NURS 203 Lecture Notes - Cystic Fibrosis, Pseudomonas Aeruginosa, Golgi Apparatus
Document Summary
Cystic fibrosis growth alteration b/c mucous in ducts of the pancreas. See atrophy b/c block lumen of exocrine ducts, and pressure goes back to the glands and that pressure atrophies the glands, leading to malabsorption. Yes b/c eventually fibrose off the islet cells, leading to type i diabetes, too. Molecular bio: c"some 7 with 3 nucleotide deletion, and those 3 nucleotides codes for phenylalanine. So, you are def of phenylalanine in the cystic fibrosis transmembrane regulator protein (cftr). Most things, after they are made in the ribosome in the rer, have posttranslational modifications in the golgi apparatus, which is where the real defect is. The real problem is when it gets to the golgi apparatus it"s supposed to be modified and secreted to the cell surface. It ends up being degraded in the cell, and you end up having the cftr.
