CA1-Ward Case #1(July 2,2011) Prepared by: Charmaine Kaye Gayacao,BSN-IV

Bronchial Asthma I. Objectives: A. The importance of case study in Bronchial Asthma is to be used as a creative alternative to traditional approaches to description, emphasizing the patient's perspective as central to the process B. The goal of the case study in Bronchial Asthma is to describe as accurately as possible the fullest, most complete description of the case. C. The patient centered objectives are to minimize morbidity by maintaining the best result with a minimum of treatment i.e. continual review of dosage requirements with gradual stepwise reduction to minimum medication. II. Introduction A. Medical Background Bronchial asthma is a condition of the lungs characterized by widespread narrowing of the airways due to spasm of the smooth muscle, edema of the mucosa, and the presence of mucus in the lumen of the bronchi and bronchioles. It is caused by the local release of spasmogens and vasoactive substances in the course of an allergic reaction. B. Synonyms Exercise-Induced Asthma- (EIA) is a condition of respiratory difficulty that is related to histamine release,triggered by aerobic exercise, and lasts several minutes. Causes include medical conditions, environmental factors, and medications. C. Causes In most cases of asthma in children, multiple triggers or precipitants exist, and the patterns of reactivity may change with age. Treatment can also change the pattern. Certain viral infections, such as respiratory syncytial virus (RSV) bronchiolitis in infancy, predispose the child to asthma. y Respiratory infections: Most commonly, these are viral infections. In some patients, fungi (eg, allergic bronchopulmonary aspergillosis), bacteria (eg, mycoplasmata, pertussis), or parasites may be responsible. Most infants and young children who continue to have a persistent wheeze and asthma have high immunoglobulin E (IgE) production and eosinophilic immune responses (in the airways and in circulation) at the time of the first viral URTI. They also have early IgE-mediated responses to local aeroallergens. y Allergens: In patients with asthma, 2 types of broncho-constrictor responses to allergens exist such as: pollens, poison ivy, dust mites, molds, grass pollens, and pet dander y Early asthmatic responses occur via IgE-induced mediator release from mast cells within minutes of exposure and last for 20-30 minutes. y Late asthmatic responses occur 4-12 hours after antigen exposure and result in more severe symptoms that can last for hours and contribute to the duration and severity of the disease. Inflammatory cell infiltration and inflammatory mediators play a role in the late asthmatic response. Allergens can be foods, household inhalants (eg, animal allergens, molds, fungi, roach allergens, dust mites), or seasonal outdoor allergens (eg, mold spores, pollens, grass, trees). y Irritants: Tobacco smoke, cold air, chemicals, perfumes, paint odors, hair sprays, air pollutants, and ozone can initiate BHR by inducing inflammation. y Weather changes: Asthma attacks can be related to changes in atmospheric temperature, barometric pressure, and the quality of air (eg, humidity, allergen and irritant content).

George Dewey Medical College 1 | P a g e

CA1-Ward Case #1(July 2,2011) Prepared by: Charmaine Kaye Gayacao,BSN-IV

y Exercise: Exercise can trigger an early asthmatic response. Mechanisms underlying exerciseinduced asthmatic response remain somewhat uncertain. Heat and water loss from the airways can increase the osmolarity of the fluid lining the airways and result in mediator release. Cooling of the airways results in congestion and dilatation of bronchial vessels. During the rewarmingphase after exercise, the changes are magnified because the ambient air breathed during recovery is warm rather than cool. Emotional factors: In some individuals, emotional upsets clearly aggravate asthma. Gastroesophageal reflux (GER): The presence of acid in the distal esophagus, mediated via vagalor other neural reflexes, can significantly increase airway resistance and airway reactivity. Allergic rhinitis, sinusitis, and chronic URTI: Inflammatory conditions of the upper airways (eg, allergic rhinitis, sinusitis, or chronic and persistent infections) must be treated before asthmatic symptoms can be completely controlled. Nocturnal asthma: Multiple factors have been proposed to explain nocturnal asthma. Circadian variation in lung function and inflammatory mediator release in the circulation and airways (including parenchyma) have been demonstrated. Other factors, such as allergen exposure and posturerelated irritation of airways (eg, GER, sinusitis), can also play a role. In some patients, abnormalities in CNS control of the respiratory drive may be present, particularly in patients with a defective hypoxic drive and obstructive sleep apnea

