Bronchial Asthma Female/ 18 yrs Diagnosis: Bronchial asthma An 18 year old girl was brought to the clinic for complaints of Bronchial Asthma. When patient reported to us, she was having a very severe attack of Asthma. She complained of breathlessness that was worse from cold drink, cold water, draft of air, monsoon, getting wet, at midnight. Her complaints were better during the dry climate and when traveling out of Philippines. The complaints would also be relieved by taking warm drinks and tea. The cough was productive with white expectoration. The patient's peculiar features at the time of the Asthma attack were extreme anxiety and fear of death. She felt thirsty for little water at a time. She was feeling sensitive to cold and extremely restless due to the complaints. The patient also had complaints of cold with watery discharge from the nose and cracking of the joint accompanied by pain. She had a normal appetite with liking for sweets, fast food and tea and was averse to eating vegetables. She would occasionally be constipated. Her sweat was profuse in the summers, especially in underarms. Her sleep would be frequently disturbed due to the asthma attacks and due to thoughts on her mind. She would often dream of flying, water and God. Her birth history was normal. Birth weight: 8 pounds Age of talking: 1 year Age of teething: 8 months
Transcript
Bronchial Asthma
Female/ 18 yrsDiagnosis: Bronchial asthma
An 18 year old girl was brought to the clinic for complaints of Bronchial Asthma. When patient reported to us, she was having a very severe attack of Asthma.
She complained of breathlessness that was worse from cold drink, cold water, draft of air, monsoon, getting wet, at midnight. Her complaints were better during the dry climate and when traveling out of Philippines. The complaints would also be relieved by taking warm drinks and tea. The cough was productive with white expectoration. The patient's peculiar features at the time of the Asthma attack were extreme anxiety and fear of death. She felt thirsty for little water at a time. She was feeling sensitive to cold and extremely restless due to the complaints. The patient also had complaints of cold with watery discharge from the nose and cracking of the joint accompanied by pain.
She had a normal appetite with liking for sweets, fast food and tea and was averse to eating vegetables. She would occasionally be constipated. Her sweat was profuse in the summers, especially in underarms.
Her sleep would be frequently disturbed due to the asthma attacks and due to thoughts on her mind. She would often dream of flying, water and God.
Her birth history was normal.Birth weight: 8 poundsAge of talking: 1 yearAge of teething: 8 months
Bronchial Asthma
Asthma is a chronic, reversible, obstructive airway disease, characterized by wheezing. It is caused by a spasm of the bronchial tubes, or the swelling of the bronchial mucosa, after exposure to various stimuli.
Asthma is the most common chronic disease in childhood. Most children experience their first symptoms by 5 years of age.
ETIOLOGY:
Asthma commonly results from hyper responsiveness of the trachea and bronchi to irritants. Allergy influences both the persistence and the severity of asthma, and atrophy or the genetic predisposition for the development of an IgE-mediated response to common airborne allergens is the most predisposing factor for the development of asthma.
CLASSIFICATION:
1. Extrinsic Asthma - called Atopic/allergic asthma. An “allergen” or an “antigen” is a foreign particle which enters the body. Our immune system over-reacts to these often harmless items, forming “antibodies” which are normally used to attack viruses or bacteria. Mast cells release these antibodies as well as other chemicals to defend the body.
Common irritants:
Cockroach particles Cat hair and saliva Dog hair and saliva House dust mites Mold or yeast spores Metabisulfite, used as a preservative in many beverages and some foods Pollen
2. Intrinsic asthma - called non-allergic asthma, is not allergy-related, in fact it is caused by anything except an allergy. It may be caused by inhalation of chemicals such as cigarette smoke or cleaning agents, taking aspirin, a chest infection, stress, laughter, exercise, cold air, food preservatives or a myriad of other factors.
Smoke Exercise Gas, wood, coal, and kerosene heating units Natural gas, propane, or kerosene used as cooking fuel Fumes Smog
The main function of the respiratory system is to move air into the lungs so that oxygen can enter the body and carbon dioxide can be exhaled. During breathing, air passes from the nose and mouth into the pharynx and through the larynx into the trachea. The trachea bifurcates to carry air into each lung. These two tubes are the main stem bronchi; there is a single left main stem bronchus and a single right main stem bronchus for the left and right lungs, respectively.
