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Bronchial obstruction

Foreign body or tumor in tracheal or bronchial obstruction... [Pg.8]

Fatal anaphylaxis occurs mostly due to bronchial obstruction or cardiac arrest, but also disseminated intervascular coagulation as well as adrenalin overdose [2, 7, 21, 31]. When anaphylactic reactions are survived, long-lasting sequels are rare. However,... [Pg.8]

An MRL of 0.07 ppm has been derived for acute-duration inhalation exposure to hydrogen sulfide. This MRL is based on a LOAEL of 2 ppm for respiratory effects—bronchial obstruction (30% change in airway resistance) in 2/10 persons with asthma reported in the Jappinen et al. 1990 study (Table 2-1 LSE 16). An uncertainty factor of 30 was applied,... [Pg.95]

Based on a LOAEL of 2 ppm for respiratory effects—bronchial obstruction (30% change in airway resistance) in 2/10 persons with asthma in the Jappinen et al. (1990) study, an acute inhalation MRL of 0.07 ppm was derived. An uncertainty factor of 30 was applied to the LOAEL 10 for the use of a LOAEL and 3 for human variability. Since persons with severe asthma were excluded from the study, an uncertainty factor of 3 is needed to protect all sensitive individuals including children. Further details on the derivation of this MRL can be found in the MRL worksheets in Appendix A of this profile. Based on aNOAEL of 30.5 ppm for respiratory effects in mice observed in the CUT (1983a) study, an intermediated MRL of 0.03 ppm was derived. The NOAEL is adjusted for intermittent exposure and the NOAEL[hec] is calculated. An uncertainty factor of 30 is then applied 3 for extrapolating from animals to humans and 10 for human variability. Further details on this MRL can be found in the MRL worksheets in Appendix A of this profile. [Pg.168]

It was found that nitric oxide plays a very important role in cystic fibrosis. In contrast to most inflammatory airway diseases (for example, asthma), exhaled NO decreased in cystic fibrosis, and nitric oxide deficiency may contribute to the bronchial obstruction [278]. Bebok et al. [279] demonstrated that NO levels in the vicinity of airway cells during inflammation are... [Pg.934]

Some studies of survivors of massive chlorine exposures have shown either persistent obstructive or restrictive deficits, but pre-exposure data on these patients were not available. Persistent respiratory symptoms, bronchial obstruction, and bronchial hyperresponsiveness were observed in 82%, 23%, and 41 % of chronically exposed pulp mill workers, respectively, 18-24 months after cessation of exposure." In most cases it is not known whether prolonged symptoms after chlorine exposure are due to aggravation of preexisting conditions such as tuberculosis, asthma, chronic obstructive pulmonary disease, or heart disease." "... [Pg.139]

Respiratory Bronchospasm dyspnea cough bronchial obstruction wheezing nasal stuffiness pharyngitis laryngospasm with respiratory distress asthma rhinitis sinusitis. [Pg.528]

Bronchial obstruction as seen in a variety of pulmonary disorders will be associated with greater local airflows and turbulence and this will result in localized deposition in the larger airways of the TB region. The bronchoconstriction of asthma has a greater influence on exhalation than inhalation and thus deposition by sedimentation may be greater than normal. [Pg.254]

Jappinen et al. (1990) exposed 10 subjects who had asthma to 2 ppm hydrogen sulfide for 30 min. On average, airway resistance was increased by 26.3% and specific airway conductance was decreased by 8.4% in the exposed subjects compared with control subjects. Although the changes were not statistically significant, 2 subjects showed changes of more than 30% in airway resistance and specific airway conductance, which indicate bronchial obstruction (Jappinen et al. 1990). [Pg.214]

Clavulanic acid has a very low immunogenic and allergenic potential in animals. The possible impact of its co-administration with other beta-lactam antibiotics is unknown (53). Two patients with IgE-mediated hypersensitivity to oral co-amoxiclav and positive skin tests for clavulanic acid, but not for penicillins, both tolerated oral amoxicillin. One patient was also challenged with clavulanic acid and developed urticaria, conjunctivitis, and bronchial obstruction (54). Since co-amoxiclav has been widely used since its introduction in 1981, the frequency of hypersensitivity reactions is low. The clinical data available on sulbactam and tazobactam are stiU hm-ited and do not allow an assessment of the frequency and pattern of associated hypersensitivity reactions (55). [Pg.504]

Malolepszy J, Boszormenyi Nagy G, Selroos O, Larsso P, Brander R. Safety of formoterol Turbuhaler at cumulative dose of 90 microg in patients with acute bronchial obstruction. Eur Respir J 2001 18(6) 928-34. [Pg.806]

Symptoms suggestive of bronchial obstruction occur only very rarely during isoniazid treatment (1). [Pg.1924]

Bronchospasm may be a consequence of penicUhn allergy (7-12). Acute severe dyspnea with cyanosis has also been observed without symptoms of bronchial obstruction or pulmonary edema (13). Specific mechanisms for such cases have yet to be identified. [Pg.2757]

Respiratory symptoms from rifampicin are very rare. They can be part of a flu-like illness with bronchial obstruction (18,19). [Pg.3041]

Cardiovascular reactions to tetracyclines have often been associated with other symptoms of hypersensitivity, such as urticaria, angioedema, bronchial obstruction, and arterial hypotension (37,56). Such reactions occurred in patients who had tolerated tetracyclines previously and were therefore considered as anaphylactic. [Pg.3334]

There have been a few cases of acute bronchial obstruction after the administration of a tetracycline (57). [Pg.3334]

In a comparison of different dosage regimens, inhaled tobramycin caused bronchial obstruction (12). However, after 10 minutes of inhalation, lung function returned to baseline the effect was independent of dose. [Pg.3437]

