Obstructive Pulmonary Diseases

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LEARNING OBJECTIVES
1.Describe the etiology, pathophysiology, clinical mannifestation, and collaborative care of asthma. 2. Describe the nursing management of the patient with asthma. 3. Diffrentiete between the etiology, pathophysiology, clinical manifestation, and collaborative care of the patient with chronic obstructive pulmonary disease (COPD). 4. Describe The effects of cigarettes smoking on lungs. 5. Identify the indication for O2 therapy, methods of delivery, and complication of O2 administration. 6. Explain the nursing management of the patient with the COPD. 7. Describe the pathophysiology, clinical manifestations, collaborative care and nursing management of the patient with cystic fibrosis. 8. Describe the pathophysiology, clinical manifestations, collaborative care, and nursing management of the patient with Bronchiectasis.

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when you can t breath , nothing else matters, is the mantra of the American lung Association. More than 35 million Americans are living with chronic lung disease. Obstructive pulmonary diseases , the most common chronic lung disease, Include diseases characterized by increase to air flow as a result of air way obstruction or air way narrowing. Airway obstruction may result from accumulate secretion, edema, and swelling of the inner lumen of airways. Bronchospam, or destruction of lung tissue. Type of the obstructive lung disease are asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis, and bronchiectatis.

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Asthma is the chronic inflammatory disorder of the airway. The chronic inflammation causes an increase in airway hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night or in the early morning. Asthma affect an estimated 20 million America. Women are 30% greater prevalence of asthma then men. Asthma affects school attendance, occupational choices, physical activity, and other quality-of-life issues.

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TRIGGER OF ASTHMA ATTACKS  

Allergens: Approximately 40% of all cases asthma related to an allergic response. Allergic asthma may be seasonal and related to allergies such as tree or weed pollen. Nonseasonal forms of asthma may be year round (perennial) and related to allergens such as dust mites, mold animals, feather, and cockroaches. Exercise: Asthma that is include or exacerbated during physical exertion is call exercise- induced asthma (EIA). Airway obstruction may occur due to change in the airway mucosa cause by hyper ventilation occurring during exercise with either cooling or rewarming of air and capillary leakage airway wall.

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TRIGGER OF ASTHMA ATTACKS (CON)  

Air Pollutants: Various air pollutants, cigarette or wood smoke, vehicle exhaust, elevated ozone level, sulfur dioxide, and nitrogen dioxide can trigger asthma attack. Occupational Factors: Occupational asthma is the most common form of occupational lung disease. These exposure in the workplace can also aggravate preexisting asthma. These agent are diverse, such as wood and vegetable dusts(flour), pharmaceutical agent, laundry detergents, animal and insect dusts, secretions and serum(e.g., chicken and crabs), metal salts, chemicals, paints, solvent, and plastics.

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TRIGGER OF ASTHMA ATTACKS (CON)
‡ Respiratory Infection: Respiratory infection (i.e.,

viral and not bacterial) or allergy to microorganisms is the major precipitating factor of an acute asthma attack. Infections cause inflammatory changes in the tracheobronchial system and alter the mucociliary mechanism. The patient with asthma should avoid people with cool or flu, get yearly influenza vaccinations, and avoid taking over counter (OTC) cold remedies unless approved by health care provider. ‡ Nose and sinus problems: Some patients with asthma have chronic sinus and nasal problem , Nasal problem include allergic rhinitis, which can be can be seasonal or perennial, and nasal polyps. Treatment of allergic rhinitis may reduce the frequency of asthma exacerbation. Sinus problems are usually related to inflammation of the mucous membranes, most commonly from noninfectious causes such as allergies.

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TRIGGER OF ASTHMA ATTACKS (CON) 

Drug and food Addictives: sensitivity to specific drugs may occur in some asthmatic person, especially those with nasal polyps and sinusitis. Some people with asthma have what is termed the asthma traidnasal polyps, asthma and sensitivity to non steroidal inflammatory drugs (NSAIDs).