All bronchial branching occurs as bifurcations This pattern is repeated as air moves down the bronchi and into the periphery of the lungs. With each branching, the tubes become smaller in diameter and eventually microscopic, until they end in the alveolar chambers that are, themselves, microscopic in size.
Gas exchange occurs within about 300 million alveoli. The alveoli have very thin walls to allow oxygen and carbon dioxide to cross between the lung capillaries and the alveolar spaces. The central function of respiration — gas exchange — takes place in the alveoli. Besides conducting air to and from the alveoli, the bronchi also serve to protect the alveoli. The bronchi warm and moisten the air before it enters the alveoli. The alveolar structures are delicate and can easily be damaged by cold, dry air.
Clearing airborne particles
Air passages have a self-cleaning mechanism to remove small, inhaled airborne particles. Among the cells that line the inside of the respiratory passages, from the nasal lining through the trachea and bronchi, are those that secrete mucus and others with cilia.
The purpose of mucus is to coat the lining of the airway to create a sticky surface that can collect foreign particles from inhaled air. Mucus-secreting cells are present on the airway surface and in specialized mucus glands found deep within the bronchial wall. However, most cells that line the airway have cilia on their surface that constantly move in a regular, sweeping fashion. Fine airborne particles land on the airway lining and are trapped in mucus, which is then swept upward by the movement of these cilia. Eventually, the mucus is brought far enough up in the respiratory system to be coughed out of the respiratory system or — more commonly — swallowed. This self-cleaning mechanism is called mucociliary clearance. Minute foreign particles that are not removed
by the airway lining can reach the alveoli, where they are phagocytosed by large scavenging cells called alveolar macrophages for removal from the airway.
Controlling airway caliber
Smooth muscle in the bronchial wall can contract or relax, without conscious control, to result in constriction or dilation of the airwayThe airway smooth muscle allows the body to change airway diameter for different environmental conditions. The body may respond to an inhaled noxious stimulus — such as smoke or another toxic irritant — by causing the airways to constrict. This "clamp down" of the airway smooth muscle, sometimes termed bronchospasm, can serve to protect the delicate alveoli from toxic damage.
The Action of Breathing
Muscles
The diaphragm and the intercostal muscles are the principal muscles involved in breathing. During normal breathing, inspiration is an active process that involves contraction of the diaphragm (to expand the chest cavity downward) and the intercostal muscles (to expand the chest cavity up and outward). Expiration is largely passive, during which time the diaphragm and intercostal muscles relax.
Neural control
The respiratory center controls the rate and depth of breathing. During inspiration, motor impulses travel from the respiratory center to the diaphragm and external intercostal muscles, which contract and cause the lungs to expand. This expansion stimulates stretch receptors in the lungs to send inhibiting impulses to the respiratory center, thus preventing overinflation.
An increase in carbon dioxide levels will stimulate an increase in the rate or depth (or both) of breathing. A decrease in oxygen levels will cause an increase in the rate of breathing. In the control of the airways, different autonomic nerve systems are also involved.
Parasympathetic nerves
Parasympathetic nerves are characterized by their use of the neurotransmitter acetylcholine. The vagus nerve sends motor fibers from the brain to smooth muscle cells in the bronchial walls. Stimulation of the vagus nerve releases acetylcholine, which binds to specific "cholinergic" receptors on smooth muscle cells within the bronchial walls and, thus, constricts the airways. Simply stated, cholinergic stimulation causes bronchoconstriction through airway smooth muscle contraction.
Sympathetic nerves
Sympathetic nerves are characterized by the use of catecholamine neurotransmitters. Also produced by the adrenal glands, catecholamines act by binding to "adrenergic" receptors. The sympathetic system sends nerves to blood vessels and glands in the lungs, but not to the bronchial smooth muscle. Thus, sympathetic nerves cannot directly control airway diameter. Instead, sympathetic nervous effects (such as bronchodilation) are caused when catecholamines, such as epinephrine, are released into the bloodstream by the adrenal glands.
The Immune System
The three main components of the immune system are antibodies, inflammatory cells, and inflammatory mediators. Antibodies are the specific proteins created by the immune system to identify and bind to foreign and potentially invading substances. Inflammatory cells circulate in the bloodstream and can "sense" the body's surroundings or exposures to create immune responses directed against those exposures. Inflammatory mediators are chemical substances that are secreted by immune cells to induce (or respond to) an ongoing immune response generated against a specific exposure to the body.
