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Definition and classification of OA
OA is a disease characterized by variable airflow limitation and/or airway hyperresponsiveness due to causes and conditions attributable to a particular environment and not to stimuli encountered outside the workplace. Two types of OA are distinguished (4):
Immunological OA. This type is characterized by a latency period (interval between onset of exposure and symptoms) that may vary from a few weeks to several years.
Non-immunological OA. This category includes asthma that occurs after single (reactive airways dysfunction syndrome or RADS) (5) or multiple (irritant-induced asthma) exposures to irritants at high concentrations.
OCCUPATIONAL ASTHMA
Occupational asthma is caused by sensitisation to an agent inhaled in the workplace and usually presents with cough, wheezing and variable shortness of breath. Symptom onset is slow and may only occur after years of repeated exposure to chemicals and allergens in the work environment. Two distinct types of occupational asthma occur namely Non-allergic Reactive Airways and Allergic Asthma. Allergic asthma takes longer to develop than non-allergic Reactive Airways Disease Syndrome (RADS) which may develop more rapidly due to workplace associated irritants such as chlorine, ammonia fumes or dust. Sometimes pre-exiting mild asthma is exacerbated in the workplace and smokers are more at risk for developing occupational asthma.
SYMPTOMS
in most people with occupational asthma, the symptoms appear a short time after beginning work and subside after leaving work.
These are the most common symptoms of occupational asthma. Most people do not have all these symptoms.
· Coughing
· Wheezing
· Chest tightness
· Chest pain
· Prolonged shortness of breath
· Extreme fatigue
Allergy symptoms that occur at work but get better away from work also may be a sign of irritants in the air that could provoke asthma symptoms. The following symptoms could occur:
· Eyes: itchy, burning, or watery
· Nose: itchy or stuffy, sneezing
· Skin: itchy, red, or irritated
Diagnosis
· Spirometry: The spirometer is a device that measures how much air you can exhale and how forcefully you can breathe out. Spirometry is a good way to see how much your breathing is impaired during an attack. This test must be done in the medical office; you may exercise on a treadmill or stationary bicycle or perform the tests before and after using an inhaled medication.
· Peak flow meter: This is another way of measuring how forcefully you can breathe out during an attack. This device is small and portable and can be used "in the field." This device can be very helpful. It is inexpensive and monitoring can be done at various times of the day to help detect any patterns associated with the reactive airways process.
Medications
Controller medications are for long-term control of persistent asthma. They help to keep airways open and reduce the inflammation in the lungs that underlies asthma attacks. Controller medications include long-acting beta-agonists and anti-inflammatory medicines.
Long-acting beta-antagonists: This class of drugs is chemically related to adrenaline, a hormone produced by the adrenal glands. Inhaled long-acting beta-agonists work to keep breathing passages open for 12 hours or longer. They relax the muscles of the breathing passages, dilating the passages and decreasing the resistance to exhaled airflow, making it easier to breathe. They also may help to reduce inflammation, but they have no effect on the underlying cause of the asthma attack. Side effects include rapid heartbeat and shakiness. Salmeterol (Serevent) andformoterol (Foradil) are long-acting beta-agonists.
Anti-inflammatory medicines minimize the inflammation that underlies an acute asthma attack. Generally these medications do not help during an attack, but you should continue to take them during an attack.
· Inhaled corticosteroids are the main class of medications in this group. The inhaledsteroids act locally by concentrating their effects directly within the breathing passages, with very few side effects outside of the lungs. Beclomethasone (Vancenase, Beclovent), fluticasone(Flovent), budesonide (Pulmicort), and triamcinolone (Azmacort) are examples of inhaled corticosteroids.
· Other anti-inflammatory drugs used to treat asthma include oral steroids,leukotriene inhibitors, methylxanthines, and cromolyn sodium. For more information about these medications, see Asthma and Understanding Asthma Medications.
Rescue medications are bronchodilators. They quickly open the airways closed off by swelling, bronchospasm, and mucus. These are taken after an asthma attack has already begun. These do not take the place of anti-inflammatory drugs. Do not stop taking your anti-inflammatory drug(s) during an asthma attack.
· Short-acting beta2-agonists are the most commonly used rescue medications. This class of drugs is chemically related to adrenaline, a hormone produced by the adrenal glands. Inhaled beta2-agonists work rapidly (within minutes) to open the breathing passages. They relax the muscles of the breathing passages, dilating the passages and decreasing the resistance to exhaled airflow, making it easier to breathe. They do not reduce inflammation and have no effect on the underlying cause of the asthma attack. Side effects include rapid heart beat and shakiness. Albuterol (Proventil HFA, Ventolin HFA, ProAir) is the most frequently used beta2-agonist medication.
