Respirtory part2


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  • S/S Frequent cough with clear to purulent sputum, have fever, H/A, SOB – DOE,

    Supportive care, uusally a self limiting disease – fluids, rest, antiinflammatory meds
    COPD patients with bronchitis get antibiotics also

    Will discuss Chronic Bronchitis in Chapter 29
  • MDR
    Resistant to two best antibiotics used to cure TB: Isoniazid (INH) and rifampin (RIF)
    The result? This form of TB is more difficult to tx and requires up to two years of multidrug tx (NIH,2008)

    A less common for incidence of XMDR TB
    The TB bacteria have changed enough to be immune to not only the two drugs listed earlier but to most of the alternative drugs used to fight MDR TB such as Fluoroquinolone, amikacin, kanamycin, or capreomycin

    Extremely challenging to treat!
    May have to lock up the patient until the disease becomes inactive
  • TB is missed in HIV patients– Misdiagnosis because of lack of s/symptoms are similar and looks like pneumocysitis jiroveci pneumonia
    Reason for Emergence of TB – poor compliance with treatment, no follow up after tx, wrong drugs used

    Vulnerable populations
    Poor, underserved, minorities
    Homeless, inner-city residents, older adults, foreign-born persons, those in institutions (SNF, prison)
    Immunosuppression for any reason: HIV, CA, increases risk of TB.
    Additional Risks:
    Children under five years old
    IV drug user or ETOH abuser
  • Coughs, sneezes, speaks or sings

    After TB enters the alveoli, it can spread via the lymphatic system to other lobes, kidneys, epiphysis of bone, cerebral cortex and adrenal glands
    It is harbored in granuloma which prevent replication (not killed, just islolated). Pt has an infection (inactive). PPD will detect in 2-12 weeks of exposure.
    .Active infection may never happen. Can not spread to others in the beginning stages. Considered a latent TB infection.
    TB disease is active, can be transmitted through repeated close contact.
  • Early – no symptoms, inactive no symptoms

    Active Disease: fatigue, malaise, anorexia, unexplained wt loss, low-grade fevers, and night sweats
    Sudden acute manifestations: high fever, chills, flu-like symptoms, cough

    Miliary TB – Invasion of the blood stream to other organs
  • Can be (+) 2 to 12 weeks after initial exposure
    Once (+), always (+)
    Assessment of PPD test looks at induration, not redness of injection site.
    Acid-Fast bacilli – AFB – found in sputum – need 3 cultures over 3 days
    BCG (vaccine) – new- used in high risk areas on children
  • Treatments - Maybe treated as inpatient - or as outpatient; mainly with a number of medications in 2 phases:
    1st phase → 4 drugs - Isonizid (INH), rifampin, ethambutol, pyrazinamide; 6 months
    2nd phase → INH & rifampin or any combination of these drugs

    Once a week with Directly observed therapy – watch the pt. swallow the drug

    Side effects – liver toxicity- non-viral hepatitis
    Prevention to active disease after exposure – Have not converted on PPD test yet – Isoniazid QD 6 – 9 months
  • Patients who are admitted with a medical Dx of respiratory disease of unknown origin and/or who have manifestations that may indicate TB, should be isolated in negative pressure flow rooms (keeps air from flowing from the room to the outside) till the Dx is confirmed
    Nursing planning:
    Single private room
    Negative air pressure
    HEPA masks – need to be fitted
    Hand washing
    Patient Can have disease relapse after tx

  • Pneumoconiosis: ‘dust in the lungs’. – diffuse pulmonary fibrosis
    Most exposures cause fibrosis – scarring after inflammatory response to the irritant
    Also hypersensitivity and pulmonary edema responses

    Occupational asthma
    Coal workers – coal dust
    Farmers – moldy hay
    Hantavirus - inhaling rat dropping particles
    Silicosis – mining for gold, copper, tin, coal, pottery making

    Latent S/S after many years of exposure. Dyspnea and cough, chest pain can come later
    Some involve simple skin tests like coccidiomycosis which affects farmers

    Supportive care, reduce irritants, prevention (wear masks),

  • Pathogenesis of primary lung cancer is believed to arise from bronchial epithelial cells. These cells grow slowly and may take 8 to 10 years for a tumor to reach 1 cm in size (smallest detectable by CXR)
    Changes in bronchial system show nonspecific inflammatory changes w/hypersecretion of mucus, desquamation of cells, reactive hyperplasia of basal cells, and metaplasia of normal respiratory epithelium to stratified squamous cells

    Metastasis primarily by direct extension and via blood/lymph systems
    Most common sites for metastasis are: liver, brain, bones, scalene lymph nodes, and adrenal glands
  • Lung cancer now surpassed breast cancer in leading cause of cancer deaths for women.
    5 year survival rate is 15 %
  • Tobacco smoke contains 60 carcinogens along w/carbon monoxide and nicotine which interfere w/normal cell development
    The smoke is an irritant which causes a change in the bronchial epithelium which usually returns to normal w/cessation
    Ten years after cessation of smoking risk of lung cancer mortality is reduced 30% to 50%
    Total risk of developing lung CA is based on total exposure, age of starting to smoke, depth of inhalation, how many cigs per day, type of cig, use of unfiltered cigs, passive exposure from others -home/office
    Pipes and cigars are included in risk factors
    Environmental irritants – asbestos, radon, nickel Iron, chromates, air pollution, arsenic
  • CXRs may identify a lung mass or infiltrate and show obstructive features such as atelectasis, pneumonia and metastasis
    CT- most effective noninvasive test
    MRI shows same as CT
    sputum studies
    Bronchoscopy (biopsy) provide the definitive diagnosis

