Lower Respiratory Disorders - Pharmacology

Lower respiratory disorders are conditions that obstruct or restrict tracheobronchial tubes and prevent the exchange of gas within the lungs. These conditions are referred to as chronic obstructive pulmonary disease (COPD) and include chronic bronchitis, bronchiectasis, emphysema, and asthma.

COPD obstructs the patient’s airway by increasing resistance of the airflow during inspiration and expiration. The result is an impairment of oxygen reaching lung tissues that can in some cases irreversibly damage lung tissues.

The airway obstruction occurs when the bronchioles constrict (bronchospasm) and mucous secretions increase causing the patient to experience difficulty breathing (dyspnea).


Pneumonia is an infection in the lungs that can be caused by a variety of microorganisms including viruses, bacteria, or fungus. It often starts after an upper respiratory infection. Symptoms can occur 2 to 3 days after a cold or sore throat. Symptoms include fever, chills, cough, rapid breathing, wheezing and/or grunting respirations, labored breathing, vomiting, chest pain, abdominal pain, loss of appetite, decreased activity, and, in extreme cases, signs of hypoxia (low oxygen levels) or cyanosis such as a bluish tint around the mouth or fingernails. There are vaccines to prevent certain types of pneumonia. Pneumonia is treated based on the underlying cause. Viral pneumonia is usually treated symptomati-cally. That is, bronchodilators, antipyretics (fever reducing), analgesics such as ibuprofen, cough medications that include expectorants, mucolytics, as well as suppressants to help the patient sleep. Bacterial and fungal pneumonia are treated with antimicrobials as well as the above treatment for viral pneumonia. The antimicrobial is chosen based on the specific microorganism causing the pneumonia. Antimicrobials are discussed in Chapter (Antimicrobials Fighting Infection) . Antipyretics such as ibuprofen are discussed in Chapter (Inflammation) . Pneumonia is contagious and is spread from person to person via droplets in the air from coughing and sneezing.


Tuberculosis (TB) is caused by the acid-fast bacillus Mycobacterium tuberculosis. The pathogen is frequently referred to as the tubercle bacillus. It is a major health problem in the world and kills more persons than any other infectious disease. More than 11/2 billion people in the world may have TB and many do not know it. Each year there are more than 8 million new bases of TB. Many of the new cases of TB can be attributed, in part, to the increased number of persons with acquired immunodeficiency syndrome (AIDS). Active TB develops in these people because of their compromised immune system. It can also be attributed to the increasingly crowded living conditions in urban areas. Individuals susceptible to TB are those with alcohol addiction, AIDS, and those in a debilitative condition.

Tuberculosis is transmitted from one person to another by droplets dispersed in the air through coughing and sneezing. The organisms are inhaled into the alveoli (air sacs) of the lung. The tubercle bacilli can spread from the lungs to other organs of the body via the blood and lymphatic system. If the body’s immune system is strong or intact, the phagocytes stop the multiplication of the tubercle bacilli. When the immune system is compromised, the tubercle bacilli spread in the lungs and to other organs. Dissemination of tuberculosis bacilli can be found in the liver, kidneys, spleen, and other organs. Symptoms of TB include anorexia, cough, sputum production, increased fever, night sweats, weight loss, and positive acid-fast bacilli (AFB) in the sputum. Medication to treat and prevent TB is discussed in(Antimicrobials Fighting Infection).


Chronic bronchitis is an inflammation of the bronchi that persists for a long period of time or repeatedly occurs. It is a form of COPD. Smoking is the main cause for bronchitis. Second-hand smoke may also cause chronic bronchitis. Air pollution, infection, and allergies make it worse. Patients who develop chronic bronchitis have excess mucous production that irritates the bronchial causing the patient to have a persistent productive cough.

Patients exhibit a gurgling lung sound (rhonchi) both on inspiration and expiration. The excess mucus blocks the airway causing a build up of carbon dioxide in the blood (hypercapnia) and a decrease in oxygen (hypoxemia) which leads to respiratory acidosis.