· Anticholinergics are another class of drugs useful as rescue medications during asthma attacks. Inhaled anticholinergic drugs open the breathing passages, similar to the action of the beta2-agonists. Inhaled anticholinergics take slightly longer than beta2-agonists to achieve their effect, but they last longer than the beta2-agonists. An anticholinergic drug is often used together with a beta2-agonist drug to produce a greater effect than either drug can achieve by itself. Ipratropium bromide (Atrovent) is the inhaled anticholinergic drug currently used as a rescue asthma medication.
· Tiotropium (Spiriva), a long-acting anticholinergic, is now also being used as a maintenance medicine in more severe cases of asthma.
· Combination therapy which includes a long-acting beta2 agonist and inhaled corticosteroid available in a single inhaler is now commonly used in asthma (for example, Advair, Symbicort, Dulera).
OCCUPATIONAL RHINITIS
Occupational rhinitis (OR) is an inflammatory disease of the nose, which is characterized by intermittent or persistent symptoms, arising out of causes and conditions attributable to a particular work environment and not to stimuli encountered outside the workplace. Its clinical symptoms (nasal congestion, sneezing, rhinorrhea, itching, nasal airflow limitation) are very similar with the symptoms of the allergic rhinitis caused by other (classical) agents. It can be produced by both high and low molecular weight agents. For example, according to the publications, its prevalence among bakers can be 18-29%, and among workers with diisocyanates (painters, urethane mould workers) 36-42%. Risk factors are atopy, high concentration and multiple irritant agents in the air of workplace. Atopy has been associated with an increased risk of specific sensitization to a variety of HMW agents. Beside of the clinical and occupational history, objective investigations have to be used as well, for the diagnosis of OR. The gold standard for confirming the diagnosis of OR is the nasal provocation test. Objective methods that can be used for assessing nasal patency during the investigation of OR include rhinomanometry, acoustic rhinometry, peak nasal inspiratory flow, and gravimetry of the nasal secret. The management of the OR needs environmental interventions. These are: increasing the ventilation, decreasing the time of exposure, substitution of the irritant agent, investigation of possible asthma in all workers with OR. Medical treatments are: oral antihistamines, local (nasal) corticosteroids, combined (antihistamine+membrane-stabilizer) eyedrops.
OCCUPATIONAL LARYNGITIS/VOCAL CORD DYSFUNCTION
Occupational laryngitis is inflammation of the larynx caused by exposure to several irritants: formaldehyde, glutaraldehyde, formaldehyde, glutaraldehyde, isopropylic alcohol, peracetic acid-hydrogen peroxide mixture. These substances are used as cleaning and antiseptic agents in healthcare settings and some ones can also be found in many indoor environments. The disease is also found in people who use their voices as a tool in their professions(teaching, singing, public speaking). Typical symptoms of VCD include wheezing, dysphonia, choking feeling, throat tightness, stridor, dyspnoea, suprasternal and neck muscle retraction, anxiety and cough.
Diagnosis for Laryngitis
The initial work-up and evaluation of the patient with hoarseness is guided by the chronicity of the condition, so a comprehensive history is essential, as is examination of the larynx. Indirect laryngoscopy with a head light and a warmed laryngeal mirror provides the quickest and best view of the hypopharynx and larynx. This may be difficult for the primary care provider, so referral to otolaryngology may be necessary. Hoarseness lasting more than 3 weeks without a history of acute infection warrants referral and further evaluation.
Indirect laryngoscopy confirms the diagnosis by revealing red, inflamed and, occasionally, hemorrhagic vocal cords, with round, rather than sharp, edges and exudate. Bilateral swelling may be present.In severe cases, or if toxicity is a concern, a culture of the exudate is obtained.
Other pertinent physical examination includes the oropharynx, thyroid, and cervical lymph nodes. If there is an unexplained neck mass or suspicious lymph node, careful evaluation may include assessment of thyroid-stimulating hormone if hypothyroidism is suspected, and smallneedle biopsy of any questionable mass.
The differential diagnosis of hoarseness should be evaluated in terms of acute and chronic etiologies. Acute hoarseness differential diagnoses include acute laryngitis, acute laryngeal edema, and acute epiglottitis. Chronic hoarseness may point to chronic laryngitis (such as vocal abuse, allergy), laryngeal carcinoma, lesions of the vocal cords, trauma to the vocal cords, systemic disease (such as hypothyroidism, rheumatoid arthritis, vitalization), or psychogenic disorder.
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