Cavities in the sinuses, the nose, and the back of the throat grow bigger, thus creating more space within the head to allow the voice to resonate. Occasionally, voice change is accompanied by unsteadiness of vocalization in the early stages of untrained voices. Due to the significant drop in pitch to the vocal range, people may unintentionally speak in head voice or even strain their voices using pitches which were previously chest voice, the lowest part of the modal voice register. History
Historical changes in the average age of puberty have had profound effects on the composing of music for childrens voices. The composer Joseph Haydn was known for typically singing parts in high pitches throughout his 17th year. Unchanged voices were in high demand for church choirs, which historically excluded women. The British cathedral choir ideal remains based on boy sopranos (or trebles), with the alto part executed by adult countertenors. In German-speaking countries, however, the alto parts are also sung by boys. Historically, a strategy for avoiding the shift altogether was castration. Castrati are first documented in Italian church records from the 1550s. Mozarts Exultate Jubilate, Allegris Miserere and parts of Handels Messiah were written for this voice, whose distinctive timbre was widely exploited in Baroque opera. In 1861, the practice of castration became illegal in Italy, and in 1878 Pope Leo XIII prohibited the hiring of new castrati by the church. The last castrato was Alessandro Moreschi, who served in the Sistine Chapel Choir.
Urinary fractional excretion potassium is high or inappropriately normal in the context of hypokalaemia, and high levels of urinary sodium and chloride are observed. Other clinical indicators include elevated serum renin and aldosterone in the bloodstream, and metabolic alkalosis. The symptomatic features of this syndrome are highly variable ranging from asymptomatic to mild manifestations (weakness, cramps) to severe symptoms (tetany, paralysis, rhabdomyolysis). Symptom severity is multi-factorial, with phenotypic expression varying amongst individuals within the same family. Genetic testing is another measure of identifying the underlying mutations which cause the pathologic symptoms of the disease. This mode of testing is available at select laboratories.Work-up to exclude the differential diagnosis of the electrolyte abnormalities is key. In Gitelman syndrome hypocalciuria is present, and a urine calcium:creatinine ratio may help distinguish it from Bartter syndrome as the two disorders can be clinically indistinguishable. Additionally in Bartter syndrome maximal urine concentrating ability is lost. Laxative abuse can mimic the serum electrolyte abnormalities, but fractional excretion of potassium will be low
Diuretic abuse could be suspected if urinary chloride excretion varies by time of day but may require a diuretic assay to detect
Surreptitious vomiting can cause metabolic alkalosis and hypokalaemia, but urinary chloride levels will be low
Medication history; Proton-pump inhibitors can cause an isolated hypomagnesaemia phenotype, and aminoglycosides such as gentamicin can cause a transient metabolic alkalosis with hypokalaemia and hypomagnesaemia that resolves 2–6 weeks after drug termination.