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Lung Disorders

Lung Disorders. COMMON MANIFESTATIONS OF LUNG DISEASE. DYSPNEA. Brought about by several physiologic processes: Increased respiratory effort due to: 1) AIRWAY OBSTRUCTION: COPD, asthma. 2) DECREASED PULMONARY COMPLIANCE: interstitial fibrosis, CHF.

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Lung Disorders

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  1. Lung Disorders

  2. COMMON MANIFESTATIONS OF LUNG DISEASE

  3. DYSPNEA • Brought about by several physiologic processes: • Increased respiratory effort due to: • 1) AIRWAY OBSTRUCTION: COPD, asthma. • 2) DECREASED PULMONARY COMPLIANCE: interstitial fibrosis, CHF. • 3) DECREASED CHEST WALL COMPLIANCE: obesity, pleural disease. • 4) WEAKNESS OF RESPIRATORY MUSCLES: neuromuscular weakness, inanition,, chronic respiratory failure.

  4. DYSPNEA ACUTE DYSPNEA • Short list: • Asthma, infection. • Pulmonary edema. • Pneumothorax. • Pulmonary embolus. • ARDS, panic attack.

  5. DYSPNEA EVALUATION • CBC, renal function, CXR, spirometry, oximetry. • If > 40 or family Hx → EKG. • ABG’s, V/Q Scan, stress testing, echocardiography where appropriate based on Signs / Sxs.

  6. DYSPNEA TREATMENT • O2 if hypoxemic. • Treat dyspnea-related anxiety w/ “judicious” use of benzodiazepines, Ativan 0.5-1.0 mg q6-8. • Pulmonary “rehab,” more appropriate breathing techniques, energy-conserving techniques, etc. • Um, smoking cessation.

  7. COUGH CHRONIC COUGH • Most commonly from COPD. • In the non-smoker: • GERD, post-nasal drip, asthma. • Side-effect of ACE Inhibitors. THE EVAL • Postnasal drip: sinus series, Rx as sinusitis. • PFT’s: asthma, COPD. • GERD: barium swallow vs empiric Rx. • CXR: for patients w/ other Sxs, hemoptysis, fever, weight loss, etc

  8. COUGH TREATMENT • Dependent upon the cause. • Elimination of irritant: tobacco, allergen, environmental, occupational. • D/C beta blockers, ACE inhibitors. • Post-nasal drip: antihistamines, decongestants, intranasal steroids. • Chronic sinusitis: prolonged antibiotic Rx, 2-4 weeks. • Asthma: inhaled steroids and bronchodilators. If not better another cause needs to be considered. • GERD- proton pump inhibitors, H2 blockers may not cut it.

  9. HEMOPTYSIS • Coughing up of blood “that originates below the vocal cords.” • Dual circulation: • 1) PULMONARY ARTERIES- from the right ventricle under low pressure to the pulmonary parenchyma. • 2) BRONCHIAL ARTERIES- from the aorta under systemic pressure to the airways, blood vessels, hilum, and visceral pleura. • The bronchial circulation is only 1-2% of total pulmonary flow, but is common source of hemoptysis.

  10. HEMOPTYSIS • CHASING DOWN THE CAUSE ANATOMICALLY • 1) FROM THE AIRWAYS: chronic bronchitis, bronchiectasis, bronchogenic carcinoma. • 2) FROM THE PULMONARY VASCULATURE: left v. failure, mitral stenosis, PE, AVM. • 3) FROM THE PULMONARY PARENCHYMA: pneumonia, inhalation of crack, autoimmune disease such as Goodpasture’s Syndrome and Wegener’s Granulomatosis.

  11. HEMOPTYSIS CLINICAL FINDINGS • In acute bronchitis in an otherwise healthy person, no big work up needed as long as it resolves w/ the illness. • Hemoptysis is frequently a sign of serious disease. • Identify the patient at risk for pathology. • CXR, CBC w/ platelets, renal function, UA. • Flexible bronchoscopy. • Chest CT.

  12. HEMOPTYSIS TREATMENT • Mild hemoptysis- identify the cause. • Massive hemoptysis- secure the airway, intubation, suction, ventilation. • Bronchoscopic control sometimes possible. • Selective arterial embolization.

