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Author Topic: What are the consequences of urinary and biliary reabsorption?  (Read 571 times)

Offline rockhard94

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CONTEXT (correct if any of this is wrong):
Renal absorption: The primary filtrate flows into the proximal tubule where solutes (amino acids, glucose, salt ions) are reabsorbed by specific active transporters ∴ creation of hypertonicity in the medullary interstitium, which allows for reabsorption of water in the peritubular capillaries by osmosis. as water is reabsorbed (out of the tubule into the capillaries), the concentration of the filtrate increases, thus creating a gradient between the tubule and the surrounding interstitial space. Whether or not (or the extent to which) the drug will travel downhill this concentration gradient, across the tubular epithelium towards the peritubular capillaries (i.e. be reabsorbed), depends on its membrane permeability (ionisation, hydro/lipo solubility, etc.).

Intestinal/biliary absorption (simplified here): Drugs are absorbed by active transporters mainly found on the microvilli of the Jejenum (& ileum for vitamins and such) and transfered to the capillaries of the G.I. tract. This "drug-rich" blood flows into the superior mesenteric vein and ultimately to the portal hepatic vein. It then flows into the liver sinusoids where the biliary flux (bile canaliculi) can take drugs away from hepatocytes and store them into the gallbladder OR excrete them in the common hepatic duct. The common hepatic duct is connected to the Duodenum ∴ enterohepatic cycle (which I guess is what is considered as biliary reabsorption?)

My question is: What are the (physiological) consequences of Urinary & Biliary Reabsorption?

Thanks to all


« Last Edit: 12/02/2016 05:49:52 by rockhard94 »


 

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