causes |
Pathophysiology
A. Non-IgE, non-allergic asthma Precipitating Factors A. Irritant exposure 1. Pollution 2. Fumes 3. Tobacco smoke B. Infection C. Gastroesophageal reflux Epidemiology A. Much more common in adults than children B. Onset age over 40 years old |
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Symptomes of asthma
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Episodic wheeze, chest tightness, shortness of breath, or cough.
Symptoms worsen in presence of aeroallergen, irritants, or exercise. Symptoms occur or worsen at night, awakening the patient Patient has allergic rhinitis or atopic dermatitis. Close relatives have asthma, allergy, sinusitis, or rhinitis. |
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Diagnosis of asthma
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The diagnosis of asthma is made with an increase of FEV1 of 12% or a min of FEV1 of 200ml after bronchodilator theraphy.
Bronchodilator theraphy can be a simple can be a simple nebulized treatment or Albutarol through a spacer or chamber Pts who are suspected of having asthma but have normal spirometry can undergo a methacholine challenge. The lower the concentration of methacholine to cause a 20% drop in the FEV1 the more likely the patient has asthma. When patient have possibly COPD or Asthma a diffusing capacity for carbon monoxide (Dlco) can be used Asthma= Dlco is normal or Increased COPD=Dlco is decreased |
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Diff diagnosis btwn COPD and asthma
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When patient have possibly COPD or Asthma a diffusing capacity for carbon monoxide (Dlco) can be used
Asthma= Dlco is normal or Increased COPD=Dlco is decreased |
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PE with asthma
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Hyperexpansion of the thorax
Sounds of wheezing during normal breathing or a prolonged phase of forced exhalation Increased nasal secretions, mucosal swelling, sinusitis, rhinitis, or nasal polyps Atopic dermatitis/eczema or other signs of allergic skin problems |
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History of severe exacerbations that increase risk of death
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Past history of sudden severe exacerbations
Prior intubation for asthma Prior admission for asthma to an intensive care unit > 2 hospitalizations in the past year > 3 emergency care visits in the past year Hospitalization or emergency visits in past month |
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Complicating health problems with asthma
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Comorbidity (e.g., cardiovascular diseases or COPD)
Serious psychiatric disease, including depression, or psychosocial problems Illicit drug use |
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Ominous Signs in Asthma
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Fatigue
Pulsus paradoxus Diaphoresis is excessive sweating Inaudible breath sounds Unable to lie flat Cyanosis |
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Athma triggers
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smoking
colds, flu, bronchitis, pollen, outdoor pollutants, air pollution animals mice, rats, cockroaches indoor mold wood smoke, strong odors, and spray exercise, sport Others: cold weather, strong emotions |
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Treatment of asthma
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1. Allergens
Avoid known trigger factors (e.g., perfumes, cold air) 2. Tobacco Smoke Strongly advise patient and others living in the home to stop smoking. Discuss ways to reduce exposure to other sources of tobacco smoke, such as from day care providers and the workplace. 3. Rhinitis Intranasal steroids. Antihistamine/decongestant combinations may also be used. 4. Sinusitis Medical measures to promote drainage. Antibiotic therapy is appropriate when complicating acute bacterial infection is present. 5. Gastroesophageal reflux No eating within 3 hours of bedtime, head of bed elevated 6 to 8 inches, and appropriate medications (e.g., H2-antagonist) 6. Sulfite sensitivity No eating shrimp, dried fruit, process potatoes. No drinking of beer or wine. 7. Medication interactions No beta-blockers (including ophthalmological preparations) Aspirin and other nonsteroidal anti-inflammatory medications. Inform adult patients with severe persistent asthma, nasal polyps, or a history of aspirin sensitivity of the risk of severe and even fatal episodes from using these drugs. Usually safe alternatives are acetaminophen or salsalate. 9. Occupational exposures Discuss with asthma patients the importance of avoidance, ventilation, respiratory protection, and a tobacco smoke-free environment. If occupationally induced asthma, recommend complete cessation of exposure to initiating agent. Obtain permission from patient before contacting management or onsite health professionals about workplace exposure. |
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Treatment: Step 1 – mild intermittent
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No daily medication needed