    Dx - Unfortunately, by the time the Dx is made, it is often too late especially if it is small cell, because of its rapid growth. CXRs are the least reliable because when seen here, the tumor is usually large and mets has occurred. However, as with any cancer, the earlier caught, the better the prognosis.
  • Early – no symptoms Clinically silent for majority of course
    Nonspecific and appear in late stages – Fatigue, wt loss, hoarseness, N/V, lymph nodes enlarged

    Chest pain may be present and dyspnea and an auscultatory wheeze if there is a bronchial obstruction

    Basic problem is that lung tissue cannot exchange O2 and CO2, there is obstruction of air flow & because of the lymphatic system metastasis occurs easily

    With centrally located tumors, there is usually some degree of coughing, wheezing, stridor and dyspnea;
    if the vascular nerves are affected there may be shoulder, arm, chest and back pain and
    hemoptysis is seen with squamous and small cell tumors;
    Small cell tumors may invade the pericardium & there will be cardiac manifestations, e.g., arrhythmias

    Paraneoplastic syndrome – cancers produce active substances – hormones, enzymes, or the body makes them in response to the Cancer.
    Messes up many body systems and can only be controlled if the tumor is removed.
  • Staging - TMN system- Oncology lecture
    Treatment Modalities
    RT - mostly for palliation although may be used in conjunction with surgery or chemotherapy
    Chemotherapy - works best with small cell
    Surgery - best with NSCLC especially if there is no distant metastasis; however only about 25% of patients are candidates and 5 year survival is about 40%
    Laser surgery – remove bronchial obstructions
    Resections - Wedge, Segmental, Lobe, Pneumonectomy
  • Preop - PFTs, ABGs,
    Pre-op education: coughing & breathing exercises, stop smoking, IS, what is a chest tube
    Interventions: meds, electrolytes, cbc,

    Postop - the usual, e.g., VS, labs, DB & C, pain management, dressings and CHEST TUBES

  • Asthma is a chronic inflammatory lung disease that results in recurrent episodes of airflow obstruction, but it is usually reversible. 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. Thick mucous is produced from the inflammation.
    The severity of the attack will affect the patient’s alertness, breathlessness, ability to talk, wheeze, use of accessory muscles, RR, P, PaO2, PaCO2
  • About 40% of cases are related to an allergic response. May be seasonal or year round depending on exposure to allergen
    Induced or exacerbated after exercise or Pronounced with exposure to cold air
    Can trigger asthma attacks
    Cigarette or wood smoke * Vehicle exhaust
    Elevated ozone levels * Sulfur dioxide
    Most common form of occupational lung disease from Exposure to diverse agents. Arrive at work well but experience a gradual decline over the course of the day
    Major precipitating factor of an acute asthma attack
    ↑ inflammation and hyperresponsiveness of the tracheobronchial system
    Allergic rhinitis and nasal polyps * Large polyps are removed
    Sinus problems are usually related to inflammation of the mucous membranes
    Asthma triad: nasal polyps, asthma, and sensitivity to aspirin and NSAIDs
    Wheezing develops in about 2 hr
    Sensitivity to salicylate acid - Found in many foods, beverages, and flavorings
    Food allergies may cause asthma symptoms
    GERD: mechanism is unknown
    Reflux of acid could be aspirated into lungs, causing bronchoconstriction
    Psychologic factors can worsen the disease process
    Attacks can trigger panic and anxiety
  • Primary response is chronic inflammation from exposure to allergens or irritants Leading to airway hyperresponsiveness and acute airflow limitations.
    Inflammatory mediators cause (early-phase response)
    Vascular congestion
    Edema formation
    Production of thick, tenacious mucous
    Bronchial muscle spasm
    Thickening of airway walls
    Late-phase response
    Occurs within 4-10 hours after initial attack
    Only occurs in 30%-50% of patients
    Can be more severe than early-phase and last for 24 hours or more
    If airway inflammation is not treated or does not resolve, it may lead to irreversible lung damage

