some babies are born with a lung disease, what is it called?
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I wonder if you are thinking about RDS or respiratory distress syndrome.  Infant RDS is a life threatening lung disorder that commonly affects premature infants.  This is caused by low blood oxygen levels in the air sacs of the lungs.
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Pleuro means lungs\nParenchymatosis means the bulk tisse inside lungs\nosis means condition of (-itis means inflammation)
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Pulmonary fibrosis, a progressive scarring of the lungs.
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Chronic obstructive pulmonary disease (COPD) is a general term for a group of diseases that cause progressive damage to your lungs. These diseases include chronic bronchitis, asthma and emphysema. Of the more than 16 million Americans with COPD, nearly 3 million have symptomatic emphysema and millions more are in the early stages of the disease before signs and symptoms appear.\n\nUnlike asthma, which occurs when the muscles in your airways tighten, emphysema causes a loss of elasticity in the walls of the small air sacs in your lungs. Eventually, the walls stretch and break, creating larger, less efficient air sacs that aren't able to handle the normal exchange of oxygen and carbon dioxide.\n\nWhen emphysema is advanced, you must work so hard to expel air from your lungs that breathing can consume up to 20 percent of your resting energy. Unfortunately, because emphysema develops gradually over many years, you may not experience symptoms such as shortness of breath until irreversible damage has already occurred. Treatments focus on relieving symptoms and avoiding complications.\n\nreduced capacity for physical activity, both of which are likely to become worse as the disease progresses. In time, you may have trouble breathing even when lying down, and it may be especially hard to breathe during and after respiratory infections, such as colds or the flu.\n\nOther signs and symptoms of emphysema include:\n\nChronic, mild cough. You may produce sputum or phlegm when you cough. \nLoss of appetite and weight loss. It's a vicious cycle. Emphysema can make eating more difficult, and the act of eating can rob you of your breath. The result is that you simply may not feel like eating much of the time. \nFatigue. You're likely to feel tired both because it's more difficult to breathe and because your body is getting less oxygenWhen you inhale, air travels to your lungs through two major airways called bronchi. Inside your lungs, the bronchi subdivide like the roots of a tree into a million smaller airways (bronchioles) that finally end in clusters of tiny air sacs (alveoli). You have about 300 million air sacs in each lung. Within the walls of the air sacs are tiny blood vessels (capillaries) where oxygen is added to your blood and carbon dioxide — a waste product of metabolism — is removed. The air sac walls also contain elastic fibers that help them expand and contract like small balloons when you breathe.\n\nWhat happens in emphysema\nIn emphysema, inflammation destroys these fragile walls of the air sacs, causing them to lose their elasticity. As a result, the bronchioles collapse, and air becomes trapped in the air sacs, which overstretches them and interferes with your ability to exhale (hyperinflation).\n\nIn time, this overstretching may cause several air sacs to rupture, forming one larger air space instead of many small ones. Because the larger, less-elastic sacs aren't able to force air completely out of your lungs when you exhale, you have to breathe harder to take in enough oxygen and to eliminate carbon dioxide.\n\nThe process works something like this: Normally, you exhale in two ways, actively and passively. When you exert yourself and need more oxygen, your chest muscles contract, forcing air out rapidly. On the other hand, when you sit quietly, your diaphragm contracts and your chest muscles expand to take air in, but your muscles don't actively contract to let the air out. Instead, the elastic tissue around your air sacs contracts, and your lungs passively shrink.\n\nBut if you have emphysema, many of these elastic fibers have been destroyed, and you must consciously force air out of your lungs. The forced exhalation compresses many of your small airways, making expelling air even more difficult.\n\nMost common cause is smoking\nCigarette smoke is by far the most common cause of emphysema. The damage begins when tobacco smoke temporarily paralyzes the microscopic hairs (cilia) that line you
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Congenital diseases are ones inherited from your parents.  Basically, it means you were born that way and it may be an insult to the parents of the person also...
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COPD is generally one of two related conditions, either chronic bronchitis or emphysema, although in some cases asthma can become a form of COPD if there is permanent damage to the airways from chronic inflammation. And sometimes there can be overlap - patients with chronic bronchitis may also have symptoms of emphysema, for example.\n\nYes, in rare cases (less than 1%) COPD can be hereditary. If it is due to asthma, then again it can be hereditary, since asthma does tend to run in families.\n\nAs you probably already know, smoking accounts for the majority of COPD (like 90%). \n\n"Another well-established cause of COPD is a deficiency of alpha-1 antitrypsin (AAT). AAT deficiency is a rare genetic (inherited) disorder that accounts for less than 1% of the COPD in the United States.\n\nAs discussed previously, normal function of the lung is dependent on elastic fibers surrounding the airways and in the alveolar walls. Elastic fibers are composed of a protein called elastin. An enzyme called elastase that is found even in normal lungs (and is increased in cigarette smokers) can break down the elastin and damage the airways and alveoli. Another protein called alpha-1 antitrypsin (AAT) (produced by the liver and released into the blood) is present in normal lungs and can block the damaging effects of elastase on elastin.\n\nThe manufacture of AAT by the liver is controlled by genes which are contained in DNA-containing chromosomes that are inherited. Each person has two AAT genes, one inherited from each parent. Individuals who inherit two defective AAT genes (one from each parent) have either low amounts of AAT in the blood or AAT that does not function properly. The reduced action of AAT in these individuals allows the destruction of tissue in the lungs by elastase to continue unopposed. This causes emphysema by age 30 or 40. Cigarette smoking accelerates the destruction and results in an even earlier onset of COPD.\n\nIndividuals with one normal and one defective AAT gene have AAT levels that are lower than normal but higher than individuals with two defective genes. These individuals are not believed to have an increased risk of developing COPD if they do not smoke cigarettes; however, their risk of COPD probably is higher than normal if they smoke." from \nhttp://www.medicinenet.com/chronic_obstructive_pulmonary_disease_copd/page4.htm
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collapsed lungs have nothing to do with genetics or relation to someone that had a collapsed lung. They are caused by disease and trauma and thats about it. Yeah sure you have the possiblity of getting sick or getting in a car wreck and getting one that way but it has nothing to do with your mother's first child.