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TRIGGER OF ASTHMA ATTACKS (CON)   

Gastroesophageal Reflux Disease: The exact mechanism by which gastroesophageal reflux disease (GERD) triggers asthma is unknown. It is postulate that reflux of stomach acid to the esophagus can be aspirated in to the lungs, causing reflex vagal stimulation and bronchoconstriction. Psychologic Factor : Another factor often in relationship to the etiology of asthma is psychology or emotional stress. Emotional expressing like Crying, laughing, anger and fair can lead to hyperventilation and hypocapnia. Which can cause airway narrowing. (See Table 29-1)

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TABLE 29-1

Triggers of Acute Asthma Attacks

Allergen inhalation ‡ Animal dander (e.g., cat, mice, guinea pig) ‡ House dust mite ‡ Cockroaches ‡ Pollen ‡ Mod Air pollutants ‡ Exhaust fumes ‡ Perfumes ‡ Oxidants ‡ Sulfur dioxides ‡ Cigarette smoke ‡ Aerosol Sprays Viral upper respiratory infection Sinusitis Exercise and cold, dry air Stress Drugs ‡ Aspirin ‡ Nonsteroidal antiinflammatory drugs ‡ -Adrenergic blockers Occupational exposure ‡ Metal salts ‡ Wood and vegetable dusts ‡ Industrial chemical and plastics ‡ Pharmaceutical agents Food additives ‡ Sulfites ( bisulfites and metabisulfites ) ‡ Beer, wine, dried fruit, shrimp, processed potatoes ‡ Monosodium glutamate ‡ Tartrazine Hormones/menses Gastroesophangeal reflux disease (GERD)

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PATHOPHYSIOLOGY   

The primary pathophysiology of asthma is chronicle inflammation. Lead to airway hyperresponsiveness and acute airflow limitation. Example of cell in asthma are mast cell, macrophage, eosinophils, neutrophils , T and B lymphocytes and epithelia cell of airway. The inflammatory process begins, mast cells (found beneath the basement membrane of the bronchial wall) degranulate and release multiple inflammatory mediators. See Fig. 29-1 and 29-2
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Triggers ‡ Infection ‡ Allergic ‡ Exercise ‡ Irritants

Immune activation (IL-4, IgE production)

Mast cell degranulation

Inflammatory mediators

Vasodilation Increase capillary permeability

Cellular infiltration (neutrophils, lymphocyte, eosiniphils)

Bronchospam Vascular congestion Mucus secretion Impaired Mucociliary function Thickening of airway walls

Autonomic nervous System effects

Bronchial hyperresponsiveness Airway obstruction

Airway remodeling

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Pathophysiology of asthma. IL, Interleukin

FIG. 29-2

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CLINICAL MANIFESTATION  

 

The characteristic clinical manifestations of asthma are wheezing, cough, dyspnea, and chest tightness. Difficulty with air movement in the out of lung. Reveals sigh of hypoxemia during acute attacks. Some patients with asthma, cough is usually symptom and this termed cough variant asthma.

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CLASSIFICATION OF ASTHMA
Asthma can be classification as mild intermittent, mild persistent, moderate persistent , or severs persistent, (See Table 29-2)

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TABLE 29-2
Cassification
Step1 Mild intermittent

Classification of Asthma Severity
Symptoms Nighttime Symptom Pulmonary Function*

Symptom”2 times/wk Asymptomatic and normal PEFR between exacerbations Exacerbation brief (hours to days) Intensity of exacerbations varies

”2 time/mo

FEV /PEFR•80% of predicated PEFR variability <20%

Step2 Mild persistent

Symptoms> 2 times/wk but <1 time/day Exacerbations may affect activity

>2 time/mo

FEV1/PEFR •80% of predicate PEFR variability 20%-30%

Step3 Moderate persistent

Daily symptom Daily use of inhaled short-acting 2 agonist Exacerbations affect activity Exacerbations at least 2 times/wk and may last for days