Antibodies
An antibody, or an immunoglobulin (Ig), is a small protein molecule created by the immune system to have a close structural "fit" to the surface of a foreign substance. The foreign substance is an antigen. The primary job of antibodies is to bind to an infectious agent (a virus, bacteria, or parasite) and, in so doing, to notify and trigger the rest of the immune system to fight off this invader. The aspect of the immune system that depends on antibodies to identify a foreign substance is sometimes termed the humoral immune system. The so-called "humoral response" refers to the creation, by the immune system,
of antibodies that can be the first step for the body to detect — and subsequently eliminate — a foreign substance.
Antibodies are created and secreted by B cells. Each individual B cell responds to a unique antigenic structure by secreting an antibody that corresponds to that structure. Once a foreign antigen interacts by binding to the B cell bearing the antibody with the best "fit," that B cell is activated to divide repeatedly (termed B cell proliferation).
The body manufactures five classes of antibodies, namely IgM, IgG, IgA, IgD, and IgE. For certain infections, generating antibodies of the IgM and IgG classes is essential for the body to fight off the infection quickly and successfully. Nonetheless, each class of antibody is specialized to perform particular functions in the immune response.
Immunoglobulin E
The antibody class of allergic diseases, including allergic asthma, is IgE. It is fundamental to the allergic immune response. Any true allergic reaction occurs because IgE antibodies are binding specifically to the substance that is stimulating the allergic reaction.
Although the usual antibody response to an antigen is to generate IgM or IgG antibodies (or both), it is unclear why some antigens in some patients lead to generation of a specific IgE antibody response. An antigen that stimulates an IgE antibody response is more specifically termed an allergen. These IgE antibodies are generally directed against substances that are not harmful to the body, including pollens; fur from cats; certain mold spores; certain foods; certain drugs; and (most commonly) droppings from microscopic dust mites. Only certain people have apparently inherited a tendency to generate IgE antibodies to innocuous allergens. This is also known as atopy.
IgE usually occurs in very minute concentration in serum, amounting only to nanograms per milliliter — for total serum IgE, in contrast to milligrams per milliliter — for serum IgM or IgG. More important than the level of circulating IgE is the level of IgE that is bound to the surface of certain inflammatory cells that are central to an allergic reaction. The most important of these cells in an immediate hypersensitivity reaction is the mast cell. After initial exposure of the patient to an allergen, the primary immune response is to generate unique IgE antibodies that become bound to the surface of mast cells. These mast cells live within various tissues of the body, including in the bronchi.
If the patient is later re-exposed to an allergen by inhalation, the allergen binds to the surface-bound IgE on mast cells in the bronchi. Binding of at least two IgE molecules, bridged by a single allergen molecule, is termed cross-linking. Cross-linking of IgE by allergen on the surface of the mast cell is the initial biologic event of an allergic reaction An allergic reaction can be technically referred to as an "immediate hypersensitivity" reaction; this term derives from the two key aspects of an allergic reaction:
The reaction occurs very quickly after exposure to the substance that stimulates the reaction (allergen). The reaction may occur (and may be life-threatening) 5-10 minutes or less after exposure to the allergen and, thus, is termed immediate.
The person having the allergic reaction is more sensitive (i.e., shows hypersensitivity) to the offending substance than one who is not allergic. A person without allergies would be expected to have absolutely no discernible reaction to the very same substance that could be fatal to one who has exquisite allergic sensitivity to that substance.
Inflammatory cells
Participants in the immune system include several types of cells. Two classes of cells include granulocytes and lymphocytes. Granulocytes include a number of cell types that are all characterized by containing many granules. The most important granulocytes in asthma are mast cells and eosinophils. Lymphocytes lack granules and manufacture other kinds of proteins that are involved in the inflammatory process.
Mast cells
A mast cell becomes "sensitized" to an allergen when the IgE specific for that allergen circulates in the bloodstream and eventually lands on the surface of the mast cell; the latter is fixed in a particular tissue location (e.g., a bronchial wall). Cross-linking of surface IgE by an allergen molecule triggers a rapid activation (<15 minutes) of the mast cell, which then releases numerous inflammatory mediators into the tissue surrounding the cell.