Brochiecstasis is the enlargement and distension of the airways so that pockets are formed where infection can develop. This condition alters the lining of the airways and damages the lung’s ability to filter air. Dust, mucus, and bacteria accumulate in the lungs, causing infection.


Emphysema is a progressive COPD. The alveoli become enlarged and damaged, trapping air in the over expanded alveoli preventing an adequate exchange of oxygen and carbon dioxide. Emphysema is caused by smoking cigarettes, by inhaling contaminants from the environment, or by the lack of the alpha1-antitrypsin protein. The lung contains bacteria that release proteolytic enzymes that destroy alveoli. The alpha1 -antitrypsin protein inhibits proteolytic enzymes and protects the alveoli.

Excess mucus as well as the residue from cigarette smoking and airborne pollutants find their way down the airways and plug the terminal bronchioles. The network of alveoli then loses their fiber and become inelastic and unable to spring back to size after expanding during inspiration. Alveoli enlarge as many of the alveolar walls are destroyed. Air becomes trapped in the overexpanded alveoli leading to inadequate gas exchange (O2 and CO2).


Acute asthma is a reactive airway disease (RAD) that occurs when lung tissue is exposed to extrinsic (environmental) or intrinsic (internal) factors that stimulate the bronchoconstrictive response. This causes bronchospasms that result in the patient wheezing and having difficulty breathing. More than 500,000 patients are hospitalized and 5000 die from asthma each year making acute asthma the third leading cause of preventable hospitalizations in the United States.

There are a variety of allergens (something that causes an allergic reaction) that can trigger an asthma attack. These include humidity, air pressure changes, temperature changes, smoke, fumes (exhaust, perfume), stress, emotional upset, and allergies to animal dander, dust mites, and drugs such as aspirin, indometh-acin, and ibuprofen.

Allergens attach to mast cells and basophils in connective tissues causing an antigen-antibody reaction to occur. Mast cells stimulate release of chemical mediators. These chemicals constrict the bronchi, increase mucous secretions, stimulate the inflammatory response, and cause pulmonary congestion.

Chemical mediators include histamines (proteins that are potent vasodilators), cytokines (small proteins that mediate and regulate the immune system, inflammatory response and hematopoiesis [red cell production]), serotonin (CNS neurotransmitter), ECF-A (eosinophil chemotatic factor of anaphylaxis) and leukotrines. Histamine and ECF-A are strong bronchoconstrictors that stimulate the contraction of bronchial smooth muscles. Cyclic adenosine monophosphate (cyclic AMP or cAMP) maintains bronchodilation. Histamines, ECF-A, and leukotrienes inhibit the action of cAMP resulting in bronchoconstriction. An increase in the serum level of eosinophils indicates that the inflammatory response has occurred. The first line of treatment for an acute asthma attack is administering sympathomimetics (beta-adrenergic agonists), which promote the production of cAMP and thereby cause bronchodilation.

Long-term management includes controlling extrinsic factors that caused the attack, educating the patient and the patient’s family, school officials, and employers about how to reduce exposure to those factors, and using various combinations of medications depending on the severity of the disease.

Medications to treat COPD

There are four types of medications used to treat this disease.


Bronchodilators relax smooth muscles around the bronchioles restoring airflow to the lungs. Sympathomimetics are bronchodilators that increase the production of cyclic AMP, causing dilation of the bronchioles by acting as adrenergic agonistic.

Some sympathomimetics are selective to particular adrenergic receptors, which are referred to as alpha1, beta2 and beta2-adrenergic. Other sympathomimetics are non-selective sympathomimetic that affect all types of adrenergic receptor sites.

Epinephrine (adrenalin) is a non-selective sympathomimetic that is given subcutaneously, IV, or via an endotracheal tube in emergency situations to restore circulation and increase airway patency.

