ECF Volume Regulation 2 Flashcards

1
Q

What is the net result of aldosterone action?

A

Promoting Na+ reabsorption

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2
Q

What promotes Na+ excretion?

A

ANP - Atrial Natriuretic Peptide

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3
Q

Describe what happens if a subject on a normal diet is given aldosterone

A

If aldosterone levels are high, H20 and Na+ reabsorption are promoted at the expense of K+ which is excreted. This gain in H20 and Na+ results in weight gain and increased BV and BP. This is detected by the atrial stretch receptors which produce ANP, causing a loss of Na+ and H20, BUT, the aldosterone levels are still high so K+ will still be excreted and the patient will be K+ depleted

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4
Q

What is the relevance of aldosterone physiology in Conn’s disease?

A

In Conn’s there is hypersecretion of aldosterone due to a primary adrenal cortex tumour which results in an increase in Na+ and H20, which is corrected by ANP, but there is K+ depletion caused by the aldosterone which the ANP does not correct

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5
Q

Why is ANP able to override the the effects of aldosterone on Na+ reabsorption? (think emergency response)

A

Because there is ECF volume expansion - this takes priority over osmolarity

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6
Q

Describe the responses, and their effect on the kidneys, of the body to increased blood volume

A

Increased BV

  • > increased atrial stretch
  • > cells release ANP

ANP acts on;
1. Hypothalamus - less vasopressin secretion (ADH) to reduce blood volume by increasing water excretion

  1. Kidney - increased GFR and decreased renin* ** to reduce reabsorption of Na and H20 and promote excretion
  2. Adrenal Cortex - less aldosterone production to reduce reabsorption *the decreased renin from the kidney also inhibits the aldosterone release
  3. Medulla Oblongata - decreased blood pressure ** decreased renin also aids this
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7
Q

Describe osmotic diuresis in uncontrolled DM with respect to the glucose uptake

A

In uncontrolled DM the BG increases past Tm, so the excess remains in the tubule. This means that there is an increased concentration in the tubule and this creates higher osmolarity which keeps more water in the tubule with the glucose. This dilutes the contents of the tubule and thereof the sodium concentration is lowered. This disrupts the sodium gradient for Na and therefore less is reabsorbed. Because glucose and sodium there the same symporter, the glucose is also reabsorbed less, creating an excess of water, salt and glucose in the tubule

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8
Q

Describe the effects of diuretic osmosis in uncontrolled DM on the contents of the descending limd of the LoH

A

The movement out of the H20 from the tubule into the interstitial is decreased thanks to the shallower gradient caused by the osmotic pull of the Na+ and glucose in the limb. This keeps the fluid in the descending dilute and reduces the gradient of the interstitium

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9
Q

Describe the effects of diuretic osmosis in uncontrolled DM on the contents of the ascending limb of the LoH

A

As a result of the fluid being less concentrated in the descending lime, the problem persists into the ascending limb. Because the NaCl pumps in the ascending limb are gradient dependant, medullary interstitial gradient is much less. As a result there is significantly less NaCl+ and H20 reabsorbed fro the loop of Henle, resulting in the abolishing of the interstitial gradient and the ability of the kidney to concentrate urine over a wide range

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10
Q

What is the response of the macula densa which perpetuates the problem of osmotic diuresis?

A

Under normal conditions, a large volume of Na and H20 delivered to the distal tubule means that there is excess ECF volume and therefore that they need gotten rid of. It activate this mechanism and surpasses renin production to decrease reabsorption of Na and H20, which in the normal situation would be correct but here makes it even worse by keeping more and more Na and H20 in the nephron, creating more and more dilute but isotonic urine and destroying the interstitial gradient of the LoH

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11
Q

Give the overview flow diagram of osmotic diuresis in uncontrolled DM

A
Decreased proximal tubule reabsorption
\+
Decreased LoH reabsorption
\+ 
Decreased distal tubule reabsorption 
=
Destruction of the interstitial gradient
=
Loss of the kidneys ability to concentrate urine based on fluid levels 
= Excretion of 6-8litres dilute, isotonic urine per day
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12
Q

Does ADH have a role in correcting osmotic diuresis? Why?

A

No, the ADH can only be effective when the interstitial gradient is intact, so it can exert no corrective effect

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13
Q

What is the result of uncorrected osmotic diuresis in patients with uncontrolled DM?

A

A raging thirst is one of the first signs, and the resulting hypotension that is caused by the extreme levels of urine excretion will eventually cause HYPERglycaemic coma

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14
Q

How does hyperglycaemic coma differ from hypoglycaemia coma?

A

Hyperglycaemic coma results from inadequate blood flow to the brain as a result of extreme urine excretion - there is no lack of glucose

Hypoglycaemic coma results from inadequate glucose supply for the brain

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