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Weekly endorsement during our rotation in the Department of Family and Community Medicine. This is the case of a 72-year-old male who came in due to difficulty of breathing

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  • Congestive heart failureCongestive heart failure (CHF) may produce wheezing and often may be difficult to differentiate from emphysema. A history of orthopnea and paroxysmal nocturnal dyspnea, fine basal crackles on chest auscultation, and typical findings on chest radiographs can lead to the diagnosis of CHF.One crude bedside test for distinguishing chronic obstructive pulmonary disease (COPD) from CHF is peak expiratory flow. If patients blow 150-200 mL or less, they are probably having a COPD exacerbation; higher flows indicate a probable CHF exacerbation.According to a prospective study in Slovenia by Prosen et al, heart failure–related acute dyspnea could be distinguished from pulmonary-related acute dyspnea in an emergency setting by the presence of a comet-tail sign on bedside lung ultrasonography. The absence of a comet-tail sign correctly ruled out heart failure–related dyspnea even in patients with a history of heart failure.[40]BronchiectasisPatients with bronchiectasis have chronic production of copious purulent sputum, coarse crackles and clubbing upon physical examination, and abnormal findings on chest radiographs and computed tomography (CT) scans.BronchiolitisobliteransBronchiolitisobliterans is observed in younger persons who do not smoke and in persons with collagen-vascular diseases. A CT scan characteristically shows areas of mosaic attenuation without evidence of generalized emphysema.Chronic asthmaThe delayed onset of severe asthma may be difficult to distinguish from COPD in older patients, but the important distinction is a significant bronchodilator response and normal diffusion (ie, diffusing capacity
  • The dominant paradigm of the pathogenesis of emphysema comprises four interrelated events(1) Chronic exposure to cigarette smoke may lead to inflammatory cell recruitment within the terminal air spaces of the lung. (2) These inflammatory cells release elastolyticproteinases that damage the extracellular matrix of the lung. (3) Structural cell death results from oxidant stress and loss of matrix-cell attachment. (4) Ineffective repair of elastin and other extracellular matrix components result in air space enlargement that defines pulmonary emphysema.
  • The chronic airflow limitation characteristic of COPD is caused by a mixture of small airways disease and emphysema. Chronic inflammation causes structural changes and narrowing of the small airways. Destruction of the lung parenchyma, also by inflammatory processes, leads to the loss of alveolar attachments to the small airways and decreases lung elastic recoil.
  • COPD can coexist with asthma, airway inflammation. The underlying chronic airway inflammation is very different in these two diseases. The pathology of chronic airflow limitation in asthmatic and COPD patients is markedly different, suggesting that the two disase entities may remain different even when presenting with similarly reduced lung function.
  • The hairs and turbinates of the nares capture larger inhaled particles before they reach the lower respiratory tract. The branching architecture of the tracheobronchial tree traps particles on the airway lining, where mucociliary clearance and local antibacterial factors either clear or kill the potential pathogen. The gag reflex and the cough mechanism offer critical protection from aspiration. In addition, the normal flora adhering to mucosal cells of the oropharynx, whose components are remarkably constant, prevents pathogenic bacteria from binding and thereby decreases the risk of pneumonia caused by these more virulent bacteria.
  • COPD

    1. 1. Igbaras, Iloilo CC Jackie Lou C. Acha
    2. 2. General Data  M.E.  72 years old  Male  Mantangan, Igbaras Chief complaint: Difficulty of breathing
    3. 3. History of Present Illness  1 week PTC (+) productive cough with whitish phlegm (+) intermittent undocumented fever x 1 day relieved by Paracetamol (+) chills (+) headache (+) body malaise (+) loss of appetite
    4. 4. History of Present Illness  Day of consult (+) persistent cough, loss of appetite, body malaise (+) sudden onset DOB
    5. 5. History of Present Illness  Pertinent negatives (-) chest pain/tightness (-) dizziness (-) hemoptysis (-) weight loss (-) orthopnea (-) PND
    6. 6. Past Medical History  Diagnosed with bronchial asthma 3 years PTC (-) HPN (-) DM (-) FDA (-) PTB
    7. 7. Family History (+) Bronchial asthma – maternal aunt (-) DM (-) HPN (-) FDA (-) heredo-familial diseases
    8. 8. Personal/Social History - High school graduate - Works as a farmer (+) 8.5-pack-year smoker - smokes 3 sticks per day since 15 years old up to present (+) alcoholic beverage drinker - ½ bottle whisky, 1-2x a week since 15 years old
    9. 9. PHYSICAL EXAMINATION - General Appearance - Awake, conscious, coherent - In CPD - Prefers to sit with upper body forward
    10. 10. PHYSICAL EXAMINATION - Vital Signs - Temperature - 37.8 degrees Celsius - RR - 28 cpm - CR - 120 bpm - O2 sat - 97%