All patients Short-acting bronchodilator: Inhaled beta2-agonist (2-4 puffs) as need for symptoms. Intensity of treatment will depend on severity of exacerbation. |
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Treatment: Step II – mild persistent
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Daily Medication of asthma:
Anti-inflammatory: either inhaled steroid (low dose)* or cromolyn (adult:2-4 puffs tid-qid; child: 1-2 puffs tid-qid) or nedocromil (adult: 2-4 puffs bid-qid; child:1-2 puffs bid-qid) (children usually begin with a trial of cromolyn or nedocromil) Sustained – release theophylline to serum concentration of 5-15 mcg/mL is an alternative, but not preferred, therapy. Zafirlukast or Zileuton may also be considered for those > 12 years old, although their position in therapy is not fully established. Proventil for acute |
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Treatment: Step III – moderate persistent
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Daily medication:
Either Anti-inflammatory: inhaled steroid (medium dose)* AND Inhaled steroid (low-to-medium dose)* and add a long-acting bronchodilator, especially for nighttime symptoms: either long-acting inhaled beta2-agonist (adult: 2 puffs q 12 hours; child: 1-2 puffs q 12 hours), sustained-release theophylline, or long-acting beta2-agonist tablets. If needed Anti-inflammatory: inhaled steroids (medium-to-high dose)* AND Long-acting bronchodilator, especially for nighttime symptoms, either long-acting inhaled beta2-agonist, sustained-release theophylline, or long-acting beta2-agonist tablets. |
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Treatment: Step IV – severe persistent
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Daily medications:
Anti-inflammatory: inhaled steroid (high dose)* AND Long-acting bronchodilator: either long-acting in haled beta2 agonist (adult: 2 puffs q 12 hours; child: 1-2 puffs q 12 hours), sustained-released theophylline, or long-acting beta2-agonist tablets AND Steroid tablets or syrup long term; make repeated attempts to reduce systemic steroid and maintain control with high dose inhaled steroid |
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Triad of asthma
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Asthma
Aspirin sensitivity Nasal Polyposis |
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Differential Diagnosis of COPD
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COPD
LV failure Pulmonary embolism Bronchiectasis Anaphylaxis Inhalation lung injury Partial obstructions Cancer Foreign body aspiration Laryngeal disorders Parasites |
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Some drugs can bring on asthma symptoms
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Aspirin – contained in many medications, such as pain relievers.
Non-steroidal anti-inflammatory drugs – such as Ibuprofen, Naproxen Beta blockers – often used to control high blood pressure Beta blocker eye drops – to treat the eye condition glaucoma Ace inhibitors – often used to control high blood pressure |
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Hospital Treatment for asthma
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1. Nebs with Proventil / Atrovent
2. Antibiotic - if you think there is infection 3. IV steroids 4. O2 5. Peak flow IV hydration |
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Definition of COPD
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A generalized increased resistance to airflow during expiration and includes chronic bronchitis, emphysema, chronic asthma, and bronchiolitis. COPD occurs in 10% to 15% of cigarette smokers.
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Chronic Bronchitis definition
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A. Characterized by chronic cough productive of mucus for at least 3 months in each of last 2 years.
2. Results from prolonged exposure to pulmonary irritants including cigarettes and allergens, pollution, recurrent infections. 3. Have inflammatory changes in bronchial mucosa. |
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Definition of emphysema
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3. Emphysema
A. Characterized by destruction of the lung parenchyma beyond the terminal bronchioles with coalescence of alveoli. 2. Divided into: 1. Panlobular, which is the result of alpha-antitrypsin deficiency. 2. Centrilobular, which is the result of smoking and of chronic bronchitis. |
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4th leading cause of death in the US, accounting for 100,360 deaths in 1996
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COPD
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What is the most important risk factor for COPD
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smoke
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There is a close relationship between_____ and COPD,
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lung cancer
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Age for COPD: Occurs more predominantly in individuals
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over 40 years of age.
