Asthma

Asthma is a disease that is caused by an overreaction of the airways to irritants or other stimuli. In normal lungs, irritants may have no effect. Asthma is considered both chronic and inflammatory and a type of chronic obstructive pulmonary disease (COPD). As a result, the client with asthma experiences bronchoconstriction, increased mucus secretions, mucosal edema, and air hunger. The episodes of asthma are usually recurrent and attacks may be due to exposure to irritants, fatigue, and/or emotional situations. Asthma is classified as either intrinsic or extrinsic clients have a combination of extrinsic and intrinsic asthma.

Intrinsic(nonatopic) asthma
Caused by anything except an allergy Can be caused by chemicals such as cigarette smoke or cleaning agents, taking aspirin, a chest infection, stress, laughter, exercise, cold air, or food preservatives. May be due to irritation of nerves or muscles of the airway Most episodes occur after an infection of the respiratory tract.

Extrinsic(atopic) asthma
Associated with allergens like pollen, pet dander, dust mites Starts in childhood/teenage years

Familial predisposition: one-third of clients have at least one family member with a diagnosis of asthma Usually have other allergy problems like hay fever, hives, allergic rhinitis, or eczema.

What cause it and Why?

Airway inflammation occurs due to cells that cause inflammationmainly lymphocytes, eosinophils, and mast cells. The inflamed airway becomes damaged and narrowed, which increases the work of breathing.

Causes

Why

Environmental irritants: pet dander, dust and Allergens cause histamine release, smooth dust mites, cockroaches, fungi, mold, pollen, muscles swell, airway narrows, poor gas feathers, smoke, foods, cold air, food additives. exhange results. Stress Exercise Hormones released during stressful times can influence gas exchange Increases work of breathing, making air exchange more difficult

Pathophysiology:
The pathophysiology of asthma is complex and involves the following components:
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Airway inflammation Intermittent airflow obstruction Bronchial hyperresponsiveness

Airway inflammation
The mechanism of inflammation in asthma may be acute, subacute, or chronic, and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity. Varying degrees of mononuclear cell and eosinophil infiltration, mucus hypersecretion, desquamation of the epithelium, smooth muscle hyperplasia, and airway remodeling are present. Some of the principal cells identified in airway inflammation include mast cells, eosinophils, epithelial cells, macrophages, and activated T lymphocytes. T lymphocytes play an important role in the regulation of airway inflammation through the release of numerous cytokines. Other constituent airway cells, such as fibroblasts, endothelial cells, and epithelial cells, contribute to the chronicity of the disease. Other factors, such as adhesion molecules (eg, selectins, integrins), are critical in directing the inflammatory changes in the airway. Finally, cell-derived mediators influence smooth muscle tone and produce structural changes and remodeling of the airway.

Airflow obstruction
Airflow obstruction can be caused by a variety of changes, including acute bronchoconstriction, airway edema, chronic mucous plug formation, and airway remodeling. Acute bronchoconstriction is the consequence of immunoglobulin E-dependent mediator release upon exposure to aeroallergens and is the primary component of the early asthmatic response. Airway edema occurs 6-24 hours following an allergen challenge and is referred to as the late asthmatic response. Chronic mucous plug formation consists of an exudate of serum proteins and cell debris that may take weeks to resolve. Airway remodeling is associated with structural changes due to long-standing inflammation and may profoundly affect the extent of reversibility of airway obstruction. Airway obstruction causes increased resistance to airflow and decreased expiratory flow rates. These changes lead to a decreased ability to expel air and may result in hyperinflation. The resulting overdistention helps maintain airway patency, thereby improving expiratory flow; however, it also alters pulmonary mechanics and increases the work of breathing.

Bronchial hyperresponsiveness
Hyperinflation compensates for the airflow obstruction, but this compensation is limited when the tidal volume approaches the volume of the pulmonary dead space; the result is alveolar hypoventilation. Uneven changes in airflow resistance, the resulting uneven distribution of air, and alterations in circulation from increased intra-alveolar pressure due to hyperinflation all lead to ventilation-perfusion mismatch. Vasoconstriction due to alveolar hypoxia also contributes to this mismatch. Vasoconstriction is also considered an adaptive response to ventilation/perfusion mismatch.

In the early stages, when ventilation-perfusion mismatch results in hypoxia, hypercarbia is prevented by the ready diffusion of carbon dioxide across alveolar capillary membranes. Thus, patients with asthma who are in the early stages of an acute episode have hypoxemia in the absence of carbon dioxide retention. Hyperventilation triggered by the hypoxic drive also causes a decrease in PaCO2. An increase in alveolar ventilation in the early stages of an acute exacerbation prevents hypercarbia. With worsening obstruction and increasing ventilation-perfusion mismatch, carbon dioxide retention occurs. In the early stages of an acute episode, respiratory alkalosis results from hyperventilation. Later, the increased work of breathing, increased oxygen consumption, and increased cardiac output result in metabolic acidosis. Respiratory failure leads to respiratory acidosis.

Signs and Symptoms:

The asthmatic response usually maxes out in a few hours, but can last for days and weeks, whereas the symptoms of asthma usually occur suddenly after exposure to triggers.Most attacks occur in the morning.

