Presentation on theme: "Asthma and Smoking John King, M. D. March 27, 2007."— Presentation transcript:
Asthma and Smoking John King, M. D. March 27, 2007
Asthma and Smoking Asthma is a chronic inflammatory disease characterized by bronchial hyper reactivity and reversible airflow obstruction if treated. Bronchial asthma is a condition of intermittent reversible airflow obstruction affecting only the airways, not the alveoli. Complex molecular and cellular immunologic factors mediate asthma. Immunologic factors include mast cells, eosinophils, thymphocytes, macrohsyes, neutrophils.
Asthma and Smoking Many people with asthma have concurrent airway inflammation and airway hyperresponsiveness. Asthma may occur in some patients after taking aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) Severe airway obstruction may be fatal.
Asthma and Smoking Asthma obstruction can occur in two ways. 1. Inflammation obstructs the lumen or the insides of the airways 2. Airway hyperresponsiveness results in airway obstruction by constricting bronchial smooth muscle, causing a narrowing of the airway from the outside
Assessment Information to obtain during history gathering phase includes. 1. Pattern of episode of dypsnea, chest tightness, coughing, wheezing and excessive amounts of mucous production 2. When symptoms occur (e.g., continuously, seasonally, in association with specific activities, or more often at night) children with parents who smoke in the house are more likely to have nocturnal asthma. 3. Triggers include, carpet, animal inside the house, smells and roaches.
Assessment Clinical manifestations during an asthma attack include 1. Audible wheezing upon expiration 2. Increased respiratory rate 3. Increased coughing if inflammation is present. 4. Use of accessory muscles to assist in respiratory effort 5. Muscle retraction at the sternum, suprasternal notch, and between the ribs
Assessment 6. Barrel chest in patient with persistent or severe asthma (See Figure 30-3, p. 588) 7. Increased anterior- posterior (A-P) diameter of the chest
Assessment 8. Longer respiratory cycle, which requires greater effort 9. Possible cyanotic nail beds and circumoral cyanosis 10. Possibly unable to complete a sentence of more than 5 words per breath 11. Pulse oximetry showing oxygen desaturation 12. Hypoxemia evidenced by change in level of consciousness and tachycardia
Assessment Other assessment data includes 1. Arterial blood gases (ABGs) 2. Pulmonary function tests 3. Chest x-ray examination 4. Therapeutic levels of selected medication
Assessment Other allergic symptoms such as allergic rhinitis, skin rash, or pruritus may occur with atopic or allergic asthma.
Asthma and Smoking Lung and airway changes related to aging is thought to be related to a change in the sensitivity of beta adrenergic receptors, which when stimulated relax smooth muscle and cause bronchodilation. As these receptors become less sensitive, that can no longer respond as quickly or strongly to naturally occurring agonist (epinephrine, dopamine) and beta-adrenergic medications
Considerations for Older People Asthma occurs as a new disorder in about 3% of people over the age of 55. Another 3% of people over the age of 60 have asthma as a chronic disorder Three factors attributed to adult onset asthma include: 1. Longstanding untreated asthma 2. Smoking with a known history of childhood asthma 3. Medication: (eg) Beta blockers, premarin and aspirin.
ASTHMA and Smoking Status Asthmaticus Status asthmaticus is a severe, potentially life threatening acute episode of airway obstruction that tends to intensify once it begins and often does not respond to common therapy 1) Clinical manifestations include extremely labored breathing and wheezing, use of accessory muscles and distended neck veins. 2) The patient may develop a pneumothorax and cardiac or respiratory arrest
ASTHMA and Smoking Status Asthmaticus Most smokers/ second hand smoke present to the ER with a more severe form of asthma: Status asthmaticus is treated with intravenous fluids, systemic bronchodilators, steroids, epinephrine, and oxygen The patient may require intubation If status asthmaticus is not reversed it may lead to cor pulmonale, pneumothorax, and cardiac or respiratory arrest
ASTHMA and Smoking Interventions The goal of therapy is to improve airflow, relieve symptoms, and prevent episodes by including the patient as a key partner in the management plan.
