Question

A 56-year-old man with a history of smoking rush to ER at FUMC with shortness of breathandcough for several days. His symptoms began 3 days ago with runny nose. He reports a chronic morning cough productive of white sputum, which has increased over the past 2 days

Past Medical History
He has had similar episodes each time of raining season for the past 4 years. He always experiences fatigue, worsening cough, increased breathlessness and waking up in the morning with headache.
Family History
(+) Tuberculosis
(+) Hypertension
(-) Cancer
Personal and Social History
He has smoked 1 to 2 packs of cigarettes per day for 40 years and continues tosmoke. He denies hemoptysis, chills, or weight loss and has not received any relief fromover-the-countercough preparations.

Chest x-ray shows hyperinflation and right lobe pneumonia.
ABG results wasPh7.24,PO2-35 mmHg, PCO2 60mmHg, HCO3 30, O2 sat - 85%.
Spirometry with FEVI 35% predicted that does not change significantly after inhaled bronchodilators. ECG was ordered.
Physical Examination:
Took vital signs which are: BP: 130/80, T: 37.5 Celsius, PR:89, RR:30.
Examination displayed tachypnea, respiratory distress, use of accessory muscles, and intercostal retraction. Barrel chest is a common observation
1.Conceptualize the pathophysiological alterations distinct to the case (flow chart) and explanation.

Answer 1

The above given case look like a Chronic Obstructive pulmonary disease ( COPD) or Emphysema.

   Given presentation like chest X-ray have shown lungs hyperinflation, excessive work of accessory mussels and tachypnea and Barrel chest presentation commonly seen in COPD.

Chronic Obstructive Pulmonary Disease ( COPD) As a disease state characterised by airflow limitation that is not fully reversible.

- COPD includes emphysema, an anatomically defined condition characterised by destruction and enlargement of alveoli,

- chronic bronchitis a clinically defined condition with chronic cough and phlegm,

- a small airway disease in which small bronchioles narrowed.

- COPD only present if chronic air flow obstruction occurs,

- COPD is not occurred in chronic bronchitis without chronic airflow obstruction.

Risk factors: 1. cigarette smoking,

2. Airway responsiveness and COPD,

3. Respiratory Infections,

4. Occupational exposures,

5. Ambient air pollution,

6. Passive or second hand smoking exposure.

Genetic considerations:  although smoking is the major environmental risk factor for the development of COPD, severe Alpha 1 antitrypsin deficiency is a proven genetic risk factor for COPD.

( by 1964, the advisory committee to the surgeon general of the United States had concluded that cigarette smoking was a major risk factor for mortality from chronic bronchitis and emphysema,

- studies have shown accelerated decline in the volume of air exhaled within the first second of the FEV1 in a dose relationship to the intensity of cigarette smoking, which typically expressed a pack years.)

PATHOPHYSIOLOGY : Persistent reduction in forced expiratory flow rates is the most typical finding in COPD,

- Increases the RV ( Residual volume) and RV/TLC ( total lung capacity ) ratio.

- processes in the lungs and airways important in the pathogenesis of COPD include inflammation, immune reactions, imbalance of proteinases and anti proteinases, turnover of extra cellular matrix, oxidative stress and apoptosis,

- pathologic features include destruction of alveolar tissue and small airways, airway wall inflammation, edema and fibrosis and intraluminal mucus,

- pulmonary function changes include decreased maximal expiratory airflow, hyperinflation, air trapping and alveolar gas exchange abnormalities,

- an increased incidence of osteoporosis, skeletal muscle dysfunction and CAD occur in COPD, perhaps indicating a systemic component of the inflammation.

Prevention: absistence from smoking is the most effective measure for preventing COPD,

- The US department of health and human services has developed telephone based support system ( 1-800-QUIT NOW) with an Internet analog (1800 quitnow.cancer.gov)

Diagnosis : Clinical presentation: History: common symptoms of COPD are dyspnea on exertion, cough, sputum production, and wheezing,

- exertion gradually progress over years,

- search for comorbid conditions such as gastroesophageal reflux, congestive heart failure or sleep disordered breathing,

- should obtain a lifelong smoking Hx and quantify exposure to environmental and occupational risk factors,

- weight loss often occurs in pts with end stage COPD, but other etiologies such as malignancy and depression should be sought.

Physical examination: until significant reduction of lung function occurs eg: FEV1 < 50% predicted,

- patients with severe COPD may exhibit prolonged > 6 seconds breath sounds on a maximal forced exhalation, decreased breath sounds, use of accessory muscle of respiration, and hyper per resonance to chest percussion. Expiratory wheezing may or may not present,

- sign of Pulmonary hypertension and right heart failure may be present,

- clubbing is not a feature of COPD, so its presence should prompt an evaluation for other conditions especially lung cancer.

Differential Diagnosis: 1. Airway tumours,

2. Asthma,

3. Chronic pulmonary thromboembolic disease,

4. Congestive heart failure,

5. Cystic fibrosis,

6. Constrictive brochiolitis,

7. Diffuse chronic parabrochiolotis,

8. Eosinophilic granuloma,

9. Ischemic heart disease,

10. Mycobacterium infection,

11. Tracheo brancho malacia,

12. Treacheal stenosis all are must be considered as part of differential in the work up of COPD.
Diagnostic Testing: 1) Pulmonary Function Testing - must be presence of EFV1 /FVC ratio is limited,

- FEV1 is usually redused.

2) Laboratories: ABG recommended for presence and severity of hypoxemia and hypercapnia,

- annual monitoring may be considered,

- elevated venous bicarbonate may signify chronic hyper capnia,

- polycythemia may reflect a physiologic. Response to chronic hypoxemia and inadequate supplemental oxygen use.

3)Imaging:  chest X-ray is not sensitive but useful for evaluating alternative diagnosis,

- CT detect emphysema, COPD and conditions associated with Tobacco smoking,

- with increasing severity of COPD, patients often develop radiographic signs of thoracic hyperinflation, including flattening of diaphragm, increased retrosternal / retro cardiac air spaces, and lung hyperlucency with diminished vascular markings. Bullae may be visible, In severe disease chest CT is utilised to determine candidacy for lung volume reduction surgery ( LVRS).

Treatment: aims of treatment is

- improve quality of life,

- decrease the frequency and severity of Acute exacerbation,

- slow the progression of disease,

- prolong the survival.

MEDICATIONS: 1. Inhaled bronchi dialators : work mainly by relaxing airway smooth muscle tone, this results In a reduction in Expiratory air flow obstruction.

- use of metered dose inhalers (MDI),

- Long acting inhaled anticholinergic agents result in significant improvement in lung function, QOL, COPD exacerbation, although rate of decline of FEV1 is unaffected,

- Long acting B adrenergic agonists,

2. Inhaled corticosteroids:

3. Combination therapy; of inhaled cortico steroids and long acting b adrenergic agonists,

4. Macrolide antibiotics: azithromycin or clarithromycin,

5. PDE4 inhibitors: like Roflumilast - 500mg,

6. Theophylline,

7. Systemic corticosteroids,

8. Intravenous alpha 1 antitrypsin,

9. Others like : supplemental oxygen,

pulmonary rehabilitation ,

Vaccinations.

10. Surgical therapy : Lung transplantation and LVRS.