Asthma types

Sudden severe attack Sudden severe attacks on a background of well controlled asthma Brittle asthma Type 2... 

Bronchial asthma types, modes of prevention, agents used for treatment and their use in asthma of varying degrees of severity... 

Thrasher et al. 1987, 1990). Elevated serum levels of IgE antibodies and respiratory tract symptoms were foimd in groups of children exposed to classroom air concentrations of 0.075, 0.069, and 0.043 ppm formaldehyde (Wantke et al. 1996a). However, the relevance of these findings to the possibility of respiratory tract sensitization to formaldehyde is uncertain because the elevated levels of IgE were not correlated with the number and severity of symptoms, and the symptoms were more indicative of irritant responses than asthma-type responses expected to be mediated through IgE antibodies. 

Another group of researchers found that patients with asthma can be subdivided into two types based on the amount of muscle present in the airways at autopsy. Their data are presented in Table 5. Lungs were selected from patients with or without bronchial asthma. Type 1 patients showed an increase in the amount of muscle in the larger airways, whereas type 2 patients demonstrated an increase in the amount of muscle in large and smaller airways (21). 

Properties Yel. liq. solvent-like odor sp.gr. 0.96 g/ml dens. 7.99 Ib/gal vapor pressure 6 mm Hg flash pt. (Seta) 30 C ref. index 1.480 Toxicology Inh. and/or repeated skin contact h caused injury to liver, kidney, brain, respiratory system, blood and/or bone marrow in lab animals may aggravate some skin and asthma-type condtions TSCA listed Precaution Flamm. flamm. limits 1.0-10.8% vol. in air eliminate all sources of ignition ventilate if indoors keep away from strong oxidizing materials... 

Acute effects are of short duration and appear fairly rapidly, usually during or after a single or short-term exposure to a hazardous substance. Such effects may be severe and require hospital treatment but are usually reversible. Examples include asthma-type attacks, nausea and fainting. 

Toxicology May aggravate some skin and asthma-type conditions, and pre-existing iiver and/or kidney disorders TSCA iisted Precaution Contains43% Stod, soiv, 5% 2-butoxyethanoi flamm. fiamm. iimits 0,6-10,6% voi, in air... 

Rhinitis is characterized by nasal stuffiness with partial or full obstmction, and itching of the nose, eyes, palate, or pharynx, sneezing, and rhinorrhoea. If left untreated it can lead to more serious respiratory diseases such as sinusitis or asthma. Although several types of dmgs are available for treatment, nasal spray topical corticosteroids are widely regarded as the reference standard in rhinitis therapy (250). 

Patients having high plasma renin activity (PRA) (>8 ng/(mLh)) respond best to an ACE inhibitor or a -adrenoceptor blocker those having low PRA (<1 ng/(mLh)) usually elderly and black, respond best to a calcium channel blocker or a diuretic (184). -Adrenoceptor blockers should not be used in patients who have diabetes, asthma, bradycardia, or peripheral vascular diseases. The thiazide-type diuretics (qv) should be used with caution in patients having diabetes. Likewise, -adrenoceptor blockers should not be combined with verapamil or diltiazem because these dmgs slow the atrioventricular nodal conduction in the heart. Calcium channel blockers are preferred in patients having coronary insufficiency diseases because of the cardioprotective effects of these dmgs. 

Chronic Pulmonary Toxicity Chronic damage to the lungs may be due to several subsequent exposures or due to one large dose that markedly exceeds the capacity of pulmonary defense, clearance, and repair mechanisms. Chronic pulmonary toxicity includes emphysema, chronic bronchitis, asthma, lung fibrosis, and lung cancer. The single most important reason for chronic pulmonary toxicity is tobacco smoke, which induces all types of chronic pulmonary toxicity, with the exception of fibrosis. 

In addition to the proteins discussed above, a large number of reactive chemicals used in industry can cause asthma and rhinitis. Hypersensitivity pneumonias have also been described. Isocyanates and acid anhydrides are industrial chemicals that cause occupational asthma. Acid anhydrides, such as phthalic anhydride, seem to cause mainly type I reactions, whereas the IgE-mediated mechanism explains only a part of the sensitizations to isocyanates. Several mechanisms have been suggested, but despite intensive research no models have been generally accepted. The situation is even more obscure for other sensitizing chemicals therefore, the term specific chemical hypersensitivity is often used for chemical allergies. This term should not be confused with multiple chemical sensitivity (MCS) syndrome, which is a controversial term referring to hypersusceptibility to very low levels of environmental chemicals. ... 