  • Recurrent episodes of wheezing, breathlessness, cough, and tight chest May be abrupt or gradual
    Lasts minutes to hours
    Inspiration-expiration ratio of 1:2 to 1:3 or 1:4
    Bronchospasm, edema, and mucus in bronchioles narrow the airways. Air takes longer to move out
    Wheezing is unreliable to gauge severity. Severe attacks may have no audible wheezing. Usually begins upon exhalation – exp. wheezing
    Cough variant asthma
    Cough is only a symptom and is non-productive. Bronchospasm is not severe enough to cause airflow obstruction
    Difficulty with air movement can create a feeling of suffocation. Patient may feel increasingly anxious
    An acute attack usually reveals signs of hypoxemia
    ↑ anxiety
    Inappropriate behavior
    More signs of hypoxemia
    ↑ pulse and blood pressure
  • Causes of status asthmaticus
    Viral illnesses
    Ingestion of aspirin or other NSAIDs
    Environmental pollutants or allergen exposure
    Emotional stress
    Abrupt discontinuation of drug therapy
    Abuse of aerosol medication
    Ingestion of β-adrenergic blockers
    Wheezing can be heard. IF wheezing is not heard, it could be a life threatening emergency indicating lack of over-inflation of the lungs, inability to exhale, feelings of tightness,
    Stress on thorax can increase intrathoracic pressure that leads cardiac dysrhythmias,& HTN
    Beginning stages of attack – hypoxemia with hypocapnia, caused by high RR- pH alkalosis. The patient compensates by active diffusion though “Dead space areas” (Nares, trachea, bronchi).
    Fatigue causes more CO2 retention but the body has compensated by diffusion so now it has increased capnia. Patient can go rapidiy downhill to resp. failure and need venting to breath.
  • Patient will usually have asthma symptoms from poor control of disease that has been progressively getting worse over time.
    Symptoms are the same but are more severe and prolonged. There is anxiety and fear of suffocation, which increases O2 needs.
    Retractions, nasal flaring, sweating (or not,) hyperinflation seen on x-ray.
  • Severe muscle fatigue leading to resp. arrest. (cardiac failure)
  • read
  • P. 873 for skills
    A drop in systolic BP during the inspiratory cycle greater than 10mm Hg
    Normally it does drop but less than 10
  • (FEV1 Forced expiratory volume in one second)
    peak expiratory flow rate or FEV1 measured

    Esinophils for allergy Response
    Can have asthma and an infection (maybe cause of the asthma)
  • Medications are divided into two general classifications:
    long-term–control medications to achieve and maintain control of persistent asthma, and
    (2) quick-relief medications to treat symptoms and exacerbations.
  • Because chronic inflammation is a primary component of asthma, corticosteroids, which suppress the inflammatory response, are the most potent and effective antiinflammatory medication currently available to treat asthma
  • Inhaled form is used in long-term control
    Systemic form to control exacerbations and manage persistent asthma
    Reduce bronchial hyperresponsiveness
    Decrease mucus production
    Taken on a fixed schedule
    Mast cell stabilizers - Mast cell stabilizers are nonsteroidal antiinflammatory drugs that inhibit the IgE-mediated release of inflammatory mediators from mast cells and suppress other inflammatory cells (e.g., eosinophils).
    Long-term administration can prevent and reduce bronchial hyperreactivity
    Effective in exercise-induced asthma when used 10-20 minutes before exercise
  • The use of leukotriene modifiers can successfully be used as add-on therapy to reduce (not substitute for) the doses of inhaled corticosteroids.

    Have both bronchodilator and anti-inflammatory effects
    Not indicated for acute attacks
    Used for prophylactic and maintenance therapy

    Monoclonal - Subcutaneous administration every 2-4 weeks
  • Short-acting inhaled β2-adrenergic agonists are the most effective drugs for relieving acute bronchospasm. They are also used for acute exacerbations of asthma and labled Rescue Drugs

    β2 agonists (albuterol) - act on the smooth muscles and cause dilation, enhance mucous clearance and respiratory muscles;
    have rapid onset and few side effects → tachycardia, tremors, nervousness
  • β-adrenergic agonists - Anticholinergics (Atrovent) - have greater broncho-dilator effects and fewer side effects than β2 agonists such as:dry mouth, H/A, nervousness; work by blocking cholinergic receptors in the larger airways
    They block the bronchoconstricting influence of parasympathetic nervous system.
    Epinephrine – racemic
  • Correct administration of drugs is a major factor in success
    Using an MDI with a spacer is easier and improves inhalation of the drug
    DPI (dry powder inhaler) requires less manual dexterity and coordination
  • Overall Goals
    No recurrent exacerbations of asthma or decreased incidence of asthma attacks
    Adequate knowledge to participate in and carry out management
  • read
  • Oxygen should be monitored with pulse oximetry or ABGs in severe cases
    Treatment is based on severity of symptoms and the response to medications. PFTS is one way to check for severity of lung dysfunction.
    2 main types of medications: Rescue drugs
    Albuterol - B-adrenergic agonists by inhalation, MDI or nebulizer
    Corticosteroids- inhaled or by IV
    Atrovent every other tx

    Racemic Epinephrine –Status asthmaticus – cardiac stimulant, vasopressor, beta angeneric agonist
  • Acute asthma episode
    Can be severe enough to require intubation and mechanical ventilation. Used when there is no response to other treatment
    Louder wheezing may occur in airways that are responding to therapy
    With progression, normal breath sounds return and wheezing subsides
  • Click to start on page
  • Education: Start at time of diagnosis & Integrate through care
    Self-management is the goal - Tailored to needs of patient
    Teach patient to identify and avoid known triggers
    Prompt diagnosis and treatment of upper respiratory infections and sinusitis may prevent exacerbation
    Seek medical attention for bronchospasm or when severe side effects occur
    Fluid intake of 2 to 3 L every day
    Take β-adrenergic agonist 10 to 20 minutes before exercising
    Peak flow should be monitored daily, and a written action plan should be followed according to results of daily PEFR