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Role of Cigarette Smoking
in COPD |
COPD 30 times higher in smokers
80% - 90% from COPD related to smoking Dose - response relationship between # of packs/year and rate of decline in spirometric values Stopping smoking can improve pulmonary function |
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Diseases of Air flow Limitations
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Chronic Obstructive Pulmonary Disease (COPD)
Chronic bronchitis Emphysema Asthma Mixtures of these three diagnoses Cystic fibrosis antitrypsin deficiency |
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Mechanisms of Air Flow
Limitation |
Three major changes in lung and connecting airways that cause a decrease in air flow
1. Enlarged bronchial mucous with excess mucus production, inflammation, bronchial wall thickening & smooth muscle hypertrophy 2. Acinar enlargement (emphysema) 3. Narrowing of small airways from inflammation and fibrosis |
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Definition = Chronic cough associated with sputum production for more than 90 days on 2 successive years
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Chronic Bronchitis
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Chronic Bronchitis
Morphology Characteristics: |
Hyperemia and edema of mucous membranes of the lung
Mucinous secretions or casts filling airways |
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Chronic Bronchitis
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Definition = Chronic cough associated with sputum production for more than 90 days on 2 successive years
Morphology Characteristics: Hyperemia and edema of mucous membranes of the lung Mucinous secretions or casts filling airways Increase in size of the mucous glands Bronchial/bronchiolar mucous plugging, inflammation, and fibrosis Dysplasia of bronchial epithelium |
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Chronic irritation of the airways by inhaled substances cause:
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Hypersecretion of mucus
Hypertrophy of mucous glands Goblet cell metaplasia in bronchiolar epithelium Bronchiolitis CO2 from smoking binds of hemoglobin, lowering the O2 carrying capacity of the blood |
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Definition = Abnormal enlargement of air spaces distal to the terminal bronchioles, with destruction of their walls.
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Emphysema
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Three classifications of emphysema
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1. Centrilobular (Centriacinar)
2. Panacinar (Panlobular) 3. Distal Acini (Paraseptal, Periacinar or Subpleural) |
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Centriacinar Emphysema
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Destruction & enlargement of central and proximal parts of the respiratory unit (acinus). Sparing distal alveoli.
Predominant in upper lobes, and apices Associated with smoking |
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Panacinar Emphysema
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Uniform (entire) destruction and enlargement of acinus
Predominance in lower basal zones Strong association with alpha-1-antitrypsin deficiency |
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Diaphragmatic Movement
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70% - 80% work to breath
Effects ability of the diaphragm to shorten due to hyperinflation Flattens and can actual invert the diaphragm Over time changes the fiber type |
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Antitrypsin Deficiency
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Antitrypsin is a glycoprotein that functions in the lung as an antiprotease to inhibit neutrophil elastase and protect the alveolar wall.
Antitrypsin deficiency (AAT) is autosomal disease increases in elastase or decreases in antitrypsin or both lead to panacinar emphysema |
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Signs of COPD
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In the prominent bronchitis group, there are some classical signs of disease.
Productive cough, with progression over time prior to dyspnea (SOB) General physical traits such as obesity, cyanosis, accessory muscle use, coarse rhonchi and evidence of cor pulmonale History of frequent, recurrent pulmonary infections with a progressively worsening cough and cardiac/respiratory failure over time |
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Laboratory Data
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A. With acute exacerbations, CBC count, ABG, CXR, and EKG are indicated depending on the clinical situation.
1. Hypercapnia with acidosis is suggestive of acute decompensation 2. A high CO2 level with a normal pH is suggestive of a compensated chronic state. 2. ECG may show multifocal atrial tachycardia, and if it is present, one should be aware of the possibility of theophylline toxicity. 3. Bedside peak flows can document response to treatment. |
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In the emphysemic, there is a somewhat different set of classical signs and historical points:
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There is usually a long history of dyspnea with late onset of cough without sputum production.
Physically, the physician may note thin, pursed lip breathing, accessory muscle use, hyperresonant barrel chest,wheezing and distant heart sounds. The course is that of progressive dyspnea with occasional mucopurulent relapses and eventual cachexia and respiratory failure. |
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Intermittent dyspnea
Pedal edema Plethora Cyanosis Wheezing Weight loss Diminished breath sounds |
COPD
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COPD signs and symphtoms
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Intermittent dyspnea
Pedal edema Plethora: excess of blood Cyanosis Wheezing Weight loss Diminished breath sounds |
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Blue Bloaters
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COPD
The blue bloaters appear somewhat cyanotic and may have coarse rhonchi with signs of right heart failure. It may be difficult to distinguish between CHF and COPD since both sound rhonchorous and have signs of right-sided failure. One crude bedside test is peak flow. If they blow 150-200 or less, they are probably having a COPD exacerbation; if higher, they are probably having a CHF exacerbation. |
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Pink Puffers):
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Emphysema
The pink puffers will look much more like a COPD exacerbation, with thin, pursed lip breathing, tripoding, barrel chest and very distant heart sounds. |
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Arterial Blood Gas (ABG):
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An ABG gives the best clues as to acuteness and severity of COPD. In general, there is renal compensation even in the chronic CO2 retainers (bronchitics) such that the pH is usually near normal. Any pH in general below 7.3 should be considered a sign of acute respiratory compromise.