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The below links should give you an overview, and refer you to other sources for more info.  Of course, the best info will come from a physician:\n\nhttp://www.answers.com/bronchiectasis\n\nhttp://www.lungusa.org/site/pp.asp?c=dvLUK9O0E&b=35009\n\nhttp://www.nlm.nih.gov/medlineplus/ency/article/000144.htm\n\nhttp://www.bronchiectasis.info/\n\nhttp://www.nhlbi.nih.gov/health/dci/Diseases/brn/brn_whatis.html\n\nhttp://images.google.com/images?q=bronchiectasis&hl=en&btnG=Search+Images
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have you ever heard of pnemoconiosis, or pulmonary fibrosis. it is a restrictive lung disease that can be cause by exposure to certain enviromental causes. The one that i am most familar with is black lung from working in coal dust (most cases of pulmonary fibrosis in my area is from that). But surly sand would cause the same effect if you are exposed to a lot of sand storms.
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high blood pressure, decreased fertility, heart disease, asthma, lung disease, emphysema, chronic pneumonia, various cancers, etc.\nWomen are likely to have babies that are low birthweight also.
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If you are talking about pneumonoultramicroscopicsilicovolcanoconiosis, it's a pnuemoconiosis caused by the inhallatation of very fine silicate or quartz dust.  In other words, a black lung disease
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no, but it can aggravate them. For example, i have had pneumonia twice because my lungs are weak and prone to that, also I frequently get bronchitis.
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pneumonoultramicroscopicsilicovolcanoconiosis \n\nMeaning? \n\nA lung disease.
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Lung infiltrates is a term that is used to describe the appearance of any abnormal substance that has accumulated in the lungs.  Lungs usually appear very dark on an xray because they contain mostly air which allows the xrays through very easily.  If the lungs start accumulating fluid or pus, for example, fewer of the xrays will make it through to the film and those areas appear whiter.  The white areas are called infiltrates.  Infiltrates can represent many things including pneumonia and other infections, tuberculosis, pulmonary edema, and hemorrhage, just to name a few.
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hemoglobin carries oxygen and crosses the placenta from mother to child.  they don't actually breathe until they are born, until that time their oxygen comes from their mothers.
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Cystic fibrosis (CF), also called mucoviscidosis, is an autosomal recessive hereditary disease that affects the lungs, sweat glands and the digestive system.\n\nCF was first described as a disease in the late 1930s. It is the most common genetic disease among people with European ancestry. Approximately one in every 25 people of European descent is a carrier for the cystic fibrosis gene, having one normal gene and one CF gene. Since cystic fibrosis is recessive, both copies of the gene have to be CF genes to cause the symptoms that occur in about 1 in every 2500 children. The high incidence of this lethal gene can be explained by the fact that CF carriers, who don't show any symptoms, enjoy some protection against cholera, since the extreme water loss in the intestines is prevented. People from areas where cholera is not a problem show a much lower incidence of CF. Genetic counseling and genetic testing is recommended for families who may be carriers of cystic fibrosis.\n\nIn 1988, the gene for CF was discovered by Francis Collins and Lap-Chee Tsui on the seventh chromosome of the human genome.
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Q. What is Emphysema?\nFAQ\n\nFrom Stacey Lloyd,\nYour Guide to Lung Diseases.\n\nA.\n\nEmphysema is a lung disease in which the walls of the alveoli (air sacs) in the lungs fracture or burst. As these alveoli break, the remaining alveoli become enlarged to make up for the loss. This results in a fewer number of alveoli, with many enlarged. \nWhen alveoli are enlarged, they loose their elasticity. A loss of elasticity in the alveoli results in the inability to eliminate air from the lungs. Therefore, patients must use force (energy) to expel this air. \n\nFurthermore, the loss of elasticity in the lungs affects the smaller bronchial tubes. To push air out of the bronchial tubes, a higher pressure must be developed inside the chest. \n\nThis higher pressure tends to collapse the smaller bronchial tubes, making it even more difficult to empty air from the alveoli. \nCoughing becomes very difficult and ineffective in expelling mucus, leaving the lungs more susceptible to lung infections, such as pneumonia. \n\n( http://lungdiseases.about.com/od/emphysema/f/emphysema_expl.htm )\n\nWhat causes emphysema?\nEmphysema can be caused by one or a combination of these things:\n\nCigarette smoking: Most cases of emphsyema are caused by cigarette smoking. Cigarette smoke reaches deep into the lungs and causes permanent damage. If you have emphysema from cigarettes, the best way to stop your lung damage is to quit smoking as soon as possible. It's never too late to quit smoking. \nAlpha-1 Antitrypsin deficiency: Some people have emphsyema because of a rare genetic disorder called Alpha-1 Antitrypsin deficiency. People with Alpha-1 are missing an enzyme that protects their lungs. Some people with Alpha-1 deficiency get emphysema without ever having smoked. Other people get emphsyema from the combination of smoking and having Alpha-1 deficiency. \nAir pollution: There is some evidence that air pollution can contribute to people getting emphysema, especially if the person also smokes. ( http://www.lung.ca/diseases-maladies/a-z/emphysema-emphyseme/index_e.php#causes )