Body Fluid Osmolarity Flashcards
(49 cards)
T or F. a change in TBW is uniformly distributed in different body fluid compartments resulting in uniform change in fluid osmolarity in different compartments
T. Because cell membranes are highly permeable to water,So an excessive water intake would increase TBW resulting in a decrease in body fluid osmolarity in different compartments and vice versa
How does the kidney respond to a decrease in fluid osmolarity?
by increasing water excretion in the urine.
How does the kidney respond to a change in fluid osmolarity?
This is a centrally regulated process. ADH secreted by the pituitary gland regulates water reabsorption in kidney. Thirst center regulates water intake.
What is the normal intake/production of water daily?
Normal daily water intake is about 2000 ml (1500 drinking and 500 food) and 400 ml is produced in the body during metabolic processes.
What is the normal distribution of water output daily?
urine-1500mlbreathing-400mlskin-400ml (burn can drastically increase)feces-100ml
Does the kidney have a high capacity to excrete water?
Yes, Excessive water driniking or lack of ADH may increase GFR by 10% which is equal to 18 L/day.
Eqn for plasma osmolarity
2[Na+] + glucose concentration in mg/dl divided by 18 + BUN in mg/dl divided by 2.8.normal is ~285mOsmNa 137, glucose 100, and BUN 15
Changes in osmolarity is sensed by what?
osmoreceptors. The Osmoreceptors on supraoptic and paraventricular nuclei of the hypothalamus are stimulated by an increase in body fluid osmolarity. Increase in osmolarity also stimulates osmoreceptors in the thirst center I the hypothalamus. The result is change in behavior encouragig to drink more water.
What does activation of the supraoptic and paraventricular nuclei of the hypothalamus cause?
Activation at the cell body of supraoptic nerves transmits signal to the nerve ending that is located in the posterior pituitary gland. The final cellular signal in the nerve ending is increase in intracellular calcium. Elevated intracellular calcium stimulates membrane fusion of ADH containing vesicles resulting in exocytosis of ADH into ECF.
What does ADH do?
ADH acts on the CD epithelial cells and increases water reabsorption.Increase in water reabsorption corrects the osmolarity back to normal.
What is the composition of ADH?
small peptide consisting of 9 amino acids with a MW of 1100 daltons.
T or F. The basolateral membranes of the CD epithelial cells have the receptors for vasopressin
T.
How is ADH released from the pituitary transported to the kidney?
By circulation. It binds to vasopressin receptors on the BL membrane and activates the intracellular signaling. It first activates the adenylate cyclase that converts ATP into cAMP.
What does increased cAMP in the CD epithelial cells stimulate?
cAMP activates protein kinase A which phosphorylates vesicles containing aquaporin-2 in their membranes and makes them fuse to plasma membrane on the luminal side, thus increases water permeability of the cells.
How quick is this whole process?
This is a rapid process, takes less than 10 min to increase water permeability once the plasma ADH level is increased
What are the types of vasopressin receptors?
There are 3 types of vasopressin receptors, V1, V2 and V3. It is the V2 receptors on the basolateral membrane that is involved in cAMP production and aquaporin translocation to luminal membrane.
What do V1 and V3 do?
V1 and V3 receptors are G-protein coiupled receptors. V1 receptors seem to present in the luminal membranes, but its function is unclear at this point.
What happens to ADH once it functions?
ADH released by stimulation of hypothalamus is rapidly degraded in the PT and liver, thus avoiding sustained presence of high plasma ADH. Rapid degradation help bring the ADH level back to normal.
Does increase in plasma osmolarity lead to concentrated or diluted urine?
concentrated. Make sure you know howUrinary osmolarity can go as high as 1200 mOM.
Describe the relationship between plasma AVP (y) and plasma osmolality (x).
up to pOsm of 270, AVP is negligible. Above 270 mOsM osmolarity ADH level increases proportionally to reach maximum of 18 pM at 290 mOsM plasma osmolarity. Above this plasma osmolarity, AVP levels will not increase any more.
In addition to plasma osmolarity, ADH secretion is also regulated by plasma volume. How?
A decrease in ECFV by 1.5 L (from normal) has only a little effect on ADH level. But, further decrease in ECFV increases plasma ADH concentration, which can be as high as 50 pg/ml. Therefore, the threshold for ADH secretion by reduction in ECFV is very high.
Greater than 10-15% decrease in ECFV is required to have a strong increase in plasma ADH.
Second, a 25% decrease in ECFV can increase plasma ADH level to 50 pg/ml, which is almost 3 fold higher than the highest concentration achieved by osmolarity changes.
Can osmolarity and volume be reduced at the same time?
Yes, A clinical condition that may reflect such a situation is of severe decline in ECFV due severe diarrhea, but with reduced plasma osmolarity due to loss of salts in diarrhea. Based on osmolarity there should reduced plasma ADH causing diuresis. But, that would result in further reduction of volume. On the other hand, reduction of plasma volume should increase plasma ADH and increase water reabsorption. So, which effect prevails?Under condition of severe loss of ECFV its effect on ADH release overrides osmolarity effect on ADH secretion. In other words, it does not matter what the osmolarity is at low ECFV, the AVP level rises high.
How does excessive vomiting lead to hypoatremia?
Assume the lid loss in vomit is isotonic.The ECFV depletion (but not osmolarity because we assume no change) is large enough to stimulate ADH release.ADH indcues concentration of urine and dilution of plasma.Therefore body water is conserved and the ECFV is increased.The result is reduced osmolarity and hyponatremia