  • Fourth leading cause of death in US
    More than 50% die within 10 years of diagnosis

  • Most of the observations, S/s and treatment are the same with emphysema and COPD disease. So they will be discussed as one disease.
    Emphysema - alveolar sacs are destroyed causing over-distention of the air spaces & obstruction of the airways; have a lot of dyspnea even in the early stages as well as the “barrel chest.”
  • Centrilobular (central part of lobule)
    Dilation and destruction of respiratory bronchioles and pulmonary capillary bed
    Prominent in upper lobes with little involvement of the alveolar sacs;
    Panlobular (destruction of whole lobule)
    Affects respiratory bronchioles, alveolar ducts, and alveolar sacs. Panlobular involves the lower lung → alveoli & bronchioles; both seen in smokers
    It destroys the alveoli in the lower lobes and there is a lot of bleb formation; seen more with patients who have an AAT defect. (Proteinase inhibitors).
    Blebs (pockets of air) form between the alveolar spaces & bullae form between the lung parenchyma
  • Smoking: Clinically significant airway obstruction develops in 15% to 20% of smokers
    80% to 90% of COPD deaths are related to tobacco smoking
    Non-modifiable Heredity and aging
  • Effects of nicotine
    Stimulates sympathetic nervous system. Increases HR
    Causes peripheral vasoconstriction. Increases BP and cardiac workload
    ↓ Amount of functional hemoglobin
    ↑ Platelet aggregation. Compounds problems in CAD
    Effects on respiratory tract
    Increased mucus production
    Hyperplasia of mucus glands
    Lost or decreased ciliary activity
    Carbon monoxide
    ↓ O2 carrying capacity
    ↑ Heart rate
    Impaired psychomotor performance and judgment

  • Recurring infections impair normal defense mechanisms. Intensify pathologic destruction of lung tissue
    COPD patients are Prone to ↑ infection which leads to further mucous production; with each episode of infection the bronchial walls become thickened and inflamed, obstructing the airways during expiration, collapsing the airways, and trapping air leading to a V/Q mismatch, ↓ PaO2 and ↑ PaCO2
    Heredity - α-Antitrypsin (AAT) deficiency
    Genetic risk factor for COPD. Accounts for <1% to 2% of COPD
    Some degree of emphysema is common due to physiologic changes of aging lung tissue. Natural changes in the aging lungs
    Gradual loss of elastic recoil
    Lungs become rounded and smaller
    Loss of alveolar supporting structures
    Decreased number of functional alveoli
    Decreased arterial O2 levels
    Thoracic cage changes from osteoporosis and calcification of costal cartilages
  • Main: Inability to expire air (largely irreversible) is the main characteristic of COPD
    Supporting structures of lungs are destroyed
    Air goes in easily but remains in the lungs
    Bronchioles tend to collapse , trapping air
    Causes barrel-chest look

    Pulmonary vascular changes
    Blood vessels thicken
    Surface area for diffusion of O2 decreases
    Increased RR
  • Commonly emphysema and chronic bronchitis coexist
    Distinguishing symptoms can be difficult with comorbidities
    Patient get used to having increased Co2 retention.
    The airways are remodeled, from the inflammatory process and become thickened.