ASTHMA and Smoking Interventions Patient education includes 1. How to assess symptom severity at least twice daily with a peak flow meter 2. How to adjust medication (s) to manage inflammation and bronchoconstriction to prevent or relieve symptoms
ASTHMA Interventions 3. How to use symptom and intervention diary to learn his or her triggers of asthma attack symptoms, early cues for impending attacks, and personal response to medication 4. How to use a metered dose inhaler 5. How to determine when to consult the health care provider
ASTHMA Interventions Drug therapy includes bronchodilators, which increase bronchiolar smooth muscle relaxation. Bronchodilators have no effect on inflammation. 1. Short-acting beta 2 agonist are more useful when an attack begins or as premedication when the client is about to enter an environment or begin an activity that is likely to produce an asthma attack 2. Long-acting beta 2 agonist delivered by MDI directly to the bronchioles, are useful in preventing an asthma attack, but have no value during an acute attack.
ASTHMA and Smoking Interventions 3. Cholinergic antagonists allow for increased bronchodilation and decreased pulmonary secretions 4. Anti-inflammatory agents decrease the general allergic inflammatory responses in the airways; they may be administered systemically or as an inhalant (eg.) oral steroids, inhaled corticosteroids (ICS), theophylline 5. Corticosteroids decrease inflammatory and immune responses
ASTHMA and Smoking Interventions 6. Nonsteroidal inhaled anti-inflammatory agents are helpful in preventing an asthma episode. 7. Mast cell stabilizers prevent mast cell membranes from opening when an allergen binds to IgE; they are helpful for preventing symptoms of atopic asthma but not useful during an acute asthma attack 8. Leukotriene antagonists are used to prevent persistent asthma
ASTHMA and Smoking Interventions Regular exercise, including aerobic exercise, is encouraged; the client’s exercise routine is adjusted to ensure that it does not trigger an episode-fro example, adjusting the environment in which the activity takes place Supplemental oxygen with high flow rates or concentration may be used during an asthma attack.
ASTHMA and Smoking National Heart, Lung, and Blood Institute/ American Thoracic Society/American Academy of Allergy, Asthma & Immunology (NHLBI/ATS/AAAAI) Task Force. Proposed definition for asthma in order to standardize nomenclature for specific phenotypes of asthma. Infection induced Asthma 1. New on set asthma RSV, parainfluenza, metapneunovirus 2. Exacerbation RSV, Rhinovirus, Influenza, parainfluenza, coronavirus. 3. Associated with persistent/chronic disease: Chlamydia pneumoniae, Mycoplasma pneumoniae adenovirus. 4.Biomarkers 1. Viral or bacterial cultures 2. Immunofluorescence 3. polymerase chain reaction from respiratory secretion 4. Serologic diagnosis
ASTHMA and Smoking Allergic Asthma IgE- Medicated Asthma 1. +Allergen sensitization by one positive skin-prick test. 2. IGE sensitivity to specific environmental allergens, pollen, weeds, mites mold (Aspergillus), and pet dander. 3.Childhood onset asthma, allergic rhinosinusitis, and symptom provocation by environmental triggers. 4. Exercise related symptoms 5. Sinusitis and nasal polyps
ASTHMA and Smoking Biomarkers: 1. Peripheral eosinophilia 2. Elevated IGE in serum 3. Th2-type cytokines (T-helper type 2 lymphocyte) 4. Mast-cell markers
ASTHMA and Smoking Non-allergic Asthma 1. Diagnosis already confirmed 1. Negative skin prick or RAST ( radioallergosorbent test) testing seasonal and perennial allergens 2. Normal to Low IGE 3. No history of triggers or seasonality 4. Adulthood asthma 5. No sensitivity to aspirin Biomarkers: 1. Low or normal total IGE levels 2. Mucosal IGE synthesis or tissue eosinophilia
ASTHMA and Smoking Definition of Aspirin-Sensitive Asthma 1. Documented asthma is in response to asthma 2. Probable aspirin sensitivity if sinus disease or nasal polyps 3. >age 20 Biomarkers: 1. Increase levels of urine leukotrienes ( eg, Leukotriene E4) 2. CT scanning pansinusitis or nasal polyps 3. Aspirin or lysine-aspirin challenge
Asthma and Smoking Relationship of Smoking and Cancer of The Lung by: Alton Ochsner, M.D. Annual consumption of cigarettes per capita in the U.S. in persons 15 years and older.
