Reg of Body Fluid Osmolality Flashcards
1st Step
Tubular fluid enters the descending limb from the PT, it is isotonic
2nd Step
The active salt pumps in the TAL transport NaCl out of the lumen until the surrounding interstitium fluid is 200mOsm/L more concentrated than the tubular fluid
Water can not follow from the TAL
Net diffusion of water occurs int he descending limb into the interstitium
3rd Step
Passive movement of water continues until the the osmolarities of the fluid in the descending limb and the interstitium are equilibrated
4th Step
A mass of 200mOsm/L fluid exits the TAL and enters the DT. A new mass of 300mOsm/L, isotonic, fluid enters the descending limb.
At bottom of limb, a comparable mass of 400 moves around the bottom of the loop
5th Step
Additional flow of fluid into the LoH from the PT, which causes the hyperosmotic fluid previously formed in the descending limb to flow into the ascending limb
Ions are pumped from the ascending limb until a 200 mOsm/L gradient is established. Interstitial osmolarity rising to 500mOsm/L
7th Step
Steps 4-6 are repeated until max concentration is 1200-1400 mOsm/L at the bottom of the loop
Vasa Recta
Blood supply to the medulla, is highly permeable to salute and water
removes water and solutes that are continuously added to the medullary interstitium by the nephron
Ability to maintain gradient is flow dependent
Increase in flow dissipates the medullary gradient, called medullary washout
Decrease in blood flow decreases salt and solute transport by nephron, reducing ability to concentrate urine
Urea Recycling
Urea reabsorption occurs in medullary CD and thin descending limb
UT-A1 and UT-A3—> transporters in medullary CD
UT-A2 in thin limb
Some of the urea that moves into the medullary interstitium eventually diffuses into the thin loop and passes upward thru the TAL to the DT and eventually CD
ADH
Secreted in response to osmotic stims, sensed by supraoptic and paraventricular nuclei of hypothalamus
Secreted from posterior pituitary gland
Osmoreceptors
Sensitive to small changes in plasma osmolality -1-2% can cause release of ADH
Activate ADH path before thirst path
Aldosterone
Release from adrenal cortex
Increase ENaC channels, which increases the amount of Na being reabsorbed
Increases reabsorption of Na and secretion of K
Aquaporin-2 Insertion
Aquaporin channels are inserted into the apical membrane of principal cells
Less ADH=Less aquaporin insertion
Central Diabetes Insipidus
Inability to release ADH
Tx by desmopressin
Nephrogenic DI
Inability of kidneys to respond to ADH
Either failure of the countercurrent mechanism or failure of the distal and collecting tubules to respond to ADH
SIADH
Excessive release of ADH, which causes excessive water retention and disrupting the electrolyte balance
Fluid shifts into the cells causing them to swell
Body holds on to electrolyte free water
Major cause of low sodium levels
Water is retained while Na is excreted