    Systemic effects of inflammation are skeletal muscle wasting> no known reason> adds to decrease in activity
  • Intermittent cough is earliest symptom
    Dyspnea usually prompts medical attention
    Occurs with exertion in early stages
    Present at rest with advanced disease
    Causes chest breathing
    Use of accessory and intercostal muscles
    Inefficient type of breathing
    Characteristically underweight with adequate caloric intake
    Chronic fatigue
  • The diagnosis of COPD is confirmed by pulmonary function tests. Goals of the diagnostic workup are to confirm the diagnosis of COPD via spirometry, evaluate the severity of the disease, and determine the impact of disease on the patient’s quality of life. When the FEV1/FVC ratio is less than 70%, it suggests the presence of obstructive lung disease. (useful in differentiating between obstructive and restrictive pulmonary dysfunction.)
    Patients seem to have an easy time getting a breath in, but have difficulty getting it out. This causes the prolonged exp. phase.
  • Exacerbations of COPD are signaled by a change in the patient’s usual dyspnea, cough, and/or sputum that is different than the usual daily patterns. These flares require changes in management.
    Frequent exacerbations associated with poorer outcomes. Primary causes are:
    Tracheobronchial infection, Air pollution
    A respiratory failure: Caused by
    Overuse of sedatives, benzodiazepines, and opioids – suppress ventilatory drive
    Surgery or severe, painful illness involving chest or abdomen
    Discontinuing bronchodilator or corticosteroid medication
    Complications: Polycythemia-compensation for hypoxemia
    GERD: Increased incidence with COPD patients who chronically retain CO2. Commonly in duodenum and painless
    Depression may be four times more likely for COPD patients
    Anxiety complicates treatment for symptoms of : Dyspnea & Hyperventilation
    Cor pulmonale is hypertrophy of the right side of the heart, with or without heart failure, resulting from pulmonary hypertension and is a late manifestation of chronic pulmonary heart disease. HTN of the pulmonary vasculature increases the pressure in the R atrium. This leads to hypertrophy of the right side of the heart. S & S - peripheral edema, hepatomegaly, splenomegaly, JVD
    Treatments - diuretics and digoxin
  • The diagnosis of COPD is confirmed by pulmonary function tests. Goals of the diagnostic workup are to confirm the diagnosis of COPD via spirometry, evaluate the severity of the disease, and determine the impact of disease on the patient’s quality of life.
    Diagnosis confirmed by pulmonary function tests. When the FEV1/FVC ratio is less than 70%, it suggests the presence of obstructive lung disease.
    Chest x-rays, spirometry, history, and physical examination are also important in the diagnostic workup
    6-minute walk test to determine O2 desaturation in the blood with exercise
    ECG can show signs of right ventricular failure
  • read
  • Irritants should be evaluated and avoided
    Exacerbations treated promptly
    Smoking cessation
    Most effective intervention
    Accelerated decline in pulmonary function slows and usually improves
    Drug therapy
    Bronchodilators - Relaxes smooth muscle in the airway - Improves ventilation of the lungs
    Drug therapy
    Inhaled corticosteroid therapy - Used for moderate-to-severe cases
    Although patients with COPD do not respond as dramatically as those with asthma to bronchodilator therapy, a reduction in dyspnea and an increase in FEV1 are usually achieved. Presently no drug modifies the decline of lung function with COPD.
    O2 therapy is used to
    Reduce work of breathing *Maintain PaO2
    Reduce workload on heart
  • Chronic O2 therapy from O2 toxicity can lead to ARDS. Amount administered should just be enough to maintain PaO2 within normal or acceptable range. O2 therapy above 50% is considered toxic.
    Periodic reevaluations are necessary to determine duration of use

    CO2 narcosis – Normally co2 accumulation is the major stimulent of the respiratory center. Some patients develop a tolerance for high Co2 levels. Anyway you never deprive a patient of O2 if needed. The lowest level should be used. Many COPD patients require high flow rates and higher concentrations to live. ABG’s determine the rate and concentration of O2
  • Surgical therapy
    Lung transplantation
    Single lung—most common due to donor shortages
    Prolongs life
    Improves functional capacity
    Enhances quality of life
  • Breathing retraining - Decreases dyspnea, improves oxygenation, and slows respiratory rate
    Pursed-lip breathing is a technique that is used to prolong exhalation and thereby prevent bronchiolar collapse and air trapping. Often instinctively patients will perform this technique.

    Effective coughing - Main goals
    Conserves energy
    Reduces fatigue
    Facilitates removal of secretions
  • Click to start on page

  • Pulmonary rehabilitation – p 652-53
    Increases exercise performance
    Reduces dyspnea
    Improves quality of life
    Activity considerations
    Exercise training leads to energy conservation
    In upper extremities it may improve muscle function and reduce dyspnea
    Modify ADLs to conserve energy
    Walk 15 to 20 minutes a day at least three times a week
    Adequate rest should be allowed
    Sexual activity
    Plan when breathing is best
    Do not assume dominant position or prolong foreplay
    Can be difficult because of medications, postnasal drip, or coughing
    Nasal saline sprays, decongestants, or nasal steroid inhalers can help
  • Bronchiectasis is characterized by permanent, abnormal dilation of one or more large bronchi. The pathophysiologic change that results in dilation is destruction of the elastic and muscular structures supporting the bronchial wall.
    The hallmark of bronchiectasis is persistent or recurrent cough with production of large amounts of purulent sputum, which may exceed 500 ml/day.
    Bronchiectasis is difficult to treat. Therapy is aimed at treating acute flare-ups and preventing decline in lung function.
    Antibiotics are the mainstay of treatment and are often given empirically, but attempts are made to culture the sputum.
    Long-term suppressive therapy with antibiotics is reserved for those patients who have symptoms that recur a few days after stopping antibiotics.
    An important nursing goal is to promote drainage and removal of bronchial mucus.
  • Respirtory part2