    11. 11. PHYSICAL EXAMINATION - Skin - warm to touch, dry, wrinkled, good skin turgor - no skin lesions or edema noted
    12. 12. PHYSICAL EXAMINATION - HEENT • Head: Normocephalic, no lesions or masses • Eyes: Anicteric sclerae, pinkish conjunctivae Pupils ~3 mm diameter, equally reactive to light and accommodation, both direct and consensus • Ears: No ear discharges • Nose: no discharges, non hyperemic nasal mucosa, (-) alar flaring
    13. 13. PHYSICAL EXAMINATION - HEENT • Mouth - moist lips and buccal mucosae - non-hyperemic, non-enlarged tonsils • Neck (+) Left cervical lymphadenopathy (-) NVE
    14. 14. PHYSICAL EXAMINATION - Chest P.E. • Heart - adynamic precordium -PMI at 5th ICS Left MCL -NCRRR -no murmurs
    15. 15. PHYSICAL EXAMINATION - Chest P.E. • Lungs - Symmetrical chest expansion (+) suprasternal, supraclavicular retractions - Resonant lungs - Equal vocal and tactile fremiti (+) wheezing on all lung fields (+) fine crackles at the R lung base
    16. 16. PHYSICAL EXAMINATION - Abdomen - No lesions - Normoactive bowel sounds - Soft, nontender abdomen; no palpable masses - Liver not enlarged; spleen and kidneys non palpable
    17. 17. PHYSICAL EXAMINATION - Extremities Grossly normal, no deformities No edema Warm to touch CRT < 2 seconds Full pulses
    18. 18. Primary Impression T/C Chronic Obstructive Pulmonary Disease in Acute Exacerbation; Community Acquired Pneumonia - Moderate Risk
    19. 19. Differentials  Congestive heart failure  Bronchiectasis  Chronic asthma  Pulmonary tuberculosis
    20. 20. Chronic Obstructive Pulmonary Disease A disease state characterized by airflow limitation that is not fully reversible -Harrison’s A common preventable and treatable disease characterized by persistent 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 - GOLD
    21. 21. COPD  Emphysema - an anatomically defined condition characterized by destruction and enlargement of the lung alveoli  Chronic bronchitis - clinically defined condition with chronic cough and phlegm  Small airways disease - a condition in which small bronchioles are narrowed
    22. 22. COPD  Emphysema - a pathological term - often (but incorrectly) used clinically - describes only one of the several structural abnormalities present in COPD patients
    23. 23.  Chronic bronchitis  Presence of cough or sputum production for at least 3 months in each of the 2 consecutive years  An independent disease entity that may precede or follow the development of airflow limitation  Also exists in patients with normal spirometry
    24. 24. Epidemiology  COPD is a leading cause of morbidity and mortality worldwide  Estimates suggest that COPD will rise from the sixth to the third most common cause of death worldwide by 2020  due to continued exposure to COPD risk factors and the changing age structure of the world’s population
    25. 25. Risk Factors  Cigarette Smoking- major risk factor  Airway responsiveness  Respiratory infections  Occupational exposures  Ambient air pollution  Passive or second-hand smoke exposure  Genetic – Severe α 1 antitrypsin ( α 1AT) deficiency
    26. 26.  Effects of smoking on pulmonary function depend on  Intensity of smoking exposure  Timing of smoking exposure during growth  Baseline lung function
    27. 27. (Intensity of smoking) (Timing of smoking exposure) (Baseline lung function) Natural History of COPD
    29. 29.  Oxidative Stress Oxidative stress may be an important amplifying mechanism in COPD. Oxidants are generated by cigarette smoke and other inhaled particulates, and released from activated inflammatory cells such as macrophages and neutrophils  Protease-Antiprotease Imbalance Protease-mediated destruction of elastin, a major connective tissue component in lung parenchyma, is an important feature of emphysema and is likely to be irreversible
    30. 30. Protease-Antiprotease Imbalance
    31. 31. Chronic airflow limitation Inflammation Small airway disease -Airway inflammation -Airway fibrosis -Luminal plugs -Increased airway resistance Parenchymal destruction -Loss of alveolar attachments -Decrease of elastic recoil Airflow limitation Decreased FEV1 Decreased gas transfer
    32. 32. Diagnosis  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 in this clinical context  Post-bronchodilator FEV1/FVC <0.70 is confirmatory
    33. 33. Key indicators for considering a diagnosis of COPD  Dyspnea  Progressive (worsens over time)  Usually worse with exercise  Persistent (present every day)  Described by the patient as an ○ “Increased effort to breathe” ○ “Heaviness”, “air hunger”, or “gasping”
    34. 34. Key indicators for considering a diagnosis of COPD  Chronic cough  May be intermittent and may be unproductive  Chronic sputum production  Any pattern  History of exposure to risk factors  Tobacco smoke, occupational dusts and chemicals, smoke from home cooking and heating fuels
    35. 35. Spirometric Classification of COPD Severity Based on Post-Bronchodilator FEV1  Stage I: Mild COPD –  Characterized by mild airflow limitation (FEV1/FVC < 0.70; FEV1 ≥ 80% predicted).  Symptoms of chronic cough and sputum production may be present, but not always. At this stage, the individual is usually unaware that his or her lung function is abnormal.