Signs and Symptoms Wheezing (most noted on expiration) and bronchospasm

Breathlessness Cough (productive or nonproductive) Mucus production and Mucosal edema

Why Leukotrienes, histamine, and other chemicals from the lungs mast cells cause bronchospasm and smooth muscle swelling, which narrows the airway. Poor gas exchange Excess mucus production

Histamine and leukotrienes increase mucus production; excess secretions narrow the airway further. Histamine causes swelling of airway in the smooth muscle of the larger bronchi. Sudden shortness of breath Hypoxia Increased respiratory rate with use of accessory Hypoxia due to worsening asthma or drug muscles toxicity Prolonged expiratory phase Lungs trying to push air out Increased pulse Triggered by hypoxia; heart pumps harder and faster to move the limited oxygen to the vital organs. Air travels into slightly opened airway lumen; on exhalation the bronchi collapse due to increased intrathoracic pressure. This causes air to become trapped. As above (air trapping in lungs) No air movement; PCO2 will increase drastically Hyperventilation causing excessive loss of CO2 (acid)

Lung hyperinflation

Barrel chest Silent chest: life threatening Respiratory alkalosis

Status asthmaticus: severe attack

Lack of response to medications; fatal if not corrected at once

Tests:
1.) Skin testing for allergens. 2.) Pulmonary function tests (PFTs): PFTs measure how well the client is able to inhale and exhale air and how well the lungs are able to provide gas exchange. PFTs are usually diagnostic only during the attack itself. PFTs may show decreased peak flows, decreased vital capacity, and increased total lung capacity. 3.) Spirometry to assess amount of airway obstruction. 4.) Chest x-rays: helpful in determining lung hyperinflation (due to restrictive airflow), accumulation of secretions, and atelectasis. Treatments for asthma are usually determined by the extent of the disease process: 1.) Desensitization if due to allergies. 2.) Prevention: If the environmental trigger is identified, avoidance of the precipitating irritant is the best course of action. 3.) Medications used to manage asthma on a daily basis are not used for treatment during an attack.

Class Bronchodilators

Medications Theophylline (Aquaphyllin), aminophylline (Phyllocontin)

Beta-adrenergic agonists

Albuterol (Proventil), epinephrine (AsthmaHaler Mist)

Corticosteroids

Prednisone (Apoprednisone), hydrocortisone (Cortef), methylprednisolone (Solu-Medrol), beclomethasone (Beclodisk)

Mast cell stabilizers

Cromolyn (Nasalcrom), nedocromil (Tilade)

Leukotriene modifiers

Leukotriene receptor antagonists (LTRAs)

Zileuton (Zyflo), Montelukast sodium (Singulair), zafirlukast (Accolate) Montelukast sodium (Singulair)

Action Stimulate beta-adrenergic receptors, which causes dilation of the airways; monitor blood levels with these drugs to prevent toxicity. Acts on beta2-adrenergic receptors in the lungs. As a result, other organs are not affected by these drugs; fewer side effects. First-line drugs to reduce inflammation and swelling; inhaled form used for prevention (goes directly into the airway); this method limits systemic effects of steroids. Oral form used for severe cases of asthma. Decrease histamine, leukotrienes, bradykinins, and prostaglandins, which inflame the airway; used prophylactically. Decrease bronchoconstriction and inflammation caused by leukotrienes; asthma preventative Decrease bronchoconstriction and inflammation; prevent client from having to take as many

high-dose inhaled steroids.

Treatment:
The goal of treatment is to avoid the substances that trigger your symptoms and control airway inflammation. There are two basic kinds of medication for treating asthma:
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Control drugs to prevent attacks Quick-relief drugs for use during attacks

Control drugs for asthma control your symptoms if you don't have mild asthma. You must take them every day for them to work. Take them even when you feel okay.

The most common control drugs are:

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Inhaled corticosteroids (such as Asmanex, Alvesco, Qvar AeroBid, Flovent, Pulmicort) prevent symptoms by helping to keep your airways from swelling up. Long-acting beta-agonist inhalers also help prevent asthma symptoms. Do not take longacting beta-agonist inhaler drugs alone. These drugs are almost always used together with an inhaled steroid drug. It may be easier to use an inhaler that contains both drugs.

Other control drugs that may be used are:

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Leukotriene inhibitors (such as Singulair and Accolate) Omalizumab (Xolair) Cromolyn sodium (Intal) or nedocromil sodium (Tilade) Aminophylline or theophylline (rarely used anymore)

Quick-relief drugs work fast to control asthma symptoms:

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You take them when you are coughing, wheezing, having trouble breathing, or having an asthma attack. They are also called "rescue" drugs. They also can be used just before exercising to help prevent asthma symptoms that are caused by exercise. Tell your doctor if you are using quick-relief medicines twice a week or more to control your asthma symptoms. Your asthma may not be under control, and your doctor may need to change your dose of daily control drugs.

Quick-relief drugs include:

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Short-acting bronchodilators (inhalers), such as Proventil, Ventolin, and Xopenex Your doctor might prescribe oral steroids (corticosteroids) when you have an asthma attack that is not going away. These are medicines that you take by mouth as pills, capsules, or liquid. Plan ahead. Make sure you do not run out of these medications.

A severe asthma attack requires a check-up by a doctor. You may also need a hospital stay, oxygen, breathing assistance, and medications given through a vein (IV). Prevention:

You can reduce asthma symptoms by avoiding known triggers and substances that irritate the airways.
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Cover bedding with "allergy-proof" casings to reduce exposure to dust mites. Remove carpets from bedrooms and vacuum regularly. Use only unscented detergents and cleaning materials in the home. Keep humidity levels low and fix leaks to reduce the growth of organisms such as mold. Keep the house clean and keep food in containers and out of bedrooms -- this helps reduce the possibility of cockroaches, which can trigger asthma attacks in some people. If a person is allergic to an animal that cannot be removed from the home, the animal should be kept out of the bedroom. Place filtering material over the heating outlets to trap animal dander. Eliminate tobacco smoke from the home. This is the single most important thing a family can do to help a child with asthma. Smoking outside the house is not enough. Family members and visitors who smoke outside carry smoke residue inside on their clothes and hair -- this can trigger asthma symptoms.

Persons with asthma should also avoid air pollution, industrial dusts, and other irritating fumes as much as possible.