    1. 1. Respiratory System NURS156 Chapter 28 & 29 albuterol Kapi’olani Community College corticosteroids for pretty much every resp
    2. 2. Chapter 28 Lower Respiratory problems Acute Bronchitis Tuberculosis (pgs 569-575) Environmental Lung Diseases Lung Cancer Chest Tubes
    3. 3. Acute Bronchitis (p 561) Inflammation of bronchi usually d/t infection Usually caused by virus (rhino or influenza) Bacterial cause are common: in smokers Acute Exacerbation of Chronic Bronchitis (AECB)- an acute infection along w/chronic bronchitis more sputum from bac supportive care: fluids, rest, meds
    4. 4. M. tuberculosis Caused by Mycobacterium tuberculosis Remains one of major causes of disability and death worldwide In 2006, 9.2 million new cases were diagnosed and 1.7 million died (NIH, 2008). requires 2years of Types of TB include: multi drug therapy -Multidrug-Resistant TB (MDR TB) -Extensively Drug-Resistant TB (XDR TB)
    5. 5. TB in the population High rates of TB among HIV population Why is this population more vulnerable? poor compliance of Emergence of MDR strains treatment What caused this to happen? wrong drugs given because harder to diagnosis when body does not produce antigen immune response
    6. 6. Tuberculosis Tuberculosis (TB) - communicable airborne disease caused by M. tuberculosis droplets inhaled when someone _coughing, sneezing, yelling__ Affects the __ of the lungs first and bacilli not phagocytized wander through the lymphatic system to other parts of the lung and body and lay dormant harbored in granulona to issolate the TB when in body active infection may never happen. must be in active stage to transmit
    7. 7. manifestations Early stages: no sx Active stage: fatigue, malaise, anorexia, unexplained wt loss, low-grade fevers, and night sweats Most common: frequent cough that produces white, frothy sputum Hemoptysis is seen in advanced cases HIV pts may present differently
    8. 8. Diagnostic tests PPD- (+) if induration develops at injection site 48 to 72 hours after test AFB (acid fest bacilli test) CXR to view lesions/scars Lung Scan Bacille Calmette-Guerin Vaccine Sputum culture- confirms diagnosis only way to confirm diagnosis and differenciate bet ween pneumonia
    9. 9. First Line TB Drugs Isoniazid side effects: liver toxicity Rifampin and non viral hepatitis Ethambutol Pyrazinamide DOT, side effects, prevention to active disease directly observed therapy
    10. 10. Nursing concerns Preventive isolation Particulate respirators - masks with special filters that filter droplet nuclei NEGATIVE AIRBORN isolation for details check PRESSURE ROOM!! fundamental text Community Concerns- all contacts with the patient need to be notified and possibly put on medications for prevention → 300mg Isonizid
    11. 11. Occupational Lung Disease (pg 577-578 & 561) Caused by inhaling dust or chemicals Longer exposure= greater damage Occupational/environmental asthma Pneumoconiosis: ‘dust in the lungs’ Chemical pneumonitis: exposure from toxic chemicals Hypersensitivity pneumonitis/extrinsic allergic alveolitis: inhaling antigen cause fibrosis; scaring hardened tissue
    12. 12. Lung Cancer Lung Cancer - affects the epithelium Four Major Types  Small cell/Oat cell (SCLC) NON- Small Cell (NSCLC)  Squamous/Epidermoid  Adenocarcinoma  Large Cell/Undifferentiated  NSCLC are S-L-O-W growing
    13. 13. Statistics Leading cause of cancer or related deaths Accounts for 28% of all cancer deaths Approx. 172,570 new cases are diagnosed each yr 58% of deaths are in men w/African- Americans having the highest rate and Hispanics the lowest Lung cancer now surpassed breast cancer Most common in persons >50 years old w/long hx of cigarette smoking
    14. 14. Etiology Cigarette smoking-#1 risk factor! Responsible for 80% to 90% of all lung cancers Tobacco smoke contains 60 The smoke is an irritant Ten years after cessation risk of lung cancer mortality is reduced 30% to 50%
    15. 15. Diagnostic tests CXRs CT- most effective noninvasive test MRI shows same as CT Bronchoscopy or sputum studies provide the definitive diagnosis usually by dx too late
    16. 16. Lung Cancer S/S Respiration decreased Symptoms – Dyspnea, hemoptysis, coughing, wheezing, fatigue, weight loss, SOB, sometimes shoulder pain. Paraneoplastic syndrome
    17. 17. Lung Cancer- treatment Staging - TMN system Treatment Modalities RT - mostly for palliation although may be used in conjunction with surgery or chemotherapy Chemotherapy - works best with small cell Surgery: better with non small cell only 25% eligible Laser surgery Resections - Wedge, Segmental, Lobe, Pneumonectomy
    18. 18. Lung Cancer – nursing care Preop diagnostic tests Education...for pre and post op...what to expect, deep breathing for post with practice, inspirometer, chest tube expectations. Postop Monitoring, labs, DB & C, pain management, dressings
    19. 19. Chapter 29 Obstructive Pulmonary Diseases Asthma COPD- Chronic Obstructive Pulmonary Disease Chronic Bronchitis Emphysema Bronchietasis Medications
    20. 20. Asthma – Definition Chronic inflammatory disorder of airways  Causes airway hyperresponsiveness leading to wheezing, breathlessness, chest tightness, and cough Affects about 20 million Americans Women and African Americans have a 30% or greater prevalence
