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  #1  
Old 08-26-2012
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with SIADH inaproprately concentrated urine develops how does it develops?
its because of ADH or ANP?
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Old 08-26-2012
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i think it's due to ADH....
SIADH is an abnormal condition in which ADH excess takes place...leading to excess reabsorption of water leaving concentrated urine.......
ANP is released by atria when BP increases..it causes vasodilation of afferent arteriole and constrict efferent arteriole....hence, increase GFR and also increases water excretion ..... and decreases BP
ADH causes hyperosmolar urine and ANP causes hypoosmolar urine i guess...
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Old 08-26-2012
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In SIADH, the extra ADH leads to excessive water absorption from the kidneys, causing a mild subclinical hypervolemia initially in the disease. The excess body water suppresses the renin-aldosterone axis, causing low aldosterone. As aldosterone is responsible for sodium absorption from the distal tubule, low aldosterone levels lead to natriuresis (salt-wasting via the urine). Eventually, most patients with SIADH will equilibrate with a near-normal total body volume and low plasma osmolality (because of the salt-wasting); thus SIADH causes euvolemic hyponatremia Characteristically, patients with SIADH do not have gross hyperolemia or peripheral edema.

Hope that helped.
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Old 08-27-2012
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Quote:
Originally Posted by Step-step View Post
In SIADH, the extra ADH leads to excessive water absorption from the kidneys, causing a mild subclinical hypervolemia initially in the disease. The excess body water suppresses the renin-aldosterone axis, causing low aldosterone. As aldosterone is responsible for sodium absorption from the distal tubule, low aldosterone levels lead to natriuresis (salt-wasting via the urine). Eventually, most patients with SIADH will equilibrate with a near-normal total body volume and low plasma osmolality (because of the salt-wasting); thus SIADH causes euvolemic hyponatremia Characteristically, patients with SIADH do not have gross hyperolemia or peripheral edema.

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yes, you are true...and about ANP
it is another counterregulatory system like renin-angiotensin-aldosterone system.....when blood volume increase it releases and increase GFR... and it promote diuresis by not activating RAA system( so, sodium excretion occurs along with water)....decreases BP hypovolemic hyponatremia
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Old 08-27-2012
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Quote:
Originally Posted by venky2600 View Post
yes, you are true...and about ANP
it is another counterregulatory system like renin-angiotensin-aldosterone system.....when blood volume increase it releases and increase GFR... and it promote diuresis by not activating RAA system( so, sodium excretion occurs along with water)....decreases BP hypovolemic hyponatremia
What you're trying to say makes sense too... but, I'll stick to the uworld explanation.
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Old 08-29-2012
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Quote:
Originally Posted by riya_rai84 View Post
with SIADH inaproprately concentrated urine develops how does it develops?
its because of ADH or ANP?
Pathophysio QBANK concept:

SIADH:
volume expansion leads to increase secretion of ANP by atrial myocytes,increased ANP is one of the factor that causes the kidney to increase sodium excretion and produce an inapropriately concentrated urine
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Old 08-30-2012
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^I DISAGREE.


SIADH---> ADH acts in the distal portion of the renal tubule as well as on the collecting duct and causes retention of water, but not solute, which means: More concentrated urine.


ANP will increase, trying to excrete more fluid, by:
  • Dilates the afferent glomerular arteriole, constricts the efferent glomerular arteriole, and relaxes the mesangial cells.
  • Increases blood flow through the vasa recta
  • Decreases sodium reabsorption
  • Inhibits renin secretion, thereby inhibiting the renin-angiotensin-aldosterone system.
  • Reduces aldosterone secretion by the adrenal cortex
  • and a million other things
this is all secondary, a compensatory mechanism, and should not be considered as being part of the SIADH- syndrome




...I think.
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Old 08-30-2012
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Quote:
Originally Posted by BritneySpears View Post
^I DISAGREE.


SIADH---> ADH acts in the distal portion of the renal tubule as well as on the collecting duct and causes retention of water, but not solute, which means: More concentrated urine.


ANP will increase, trying to excrete more fluid, by:
  • Dilates the afferent glomerular arteriole, constricts the efferent glomerular arteriole, and relaxes the mesangial cells.
  • Increases blood flow through the vasa recta
  • Decreases sodium reabsorption
  • Inhibits renin secretion, thereby inhibiting the renin-angiotensin-aldosterone system.
  • Reduces aldosterone secretion by the adrenal cortex
  • and a million other things
this is all secondary, a compensatory mechanism, and should not be considered as being part of the SIADH- syndrome
...I think.
ya you are right this is all because of 2ndary compensatory mechanism.

http://quizlet.com/12760653/hurst-re...s-flash-cards/

What is ANP?
Atreial Natriuetic Peptide
-found in atria
-oppisite of aldosterone causes excretion of Na & H2O

What is ADH?
Antidiuretic Hormone
causes body to retain water
found in pituitary

What happens with too much ADH?
Fluid volume excess/ retain water
Urine concentrated & blood diluted

What disease is caused from too much ADH?
SIADH - syndrome of inappropriate ADH secretion
(think...too many letters...too much water)
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