Regulation of Water Balance Flashcards
certain cells can respond acutely to osmotic changes. how do individual cells respond to osmotic swelling/shrinkage
swelling- extrusion of electrolytes
shrinkage- electrolyte take up
which organs are allowed to autoregulate cell volume? why can’t more cells do this?
only the brain and the small intestines.
other cells in the body are not permitted to do this because their combined changes would result in dramatic osmostic changes globally.
what does brain autoregulation have to “take into consideration”
the brain requires certain ion gradients to function and cannot use them to fix osmolality. it therefore uses small organic molecules instead.
what is the solute that is responsible for tonicty under normal conditions?
Na
how does the body respond to hypoatremia and hyperatremia?
hypo- low salt concentration- actually a sign of overhydration
hyper- high salt concentration- actually a sign of dehydration
symptoms of hypoatremia
salvation bradycardia twitching muscles high BP hypoventalation nausea headache lethargy apathy agitation
symptoms of hyperatremia
fever tachycardia low NP hyperventilation thirsty dry mucous swollen tongue weakness seizures delirium coma
how do the responses to over and dehyrdration differ?
the body is good at excreting excess water and kidney output can be increased substantially
conversely, the body is not good at minimizing kidney output. thus, it requires a two-fold response of increasing thirst and increasing ADH (decreasing output)
where are the receptors for sensing osmolality?
in the brain- two separate receptors- one for thirst and one for ADH.
these receptors have different sensitivities, with ADH being more sensitive
how does the body prevent over-drinking?
cold receptors in the mouth and stretch receptors in the esophogus
how does the regulation of thirst and ADH change with blood volume?
normally, the body prioritizes preserving plasma osmolality and thus cell volume at the expense of ECFV. however, as ECFV or blood pressure drops below a certain threshold, the priorities switch, and the body allows non-osmotic intake to prevent CV collapse.
CV control centers have inputs to the osmotic receptors, and stimulate them such that you have a massive increase in ADH (to get its vasoconstritive effects) and thirst
what effect does angiotensin 2 have on osmoreceptors?
it increases thirst
what is counter current exchange?
the mechanism in the kidneys whereby the vasa recta (medullary blood supply) has an ascending and a descending limb, each of which equilibrates with the interstitium osmotically so that no solute is lost when the vasa recta leaves the kidney, preserving the hypertonic environment
what is counter current multiplication
this involves two ideas
- the difference in permeability between the ascending and descending LOH. The descending loops is permeable only to water, whereas the ascending is permeable only to salt. Salt gets pumped out in the ALH, especially the thick limb, creating a hypotonic urine in the collecting tubule. this creates a hypertonic interstitium of approx 600 osm that helps reabsorb water in the descending limb and potentially the CD
- under ADH, the urine wants to be reconcentrated. aquaporin channels open on the in the CT and CD, allowing water to be reabsorbed as it flows through the CD. ADH also makes the terminal CD permeable to urea, which is concentrated inside the tubule at this point and escapes into the interstium, doubling the medullary oncotic pressure (1200). the urea is reabsorbed by the thin LOH and thus recycled.
besides increasing water and urea reabsorption, what are two other mechanisms for ADH urine concentration
- constricts juxtamedullary glomeruli efferent arterioles, increasing GFR in long LOH for increased Na reab, and decreasing vasa recta flow for decreased solute loss
- directly increases Na absorpotion in ascending LOH
