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[醫(yī)學(xué)]chapter8urineformationandexcretion-20xx-update(編輯修改稿)

2025-04-18 00:08 本頁面
 

【文章內(nèi)容簡介】 腎血管收縮 A 23yearold man has been admitted to the surgical floor after suffering multiple injuries in a motor vehicle accident. Plain film radiographs have not indicated any fractures. At the time of admission, his abdomen had some bruising but no distension or tenderness. After 8 hours of observation,the nurse calls the physician because the patient’s urine output has been decreasing steadily. His blood pressure is normal but lower than it was when he presented to the hospital,and he has a slightly increased heart rate. His abdomen is now distended and tender. An intravenous (IV) fluid bolus of normal saline is performed ,and his urine output increases to a normal range. The surgeon makes a diagnosis of hypovolemia(低血容量) that probably is due to intraabdominal hemorrhage and prepares the patient for exploratory surgery. CASE analysis 2 Clinical correlation: Monitoring the urine output is an easy way to assess a patient’s fluid status. Decreasing urine output may be due to hypovolemia or injury to the urinary tract system. Depressor reflex Reninangiotensin aldosterone system The blood pressure remained relatively normal initially: Reabsorption and secretion in the renal tubule and collecting duct 1. Reabsorption in the renal tubule and collecting duct 1) Type of the reabsorption Material transportation: Passive amp。 Active reabsorption Pathways: Transcellular amp。 Paracellular 2) Reabsorption in renal tubule and collecting duct ?Sodium reabsorption Site: 65% 25% 12% ?Front half segment of proximal tubuleactive transport Mechanism for sodium reabsorption : ?Second half segment of proximal tubule passive reabsorption Paracellular pathway: Cl: down the concentration gradient Na+: down the electric potential gradient ?Thick ascending limb of the loop 1Na+:2Cl:1K+ ?Early distal tube: Na+Cl cotransporter ?Late distal tube: Na+ channel ( potassiumsparing diuretics) ?chloride reabsorption 99% reabsorbed Mechanism: TAL (thick ascending limb) active transportation mechanism: Na+/K+ 2Cl cotransport Other tubular segments passive transportation Cl is passively reabsorbed mainly through the paracellular pathway 99% reabsorbed Mechanism: move passively Collecting duct regulated by ADH ?Water reabsorption by osmosis A model of the role of the kidneys in water balance ? Glucose reabsorption Site: Proximal tubule (Proximal convoluted tubule) Completely reabsorbed Mechanism: Active process (secondary) Cotransporter Facilitated by the presence of sodium ? When filtered load reaches 200 mg/dl glucose begins to appear in the urine (threshold). ? Transport maximum is 375 mg/min plasma [glucose] glucose in urine Normal range 80 ~ 120 mg/100ml () Increase 160 ~ 180 mg/100ml () 180 ~ 200 mg/100ml (+) Renal glucose threshold: When the plasma glucose level increases up to a value above160~180mg/dl, glucose can first be detected in the urine. This value is called renal glucose threshold. Maximal rate of glucose transport: Maximal tubular reabsorption of glucose (Tm or TmG) normal value: male : 375 mg/min female: 300 mg/min ?HCO3 reabsorption Site: 80% reabsorbed at proximal tubule reabsorption form: CO2 depend on H+ secretion Acetazolamide(乙酰唑胺 ) inhibit
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