RESIDUAL VOLUME INCREASE BRONCHIAL OBSTRUCTION OF AIRFLOW... [Pg.356]

Figure 4 contains data from a subject exposed 1 hour to 6 p.p.m. of ozone, which may be regarded as a typical example of the effects of ozone above 5 p.p.m. First, the vital capacity is diminished from 5030 cc. down to 2905 cc. or to 57.7% of its original value. At the same time, the residual capacity is increased from 1730 to 2570 cc. The smaller vital capacity can easily be felt subjectively one is unable to expire very deeply. It should be assumed that the increase of residual capacity is nothing more than the decrease of vital capacity. But in summing up both to the total capacity, they do not compensate each other the total capacity is smaller after ozone exposure. There is one possible explanation The decrease of the vital capacity is caused by edematous fluid, the increase of the residual capacity by a bronchial obstruction which will not permit a complete opening of entries into the alveoli. Histological studies on animals after ozone exposure show that the alveoli may be filled with edematous fluid, but a real obstruction has not been observed. [Pg.357]

Booij Noord, H., de Vries. K., Sluiter, H.J. and Orie. N.G.M. (1972). Late bronchial obstructive reaction to experimental inhalation of house dust mite extract. Clin. Allergy 2,43-61. Boucek, RK. and Nobel, N.L. (1973). Histamine, norepinephrine and bradykinin stimulation of fibroblast growth and modification of serotonin response. Proc. Soc. Exp. Biol. Med. 144, 929-933. [Pg.74]

The acute MRL was established based on effects reported in humans with the critical effect of respiratory effects-bronchial obstruction (30% change in airway resistance). It is intended to protect for exposure occurring up to 14 days. [Pg.1361]

The problems of transplanted organs are legion, and lung transplantation is probably one of the most difficult transplants to maintain. Aerosol applications may play a role. Major problems include transplant rejection, pulmonary hypertension, infection, and progressive bronchial obstruction caused by an immune response in the airways. [Pg.456]

The main effect of lewisite on the upper respiratory tract is to produce necrosis of the epithelium, which is accompanied by the formation of a false diphtheria-type membrane which consists of sloughed epithelial cells, together with inflammatory cells and mucus. The membrane may become detached and cause bronchial obstruction. Widespread edema and congestion of the lungs occurs and they may acquire a greyish-red to purple hue. Areas of atelectasis and secondary emphysema are common. Secondary bronchopneumonia is common and a frequent cause of death (Vedder, 1926). [Pg.469]

However, the low intrinsic activity of this steroid hindered its widespread use. The glucocorticoid receptor affinity and the topical anti-inflammatory potency of fluocortin butyl (30)are severalfold lower than those of dexa-methasone (126). Fluocortin butyl ameliorated allergic rhinitis at daily doses of 2-8-mg divided into two to four daily inhalations (129, 130), but it did not protect against bronchial obstruction in bronchial provocation tests, even at 8-mg doses divided into four daily inhalations, in contrast to a 10 times lower dose of beclomethasone dipropionate (131). [Pg.550]

Bronchodilation is another property of belladonna alkaloids of potential usefulness. Due to relaxation of the smooth musculature of bronchial passageways, this effect has found applications in asthma and other pulmonary obstructive conditions. At one time the smoking of cigarettes made of stramonium leaves was popular. More recently, atropine, quater-nized with isopropyl bromide (Ipratropium, Fig. 8-13) has been introduced as an aerosol for inhalation. This renewed interest in antimuscarinics resulted in part from clarifications of the role of the parasympathetic system in bronchial obstructions. The availability of a potent agent such as atropine in a poorly absorbed form (i.e., quatemized) would minimize systemic effects following inhalation. Ipratropium bromide does not cross the BBB. It is longer acting and more bronchoselective than atropine methylbromide and exhibits no CNS effects. [Pg.364]

Timolol is contraindicated in patients with nnstabilized cardiac failure or bronchial obstruction, AV condnction disturbances of the second and third grade, nnstable insnlin-dependent diabetes, and severe peripheral arterial obstruction. The most common side effects are mnscnlar fatigne, cold hands and feet, symptomatic hypotension, and bradycardia. [Pg.693]

Bronchoconstriction, inflammation and loss of lung elasticity are the three most common processes that result in bronchial obstruction. Therapy for obstructive limg disease is aimed at preventing or reversing these processes. [Pg.85]

Systematic follow-up studies have been reported on after effects of exposure to the toxic gas on the population of Bhopal (Gupta et al. 1988 Rastogi et al. 1988 Sri-vastava et al. 1989 Saxena et al. 1988). The symptoms pertained to respiratory, gastrointestinal, cardiovascular, and musculoskeletal systems. The respiratory impairment involved bronchial obstruction, pulmonary defect, and ventilatory disorder. Behavior studies showed that visual perceptual response was severely affected. Among the biochemical parameters, there was an increase in hemoglobin values, lymphocyte and eosinophil counts, serum ceruloplasmin, and creatinine content in urine, while a decrease in blood glutathione was observed in the exposed people. [Pg.555]


See other pages where Bronchial obstruction is mentioned: [Pg.174]    [Pg.38]    [Pg.49]    [Pg.117]    [Pg.123]    [Pg.214]    [Pg.355]    [Pg.296]    [Pg.1412]    [Pg.46]    [Pg.96]    [Pg.97]    [Pg.727]    [Pg.2757]    [Pg.3218]    [Pg.131]    [Pg.121]    [Pg.224]    [Pg.224]    [Pg.244]    [Pg.535]   
See also in sourсe #XX -- [ Pg.279 ]

See also in sourсe #XX -- [ Pg.534 ]




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Obstruction

Obstructive

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