Selective beta2-adrenergic agonists have fewer side effects then epinephrine and are given by aerosol or as a tablet. These include albuterol (Proventil, Ventolin), isoetharineHCl (Bronkosol), metaproterenol sulfate (Alupent), samleterol (Serevent), and Terbulaline SO4 (Brethine).

Ipratropium bromide (Atrovent) is an anticholinergic drug that inhibits vagal-mediated response by reversing the action of acetylcholine, producing smooth muscle relaxation. It is a newer medication that dilates bronchioles with few systemic effects. Ipratropium bromide (Atrovent) is used five minutes before glucocorticoid (steroid) or cromolyn are inhaled so the bronchioles dilate enabling the steroids to be deposited in the bronchioles. Sometimes ipratropium bromide is combined with albuterol sulfate (Combivent) to treat chronic bronchitis for more effective and longer duration than if each is used alone.

Methylxanthine (xanthine) derivatives are a second group of bronchodilators used to treat asthma. They include aminophylline, theophylline, and caffeine, which stimulate the central nervous system (CNS) to increase respirations, dilate coronary and pulmonary vessels, and increase urination (diuresis).

Leukotriene Modifiers

Bronchoconstrictors cause the contraction of smooth muscle around the bronchi restricting airflow to the lungs. Leukotriene (LK) is the primary bronchocon-strictor that increases migration of eosinophils, increases mucous production, and increases edema in the bronchi resulting in bronchoconstriction.

There are two types of Leukotriene (LK) modifers: LT receptor antagonists and LT synthesis inhibitors. These are effective in reducing the inflammatory symptoms of asthma triggered by allergic and environmental stimuli.

Leukotriene (LK) modifiers include Zafirlukast (Accolate), zileuton (Zyflo) and nontelukast sodium (Singulair).


Chronic obstructive pulmonary disease causes inflammation in the respiratory tract that results in respiratory distress for the patient. Glucocorticoids (steroids) are the primary medication given to reduce the inflammation. You’ll learn more about glucocorticoids (steroids) in(Inflammation).

Glucocorticoids (steroids) can be administered orally, via aerosol inhalation, intramuscularly, and intravenously. Glucocorticoids used for aerosol inhalation use beclomethasone (Beconase, Vanceril), dexamethasone (decadron), flunisolide(Aerobid, Nasalid), or triamcinolone (Azmacort, Kenalog, Nasacort).

Glucocorticoids used for other routes include betamethasones (Celestone), cortisone acetate (Cortone acetate, Cortistan), dexamethasone (Decadron), hydrocortisone (Cortef, Hydrocortone), methylprednisolone (Medrol, Solu-Medtol, Depo-Medrol); and prednisolone, prednisone, and triamcinolone (Aristocort, Kenacort, Azmacort).


As you learned previously in this chapter, an expectorant—referred to as mucolytics—liquefies and loosens thick mucous secretions so they can be removed through coughing. A commonly prescribed expectorant for chronic obstructive pulmonary disease is acetylcysteine (Mucomyst), which is administered by nebulizor five minutes after the patient receives a bronchodilator.

Acetylcysteine should not be mixed with other medications and can cause nausea, vomiting, oral ulcers (stomatitis), and a runny nose. Acetylcysteine is also an antidote for acetaminophen overdose if given within 12 to 24 hours after the overdose.

Mast Stabilizer Drugs

Mast cells release histamines, leukotrienes and other mediators of the inflammatory process. Mast cell stabilizer drugs inhibit the early asthmatic response and the late asthmatic response. They have no bronchodilator effect nor do they have any effect on any inflammatory mediators already released in the body. They are indicated for the prevention of bronchospasms and bronchial asthma attacks. They are administered by aerosol inhalation. The exact action of the drugs have not been determined. However, they are believed to have a modest effect in lowering the required dose of corticosteroids. The most common mast stabilizer drugs are cromolyn (Intal) and nedocromil (Tilade).

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