Cystic Fibrosis (often referred to as 'CF') is an inherited condition. It has an autosomal recessive pattern of inheritance - sounds fancy we know, all it means is that a person with CF has received a faulty gene from both their mother and their father. If they receive one faulty gene from their mother, but the normal gene from their father - they will not have the disease, instead they will be a carrier of the mutation. In places such as Ireland, one in every twenty people are carriers of the faulty, CF gene. If a couple are both carriers of the CF gene, the chances of their child having cystic fibrosis is 25%. Just for you curious geeks out there, the most common gene mutation is 'ΔF508', a deletion of part of the CFTR gene on Chromosome 7. 

The CFTR gene (cystic fibrosis transmembrane conductance regulator) is a gene responsible for the production of a protein that lines mucous and sweat producing cells. It ensures that our mucous isn't too thick. Not only in our lungs, but all over the body. 
It also controls the amount of salt released in our sweat - which is why a helpful test for diagnosing CF is "the sweat test", whereby an abnormally salty sample can suggest CF.

A problem with the CFTR gene will render the mucous thicker than it should be, leading to clogging problems in the lungs airways, in the intestines, in the pancreas (preventing the delivery of digestive enzymes), etc. The result - cystic fibrosis affects more than just the lungs, but let's start with them. 

Thickened mucous in the lungs airway increases the risk of developing both common and uncommon chest infections - as the excess mucous acts as a bacterial breeding ground. CF patients can often end up in hospital a few times a year being treated for infections with IV antibiotics. To prevent this, one of the mainstays of treatment is respiratory physiotherapy - essentially techniques to keep the chest as clear as possible. To aid the patients efforts, many medications are utilised to thin the mucous.

There are constant improvements in the expensive medications also, the ones that attempt to replace the function of the faulty CFTR gene (such as manipulation of the chloride channels) - essentially trying to thin the mucous at the source. 

Aside from the lungs, CF patients often experience issues with their digestion. The thickened mucous in the bowel makes the progression of food content through the intestines more challenging, and when the food finally makes its way through, it cannot be effectively broken down and absorbed due to the blockage of pancreatic enzymes. 
Creon is a mainstay of CF treatment for this reason - it acts as a substitute for the pancreatic enzymes, allowing appropriate digestion. This is supplemented with various vitamins. 

There is certainly more to know than what we have covered here, as any CF patient would tell you - but we hope it acts as a good, simple introduction!