As the disease progresses, occurrence of secondary symptoms such as dysphagia, pneumonia, acute respiratory distress syndrome, failure to thrive, and recurrent upper respiratory infections can be diagnosed. The risk of laryngeal papillomatosis spreading to the lungs is higher in the juvenile-onset than the adult-onset. In children, symptoms are usually more severe and often mistaken for manifestations of other diseases such as asthma, croup or bronchitis. Therefore, diagnosis is usually delayed. Cause
Laryngeal papillomatosis is caused by human papillomavirus (HPV) infection, most frequently types 6 and 11 although genotypes 16, 18, 31, and 33 have also been implicated. HPV-11 is associated with more aggressive forms of papillomatosis, which may involve more distal parts of the tracheobronchial tree. The mode of viral inoculation is hypothesized to vary according to age of disease onset. The presence of HPV in the respiratory tract does not necessarily result in the development of laryngeal papillomatosis. Other factors that could be involved include immunodeficiency or other similar infections. For example, laryngeal papillomatosis may become more aggressive due to the presence of certain viruses (e.g., herpes simplex virus, Epstein–Barr virus).The disease occurs in two forms, juvenile and adult papillomatosis, based on whether it develops before or after 20 years of age. The juvenile form is generally transmitted through contact with a mothers infected vaginal canal during childbirth. Less is known about transmission in the adult form of this disease, though oral sex has been implicated as a potential mode of transmission.
Post-Partum Hemorrhaging (PPH) is believed to be a predictor of Sheehan’s syndrome, so the symptoms of anaemia, obesity, and advanced maternal age may increase the risk of Sheehan Syndrome. Atony of the uterus may be related to PPH that could induce Sheehan’s syndrome. This results in the abnormally prolonged flow of blood to the placenta after delivery. Pathophysiology
Sheehans syndrome is caused by damage to the pituitary, thereby causing a decrease in one or more of the hormones it normally secretes. The anterior pituitary is supplied by a low pressure portal venous system. A 1995 study found that 56.2% of patients with diagnosed Sheehan’s syndrome experienced a loss of all pituitary hormones (with the remaining 43.8% having selective pituitary insufficiency). Since the growth hormone-secreting cells are located at the periphery of the pituitary (and are therefore most likely to be affected by ischemia), all of the patients experienced growth hormone deficiency. Diagnosis
Hormonal assays are conducted to determine a patient has low levels of T4, TSH, estrogen, gonadotropin, cortisol, and ACTH depending on the extent of necrosis. It might be difficult to detect damage to these hormone pathways if hormone levels are at the borderline of the abnormal range. In this case, stimulation tests will be done to determine if the pituitary is responsive to hypothalamic hormones. For example, to determine deficiencies in cortisol release, synthetic ACTH might be administered, and hormonal assays will be conducted to determine the strength of the response. Additionally, MRI of the pituitary and hypothalamus: this helps to exclude tumor or other pathologies.