>1times/wk

FEV1/PEFR •60% but 80^% of predicate PEFR variability >30%

Step4 Sever persist

Continual symptoms Limited physical activity Frequent exacerbation

Frequent

FEV 1/PEFR ” 60% Of predicate PEFR variability > 30%

COMPLICATIONS  

Sever Acute asthma can result in complications such as rib fracture, pneumothorax, pneumomediastinum, atelectasis, pneumonia, and status asthmaticus. Status asthmaticus : is a severe, life threatening asthma attack that is refractory to usual treatment and place the patient at risk for developing respiratory failure.
‡

Cause of status asthmaticus include viral illness, ingestion of aspirin or other NSAIDs, emotional stress, increase enviromental pollutans or other allergen expose, abrupt discontinuation drug therapy , and ingestion of adrenergic blockers.

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COMPLICATIONS (CON)

Status asthmaticus (cont)
Clinical manifestation status asthmaticus result from increase airway resistance as consequence of edema, mucous plugging, and severe with subsequent air trapping , hyperinflation, hypoxemia, and respiratory acidosis. y Complication of status asthmaticus include pneuthorax, pneumomediastinum, acute core pulmonale with right ventricular failure, and sever respiratory muscle fatigue leading to respiratory arrest. Death from status asthmaticus is usually the result of respiratory arrest or cardiac failure.
y
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DIAGNOSTIC STUDY 
 

  

  

History and physical examination Pulmonary function studies including response to bronchodilator therapy Peak expiration flow rate (PEFR) Chest x-ray Measurement of ABGs or oximetry (if sever exacerbation) Allergy skin testing ( if indicate) Blood level of eosinophils and IgE ( if indicate) Nitric oxide levels Table 29-04

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TABLE 29-04

COLLABORATIVE CARE

Asthma

Diagnostic History and physical examination Pulmonary function studies including response to bronchodilator therapy Peak expiration flow rate (PEFR) Chest x-ray Measurement of ABGs or oximetry (if sever exacerbation) Allergy skin testing ( if indicate) Blood level of eosinophils and IgE ( if indicate) Nitric oxide levels Collaborative Therapy Mild Intermittent or Persistent Asthma Identification and avoidance/elimination of triggers Desensitization (immunotherapy) if indicate Patient and family teaching Drug therapy (see Table 29-5, 29-6, and 29-7) Asthma action plan (see Table 29-13) Status Asthmaticus SaO2 Monitoring ABGs Inhaled -adrenergic agonists or anticholinergic agent O2 by mask or nasal prongs IV or oral corticosteroids IV fluids IV magnesium Intubation and assisted ventilation

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ABGs, Arterial blood gases, IgE, immunoglobulin E: SaO2, Oxygen saturation

COLLABORATIVE CARE

Desirable therapeutic out come include
1. 2. 3. 4. 5. 6.

Control or elimination of chronic symptoms such as cough, Dyspnea, and nocturnal awakenings; Attainment of normal or nearly normal lung function ; Restoration or maintenance of normal levels of activity; Reduction in the number of, or elimination of, recurrence exacerbation; Reduction in the number of, or elimination of, ED visits and acute care hospitalizations; and Elimination or reduction of side effects of medication.

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COLLABORATIVE CARE (CON)
The patient who has persistent air flow obstruction and frequent attacks of asthma should be taught to avoid trigger of acute attacks and to predicate before exercising. Mild Intermittent or Persistent Asthma

y y y y y

Identification and avoidance/elimination of triggers Desensitization (immunotherapy) if indicate Patient and family teaching Drug therapy (see Table 29-5, 29-6, and 29-7) Asthma action plan (see Table 29-13)
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COLLABORATIVE CARE (CON)

Status Asthmaticus y SaO2 Monitoring y ABGs y Inhaled -adrenergic agonists or anticholinergic agent y O2 by mask or nasal prongs y IV or oral corticosteroids y IV fluids y IV magnesium y Intubation and assisted ventilation Acute Asthma Episode y Measuring FEV1 or PEFR y O2 therapy y The administration should be monitored by pulse oxmetry to keep the SpO2 >90%(or 95% in pregnant women and patients with coexisting heart disease y Inhaled 2 adrenergic agonists administered by metered dose inhaler (MDI) y Aerosolize medications by nebulizer therapy or by MDI with a spacer are given every 20 minutes for 1 hour.