  13. UPPER AIRWAY OBSTRUCTION ACUTE • Can be life-threatening. • CAUSES: Foreign body, laryngospasm, laryngeal edema from burns, angioedema, trauma to the pharynx/larynx, infections (retropharyngeal abscess, etc), acute allergic laryngitis.

  14. ASTHMA • Chronic, inflammatory disorder of the airways. • Reversible airway hyper-responsiveness, airway edema, bronchoconstriction, mucous production. • 5% of the population, 5000 deaths annually. • Prevalence, # hospitalizations, and deaths all increased over the last 20 years. • See text for histopathology, underlying inflammatory changes, mast cells, etc.

  15. ASTHMA • Genetic predisposition, atopy. • Most common trigger is inhaled allergens. • Other triggers: exercise, URI’s, rhinitis, sinusitis, postnasal drip, GERD, changes in weather, stress. • Also: tobacco smoke, ozone, SO2, NO2. • Some cases due to use of aspirin, NSAID’s, tartrazine dyes. • Catamenial. • “Cardiac asthma.”

  16. Allergens O “Seasonal pollens O Year round allergens – dust mites, moulds, pets, and insect parts O Foods – fish, egg, peanuts, nuts, cow’s milk, and soy O Additives – sulphites O Work related agents – latex, flour Irritants O Respiratory infections – viral colds, bronchitis, and sinusitis O Drugs – aspirin, NSAIDs, betablockers O Tobacco smoke O Outdoor factors – haze and smog, weather changes, exhaust fumes from vehicles O Indoor factors — paint, detergents, deodorants, chemicals and perfumes O GERD O Temperature change – night-time O Exercise in cold dry conditions O Work-related factors – chemicals, dusts, gases, and metals O Emotional factors – laughing, crying, yelling and distress O Hormonal factors – premenstrual syndrome Asthma

  17. Clinical consequences of airway remodeling in asthma

  18. ASTHMA SIGNS / SYMPTOMS • Wheezing, difficulty breathing, chest tightness, cough. • Extreme variability in symptoms from one patient to the next. • Worse at night, bronchoconstriction max between 3-4 AM. • COEXISTING CONDITIONDS: nasal polyps, eczema, atopic dermatitis, other allergic skin disorders.

  19. ASTHMA SIGNS / SYMPTOMS • Wheezing may be absent when bronchoconstriction is extreme, as not enough air is flowing to produce wheezing. This portends respiratory failure. • Here we find globally diminished breath sounds and prolonged expiration. PFT’s • FEV1, FVC, (FEV1 / FVC). • Peak expiratory flow meters for home monitoring.

  20. ASTHMA COMPLICATIONS • Exhaustion. • Dehydration, airway infection. • Cor pulmonale. • Pneumothorax.

  21. ASTHMA LONG-TERM TREATMENT • GOALS: • 1) Minimize chronic Sxs that impair normal activity. • 2) Prevent recurrences. • 3) Minimize need for ER / hospitalizations. • 4) Maintain near-normal pulmonary function. • Daily anti-inflammatory therapy w/ inhaled corticosteroids.

  22. ASTHMA LONG-TERM TREATMENT • Therapy dictated by algorithms set forth by the Expert Panel Report 2 from the NAEPP, step-wise fashion (“stair-step”). • Amount of medication and dosing based on severity of Sxs. • Begin therapy at a higher level of intensity then back down.

  23. ASTHMA PHARMACOLOGIC AGENTS • 2 CATEGORIES: • 1) Those that promote long-term control- address airway inflammation. • 2) Those that offer quick relief- bronchodilators

  24. ASTHMA PHARMACOLOGIC AGENTS • LONG-TERM CONTROL MEDICATIONS. • QUICK RELIEF MEDICATIONS.

  25. ASTHMA PHARMACOLOGIC AGENTS • LONG-TERM CONTROL MEDICATIONS. ANTI-INFLAMMATORY AGENTS LONG-ACTING BRONCHODILATORS LEUKOTRIENE MODIFIERS DESENSITIZATION MISCELLANEOUS

  26. ASTHMA PHARMACOLOGIC AGENTS – LONG-TERM • LONG-ACTING BRONCHODILATORS • 1) MEDIATOR INHIBITORS- cromolyn sodium, nedocromil. Modulate mast cell and eosinophil function. • 2) BETA ADRENERGIC AGENTS- inhaled,long-acting. Onset of action is delayed, not for acute bronchoconstriction, exacerbations. Combined w/ inhaled corticosteroids.