Asthma and Smoking A nnual Consumption Cigarettes Per capita in U.S. in Persons 15 Years and Older
Asthma and Smoking Relationship of Smoking and Lung Cancer by Alton Ochsner, M. D. The American Surgeon Vol. 21, 1955
Asthma and Smoking Relationship of Smoking and Lung Cancer by Alton Ochsner, M. D. The American Surgeon Vol. 21, 1955
Asthma and Smoking Death From Cancer of Lung in White Males In U.S. Relationship of Smoking and Lung Cancer by Alton Ochsner, M. D. The American Surgeon Vol. 21, % Increase
Asthma and Smoking Nicotine in Cigarettes up 10% from 1998 to 2004 Minority – Aimed Brands tally Highest Amount 1. Marlboro 2. Kool Menthol Lights Newport menthol filter 100’s and Camel nonfilters were tied for the highest nicotine at 2.9 milligrams. And rose to 3.2 milligrams. The Washington Post By David Brown August 31, 2006
Asthma and Smoking Is The Public Health Message On Secondhand Smoke Based On Science? No, it’s driven by politics, not good science. Stated by Jerome C. Arnett Jr., M.D. Public health messages are based on solid evidence. Stated by Peter Tuteur, M.D. Internal Medicine News February 15, 2007
Asthma and Smoking Secondhand Smoking Secondhand smoke is called: Passive Involuntary Secondhand smoking The non-smoker breathes “Sidestream” smoke from the burning tip of the cigarette. “Mainstream” smoke that has been inhaled and then exhaled by the smoker. Secondhand Smoke (SHS) Is a major source of indoor air pollution.
Asthma and Smoking Secondhand Smoking Tobacco Smoke Contains over 4000 chemicals in the form of particles and gases. 85% of the smoke in a room results from sidestream smoke. Particulate phase includes tar (itself composed of many chemicals) nicotine, benzene and benzo(a)pyrene. Gas phase includes carbon monoxide, ammonia. dimethylnitrosamine, formaldehyde, hydrogen cyanide and acrolein. Some of these are marked irritant properties and are known or suspected carcinogens (cancer causing substances). The Environmental Protection Agency (EPA) in the USA has classified environmental tobacco smoke as a class A (known human) carcinogen along with asbestos, arsenic, benzene and radon gas,
Asthma and Smoking Secondhand Smoking Secondhand Smoke Definition Environmental tobacco smoke (ETS) is a mixture of the smoke given off by the burning end of a cigarette, pipe or cigar. It is involuntarily inhaled by nonsmokers
Asthma and Smoking Secondhand Smoking Environmental Protection Agency (EPA) classified secondhand smoke as: Known cause of cancer in humans Causes disease and premature death in children and adults who do not smoke. Causes approximately 3400 lung cancer deaths and 22, ,600 heart disease deaths in adult nonsmokers in the U.S. each year.
Asthma and Smoking Secondhand Smoking Approximately 26 % of adults in the United States currently smoke cigarettes, and 50% to 67% of children under five years of age live in homes with at least one adult smoker.
Asthma and Smoking Secondhand Smoking Exposure Environmental Tobacco Smoke (ETS) Decreases lung efficiency and impairs lung function in children of all ages. Increases both the frequency and severity of childhood asthma. Aggravate sinusitis, cystic fibrosis, and chronic respiratory problems such as cough and postnasal drip. Increases the number of children’s colds and sore throats. ETS exposure increases the likelihood of bronchitis and pneumonia.
Asthma and Smoking Secondhand Smoking Scientific Committee on Tobacco and Health (SCOTH) Recent reviews by SCOTH found that the conclusions of its initial report still stand i.e. that there is a “causal effect of exposure to secondhand smoke on the risks of lung cancer, ischaemic heart disease and a strong link to adverse effects in children”