PP552 Principles of Human Disorders and Pharmacotherapeutics CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) Karen J. Tietze, B.S., Pharm.D.

Professor of Clinical Pharmacy The GOALS of this lecture are to: 1.Review the epidemiology, etiology, pathophysiology, and signs and symptoms of COPD. 2.Review COPD therapeutics. OBJECTIVES Upon completion of the readings, lecture, lab, and case studies, the student will be able to: 1. Define chronic obstructive pulmonary disease, chronic bronchitis (old term), and emphysema (old term) a. COPD i. COPD is a preventable and treatable disease with some significant extra-pulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases. 1. KEY POINT IS THAT COPD IS NOT REVERSIBLE, asthma is reversible (except in stage 4) 2. COPD is a chronic disease where progression can only be slowed down and not really stopped. 3. Asthma is majority all inflammatory etiology but in COPD its just a part of the disease state. b. Chronic Bronchitis (old term) - BLUE BLOATER (blue cause not enough O2) - Can treat this part of COPD! i. Defined as the presence of cough and sputum production for at least 3 months in each of 2 consecutive years, is not necessarily a/w airflow limitation. 1. Gas exchange suffers because of mucous interference 2. Can lead to right sided heart failure as V/Q matching problem occurs 3. Pulmonary hypertension 4. Bloated cause of all the fluid in the lung, blue cause of no O2 c. Emphysema (old term) - Pink Puffer - Presumptive diagnosis i. Destruction of the alveoli, is a pathological term. 1. Three types: UNTREATABLE PART OF COPD a. Centriacinar - a/w long-term smoking b. Panacinar i. a/w alpha 1-antitrypsin deficiency 1. It is a genetic disorder where there is a lack of a liver protein that blocks the destructive effects of certain enzymes. The condition may lead to emphysema and liver disease, and in rare cases, skin disease. Can be treated if detected early. 2. c. Distal acinar 2. Clinically means abnormal permanent enlargement of airspace distal to terminal bronchioles with destruction of airway and alveolar walls but without obvious fibrosis. i. Permanent damage to alveoli, no way to repair it 3. Loose alveolar surface area, limiting gas exchange 4. EXTRA INFO: Acinar = pertaining to one of the small sacs, in this case alveoli 2. List the airway changes associated with COPD and state the pathogenesis of each change

Noxious particles and Gases Lung Inflamation (the presence of host factors can increase severity and chances of inflamation)

Oxidative stress Proteinases (antioxidants usually take care of it) (cleave proteins or antiproteinases usually take care of this) COPD Pathology (Repair mechanisms usually take of this but the body can be overwhelmed and cant stop progresion)

a. Pathogenesis of COPD i. Noxious agents are the triggers ii. Resulting in COPD Inflammation iii. Responded to by CD+8 Lymphs, macrophages, neutrophils iv. The mediators involved are LTB4, IL-8, TNF-alpha v. The result is irreversible air flow limitation vi. This is due to airway fibrosis and narrowing (scrar tissue); alveolar destruction - loss of elastic recoil due to scar tissue; small airway collapse as alveolar support is gone 3. Identify/state the signs and symptoms associated with COPD. a. Tripoding position...elbows on thighs and hands on chin...this raises the clauvical and expands the thorax, improving air flow b. Key Indicator - Spirometry - PFTs i. Chronic cough with huge amounts of sputum ii. Dyspnea on Exertion (DOE) - air hunger, chest heaviness (ASTHMA is more of a chest tightness, cant expand chest type of thing) iii. PFTs establish it - Airflow limitation - DIAGNOSTIC 1. Decreased: FEV1, FVC, FEV1/FVC<80% predicted; NOT REVERSIBLE W/ASTHMA DRUGS c. Physical Exam i. NOT DIAGNOSTIC ii. May see barrel chest iii. Right sided heart failure 1. central cyanosis, ankle swelling, increased JVP, displaced PMI- dwn left 2. Look for the classic signs of HF (above) d. Chest X-Ray i. NOT DIAGNOSTIC ii. Low, flat diaphragms (due to air trapping) iii. Airway destruction (bullae) iv. Right sided heart failure e. Arterial Blood Gas i. Usually Compensated low O2 1. Central resp. becomes insensitive to CO2 ...its rises and rises triggering breathing factors in CNS...usually higher breathing rate is triggered but not for this type...they are insensitive to the chronic high levels of CO2 - body adjusts to a new normal - May be treated with oxygen therapy: becareful as they may stop breathing with the increased O2 levels when above ii. If CO2 retainer will show compensated Resp. acidosis (small % of COPDers)

prescribed range. Body has adjusted to having a certain amount of CO2 with CO2 retainers. If it there is not much CO2, no longer a trigger to breathe, can be fatal! 4. Given a specific patient case, determine the most likely cause of the patient's COPD. a. See Notes 5. Differentiate between emphysema, chronic bronchitis and asthma in-terms of etiology, pathophysiology, clinical manifestations, and laboratory findings. a. See notes 6. Given a specific patient case, determine the GOLD severity of illness classification. a. Table 4, P.4 Bottom 7. Based on the GOLD severity of illness classification (see #6 above), create a comprehensive treatment plan including drug(s), dose(s), route(s) of administration, duration of therapy and appropriate alternative drugs, if any. State the rationale for each medication. a. Table 5, P.5 Top 8. Given a specific patient case, determine if the patient qualifies for long-term oxygen therapy. a. Chronic oxygen therapy is indicated if: i. PaO2 < 55 mmHg or SaO2 < 88% with or without hypercapnia [too much CO2 in the blood] ii. PaO2 55-60 mmHg or SaO2 is less than or equal to 88% if evidence of pulmonary HTN, peripheral edema suggesting CHF, or polycythemia [Abnormal increase in blood cells (primarily red blood cells) resulting from excess production by the bone marrow]. (NOTT data) 9. Create a patient-specific monitoring plan. a. See Notes

Prior Learning Requisites: Pulmonary physiology (ventilation, diffusion, perfusion, ventilation-perfusion relationships, mechanics of breathing, control of breathing), pulmonary physical assessment skills, arterial blood gas assessment, pulmonary function assessment skills.

Required Reading:Bourdet SV, Williams OM. Chronic obstructive lung disease. In: Pharmacotherapy .. DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. New York: McGraw-Hili. 2005: 537 -554. Supplemental Reading: Global Initiative for Chronic Obstructive Lung Disease (GOLD Guidelines). NHLBIIWHO Workshop Report. Executive Summary. December 2006 update. National Institutes of Health. Report available at www.goldcopd.com.

Brewis RAL. Lecture Notes on Respiratory Disease. 3rd ed. 1985 Blackwell Scientific Publication, p. 45.