  27. ASTHMA PHARMACOLOGIC AGENTS – LONG-TERM • LONG-ACTING BRONCHODILATORS • 3) PHOSPHODIESTERASE INHIBITORS- Theophylline. • Mild bronchodilator. • Control of nocturnal symptoms. • Used in patients w/ moderate to severe persistent asthma along w/ inhaled steroids and beta blockers. • See text re serum concentrations, effects of other meds.

  28. ASTHMA PHARMACOLOGIC AGENTS – LONG-TERM • LEUKOTRIENE MODIFIERS • Singulair (montelukast), Zileuton. • Leukotrienes- think of them as a delayed-onset histamine → vasodilatation, increased capillary permeability, mucous production, and bronchoconstriction. • Can minimize need for “rescue” treatment in acute exacerbations; alternatives to inhaled steroids.

  29. ASTHMA PHARMACOLOGIC AGENTS – LONG-TERM • DESENSITIZATION • Immunotherapy, “allergy shots.” • When response to meds for long-term control is not optimal, ie you’ve tried everything else without adequate control. This is the top rung of the outpatient “stair step.” • MISCELLANEOUS • Oral sustained-release beta2 agonists. • Omalizumab- a recombinant antibody that binds IgE.

  30. ASTHMA QUICK-RELIEF MEDICATIONS • 1) BETA-ADRENERGIC AGENTS • 2) SYSTEMIC CORTICOSTEROIDS.

  31. ASTHMA QUICK-RELIEF MEDICATIONS • 1) BETA-ADRENERGIC AGENTS • Short-acting, inhaled bronchodilators. • For exacerbations only. (“rescue”) • β-1 vs β-2. • Albuterol, terbutaline, bitolterol, pirbuerol. • If need is often for these, long-term control efforts need to be ramped up.

  32. ASTHMA QUICK-RELIEF MEDICATIONS • 2) SYSTEMIC CORTICOSTEROIDS • For moderate to severe exacerbations, lack of response to inhaled short-acting β2 therapy. • Sometimes necessary for the long-term control of patients w/ severe asthma. • PO vs. IV. • Adrenal suppression.

  33. ASTHMA • ASSESSMENT, MONITORING, PREVENTION. • Periodic clinical assessments and self-assessments (peak flow meters) are the primary methods of monitoring asthma • Written action plan for self-monitoring, changes to therapy, and treatment of exacerbations. • Asthmatics should receive vaccinations for influenza and pneumococcal pneumonia.

  34. COPD • Airflow obstruction due to emphysema and chronic bronchitis. Most have features of both. • Usually progressive, has variable amounts of airway inflammation, some of which may be reversible. • COPD and asthma combined = the 4th leading cause of death in the U.S. • Death rate is increasing, esp in elderly men. • Almost all due to smoking. • Other causes:

  35. COPD SIGNS & SYMPTOMS • Present in the 5th and 6th decades of life. • Excessive cough, shortness of breath, and sputum production. • Symptoms often present 10 years or more. • Progressively worsening dyspnea: w/ exertion → w/ mild exertion → at rest. • Late stages → complicated by pneumonia, pulmonary hypertension, cor pulmonale, chronic respiratory failure.

  36. COPD SIGNS & SYMPTOMS • See text for comparison of “pink puffer” (emphysema) vs “blue bloater” (chronic bronchitis). • Thin, uncomfortable, quiet chest- emphysema. • Obese, noisy chest, rhonchi, wheezes- chronic bronchitis. • In reality, most patients have features of both.

  37. COPD IMAGING • Plain X-rays not sensitive enough for a Dx, but show: • Hyperinflation, flattening of the diaphragm. • Bullae- when present in the right clinical setting → diagnostic of emphysema.

