Keef 7 Flashcards
How does a hemorrhage that decreases extracellular fluid volume affect ADH release?
The decrease in EFV will decrease BP & baroreceptor reflexes will cause an increase in ADH & an increase in the tubular permeability to water. This increases water reabsorption.
If you consume isotonic saline…why isn’t ADH enough to regulate EFV volume?
B/c osmolarity doesn’t change & only ECF compartment is expanded. When water is excreted the osmolarity of the ECF raises & the body thinks that ADH is necessary & that more water needs to be reabsorbed. Once this water is excreted…the plasma osmolarity will just increase again. It is cyclical & useless b/c it needs to include the issue of sodium reabsorption.
Why does water follow sodium? How does an increase in sodium reabsorption lead to an increase in water reabsorption?
b/c EFV is low & aldosterone is triggered to cause sodium reabsorption. this will increase the plasma osmolarity & trigger the release of ADH & water reabsorption in the collecting duct. Thus, EFV is restored w/ proper osmolarity.
Glomerulotubular balance assures what about sodium reabsorption in the proximal tubule?
That no matter what the filtered load…the same percentage of salt will be reabsorbed every time. 67%
When you have a low EFV what naturally happens to your sodium reabsorption? What does this mean graphically?
It increases at each point of filtered load.
It has a steeper slope if the x axis is filtered load & the y axis is sodium reabsorption.
When you have a high EFV what naturally happens to your sodium reabsorption? What does this mean graphically?
It decreases at each point of filtered load.
It has gentler slope if the x axis is filtered load & the y axis is sodium reabsorption.
If you eat a ton of potato chips why is there an increase in your ECF volume?
Sudden increase in sodium consumption.
Plasma sodium conc’n will increase.
Plasma osmolarity will increase.
Fluid will shift at first form the IFC to the EFC.
ADH release will increase & increase water consumption & water reabsorption.
All of these will act to increase your EFC volume.
Later, other mechanisms will compensate to correct this.
What cells does aldosterone act on?
The principal cells in the collecting duct
Is the receptor for aldosterone extracellular or intracellular?
Intracellular
How does aldosterone increase sodium reabsorption once it binds to its receptor in the principal cells?
In the nucleus, synthesis of sodium channels & sodium potassium pumps are increased.
Sodium channels conductance is increased.
The mitochondria are told to make more ATP, which also helps the pumps.
Ultimately, what 3 things does aldosterone affect?
Increases sodium reabsorption
Increases potassium secretion
Increases H+ secretion
What 3 states does aldosterone promote?
BP to be raised thru sodium reabsorption
Hypokalemia thru potassium secretion
Alkalosis thru H+ secretion
Where is aldosterone secreted from?
Adrenal cortex
What are the primary regulators of aldosterone secretion?
High potassium conc’n in the plasma
Ang II
What are 2 less important regulators of aldosterone secretion?
Low sodium conc’n in the plasma
ACTH
What would be a condition that would promote hypoaldosteronemia? What 3 conditions would this cause?
Addison’s Disease
Acidosis
Hyperkalemia
Low BP…hypotension
What 3 conditions would hyperaldosteronemia promote?
Alkalosis
Hypokalemia
Hypertension
What is something that might cause primary hyperaldosteronemia? What would this mean for renin?
An adrenal gland tumor that causes continued secretion of aldosterone.
This would cause HTN & would cause renin release to be low.
What is something that might cause secondary hyperaldosteronemia? What would this mean for renin?
Renal artery stenosis.
High renin leading to the high aldosterone.
Would too much aldosterone cause pitting edema?
NO
What does Ang II really do that helps with sodium reabsorption?
It acts directly on the PCT to increase sodium reabsorption.
It constricts the efferent arteriole @ the glomerulus so that there is low pressure in the peritubular capillaries & this also favors reabsorption.
Stimulates aldosterone release
What does atrial natriuretic factor (anti-aldosterone) do to decrease sodium reabsorption?
Acts on the late collecting tubules via a membrane receptors that activates guanylate cyclase & increases cGMP…this decreases sodium reabsorption.
It also increases GFR @ the glomerulus.
It causes natriuresis: excretion of sodium.
What is the difference b/w where aldosterone, ADH, & ANF work?
Aldosterone works late DCT & cortical collecting duct & a little medullary
ADH works the collecting duct: cortical & medullary
ANF works the late collecting duct.
Why does congestive heart failure lead to high plasma sodium conc’n & edema?
Congestive heart failure decreases cardiac output.
This causes a shift in the blood from the arterial to the venous side…it is just stored there.
Baroreceptors perceive–oh no! low blood volume
Increases sodium reabsorption
Plasma osmolarity increases
ADH is released
Extra water is reabsorbed
Now so much water in the body that edema is caused.
Why do patients w/ CHF often need to take diuretics?
b/c of their edema! low perceived blood volume leads to sodium & water reabsorption.
Aside from renin, what important substance is released from the kidney? What other organ can also release it? Who is better at it?
Erythropoietin. 90% is released from the kidney
10% is released from the liver
What exact part of the kidney releases erythropoietin?
fibroblast-like cells in the outer cortex & the medulla
What prompts the release of erythropoietin?
Decreased tissue oxygenation
When you lose a bunch of nephrons…what happens to GFR? What happens to sodium filtered load? What happens to sodium excretion rate? What happens to sodium fractional excretion?
GFR decreases b/c nephrons lost.
Filtered Load decreases b/c GFR decreases
Sodium excretion rate is maintained
Fractional excretion increases (offsets decreased filtered load & allows the maintenance of excretion rate).
What is the equation for filtered load?
Filtered Load = GFR X Pconc’n
What is the equation for excretion rate?
Excretion = Filtered Load X Fractional Excretion
What are 2 substances whose conc’n significantly increases in the plasma when nephrons are lost?
Creatinine & BUN
B/c creatinine isn’t reabsorbed once it is in the tubules…how does it maintain its excretion rate with nephron loss?
it increases its filtered load by increasing its plasma conc’n.
This allows a greater amount of creatinine to get into the tubules & be excreted.
