Session 6: Group Work Flashcards
Which two physiological mechanisms exist to help maintain plasma osmolality?
Thirst
ADH leading to urination
Which of the two physiological mechanisms that control plasma osmolality is its first line of defence.
ADH
Where is the hormone that regulates water reabsorption made?
(ADH)
Made in hypothalamus specifically the supraoptic nucleus and the paraventricular nucleus.
Where after synthesis is ADH stored?
In the posterior pituitary gland
What is the most important physiological effect of this hormone?
Water reabsorption by upregulation of aquaporin on the apical membrane in the collecting duct.
Also causes vasoconstriction
Describe the action of this hormone in the kidney.
Increased expression aquaporin channels on the apical membrane in the collecting duct. This increases water permeability and more water can be reabsorbed.
How would you describe the osmolality of the glomerular filtrate (tubular fluid) as it reaches the top of the ascending limb of the loop of Henle compared to plasma?
Hypo-osmotic
How would you describe the interstitial osmolalility changes that occur from the cortex to the papillary region of the kidney?
Increases in concentration as you go further down into the medulla
How does this corticomedullary concentration gradient allow the kidney to produce concentrated urine?
Allows an increasing concentration of urine as the urine descends the collecting duct.
Since the collecting duct is descending as well and the interstitium in the collecting duct is very concentrated the urine will be hypo-osmotic compared to it. This allows water reabsorption in the collecting duct.
What role does urea play in the concentrating ability of the kidney.
Works as an osmotic agent to concentrate urine further.
It is then recycled in response to ADH.
Explain why water leaving the descending limb of the loop of Henle and the collecting duct does not dilute the concentration of the interstitial fluid thus destroying the concentration gradient. (Counter current mechanism)
Because the water does not stay in the interstitium. The water moves into the concentrated vasa recta as it ascends the descending limb. This allwows the concentration gradient to be maintained.
What effect has the elevated serum glucose had on her plasma osmolality?
Her plasma osmolality has increased leaving her plasma hyperosmotic.
In the nephron, what is the site of glucose reabsorption?
PCT
What normally happens to the total volume of filtrate by the end of this region?
Decrease total volume as there is a lot of reabsorption of ions, glucose and amino acids. There are also aquaporin channels so water can move down the concentration gradient.
65% water is reabsorbed.
What has happend to the osmolality of the filtrate at the end of this region?
It is isosmotic
Can you explain why the patient would complain of polyuria?
Not all glucose is being reabsorbed because it has reached its reabsorption limit.
This means that there will be glucose in the urine. The glucose is an osmotic agent and will lead to water moving into the tubule or rather staying in the tubule.
This leads to increase urination.
What effect on the patient’s plasma volume will have occurred following the change to the volume of urine produced?
Decrease in plasma volume and decrease in BP
Can you explain why your patient has polydipsia?
Hypothalamic osmoreceptors detect hyperosmotic plasma. This stimulates the hypothalamus to produce ADH or PP to secrete ADH.
Baroreceptors will detect low plasma volume in the carotid sinus and the aortic arch. This leads to the same response as with the osmoreceptors.
Also baroreceptors in the kidneys will be stimulated to start the RAAS system.
If the ADH can’t keep up with the water loss, thirst will be induced by the hypothalamus instead.
Think about his electrolytes and osmolality. What conclusion do you draw about this patents water balance and why?
He does not get enough water. Water is low and he is dehydrated.
Using your knowledge about ADH, can you think of an explanation for his clinical presentation and blood and urine results?
ADH is not working.
Probably something wrong with hypothalamus or PP due to trauma
Describe the changs in plasma osmolality and urine osmolality in this patient.
Plasma has decreased
Urine has increased
What is your interpretation of her urine sodium result and what can you infer from this?
That her kidneys are working and doing what they are told.
In this patient what is the most likely underlying cause?
SIADH
