Regulation of ECF Volume 2 Flashcards Preview

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Flashcards in Regulation of ECF Volume 2 Deck (13):

What does the regulation of Na+ correspond with?

Regulation of ECF volume


What effects do aldosterone and ANP have?

Why do these effects have clinical significance?

Alsosterone promotes :
-Na+ reabsorption
-K+ secretion

Atrial naturitic peptide promotes:
-Na+ excretion

If aldosterone is given -> increased weight because of water retention

Stimulation of ANP release from atrial cells -> loss of Na+ and H2O (Natiuresis)

BUT aldosterone -> continued K+ loss because still increased K+ secretion


What is "aldosterone escape"?

ANP overrides aldosterone effects on Na+ reabsorption because of volume expansion = "Aldosterone escape"

Give aldosterone -> weight gain but then after a couple of days natiuresis


How does aldosterone escape effect Conn's syndrome?

Patients with Conn's syndrome (primary hyperaldosteronism) due to a tumour of the adrenal cortex, they are K+ depleted, but nor hypernatraemic.

ANP is secreted by atrial cells in response to expansion of ECF volume and causes natiuresis, loss of Na+ and H2O in urine.

Actions may be to inhibit secretion of renin, generally oppose the actions of angiotensin II


What effect does uncontrolled diabetes mellitus have on the kidney?

Osmotic diuresis
-Renal function is disrupted
-Can produce hyperglycaemic coma


How does uncontrolled DM effect the kidneys ability to reabsorb glucose from the proximal tubule?

[BG] not kept within strict control, high plasma glucose levels exceeds the maximim reabsorpive capacity in the proximal tubule

Therefore glucose remains in the tubule and exerts an osmotic effect to retain H2O in tubule

[Na+] in the lumen is decreased becuase of H2O

Since Na+ gains access to the proximal tubule cells by passive diffusion down a concentration gradient created by the active transport out of the basolateral surfaces, Na+ reabsorption will be decreased

-> Decreased ability to reabsorb glucose since it shares a simper with Na+


How does uncontrolled DM effect the loop of Henle?

In the DESCENDING limb of the loop of Henle, movemnt of H2O out of the tubule into the interstitium is reduced because the glucose and excess Na+ exert an osmotic effect to retain H2O.

Therefore fluid in the descending limb is not so concentrated.

This means that the fluid delivered to the ASCENDING limb is less concentrated.
Since the NaCl pumps in ascending limb are gradient limited, medullary interstitial gradient is much less

Therefore there is a considerable reduction in the volume of NaCl and H2O reabsorbed from the loop of Henle

No a large volume of NaCl and H2O is delviered to the distal tubule
AND the interstitial gradient is gradually abolished


What does the 200mOsmole gradient at each horizontal level of the ascending limb of the loop of Henle represent?

The pumping of the active pumps


How does uncontrolled DM effect Na+ reabsorption at the distal tubule?

Under normal conditions, a large volume of NaCl and H2O delivered to the distal tubule means there is excess ECF volume and therefoe need to get rid of NaCl and H2O.

The macula densa will detect the high rate of delivery of NaCl so that renin secretion will be suppressed and therefore Na+ reabsorption at the distal tubule will be decreased


How does uncontrolled DM effect the ability of ADH to conserve H2O at the collecting duct?

Loss of interstitial gradient so H2O wont be reabsorbed


How does uncontrolled DM effect the release of ADH?

A large volume of nearly isotonic urine will be excreted -> decrease in plasma volume

This stimulates ADH release via baroreceptors but CANNOT BE EFFECTIVE because interstitial gradient has run down


How does uncontrolled DM ultimately lead to hyperglycaemic coma?

Patients with uncontrolled DM can produce 6-8l/day, causing severe salt and water depletion.

Hypotension may be so severe as to cause hyperglycaemic coma.

This is due to inadequate BF to the brain whereas a hypoglycaemic coma is due to inadequate glucose for the brain


How do loop diuretics effect K+?

The active transport mechanism that operates on the luminal surface of the thick ascending loop of Henle, actually involves K+ ions as well as NaCl, i.e. Na+ K+ 2Cl- co-transporter

This is a passive process (energy from Na+/K+ATPase on basolateral membrane)

Therefore loop diuretics can cause K+ ion wasting