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DRUG THERAPY

Persistent Asthma require daily long-term therapy in addiction to appropriate to manage acute asthma . Medication are divide into two general classifications:
Long-term-control medications to achieve and maintenance control of persistent asthma. 2) Quick-relief medication to threat symptoms and exacerbations
1)

See Table 29-6

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DRUG THERAPY TABLE Long-Term Control versus Quick relief 29-6 Of Asthma Long-term Control Medications Antiinflammatory Drugs Corticosteroids (inhaled or oral) Cromolyn (Intal) and nedocromil (Tilade) Leukotriene modifiers Omalizumab(xolair) Bronchodilators Long-acting inhaled 2-adrenergic agnosists Anticholinergics (inhaled) Antiinflammatory Drugs Corticosteroids (systemic)*
*Considered quick-relief drugs when used in a short burst (3 to 6 days) at the start of therapy or during a period of gradual deterioration. Corticosteroids are not use for immediate relief of an ongoing attack.

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PATIENT
TEACHING RELATE TO DRUG THERAPY
Information about a bout medication should include name, dosage, method of administration, and schedule. Teaching May include :

y y y y y y

Purpose side effect appropriate action if side effect occur Consequent of improper use The importance of refilling the prescription before medication run out. and How to use :
Metered-Dose Inhaler (MDI) Dry Powder Inhaler(DPI)

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NURSING MANAGEMENT

Asthma
y

y

Nursing Assessment if patient can speak and is not in acute distress, a detailed health history, include identify of any precipitating factors and what has helped alleviate attacks in the past, can be taken. Subjective and objective data that should be obtained from the patient with asthma. (See table 29-12 pg624 for More detail) Nursing Diagnosis

Ineffective airway clearance relate to Bronchospam, excessive mucus production, tenacious secretion and fatigue as evidenced by ineffective cough, inability to raise secretion, adventitious sounds. Anxiety related to difficulty breathing, perceived or actual loss of control and fear of suffocation as evidenced by restlessness, elevated pulse, respiratory, rate, and blood pressure. Deficient knowledge relate to lack of information and education about asthma and its treatment as evidence by frequent question regarding all aspects all aspect of long term management.

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NURSING MANAGEMENT (CON)

Asthma (con)
y

Planning The overall goal that are the patient with asthma will 1. Maintains >80% of personal best PEFR or FER1 , 2. Have minimal symptom during the day and night, 3. Maintain acceptable activity level (including exercise and other physical activity), 4. Have no recurrent exacerbation of asthma or decreased incidence of asthma attacks, 5. Have adequate knowledge to participate in and carry out management
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NURSING MANAGEMENT (CON)
Nursing Implementation
y

Health promotion The nursing role in preventing asthma attacks or decreasing the severity focuses primary on teaching the patient and family. Patient should be taught to identify and avoid know personal trigger for asthma ( e.g. cold air aspirin, foods, cats, indoor air pollution)(See Table 29-1). The patient to be encourage to maintain fluid intake of 2 to 3 L per day, good nutrition and adequate rest.

y

A cute intervention During an acute attacks of asthma it is important to monitor the patient respiratory and cardiovascular system, Include auscultation lung sound taking the pulse rate, respiratory rate, BP; and monitoring ABGs, pulse oximetry and PEFR. Nursing intervention include administrating O2 , bronchodilator s and medications as ordered and going patient monitoring ( especially lung auscultation ), including the effectiveness of this interventions.

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NURSING MANAGEMENT (CON)
Nursing Implementation (con)
‡

Ambulatory and Home care :
‡

‡

‡

‡

the patient with asthma usually take several medications with difference route of administration and time frame for dosage. The patient with asthma must learn about the numerous medications and develop self management strategies. Good nutrition is important, physical exercise ( e.g swimming , walking, stationary, cycling ) Write asthma action plan (see table 29-13) should be develop with patient and family

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Chronic Obstructive Pulmonary Disease (COPD) is the preventable and treatable disease state characterized by airflow limitation that is not fully reversible.

