Asthma factors

Intrinsic asthma, also called idiopathic asthma, usually develops in adulthood. In intrinsic asthma allergic factors are not demonstrable. Episodes of intrinsic asthma may be triggered by a variety of stimuli, eg, emotional state, exposure to cold air, or inert dusts. Both intrinsic and extrinsic asthmatics can be prone to exercise-induced attacks. Individuals who experience a combination of extrinsic and intrinsic asthmatic reactions have mixed asthma. Status asthmaticus refers to an especially acute life-threatening asthma attack which is resistant to normal treatments and which may require hospitalization in order to stabilize the patient. 

Asthma A diseased condition of the lungs caused by pollution and other factors. 

Platelet activating factor (PAF) was first identified by its ability (at low levels) to cause platelet aggregation and dilation of blood vessels, but it is now known to be a potent mediator in inflammation, allergic responses, and shock. PAF effects are observed at tissue concentrations as low as 10 M. PAF causes a dramatic inflammation of air passages and induces asthma-like symptoms in laboratory animals. Toxic-shock syndrome occurs when fragments of destroyed bacteria act as toxins and induce the synthesis of PAF. This results in a drop in blood pressure and a reduced... 

Mixed asthma (caused by both intrinsic and extrinsic factors)... 

In patients with chronic asthma, question the patient concerning allergies, frequency of attacks, severity of attacks, factors that cause or relieve attacks, and any antiasthma drugs used currently or taken previously. 

Influenza vaccine. Influenza vaccine is recommended annually for children age > 6 months with certain risk factors (including but not limited to asthma, cardiac disease, sickle cell disease, HIV, diabetes see MMWR. 2001 50(RR-4) 1-44), and can be administered to all others wishing to obtain immunity. Children aged <12 years should receive vaccine in a dosage appropriate for their age (0.25 mL if age 6-35 months or 0.5 mL if age >3 years). Children aged <8 years who are receiving influenza vaccine for the first time should receive two doses separated by at least 4 weeks. 

The role of atopy in anaphylaxis has not completely been resolved. On the one hand there is for example no evidence of a higher risk of severe reactions in venom-allergic patients. A recent study by Sturm et al. [38] indicated that patients with high total IgE levels predominantly developed mild to moderate reactions. By contrast, atopy may increase the risk and severity of systemic reactions in beekeepers and their family numbers [39]. On the other hand, atopy and in particular allergic asthma are risk factors for food allergy and therefore are also important risk factors for food-induced anaphylaxis. This is most likely also true for exercise-induced anaphylaxis, but also non-IgE-dependent anaphylaxis induced by NSAIDs or contrast media. 

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. 

People known to be at risk for anaphylaxis should wear up-to-date medical identification such as a bracelet or other jewelry, or carry an Anaphylaxis Wallet Card listing their confirmed trigger factor(s), relevant co-morbidities such as asthma, and concurrent medications [45]. 

Other therapeutic uses of cannabinoid agonists have been reported. The potential of cannabinoids as a treatment for asthma is supported experimentally. A CBi agonist, (i )-methanandamide (21), inhibited nerve growth factor (NGF)-induced airway hyperresponsiveness in vivo [251]. The antipruritic effect of cannabinoids has been reported, the action being mediated by both CBi and CB2 pathways [252]. Treatment with cannabis extract improved urinary tract symptoms of multiple sclerosis patients significantly in an open-label pilot study [253]. 

Asthma results from a complex interaction of genetic and environmental factors however, the underlying cause is not well understood. There appears to be an inheritable component, as the presence of asthma in a parent is a strong risk factor for the development of asthma in a child. This risk increases when a family history of atopy is also present.13 Approximately 50% of asthma can be attributed to atopy, and atopic asthma is more common in children than adults.3 Furthermore, atopy in childhood asthma is the strongest prognostic factor for continued asthma as an adult.1,3... 

Genetic factors cannot explain the recent rapid rise in asthma prevalence. Asthma appears to require both genetic predisposition and environmental exposure. Many patients with occupational asthma develop the disease late in life upon exposure to specific allergens in the workplace. Environmental influences in utero or in infancy may contribute to the development of asthma. Maternal smoking during pregnancy or exposure to secondhand smoke after birth increases the risk of childhood asthma.3 Adult-onset asthma is not uncommon and may be related to atopy, nasal polyps, aspirin sensitivity, occupational exposure, or a recurrence of childhood asthma. 

Th2 lymphocytes are one of the primary factors initiating and perpetuating the inflammatory response.7 In addition, proinflammatory mediators such as the leukotrienes generated during mast cell degranulation can increase vascular permeability, leading to airway edema and increased mucus production.8 Eosinophilic infiltration of the airways is a hallmark of asthma, and activated eosinophils can cause bronchoconstriction and AHR.9... 

Major factors that may contribute to the severity of asthma include allergens typically associated with atopy chemical exposures in occupational environments and exposure to tobacco smoke, irritants, and indoor and outdoor pollution. Other factors include concurrent disease states or medications that may worsen asthma severity. 

Provide education on self-management or parent education on asthma management and controlling environmental factors that make asthma worse (e.g., allergens and irritants). 

Gather patient history. Assess factors involved in drug selection. Inquire about social history and alcohol use. Ask the patient about drug allergies and chronic health problems such as asthma. 

Improvement in symptoms should occur within 48 to 72 hours after initiation of therapy for most patients with CAP. Response to therapy could be slowed in patients with underlying pulmonary disease such as moderate to severe asthma, COPD, or emphysema. In patients not responding to therapy with no underlying factors that would suggest a slowed response to therapy, then other infectious and noninfectious reasons must be considered. The infection could be caused by a pathogen not covered by the initial therapy, a drug-resistant isolate could be present, or more severe infection could be present (nonpulmonary), and the patient should be... 

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,... 

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