Saussurea Cappa Clarke. The root contains saussurine i which, according to Prasad, accounts for the effect of the drug in controlling attacks of bronchial asthma, especially of the vagotonic type. ((1) Ghosh, Chatterjee and Dutta, J. Ind. Chem. Soc., 1929, 6, 517 (2) Ind. J. Pharm., 1945, 7, 81.)... 

FIGURE 9.11 An example of a cellular system designed to study inflammatory processes related to asthma and arthritis. Multiple readouts (ELISA measurements) from each of four cell types are obtained under conditions of four contexts (mixture of stimulating agents). This results in a complex heat map of basal cellular activities that can be affected by compounds. The changes in the heat map (measured as ratios of basal to compound-altered activity) are analyzed statistically to yield associations and differences. 

Leukotrienes are rapidly produced and released during a Type I reaction (Fig. 3). They are responsible for a massive bronchoconstriction in allergic bronchial asthma and attract leukocytes, thus being proinflamma-tory. Consequently, antagonists of the LTC recqDtor have been proven useful in the therapy of bronchial asthma, often in combination with bronchodilators (example montelukast). 

About 90% of all asthmatics have increased serum IgE levels and suffer from Type I allergy, called extrinsic (allergic) asthma. 

Adrenergic receptor 2 Amino acid variants appear to be associated with receptor function and agonist induced down regulation. Some variants may predispose to some types of asthma and modulate action of (3-2-adrenergic drugs. 

Asthma is a reversible obstructive disease of the lower airway. With asthma there is increasing airway obstruction caused by bronchospasm and bronchoconstriction, inflammation and edema of the lining of the bronchioles, and the production of thick mucus that can plug the airway (see Pig. 37-1). There are three types of asthma ... 

Along with the bronchodilators, several types of dragp are effective in Hie treatment of asthma. These include corticosteroids, leukotriene formation inhibitors, leukotriene receptor agonists, and mast cell stabilizers. 

The thiazide diuretics are contraindicated in patients with known hypersensitivity to the thiazides or related diuretics, electrolyte imbalances, renal decompensation, hepatic coma, or anuria. A cross-sensitivity reaction may occur with the thiazides and sulfonamides. Some of the thiazide diuretics contain tartrazine, which may cause allergic-type reactions or bronchial asthma in individuals sensitive to tartrazine. 

Munthe-Kaas MC, Carlsen KH. Haland G. Devula-palli CS, Gervin K, Egeland T. Carlsen KL. Undlien D T cell-specific T-box transcription factor haplo-type is associated with allergic asthma in childrea J Allergy Chn Immunol 2008 121 51 -56. 

Three years after introduction of aspirin into therapy, Hirschberg in Poznan, now in Poland, described the first case of a transient, acute angioedema/urticaria, occurring shortly after ingestion of aspirin. Reports of anaphylactic reactions to aspirin soon followed. The other major type of adverse reaction, acute bronchospasm, was described in the second decade of the 20th century. In 1920, Van der Veer reported the first death due to aspirin. The association of aspirin sensitivity, asthma and nasal polyps was first recorded by Widal in 1922. This clinical entity, later named the aspirin triad was popularized in 1968 by Samter and Beers [3], who presented a... 

In general, treatment of the asthma underlying NSAlDs sensitivity should follow standard asthma guidelines. This type of asthma is often severe and frequently high doses of inhaled corticosteroids and daily doses of oral corticosteroids are necessary. A special treatment option is a chronic desensitization to aspirin [8]. Desensitization and aspirin maintenance is routinely used in some centers for treatment of chronic rhinusinusitis with nasal polyposis. It is the only available procedure which allows AIA patients with ischemic heart disease to use aspirin. During the state of desensitization to aspirin, not only aspirin but almost all strong NSAIDs are tolerated, so desensitization and NSAID maintenance could be used for treatment of rheumatic disease or chronic pain syndromes. 

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