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This test gives the best clues as to acuteness and severity of COPD. In general, there is renal compensation even in the chronic CO2 retainers (bronchitics) such that the pH is usually near normal. Any pH in general below 7.3 should be considered a sign of acute respiratory compromise.
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Arterial Blood Gas (ABG):
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Serum Chemistry:
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These patients tend to retain sodium, and because of diuretic use can become hypokalemic. In addition, beta andrenergics and theophylline act to lower potassium levels, so this should be monitored carefully. Beta andrenergics also increase the renal excretion of serum calcium and magnesium, which may be important in the face of hypokalemia.
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Lab Studies for asthma
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Arterial Blood Gas (ABG):
An ABG gives the best clues as to acuteness and severity. In general, there is renal compensation even in the chronic CO2 retainers (bronchitics) such that the pH is usually near normal. Any pH in general below 7.3 should be considered a sign of acute respiratory compromise. Serum Chemistry: These patients tend to retain sodium, and because of diuretic use can become hypokalemic. In addition, beta andrenergics and theophylline act to lower potassium levels, so this should be monitored carefully. Beta andrenergics also increase the renal excretion of serum calcium and magnesium, which may be important in the face of hypokalemia. CBC: Polycythemia |
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Increased bronchovascular markings and cardiomegaly
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Chronic Bronchitis:
CXR |
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Small heart, hyperinflation, flat diaphragms and, possibly, bullous changes
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emphysema CXR
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Pulse Oximetry:
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Pulse oximetry does not offer as much information as the ABG, but it can be a powerful tool for instant feedback on the patient’s status w COPD when combined with clinical observation.
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This lab test does not offer as much information as the ABG, but it can be a powerful tool for instant feedback on the patient’s status when combined with clinical observation.
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Pulse Oximetry:
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Electrocardiogram (ECG):
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In COPD patients, there is high likelihood of underlying cardiac disease. It is important to establish that the hypoxia is not resulting in ischemia and that the underlying cause of the respiratory difficulty is not cardiac in nature.
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Pulmonary Function Test (PFTs)
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Decreased FEV1 with concomitant reduction in FEV1 / FVC ratio
Poor/absent reversibility with bronchodilators FVC may be normal or reduced Normal or increased total lung capacity (TLC) Increased residual volume (RV) Diffusing capacity is normal or reduced |
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Draw the stages of COPD table.
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yonts obstructive diesases 2 ppt slide 30
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How do we stage the severity? This will give you the percentage to classify the severity of the patient.
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%=FEV1 measured/FEV1 predicted)x 100
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How do you Interpretation the PFT?
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The patient has obstruction because the FEV1/FVC ratio is less than 0.70 or 70%, it is 62%.
This does not answer if it is reversible. What stage is the COPD if we know that it is not reversible? Stage II (Moderate) because the FEV1 is 52% of predicted values. |
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TX for COPD
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The mainstays of therapy for acute exacerbations of COPD are oxygen, bronchodilators and definitive airway management.
Mainly O2, steroids and antibiotics |
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Proven benefits of O2 with what problems?
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cor pulmonale
erythrocytosis cognitive function exercise intolerance nocturnal restlessness morning headache |
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Proven benefits of O2 general****
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Longer survival
decrease hospitalization Better quality of life |
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Drug Therapy for COPD table
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yonts obstructive lecture 2, slide 38
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antibiotics tx for COPD
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1.) Long-term antibiotics are not helpful but should be used to treat acute purulent exacerbations. Amoxicillin or amoxicillin/clavulanate 500mg TID, trimethoprim-sulfamethoxazole (Septra DS) 1 PO BID, or doxycycline 100mg PO BID are recommended.
2.) Many other antibiotics also work: e.g. Levaquin, Rocephin, Fortaz 3.) The main bacteria is H. influenza (but may have others… Board Q.) in COPD |
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surgical removal of large air spaces called bullae that are filled with stagnant air, may be beneficial in selected patients. Recently, use of lasers to remove bullae has been suggested
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Bullectomy
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has been successfully employed in some patients with end-stage COPD. The 1-year survival in patients is over 70 percent.
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Lung transplantation
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programs, along with medical treatment, are useful in certain patients with COPD. The goals are to improve overall physical endurance and generally help to overcome the conditions which cause dyspnea and limit capacity for physical exercise and activities of daily living. General exercise training increases performances.