y y y

III. Etiology The complete causes of asthma are (unknown). Heredity does seem to play a role as do allergens and environmental factors. According to the latest Expert Panel Report (EPR) in 1997 from the National Heart, Lung, and Blood Institute's National Asthma Education and Prevention Program, "Atopy, the genetic predisposition for the development of an IgE-mediated response to common aeroallergens, is the strongest identifiable predisposing factor for developing asthma." There are two categories of asthma: atopic or allergic or extrinsic and non-atopic or Idiosyncratic or intrinsic. Allergic asthma is a result of an antigen\antibody reaction on mast cells in the respiratory tract. This reaction causes the release of inflammatory mediators from mast cells which elicit the clinical response associated with an asthma attack. Idiosyncratic asthma is a result of neurological imbalances in the autonomic nervous system (ANS) in which the alpha and beta adrenergic as well as the cholinergic sites of the ANS are not properly coordinated. Atopic, or "extrinsic," asthma has been thought to result from sensitization of the bronchial mucosa by tissue-specific antibodies. The antibodies produced are specific immunoglobulins of the IgE (type I) class, and the total serum IgE concentration is usually elevated. Exposure to the appropriate allergens by inhalation results in an antigen-antibody reaction, that releases vasoactive bronchoconstrictive chemical mediators, causing the characteristic tissue changes More recent work suggests that immunoglobulin G (IgG) may play a role similar to that of IgE in some cases. Approximately 50% of asthmatics are of the non-atopic ("intrinsic") type in which the bronchial reaction occurs in response to non-immunologic stimuli such as infection, irritating inhalants, cold air, exercise, and emotional upset. These patients do not demonstrate elevated IgE antibodies in their serum, and the history does not suggest hypersensitivity to specific allergens, although there may be other immunologic mechanisms that have not yet been demonstrated. A growing list of agents encountered in the work place has been shown to cause asthma. Some organic materials such as wood dust act through an immunologic mechanism, whereas certain chemicals and metal dusts apparently cause direct irritation or protein denaturation in low concentrations. Occupational asthma should be suspected when symptoms occur repeatedly at work or within several hours there after and improve away from work. Improvement may require several days Beta-adrenergic blocking agents such as propranolol cause intense bronchial constriction in patients with asthma, apparently due to parasympathetic nerve stimulation. Aspirin and nonsteroidal antiinflammatory agents may cause severe asthma in some patients.

George Dewey Medical College 2 | P a g e

CA1-Ward Case #1(July 2,2011) Prepared by: Charmaine Kaye Gayacao,BSN-IV

IV. Latest Update and Statistics of the Disease Should be the latest ( 2005 above.) V. Chain of Infection ( starting from etiologic agent reservoir, mot , poe- poe- susceptible host ) A. Pathology ( should be narrative bulleted.) Asthma is the chronic disease which involves inflammation of the pulmonary airways and bronchial hyper responsiveness. The asthma pathophysiology shows that an inflammation in the airway is an important part of the pathology of asthma. The underlying process driving and maintaining the asthmatic inflammatory process. The stimuli activate the release of inflammatory mediators from mast cells, macrophages, eosinophils and other cells in the airways. The bronchi and bronchioles are tubes through in which air must pass to reach the alveoli and it will be absorbed into the blood. The two main branches of the bronchi split so that each reaches a lung. In the airway inflammation contains the cells such as mast cells, eosinophils, epithelial cells, macrophages and activated T lymphocytes. The mucosa which contains the inflammation and thickening of airway. This can increase in the amount of mucus secretion and the contraction of the airways in the body. The inflamed airways become small and blocked. The epithelial layer of cells in asthmatic subjects is often inflamed and damaged. The contraction of airway smooth muscle is regulated by Ca2+ dependent and Ca2+ independent mechanisms. The inflammatory mediators released from inflammatory cells such as histamine and cysteinyl-leukotrienes. B. Pathogenesis The airway obstruction in asthma is due to a number of factors which include: 1) bronchospasm; 2) edema of the airway; 3) increased mucus secretions; 4) cellular, especially eosinophilic, infiltration of the airway walls; and 5) injury of the airway epithelium. Formerly, it was thought that bronchoconstriction due to smooth muscle contraction in the airway was the major contributing factor in airway obstruction with asthma. Recently, however, it has been appreciated that the obstruction of the airways in asthma, especially in its chronic form, is primarily due to an inflammatory process. The mast cell and its contents are more important in the acute bronchospasm caused by the reaction to inhaled irritants, allergens, and possibly exercise. More important in the chronic inflammation associated with asthma is the eosinophil which contains proteins that damage the epithelium of the airway. Neurogenic influences on the pathogenesis of asthma have led to the cholinergic theory. The cholinergic reflex plays a role in the acute bronchoconstrictive response to the inhalation of irritants. Recent interests in neurogenic mechanisms of asthma have focused on neuropeptides that are secreted by sensory nerves. These substances have vascular permeability and mucus secretory activity, bronchoconstrictor activity, and a bronchial vascular dilation effect. These cause narrowing of the airway and increased resistance to airflow. The chest x-ray changes seen in these patients include hyperlucency of the lung fields and hyperinflation characterized by wide intercostal spaces and flattened diaphragm. C. Non-modifiable Gender: females are more prone to have asthma

