Serious Symptoms Of Cystic Fibrosis

Frequent Shortness Of Breath

Individuals affected by cystic fibrosis can experience frequent shortness of breath as a symptom of their disease. Healthy individuals produce mucus with thin and slippery properties, and it serves as a lubricant for the respiratory and digestive tracts. When a patient's body produces thick and sticky mucus, these secretions can plug up numerous tubes in the digestive system, ducts, and lung passageways. The reduced amount of space air has to pass into the alveoli can cause the individual to feel like they cannot breathe in enough air. In addition, cystic fibrosis increases the occurrence of pneumothorax or a condition where air accumulates in the space that separates the chest wall from the lungs. This malfunction places pressure on the exterior of the lungs causing the passageways to become even more narrowed, resulting in severe chest pain and shortness of breath. An inflammatory component called neutrophil elastase can cause elastin degradation and the production of IL-8 in epithelial cells. Therefore, it acts as a secretagogue and contributes to impaired gas exchange, structural damage, and end-stage lung disease. Cystic fibrosis causes the airway walls to become thinner over time and can cause severe damage to the lungs, impairing their function. A combination of one or more of these factors can cause frequent episodes of breathlessness.

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Frequent Pneumonia

Frequent pneumonia infections can be indicative of cystic fibrosis. This symptom is most prevalent in older children and adults affected by cystic fibrosis. The thick and sticky mucus can easily accumulate and clog up the tubes within the lungs of cystic fibrosis patients. This thick mucus also commonly clogs up the openings to the sinuses, the small air pockets behind the cheekbones, nose, eyes, and forehead. Both types of blockages create a hospitable environment and breeding ground for pathogens such as bacteria and fungi. In the immune system of cystic fibrosis patients, complement receptors including CR1, C3bi, and IgG are split into simpler molecules by neutrophil elastase. This dismantling process results in the failure of a process called opsonophagocytosis, or the process of ingesting and destroying foreign pathogens and particles by phagocytes initiated by an opsonin. This malfunction results in a vicious recurrent infection and neutrophilic inflammatory cycle that results in further irritation and damage of the lung tissues. Due to this impairment, the bacteria that invade the lungs become persistent and hard to fight off, leading to repeated infections or frequent pneumonia.