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English to Italian Spanish to Italian Italian to Spanish
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Services
Interpreting, Translation
Expertise
Specializes in:
Medical (general)
Psychology
Medical: Pharmaceuticals
International Org/Dev/Coop
Science (general)
Biology (-tech,-chem,micro-)
Business/Commerce (general)
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Open to considering volunteer work for registered non-profit organizations
English to Italian: Urology (general text) General field: Medical Detailed field: Medical (general)
Source text - English Stephen W. Leslie; Shashank Singh.
Last Update: July 31, 2018.
Two hormones are involved in the determination of hourly urinary production.
Arginine vasopressin (AVP) is an antidiuretic hormone produced by the hypothalamus that is stored and released from the posterior pituitary gland (the hormone is manufactured by the magnocellular neurosecretory neurons in the paraventricular nucleus of the hypothalamus and the supraoptic nucleus). It is released when plasma osmolality decreases (hyponatremia) and when a patient has low blood pressure. AVP binds to the V2 receptors in the collecting ducts and distal renal tubules which increases water permeability and absorption in these areas, ultimately resulting in decreased urine production. A disruption of nocturnal arginine vasopressin (AVP) levels, where nocturia patients have a reduction in nighttime AVP levels, is a common etiology for nocturnal polyuria. AVP increases reabsorption of free water returned to the circulation from the filtrate in the renal collecting tubules, which results in reduced urine volume but higher urinary concentration. AVP also constricts arterioles, which increases peripheral vascular resistance and raises systolic blood pressure. AVP production is normally increased during sleep as part of the normal circadian rhythm cycle. When this surge is diminished or missing, increased nocturnal polyuria and nocturia will result. This normal diurnal variation tends to diminish or disappear in older individuals. Parkinson disease can also cause nocturnal polyuria through its effect on AVP. Other causes of decreased nocturnal AVP secretion include AVP receptor mutations, intrinsic renal disease, electrolyte abnormalities, congestive heart failure, sleep apnea, drug usage (lithium, diuretics, tetracyclines), and venous insufficiency with peripheral edema of the lower extremities.
Atrial natriuretic peptide (ANP) is a diuretic hormone made by cardiac muscle cells in the atria. It increases renal sodium excretion, which acts as a diuretic because extra water is also excreted. The muscle cells in the atria have volume receptors that respond to increased fluid and stretching of the atrial walls by releasing ANP which happens in congestive heart failure and uncontrolled hypertension. The goal of atrial ANP secretion is to reduce blood pressure and total blood volume through enhanced renal excretion of sodium and water. ANP has virtually the opposite effect of aldosterone, which increases renal sodium and water retention. ANP excretes sodium and water. Increased secretion of ANP may occur in patients with obstructive sleep apnea, which would then lead to a nocturnal natriuresis and increased nocturia. This effect occurs from increased airway resistance and negative intrathoracic pressure resulting in myocardial stretching and ANP production. Obstructive sleep apnea sufferers have been shown to have increased renal sodium and water excretion that are mediated by elevated plasma ANP levels. The ANP level can be reduced in patients with obstructive sleep apnea by the use of continuous positive airway pressure (CPAP).
Translation - Italian FONTE: Stephen W. Leslie; Shashank Singh.
Ultimo aggiornamento: 31 luglio 2018.
La produzione oraria di urine è determinata dall’azione di due ormoni.
Vasopressina (ADH): l’ADH è un ormone antidiuretico prodotto dall’ipotalamo che viene immagazzinato e rilasciato dalla neuroipofisi (l’ormone viene prodotto dai neuroni neurosecretori magnocellulari nel nucleo paraventricolare dell'ipotalamo e nel nucleo sopraottico). Viene rilasciato quando l’osmolalità plasmatica diminuisce (iponatriemia) e quando il paziente ha la pressione sanguigna bassa. L’ADH si lega ai recettori V2 nei dotti collettori e nei tubuli distali renali dove aumenta la permeabilità e il riassorbimento dell’acqua, comportando infine una riduzione della produzione di urine. Uno squilibrio dei livelli notturni di ADH, nei casi in cui i pazienti con nicturia presentano una diminuzione dei livelli notturni di ADH, è un’eziologia comune della poliuria notturna. L’ADH aumenta il riassorbimento dell’acqua libera tornata alla circolazione dal filtrato nei tubuli collettori renali, comportando la riduzione del volume di urine e l’aumento della concentrazione urinaria. Inoltre, l’ADH costringe le arteriole, fenomeno che aumenta la resistenza vascolare periferica e innalza la pressione sanguigna sistolica. La produzione di ADH aumenta normalmente durante il sonno nell’àmbito del regolare ciclo circadiano. Se detto incremento diminuisce o non si verifica, ne consegue un aumento della poliuria notturna e della nicturia. Tale variazione diurna normale tende a diminuire o a scomparire nei soggetti anziani. Anche la malattia di Parkinson può causare poliuria notturna mediante il suo effetto sull’ADH. Altre cause della riduzione della secrezione notturna di ADH comprendono mutazioni dei recettori dell’ADH, malattia renale intrinseca, squilibri elettrolitici, CHF, apnea del sonno, assunzione di farmaci (litio, diuretici, tetracicline) e insufficienza venosa con edema periferico degli arti inferiori.
Peptide natriuretico atriale (ANP): l’ANP è un ormone diuretico prodotto dai miociti atriali. Tale ormone aumenta l’escrezione renale di sodio agendo come diuretico dal momento che viene escreta anche l’acqua in eccesso. I miociti atriali presentano dei recettori di volume che rispondono all’aumento di liquido e alla distensione atriale rilasciando ANP, fenomeno che si verifica durante la CHF e l’ipertensione non controllata. La finalità della secrezione atriale di ANP è di ridurre la pressione sanguigna e il volume ematico totale mediante una maggiore escrezione renale di sodio e acqua. L’ANP ha sostanzialmente l’effetto opposto dell’aldosterone, il quale aumenta la ritenzione di sodio e acqua da parte dei reni. L’ANP espelle sodio e acqua. È possibile che si verifichi un aumento della secrezione di ANP in pazienti con apnea ostruttiva del sonno, il che può successivamente comportare natriuresi notturna e aumento della nicturia. Tale effetto si manifesta a livello di un aumento della resistenza delle vie respiratorie e della pressione intratoracica negativa, che comporta dilatazione del miocardio e produzione di ANP. È stato dimostrato che nei pazienti con apnea ostruttiva del sonno aumenta l’escrezione renale di sodio e acqua mediata da maggiori livelli di ANP nel plasma. È possibile ridurre i livelli di ANP in pazienti con apnea ostruttiva del sonno avvalendosi della pressione positiva continua delle vie aeree (CPAP).
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Translation education
Master's degree - Bologna University
Experience
Years of experience: 9. Registered at ProZ.com: Jun 2015.
Spanish to Italian (Università di Bologna, Scuola Superiore di Lingue Moderne per Interpreti e Traduttori, verified) English to Italian (Università di Bologna, Scuola Superiore di Lingue Moderne per Interpreti e Traduttori, verified) Italian to Spanish (Università di Bologna, Scuola Superiore di Lingue Moderne per Interpreti e Traduttori, verified) Italian to English (Università di Bologna, Scuola Superiore di Lingue Moderne per Interpreti e Traduttori, verified)
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Adobe Acrobat, Aegisub, memoQ, Microsoft Excel, Microsoft Word, Powerpoint, Subtitle Edit, Trados Studio
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Keywords: interpreter, translator, Italian interpreter, Italian translator, Spanish interpreter, Spanish translator