    36. 36.  Stage II: Moderate COPD –  Characterized by worsening airflow limitation (FEV1/FVC < 0.70; 50% ≤ FEV1 < 80% predicted), with shortness of breath typically developing on exertion and cough and sputum production sometimes also present.  This is the stage at which patients typically seek medical attention because of chronic respiratory symptoms or an exacerbation of their disease.
    37. 37.  Stage III: Severe COPD –  Characterized by further worsening of airflow limitation  (FEV1/FVC < 0.70; 30% ≤ FEV1 < 50% predicted), greater shortness of breath, reduced exercise capacity, fatigue, and repeated exacerbations that almost always have an impact on patients’ quality of life.
    38. 38.  Stage IV: Very Severe COPD  Characterized by severe airflow limitation (FEV1/FVC < 0.70; FEV1 < 30% predicted or FEV1 < 50% predicted plus the presence of chronic respiratory failure)  At this stage, quality of life is very appreciably impaired and exacerbations may be life threatening
    39. 39. Treatment of Stable COPD
    40. 40. COPD Exacerbations  an event in the natural course of the disease characterized by a change in the patient’s baseline dyspnea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patient with underlying COPD  Triggered by infection with bacteria or viruses, environmental pollutants, or unknown factors  Increased hyperinflation and gas trapping accounting for the increased dyspnea
    41. 41. Assessment of COPD Exacerbations
    42. 42. Management of Severe but Not life- threatening Exacerbations of COPD  Assess severity of symptoms  Administer controlled oxygen therapy  Bronchodilators  Increase doses and/or frequency  Combine beta2-agonists and anticholinergics  Use spacers or nebulizers  Add oral or IV glucocorticoids  Consider antibiotics if with signs of bacterial infection  Closely monitor condition of the patient
    43. 43. Indications for hospital admission
    44. 44. Definition  Pneumonia  Infection of the pulmonary parenchyma  Community acquired pneumonia  a lower respiratory tract infection acquired in the community within 24 hours to less than 2 weeks  It commonly presents with an acute cough, abnormal vital signs of tachypnea (respiratory rate >20 breaths per minute), tachycardia (cardiac rate >100/minute), and fever (temperature >37.8ºC) with at least one abnormal chest finding of diminished breath sounds, rhonchi, crackles, or wheeze
    45. 45. Epidemiology  Pneumonia is the third leading cause of morbidity (2001) and mortality (1998) in Filipinos -Philippine Health Statistics, DOH  The incidence rates are highest at the extremes of age
    46. 46. Risk factors for CAP  asthma  immunosuppression  institutionalization  age of 70 years  heart failure  cerebrovascular disease  alcoholism  tobacco smoking  COPD  HIV infection
    47. 47. Epidemiologic Factors Suggesting Possible Causes of CAP Factor Possible Pathogen Alcoholism Streptococcus pneumoniae, oral anaerobes, Klebsiella pneumoniae, Acinetobacter spp., Mycobacterium tuberculosis COPD and/or smoking Haemophilus influenzae, Pseudomonas aeruginosa, Legionella spp., S. pneumoniae, Moraxella catarrhalis, Chlamydia pneumoniae Structural lung disease (e.g. bronchiectasis) P. aeruginosa, Burkholderia cepacia, Staphylococcus aureus
    48. 48. Pathophysiology  Pneumonia results from the proliferation of microbial pathogens at the alveolar level and the host's response to those pathogens  Microorganisms gain access to the lower respiratory tract commonly by aspiration from the oropharynx
    49. 49. Pathophysiology  Mechanical factors are critically important in host defense  hairs and turbinates of the nares  branching architecture of the tracheobronchial tree  gag reflex and the cough mechanism  Normal flora in oropharynx
    50. 50. Pathophysiology  When barriers are overcome, resident alveolar macrophages are extremely efficient at clearing and killing pathogens  When the capacity of the alveolar macrophages to ingest or kill the microorganisms is exceeded => clinical pneumonia  The host inflammatory response, rather than the proliferation of microorganisms, triggers the clinical syndrome of pneumonia
    51. 51. Pathophysiology  The release of inflammatory mediators, such as interleukin (IL)-1 and tumor necrosis factor (TNF), results in fever  Chemokines, such as IL-8 and granulocyte colony-stimulating factor, stimulate the release of neutrophils and their attraction to the lung, producing both peripheral leukocytosis and increased purulent secretions
    52. 52. Diagnosis and Management of CAP
    53. 53. Empiric Antibiotic Therapy  For moderate-risk CAP a combination of an IV non- antipseudomonal β-lactam (BLIC, cephalosporin or carbapenem) with either an extended macrolide or respiratory fluoroquinolone is recommended as initial antimicrobial treatment
    54. 54. Prevention  Influenza vaccination is recommended for the prevention of CAP  Pneumococcal vaccination is recommended for the prevention of invasive pneumococcal disease in adults  Smoking cessation is recommended for all persons with CAP who smoke
    55. 55. What was done to the patient?  Given O2 at 2 lpm via nasal prong  Given PAI with Salbutamol + Ipratropium bromide neb 1 neb q15 mins x 3 doses  Chest physiotherapy after nebulization  Referred to Guimbal hospital for admission  Encouraged smoking and alcohol cessation