Eosinophils
The eosinophil is the inflammatory cell most closely associated with asthma. Unlike mast cells that are fixed in various tissues throughout the body, eosinophil are very mobile. In association with asthma, elevated numbers of eosinophils have been identified in various tissue compartments, including:
circulating in the peripheral blood. The increase in peripheral blood eosinophils in asthma is probably due to inflammatory cells or mediators coming from the lungs to cause increased production of eosinophils by the bone marrow.
in biopsies of lung tissue, particularly in the bronchial wall of patients with asthma.
in fluid specimens obtained from the lung using a bronchoscope. With this method, fluid that "washes out" the bronchi and alveoli — termed bronchoalveolar lavage (BAL) fluid — is obtained by inserting a fiberoptic scope down the air passages and into the lungs.
in secretions or sputum of patients with asthma. A sputum specimen is basically a coughed-up sample of the mucus that is coating the airway lining.
The mobility of eosinophils indicates that they can be stimulated to leave the bloodstream and enter the tissues. In asthma, eosinophils move from the blood into the bronchi (as documented in bronchial biopsies and in BAL fluid) and onto the surface of the airway lining (as documented in sputum). Importantly, the levels of eosinophils in each of these compartments demonstrate a rough correlation with the disease state of asthma and even with the clinical severity of asthma. When activated, eosinophils release several pre-formed mediators from within their granules. These granules contain several proteins, among which is eosinophilic cationic protein.
Eosinophils appear to play a role in virtually all types and severities of asthma. Although mast cells play a central role in allergic asthma, the activity of eosinophils is evident in both allergic and nonallergic asthma. Also, there is clear documentation of increased eosinophil numbers (sometimes termed eosinophilia) and increased eosinophil activation in the blood, lungs, and sputum of asthmatics.
Lymphocytes
Lymphocytes lack granules and manufacture other kinds of proteins that are involved in the inflammatory process. B lymphocytes have the important function of manufacturing antibodies. T lymphocytes play an essential role in events that lead to airway inflammation by orchestrating the entire inflammatory process. T cells release a variety of cytokines that communicate with most other cells in the inflammatory process. Cytokines from T cells can, for instance, activate B cells to make antibodies (even controlling the choice between making IgM, IgG, or IgE) or activate eosinophils versus neutrophils.
T cells thus initiate and orchestrate a cascade of cytokine-mediated airways inflammation. T cells and their cytokines provide a common pathway for allergic (i.e., IgE-mediated) and nonallergic asthma. They are, however, not a source of mediators of immediate hypersensitivity reactions and thus do not participate in the acute (<15 minutes) response to allergen that can cause an acute asthma attack.
Inflammatory mediators
The immunologic cascade and the ensuing inflammatory reaction comprise activation of specific inflammatory cells that also release various inflammatory mediators, such as histamine, mast cell tryptase, leukotrienes, prostaglandins, eosinophil cationic protein, and cytokines. However, these represent a small subset of the several inflammatory mediators that have been identified and studied worldwide.
Development of Asthma
Airway Inflammation
Infectious agents constantly enter the body via the respiratory system. The bronchi have several protective methods against these invaders. These include:
recruitment of inflammatory cells from the bloodstream into the bronchial wall, where they directly attack the invading organisms and secrete inflammatory chemicals that are toxic to the organisms
swelling of the bronchial wall mucus secretion constriction of the airway.
The fundamental defect in asthma is that, for reasons that are unclear, these inflammatory actions occur in the bronchi when no serious infection, toxin, or other inhaled threat to the body exists.
Airway inflammation in asthma is:
a direct response of the immune system to a trigger a cascade of immunologic events that includes inflammatory cells and mediators an immune-mediated process that leads to inflammatory changes in the airway,
including eosinophil recruitment and airway edema.
Pathophysiology of the Airway in Asthma
A cross-section of a normal airway, the lumen is free of significant mucus. The single layer of ciliated epithelial cells lines and protects the bronchial wall. The mucous gland provides a protective layer of mucus above the epithelial cells. There are few eosinophils in the bronchial wall.
The following depicts some of the histologic features of airway inflammation. Plasma leakage from blood vessels contributes to bronchial wall edema, which results in thickening of the bronchial wall. Eosinophils migrate from the bloodstream into the bronchial wall and the airway lumen and can release eosinophil cationic protein and leukotrienes. Enlarged mucus glands secrete excess mucus that can plug the airway lumen.
Moreover, as the airway walls thicken due to these inflammatory reactions, the amount of airway narrowing produced by a given amount of smooth muscle contraction in asthma is much greater than that in a normal airway. Thus, even a small contraction of bronchial smooth muscle can lead to dramatic increases in airway resistance when the bronchial walls are already thickened from the actions of inflammatory cells and airway edema.