  38. COPD COMPLICATIONS • Spontaneous pneumothorax. • Pulmonary hypertension, cor pulmonale. • Acute bronchitis, pneumonia, pulmonary thromboembolism, LV failure can worsen otherwise stable COPD. • Hemoptysis- can be from chronic bronchitis but bronchogenic carcinoma needs to be considered.

  39. COPD TREATMENT • AMBULATORY PATIENTS • 1) Smoking cessation. • 2) Oxygen therapy. • 3) Bronchodilators. • 4) Corticosteroids. • 5) Antibiotics. • 6) Other measures.

  40. COPD TREATMENT 1) SMOKING CESSATION • Requires an active, multidimensional program, not simply telling patients to quit (5%). • Nicotine gum + behavior modification = 22% sustained abstinence at 5 years.

  41. COPD TREATMENT 2) OXYGEN THERAPY • For patients w/ resting hypoxemia. • The only therapy (“drug”) that has been shown to improve the natural history of COPD in patients w/ resting hypoxemia. • Correlated w/ prolonged survival, reduced hospitalizations, better quality of life. • Esp likely to benefit- the hypoxemic patient w/ pulmonary hypertension, cor pulmonale, erythrocytosis, impaired cognitive function, exercise intolerance, nocturnal restlessness, morning headache.

  42. COPD TREATMENT 3) BRONCHODILATORS • The most important pharmacologic agents in the management of COPD. • Symptomatic improvement only. Do not alter the progressive deterioration in lung function. • Ipratropium bromide- an anticholinergic. • Albuterol, metaproterelol- short-acting β2 agonists. • Salmetrol, Formoterol- long-acting β2 agonists. • Oral theophylline- 3rd line agent.

  43. COPD TREATMENT 4) CORTICOSTEROIDS • Only useful in acute exacerbations. • More useful when the predominant component is chronic bronchitis rather than emphysema. • See text for details. • Inhaled steroids have no effect on the characteristic decline in lung function in COPD.

  44. COPD TREATMENT 5) ANTIBIOTICS • For: • 1) To treat an acute exacerbation. • 2) To treat acute bronchitis. • 3) To prevent acute exacerbations (prophylaxis). • Evidence supports use in only the 1st two. • Trimethoprim-sulfamethoxazole (Septra). • Amoxicillin-clavulanate (Biaxin).

  45. COPD TREATMENT 6) OTHER MEASURES • See text. • Graded exercise, hydration to promote clearing of secretions. • Expectorants, mucolytics, not helpful. • Cough suppressants to be avoided.

  46. PNEUMONIA • Lower respiratory tract infection. • We will look at community-acquired pneumonia. • See text for Hospital-acquired pneumonia, anaerobic pneumonia, and pneumonia in the immunocompromised.

  47. COMMUNITY-ACQUIRED PNEUMONIA • Common. • Most deadly infectious disease in the U.S. • 4th leading cause of death. • 14% mortality if hospitalization is required, < 1% if not.

  48. COMMUNITY-ACQUIRED PNEUMONIA PATHOGENESIS • Begins outside the hospital or within 48 hours after admission in a patient who has not been in a long-term care facility for 14 or more days before the onset of symptoms. • Occurs when there is a defect in one or more of the defense mechanisms: cough reflex, mucociliary clearance of secretions, immune response. • Or when there is a large inoculum or a particularly virulent organism.

  49. COMMUNITY-ACQUIRED PNEUMONIA PATHOGENESIS • THE BACTERIAL BUGS: • Strep pneumoniae- 2/3 of cases. • H. flu, Mycoplasma, Klebsiella, Chlamydia pneumoniae, Staph aureus, Legionella. • THE VIRAL BUGS: • Influenza, respiratory syncytial virus (RSV), adenovirus, parainfluenza virus.

  50. COMMUNITY-ACQUIRED PNEUMONIA PATHOGENESIS • THE SCREWY BUGS: • Chlamydia psittaci (psittacosis), Coxiella burnetti (Q fever), Francisella tularensis (tularemia aka rabbitt fever), fungi such as Blastomyces, Coccidioides, Histoplasmosis

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