vasoconstriction, phosphodiesterases which increase cellular proliferation, increased serotonin levels which cause vasoconstriction all of which add to the pathogenesis of this disorder. The higher pressure in the pulmonary artery causes the right ventricle to work harder. It must push against the increased pressure. The right ventricle will compensate for the increased workload by enlarging and will eventually fail, causing cor pulmonale. o On CXR one will see an enlarged right ventricle and pulmonary artery. Non-specific manifestations include fatigue, chest pain, tachypnea, dyspnea on exertion, palpitations and cough. They will have signs of right sided heart failure as well. · Discuss the etiology, pathophysiology and clinical manifestations of Cor Pulmonale. o This condition is secondary to pulmonary artery hypertension. The right ventricle in normal physiology is not made to push against high pressures. In the setting of PAH, it must push against the higher pulmonary artery pressure and eventually fails. The person will have symptoms of right sided heart failure.
5 . Differentiate between the etiology, clinical manifestations, and pathophysiology of select pulmonary disorders in children. o Croup - upper respiratory infection which may be caused by a virus or bacteria that leads to inflammation and obstruction. Viral croup causes a subglottic edema which can lead to obstruction. · Clinical manifestations start with rhinorrhea, sore throat, and low- grade fever. They then develop a seal like, barking cough, hoarse voice and inspiratory stridor. Most cases resolve spontaneously; however, if they have upper airway obstruction, this must be treated. o Cystic Fibrosis - autosomal recessive disorder which results from a defective gene on chromosome 7. It is more common in Caucasians and the median age of diagnosis is 4 months old. The average life span is 30 years old. · CF affects the airways, gastrointestinal tract and reproductive tract. The cystic fibrosis transmembrane conductance regulator gene mutation results in the production of an abnormal protein called the cystic fibrosis transmembrane conductance regulator protein. This protein makes the chloride channel on the surface of many epithelial cells, especially those which line the airways, bile ducts, the pancreas, sweat ducts, paranasal sinuses and the vas deferens. Chloride intracellular balance is maintained in these cells by the chloride channels. The mutation results in a failure of the chloride channels. When the chloride channels fail, they are unable to secrete chloride out of the cell and the cell increases absorption of sodium. ↑ Na+ intracellularly → water moves intracellularly → less water on the epithelial surface tissues → increased viscosity of secretions from these tissues. · Effects in lungs Occlusion of airways, chronic inflammation, decrease in elastic recoil (difficulty with exhalation), and increased susceptibility to infections.
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- pulmonary edema