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ETIOLOGY
Cigarette Smoking : A major risk factor for developing COPD. Cigarette smoking has also been implicate as a factor in cancer of the mouth, pharynx, larynx , esophagus, pancreas, kidney, stomach ,colon, cervix, uterus and bladder.  Nicotine :is acts by stimulating the sympathetic nerves system, result in increase heart rate, increase peripheral vasoconstriction, increase BP, increase cardiac workload and also decrease the amount of functional hemoglobin and increase platelets aggregation. 

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ETIOLOGY (CON)
Occupational Chemical and Dusts If a person has intense or prolong exposure to various dusts, vapors, irritants, or fumes in the workplace, COPD can develop independently of cigarette smoking.  Air Pollution: Many women who have never smoked, are developing COPD because of cooking with this fuels in poorly ventilate area.  Infection: Sever recurring respiratory tract infections in childhoods has been associated with reduced lung function and increased respiratory symptom in adulthood.
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ETIOLOGY (CON)
Occupational Chemical and Dusts (cont)  heredity 1 antitrypsin(AAT) deficiency is the genetic risk factors the leads to COPD. AAT is the serum protein produce by the liver and normally found in the lung. Sever AAT deficiency leads to premature bullous emphysema in the lungs found via radiology testing.  Aging : some of emphysema is common in the lungs of older person, even a nonsmoker.

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PATHOPHYSIOLOGY
The pathogenesis of COPD is complex and involve many mechanism. 1. The inflammatory process : Start with inhalation of noxious particle and gases( ex: cigarette smoke, air pollution) 2. The airway become inflamed : resulting in increase number of enlarged goblet cells. This result in excess mucus production( or chronic bronchitis). 3. Destruction of the lung: Parenchyma in COPD patient result in emphysema with significant loss of attachment, which could be likened to robber bands connecting airways open. (See fig. 29-7)

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CLINICAL MANIFESTATIONS
Clinical manifestation is a diagnosis of COPD should be considered in any patient who has symptoms of cough, sputum production, or dyspnea and or a history of exposure to risk factor for the disease.  Dyspnea usually occurs with exertion.  The cough initially may be intermittent. Later it is present everyday, but the seldom present during the night. In some people the cough may be nonproductive.  Wheezing and chest tightness may be present, but may vary by time of the day or from day to day, especially in patient with more severe disease.

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CLASSIFICATION OF COPD

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COMPLICATIONS 
   

Cor pulmonale Exacerbation of COPD Acute respiratory failure Peptic ulcer and gastroesophageal reflux disease Depression/anxiety

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DIAGNOSTIC STUDIES
‡ ‡ ‡ ‡ ‡ ‡

History and physical examination Pulmonary function test Chest X-ray Serum antitrypsin level Sputum specimen for gram stain and culture
‡

ABGs

ECG ‡ Exercise testing with oximetry ‡ Echocardiogram or cardiac nuclear scans
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COLLABORATIVE CARE
The primary goals of care for The COPD patient are to 1. Prevent disease progression, 2. Relieve symptoms and improve exercise tolerance, 3. Prevent and treat complication, 4. Promote patient participation in care , 5. Prevent and treat exacerbation, 6. Improve quality of life.

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COLLABORATIVE CARE (CON)
Smoking cessation : cessation of cigarette smoking in all stage of COPD in the single most effective and cost-effective intervention to reduce the risk of developing COPD and stop the progression of disease. Drug therapy :medication of COPD can reduce or abolish symptoms, release the capacity to exercise, improve overall health, and reduce the number of severity exacerbation.

y

Bronchodilator medications commonly used are 2-adrenergic agonists, anticholinergic agents, and methlylxanthines ( see Table 29-7)
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COLLABORATIVE CARE (CON)  