    21. 21. Triggers of Asthma Allergens: 40% of cases Exercise Air Pollutants Occupational Factors Respiratory Infection Nose and Sinus Problems ie. Rhinotic pollops Drugs and Food Additives Gastroesophageal Reflux Disease Emotional Stress
    22. 22. Pathophysiology thick tenacious (sticky)mucous edema o Primary response bronchio spasms Hyper-responsivenes o Inflammatory mediators o Late-phase response
    23. 23. Factors Causing Airway Obstruction in Asthma Fig. 29-3
    24. 24. Clinical Manifestations Unpredictable and variable Expiration may be prolonged (3-4x longer) Wheezing is unreliable to gauge severity Cough variant asthma feeling of suffocation hypoxemia: sx, in rr and pulse, increased CO2, decreased O2, restless, anxious, inappropriate behavior.
    25. 25. Complications-Status asthmaticus triggered more Status asthmaticus easily by viral infections and  Severe, life-threatening attack ingestion of aspirin unresponsive to usual treatment  Patient at risk for respiratory failure  As attack severity ↑, work of breathing ↑, patient tires, and it is harder to overcome the ↑ resistance to breathing  Ultimately the patient deteriorates to hypercapnia (too much CO2) and hypoxemia
    26. 26. Complications Clinical manifestations of status asthmaticus result from  Increased airway resistance from edema  Mucous plugging  Bronchospasm  Respiratory acidosis
    27. 27. Complications of status asthmaticus Complications of status asthmaticus  Acute cor pulmonale  Severe respiratory muscle fatigue leading to respiratory arrest  Death is usually result of respiratory arrest or cardiac failure
    28. 28. **Red Flags** • Heart rate >120 bpm • Respiratory rate >30 bpm • Pulsus paradoxus • Wheezes to silent breath sounds • Speaks in words not sentences • O2 sat <90% • Cant converse • These signs warrant immediate medical intervention to prevent respiratory failure
    29. 29. Pulses paradoxus see page 873 Usually during the inspiration phase the pulse becomes weaker as one inhales and stronger as one exhales. Pulses paradoxus is an exaggeration of this normal variation in pulse. This could also indicate other serious conditions such as: cardiac tamponade, pericarditis, chronic sleep apnea, croup, COPD, and asthma
    30. 30. Diagnostic Studies Detailed history and physical exam Pulmonary function tests (FEV measuring how much air u can breath out in one second) Peak flow monitoring Chest x-ray ABGs Oximetry Allergy testing Blood levels of eosinophils Sputum culture and sensitivity
    31. 31. Drug Therapy Long-term control medications  Achieve and maintain control of persistent asthma Quick-relief medications  Treat symptoms of exacerbations
    32. 32. Drug Therapy 4 Types of Antiinflammatory Drugs  Corticosteroids (suppress inflammatory response) side effects to steroids:  Mast cell stabilizers lowers immune response and healing time  Leukotriene modifiers round face and thin skin. faster metabolism, and  Monoclonal antibody to IgE appetite high glucose levels
    33. 33. Drug Therapy Corticosteroids Suppress inflammatory response  Inhaled  Systemic form Mast cell stabilizers  Inhibit IgE-mediated release of inflammatory mast cells non-steroidal
    34. 34. Drug Therapy Leukotriene modifiers or inhibitors  Blocks action of leukotrienes- potent bronchoconstrictors add on therapy to induce but not sub for steroids Monoclonal antibody to IgE  ↓ circulating free IgE levels  Prevents IgE from attaching to mast cells, preventing release of chemical mediators
    35. 35. Drug Therapy 3 Types of Bronchodilators  β2-adrenergic agonists aka rescue drugs  Methylxanthines – rarely used  Anticholinergics β-adrenergic agonists (e.g., albuterol, metaproterenol)  Effective for relieving acute bronchospasm  Onset of action in minutes and duration of 4-8 hours  side: tacycard, restlessness
    36. 36. Drug Therapy Anticholinergic drugs (e.g., ipratropium, atrovent)  Block action of acetylcholine  Usually used in combination with a bronchodilator  Most common side effect is dry mouth, headache, nervousnes
    37. 37. Patient Teaching Correct administration of drugs is a major factor in success  Inhalation of drugs is preferable to avoid systemic side effects
    38. 38. Nursing Management Nursing Diagnoses Ineffective airway clearance Anxiety Deficient knowledge Overall Goals  Maintain greater than 80% of PEFR  Have minimal symptoms  Maintain acceptable activity levels
    39. 39. Collaborative Care Desired therapeutic outcomes  Control or eliminate symptoms  Attain normal lung function  Restore normal activities  Reduce or eliminate exacerbations and side effects of medications  Avoid triggers of acute attacks  Premedicate before exercising  Choice of drug therapy depends on symptom severity
    40. 40. Collaborative Care Acute asthma episode • O2 therapy should be started • Treatment depends on severity and response • Inhaled β-adrenergic agonists by metered dose inhaler • Corticosteroids
    41. 41. Collaborative Care Status asthmaticus  Most therapeutic measures are the same as for acute episode  ↑ in frequency and dose of bronchodilators  IV corticosteroids are administered every 4-6 hours  Continuous monitoring  IV fluids - insensible loss of fluids
