3220: asthma/ pulmonary disorder

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jam110007
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3220: asthma/ pulmonary disorder
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2013-09-24 21:11:54
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3220 exam 1
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  1. restrictive lung disease
    • - lungs stiff, noncompliant
    • - more effort during inspiration 
    • - often a V/Q mismatch =>reducing diffusion of oxugen into the blood
    • - examples: pulmonary fibrosis, cystic fibrosis
  2. obstructive lung disease
    • - airway obstruction that is worse with expiration 
    • - more force is required and emptying [expiration] of lungs is slowed
    • - shared symptom of all three is dyspnea, and shared sign is wheezing
    • - increased work of breathing, V/Q mismatch
    • - asthma, emphysema, and bronchitis 

    sometimes air trapping can occur
  3. asthma
    • - chronic inflammatory disorder of the bronchial mucosa that causes hyperreponsiveness and constriction of the airway 
    • - occurs in all ages, but common in children and urban areas
    • - cause is unclear, probably a combination of an immune response, genetics, envrionment
  4. asthma death rates ____ and incidences ____
    decreased, increased
  5. asthma: early response
    - antigen response activates B cells to produce IgE. inflammatory mediators are released causing vasodilatio, edema, and mucus secreation
  6. asthma: late response
    - begins 4-8 hours later with a letent release of inflammatory mediators
  7. how does IgE play a role?
    they cause mast cells to release histamine which can lead to inflammation
  8. airway obstructions can be due to
    - Edema of bronchial wall

    - excess Mucus production

    - Smooth muscle contraction [bronchospasm occurs making it difficult for expiration]

    - Hypertrophy [of the walls of the bronchi]

    - Can be gradual or abrupt!!
  9. airway inflammation can be due to
    • - Release of inflammatory mediators from mast cells [histamine], macrophages, epithelial cells
    • - Reduced mucociliary clearance [cilia are damaged causing a reduced clearanc
  10. characteristics of asthma
    • - vascular leakage 
    • - histamine
    • - mast cells
    • - swollen endothelium 
    • - mucus
  11. signs and symptoms of asthma
    - cough, wheezing [b/c its hard to expire], chest tightness
  12. asthma classified by severity
    • - mild intermittent
    • - mild persistent
    • - moderate persistent 
    • - severe persistent
  13. mild intermittent asthma
    less than twice a week
  14. Mild persistent asthma
    3-6 times/week
  15. Moderate persistent asthma
    have normal or below normal gas exchange plus signs/symptoms daily, sometimes at night
  16. Severe persistent asthma
    below normal gas exchange plus continuous signs/symptoms and frequently at night
  17. Status Asthmaticus
    • - It’s an Acute attack that doesn’t respond to treatment [as far as steroids or bronchodialators]
    • - Respiratory distress
    • - wheezing or absent breath sounds
    • - Pulsus paradoxus [difficult to measure, systolic b/p will drop 10 points on inspiration]
    • - Chest wall contractions
    • - expiratory flow is decreased acidotic
  18. Why is there an increased incidence of asthma?
    • A. Gastroesophageal reflux disease
    • B. Hygiene hypothesis
    • C. Cockroaches, house dust
  19. Hygiene Hypothesis
    - Increased exposure to high levels of allergens during childhood increases the risk for asthma

    - Decreased exposure to certain infectious organisms also increases the risk for asthma
  20. GENETICS OF ASTHMA
    - Sensitivity to specific allergens, including pollen, dander, dust, mold, cockroach allergen

    - Can be associated with other hereditary allergies, eg. Eczema, allergic rhinitis
  21. asthma & Environment
    • - Reaction to internal, nonallergen factors
    • - Usually occur after a severe respiratory infection
    • - Most asthmatics have genetically induced and environmentally induced asthma
  22. Other risk factors of asthma
    - Age of onset

    - Levels of allergen exposure

    - Urban residence

    - Air pollution

    - Tobacco smoke

    - Recurrent infections

    - Obesity
  23. AIRWAY TRIGGERS for asthma
    - Allergens

    - Cold air – airways are dry thus decreasing mucus production. Also may have bronchospasms.

    - Exercise

    - Laughing [extreme emotion]
  24. diagnosing asthma how?
    • - Pulmonary function tests
    • - Serum IgE levels
    • - Chest xray
    • - ABG analysis [blood gas]
    • - Allergen testing
  25. Pulmonary Function Tests
    - Spirometry: Helpful for patients with respiratory symptoms or those at risk

    - Measures volume of air that patient can expel from the lungs after a maximal inspiration

    - Forced Vital capacity (FVC): total volume of air that pt can forcibly exhale in one breath

    - Forced Expiratory Volume in 1 second(FEV1)

    - FEV1/FVC expressed as a fraction. Normal is between 0.7 and 0.8
  26. SPIROMETRY FINDINGS IN ASTHMA
    - Decreased expiratory flow rate (EFR)

    - Decreased FEV

    - Decreased FVC [force vital capacity]