Bronchial hyperreactivity
Hyperreactivity of the airways to several stimuli is a hallmark of clinical asthma, and it appears bronchial hyperreactivity (BHR) is caused by airway inflammation. Studies have shown that the degree of BHR correlates, for instance, with the number of inflammatory cells recovered in BAL fluid from the airways of asthmatic patients
Clinically, the degree of BHR (measured in research studies by methacholine challenge) has been shown to correlate with general asthma severity, with morning peak expiratory flow rate (PEFR), with the degree of diurnal variation of PEFR, and with the frequency of inhaled beta-agonist use (when taken by patients as needed for symptoms). The degree of BHR appears to decrease when asthma is well controlled with medication. The ultimate result and significance of BHR is the airflow obstruction that occurs when an asthmatic is exposed to a trigger.
Bronchoconstriction
Inhalation of an allergen solution by a patient with allergic asthma causes prompt and significant bronchoconstriction. After this bronchial allergen challenge, there is a rapid decline in forced expiratory volume in 1 second (FEV1) that begins within 15 minutes and generally subsides within the first hour. This bronchial manifestation of immediate hypersensitivity has been termed an early asthmatic reaction (EAR), or the early phase response. After this phase resolves (spontaneously or with a beta-agonist, if needed), the FEV1 reaches a level that is at or close to the pre-challenge baseline.
In about 50% of patients, there can be a spontaneous return of bronchoconstriction that occurs several hours after the allergen challenge (and after the EAR has resolved) (see figure above). This late phase response usually occurs 6-24 hours after exposure to the allergen and is termed the late asthmatic response (LAR). This late decline in FEV1 may be less severe than during the EAR but is generally more prolonged, lasting several hours.
The EAR results from binding of inhaled allergen to mast cell membrane-bound IgE with subsequent release of mediators (e.g., histamine, leukotrienes, and prostaglandins). Among these mediators, the cysteinyl leukotrienes appear to account for a significant part of the early bronchoconstrictor response.
The LAR to an allergen is typified not only by a decline in FEV1 but also by the influx of inflammatory cells, most notably eosinophils, and airway edema. The intensity of LAR inflammation correlates with the degree of airflow obstruction that occurs during the LAR. Note that the airflow obstruction of the LAR usually lasts longer, as much as several hours or more.
The LAR often resembles asthma, which is a chronic inflammatory disease. It is possible that repeated or prolonged episodes of LAR may approximate the events in the airways in both chronic allergic and nonallergic asthma.
"Airway remodeling"
The term airway remodeling is widely used to refer to the development of specific structural changes in the airway wall in asthma accompanying long-standing and severe airway inflammation. Airway remodeling and fibrosis may be the cause of "fixed" airflow obstruction in asthma that is not reversible with steroids, bronchodilators, or both. Interest has especially been focused on subepithelial collagen deposition, myofibroblast accumulation, airway smooth muscle hyperplasia and hypertrophy, mucous gland and goblet cell hyperplasia, and epithelial disruption.
Although the presence of these features is accepted, further studies are required to define the changes that occur at the pathologic and ultrastructural levels and to determine whether these changes occur in small airways. The natural history of the response has not been well described. Remodeling occurs in the airways of asthmatic children and adults with newly diagnosed asthma, and studies that have attempted to relate the extent of remodeling to disease severity have produced conflicting findings. The role of remodeling in the progressive decline in lung function that leads to fixed airflow obstruction in some patients is also unclear.
Epidemiologic studies are currently hindered by the lack of a useful noninvasive marker of remodeling. Airway remodeling is frequently assumed to be a consequence of chronic inflammation, although the relationship between the remodeling and inflammatory components in asthma is unclear. The cellular and molecular events underlying the remodeling process are also poorly understood. The ability of antasthmatic therapies to prevent or reverse airway remodeling is uncertain.
Pathophysiology
1. An asthma attack may occur spontaneously or in response to a trigger. Either way, the attack progresses in the following manner:
There is an initial release of inflammatory mediators from bronchial mast cells, epithelial cells, and macrophages, followed by activation of other inflammatory cells
Alteration of autonomic neural control of airway tone and epithelial integrity occur and the increased responsiveness in airways smooth muscle results in clinical manifestations (e.g. wheezing and dyspnea)
2. Three events contribute to clinical manifestations
Bronchial spasm Inflammation and edema of the mucosa Production of thick mucus, which results in increased airway resistance,
premature closure of airways, hyperinflation, increased work of breathing, and impaired gas exchange
3. If not treated promptly, status asthmaticus - an acute, severe, prolonged asthma attack that is unresponsive to the usual treatment - may occur, requiring hospitalization.