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Pulmonary rehabilitation
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Long-term Management of COPD
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A. All patients with COPD should have a Pneumovax and yearly flu shot.
2. Patients should be educated about their disease and should be taught that if they start having difficulties with breathing they should contact their health care professional. 3. Low-flow O2 has been shown to be useful in reducing pulmonary arterial resistance, which, if uncontrolled,leads to cor pulmonale. 1. Use continuous oxygen in those with either a PO 2 <55 mm Hg, an O2 saturation of <89%, or a PO2 <59 mm Hg with evidence of cor pulmonale (peripheral edema, HCT >55, P pulmonale on ECG). 2. O2 saturation should be kept above 90% (PO2 of 60 to 80 mm Hg). 3. Usually can be accomplished with 2 L/min O2 but titrate to patient’s needs. 4. Survival significantly enhanced with oxygen use 24 hours a day. Patients should be encouraged to use oxygen at least 15 hours a day. |
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Complications from COPD
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Some of the complications that must be anticipated in the treatment of COPD patients are as follows:
the incidence of pneumothorax due to bleb formation is fairly high and should be looked for in all COPD patients with increased shortness of breath. In patients who require chronic steroid use, the possibility of adrenal crisis is very real. At the very least, patients with steroid-dependent COPD should receive stress dosing in the event of an exacerbation or any other stressor. Infection is common Cor pulmonale Secondary polycythemia- An abnormally increased concentration of hemoglobin in the blood Bullous lung disease Acute or chronic respiratory failure Pulmonary hypertension Malnutrition |
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What are the most important predictors of COPD prognosis?
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The patient’s age and post-bronchodilator FEV1 are the most important predictors of prognosis. Young age and FEV1 >50% predicated have a good prognosis. Older patients and those with more severe lung disease do worse.
Supplemental oxygen, when indicated, has been shown to increase survival. Smoking cessation improves prognosis. Cor pulmonale, hypercapnia, tachycardia and malnutrition indicate a poor prognosis. |
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Medical/Legal Pitfalls:
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Be wary of discharging patients with exacerbations when they do not feel comfortable with their breathing, regardless of their oxygen saturation, ABG or other test results.
Always look for underlying cardiac ischemia with acute exacerbations. With hypoxia and distress, many of these patients can have some underlying ischemia that can go unrecognized. |
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A form of obstruction that is similar to COPD but is not classified as COPD.
It basically deals with airway dilation and destruction. The presentation is very similar to COPD |
Bronchiectasis
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What can cause bronchiectasis?
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A single infection can cause bronchiectasis. Examples of agents than can cause bronchiectasis;
Tuberculosis Mycobacterium avium complex (MAC) Pertusis Bacterial Pnemonias Mycoplasma Allergic bronchopulmonary aspergillosis |
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The halmark is cough and daily production of mucopurulent and tenacious sputum.
Dyspnea Wheezing Pleuritic chest pain |
Bronchiectasis
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Bronchiectasis sympthoms
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The halmark is cough and daily production of mucopurulent and tenacious sputum.
Dyspnea Wheezing Pleuritic chest pain |
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Cough 98%
Daily sputum production 78% Dyspnea 62% Rhinosinusitis 73% Hemoptysis 27% Recurrent Plurisy 20% |
Bronchiectasis
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PE with Bronchiectasis
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Crackles 75%
Wheezing 22% Digital clubbing 2% |
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Bronchiectasis Induction requires 2 factors
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An infectious insult
Airway obstruction, impaired drainage, or defect in host defense |
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LABs for Bronchiectasis
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CBC with differential
Immunoglobulin quantification (to get levels of IgG, IgM, and IgA) Sputum culture and smear for bacteria, mycobacteria, and fungi. |
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Diagnosis of Bronchiectasis
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Lab testing
Radiographic imaging Pulmonary function testing |
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Linear atelectasis
Dilated and thickened airways Irregular peripheral opacities which is usually mucopurulent plugs |
CXR Bronchiectasis
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Multidetector computed tomography (MDCT) is the imaging of choice. High resolution computed tomography (HRCT) is the second choice. The findings listed below help make the diagnosis.
Airway Dilation Lack of Tapering Bronchial wall thickening observed in dilated airways Mucopurulent plugs or debris Cysts of the bronchial wall (Sometimes they appear like grapes) |
CT scan Bronchiectasis
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