George Dewey Medical College 3 | P a g e

CA1-Ward Case #1(July 2,2011) Prepared by: Charmaine Kaye Gayacao,BSN-IV

y y y y Age: asthma can occur in any ages, but most common in children Atopy: one of the predisposing factor Environmental factors Heredity D. Modifiable factors Active/passive smoking Diet Alcoholism Exposure to allergens(dusk, pollens, animal dander) Exercise and hyperventilation

y y y y y

VI. Clinical Manifestations Asthma is characterized by recurrent attacks of dyspnea, cough, and expectoration of tenacious mucoid sputum, and usually wheezing. Symptoms may be mild and may occur only in association with respiratory infection, or they may occur in various degrees of severity to the point of being life-threatening. Classic allergic (atopic) asthma usually begins in childhood and becomes progressively more severe throughout life, although spontaneous remissions may occur in adulthood. Hay fever often accompanies atopic asthma. The acute attack is characterized by dyspnea usually associated with expiratory wheezing that may be heard without a stethoscope. Cough may be present but is usually not the predominant symptom. There is a small group of patients with asthma in whom paroxysmal cough may be the predominant symptom.When asthma becomes prolonged, with severe intractable wheezing, it is known as status asthmaticus. VII. Complications of Disease Complications of asthma may include status asthmaticus, respiratory failure, pneumonia and atelectasis. Airway obstruction particularly during acute asthmatic episodes, often results in hypoxemia, requiring the administration of oxygen and the monitoring of pulse oximetry and arterial blood gases. Fluids are administered, because people with asthma are frequently dehydrated from diaphoresis and insensible fluid loss with hyperventilation. VIII. Diagnostics and Physical Exams ( physical exam ) iapp) y Laboratory Studies The sputum is characteristically tenacious and mucoid, containing "plugs" and "spirals." Eosinophils are seen microscopically. The differential blood count may show eosinophilia. In severe, acute bronchospasm, arterial hypoxemia may be present as a result of disturbed perfusion /ventilation relationships, alveolar hypoventilation, or functional right-to-left shunts. y X-Ray Findings: Chest films usually show no abnormalities. Reversible hyperexpansion may occur in severe paroxysms, or hyperexpansion may persist in long-standing cases. Transient, migratory pulmonary infiltrations may be present. Severe attacks are sometimes complicated by pneumothorax y Differential Diagnosis Distinguish wheezing from that due to other disorders such as bronchitis, obstructive emphysema, and congestive heart failure.

Essentials of Diagnosis: Recurrent acute attacks of dyspnea, cough, and mucoid sputum, usually accompanied by wheezing. Prolonged expiration with generalized wheezing and musical rales. Bronchial obstruction reversible by drugs IX. Treatment

George Dewey Medical College 4 | P a g e

CA1-Ward Case #1(July 2,2011) Prepared by: Charmaine Kaye Gayacao,BSN-IV

y DRUG CATEGORY: BRONCHODILATORS Provide symptomatic relief of bronchospasm due to acute asthma exacerbation (short-acting agents) or long-term control of symptoms (long-acting agents). Also used as the primary medication for prophylaxis of EIA. A metered-dose inhaler (MDI) can be used for administration. y Drug Name: Albuterol (Ventolin, Proventil, Proventil-HFA): Relaxes bronchial smooth muscle by action on beta2-receptors, with little effect on cardiac muscle contractility.

References: Medical-Surgical Nursing(Brunner & Suddarth) vol.1 12th edition, date of publication

www.webmd.com classes.kumc.edu/ hubpages.com

George Dewey Medical College 5 | P a g e