1. Increased respiratory rate 2. Wheezing (intensifies as attack progresses) 3. Cough (productive) 4. Use of accessory muscles 5. Distant breath sounds 6. Fatigue 7. Moist skin 8. Anxiety and apprehension 9. Dyspnea
Steps of Clinical and Diagnostic as per National Asthma Education and Prevention Program
Mild Intermittent Asthma
Symptoms? 2 times per week Brief exacerbations Nighttime symptoms? 2 times a month
Predisposing FactorAtopy
Female gender
Contributing Factors>Respriratory infections
>Air pollution>Active/passive smoking>Others diet, small size
at birth
Inflammation
Hyperresponsiveness of airways Airflow limitation
Risk Factors for Exacerbations
AllergensRespiratory infections
Exercise and hyperventilationWeather changes
Exposure to sulfur dioxideExposure to food, additives,
medications
SymptomsWheezing
CoughDyspnea
Chest tightness
Causal Factors>Exposure to indoor
And outdoor allergens>Occupational
sensitizers
Asymptomatic and normal PEF (peak expiratory flow) between exacerbations PEF or FEV, (forced expiratory volume in 1 second)? 80% of predicted value PEF variability < 20%
Mild Persistent Asthma
Symptoms > 2 times/week, but less than once a day Exacerbations may affect activity Nighttimes symptoms > 2 times a month PEF/FEV? 80% of predicted value PEF variability 20%-30%
Moderate Persistent Asthma
Daily Symptoms Daily use of inhaled short-acting ?2 - agonists Exacerbations affect activity Exacerbations? 2 times a week Exacerbations may last days Nighttime symptoms > once a week PEF/FEV > 60%-<80% of predicted value PEF variability > 30%
Severe Persistent Asthma
Continual symptoms Frequent exacerbations Frequent nighttime symptoms Limited physical activity PEF or FEV? 60% of predicted value PEF variability > 30 %
LABORATORY AND DIAGNOSTIC FINDINGS:
Spirometry will detect:
a. Decreased for expiratory volume (FEV)
b. Decreased peak expiratory flow rate (PEFR)
c. Diminished forced vital capacity (FVC)
d. Diminished inspiratory capacity (IC)
NURSING MANAGEMENT:
1. Assess respiratory status by closely evaluating breathing patterns and monitoring vital signs
2. Administer prescribed medications, such as bronchodilators, anti-inflammatories, and antibiotics
3. Promote adequate oxygenation and a normal breathing pattern
4. Explain the possible use of hyposensitization therapy
5. Help the child cope with poor self-esteem by encouraging him to ventilate feelings and concerns. Listen actively as the child speaks, focus on the child’s strengths, and help him to identify the positive and negative aspects of his situation.
6. Discuss the need for periodic PFTs to evaluate and guide therapy and to monitor the course of the illness.
7. Provide child and family teaching. Assist the child and family to name signs and symptoms of an acute attack and appropriate treatment measures
8. Refer the family to appropriate community agencies for assistance.
Medical ManagementThere are two basic kinds of medication for the treatment of asthma:
Long-term control medications -- used on a regular basis to prevent attacks, not for treatment during an attack.
leukotriene inhibitors (e.g., Singulair, Accolate) long-acting bronchodilators (e.g., famoterol, Serevent) help open airways cromolyn sodium (Intal) or nedocromil sodium aminophylline or theophylline (not used as frequently as in the past) combination of anti-inflammatory and bronchodilator, using either
separate inhalers or a single inhaler (Advair Diskus)
Quick relief (rescue) medications -- used to relieve symptoms during an attack. short-acting bronchodilators (e.g., Proventil, Ventolin, Xopenex, and
others) oral or intravenous corticosteroids (e.g., prednisone, methylprednisolone)
stabilize severe episodes
References: Joyce Black, Medical and Surgical Nursing, 8th edition, 2005 Brunner And Suddarth, Medical and Surgical Nursing, 6th Edition, 2005 Berto, J.M.; Pelaez, A.; Fernandez E; A new indoor source of Allergic