O2 Therapy : Oxygen therapy is frequently used in the treatment of COPD and other problems associated with hypoxemia. It is a colorless, odorless, tasteless, gas that constitutes 20.95% of the atmosphere. (see TABLE 29-22, And Fig 29-11 through fig 29-11) Goals for oxygen therapy to reduce work of breathing, maintain the PaO2 , reduce workload on the heart , keeping the SaO2 during rest, sleep and exertion. The goal of oxygen administration is to supply the patient with adequate oxygen to maximize the oxygen carrying ability of the blood

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COLLABORATIVE CARE (CON)

Surgical therapy for COPD: three difference surgical procedures have been use in sever COPD.
One type of surgery is lung volume reduction surgery (LVRS). y The second surgical procedure is bullectomy. y The surgical procedure is lung transplantation.
y

Respiratory and physical therapy :
Breath retraining y Effective Coughing y Chest physiotherapy
y
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COLLABORATIVE CARE (CON)

Respiratory and physical therapy (con) :
Flutter mucus clearance device y High-frequency chest compression (ThAIRaphy vest) y Acapella y Aerosol Nebullization Therapy
y

Nutrition Therapy :
The patient with COPD should try to keep body mass index (BMI) between 21 to 25 kg /m2 y Cold food may give less than hot food. y Fluid intake should be at least 3L per day. y Fluid should be taken between milk ( rather then with them)
y

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NURSING MANAGEMENT COPD
o

Nursing assessment Subject data and object data should be obtained from person with COPD are
o

Subject data include 
    

Past health history Nutrition metabolic Activity exercise Elimination Sleeping habit Cognitive and coping stress tolerance.
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NURSING MANAGEMENT COPD (CON)
o

Objective data are including 
    

Intergumentary Respiratory Cardiovascular Gastrointestinal Musculoskeletal Possible finding Ineffective airway clearance : related to expiratory airflow obstruction, ineffective cough, decrease airway humidity and infection in airway as evidence by ineffective or absence cough, present of abnormal breath sounds or absence of breath sounds.

o

Nursing diagnosis 

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NURSING MANAGEMENT COPD (CON)
o

Nursing diagnosis (cont)  Imbalance nutrition: less than body requirement related to poor appetite, lower energy level, shortness of breath, gastric distention, sputum production.  Insomnia: related to anxiety, dyspnea, depression, hypoxemia, orthopnea as evidence by frequent awakening, prolong onset of sleep, fatigue, irritability.  Risk for infection: related to decrease pulmonary function, ineffective airway clearance, and lack of knowledge regarding sings and symptoms of infection.

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NURSING MANAGEMENT COPD (CON)
Planning The overall goals are that the patient with COPD will have 1. Prevention of disease progressive 2. Ability to perform ADLs and improve exercise tolerance 3. Relief from form symptoms 4. No complication related to COPD 5. Knowledge and ability to implement along term treatment regimen 6. Overall improve quality of life
o

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NURSING MANAGEMENT COPD (CON)
o

Nursing implementation Airway management ‡ Encourage slow, deep breathing , turning and coughing to mobilize pulmonary secretion ‡ Position patient to maximize ventilation potential ‡ Perform chest physiotherapy to used effect of gravity in remove secretions ‡ Administer bronchodilator and aerosol treatment to facilitate clearance of retained secretion and increase easy of breathing.
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NURSING MANAGEMENT COPD (CON)
Oxygen therapy ‡ Administer supplemental O2 as order ‡ set up O2 equipment and administer through a heat, humidity system ‡ Observe for signs of oxygen induced hypoventilation Nutrition therapy  Monitor food/fruits ingested and calculate daily caloric intake  Select nutrition supplement to provide nutritional between meal, snakes.  Provide food selection to stimulate the appetite  Provide appropriate formation about nutritional needs and how to meet them to ensure nutritional adequacy after discharge

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NURSING MANAGEMENT COPD (CON)
Infection control ‡ Instruct patient on appropriated hand washing technique to prevent spread of infection ‡ Encourage deep breathing and coughing to prevent stasis of respiratory secrete.

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CF is a hereditary, autosomal recessive, multisystem disease characterized by altered function of the exocrine glands primarily including lungs, pancreas and sweat glands.

