Define inhaled steroids

40 mcg inhaled twice daily, approximately 12 hours apart, is the recommended starting dose. For patients who do not respond adequately to 40 mcg after 2 weeks of therapy, increasing the dosage to 80 mcg twice daily may provide additional asthma control. The maximum recommended dosage is 80 mcg twice daily. The starting dosage is based on the severity of asthma, including consideration of the patients’ current control of asthma symptoms and risk of future exacerbation. Improvement in asthma symptoms can occur within 24 hours of the beginning of treatment and should be expected within the first or second week, but maximum benefit should not be expected until 3 to 4 weeks of therapy. Improvement in pulmonary function is usually apparent within 1 to 4 weeks after the start of therapy. The National Asthma Education and Prevention Program Expert Panel defines low dose therapy as 80 to 160 mcg/day, medium dose as 161 to 320 mcg/day, and high dose therapy as more than 320 mcg/day for children ages 5 to 11 years. The Global Initiative for Asthma (GINA) guidelines define low dose therapy as 100 mcg/day in this age group. Titrate to the lowest effective dose once asthma stability is achieved.

Family history is a risk factor for asthma, with many different genes being implicated. [67] If one identical twin is affected, the probability of the other having the disease is approximately 25%. [67] By the end of 2005, 25 genes had been associated with asthma in six or more separate populations, including GSTM1 , IL10 , CTLA-4 , SPINK5 , LTC4S , IL4R and ADAM33 , among others. [68] Many of these genes are related to the immune system or modulating inflammation. Even among this list of genes supported by highly replicated studies, results have not been consistent among all populations tested. [68] In 2006 over 100 genes were associated with asthma in one genetic association study alone; [68] more continue to be found. [69]

Lung disease: People with this condition often develop emphysema, with symptoms of a hacking cough, barrel-shaped chest, and difficulty breathing. If you have this condition and smoke or are exposed to tobacco smoke, it accelerates the appearance of emphysema symptoms and lung damage.

Liver disease: Alpha-1 antitrypsin deficiency also cause liver disease in some people with the condition, that include liver cancer, cirrhosis of the liver, an abnormally large liver (hepatomegaly), liver failure, and hepatitis. Liver damage from alpha-1 antitrypsin deficiency causes symptom of a swollen abdomen, swollen legs or feet, and jaundice.

Treatment of AATD depends upon the severity of symptoms. FDA approved drug for AATD is an orphan product called alpha-1-proteinase inhibitor (human), sold under the brand name "Prolastin."

Genetics play a role in the development of COPD. [9] It is more common among relatives of those with COPD who smoke than unrelated smokers. [9] Currently, the only clearly inherited risk factor is alpha 1-antitrypsin deficiency (AAT). [46] This risk is particularly high if someone deficient in alpha 1-antitrypsin also smokes. [46] It is responsible for about 1–5% of cases [46] [47] and the condition is present in about 3–4 in 10,000 people. [16] Other genetic factors are being investigated, [46] of which there are likely to be many. [11]

Define inhaled steroids

define inhaled steroids

Genetics play a role in the development of COPD. [9] It is more common among relatives of those with COPD who smoke than unrelated smokers. [9] Currently, the only clearly inherited risk factor is alpha 1-antitrypsin deficiency (AAT). [46] This risk is particularly high if someone deficient in alpha 1-antitrypsin also smokes. [46] It is responsible for about 1–5% of cases [46] [47] and the condition is present in about 3–4 in 10,000 people. [16] Other genetic factors are being investigated, [46] of which there are likely to be many. [11]

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