    - Increased functional residual capacity (FRC – functional residual capacity [the amount of air left in the lungs after passive expiration)

    - Increased total lung capacity (TLC)

    - Hypoxemia (O2 Sat <90%)
  27. PEAK EXPIRATORY FLOW RATE (PEFR)
    - Measures level of airway hyperresponsiveness

    - ~ FEV1 measured by spirometry

    - Measured AM, PM daily

    - Used to tailor Rx[treatment]

    • handhald device that is not used
    • to treat but based of the results their treatments can be adjusted
  28. Asthma Treatment
    • - Avoidance of triggers
    • - Beta agonist inhalers
    • - Leukotriene antagonists
  29. COPD
    • - Emphysema and Bronchitis
    • - Preventable and treatable
    • - Extrapulmonary effects [outside of the pulmonary system such as the cardiovascular system]
  30. COPD risk factors
    tobacco smoke, dusts, chemicals, indoor and outdoor air pollutionGenetics
  31. what is the GOLD definition of COPD
    “a common preventable and treatable disease, is characterized by airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individual patients”
  32. COPD Diagnosis and Assessment: Key Points
    - A clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and a history of exposure to risk factors for the disease.

    - Spirometry is required to make the diagnosis; the presence of a post-bronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation and thus of COPD. [usually done annually]
  33. Spirometry
    - Performed after the administration of an adequate dose of short acting inhaled bronchodilator

    - A post bronchodilator FEV1/FVC <.70 confirms airflow limitation
  34. CHRONIC BRONCHITIS
    • - Hypersecretion of
    • mucus and chronic productive cough that lasts for at least 3 months of the year
    • and occurs 2 years in a row

    • - Airflow
    • obstruction caused by mucus
  35. How is this different from acute bronchitis
    • - Its more of a viral infection and lasts for about a week or two
    • - Its self limiting

    While chronic bronchitis occurs for months and every year
  36. CHRONIC BRONCHITIS patho
    - Inhaled irritants cause inflammation with infiltration of neutrophils, macrophages, and lymphocytes into the bronchial wall

    - This leads to edema and increases the number of mucus cells and mucus production

    - Gas can pass during inspiration but is trapped during expiration

    - Increased airway resistance, bronchospasm, chronic inflammation

    - V/Q mismatch > PCO2 is elevated. ok ventilation but bad perfusion

    - Right ventricular decompensation (cor pulmonale) – edema occurs, liver congestion with fluid – caused by end stage bronchitis
  37. blue bloaters refer to what type of pt
    • a pt with chronic bronchitis 
    • - cyanosis
    • - peripheral edema
    • - "nonfighter" > resp drive is increased 
    • - low PO2 and high PCO2
    • - V/Q mismatch > not ventilating well
  38. CHRONIC BRONCHITIS: TREATMENT
    - STOP SMOKING!!

    • - Pursed lip breathing (to dec. PaCO2, inc. PaO2)
    • - lean forward to exhale, abdominal breathing, exhalation with exertion, inhalation/exhalation exercises

    - Ipratropium (inhaled anticholinergic – dries up secretions)

    - Bronchodilators

    - Expectorants – helps cough up secretions

    - Respiratory therapy – chest PT
  39. EMPHYSEMA: PATHOPHYSIOLGY
    • - Narrowed bronchiole (reduced patency)
    • - Decreased elastic recoil
    • - Destruction of the aveloar walls [air space], less surface and vascular for gas exchange
    • - Elastases from neutrophils
    • - Weakened lung recoil – air trapping with expiration (hyperinflation – due to air trapping)
  40. number one cause of emphysema
    smoking
  41. smoking and emphysema
    • - Smoking (98% of cases)
    • - Inc. neutrophils in lung tissue
    • - Neutrophils have proteolytic enzymes
  42. genetic predisposition and emphysema
    • - Genetic predisposition (1-2%)
    • - Alpha-1-antitrypsin deficiency – made in the liver and protects the lungs from proteolysis [have emphysema w/ no his of smoking]
    • - Proteolysis is less inhibited
  43. which pt is known at the "pink puffer"
    pt with emphysema
  44. emphysema pt physical description
    “Fighters”

    “Pink Puffer”

    • “Barrel Chest”
    • – using accessory muscle, air trapping, muscle wasting and weight loss because
    • of the hyperventilation

    “Pursed lip breathers”
  45. COPD signs and symptoms
    - Dyspnea,faint BS with limited air movement

    - Increased respiratory rate

    - Use of accessory muscles

    - Hyperresonance with percussion (hyperinflation) – air filled sound

    - Decreased forced expiratory velocity (FEV)

    - Right ventricular failure

    - Difficulty eating [due to the constant shortness of breath], weight loss

    - Pursed lip breathing

    - More comfortable sitting
  46. early phase COPD
    - Hypoxemia with respiratory alkalosis (inc. VR, over compensation)
  47. later phase COPD
    hypoxemia, respiratory acidosis

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