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ETIOLOGY AND PATHOPHYSIOLOGY
The CF gene is located on chromosome 7 and produces a protein called CF transmembrane regulator (CFTR). The CFTR protein localizes to the lining of the exocrine portion of particular organs and regulates sodium and chloride channels. y But mutation of CFTR gene alter this protein that way sodium and chloride channels are blocked. As a result, cells that line the passage and other organs produced abnormally thick and sticky mucus.
y
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CLINICAL MANIFESTATIONS
The clinical manifestations of CF are caused by the production of abnormally thick and sticky mucus of the body s organs and dependent on the severity of the disease.
‡ ‡

‡ ‡ ‡ ‡

An initial finding of meconium ileus in the newborn is present Childhood are failure to grow, clubbing, persistent cough with mucus production, tachypnea and large, frequent bowel movements. Problems with breathing are among the most serious symptoms. The first symptom of CF in the adult is frequent cough DIOS (distal intestinal obstruction syndrome) causes RLQ pain, loss of appetite, emesis and often palpable mass. The function of reproductive system are altered.

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COMPLICATIONS
Pneumothorax is common. The CF patient with lung infection present of small amount of blood in sputum is common. ‡ Respiratory failure and cor pulmonale are late complications of CF. DIAGNOSTIC STUDY
‡ ‡
‡ ‡ ‡ ‡

The sweat chloride test Chest X-ray Pulmonary function test Fecal analysis for fat

COLLABORATIVE CARE
The major objectives of therapy in CF are to ‡ Promote clearance of secretions ‡ Control infection in the lungs ‡ Provide adequate nutrition

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NURSING MANAGEMENT 

Nursing Assessment

Subjective and objective data that should obtained from the patient with CF are present in Table 29-29 

Nursing Diagnoses

‡

nursing diagnoses for the patient with CF may include, but are not limited to, the following: Ineffective airway clearance related to abundant, thick bronchial mucus, weakness and fatigue.

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NURSING MANAGEMENT 

‡

‡

‡

Nursing Diagnoses (cont d) Ineffective breathing pattern related to bronchoconstriction, anxiety and airway obstruction Impaired gas exchange related t0 recurring lung infections. Imbalanced nutrition: less than body requirement related to dietary intolerance, intestinal gas, and altered pancreatic enzyme production.

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NURSING MANAGEMENT (CON) 

Planning The overall goals that the patient with CF will have
‡ ‡ ‡ ‡ ‡ ‡

Adequate airway clearance Reduced risk factors associated with respiratory infections Adequate nutritional support to maintain appropriate BMI Ability to perform ADLs No complications related to CF Active participation in planning and implementing a therapeutic regimen
58

NURSING MANAGEMENT (CON) 

Nursing Implementation
Acute intervention for the patient with CF includes reliefs of bronchoconstriction, airway obstruction, and airflow limitation. ‡ Interventions includes aggressive CPT, antibiotics, oxygen therapy and corticosteroids in severe disease.
‡

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Table 29-29

NURSING ASSESSMENT Cystic Fibrosis

Subjective data
Important health information Past health history: recurrent respiratory and sinus infections, persistent cough with excessive sputum production Medications: use of and compliance with corticosteroids, bronchodilator, antibiotics, herbs Functional Health Patterns Health perception-Health maintenance: family history of CF, diagnosis of CF in childhood Nutritional-metabolic: dietary intolerance, voracious appetite, weight loss, heartburn Elimination: intestinal gas; large, frequent bowel movement, constipation Activity-exercise: fatigue, exercise tolerance, amount/type of exercise, dyspnea, cough, excessive mucus or sputum production, coughing up blood Cognitive-perceptual: abdominal pain Sexuality-reproductive: delayed menarche, menstrual irregularities, and secondary amenorrhea, problems conceiving or fathering a child Coping-stress tolerance: anxiety, depression, problems adapting to diagnosis

