This pathogenetic model is indirectly supported by the clinical features of IPF, including an insidious onset over several years, relatively infrequent acute exacerbations, and failure to respond to immunosuppressive therapy. However, it is the belief of some researchers that the disease is a multi-mechanistic one, wherein the trigger for the disease may stem from abnormalities in any number of wound healing pathways, including the inflammatory response. Such abnormalities could occur in any number of the nine implicated pathways (clotting cascade, antioxidant pathways, apoptosis, inflammatory cytokines, angiogenesis and vascular remodelling, growth factors, surfactant and matrix regulatory factors), and that through further investigation into all nine, novel therapies and approaches could be proposed on a unique or case-by-case basis should attempts at treating or circumventing complications in any one pathway prove unsuccessful. A number of therapies that target fibroblast activation or the synthesis of extracellular matrix are currently in early testing or are being considered for development.Familial IPF accounts for less than 5% of the total of patients with IPF and is clinically and histologically indistinguishable from sporadic IPF. Genetic associations include mutations in pulmonary surfactant proteins A1, A2, C (SFTPA1, SFTPA2B) and mucin (MUC5B). A remarkable aspect of the MUC5B variant is its high frequency of detection, as it is found in approximately 20% of individuals with Northern and Western European ancestry and in 19% of the Framingham Heart Study population. Mutations in human telomerase genes are also associated with familial pulmonary fibrosis and in some patients with sporadic IPF (e.g. the TERT, TERC genes).
Adenoiditis is the inflammation of the adenoid tissue usually caused by an infection. Adenoiditis is treated using medication (antibiotics and/or steroids) or surgical intervention. Adenoiditis may produce cold-like symptoms. However, adenoiditis symptoms often persist for ten or more days, and often include pus-like discharge from nose. The infection cause is usually viral. However, if the adenoiditis is caused by a bacterial infection, antibiotics may be prescribed for treatment. A steroidal nasal spray may also be prescribed in order to reduce nasal congestion. Severe or recurring adenoiditis may require surgical removal of the adenoids (adenotonsillectomy). Signs and symptoms
Acute adenoiditis is characterized by fever, runny nose, nasal airway obstruction resulting in predominantly oral breathing, snoring and sleep apnea, Rhinorrhea with serous secretion in viral forms and mucous-purulent secretion in bacterial forms. In cases due to viral infection symptoms usually recede spontaneously after 48 hours, symptoms of bacterial adenoiditis typically persist up to a week. Adenoiditis is sometimes accompanied by tonsillitis. Repeated adenoiditis may lead to enlarged adenoids. Complications
Complications of acute adenoiditis can occur due to extension of inflammation to the neighboring organs. Cause
Viruses that may cause adenoiditis include adenovirus, rhinovirus and paramyxovirus. Bacterial causes include Streptococcus pyogenes, Streptococcus pneumoniae, Moraxella catarrhalis and various species of Staphylococcus including Staphylococcus aureus. Pathophysiology
It is currently believed that bacterial biofilms play an integral role in the harboring of chronic infection by tonsil and adenoid tissue so contributing to recurrent sinusitis and recurrent or persistent ear disease.