Imagine you are walking through the park; it’s a warm day, you are surrounded by beautiful flowers, grass, and trees. Now imagine that these normal, everyday activities such as, walking outside on a humid day, make it more difficult for you to breathe. Instead of taking a normal breath, you are only able to inhale at thirty percent capacity. That is like breathing through the end of a tiny crimped straw. Also, imagine having to carry various inhalers and oxygen as part of an everyday routine. This is how it feels to have Alpha-1 Antitrypsin Deficiency, also known as early onset emphysema. For someone with Alpha-1 Antitrypsin Deficiency, everyday tasks can seem nearly impossible. Simply walking upstairs or raking leaves …show more content…
· Alpha-1 level test – determines the amount of Alpha-1 Antitrypsin in a persons’ blood.
To confirm the severity of the disease other tests may be done such as, chest x-rays and Computerized Automatic Tomography (CAT) scans. The chest x-ray examination may reveal a barrel-shaped chest. Also, listening to the chest with a stethoscope may reveal wheezing, crackles, or decreased breath sounds.
7.0 TREATMENT As far as treatments for Alpha-1 Antitrypsin Deficiency, there is currently no cure, but there are ways to relieve symptoms and to slow down the advancement of the lung disease. The first defense of treatment given to individuals with Alpha-1 Antitrypsin Deficiency is bronchodilators. Bronchodilators are medications used to relax the muscles around the airways, helping the airways to open up, making it easier to breathe. Bronchodilators are administered by a portable inhaler or by a nebulizer. Also there is a Proteinase Inhibitor, i.e. ProlastinÒ, available that is used as a replacement therapy for the deficient Alpha-1 Antitrypsin. ProlastinÒ is administered intravenously. Methods used intravenously are a catheter inserted into a vein in the arm, or through a subcutaneous pre-inserted port. Therapeutic administration of ProlastinÒ is typically 60mg/kg body weight weekly. In some cases, an individual might develop end stage lung disease making a lung transplant …show more content…
All my life I have grown up watching my father, Daniel Gift, suffer from this disease. Before he started showing symptoms of A1AT Deficiency, he was an active, hard working, daily exercising adult. Unfortunately he was a smoker, which increased the effects of Alpha-1 Antitrypsin Deficiency. It wasn’t until he was about 35 years old when he started showing signs of early onset emphysema. Within ten years of his diagnosis he was unable to continue working and could no longer be involved in outdoor activities with his family. In the summer my mom, sister, brother and I would go to the pool almost everyday coming home to my dad who was stuck in the house all day. The chlorine in the water and the hot sun was too much for him to handle. When inhaled the chlorine causes an asthmatic attack. The effects of the medication prevent him from being in the sun. My brother was never able to go outside and throw the football or play catch with my dad because of excursion. Also, my dad has to circumvent contact with other people to avoid contracting potential colds and