Objective data
General Restlessness, failure to thrive Integumentary Cyanosis (circumoral, nail bed) distal clubbing, salty skin Eye Scleral icterus Respiratory Sinus difficulties, persistent runny nose, diminished breast sounds, sputum (thick, white or green, tenacious), hemoptysis, of accessory muscles of respiration, barrel chest Cardiovascular Tachycardia Gastrointestinal Protuberant abdomen, abdominal distention, foul, fatty stools Possible finding Abnomal ABGs and pulmonary function tests, abnormal sweat, chloride test, chest X-ray, fecal fat analysis

work of breathing, use

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Etiology and Pathophysiology ‡ Bronchiectasis is characterized by permanent, abnormal dilation of one or more large bronchi. ‡ Pathophysiology change that results in dilation is destruction of the elastic and muscular structures supporting the bronchial wall.
61

BRONCHIECTASIS
Clinical manifestations Hallmark of brochiectasis is persist or recurrent cough with production of large amount of purulent sputum that may exceed 500 ml/day. Other manifestations of brochiectasis are dyspea, wheezing, pleuritic chest pain, and hemoptysis. On auscultation of the lungs, crackles are the most common finding.

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BRONCHIECTASIS
Diagnostic studies ‡ Chest X-ray ‡ High-resolution CT(HRCT) scan of the chest ‡ Sputum ‡ Pulmonary function Collaborative care
y Bronchiectasis is difficult to treat.

y Therapy is aimed at treating acute flare-ups and preventing decline in lung function. y Antibiotics are the mainstay of the treatment and are often given empirically.

63

NURSING MANAGEMENT
An important nursing goal is to promote drainage and removal of bronchial mucus. Various airway clearance techniques can be effectively used to facilitate secretion removal. Bed rest may be indicated during the acute phase of illness. Good nutrition is important and may be difficult to maintain because the patient is often anorexic.

64

REVIEW QUESTION
1.

Asthma is the best characterized as a. an inflammatory disease . b. a steady progression of bronchoconstriction. c. an obstructive disease with loss of alveolar walls. d. chronic obstructive disorder characterized by mucus production. In evaluating the asthmatic patient knowledge of self-care. The nurse recognize that additional Instruction is needed when the patient says, a. I use my corticosteroid inhaler when I feel short of breath. b. I get a flu shot of every year and see my health care provider if I have an upper respiratory infection. c. I use of my brochochodialator inhaler before I visit my aunt who has a cat d. I walk 30 minutes every but some time I have to use my 65 bronchodilator inhaler before walking to prevent me from getting short of breath.

2.

REVIEW QUESTION
3.

A plan of care for the patient with COPD could include
a. b. c. d.

Exercise such as walking. Chronic oral corticosteroid therapy. High flow rate of O2 administration. Breathing exercises in involve inhaling longer than exhaling

4.

The effect of cigarette smoking on the respiratory system include.
a. b. c. d.

Increased proliferation of ciliated cell Hypertrophy of the alveolar membrane. Destruction of all alveolar macrophage. Hyperplasia of goblet cells and increase production of mucus.
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REVIEW QUESTION
5.

The major advantage of venturi mask is that it can
a. b. c. d.

Deliver up to 80% O2. Provide continuous 100% humidity. Deliver the precise concentration of O2 . Be used while the patient eats and sleep.

6.

One of the most important thing that the nurse can teach a patient with COPD is to
a. b. c. d.

Move to a hot, dry climate. Perform chest physiotherapy. Obtain adequate rest in the supine position. Know the early sign/symptom Of COPD exerbation.
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REVIEW QUESTION
7.

Diagnosis studies that he nurse would expect to be abnormal in a person with CF are
a. b. c. d.

Insulin tolerance and blood glucose. Pancreatic enzyme and hormones. Sweat test and vitamin B tolerance test. Pulmonary function test and sweat test.

8.

A primary goal for the patient with bronchietatis is that the patient will.
a. b. c. d.

Have no recurrence of disease. Have normal pulmonary function. Maintain removal of bronchial secretions. Avoid environmental agents that precipitate attacks
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REFERENCE

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