    42. 42. Nursing Management Health Promotion Teach patient to identify and avoid known triggers Prompt diagnosis Adequate nutrition Adequate sleep Preventive medications Monitoring symptoms
    43. 43. COPD - Overview  increased resistance secondary to bronchial edema, ↑ mucous production, destruction of cilia, smooth muscle contraction, or↓ elastic recoil, or bronchiolar/alveolar wall damage  caused by numerous irritants especially cigarette smoke which is also a risk factor
    44. 44. COPD - Description Airflow limitation not fully reversible  Generally progressive  Abnormal inflammatory response of lungs to noxious particles or gases Includes  Chronic bronchitis  Emphysema
    45. 45. Chronic Bronchitis Presence of chronic productive cough for 3 or more months in each of 2 successive years  Other causes of chronic cough are excluded
    46. 46. Emphysema Abnormal permanent enlargement of the air space distal to the terminal bronchioles Destruction of bronchioles without obvious fibrosis
    47. 47. Emphysema - Pathophysiology Two types  Centrilobular  Panlobular
    48. 48. COPD - Etiology Risk factors  Cigarette smoking  Occupational chemicals and dust  Air pollution  Infection  Heredity  Aging
    49. 49. COPD - Cigarette Smoking Effects of nicotine  Carbon monoxide  Involuntary smoke exposure Effects on respiratory tract  Increased mucus production  Hyperplasia of mucus glands  Lost or decreased ciliary activity
    50. 50. Occupational and Environmental COPD can develop with intense or prolonged exposure to  Dusts, vapors, irritants, or fumes  High levels of air pollution  Fumes from indoor heating or cooking with fossil fuels
    51. 51. COPD Risk - Factors Infection Heredity - α1-Antitrypsin deficiency Aging
    52. 52. COPD - Pathophysiology Primary process is inflammation  Inhalation of noxious particles  Mediators released cause damage to lung tissue  Airways inflamed  Parenchyma destroyed Supporting structures of lungs are destroyed Pulmonary vascular changes
    53. 53. COPD - Pathophysiology Common characteristics  Mucus hypersecretion  Dysfunction of cilia  Hyperinflation of lungs  Gas exchange abnormalities  Skeletal muscle wasting
    54. 54. COPD - Clinical Manifestations Develops slowly Diagnosis is considered with  Cough  Sputum production  Dyspnea  Exposure to risk factors  Accessory intercostal muscles  Underweight with adequate caloric intake
    55. 55. COPD - Clinical Manifestations Physical examination findings  Prolonged expiratory phase  Wheezes  Decreased breath sounds  ↑ Anterior-posterior diameter  Fatigue Dx with pulmonary  SOB function test
    56. 56. COPD - Complications Exacerbations of COPD polycythemia Acute respiratory failure Peptic ulcer disease Depression/anxiety Cor pulmonale hypertrophy on R side of heart; late manifestation
    57. 57. COPD- Diagnostic Studies Diagnosis confirmed by pulmonary function tests Spirometry—typical findings 6-minute walk ECG
    58. 58. COPD - Collaborative Care Primary goals of care  Prevent progression  Relieve symptoms  Prevent/treat complications  Promote patient participation  Prevent/treat exacerbations  Improve quality of life and reduce mortality risk
    59. 59. COPD- Collaborative Care Irritants avoided Exacerbations Smoking cessation  Bronchodilators  corticosteroid therapy  O2 therapy pt with COPD do not respond as dramatically as pt with asthma to O2
    60. 60. COPD - Collaborative Care Complications of oxygen therapy  Combustion adapted to high CO2 levels if O2 is given decreases  CO2 narcosis CO2 concentration which decreases reflex to breath  O2 toxicity  Absorption atelectasis  Infection
    61. 61. COPD - Collaborative Care Surgical therapy  Lung volume reduction surgery C-OPD  Remove 30% of most diseased lung to enhance performance of remaining tissue  Bullectomy  Used for emphysema  Large bullae are resected to improve lung function
    62. 62. COPD Collaborative Care (Cont’d) Respiratory and physical therapy  Aerosol nebulization therapy  Chest physiotherapy  Percussion  Vibration  Postural drainage  Pursed-lip breathing slows RR and extends E  Effective coughing
    63. 63. COPD - Collaborative Care Vibration  Facilitates movement of secretions to larger airways  Mild vibration tolerated better than percussion Flutter mucus clearance device  Produces vibration in lungs to loosen mucus for expectoration  Handheld device
    64. 64. Lower Respiratory Diseases - COPD Nursing Dx  Impaired gas exchange  Ineffective airway clearance  Activity intolerance  Anxiety  Risk for infection  Imbalanced nutrition  Sexual dysfunction  Disturbed sleep pattern
    65. 65. Nursing Management - Planning Goals  Knowledge and ability to implement long-term regimen  Overall improved quality of life
    66. 66. Nursing Management Nursing Implementation Ambulatory and Home Care  Most important aspect is teaching  Pulmonary rehabilitation  Activity considerations  Sexual activity  Sleep  Psychosocial considerations
    67. 67. disease for life Bronchiectasis - longterm antibiotic therapy reser ved for worst case pt. ↑ ↑ ↑ mucous production seen in 3 layers → clear, cloudy, purulent; seen in patients who work with fine particles such as flour, aspertame, wheat hallmark- persistent and very productive cough with purulent sputum up to 500ml of mucus