Flashcards in Renal Part III Deck (21)
What is osmolality?
mol solute/ kg solvent
What is osmolarity?
Concentration of dissolved particles.
What is osmosis and osmotic pressure?
Water follows solutes, though going down its concentration gradient. The osmotic pressure is the force created by water flow and is determined by osmolarity-- not molarity.
What is tonicity?
The osmotic pressure created by solutes.
Solutions can be hypotonic, isotonic, or hypertonic
What impact does extracellular hypertonicity have on cell size? Hypotonicity?
Cells in the hypotonic solution swell while cells in the hypertonic solution shrink. Extracellular osmolarity determines the EC and IC fluid balance. Cells cannot survive significant changes in osmolarity as swelling or shrinking can disturb cell functions. NaCl ups EC osmolarity and shrinks the cells while water intake lowers EC osmolarity and expands the cells.
How does the interstitial region of the medullary pyramid become hypertonic?
The medullary interstitium is hypertonic due to accumulation of urea and NaCl. Urea enters the interstitium via the collecting duct. NaCl enters from the thick and thin portions of the ascending loop. Hyaluronic acid and albumin form a gel that suspends the water and solutes.
How is the Hypertonicity protected by the vasa recta?
Loops of the vasa recta absorb solutes in the inner medulla and release them into the outer medulla. This prevents the dissipation of the hypertonic gradient in the medulla. Organic osmolytes (betaine, urea, sorbitol, etc) prevent efflux of water and cell shrinkage in the harsh hypertonic environment.
How does urea accumulate into the interstitium?
Urea is secreted into the tubule from descending vasa recta in short nephrons. Urea is then transported out from the collecting tubules into the inner interstitial fluid, adding to its tonicity. Urea is then recirculated back into the loops either directly or through the ascending vasa recta.
What is urea?
Urea is a byproduct of protein digestion.
How does ADH regulate osmolarity?
ADH increases water permeability in collecting system by up regulating aquaporins. This increases blood volume, capillaries readily reabsorb water, which prevents dilution of interstitial osmolarity.
What is ADH?
What are the osmoreceptors?
Cells in the hypothalamus that stimulate ADH release from the Supraoptic (SO) and Paraventricular (PV) hypothalamic nuclei.
Where are the osmoreceptors?
How is ADH synthesized and released?
The SO and PV nuclei synthesize ADH, axons transport ADH into the posterior pituitary, it is then released into the blood stream.
What stimulates ADH release?
Increased plasma Na (food) increases ADH and the reabsorbed water dilutes the Na.
What inhibits ADH release?
Decreased plasma Na (drink water) decreases ADH, water is excreted. In extreme cases, baroreceptors inhibit ADH release to excrete excess fluid volume to control blood pressure.
What conditions affect ADH?
Nausea, nicotine, and morphine stimulate ADH release while alcohol inhibits ADH release.
Where is the thirst center?
In the hypothalamus, near the PV and SO
What does the hypothalamic thirst center respond to?
ECF osmolarity, drop in blood volume, angiotensin II, dryness of mouth and throat. These conditions act to dilute Na and stimulate osmoreceptors.
What are some of the consequences of excessive water intake?
Hypothalamus creates a new set point. ADH is suppressed and enhanced water excretion stimulates thirst and excessive drinking.